Oxford American Handbook of Clinical Examination and Practical Skills

Oxford American Handbook of

Clinical

Examination

and

Practical Skills

About the Oxford American Handbooks in Medicine

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Oxford American Handbook of Clinical Medicine

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Oxford American

Handbook of

Clinical

Examination and

Practical Skills

E lizabeth A. B urns, MD, MA

Professor of Family Medicine

President and CEO

Michigan State University

Kalamazoo Center for Medical Studies

Kalamazoo, Michigan

K enneth K orn, PA-C, ARNP

Adjunct Faculty, Physician Assistant Program

University of North Dakota

Grand Forks, North Dakota

and

Family Nurse Practitioner

Leon County Health Department

Florida Department of Health

Tallahassee, Florida

J ames W hyte IV, ND, ARNP

Associate Professor

College of Nursing

Florida State University

Tallahassee, Florida

with

J ames T homas

T anya M onaghan

1

3

Oxford University Press, Inc. publishes works that further

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Published by Oxford University Press Inc.

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Oxford is a registered trademark of Oxford University Press.

First published 2011

UK version 2007

stored in a retrieval system, or transmitted, in any form or by any means,

electronic, mechanical, photocopying, recording, or otherwise,

without the prior permission of Oxford University Press,

Library of Congress Cataloging-in-Publication Data

Oxford American handbook of clinical examination and practical skills / edited by

Elizabeth A. Burns, Kenneth Korn, James Whyte IV ; with James Thomas, Tanya

Monaghan.

p. ; cm.

Other title: Handbook of clinical examination and practical skills

Includes index.

ISBN 978-0-19-538972-2

1. Physical diagnosis—Handbooks, manuals, etc. I. Burns, Elizabeth A. (Elizabeth

Ann), 1950– II. Korn, Kenneth. III. Whyte, James, IV. IV. Title: Handbook of

clinical examination and practical skills.

[DNLM: 1. Clinical Medicine—methods—Handbooks. 2. Physical

Examination—Handbooks. WB 39]

RC76.O937 2011

616.07´54—dc22

2010027995

10 9 8 7 6 5 4 3 2 1

Printed in China

on acid-free paper

This material is not intended to be, and should not be considered, a

substitute for medical or other professional advice. Treatment for the

conditions described in this material is highly dependent on the individ-

ual circumstances. And, while this material is designed to offer accurate

information with respect to the subject matter covered and to be cur-

rent as of the time it was written, research and knowledge about medical

and health issues are constantly evolving and dose schedules for medica-

tions are being revised continually, with new side effects recognized and

accounted for regularly. Readers must therefore always check the product

information and clinical procedures with the most up-to-date published

product information and data sheets provided by the manufacturers and

the most recent codes of conduct and safety regulation. Oxford University

Press and the authors make no representations or warranties to readers,

express or implied, as to the accuracy or completeness of this material,

including without limitation that they make no representation or warran-

ties as to the accuracy or efﬁ cacy of the drug dosages mentioned in the

material. The authors and the publishers do not accept, and expressly dis-

claim, any responsibility for any liability, loss, or risk that may be claimed

or incurred as a consequence of the use and/or application of any of the

contents of this material.

This page intentionally left blank

vii

Preface (U.S.)

Although we would like to claim the idea for this text as our own, this is

not the case; however, the belief in the text’s adaptability for U.S. medical

providers is. The ﬁ rst edition of this text was developed for use in the

U.K., where a different model of health care exists.

In the United States, the primary care provider role was once the exclu-

sive responsibility of the traditional, medical school–educated MD or DO.

Primary care is no longer the realm of only one type of health-care pro-

vider. No longer is it the duty of only the physician to assess and care

for the patient. Now, collaborative and collegial relationships exist among

various disciplines. Cooperative-care models seek to provide optimal care.

It is from this type of model that the U.S. authors elected to remove the

term doctor from most areas of this text in preference to the term health-

care provider .

Representing the varied disciplines now likely to serve as primary care

providers, the U.S. team of authors illustrates the changing face of U.S.

health care. The authors represent educators and practitioners from

traditional allopathic medicine, nurse practitioner, and physician assistant

disciplines.

This text is not offered as the quintessential text on physical examin-

ation; it is presented, as the title states, as a handbook of physical examin-

ation and practical skills. We also believe that as U.S. health care evolves,

so will this text, with requisite changes and adaptations.

In this text, the important elements that will not change are those that

comprise an appropriate exam and quality care. No matter which discip-

line the provider represents, quality is critical.

Elizabeth Burns, MD

Kenneth Korn, PA-C, ARNP

James White, ARNP

2010

* Out of great respect for the work of James Thomas and Tanya

Monaghan, the U.S. authors chose to leave the following Preface and

Acknowledgments by the U.K. authors unchanged.

Preface

viii

Preface (U.K.)

There are very few people who, in the course of their daily work, can

approach a stranger, ask them to remove their clothes, and touch their

bodies without fear of admonition. This unique position of doctors, med-

ical students, and other health care professionals comes with many strings

attached. We are expected to act “professionally”and be competent and

conﬁ dent in all our dealings. This is hard to teach and hard to learn and

many students are rightly daunted by the new position in which they ﬁ nd

themselves.

We felt a little let down by many books during our time in medical

school, and often found ourselves having to dip into several texts to

appreciate a topic. This book, then, is the one text that we would have

wanted as students covering all the main medical and surgical subspecial-

ties. We anticipate it will be useful to students as they make the transition

to being a doctor and also to junior doctors. We hope that it will be car-

ried in coat pockets for quick glances as well as being suitable for study at

home or in the library.

The ﬁ rst three chapters cover the basics of communication skills, history

taking, and general physical examination. Chapters 4–14 are divided by sys-

tems. In each of these there is a section on the common symptoms seen

in that system, with the appropriate questions to ask the patient, details

of how to examine parts of that system, and important patterns of disease

presentation. Each of these system chapters is ﬁ nished off with an “elderly

patient”page provided by Dr. Richard Fuller. Following the systems, there

are chapters on paediatric and psychiatric patients—something not found

in many other books of this kind. The penultimate chapter—practical pro-

cedures—details all those tasks that junior doctors might be expected to

perform. Finally, there is an extensive data interpretation chapter which,

while not exhaustive, tries to cover those topics such as ECG, ABG, and

X-ray interpretation that may appear in a ﬁ nal OSCE examination.

Although we have consulted experts on the contents of each chapter,

any mistakes or omissions remain ours alone. We welcome any comments

and suggestions for improvement from our reader—this book, after all,

is for you.

James Thomas

Tanya Monaghan

2007

ix

Acknowledgments (U.S.)

The U.S. authors acknowledge the great work of the U.K. team in the

development of a unique text. The combination of examination, pro-

cedures, and data interpretation into a single handbook-sized resource

represents a new type of resource. It is recognized that this text is a

resource with the potential for substantial enhancement. Your comments

are welcome.

We would also like to thank Oxford University Press (U.S.) for the

opportunity to be involved in this adaptation of this text, with special

thanks to Andrea Seils and Staci Hou for their patience and assistance

during this process.

Colleagues providing specialty review of the Americanization of the

U.K. data and procedures also deserve special thanks.

As always, such projects represent time away from other responsibil-

ities. We acknowledge and appreciate our co-workers and family for giving

us the time to complete this project.

Finally, one last thank-you goes to the ﬁ ne U.K. authors for those

moments of humor while reviewing their text for “Britishisms.”

x

Acknowledgments (U.K.)

We would like to record our thanks to the very many people who have

given their advice and support through this project.

For contributing specialist portions of the book, we thank

Dr. Tom Fearnley (pages relating to ophthalmology), Dr. Caroline Boyes

(Chapter 16, The paediatric assessment) and Dr. Bruno Rushforth (ECG

interpretation and other parts of Chapter 18). We also thank Heidi

Ridsdale, senior physiotherapist at Leeds General Inﬁ rmary, for her help

with the oxygen/airway pages and for providing all the equipment for

the photographs. Dr. Franco Guarasci and Jeremy Robson read the NIV

and inhaler pages, respectively, for which we are very grateful. We thank

Senior Sister Lyn Dean of Ward 26 at the Leeds General Inﬁ rmary for

reading parts of Chapter 17 (Practical procedures). Our thanks also go to

Dr. Jonathan Bodansky, Mandy Garforth, and Mike Geall for providing the

retinal photographs.

An extra special word of thanks is reserved for our models Adam

Swallow, Geoffrey McConnell, and our female model who would like to

remain anonymous. Their bravery and good humour made a potentially

difﬁ cult few days very easy. They were a joy to work with. We thank the

staff at the St James’s University Hospital Medical Illustration Studio, in

particular Tim Vernon, for taking the photographs.

We would also like to thank the staff at Oxford University Press,

especially Catherine Barnes, for having faith in us to take this project on,

and Elizabeth Reeve, for her seemingly endless patience, support, and

guidance.

A special word of thanks is reserved for our ofﬁ cial “friend of the book,”

Dr. Richard Fuller, who provided all the “elderly patient”pages. Aside from

this, his steadfast and overtly biased support helped carry us through.

Finally, we would like to thank our good friend Dr. Paul Johns. He read

through much of the text and provided invaluable advice and support

from the very beginning. We wish Paul the very best with his own writing

projects and hope to work with him in the future.

Our panel of readers was responsible for conﬁ rming the medical accur-

acy of the text. Most have performed far beyond our expectations, we are

eternally grateful to them all.

Contents

xi

Contents

How to use this book xii

Detailed contents xiii

Symbols and abbreviations xx

1 Communication skills

1

2 The history

29

3 General examination

47

4 Skin, hair, and nails

75

5 Endocrine system

95

6 Ear, nose, and throat

119

7 Cardiovascular system

145

8 Respiratory system

181

9 Abdomen

203

10 Nervous system

255

11 Musculoskeletal system 337

12 Male reproductive system 375

13 Female breast 391

14 Female reproductive system 407

15 Psychiatric assessment 449

16 Pediatric assessment 479

17 Examination under special circumstances 507

18 Practical procedures 511

19 Data interpretation 591

Index 673

xii

How to use this book

The systems chapters

In each chapter, there are suggestions of what questions to ask and how

to proceed depending on the nature of the presenting complaint. These

are not exhaustive and are intended as guidance.

The history parts of the systems chapters should be used in conjunction

with Chapter 2 in order to build a full and thorough history.

Practical procedures

This chapter (Chapter 18) describes those practical procedures that the

health-care provider, whether a physician, physician assistant, nurse prac-

titioner, or member of another health-care discipline, may be expected

to perform. Some procedures should only be performed once you have

been trained speciﬁ cally in the correct technique by an experienced

professional.

Each procedure has a difﬁ culty icon as follows:

1 Requires no speciﬁ

c training, and all primary-care provider graduates

should be competent to perform this procedure.

2 Requires some skill. Providers with moderate experience should be

able to perform this procedure with ease.

3 More complex procedures that you may only come across in spe-

cialty practices and will not be required to perform without advanced

training and experience.

Reality vs. theory

In describing the practical procedures, we have tried to be realistic. The

methods described are the most commonly ones used across the profes-

sion and are aimed at helping the reader perform the procedure correctly

and safely within a clinical environment.

There may be differences between the way a number of the procedures

are described here and the way in which they are taught in a clinical skills

laboratory. In addition, local hospitals and clinics may use different equip-

ment for some procedures. Good practitioners should be ﬂ exible and

make changes to their routine accordingly.

Data interpretation

A minority of the reference ranges described for some of the biochemical

tests in the data interpretation chapter (Chapter 19) may differ slightly

from those used by your local laboratory—this depends on the equipment

and techniques used for measurement. Any differences are likely to be

very small. Always check with, and be guided by, your local resources.

xiii

Detailed contents

1 Communication skills 1

Introduction 2

Essential considerations 4

Essential rules 6

Getting started 7

General principles 9

Communicating with deaf patients 12

Cross-cultural communication 13

Interpreters 14

Imparting information 15

The importance of silence 15

Angry patients 15

Telephone and e-mail communication 16

Talking about sex 16

Breaking bad news 17

Body language: an introduction 21

Written communication 23

Law, ethics, and communication 26

2 The history 29

History-taking 30

Using this book 31

Patient proﬁ le

(PP)

31

Chief complaint (CC) 32

History of present illness (HPI) 33

Past medical history (PMH) 35

Allergies 36

Drug history 36

Alcohol 37

Smoking 38

Family history (FH) 39

Social history (SH) 41

Review of systems (ROS) 42

The elderly patient 43

The pediatric patient 45

3 General examination 47

Approaching the physical examination 48

First impressions 50

Preparing for the examination 50

Color 51

Temperature 53

xiv

DETAILED CONTENTS

Hydration 54

Edema 55

Nutritional status 56

Lymph nodes 58

Hands 62

Recognizable syndromes 68

Vitamin and trace element deﬁ ciencies 70

The elderly patient 72

4 Skin, hair, and nails 75

Applied anatomy and physiology 76

Dermatological history 78

Hair and nail symptoms 80

Examining the skin 82

Describing a lesion 84

Examining a lump 88

Examining an ulcer 90

The elderly patient 92

5 Endocrine system 95

Applied anatomy and physiology 96

Presenting symptoms in endocrinology 98

The rest of the history 100

General examination 102

Examining the thyroid 104

Eye signs in thyroid disease 106

Examining the patient with diabetes 108

The fundus in endocrine disease 110

Important presenting patterns 114

6 Ear, nose, and throat 119

Applied anatomy and physiology 120

Symptoms of ear disorders 122

Tinnitus 124

Symptoms of nasal disorders 127

Symptoms of throat disorders 129

Examining the ear 132

Examining the nose 135

Examining the nasal sinuses 137

Examining the mouth and throat 138

Important presentations 141

7 Cardiovascular system 145

Applied anatomy and physiology 146

Chest pain 148

Breathlessness and edema 150

xv

DETAILED CONTENTS

Palpitations 152

Syncope 152

Other cardiovascular symptoms 153

The rest of the history 154

General inspection and hands 155

Peripheral pulses 157

The face and neck 161

Examining the precordium 165

Auscultating the precordium 167

The rest of the body 173

Important presenting patterns 175

The elderly patient 179

8 Respiratory system 181

Applied anatomy and physiology 182

Dyspnea 184

Cough and expectoration 185

Other respiratory symptoms 187

The rest of the history 188

General appearance 190

Hands, face, and neck 191

Inspection of the chest 193

Palpation 194

Percussion 196

Auscultation 198

Important presenting patterns 200

The elderly patient 201

9 Abdomen

203

Applied anatomy 204

Esophageal symptoms 206

Nausea, vomiting, and vomitus 208

Abdominal pain 210

Bowel habit 212

Jaundice and pruritus 216

Abdominal swelling 217

Urinary and prostate symptoms 218

Appetite and weight 220

The rest of the history 221

Outline examination 223

Hand and upper limb 224

Face and chest 226

Inspection of the abdomen 229

Auscultation 231

Palpation 232

Palpating the abdominal organs 233

Percussion 239

Rectal examination 241

xvi

DETAILED CONTENTS

Hernial oriﬁ ces 243

Important presenting patterns 246

The elderly patient 252

10 Nervous system 255

Presenting symptoms in neurology 256

The rest of the history 258

The outline examination 259

General inspection and mental state 259

Speech and language 260

Cognitive function 262

Cranial nerve I: olfactory 263

Cranial nerve II: optic 264

Cranial nerve II: ophthalmoscopy 268

Pupils 273

Cranial nerves III, IV, and VI 276

Palsies of cranial nerves III, IV, and VI 280

Cranial nerve V: trigeminal 283

Cranial nerve VII: facial 285

Cranial nerve VIII: vestibulocochlear 287

Cranial nerves IX and X 289

Cranial nerve XI: accessory 291

Cranial nerve XII: hypoglossal 293

Motor: applied anatomy 294

Motor: inspection and tone 296

Motor: upper limb power 298

Motor: lower limb power 300

Tendon reﬂ exes 302

Other reﬂ exes 305

Primitive reﬂ exes 307

Sensory: applied anatomy 308

Sensory examination 312

Coordination 315

Some peripheral nerves 317

Gait 321

Important presenting patterns 323

The unconscious patient 331

The elderly patient 334

11 Musculoskeletal system 337

Applied anatomy and physiology 338

Important locomotor musculoskeletal symptoms 340

The rest of the history 344

Outline examination 346

GALS screen 347

Elbow 349

Shoulder 351

Spine 354

xvii

DETAILED CONTENTS

Hip 356

Knee 358

Ankle and foot 363

Important presenting patterns 365

The elderly patient 373

12 Male reproductive system 375

Applied anatomy and physiology 376

Sexual history 378

Symptoms 379

Examining the male genitalia 381

Important presenting patterns 386

The elderly patient 388

13 Female breast 391

Applied anatomy and physiology 392

Important symptoms 394

Inspection of the breast 397

Palpation of the breast 399

Examining beyond the breast 402

Important presentations 404

14 Female reproductive system 407

Applied anatomy 408

Applied physiology 411

History-taking in gynecology 413

Abnormal bleeding in gynecology 415

Other symptoms in gynecology 419

Outline gynecological examination 423

Pelvic examination 424

Taking a cervical smear 430

History-taking in obstetrics 433

Presenting symptoms in obstetrics 437

Outline obstetric examination 441

Abdominal examination 442

The elderly patient 447

15 Psychiatric assessment 449

Approach to psychiatric assessment 450

History 452

Mental status examination 458

Physical examination 466

Important presenting patterns 467

Medical conditions with psychiatric symptoms and signs 476

xviii

DETAILED CONTENTS

16 Pediatric assessment 479

History-taking 480

Examination: an approach 482

Respiratory system 484

Ear, nose, and throat 488

Cardiovascular system 490

Abdomen and gastrointestinal system 493

Palpation 495

Nervous system 497

Developmental assessment 500

The newborn 502

17 Examination under special circumstances 507

Overview 508

Disasters, terrorism, and public health emergencies 509

Sexual assault 510

Other thoughts 510

18 Practical procedures 511

Using this chapter 512

Inﬁ

ltrating anesthetic agents

512

Sterility and preparation 513

Hand-washing 514

Injections 516

Venipuncture 518

Peripheral IV catheterization 522

Setting up an infusion 524

External jugular vein catheterization 526

Central venous catheterization 527

Blood pressure measurement 531

Recording a 12-lead ECG 533

Arterial blood gas sampling 535

Peak ﬂ ow

measurement

537

Inhaler technique 538

Oxygen administration 544

Basic airway management 547

Tracheostomy management 555

Endotracheal (ET) intubation 557

Noninvasive ventilation (NIV) 559

Pleural ﬂ

uid sampling (thoracentesis)

561

Chest tube insertion 563

Nasogastric (NG) tube insertion 567

Ascitic tap 569

Abdominal paracentesis (drainage) 571

Male urethral catheterization 573

Female urethral catheterization 575

Suprapubic catheterization 577

xix

DETAILED CONTENTS

Basic suturing 579

Lumbar puncture 581

Pericardial aspiration 583

Deﬁ brillation 584

Knee joint aspiration 588

19 Data interpretation 591

ECG: introduction 592

Chest X-rays: introduction 616

Abdominal X-rays: introduction 641

Radiology: pelvis 646

Radiology: hips and femurs 648

Radiology: knees 650

Radiology: shoulder 652

Radiology: cervical spine 654

Radiology: thoracic and lumbar spine 656

Lung function tests 658

Arterial blood gas analysis 663

Cerebrospinal ﬂ uid

(CSF)

667

Urinalysis 669

Pleural and ascitic ﬂ uid 671

Index 673

xx

Symbols and

abbreviations

i increased

d decreased

n normal

7 approximately

b cross-reference

0 warning

2 important

ABC airway, breathing, circulation

ABG arterial blood gases

AC acromioclavicular

ACE angiotensin-converting enzyme

ACL anterior cruciate ligament

ACLS advanced cardiac life support

ACSM American College of Sports Medicine

ACTH adrenocorticotrophic hormone

AD Alzheimer’s disease

ADH antidiuretic hormone

ADL activities of daily living

ADP adenosine diphosphate

AED automated external deﬁ brillator

AF atrial ﬁ brillation

AHA American Heart Association

AITFL antero-inferior tibio-ﬁ bular

ligament

AMTS Abbreviated Mental test Score

ANCOVA analysis of covariance

ANOVA analysis of variance

AP anteroposterior

APH antepartum hemorrhage

APL antiphospholipid

ASD atrial septal defect

ASL American Sign Language

ATFL anterior taloﬁ bular

ligament

ATLS advanced trauma life support

ATP adenosine triphosphate

xxi

SYMBOLS AND ABBREVIATIONS

AV atrioventricular

AVN avascular necrosis

AVPU Alert, Voice, Pain, Unresponsive (scale)

AXR abdominal X-ray

BCC basal cell carcinoma

BCG bacillus Calmette-Guérin

bid twice daily

BiPAP bilevel positional vertigo

BMD bone mineral density

BMI body mass index

BMR basal metabolic rate

BP blood pressure

BPH benign prostatic hyperplasia

bpm beats per minute

BPV benign positional vertigo

C cervical

CABG coronary artery bypass graft

CBC complete blood count

CBRNE chemical, biological, radiological, nuclear, & explosive

CC chief complaint

CDC Centers for Disease Control and Prevention

CEA carcinoembryogenic antigen

CF cystic ﬁ brosis

CFS chronic fatigue syndrome

CHD coronary heart disease

CHF congestive heart failure

CHO carbohydrate

CIN cervical intraepithelial neoplasm

CK creatine kinase

CN cranial nerve

CNS central nervous system

COPD chronic obstructive pulmonary disease

CP cerebral palsy

CPAP continuous positive airways pressure

CPK creatine phosphokinase

CPR cardiopulmonary resuscitation

CRF corticotropin-releasing factor

CRP C-reactive protein

CSF cerebrospinal ﬂ uid

CT computerized tomography

xxii

SYMBOLS AND ABBREVIATIONS

CTD connective tissue disease

CVA cerebrovascular accident

CVP central venous pressure

CXR chest X-ray

DEXA dual-energy X-ray absorptiometry

DIP distal interphalangeal

DKA diabetic ketoacidosis

DM diabetes mellitus

DO detrussor overactivity

DOB date of birth

DUB dysfunctional uterine bleeding

DVT deep venous thrombosis

EBP epidural blood patch

ECG electrocardiogram

ECRB extensor carpi radialis brevis

ECRL extensor carpi radialis longus

ECU extensor carpi ulnaris

EDD estimated date of delivery

EIA exercise-induced asthma

EIB exercise-induced bronchospasm

EJV external jugular vein

EMG electromyography

EMR electronic medical record

ENMG electoneuromyography

EPAP expiration positive airways pressure

EPB extensor polaris brevis

EPO erythropoetin

ESR erythrocyte sedimentation rate

ET endotracheal

FCU ﬂ

exor carpi ulnaris

FDS ﬂ exor digitorum superﬁ cialis

FeCO

2

expired air carbon dioxide concentration

FeO

2

expired air oxygen concentration

FEV

1

forced expiratory volume in 1 second

FH family history

FHR fetal heart rate

FMLA Family Medical Leave Act

FPL ﬂ exor policis longus

FRC functional residual capacity

FSH follicle-stimulating hormone

xxiii

SYMBOLS AND ABBREVIATIONS

FVC forced vital capacity

G gauge

GALS gait, arms, legs, spine

GBS Guillain–Barré syndrome

GCS Glasgow Coma Scale

GEJ gastroesophageal junction

GERD gastroesophageal reﬂ ux disease

GFR glomerular ﬁ ltration rate

GH growth hormone

GI gastrointestinal

GnRH gonadotrophin-releasing hormone

hCG human chorionic gonadotrophin

Hct hematocrit

Hgb hemoglobin

HDL high-density lipoprotein

HIPAA Health Insurance Portability & Accountability Act

HPI history of present illness

HPV human papillomavirus

HR heart rate

HRT hormone replacement therapy

HT hormone therapy

HZV herpes zoster virus

Hct hematocrit

IA intra-arterial

IBD inﬂ

ammatory bowel disease

IBS irritable bowel syndrome

ICP intracranial pressure

ICU intensive care unit

ID intradermal

IGF-1 insulin-like growth factor 1

IHD ischemic heart disease

IHS Indian Health Service

IHSS idiopathic hypertrophic subaortic stenosis

IIH idiopathic intracranial hypertension

IJV internal jugular vein

ILI inﬂ uenza-like illness

IM intramuscular

IMB intermenstrual bleeding

IOC International Olympic Committee

IPAP inspiration positive airways pressure

xxiv

SYMBOLS AND ABBREVIATIONS

IRMA intraretinal microvascular abnormalities

ITB ilio-tibial band

ITBS ilio-tibial band syndrome

IUD intrauterine device

IV intravenous

IVP intravenous pyelogram

JVP jugular venous pressure

L lumbar

LBBB left bundle branch block

LBC liquid-based cytology

LDH lactate dehydrogenase

LDL low-density lipoprotein

LEP Limited English Proﬁ ciency

LFT liver function test

LH luetinizing hormone

LMA laryngeal mask airway

LMN lower motor neuron

LMP last menstrual period

LP lumbar puncture

LOC loss of consciousness

LSB left sternal border

LSE left sternal edge

LV left ventricle

LVH left ventricular hypertrophy

MALT mucosa-associated lymphoid tissue

MANOVA multivariate analysis of the variance

MCL medial collateral ligament

MCP metacarpophalangeal

MC&S microscopy, culture, and sensitivity

MDI metered-dose inhaler

MI myocardial infarction

MLF medial longitudinal fasciculus

MMSE Mini-Mental State Examination

MND motor neuron disease

MPHR maximum predicted heart rate

MRI magnetic resonance imaging

MRSA methicillin-resistant Staphylococcus aureus

MS multiple sclerosis

MSH melanocyte-stimulating hormone

MTP metatarsophalangeal

xxv

SYMBOLS AND ABBREVIATIONS

MVA motor vehicle accident

NG nasogstric

NIV noninvasive ventilation

NSAID nonsteroidal anti-inﬂ ammatory drug

NYHA New York Heart Association

OA osteoarthritis

OCD obsessive-compulsive disorder

OCP oral contraceptive pill

OSHA Occupational Safety & Health Administration

ORIF open reduction and internal ﬁ xation

OTC over the counter

PA posterior–anterior

PCL posterior cruciate ligament

PCOS polycystic ovarian syndrome

PCP primary care provider

PCR polymerase chain reaction

PCS post-concussion syndrome

PDA patent ductus arteriosis

PE pulmonary embolism

PFJ patello-femoral

PID pelvic inﬂ ammatory

disease

PIP proximal interphalangeal

PMH past medical history

PMI point of maximum impulse

PND paroxysmal nocturnal dyspnea

PP patient proﬁ le

PPH postpartum hemorrhage

PPRF parapontine reticular formation

PSIS posterior superior iliac crest

PSYM parasympathetic

PTFL posterior taloﬁ bular ligament

PTH parathyroid hormone

Q cardiac output

q4h every 4 hours

qid 4 times a day (quarter in die)

RAPD relative afferent pupil defect

RBC red blood count or cell

RICE rest, ice, compression, elevation

ROM range of motion

ROS review of systems

xxvi

SYMBOLS AND ABBREVIATIONS

RR respiratory rate

RSE right sternal edge

RV residual volume; right ventricule

SA sinoatrial

SAAG serum/ascites albumin gradient

SANE sexual assault nurse examiner

SAH subarachnoid hemorrhage

SaO

2

oxygen saturation

SC subcutaneous

SCC squamous cell carcinoma

SH social history

SI stress incontinence

SIJ sacroiliac joint

SLAP superior labrum anterior to posterior

SLE systemic lupus erythematosus

SLR straight leg raise

SOB shortness of breath

SPECT single photon emission computer tomography

STD sexually transmitted disease

STI sexually transmitted infection

SQJ squamo-columnar junction

SV stroke volume

SVC superior vena cava

SVT sustained ventricular tachycardia

T thoracic

T

3

triiodothyronine

T

4

thyroxine

TB tuberculosis

TBG thyroid-binding globulin

TBI traumatic brain injury

TGA transposition of the great arteries

TIA transient ischemic attack

tid three times daily

TPN total parenteral nutrition

TSH thyroid-stimulating hormone

TURP transurethral resection of the prostate

UAP unlicensed assistive personnel

UMN upper motor neuron

UC ulcerative collitis

UCL ulnar collateral ligament

xxvii

SYMBOLS AND ABBREVIATIONS

URI upper respiratory infection

US ultrasound

UTI urinary tract infection

UV ultraviolet

VEGF vascular endothelial-derived growth factor

VF ventricular ﬁ brillation

VIN vulval intraepithelial neoplasm

VIP vasoactive intestinal polypeptide

VO

2

oxygen uptake

VRSA vancomycin-resistant Staphylococcus aureus

VSD ventricular septal defect

VT ventricular tachycardia

WBC white blood count

WHO World Health Organization

WPW Wolff–Parkinson–White (syndrome)

Important Notes

0 Write legibly on orders, or print or enter orders via computer.

0 Date, time, and sign all patient care orders.

0 Remember, all facilities should have an approved abbreviations list—

follow it.

0 The ofﬁ

cial “Do Not Use”list of abbreviations is available at the Joint

Commission Web site at: http://www.jointcommission.org.

This page intentionally left blank

1

Communication Skills

Introduction 2

Essential considerations 4

Essential rules 6

Getting started 7

General principles 9

Communicating with deaf patients 12

Cross-cultural communication 13

Interpreters 14

Imparting information 15

The importance of silence 15

Angry patients 15

Telephone and e-mail communication 16

Talking about sex 16

Breaking bad news 17

Body language: an introduction 21

Written communication 23

Law, ethics, and communication 26

Chapter 1

CHAPTER 1 Communication skills2

Introduction

Communication skills are notoriously hard to teach and describe. There

are too many possible situations that you might encounter to be able to

draw rules or guidelines. In addition, your actions will depend greatly on

the personalities present—not least of which your own!

Using this chapter

Over the following pages, we present some general advice about com-

municating in different situations and to different people. We have

not provided rules to stick to but rather have tried to give the reader

an appreciation of the many ways in which the same situation may be

tackled.

Ultimately, skill at communication comes from practice, self-knowledge

and reﬂ ection, and a large amount of common sense.

Quite a bit has been written about communication skills in medicine and

the health sciences. Most articles suggest a mix of accepted protocols and

traditional approaches—this chapter is no different.

Communication models

There are many models of the practitioner–patient encounter that have

been discussed over the years at great length. These models are for the

hardened student of communication. We mention them here so that the

reader is aware of their existence.

Patient-centered communication

In recent years, there has been a signiﬁ cant change in the way health-

care workers interact with patients. The biomedical model has fallen out

of favor and instead, an appreciation has evolved that the patient has a

unique experience of the illness. This experience involves the social, psy-

chological, and behavioral effects of the disease. Some authors refer to this

approach as the biopsychosocial model, which focuses on the patient in a

more encompassing way.

The biomedical model

• The provider is in charge of the consultation and examination.

• Focus is on disease management.

The patient-centered model

• Power and decision-making are shared.

• Address and treat the whole patient.

The rule is: there are no rules.

INTRODUCTION

3

Box 1.1 Key points in the patient-centered model

• Explore the disease and the patient’s experience of it:

• Understand the patient’s ideas and feelings about the illness.

• Appreciate the illness’s impact on the patient’s quality of life and

psychosocial well-being.

• Understand the patient’s expectations of the encounter.

• Understand the whole person:

• Family

• Social and work environment

• Beliefs

• Find common ground on disease management.

• Establish the doctor–patient relationship.

• Be realistic:

• Priorities for treatment

• Resources

Box 1.2 Conﬁ dentiality

As a doctor, health-care provider, or student, you are party to per-

sonal and conﬁ dential information. While Health Insurance Portability

and Accountability Act (HIPAA) regulations must be followed, there are

also times when conﬁ dentiality must or should be broken (b p. 26).

The essence of day-to-day practice is:

Never tell anyone about a patient unless it is directly related to his

or her care and you have permission.

This includes relatives, which can be very difﬁ cult at times, particularly if

a relative asks you directly about something conﬁ dential.

You can reinforce the importance of conﬁ dentiality to relatives and

visitors. If asked by a relative to speak about a patient, it is a good idea

to approach the patient ﬁ rst and ask their permission, within full view of

the relative. You can also seek permission from the patient in anticipa-

tion of such queries.

This rule also applies to friends outside of medicine. As care provid-

ers, we come across many amazing, bizarre, amusing, or uplifting sto-

ries on a day-to-day basis, but like any other kind of information, these

should not be shared with anyone.

If you do intend to use an anecdote in public, at the very least you

should ensure that there is nothing in your story that could possibly

lead to the identiﬁ cation of the person involved. If you are in a small

community, it is best to avoid sharing anything, lest you undermine your

reputation as a professional.

CHAPTER 1 Communication skills4

Essential considerations

Attitudes

Patients are entrusting their health and personal information to you—they

want someone who is conﬁ dent, approachable, competent, and, above

all, trustworthy.

Personal appearance

First impressions count—and studies have consistently shown that your

appearance (clothes, hair, makeup) has a great impact on patients’ opinion

of you and their willingness to interact with you. Part of that intangible

professionalism comes from your image.

The white coat is still part of medical culture for students and most

providers. Fashions in clothing change rapidly, but some basic rules still

apply:

• Neutralize any extreme tastes in fashion that you may have.

• Men and women should wear appropriate professional attire.

• Women may wear skirts or slacks but the length of the skirts should

not raise any eyebrows.

• Necklines should not be revealing—no décolletage!

• The belly should be covered—no bare midriffs!

• The shoulders, likewise, should be covered.

• Shoes should be polished and clean.

• Clean surgical scrubs may be worn, if appropriate.

• Hair should be relatively conservatively styled and no hair should be

over the face. Wear long hair tied up.

• Your name badge should be clearly visible, even if you don’t like your

picture.

• Stethoscopes are best carried or held in a coat pocket—worn at the

neck is acceptable but a little pretentious, according to some views.

• Try not to tuck items in your belt—use pockets or belt-holders for

cell phones, keys, and wallets.

2 Psychiatry, pediatrics, and a handful of other specialties require a differ-

ent dress code, as they deal with patients who require differing techniques

for bonding with the health-care professional.

Timing

If in a hospital setting, make sure that your discussion with a patient is not

during an allocated quiet time or disturbing to the patient’s roommate.

You should also avoid mealtimes or when the patient’s long-lost relative

has just come to visit.

2 If you plan to move the patient from the bed to an exam room, ask

the supervising doctor (if not you) and the nursing staff, and let all con-

cerned know where you have gone in case the patient is needed.

Setting

Students, doctors, and other medical providers tend to see patients on

hospital ﬂ oors ﬁ lled with distractions that can break up the interaction.

ESSENTIAL CONSIDERATIONS

5

Often such meetings are necessary during the course of the day. However,

if you need to discuss an important matter that requires concentration

from both of you, consider the following conditions:

• The room should be quiet, private, and free from disturbances.

• There should be enough seating for everyone.

• Chairs should be comfortable enough for an extended conversation.

• Arrange the seats close to yours, with no intervening tables or other

furniture.

Box 1.3 Becoming a good communicator

Learning

As in all aspects of medicine, learning is a lifelong process. One part of

this process, particularly for acquiring communication skills and at the

beginning of your career, is watching others .

You should take every opportunity to observe provider–patient

interactions.

2 You should ask to be present during difﬁ cult

conversations.

Instead of glazing over during clinic visits or on rounds, you should

watch the interaction and consider if the behaviors you see are worth

emulating or avoiding. Consider how you might adjust your future

behavior.

Select the actions and words you like and use them as your own,

building up your own repertoire of communication techniques.

Spontaneity vs. learned behaviors

When you watch a good communicator, you will see them making friendly

conversation and spontaneous jokes, and using words and phrases that

put people at ease. The conversation seems natural, relaxed, and spon-

taneous. Watching that same person interact with someone else can

shatter the illusion as you see them using the same “spontaneous” jokes

and other gambits from their repertoire.

This is one of the keys to good communication—an ability to judge

the situation and pull the appropriate phrase, word, or action from your

internal catalogue. If done well, it leads to a smooth interaction with no

hesitations or misunderstandings. The additional advantage is that your

mental processes are free to consider the next move, mull over what

has been said, or assess ﬁ ndings, while externally you are partially on

autopilot, following a familiar pattern of interaction.

During physical examination this ability is particularly relevant. You

should be able to coax the wanted actions from the patient and put

them at ease while considering ﬁ ndings and your next step.

It must be stressed, however, that this is not the same as lacking con-

centration—quite the opposite.

CHAPTER 1 Communication skills6

Essential rules

Avoid medical jargon

Medical personnel are so immersed in jargon that it becomes part of their

daily speech. The patient may not understand the words or may have a

different idea of their meaning.

Technical words such as myocardial infarction are in obvious need of

avoidance or explanation. Consider also terms such as exacerbate , chronic ,

numb , and sputum —these may seem obvious in meaning to you but not

to the patient.

You may think that some terms such as angina and migraine are so well

known that they don’t need explanation, but these are very often misinter-

preted. Some examples of such words are given in Table 1.1.

Remember names

Forgetting someone’s name is what we all fear; it is relatively easy to

disguise by simple avoidance. However, using the patient’s name will

make you appear to be taking a greater interest in them. It is particularly

important that you remember the patient’s name when talking to fam-

ily members. Getting the name wrong is embarrassing and can seriously

undermine their conﬁ dence in you.

Aside from actually remembering the name, it is a good idea to have it

written down and within sight—on a piece of paper in your hand, on the

chart, or on the desk. It is a best practice to conﬁ rm the identity of the

patient, using two identiﬁ ers (name, date of birth [DOB]), before you read

results from the chart or electronic medical record (EMR). To be seen

glancing at the name is forgivable; patients would rather have you double

check than bluff your way through an interview.

Table 1.1 Some examples of differing interpretations of medical terms

Word Your meaning Patient’s understanding

Acute Rapid onset Very bad, severe

Chronic Long duration Very bad, severe

Sick Nauseated, vomiting Unwell

Angina Chest pain associated with

ischemic heart disease

Heart attack, shortness of

breath, palpitations

Migraine Speciﬁ c headache disorder Any severe headache

Numb Without sensation Weak

GETTING STARTED

7

Getting started

The start of an encounter is important but is fraught with potential difﬁ cul

-

ties. Like ever

y

thin

g

else in this cha

p

ter, there are no hard-and-

f

ast rules.

Issues

y

ou should take into consideration include the followin

g

:

•

Are you using a language the patient can understand

?

•

Can the

p

atient hear

y

ou?

Greetin

g

Beware o

f

sa

y

in

g

“

g

ood a

f

ternoon” or “

g

ood mornin

g

.” These

g

reetin

g

s

c

an be inappropriate if you are about to break some bad news or if there is

a

nother reason

f

or distress.

C

onsider instead usin

g

a sim

p

le “hello.”

Shaking hands

A traditional greeting, shaking hands will be readily accepted by most

p

atients, but it can also

p

resent challen

g

es

(

think of

p

atients with severe

a

rthritis of the hands

)

. While physical contact always seems friendly and

c

an warm a

p

erson to

y

ou, a handshake ma

y

be seen as overl

y

formal b

y

s

ome and inappropriate by others. Consider using some other form o

f

touch, such as a sli

g

ht

g

uidin

g

hand on the

p

atient

’

s arm as the

y

enter the

room or a brief touch to the forearm.

(

See also Chapter 3 (b p. 63).

• Splinter hemorrhages are tiny, longitudinal streak hemorrhages

under the nails caused by microemboli or trauma. They can be a

normal ﬁ

nding in manual workers.

• Pitting involves tiny indentations in the surface of the nail. It is a

feature of psoriasis and less commonly eczema, lichen planus, and

alopecia areata.

• Onycholysis is is premature lifting of the nail.

• Leukonychia is white discoloration of the nail. It is a sign of low

albumin or chronic ill health.

• Beau’s lines are transverse depressions in the nail. They coincide

with arrested nail growth during a period of acute illness.

• Paronychia is infection of the skin adjacent to the nail, causing pain,

swelling, redness, and tenderness.

• Koilonychia is spooning (concave indentation) of the nail. It is

associated with severe iron deﬁ ciency.

• Clubbing: See Chapter 8, Fig. 8.2 (b p. 192).

• Onychomycosis is fungal nail infection causing the nail to become

thickened, opaque, crumbly, and yellow. It often occurs with

onycholysis and may be indistinguishable from psoriatic nail changes.

CHAPTER 4 Skin, hair, and nails82

Examining the skin

Avoid focusing on the area identiﬁ ed by the patient—the whole organ

needs to be examined.

After explaining the examination and asking permission, ask the patient

to undress to their underwear and lie back comfortably on the exam table

or bed, and cover them with a sheet. Ensure that the room is warm and

private and that you have adequate lighting, preferably in the form of an

adjustable light source. You should consider having an assistant to help

with and chaperone the exam.*

The examination in dermatology consists largely of a careful, thorough

inspection along with an accurate description using recognized dermato-

logical terms.

General inspection of the skin

Begin by scanning the whole surface of the skin for any abnormal lesions.

This can be done in any order, but it will help you to build a pattern that

you can consistently remember that does not miss any areas!

Remember to inspect those areas that are usually hidden:

• Inner thighs

• Undersurfaces of female breasts

• External genitalia

• Axilla

• Gluteal cleft (between the buttocks)

0 Remember also to inspect the mucosal surfaces of the mouth, nails,

hair, and scalp.

Skin color

Skin color varies widely between individuals but should always be even in

distribution, with normal variation for sun-exposed surfaces.

Inspecting a lesion

Inspect each lesion carefully and note the following:

• Grouped or solitary? Pattern if grouped (see Figs. 4.2 . and 4.3 . , b p. 86)

• Distribution and location

• Symmetrical or asymmetrical?

• Peripheral?

• In only light-exposed areas?

• Dermatomal?

• Color

• Shape

• Size

• Surface

• Edge

• Nature of the surrounding skin

* The presence of chaperones is controversial–attitudes vary between geographic areas and institu-

tions. It is considered prudent advice that providers have a chaperone present when performing a

sexually sensitive examination. In practice, male providers performing an examination on a female

and females performing an examination on a male should consider having a chaperone present; the

need for a chaperone in other situations can be judged at the time.

EXAMINING THE SKIN

83

For each of the previous points, describe it as accurately as you can using

dermatological terms. However, if a lesion is pear shaped, it is perfectly

acceptable to call it just that!

When noting the distribution, bear in mind the type of clothing (or lack

of) is usually at that site and what other objects or substances that part of

the body would come into contact with. (Consider especially belt buckles,

watches, gloves, and jewelry.)

Palpation

Each lesion should be felt (remember to ask for, and be granted, permis-

sion ﬁ rst). It is rare to catch an infection from touching a rash or lesion,

and it’s even rarer to see a dermatologist wearing gloves. Each situation

should be judged at the time—obviously, gloves should be worn if there is

bleeding or exudate present or if you are examining the genitalia.

For each lesion, note the following:

• Tenderness (watch the patient’s face)

• Consistency

• Temperature

• Use the back of your hand (inﬂ

amed lesions are usually hot)

• Depth and height

• Mobility

• What skin layer is the lesion in? Is it attached to any underlying or

nearby structures?

• Can it be moved in all directions or only in one or two?

• Does it move with movement of underlying muscle or tendons?

Beyond the lesion

The skin condition must be seen in the context of the whole patient, and

other organ systems should be examined as necessary. Remember to pal-

pate regional lymph nodes if appropriate (See Chapter 3, Lymph Nodes,

b p. 58).

Box 4.3 Koebner’s phenomenon

This is the tendency for certain rashes or lesions to form at the site of

skin trauma, including surgical scars.

Box 4.4 Some common skin color abnormalities

• Jaundice: a yellow tinge to the skin; best appreciated at sclera

• Carotenemia: a yellow–orange tinge to the skin that is similar to that

of jaundice but the sclera are spared

• Hemochromatosis: slate-gray skin coloration

• Addison’s disease: darkened scars and skin creases on the palms and

soles–also darkening of mucosa

• Albinism: a lack of pigmentation with white skin and pink irises

• Vitilgo: autoimmune phenomenon resulting in patchy loss of skin

color

CHAPTER 4 Skin, hair, and nails84

Describing a lesion

A careful description often clinches the diagnosis in dermatology. All

lesions should be documented in accepted dermatological terms ( Figs. 4.1 ,

4.2 , and 4.3 . and Box 4.5 )

Flat, nonpalpable changes in skin color

(a)

Macule

Flat, nonpalpable

change in skin color

<0.5 cm diameter.

Freckles are

pigmented macules

Elevation due to fluid in a cavity

Blister

Fluid below the

epidermis >0.5 cm

diameter

Elevation due to solid masses

Loss of skin

Papule

A raised area <0.5 cm

diameter

Nodule

A mass or lump >0.5 cm

diameter

Callus

Hyperplastic epidermis, often found on the

soles, palms or other areas of excessive

friction and use

Erosion

Partial epidermal loss

Heals without scarring

Fissure

A linear crack

Atrophy

Thinning of the

epidermis

Loss of tissue

(epidermis/dermis + /or

subcutis)

Ulcer

Full-thickness skin loss

(see p. 90)

Wheal

Dermal edema

Plaque

A raised area >2 cm

diameter

Pustule

Visible collection of pus

in the subcutis

Bulla

Large, fluid-filled lesion

below the epidermis

>10 cm diameter

Patch

Flat, nonpalpable

change in skin color

>0.5 cm diameter

Vesicle

Fluid below the

epidermis <0.5 cm

diameter

Fig. 4.1 (a) Primary lesions.

DESCRIBING A LESION

85

Scale

A small thin piece of

horny epithelium

resembling that of a fish

Excoriation

A scratch mark

Telangiectasia

Easily visible superificial

blood vessels

Purpura

A rash caused by blood

in the skin—often

multiple petechiae

Ecchymosis

A ‘bruise,’. Technically a

form of purpura

Erythema

A reddening of the skin

due to local

vasodilatation

Petechia

microhemorrahge

1–2 mm diameter

Spider nevus

A single telangiectatic

arteriole in the skin

Lichenification

Thickening of the

epidermis with

exaggerated skin

markings (bark-like)

usually due to repeated

scratching

Crust (scab)

Dried exudate

is a crust of

blood/plasma

(b)

(c)

Fig. 4.1 (b) Secondary lesions. (c) Vascular lesions.

CHAPTER 4 Skin, hair, and nails86

Linear

Annular

Arciform

Serpiginous

Target Gyrate

Fig. 4.2 Descriptive terms for lesion shapes and patterns of grouped lesions.

Fig. 4.3 Conﬂ uence of grouped lesions. Note how the smaller lesions coalesce to

form a larger lesion.

DESCRIBING A LESION

87

For more information from the American Cancer Society, go to http://

www.cancer.org

For more information from the American Academy of Dermatology, go

to http://www.aad.org

Box 4.5 Malignant melanoma

This is an invasive malignant tumor of melanocytes, occurring mostly in

white adults, and is more common in women. Malignant melanoma can

be present on any skin surface but is most frequently seen on the trunk

of men and women and the legs of women. It can also be found in the

eyes, ears, oral and genital mucosa, and internal sites.

You should be alert to the possibility of a malignant mole if the patient

describes a newly presenting pigmented lesion.

The system most commonly used to assist in diagnosis of malignant

melanoma is the ABCD of the American Cancer Society.

ABCD

• A: asymmetry

• B: irregular border

• C: irregular color

• D: diameter >6 mm

Inclusion of an E, for evolving , is used by the American Academy of

Dermatology. Recent additions to the traditional ABCD warning signs

for malignant melanoma include the “Ugly Duckling sign” or “funny-

looking mole.”

CHAPTER 4 Skin, hair, and nails88

Examining a lump

Any raised lesion or lump should be inspected and palpated as described

previously. Note position, distribution, color, shape, size, surface, edge,

nature of the surrounding skin, tenderness, consistency, temperature, and

mobility.

When examining a lump, there are some points to pay particular atten-

tion to.

Which layer is the lump in?

• Does it move with the skin? (epidermal or dermal)

• Does the skin move over the lump? (subcuticular)

• Does it move with muscular contraction? (muscle/tendon)

• Does it move only in one direction? (tendon or nerve)

• If the lesion belongs to a nerve, the patient may feel pins and

needles in the distribution of the nerve when the lump is pressed.

• Is it immobile? (bone)

Additional characteristics to consider

• Consistency: e.g., stony, rubbery, spongy, soft (Remember, the

consistency does not always correlate with the composition—a ﬂ uid-

ﬁ

lled lump will feel hard if it is tense.)

• Fluctuation: Press one side of the lump—the other sides may

protrude.

• If the lump is solid, it will bulge at the opposite side only.

• Fluid thrill: This can only be elicited if the ﬂ uid-ﬁ

lled lesion is very

large. Examine by tapping on one side and feeling the impulse on the

other, much as you would for ascites (see Chapter 9,

b p. 240).

• Translucency: Darken the room and press a lit penlight to one side of

the lump—it will glow, illuminating the whole lump in the presence of

water, serum, fat, or lymph. Solid lumps will not transilluminate.

• Resonance: This is only possible to test on large lumps. Percuss as you

would any other part of the body (see Chapter 8, b p. 196) and listen

(and feel) if the lump is hollow (gas-ﬁ

lled) or solid.

• Pulsatility: Can you feel a pulse in the lump? Consider carefully if the

pulse is transmitted from an underlying structure or if the lump itself is

pulsating.

• Use two ﬁ

ngers and place one on either side of the lump.

• If the lump is pulsating, it will be expansile and your ﬁ ngers will

move up and outward, away from each other.

• If the pulse is transmitted from a structure below, your ﬁ ngers

will

move upward but not outward (see Chapter 9,

b p. 238).

• Compressibility: Attempt to compress the lump until it disappears. If

this is possible, release the pressure and watch for the lump reforming.

Compressible lumps may be ﬂ uid-ﬁ

lled or vascular malformations.

Note that this is not reducibility.

• Reducibility: This is a feature of hernias. Attempt to reduce the lump

by maneuvering its contents into another space (e.g., back into the

abdominal cavity). Ask the patient to cough and watch for the lump

reforming.

EXAMINING A LUMP

89

Auscultation

You should always listen with a stethoscope over any lump; you could

gain important clues regarding its origin and contents. Listen especially

for the following:

• Vascular bruits

• Bowel sounds

CHAPTER 4 Skin, hair, and nails90

Examining an ulcer

Ulcers should be examined just like any other skin lesion, noting the posi-

tion, distribution, color, shape, size, surface, edge, nature of the surround-

ing skin, tenderness, consistency, and temperature.

If the shape of the ulcer or its position is unusual or difﬁ cult to describe,

make a drawing!

Some of the following characteristics particular to ulcers need to be

considered.

Base

If the base of the ulcer can be seen (i.e., not covered with mucus, blood, or

crust), it should be carefully examined and described. Ulcers usually have

either slough or granulation tissue at the base. Look especially for bone,

tendons, and blood vessels.

Edge

Look carefully at the edge—it may help to make a quick drawing of the

edge in cross-section. Some typical edges are described as follows (also

see Fig. 4.4):

• Sloping: These ulcers are usually shallow and a sloping edge implies

that it is healing (e.g., venous ulcers).

• Punched out: This is full-thickness skin loss and typical of neuropathic

ulceration and vasculitic lesions.

• Undermined: These extend below the visible edge, creating a lip. This

is typical of pyoderma gangrenosum and infected ulceration such as

TB.

• Rolled: Here the edge is mounded but neither everted or undermined

and implies proliferation of the tissues at the edge of the ulcer. Basal

cell carcinoma typically has a rolled edge that is often described as

pearly in color with thin overlying vessels.

• Everted: The tissues at the edge of the ulcer are proliferating too fast,

creating an everted lip. This is typical of neoplastic ulceration.

Depth

Determine what layer (of skin or underlying tissues) the ulcer extends to.

If possible, estimate the depth in mm.

Discharge

Any discharge (e.g., serous ﬂ

uid, pus, blood) from the ulcer should be

examined and noted. If there is an overlying scab or crust (dried discharge

or scale), this should be carefully removed in order to examine the base

of the ulcer.

EXAMINING AN ULCER

91

Box 4.6 Leg ulcers

Leg ulcers are often a result of mixed venous and arterial disease.

However, one pathology may predominate, giving the ﬁ ndings below.

Venous ulceration

Venous hypertension causes ﬁ brin to be laid down at the pericapillary

cuff (lipodermatosclerosis), interfering with the delivery of nutrients to

the surrounding tissues. There may be brown discoloration (hemosi-

derin deposition), eczema, telangiectasia, and, eventually, ulcer forma-

tion with a base of granulation tissue and a serous exudate. Venous

ulcers occur at the medial or lateral malleoli especially. These ulcers will

often heal with time and care.

Arterial ulceration

Along with other symptoms and signs of leg ischemia (Chapter 7,

b p. 178), there may be loss of hair, and toenail dystrophy. Chronic

arterial insufﬁ ciency may lead to deep, sharply deﬁ ned, and painful ulcers

that will not heal without intervention to restore blood supply. Arterial

ulcers appear especially on the foot or mid-shin.

(a)

(b)

(c)

(d)

(e)

Fig. 4.4 Representation of some ulcer edges. (a) sloping; (b) punched out; (c)

undermined; (d) rolled; (e) everted.

CHAPTER 4 Skin, hair, and nails92

The elderly patient

While the skin may be regarded as the largest organ of the body, it is sadly

the one most often overlooked in any assessment of a patient. Many of the

functional changes in aging skin make it increasingly susceptible to injury,

with delayed resolution of wounds and consequent i in infection risk.

Systemic illnesses often manifest in skin and nail changes, and astute

assessment can resolve challenging diagnoses—e.g., erythema ab igne as a

manifestation of hot water bottle use for abdominal pain and underlying

pancreatic cancer or late-onset icthyosis associated with lymphoma.

For acutely ill older people, being alert to the existence and develop-

ment of pressure ulcers can signiﬁ cantly reduce pain and immobility as

well as delays in their recovery.

History

Symptoms

These should be taken seriously. While it is tempting to dismiss pruritus if

there is no visible skin lesion, doing so risks missing a range of important

diagnoses, including iron-deﬁ ciency anemia and liver disease.

Attributing symptoms to age-related changes in the skin should be a

diagnosis of exclusion by generalists (and avoid the term senile pruritus —

older people ﬁ nd it offensive). Always remember that many systemic dis-

eases may ﬁ rst manifest through skin changes.

Pre-existing conditions

Carefully documenting the presence of (and treatment plan for) pres-

sure ulcers is the obligation of medical and nursing staff. Do not shirk

this responsibility—it is important to plan pressure care as critically as

any other intervention. You should be particularly thorough if there is

diabetes mellitus.

Medications

It is important to ask about new changes in drugs and to carefully docu-

ment what an allergy or intolerance consists of—contact the patient’s pri-

mary provider if needed. In the presence of infusion or injection sites, it is

always important to evaluate the integrity of the site.

Functional history

Are overgrown toenails really a sign of self-neglect, or are they more likely

due to poor vision, arthritis, poor handgrip, or neuropathy? Consider ask-

ing about diet, particularly in continuing-care and nursing home residents.

Examination

General

An assessment of pressure areas is critical—ask about and look for sore

heels (and prescribe heel pads if needed). Is the skin frail, intact, marked,

or broken? Asteatosis is extremely common, especially in states of dehy-

dration. Prescribing emollients will earn the thanks of your patients (who

may be uncomfortable and itching) and colleagues.

THE ELDERLY PATIENT

93

Edema

Avoiding hurting your patient—palpate gently. Is the edema gravitational;

are there signs of venous insufﬁ ciency or hypoalbuminemia? Avoid rushing

instantly to the diagnosis of heart failure.

Gravitational eczema

This is often linked with edematous change, as above. Look for pigment

change and ensure that emollients are prescribed. For patients who may

receive compression bandaging or hosiery, check peripheral pulses care-

fully. Carefully describe any ulceration present.

ECG electrodes

If you perform an electrocardiogram (ECG), remove the electrodes imme-

diately afterward. Frail skin is easily torn and ulcerated when attempts at

removal are made the next day, merely from the thoughtlessness of the

person recording the ECG.

Skin malignancies

Common presentations

We all spend signiﬁ cant amounts of time examining and talking to our

patients. Don’t overlook the typical ulceration of a basal cell carcinoma

around the eye or nasal region and the ears.

If you suspect a skin cancer, explore the patient’s previous occupation

or lifestyle. Most importantly, if lesions are suspicious, biopsy them or

refer for further evaluation.

Atypical presentations

Atypical presentations of common problems in atypical sites are legion, so

be thoughtful and carefully examine areas where patients might not look

or be able to see (e.g., scalp, back, calves). Examine nails particularly care-

fully for signs of systemic disease or subungual melanoma.

Be careful about rushing to a diagnosis of psoriasis in a new, isolated

plaque. This is more likely to be Bowen’s disease, so seek expert review.

New onset of diffuse psoriasis-like type plaques in the mature patient with

no history of psoriasis may actually represent lesions of tertiary syphilis.

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95

Endocrine system

Applied anatomy and physiology 96

Presenting symptoms in endocrinology 98

The rest of the history 100

General examination 102

Examining the thyroid 104

Eye signs in thyroid disease 106

Examining the patient with diabetes 108

The fundus in endocrine disease 110

Important presenting patterns 114

Chapter 5

CHAPTER 5 Endocrine system96

Applied anatomy and physiology

The endocrine system is a complex, delicately balanced arrangement of

hormonal feedback loops designed to coordinate organ functions. It main-

tains the internal environment (homeostasis), controls the storage and

utilization of energy substrates, regulates growth and reproduction, and

controls the organ responses to external stimuli.

The major glands that make up the human endocrine system are the

hypothalamus, pituitary, thyroid, parathyroids, adrenals, pineal, and repro-

ductive glands, which include the ovaries and testes ( Fig. 5.1 ). The pan-

creas and the digestive system have endocrine components secreting

insulin, glucagons, gastrin, and somatostatin.

The following is a very brief overview of those aspects of the endocrine

system that may have an impact on the history and examination. Readers

wanting more extensive information on endocrine physiology are advised

to consult a more traditional physiology text.

The hypothalamopituitary axis

The hypothalamus is a collection of specialized cells located in the lower

central part of the brain and, along with the pituitary gland sitting just

below the optic chiasm, forms the primary link between the endocrine and

nervous systems. Neurons in the hypothalamus control the pituitary gland

by producing chemical releasing factors that either increase or suppress

hormone secretion.

This part of the brain is also important in the regulation of satiety,

metabolism, and body temperature.

The releasing factors produced in the hypothalamus reach the pituitary

via a short portal system running down the pituitary stalk (infundibulum).

The pituitary gland is a pea-shaped structure lying in a bony walled cavity,

the sella turcica, in the sphenoid bone at the base of the skull. It has an

anterior lobe that develops from an outgrowth of ectoderm called the

hypophyseal (Rathke’s) pouch in the roof of the mouth and a posterior lobe

that is directly linked to the hypothalamus.

Anterior pituitary hormones

• Growth hormone (GH) stimulates general body growth and regulates

aspects of metabolism.

• Thyroid-stimulating hormone (TSH) controls the production of thyroid

hormones by the thyroid gland.

• Follicle stimulating hormone (FSH) and luteinizing hormone (LH) together

act on the secretion of estrogen and progesterone from the ovaries,

maturation of oocytes, and secretion of testosterone and production

of spermatozoa in the testes.

• Prolactin initiates milk production in mammary glands.

• Adrenocorticotrophic hormone (ACTH) stimulates the adrenal cortex to

produce glucocorticoids.

• Melanocyte stimulating hormone (MSH) enhances skin pigmentation.

APPLIED ANATOMY AND PHYSIOLOGY

97

Posterior pituitary gland

Hormones released here are actually produced in the hypothalamus but

travel down axons in the pituitary stalk to be stored ready for release.

They include anitdiuretic hormone (ADH) and oxytocin.

• Oxytocin acts principally to stimulate contraction of smooth muscle

cells in the uterus during childbirth and around glandular cells of the

mammary glands to cause milk ejection.

• ADH (vasopressin) is secreted by neurosecretory cells in the

hypothalamus in response to increased blood osmotic pressure,

dehydration, and loss of blood volume. It acts to conserve body water.

Thyroid

The thyroid gland is made up of the isthmus and two lateral lobes. The

isthmus overlies the second and third rings of the trachea, while the lobes

extend from either side of the thyroid cartilage downward.

TSH stimulates the release of T

4

(thyroxine) and T

3

(triiodothyronine).

T

3

is considered the active hormone, as it is about 2–4 times more potent

than T

4

, which can be considered a prohormone. Around 80% of circulat-

ing T

3

is derived from the deiodination (removal of iodine) of T

4

. This takes

place in peripheral tissue—the remaining 20% is secreted directly by the

thyroid gland. Most circulating T

3

and T

4

is bound to proteins, including

albumin and thyroid-binding globulin (TBG).

The effects of thyroid hormones are multiple, including increased base-

line metabolism, O

2

utilization, energy turnover, and heat production.

Hypothalamus

and pituitary

Thyroid

Adrenal

Pancreas

Testicles

Fig. 5.1 The major endocrine glands of the body.

CHAPTER 5 Endocrine system98

Presenting symptoms in endocrinology

As hormones have an impact on every body system, it is necessary to

cover all areas of general health in history-taking.

This section outlines some of the more important presenting symptoms

in endocrine disease that should not be missed (if clinical suspicion of

endocrine dysfunction is high), but it is by no means exhaustive.

Appetite and weight changes

Many people do not routinely weigh themselves but may have noticed the

consequences of weight change—e.g., their clothes becoming looser or

tighter (see Box 5.1, b p. 100).

Lethargy

Lethargy or fatigue is a difﬁ cult symptom to pin down. Ask the patient

how the tiredness affects their daily life. What are they able to do before

needing to rest, and has this changed?

Fatigue may be a feature of undiagnosed diabetes mellitus, Cushing’s

syndrome, hypoadrenalism, hypothyroidism, or hypercalcemia.

Consider depression and chronic disease of any other kind (e.g., anemia,

chronic liver and renal problems, chronic infection, and malignancy).

Bowel habit

See b p. 312. Constipation is a common feature of hypercalcemia and

hypothyroidism. Hyperthyroidism and Addison’s disease may produce

diarrhea.

Urinary frequency and polyuria

See b p. 108. Common endocrine causes are diabetes mellitus and diabetes

insipidus. Hyperglycemia caused by Cushing’s syndrome can also result in

polyuria. Polyuria may also be seen in the presence of hypercalcemia.

Thirst and polydipsia

Consider diabetes mellitus, diabetes insipidus, and hypercalcemia.

Sweating

i Perspiration may be seen during episodes of hypoglycemia as well as in

hyperthyroidism and acromegaly and is associated with the other adrener-

gic symptoms of a pheochromocytoma.

Pigmentation

Localized loss of pigmentation may be due to vitiligo —an inherited autoim-

mune disorder associated with other endocrine immune diseases such as

hypo- or hyperthyroidism, Addison’s disease, and Hashimoto’s thyroiditis.

• i pigmentation: Addison’s disease, Cushing’s syndrome

• d pigmentation: generalized loss of pigmentation in hypopituitarism

Hair distribution

Hirsutism , or excessive hair growth, in a female may be due to endocrine

dysfunction. Consider polycystic ovarian syndrome, Cushing’s syndrome,

congenital adrenal hyperplasia, acromegaly, and virilizing tumors.

PRESENTING SYMPTOMS IN ENDOCRINOLOGY

99

Hypogonadism , or adrenal insufﬁ ciency, leads to decreased adrenal

androgen production and loss of axillary and pubic hair in both sexes.

Skin and soft tissue changes

Endocrine disorders cause many soft tissue changes:

• Hypothyroidism: dry, coarse, pale skin with xanthelasma formation,

and, classically, loss of outer 1/3 of the eyebrows

• Hyperthyroidism: thyroid achropachy is seen only in hyperthyroidism

due to Grave’s disease. It is ﬁ

nger clubbing and new bone formation

at the ﬁ

ngers. There is also pretibial myxedema —reddened edematous

lesions on the shins (often the lateral aspects).

• Hypoparathyroidism: generally dry, scaly skin

• Diabetes mellitus: xanthelasma, ulceration, repeated skin infections,

necrobiosis lipoidica diabeticorum —shiny, yellowed lesions on the shins

• Acromegaly: soft tissue overgrowth with skin tags at the axillae and

anus, doughy-looking hands and ﬁ ngers,

acanthosis nigricans

—velvety

black skin changes at the axilla. (Acanthosis nigricans can also be

seen in Cushing’s syndrome, polycystic ovarian syndrome and insulin

resistance.)

Headache and visual disturbance

Visual ﬁ eld defects, cranial nerve palsies, and headache may be caused by

space-occupying lesions within the skull. Pituitary tumors classically cause

a bitemporal hemianopia by impinging on the optic chiasm (b p. 266).

Blurred vision is rather nonspeciﬁ c, but consider osmotic changes in the

lens due to hyperglycemia.

Alteration in growth

Hypopituitarism, hypothyroidism, growth hormone deﬁ ciency, and steroid

excess may present with short stature. Tall stature may be caused by

growth hormone excess or gonadotrophin deﬁ ciency.

Growth hormone excess in adults (acromegaly) causes soft tissue over-

growth. Patients may notice an increase in shoe size, glove size, or facial

appearance (do they have any old photographs for comparison?).

Changes in sexual function

Altered menstrual pattern in a female may be an early symptom suggestive

of pituitary dysfunction. See b Chapter 14 for more detail.

In men, hypogonadism may result in loss of libido and an inability to

attain or sustain an erection (see b Chapter 12). Remember to look for

nonendocrine causes of sexual dysfunction, such as alcoholism, spinal cord

disease, or psychological illness (see b Chapters 11 and 15).

Flushing

Flushing may be a symptom of carcinoid tumor or menopause.

Ask about the nature of the ﬂ ushing, any aggravating or relieving fac-

tors, and, importantly, any other symptoms at the time, such as palpita-

tions, diarrhea, or dizziness. Remember to take a full menstrual history

(see b Chapter 14).

CHAPTER 5 Endocrine system100

The rest of the history

A full history should be taken (b Chapter 2). In a patient with endocrine

symptoms, you should pay special attention to the following (see also

Box 5.1).

Drug history

As ever, a detailed medication history should be sought. Remember to ask

especially about the following:

• Over-the-counter medicines

• Hormonal treatments—including oral contraceptive pill, and local and

systemic steroids

• Amiodarone

• Lithium

• Herbal or other alternative remedies

Past medical history

• Any previous thyroid or parathyroid surgery

• Any previous Iodine

131

(radioiodine) treatment or other antithyroid

drugs

• Gestational diabetes

• Hypertension

• Any previous pituitary or adrenal surgery

Family history

Ask especially about the following:

• Type 2 diabetes (Box 5.2).

• Related autoimmune disorders (pernicious anemia, celiac disease,

vitiligo, Addison’s disease, thyroid disease, type 1 diabetes)

•

Many patients will only have heard of these disorders if they have a

family member who suffers from them.

• Congential adrenal hyperplasia (CAH)

• Tumors of the MEN syndromes (Box 5.3)

Box 5.1 Weight, appetite, and endocrine disorders

• i Appetite , d weight: thyrotoxicosis, uncontrolled diabetes mellitus

• i Appetite , i weight: Cushing’s syndrome, hypoglycemia,

hypothalamic disease

• d Appetite , d weight: gastrointestinal disease, malignancy, anorexia,

Addison’s disease, diabetes mellitus

• d Appetite , i weight: hypothyroidism

THE REST OF THE HISTORY

101

Box 5.2 Diabetic history

As with other diseases, you should establish when the diagnosis was

made (and how) and the course and treatment of the disease. Additional

questions relating to disease monitoring and diabetic complications that

you should ask patients with diabetes are as follows:

• When was it ﬁ rst

diagnosed?

• How was it ﬁ rst diagnosed?

• How was it ﬁ rst managed?

• How is it managed now?

• If on insulin, when was that ﬁ rst

started?

• Are they compliant with a diabetic diet?

• Are they compliant with their diabetic medication?

• How often do they check their blood sugar?

• What readings do they normally get (if possible, ask to see their

monitoring booklet)?

• What is their latest Hb

A

1

C

(many will know this)?

• Have they ever been admitted to hospital with diabetic ketoacidosis

(DKA)?

• Do they go to a podiatrist?

• Have they experienced any problems with their feet? Do they use

any moisturizers or cream on their feet?

• Do they participate in a retinal screening program?

• Have they needed a referral to an ophthalmologist?

• In the newly diagnosed diabetic, ask about a history of weight loss

(will differentiate type 1 and type 2 diabetes).

Box 5.3 MEN syndromes

These are multiple endocrine neoplasias (MEN) that display autosomal

dominant inheritance.

• MEN 1: the “3 Ps: p arathyroid hyperplasia (100%), p ancreatic

endocrine tumors (40–70%), p ituitary adenomas (30–50%)

• MEN 2: medullary cell thyroid carcinoma (100%),

pheochromocytoma (50%), and the following:

• MEN 2a: parathyroid hyperplasia (80%)

• MEN 2b: mucosal and bowel neuromas, marfanoid habitus

CHAPTER 5 Endocrine system102

General examination

It is not possible to perform an examination of the endocrine system in the

same way that you examine other organ systems. Usually, an endocrine

examination is focused—looking for signs to conﬁ rm or refute differential

diagnoses that you have developed during history-taking or examining the

function of one or more speciﬁ c glands (e.g., thyroid).

You may, however, perform a quick screening general examination of a

patient’s endocrine status. Combine this with the examination described

in b Chapter 3.

Hands and arms

Check size, subcutaneous tissue, length of the metacarpals, nails, palmar

erythema, and sweating, tremor. Note also skin thickness (thin skin in

Cushing’s, thick skin in acromegaly) and look for signs of easy bruising.

Assess pulse and blood pressure—lying and standing. Test for proximal

muscle weakness (b p. 343).

Axillae

Note any skin tags, loss of hair, abnormal pigmentation, or acanthosis

nigricans.

Face and mouth

Look for hirsutism, acne, plethora, or skin greasiness. Look at the soft tis-

sues of the face for prominent glabellas (above the eyes) and enlargement

of the chin (macrognathism). In the mouth, look at spacing of the teeth and

if any have fallen out. Note any buccal pigmentation and tongue enlarge-

ment (macroglossia). Normally, the upper teeth close in front of the lower

set; reversal of this is termed prognathism .

Eyes and fundi

See b p. 110–113.

Neck

Note any swellings or lymphadenopathy (b p. 60). Examine the thyroid.

Palpate the supraclavicular regions and note any excessive soft tissue.

Chest

Inspect for any hair excess or loss, breast size in females, and gynecomastia

in males. Note the nipple color, pigmentation, or galactorrhea.

Abdomen

Inspect for central adiposity and obesity, purple striae, and hirsutism.

Palpate for organomegaly. Look at the external genitalia to exclude any

testicular atrophy in males or virilization (e.g., clitoromegaly) in women.

Legs

Test for proximal muscle weakness (b p. 343) and make note of any

diabetes-related changes (b p. 108 and p. 109 respoctively).

GENERAL EXAMINATION

103

Height and weight

Calculate the patient’s BMI (b p. 56).

Box 5.4 Signs of tetany

Trousseau’s sign

Inﬂ ate a blood pressure cuff just above the systolic pressure for 3 min-

utes. When hypocalcemia has caused muscular irritability, the hand will

develop ﬂ exor spasm.

Chvostek’s sign

Gently tap over the facial nerve (in front of the tragus of the ear). The

sign is positive if there is contraction of the lip and facial muscles on the

same side of the face.

CHAPTER 5 Endocrine system104

Examining the thyroid

The patient should be sitting upright on a chair or the edge of a bed.

Inspection

Look at the thyroid region. If the gland is quite enlarged (goiter), you may

notice it protruding as a swelling just below the thyroid cartilage. The

normal thyroid gland is usually neither visible nor palpable.

Thyroid gland

The gland lies 72–3 cm below the thyroid cartilage and has two equal-sized

lobes connected by a narrow isthmus.

If a localized or generalized swelling is visible, ask the patient to take a

mouthful of water and then swallow—watch the neck swelling. Also ask

the patient to protrude their tongue and watch the neck swelling.

• The thyroid is attached to the thyroid cartilage of the larynx and will

move up with swallowing.

• Other neck masses, such as an enlarged lymph node, will hardly move.

• Thyroglossal cysts will not move with swallowing but will move

upward with protrusion of the tongue.

The rest of the neck

• Carefully inspect the neck for any obvious scars (thyroidectomy scars

are often hidden below a necklace and are easily missed).

• Look for the JVP and make note of dilated veins, which may indicate

retrosternal extension of a goiter (see Box 5.5).

• Redness or erythema may indicate suppurative thyroiditis (Box 5.6).

Palpation

Thyroid gland

Always begin palpation from behind the patient. Place a hand on either

side of their neck, which should be slightly ﬂ exed to relax the sternomas-

toids. 0 Explain what you are doing.

• Ask if there is any tenderness.

• Place the middle three ﬁ

ngers of either hand along the midline of the

neck, just below the chin.

• Gently walk your ﬁ

ngers down until you reach the thyroid gland.

• The central isthmus is almost never palpable.

• If the gland is enlarged, determine if it is symmetrical.

• Are there any discrete nodules?

• Assess the size, shape, and mobility of any swelling.

• Repeat the examination while the patient swallows.

• Ask them to hold a small amount of water in their mouth, then ask

them to swallow once your hands are in position.

• Consider the consistency of any palpable thyroid tissue.

• Soft: normal

• Firm: simple goiter

• Rubbery hard: Hashimoto’s thyroiditis

• Stony hard: cancer, cystic calciﬁ cation,

ﬁ

brosis, Riedel’s thyroiditis

• Feel for a palpable thrill, which may be present in metabolically active

thyrotoxicosis.

EXAMINING THE THYROID

105

The rest of the neck

Palpate cervical lymph nodes, carotid arteries (to check for patency—can

be compressed by a large thyroid), and the trachea for deviation.

Percussion

• Percuss downward from the sternal notch.

• In retrosternal enlargement, the percussion note over the manubrium

of the sternum is dull, in contrast to the normal resonance.

Auscultation

Apply the diaphragm of the stethoscope over each lobe of the thyroid

gland and auscultate for a bruit.

• A soft bruit is indicative of increased blood ﬂ

ow characteristic of the

hyperthyroid goiter seen in Grave’s disease.

• You may need to occlude venous return within the internal jugular

vein (IJV) to rule out a venous hum.

• Listen over the aortic area to ensure that the thyroid bruit is not an

outﬂ ow obstruction murmur conducted to the root of the neck.

Box 5.5 Pemberton’s sign

This signiﬁ es thoracic inlet obstruction (e.g., retrosternal goiter).

• Ask the patient to raise both arms above the head.

• Patients with inlet obstruction may develop signs of venous

compression (facial plethora, cyanosis, dizziness, syncope).

• Look at neck veins for congestion and listen for stridor.

Box 5.6 Assessing thyroid status: examination

• Observe the patient’s composure (relaxed, agitated, ﬁ dgety?).

• Measure heart rate and note if patient is in atrial ﬁ brillation.

• Inspect hands for erythema, warmth, and thyroid acropachy

(phalangeal bone overgrowth similar to pulmonary osteopathy).

• Feel the palms—are they sweaty or dry?

• Look for peripheral tremor—ask patient to stretch out arms with

ﬁ

ngers out straight and palms down. Resting a piece of paper on

back of the hand can make a tremor more obvious.

• Inspect the face.

• Exophthalmos, proptosis ( b p. 106)

• Hypothyroid features ( b p. 114)

• Examine the eyes ( b p. 106).

• Examine thyroid and neck ( b p. 104).

• Test tendon reﬂ

exes at the biceps and ankle ( b

p. 302).

• Test for proximal myopathy by asking the patient to stand from a

sitting position.

• Look for pretibial myxedema.

CHAPTER 5 Endocrine system106

Eye signs in thyroid disease

Examination

Inspection

• Look at the patient’s eyes from the front, side, and above.

• Note whether the sclera is visible above or below the iris and whether

the eyeball appears to sit forward (proptosis—best seen from above).

• Note health of the conjunctiva and sclera, looking especially for any

ulceration or conjunctivitis.

• Ensure that both eyes can close (failure is a medical emergency).

Visual ﬁ elds

It is wise to perform a quick screening test of the visual ﬁ elds

(

b p. 264

and 265).

Eye movements

Test eye movements in all directions (b p. 276).

Lid lag (von Graefe’s sign)

• Hold your ﬁ

nger high and ask the patient to look at it and follow it

with their eyes as it moves (keeping their head still).

• Quickly move your hand downward—in this way the patient is made

to look upward and then quickly downward.

• Watch the eyes and eyelids—do they move smoothly and together?

• If lid lag is present, the upper eyelid seems to lag behind movement

of the eye, allowing white sclera to be seen above the iris as the eye

moves downward.

Findings

Proptosis

This is protrusion of the globes as a result of an increase in retro-

orbital fat, edema, and cellular inﬁ ltration (see Box 5.7). It can be formally

assessed using Hertel’s exophthalmometer.

Exophthalmos

This is more severe form of proptosis. Sclera becomes visible below the

lower edge of the iris (the inferior limbus). In very severe cases, the patient

may not be able to close their eyelids and can develop the following:

• Corneal ulceration

• Chemosis (edema of the conjunctiva and sclera caused by obstruction

of the normal venous and lymphatic drainage)

• Conjunctivitis

Lid retraction

The upper eyelid is retracted such that you are able to see white sclera

above the iris when the patient looks forward.

This condition is caused by increase tone and spasm of levator palpe-

brae superioris as a result of thyroid hormone excess (Dalrymple’s sign).

Lid lag

This is caused by sympathetic overstimulation of the muscles supplying the

upper eyelid, seen in thyroid hormone excess.

EYE SIGNS IN THYROID DISEASE

107

Box 5.7 Eye signs of thyrotoxicosis and Graves disease

A common misconception is that proptosis and exophthalmos are

caused by thyrotoxicosis, but this is not the case. Proptosis and exoph-

thalmos may be seen in 50% of patients with Graves disease, and thyro-

toxicosis may occur in Graves disease. However, proptosis may persist

once thyroid hormone levels have normalized.

Eye signs of thyrotoxicosis

• Lid retraction

• Lid lag

Eye signs of Graves disease (Graves ophthalmopathy)

• Periorbital edema and chemosis

• Proptosis/exophthalmos

• Ophthalmoplegias (particularly of upward gaze)

• Lid retraction and lid lag only when thyrotoxicosis is present

Visual blurring may indicate optic neuropathy, therefore, fundoscopy

(b p. 268) should be performed.

CHAPTER 5 Endocrine system108

Examining the patient with diabetes

As diabetes has an impact on every body system, you can make the exami-

nation of a diabetic patient complex or simple depending on the circum-

stances (Box 5.8).

In diabetes clinics, a quick screening examination is performed looking

for major complications, particularly those involving the feet.

In general, you should be alert to cardiovascular disease, renal disease,

retinal disease, peripheral neuropathy, especially sensory, health of insulin

injection sites, the diabetic foot, secondary causes of diabetes (e.g., acrome-

galy, Cushing’s syndrome, hemochromatosis), and associated hyperlipidemia.

The diabetic foot

The combination of peripheral vascular disease and peripheral neuropathy

can lead to repeated minor trauma to the feet, resulting in ulceration and

infection, which are very slow to heal. Chronic infection and other foot

complications are a major cause of morbidity and mortality in the diabetic

patient (see Box 5.8 for examination).

Box 5.8 Important points for a thorough diabetic

examination

Inspection

• Hydration, weight, facies associated with a known endocrine disease,

pigmentation (hyperpigmentation or patchy loss)

• Legs

• Muscle wasting, hair loss, skin atrophy, skin pigmentation, leg

ulceration (especially around pressure points and toes), skin infections

Injection sites

• Inspect and palpate for fat atrophy, fat hypertrophy, or local infection

Associated skin lesions

• Necrobiosis lipoidica diabeticorum—look on the shins, arms, and

back for sharply demarcated oval plaques with a shiny surface, yellow

waxy atrophic centers, and brownish-red margins with surrounding

telangiectasia. Also look for granuloma annulare.

Hyperlipidemia

• Eruptive xanthoma, tendon xanthoma, xanthelasma

Neurological examination

• Visual acuity, fundoscopy, peripheral sensory neuropathy—evidence

of injury, ulceration, and Charcot joint formation. Test muscle

strength and examine feet.

Cardiovascular examination

• Ideally, a conduct a full cardiovascular examination, including lying

and standing blood pressure measurements.

EXAMINING THE PATIENT WITH DIABETES

109

Using a 10 gram monoﬁ lament

Small, thin plastic ﬁ laments are used for testing peripheral sensation in the

diabetic foot. They are designed such that it bends under approximately

10 grams of pressure.

• Apply ﬁ

lament to the patient’s skin at spots shown in Fig. 5.2a .

• Press ﬁ rmly so that the ﬁ lament bends ( Fig. 5.2b ).

• Hold the ﬁ

lament against the skin for 71.5 seconds and ask the patient

if they can feel it.

• The ﬁ

lament should not slide, or stroke or scratch the skin.

• 0 Do not press on ulcers, calluses, scars, or necrotic tissue.

• The patient’s feet are at risk if they cannot feel the monoﬁ lament

at

any of the sites.

Box 5.9 Framework for diabetic foot examination

Inspection

• Color

• Ulceration

• Dryness

• Callous formation

• Infection

• Evidence of injury—are shoes rubbing?

• Charcot’s joints (grossly abnormal and dysfunctional joints due to

repeated minor trauma and poor healing from a loss of pain sensation)

Neurology

• 10 g monoﬁ

lament test (see below)

• Light touch sensation, pain sensation, vibration sense, and joint

position sense (proprioception)

Circulation

• Peripheral pulses (dorsalis pedis and posterior tibial)

• Temperature

• Capillary ﬁ lling

time.

(a) (b)

Fig. 5.2 (a) Sites to test with a 10 g monoﬁ lament in the diabetic patient.

(b) Apply the monoﬁ lament to the skin with enough force to make it bend.

CHAPTER 5 Endocrine system110

The fundus in endocrine disease

Diabetes mellitus

Diabetes mellitus (DM) is the most common cause of blindness in

people between ages 25 and 74 worldwide. Early diagnosis and treat-

ment of diabetic retinopathy can eliminate >95% of diabetic blindness.

For this reason, it is essential for all diabetics to undergo an annual eye

examination.

Mechanisms of damage

The precise metabolic mechanisms underlying the retinal changes seen in

diabetes are still unclear. There may be a role for aldose reductase, the

enzyme responsible for the conversion of glucose to sorbitol. High levels

of sorbitol are found in the lens, pericytes, and Schwann cells of diabetic

patients and are thought to lead to cell damage. A great deal of the dam-

age may be caused by the release of vascular endothelial-derived growth

factor (VEGF) in response to retinal ischemia.

The changes seen in the fundus of diabetic patients arise from common

microvascular lesions. These include the following:

• Microaneurysms

• Hemorrhages—dot and blot

• Hard exudates—lipid precipitated out of the plasma

• Cotton wool spots—represent ischemia and occur from interruption

of axoplasmic ﬂ

ow in the nerve ﬁ ber

layer

• Intraretinal microvascular abnormalities (IRMA)

• Venous beading

• Neovascularization

Classiﬁ

cation of diabetic retinopathy

A simple classiﬁ cation system exists and is detailed below.

Background diabetic retinopathy

Microaneurysms, hard exudates, and hemorrhages are present ( Fig. 5.3 ). It

may be extensive and widespread in severe disease.

Pre-proliferative retinopathy

Ischemia is demonstrated by cotton wool spots; venous beading may also

be present.

Proliferative

New retinal vessel formation occurs ( Fig. 5.4 ). This may progress to vitre-

ous bleeding, traction, retinal detachment, and blindness.

Maculopathy

Pathology affecting the macula causes catastrophic visual loss:

• Exudates and hemorrhages in the macular area ( Fig. 5.5 )

• 2The patient may have reduced visual acuity with no abnormality seen

on fundoscopy.

THE FUNDUS IN ENDOCRINE DISEASE

111

Fig. 5.5 Retinal photograph showing diabetic maculopathy. Thin white arrows

show hard exudates; black arrows show hemorrhages—both within the macula.

New vessels are growing into the macula (thick white arrow).

Fig. 5.3 Retinal photograph showing background diabetic retinopathy. White

arrow shows a microaneurysm, black arrows show hemorrhages.

Fig. 5.4 Retinal photograph showing proliferative diabetic retinopathy. White

arrow shows new vessels growing into an ischemic area (cotton wool spot). Dot

hemorrhages (black arrows) are also apparent.

CHAPTER 5 Endocrine system112

Further ocular manifestations of diabetes

While a great deal of focus is placed on retinal changes seen in diabetes, it

is also worth noting that diabetic patients are predisposed to a number of

other sight-threatening conditions (see Box 5.10 for prevention).

Glaucoma

• Open angle

• Neovascular secondary to rubeosis iridis—new vessel formation on

the iris and interruption of the drainage angle ( Fig. 5.6 )

Cataract

Cataract treatment can be very difﬁ cult

( Fig. 5.7

). Generally, diabetic retin-

opathy should be treated ﬁ rst before contemplating cataract surgery.

Optic neuropathy

• Acute ischemic optic neuritis

• Diabetic optic neuropathy

Cranial nerve palsy

See cranial nerve examination in b Chapter 10 for the common palsies

associated with diabetes.

Hypertensive retinopathy

This is classiﬁ ed into mild, moderate, and severe forms to better correlate

with the duration of systemic hypertension and associated risk of coronary

artery and cerebrovascular disease (see

Fig. 5.8 for treatment).

Appearance—mild

• Generalized or focal arteriolar narrowing of the retinal arterioles

• Opacity of the retinal artery walls—so-called silver/copper wiring

• Arteriovenous (AV) nicking—the retinal arteries cross the veins at a

more perpendicular angle and impinge on the surface of the vein.

Appearance—moderate

• Retinal hemorrhage.

• Cotton wool spots—small areas of ischemia with resulting disruption

of axoplasmic ﬂ

ow in the nerve ﬁ

ber layer of the retina

• Hard exudateslipid exudates

• Microaneurysms

Appearance—severe

• All the above plus optic disc swelling

Box 5.10 Avoiding visual loss in diabetes

Management of the diabetic eye requires a multidisciplinary approach

involving the primary care provider, diabetes physician, diabetes center

staff, optician, ophthalmologist, and, not least of all, the patient.

Ocular examination at the time of diagnosis and yearly screening

thereafter coupled with tight control of weight, blood pressure, chol-

esterol, and blood glucose can help the patient to avoid the devastating

consequences of diabetic eye disease.

THE FUNDUS IN ENDOCRINE DISEASE

113

Fig. 5.6 Retinal photograph showing close-up of the optic disc in glaucoma. Note

how the disc is sunken—the vessels appear to disappear into it (left side of picture).

(a) (b)

Fig. 5.7 Cataract. (a) External appearance. (b) Fundoscopy becomes very difﬁ cult

or impossible.

Fig. 5.8 Retinal photograph showing proliferative diabetic retinopathy treated

with laser therapy. Note the multiple rounded scars on the retina.

CHAPTER 5 Endocrine system114

Important presenting patterns

Hypothyroidism

Causes

These include dietary iodine deﬁ ciency, autoimmune thyroiditis (Hashimoto

thyroiditis), lymphocytic thyroiditis (10% of postpartum women), drugs

(amiodarone, interferon alpha, thalidomide, dopamine, lithium), radio-

active iodine treatment, surgical thyroid injury, external irradiation (e.g.,

for head and neck neoplasms or breast cancer), and pituitary adenoma.

Symptoms

Symptoms include tiredness, weight gain, anorexia, cold intolerance, poor

memory, depression, d libido, goiter, puffy eyes, brittle hair, dry skin,

arthralgia, myalgia, muscle weakness, constipation, and menorrhagia.

Signs

A croaking voice, mental and physical sluggishness, and pseudodementia

“myxedema madness” can be present.

Inspection

• Coarse, cool dry skin (look for yellowish tint of carotenemia “peaches

and cream” complexion), palmar crease pallor, peripheral cyanosis,

puffy lower eyelids, loss of outer 1/3 of eyebrows, thinning of scalp

hair, tongue swelling, xanthalasma

Cardiovascular and chest

• Mild hypertension, pericarditis, pleural effusion, low cardiac output,

cardiac failure, bradycardia, small-volume pulse

Neurological

• Carpal tunnel syndrome, peripheral neuropathy, cerebellar syndrome,

proximal muscle weakness, myotonia, muscular hypertrophy,

delayed ankle jerks, bilateral neural deafness (seen in congenital

hypothyroidism)

Hyperthyroidism

Causes

These include Graves disease, chronic thyroiditis (Hashimoto thyroiditis),

sub acute thyroiditis (de Quervain thyroiditis), postpartum thyroiditis,

drugs (iodine-induced, amiodarone), bacterial thyroiditis, postviral thy-

roiditis, idiopathic, toxic multinodular goitre, malignancy (toxic adenoma,

TSH-producing pituitary tumours).

Symptoms

Symptoms include weight loss, i appetite, irritability, restlessness, muscle

weakness, tremor, breathlessness, palpitations, sweating, heat intolerance,

itching, thirst, vomiting, diarrhea, eye complaints (Graves ophthalmopa-

thy), oligomenorrhea, loss of libido, and gynecomastia.

Signs

Irritability and weight loss can occur.

IMPORTANT PRESENTING PATTERNS

115

Inspection

• Onycholysis, palmar erythema, tremor, sweaty palms, thyroid

acropachy, hyperkinesis, gynecomastia, pretibial myxedema, Graves

ophthalmopathy

Cardiovascular and chest

• Resting tachycardia, high cardiac output, systolic ﬂ ow

murmurs

Neurological

• Proximal myopathy, muscle wasting, hyperreﬂ exia in legs

Polycystic ovarian syndrome (PCOS)

PCOS is caused by abnormal metabolism of androgens and estrogen with

abnormal control of androgen production.

Symptoms

These include oligomenorrhea with an ovulation and erratic periods, and

infertility. Some patients present with hirsutism.

Signs

Obesity (50%), male-pattern hair growth, male-pattern baldness, increased

muscle mass, deep voice, clitoromegaly, and acanthosis nigricans are

among the signs of PCOS.

Glucocorticoid excess (Cushing’s syndrome)

Causes

Causes include high ACTH production from a pituitary adenoma and

ectopic ACTH (e.g., small cell lung cancer). Primary hypercortisolemia

caused by adrenal hyperplasia, adrenal tumor (adenoma or carcinoma), use

of exogenous steroids, ectopic (CRF) production (very rare), depression,

and alcohol use can also contribute to excessive glucocorticoid levels.

Symptoms

These include weight gain (central or upper body), change in appearance,

menstrual disturbance, thin skin with easy bruising, acne, excessive hair

growth, muscle weakness, d libido, depression, and insomnia.

Signs

There are supraclavicular fat pads, moon face, thoracocervical fat pads

(“buffalo hump”), centripetal obesity, hirsutism, thinning of skin, easy

bruising, purple striae, poor wound healing, skin infections, proximal mus-

cle weakness (shoulders and hips), ankle edema, hypertension, fractures

due to osteoporosis, hyperpigmentation (if raised ACTH), and glycosuria.

Hypoadrenalism (Addison’s disease)

Causes

These include autoimmune adrenalitis (up to 80% of U.S. cases), tubercu-

losis, metastatic malignancy, amyloidosis, hemorrhage, infarction, bilateral

adrenalectomy, and HIV.

CHAPTER 5 Endocrine system116

Symptoms

Anorexia, weight loss, tiredness, nausea, vomiting, diarrhea, constipation,

abdominal pain, confusion, erectile dysfunction, amenorrhea, dizziness,

syncope, myalgia, and arthralgia can occur.

Signs

These include skin pigmentation (especially on sun-exposed areas, mucosal

surfaces, axillae, palmar creases, and in recent scars), cachexia, loss of

body hair, postural hypotension, low-grade fever, and dehydration.

Growth hormone excess (acromegaly)

Causes

Pituitary tumor (>95%), hyperplasia due to GHRH excess (very rare), and

tumors in the hypothalamus, adrenal, or pancreas are possible causes.

Symptoms

These include headache, diplopia, change in appearance, enlarged extremi-

ties, deepening of the voice, sweating, tiredness, weight gain, erectile

dysfunction, dysmennorrhea, galactorrhea, snoring, arthralgia, weakness,

numbness, paresthesia, polyuria, and polydipsia.

Signs

These include prominent supraorbital ridges, a large nose and lips, protru-

sion of the lower jaw (prognathism), interdental separation, macroglos-

sia, spade-like hands, doughy soft tissue, thick oily skin, carpal tunnel

syndrome, hirsutism, bitemporal hemianopia (if pituitary tumor impinges

on optic chiasm), cranial nerve palsies (particularly III, IV, and VI), and

hypertension.

Prolactinoma

This is a pituitary tumor (the most common hormone-secreting tumor).

Symptoms

Symptoms depend on the patient’s age, sex, and degree of prolactine-

mia. In females there is oligomenorrhea, vaginal dryness, dyspareunia, and

galactorrhea. In males there is d libido, erectile dysfunction, infertility, and

galactorrhea. If prolactinoma occurs before puberty in males, they may

have a female body habitus and small testicles.

Signs

Visual ﬁ eld defects (bitemporal hemianopia), cranial nerve palsies (III, IV,

and VI), and galactorrhea can occur. Males may have small testicles and a

female pattern of hair growth.

Hypercalcemia

Causes

Common causes include hyperparathyroidism and malignancy (PTHrp

production or metastases in bone). Less common causes are vitamin D

intoxication, granulomatous disease, familial hypocalciuric hypercalemia.

Rarely, hypercalcemia results from certain drugs (e.g., bendroﬂ uazide),

hyperthyroidism, or Addison’s disease.

IMPORTANT PRESENTING PATTERNS

117

Symptoms

These depend largely on the underlying cause. Mild hypercalcemia is

asymptomatic. Higher levels may cause nausea, vomiting, drowsiness, con-

fusion, abdominal pain, constipation, depression, muscle weakness, myal-

gia, polyuria, headache, and coma.

Signs

Often there are signs of the underlying cause. There are no speciﬁ c signs

of hypercalcemia.

Hypocalcemia

Causes

These include hypoalbuminemia, hypomagnesemia, hyperphosphatemia,

surgery to the thyroid or parathyroid glands, parathyroid hormone (PTH)

deﬁ ciency or resistance, and vitamin D deﬁ ciency.

Symptoms

Depression, paresthesia around the mouth, and muscle spasms occur.

Signs

Carpopedal spasm (ﬂ exion at the wrist and the ﬁ ngers) occurs when

blood supply to the hand is reduced by inﬂ ating a sphygmomanometer cuff

on the arm (Trousseau’s sign). There is also nervous excitability—tapping

a nerve causes the supplied muscles to twitch (Chvostek’s sign—tapping

the facial nerve at the parotid gland about 2 cm anterior to the tragus of

the ear causes the facial muscles to contract).

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119

Ear, nose, and throat

Applied anatomy and physiology 120

Symptoms of ear disorders 122

Tinnitus 124

Symptoms of nasal disorders 127

Symptoms of throat disorders 129

Examining the ear 132

Examining the nose 135

Examining the nasal sinuses 137

Examining the mouth and throat 138

Important presentations 141

Chapter 6

CHAPTER 6 Ear, nose, and throat120

Applied anatomy and physiology

Following is a brief review of anatomy relevant to clinical examination.

Ear

The ear is involved in both balance and hearing and is divided into the

external, middle, and inner ear.

The external ear is composed of the pinna (auricle), external auditory

meatus, and the lateral wall of the tympanic membrane.

The auricle is divided into the antihelix, helix, lobe, tragus, and concha

(see Fig. 6.2 , b p. 133) and is composed of ﬁ brocartilage. The ear lobe

is adipose only.

The tympanic membrane is a thin, gray, oval, semitransparent mem-

brane at the medial end of the external acoustic meatus 71 cm in diameter.

It detects air vibrations (sound waves). These tiny movements are then

transmitted to the auditory ossicles.

The middle ear lies in the petrous part of the temporal bone and is

connected to the nasopharynx via the Eustachian tube. It connects with

the mastoid air cells.

The tympanic cavity contains three tiny bones (ossicles: the malleus,

incus, and stapes) that transmit vibrations to the cochlea and two small

muscles (stapedius and tensor tympani). The chorda tympani branch of the

facial nerve passes through here before it exits the skull.

The inner ear (vestibulocochlear organ) is involved in the reception of

sound and maintenance of balance. It consists of a series of interconnect-

ing bony-walled, ﬂ uid-ﬁ lled chambers (vestibule, semicircular canals, and

cochlea). Within the bony labyrinth is a further series of interconnecting

membranous chambers (membranous labyrinth: saccule, utricle, cochlear

duct, and semicircular ducts).

The vestibule and semicircular canals contain the peripheral balance

organs. These have connections to the cerebellum and are important in

the maintenance of posture and ﬁ xed gaze. The sensory impulses are con-

ducted by the cochlear and vestibular divisions of cranial nerve VIII.

Nose and paranasal sinuses

The main functions of the nose and nasal cavities are olfaction, respiration,

and air ﬁ ltration.

The upper 1/3 of the external nose is bony; the rest is cartilaginous. The

inferior surface holds the anterior nares (nostrils), which are separated

from each other by the bony and cartilaginous nasal septum. The lateral

wall of each cavity supports a series of three ridges called turbinates (supe-

rior, middle, and inferior).

The paranasal sinuses are air-ﬁ lled extensions of the nasal cavity. They

are named according to the bones in which they are located: frontal, eth-

moid, sphenoid, and maxilla (see Fig. 6.1 ). Their purpose is thought to

include protection of intracranial structures and the eyes from trauma, an

aid to vocal resonance, and reduction of skull weight.

Mouth and throat

The oral cavity comprises the lips, the anterior 2/3 of the tongue, hard

palate, teeth, and alveoli of the mandible and maxilla.

APPLIED ANATOMY AND PHYSIOLOGY

121

The tongue is involved with mastication, taste, swallowing (deglutina-

tion) and articulation.

Two sets of teeth develop within a lifetime. The ﬁ rst set is deciduous

(milk teeth). The incisors are the ﬁ rst to erupt at 76 months of age; the

rest follow within 3 years. In the permanent set, the ﬁ rst molar or central

incisor erupts ﬁ rst (76 years), the second molar erupts at 711 years of age;

the third molar emerges at 718 years (wisdom teeth).

The pharynx is divided into three parts: nasopharynx, oropharynx, and

hypopharynx. The nasopharynx lies posterior to the nose and superior to

the soft palate. The oropharynx lies posterior to the oral cavity, extend-

ing from the soft palate to the epiglottis, and contains the tonsils. The

hypopharynx lies posterior to the larynx, extending from the epiglottis

to the inferior border of cricoid cartilage, where it is continuous with the

esophagus.

The larynx lies at the level of the bodies of C3–C6 vertebrae. It con-

nects the inferior part of the pharynx with the trachea. It functions to pre-

vent food and saliva from entering the respiratory tract and as a phonating

mechanism for voice production. It is supported by a framework of hyaline

cartilage connected by ligaments.

The thyroid cartilage is the largest of the laryngeal cartilages and can be

seen as the Adam’s apple. The nervous supply of the larynx is from cranial

nerve X (sensory and motor).

The epiglottis is attached to the thyroid cartilage and occludes the laryn-

geal inlet during swallowing.

Salivary glands

The main salivary glands are the parotid, submandibular, and sublingual.

The sublingual glands are the smallest; their ducts open onto the ﬂ oor

of the mouth, as do the ducts of the submandibular glands. The parotid

glands are the largest ones. The parotid ducts cross the masseter muscles

and open into the oral cavity opposite the upper second molar teeth.

Frontal

Ethmoid

Maxillary

Fig. 6.1 Surface anatomy of the facial sinuses.

CHAPTER 6 Ear, nose, and throat122

Symptoms of ear disorders

Otalgia

Earache (otalgia) is common in both children and adults and may be oto-

logical (local) or nonotological (referred) in cause ( Box 6.1 ).

Take a standard pain history, as on b p. 34.

Ask about associated discharge, hearing loss, previous ear operations,

use of Q-tips, trauma, swimming, and air travel.

2 Remember that the ear has a sensory supply from cranial nerves V,

IX, and X and from the second and third cervical nerves, so otalgia may be

referred from several other areas.

Otorrhea

This is discharge from the external auditory meatus. Ask about other ear

symptoms, when the discharge began, and any precipitating or exacerbat-

ing factors. Ask especially about the nature of the discharge:

• Watery: eczema, cerebrospinal ﬂ uid

(CSF)

• Purulent: acute otitis externa

• Mucoid: chronic suppurative otitis media with perforation

• Mucopurulent or blood-stained: trauma, acute otitis media, cancer

• Foul-smelling: chronic suppurative otitis media ± cholesteatoma

Hearing loss

Deafness or total hearing loss is unusual. Hearing loss is usually described

as being mild, moderate, or profound. Hearing loss may be conductive,

sensorineural, mixed, or nonorganic.

Conductive hearing loss may be due to pathology of the ear canal, ear-

drum, or middle ear ( Box 6.2 ). Sensorineural hearing loss is caused by

disease in the cochlea or the neural pathway to the brain.

Box 6.1 Some causes of otalgia

Otological

• Acute otitis externa

• Acute otitis media

• Perichondritis

• Furunculosis

• Trauma

• Neoplasm

• Herpes zoster

Nonotological causes (referred)

• Cervical spine disease

• Tonsillitis

• Dental disease

• Temporomandibular joint disease

• Neoplasms of the pharynx or larynx

SYMPTOMS OF EAR DISORDERS

123

Take a full history as in b Chapter 2. In particular, note the following:

• CC : As well as the usual questions, establish the following:

• Time and speed of onset

•

Is it partial or complete?

•

Are both ears affected or just one?

•

Is there associated pain, discharge, or vertigo?

• PMH : especially tuberculosis and septicemia

• FH : Hearing loss may be inherited (e.g., otosclerosis).

• Drug history : Certain drugs, particularly those toxic to the renal

system, affect the ear (e.g., aminoglycosides, some diuretics, cytotoxic

agents). Salicylates and quinine show reversible toxicity.

• SH : occupation and leisure activities should not be overlooked.

Prolonged exposure to loud noise (e.g., heavy industrial machinery)

can lead to sensorineural hearing loss. The Occupational Safety and

Health Administration (OSHA) requires ear protection or limited

exposure at levels of 90 dB or greater.

0 OSHA mandated limits are available at http://www.osha.gov.

Nonorganic hearing loss

0 Diagnose only after fully excluding an organic cause. In such cases, there

may be a discrepancy between the history and clinical and audiometric

ﬁ ndings.

Box 6.2 Some causes of hearing loss

Conductive

• Cerumen

• Otitis externa, if ear is full of debris

• Middle ear effusion

• Trauma to ossicles

• Otosclerosis

• Chronic middle ear infection (current or previous)

• Tumors of the middle ear

Sensorineural

• Presbycusis

• Vascular ischemia

• Noise exposure

• Inﬂ

ammatory or infectious diseases (e.g., measles, mumps meningitis,

syphilis)

• Ototoxicity

• Acoustic tumors (progressive unilateral hearing loss, but may be

bilateral)

CHAPTER 6 Ear, nose, and throat124

Tinnitus

This is the perception of abnormal noise in the ear or head and may be

caused by almost any pathology in the auditory apparatus ( Box 6.3 ).

As well as taking the full standard history, ask the patient about the

character of the tinnitus, associated hearing loss, how the tinnitus bothers

them (i.e., whether sleep or daily living is affected), and any previous his-

tory of ear disease.

Rushing, hissing, or buzzing tinnitus is most common and is usually

associated with a hearing loss. It is caused by pathology in the inner ear,

brainstem, or auditory cortex (although it can sometimes appear with

conductive hearing loss).

Pulsatile tinnitus is caused by noise transmitted from blood vessels close

to the ear. These include the internal carotid artery and internal jugular

vein (the latter can be diagnosed by abolition of the noise by pressure on

the neck). Occasionally, pulsatile tinnitus can be heard by an observer, by

using a stethoscope over the ear or neck.

Cracking and popping noises can be associated with dysfunction of the

Eustachian tube or rhythmic myoclonus of the muscles in the middle ear

or attached to the Eustachian tube.

2 Remember to distinguish tinnitus from complex noises (e.g., voices,

music) that may constitute auditory hallucinations and point to a psychi-

atric diagnosis.

Injury to the ear

• Trauma may be self-inﬂ icted, especially in children; foreign bodies

inserted in the ear can damage the meatal skin or the eardrum.

• Head injuries can cause temporal bone fractures, with bleeding from the

ear. Fracture may be associated with dislocation of the ossicles or may

pass through the labyrinth, causing severe vertigo and complete deafness.

• Temporary or permanent facial nerve palsy may also occur.

Deformity of the ear

• This may be either congenital or acquired (usually traumatic).

• There may be complete or partial absence of the pinna (anotia or

microtia), accessory auricles (anterior to the tragus) or a preauricular

Box 6.3 Some causes of tinnitus

• Presbycusis

• Noise-induced hearing loss

• Menière’s disease

• Ototoxic drugs, trauma

• Any cause of conductive hearing loss

• Acoustic neuromas

Pulsatile tinnitus

• Arterial aneurysms

• Arteriovenous malformations

• Glomus tumors of the middle ear

TINNITUS

125

sinus. Protruding ears may cause social embarrassment and can be

surgically corrected.

• Small auricles are seen in Down syndrome, often with a rudimentary

or absent lobule.

Dizziness

The term dizziness can mean different things to different people and must

be distinguished from light-headedness, presyncope, and simple unsteadi-

ness. Two features of dizziness suggest that it arises from the vestibular

system:

• Vertigo (a hallucination of movement, most commonly rotational)

• Dizziness related to movement or position change

Both of these symptoms can occur together, separately in time, or alone in

different people. Disequilibrium (unsteadiness or veering) may accompany

vestibular dizziness.

Important points from the history

Obtain a precise history, aiming to establish whether or not the dizziness

is due to vestibular disease ( Boxes 6.4 and 6.5 ). Ask about the following:

• Nature and severity of the dizziness

• Whether it is persistent or in intermittent attacks

• Duration of attacks (seconds, hours, or days)

• Pattern of events since the onset

• Relation to movement or position, especially lying down

• Associated symptoms (e.g., nausea, vomiting, hearing change, tinnitus,

headaches)

• History, including alcohol or drug use

• Other ear problems or previous ear surgery

Peripheral vestibular lesions

Vertigo caused by vestibular problems is most commonly rotational but

may be swaying or tilting. Whether it is movement of the person or sur-

roundings is irrelevant.

Any rapid head movement may provoke the dizziness, but dizziness

provoked by lying down, rolling over, or sitting up is generally speciﬁ c

to

benign paroxysmal positional vertigo.

Box 6.4 Some otological causes of dizziness

• Benign paroxysmal positional vertigo

• Menière’s disease

• Vestibular neuronitis

• Trauma (surgery or temporal bone fracture)

• Perilymph ﬁ stula

• Middle ear infection

• Otosclerosis

• Syphilis

• Ototoxic drugs

• Acoustic neuromas

CHAPTER 6 Ear, nose, and throat126

Central vestibular lesions

These are not always easy to distinguish on the history, with vertigo being

less evident. Gait disturbances, along with other neurological signs and

symptoms, might suggest the presence of a central vestibular lesion.

Box 6.5 Some nonotological causes of dizziness and

disequilibrium

• These are often more disequilibrium than dizziness.

• Aging (poor eyesight and proprioception)

• Cerebrovascular disease

• Parkinson’s disease

• Migraine

• Epilepsy

• Demyelinating disorders

• Hyperventilation

• Drugs (e.g., cardiovascular, neuroleptic drugs, alcohol)

SYMPTOMS OF NASAL DISORDERS

127

Symptoms of nasal disorders

Nasal obstruction

As well as the full history (b Chapter 2), establish the following:

• Is the nose blocked constantly or intermittently?

• Constant: long-standing structural deformity such as deviated

septum, nasal polyps, or enlarged turbinates

• Intermittent: allergic rhinitis or common cold

• Unilateral or bilateral obstruction?

• Associated nasal discharge

• Relieving or exacerbating factors

• Use of nose drops or any other nasal substance (e.g., “hufﬁ ng,”

glue-

snifﬁ

ng, or drug-snorting)

2 Don’t miss a previous history of nasal surgery.

Nasal discharge

Ask about the speciﬁ c character of the discharge, which is often very help-

ful in deciding etiology. See Box 6.6 .

The terms catarrh and postnasal drip should be reserved only for com-

plaints of nasal discharge ﬂ owing backward into the nasopharynx.

Epistaxis

This is a nasal hemorrhage, or nosebleed. The anterior septum, known

as Kiesselbach’s plexus or Little’s area, is the point of convergence of the

anterior ethmoidal artery, the septal branches of the sphenopalatine and

superior labial arteries, and the greater palatine artery. This is a common

site of bleeding.

Epistaxis is most commonly due to spontaneous rupture of a blood ves-

sel in the nasal mucous membrane.

Explore the possible causes ( Box 6.7 ) during history-taking.

Box 6.7 Some causes of epistaxis

• Trauma from nose-picking, surgery, or infection

• Prolonged bleeding may be caused by hypertension, alcohol,

anticoagulants, coagulation defects, and hereditary telangiectasia.

• Neoplasia and angiomas of the postnasal space and nose may

present with epistaxis.

Box 6.6 Some causes of nasal discharge

• Watery or mucoid: allergic or infective (viral) or vasomotor rhinitis

•

A unilateral copious watery discharge may be due to CSF rhinorrhea.

• Purulent: infective rhinosinusitis or foreign body (especially if

unilateral)

• Blood stained: (with unilateral symptoms) tumors, a bleeding

diathesis, or trauma

CHAPTER 6 Ear, nose, and throat128

Sneezing

Sneezing is a very frequent accompaniment to viral upper respiratory tract

infection and allergic rhinitis. It is commonly associated with rhinorrhea

and itching of the nose and eyes.

Ask about exacerbating factors and explore the timeline carefully, look-

ing for precipitants.

Disorders of smell

Patients may complain of a decreased sense of smell (hyposmia) or, more

rarely, a total loss of smell (anosmia) . Ask about the exact timing of the

hyposmia and any other associated nasal symptoms.

Anosmia is most commonly caused by nasal polyps but may be caused

by head injury disrupting the olfactory ﬁ bers emerging through the cribi-

form plate. It may also complicate a viral upper respiratory tract infection

(viral neuropathy).

Cacosmia is the hallucination of an unpleasant smell and may be caused

by infection interfering with the olfactory structures.

Nasal deformity

Nasal deformity may occur as a result of a trauma causing pain ± swelling

± epistaxis ± displacement of nasal bones and septum.

Disruption of the bones and nasal septum may produce a “saddle”

deformity. Other causes of a saddle nose include Wegener’s granuloma-

tosis, congenital syphilis, and long-term snorting of cocaine.

Rosacea (acne rosacea) can cause an enlarged, red, and bulbous rhino-

phyma. Widening of the nose is an early feature of acromegaly.

Nasal and facial pain

Facial pain is not normally due to local nasal causes. More frequently, it is

related to infection within the sinuses, trigeminal neuralgia, dental infec-

tion, migraine, or mid-facial segment pain.

SYMPTOMS OF THROAT DISORDERS

129

Symptoms of throat disorders

Oral pain

• The most common cause of pain in the oral cavity is dental caries and

periodontal infection. Periodontal disease can cause pain with tooth-

brushing and is associated with halitosis.

• Gum disease is a common cause of oral pain.

• In elderly patients, dentures may cause pain if improperly sized or if

they produce an abnormal bite.

• Take a full pain history (b p. 34) and ask about other mouth and

throat symptoms.

Throat pain

• A sore throat is an extremely common symptom. Clarify the full

nature of the pain as discussed on b p. 34. It is important to establish

exactly where the pain is felt.

• Most acute sore throats are viral in origin and are associated with

rhinorrhea and a productive cough. Consider infectious mononucleosis

in teenagers.

• Acute tonsillitis is associated with systemic symptoms such as malaise,

fever, and anorexia.

• Consider malignancy in adults with a chronically sore throat (see also

Box 6.8 ).

• Ask about symptoms associated with cancer, such as dysphagia,

dysphonia, weight loss, and a history of smoking or excessive

alcohol.

2 It is important to remember that oral and throat problems may be

indicative of sexually transmitted infections. Tactfully ask about sexual

encounters, if indicated. Such questioning is often difﬁ cult for new provid-

ers, but one can preface the question with a brief comment as to why such

questions need to be asked.

2 Throat pain often radiates to the ear because the pharynx and external

auditory meatus are innervated by the vagus (X) nerve.

Lumps in the mouth

• Lips are a common site for localized malignancy, e.g., basal cell

carcinoma (BCC), squamous cell carcinoma (SCC).

• Tongue : lumps here are nearly always neoplastic.

• Oral cavity : blockage of a minor salivary gland might give rise to a cystic

lesion called a ranula and is usually sited in the ﬂ oor of the mouth.

Box 6.8 Questions regarding chronic pharyngitis

• Ask about irritants such as tobacco smoke and alcohol.

• Consider chronic tonsillitis, postnasal drip from chronic sinusitis, acid

reﬂ ux, and chronic noninfective laryngitis.

CHAPTER 6 Ear, nose, and throat130

Most malignant lesions on the ﬂ oor of the mouth present late: pain,

dysphagia, and odynophagia (pain on swallowing) are common symptoms.

The buccal lining is also another very common site for cancer.

Globus hystericus (globus pharyngeus)

This is the sensation of a lump in the throat (globus hystericus or globus

syndrome). It is important to ask about symptoms of gastroesophageal

reﬂ ux (GER) (b p. 206) or postnasal drip.

It is occasionally associated with a malignancy. Ask about dysphagia,

odynophagia, hoarseness, and weight loss.

Lumps in the neck

Neck lumps are usually secondary to infection but a minority are due

to malignant disease. The most common cause of neck swelling is lymph

node enlargement. A comprehensive history and examination of the head

and neck is important.

2 In the adult, remember that metastatic neck disease may represent

spread from structures below the clavicle, including lung, breast, stomach,

pancreas, kidney, prostate, and uterus. If malignancy is suspected, the his-

tory and examination should include a search for symptoms and signs in

other systems.

As well as the full standard history, ask especially about the following:

• Duration of the swelling

• Progression in size

• Associated pain or other symptoms in the upper aerodigestive tract

• Odynophagia

• Dysphagia

• Dysphonia

• Systemic symptoms (weight loss, night sweats, malaise)

• Smoking and alcohol habits

Dysphonia

This is an alteration in the quality of the voice. The history should be

aimed at identifying any of the several possible causes:

• Inﬂ ammatory : acute laryngitis, chronic laryngitis (chronic vocal abuse,

alcohol, smoke inhalation)

• Neurological

• Central : pseudobulbar palsy, cerebral palsy, multiple sclerosis, stroke,

Guillain–Barré syndrome, head injury

• Peripheral : lesions affecting cranial nerve X and recurrent laryngeal

nerves (e.g., lung cancer, post-thyroidectomy, cardiothoracic and

esophageal surgery), myasthenia gravis, motor neuron disease

• Neoplastic : laryngeal cancer, for example

• Systemic : rheumatoid arthritis, angiogenic edema, hypothyroidism

• Psychogenic : These are dysphonias in the absence of laryngeal disease

and are mainly due to an underlying anxiety or depression (i.e.,

musculoskeletal tension disorders, conversion voice disorders). Like all

other nonorganic disorders, you must rule out organic pathology.

SYMPTOMS OF THROAT DISORDERS

131

Halitosis

This is offensive-smelling breath. It is commonly caused by poor den-

tal hygiene or diet. Tonsillar infection, gingivitis, pharyngeal pouch, and

chronic sinusitis with purulent postnasal drip can also cause bad breath.

Stridor

This is a noise from the upper airway (see also b p. 187) and is caused by

narrowing of the trachea or larynx. The main causes of stridor in adults are

laryngeal cancer, laryngeal trauma, epiglottitis, and cancer of the trachea

or main bronchus.

CHAPTER 6 Ear, nose, and throat132

Examining the ear

Inspection and palpation

• Brieﬂ y inspect the external structures of the ear ( Fig. 6.2 ), paying

particular attention to the pinna, noting its shape, size, and any deformity.

• Carefully inspect for any skin changes suggestive of cancer.

• Don’t forget to look behind the ears for any scars or a hearing aid.

• Gently pull on the pinna and push on the tragus and ask the patient if

it is painful.

• Pain indicates infection of the external auditory meatus

• Palpate the area in front of the tragus and ask if there is any pain.

• Pain indicates temporomandibular joint disease.

• Look for any discharge.

Otoscopy

The otoscope allows you to examine the external auditory canal, the ear-

drum, and a few middle ear structures.

Otoscope

The otoscope consists of a light source, removable funnel-shaped specu-

lum, and viewing window that often slightly magniﬁ es the image. On many

otoscopes, the viewing window can be slid aside for insertion of instru-

ments (e.g., curettes and swabs) down the auditory canal ( Fig. 6.3 ).

Technique

The following is the method for examining the patient’s right ear.

Examination of the left ear should be a mirror image of this.

• Explain the procedure to the patient and obtain verbal consent.

• Turn the light source on.

• Place a clean speculum on the end of the scope.

• Gently pull the pinna upward and backward with your left hand.

• This straightens out the cartilaginous part of the canal, allowing

easier passage of the scope.

• Holding the otoscope in your right hand, place the tip of the speculum

in the opening of the external canal. Do this under direct vision before

looking through the viewing window.

• Slowly advance the otoscope while looking through it.

• It is often helpful to stabilize the otoscope by extending the little

ﬁ

nger of the right hand and placing it on the patient’s head.

• Inspect the skin of the auditory canal for signs of infection, wax, and

foreign bodies.

• If wax is causing obstruction, it may be necessary to perform ear

lavage before continuing.

• Examine the tympanic membrane ( Fig. 6.4 ).

• A healthy eardrum should appear grayish and translucent.

• Look for the light reﬂ

ex. This is the reﬂ

ection off the surface of the

drum visible just below the malleus.

• Notice any white patches (tympanosclerosis) or perforation.

• A reddened, bulging drum is a sign of acute otitis media.

• A dull gray, yellow drum may indicate middle ear ﬂ uid.

EXAMINING THE EAR

133

Triangula

r

fossa

External

auditory

meatus

Tragus

Lobule

Helix

Concha

Antihelix

Antitragus

Fig. 6.2 The surface anatomy of the normal ear.

Insufflator port for

pneumatic otoscopy

Removable specula—

choice of sizes

Built-in bulb here

On/off switch.

These often slide side-to-side

for variable illumination

Batteries housed here

Magnified viewing

lens—can slide open

to insert the instruments

Fig. 6.3 A standard otoscope.

Posterior fold

Short process

of malleus

Umbo

Pars flaccida

Anterior fold

Handle of malleus

Cone of high reflex

Fig. 6.4 The appearance of the normal eardrum on otoscopy.

CHAPTER 6 Ear, nose, and throat134

A note on pneumatic otoscopy: Remember that this simple evaluation,

when used by a reasonably skilled provider, may help avoid the necessity

of sending the patient for a costly procedure. Simple procedures can be

accurate and cost-effective.

Box 6.9 Testing auditory and vestibular function

See b Chapter 10, Cranial Nerve VIII (b p. 287).

EXAMINING THE NOSE

135

Examining the nose

External inspection

• Inspect the external surface and appearance of the nose, noting any

disease or deformity.

• Stand behind the patient and look down over their head to detect any

deviation.

Palpation

• Gently palpate the nasal bones and ask patient to alert you to any pain.

• If a visible deformity is present, palpate to determine if it is bony (hard

and immobile) or cartilaginous (ﬁ rm but compressible).

• Feel for facial swelling and tenderness.

• Tenderness suggests underlying inﬂ ammation.

Nostril patency

Assess whether air moves through both nostrils effectively.

• Push on one nostril until it is occluded.

• Ask the patient to inhale through their nose.

• Then repeat on the opposite side.

Air should move equally well through each nostril; however, remember

that nasal cycling may occur in a substantial portion of the population.

Internal examination

The postnasal space (nasopharynx) can be examined using ﬁ ne-bore

endoscopy. This is done by trained professionals; the student or nonspe-

cialist should examine the anterior portion of the nose only.

• Ask the patient to tilt their head back.

• Push up slightly on the tip of the nose with the thumb (see Fig. 6.5 ).

• You should now be able to see just inside the anterior vestibule.

• In adults, you can use a nasal speculum (see Fig. 6.6 ) to widen the

nares to enable easier inspection.

• Pinch or release the speculum to the closed position, place the prongs

just inside the nostril, and squeeze or release your grip gently, allowing

the prongs to spread apart.

• Look at the following:

• Color of the mucosa

• Presence and color of any discharge

• Septum (which should be in the midline)

• Any obvious bleeding points, clots, crusting, or perforation

• Middle and inferior turbinates along the lateral wall for evidence of

polypoid growth, foreign bodies, and other soft tissue swelling

Testing olfaction

This is described in b Chapter 10, Cranial Nerve I (b p. 263).

CHAPTER 6 Ear, nose, and throat136

Fig. 6.6 A standard nasal speculum and Thudicum speculum.

Fig. 6.5 Examination of the anterior vestibule: press nose upward with your thumb.

EXAMINING THE NASAL SINUSES

137

Examining the nasal sinuses

The reader should revisit the anatomy of the sinuses and Fig. 6.1 on

b p. 121. The frontal and maxillary sinuses are the only two that can be

examined, albeit indirectly.

Palpation

• Palpate and percuss the skin overlying the frontal and maxillary sinuses.

• Tap on the upper teeth (which sit in the ﬂ oor of the maxillary sinus).

• In both of the above, pain suggests inﬂ ammation (sinusitis).

CHAPTER 6 Ear, nose, and throat138

Examining the mouth and throat

Ensure that the room is well lit. You should have an adjustable light-source.

An otoscope or penlight should be adequate for nonspecialists.

Inspection

Face

Look at the patient’s face for obvious skin disease, scars, lumps, signs of

trauma, deformity, or facial asymmetry (including parotid enlargement).

Lips, teeth, gums

Inspect the lips at rest ﬁ rst.

• Ask the patient to open their mouth and take a look at the buccal

mucosa, teeth, and gums.

• Note signs of dental decay or gingivitis.

• Ask the patient to evert the lips and look for any inﬂ ammation,

discoloration, ulceration, nodules, or telangiectasia.

Tongue and ﬂ

oor of the mouth

Inspect the tongue inside and outside the mouth. Look for any obvious

growths or abnormalities.

• Included in this should be an assessment of cranial nerve XII (b p. 293).

• Ask the patient to touch the roof of the mouth with their tongue.

• This allows you to look at the underside of the tongue and ﬂ oor of

the mouth.

Oropharynx

In order to look at the posterior oropharynx ( Fig. 6.7 ), ask the patient to

say “aaah” (which elevates the soft palate).

Hard palate

Soft palate

Uvula

Posterior arch

(pilla)

Tonsillar fossa

Anterior arch

(pilla)

Oropharynx

Fig. 6.7 The normal appearance of the oral cavity.

EXAMINING THE MOUTH AND THROAT

139

• Use of a tongue depressor may provide a better view or it may just

serve to gag the patient.

Uvula

The uvula should hang down from the roof of the mouth, in the mid-

line. With an “aaah” the uvula rises up. Deviation to one side may be

caused by cranial nerve IX palsy (see b p. 289 for more detail), tumor,

or infection.

Soft palate

Look for any cleft, structural abnormality, or asymmetry of movement and

note any telangiectasia.

Tonsils

Inspect the tonsils, noting their size, color, and any discharge.

• The tonsils lie in an alcove between the posterior and anterior pillars

(arches) on either side of the mouth.

Palpation

This is reserved for any abnormal or painful areas detected on initial

inspection.

• Put on gloves and palpate the area of interest with both hands (one hand

outside on patient’s cheek or jaw and the other inside the mouth).

• Note the characteristics of any lump (b p. 88).

The rest of the neck

Palpate the cervical and supraclavicular lymph nodes (b p. 58) and

thyroid (b p. 104) and look for any additional masses (describe each

as on b p. 98).

Findings

• Mucosal inﬂ ammation: bacterial, fungal (candidiasis), and viral (e.g.,

herpes simplex) infections, or after radiotherapy treatment

• Oral candidiasis: radiotherapy, use of inhaled steroids, and

immunodeﬁ

ciency states (e.g., leukemia, lymphoma, HIV)

• Gingivitis: inﬂ

ammation of the gums may occur in minor trauma (teeth

brushing), vitamin and mineral deﬁ

ciency, or lichen planus (see also

Box 6.10 ).

• Tonsillitis: mucopus on the pharyngeal wall implies bacterial infection.

Posterior pharyngeal wall vesicles may imply a viral origin. In teenagers

think of infectious mononucleosis, particularly if the tonsils are covered

with a white pseudomembranous exudate.

Box 6.10 Gum changes in systemic conditions

• Chronic lead poisoning: punctuate blue lesions

• Phenytoin treatment: ﬁ rm and hypertrophied

• Scurvy: soft and hemorrhagic

• Cyanotic congenital heart disease: spongy and hemorrhagic

CHAPTER 6 Ear, nose, and throat140

• Acute tonsillitis is often associated with systemic features of

malaise, fever, anorexia, cervical lymphadenopathy, and candidiasis.

Remember to consider HIV or other immune disorders in the

presence of candidiasis!

• See Box 6.11 for causes of neck masses.

Box 6.11 Some causes of neck masses

Midline

• Lesions of the thyroid gland, thyroglossal cysts (lump moves when

patient sticks out tongue), midline dermoids, submental lymph

nodes, parathyroid gland enlargement (very rare)

Lateral

• Neoplasia (primary cancer, lymphoma, schwannoma, metastatic

cancer), infection (mumps, glandular fever, TB, HIV), autoimmune

(e.g., Sjogren’s syndrome), normal variants (transverse process of C2,

cervical rib, elongated styloid process), sarcoidosis, branchial cyst

IMPORTANT PRESENTATIONS

141

Important presentations

Otitis externa

This is inﬂ ammation of the outer ear and is commonly caused by bacterial

infection of the ear canal (e.g., Streptococci, Staphylococci, Pseudomonas )

and fungi. Heat, humidity, swimming, and any irritants causing pruritis can

all predispose a patient to otitis externa.

Otitis externa often occurs in patients with eczema, seborrheic derma-

titis, or psoriasis due to scratching. Symptoms can vary from irritation to

severe pain ± discharge.

Pressure on the tragus or movement of the auricle may cause pain.

Malignant otitis externa is a very aggressive form caused by a spreading

osteomyelitis of the temporal bone (usually Pseudomonas pyocaneus ). The

infection may spread to involve the middle ear and lower cranial nerves. It

is seen in immunocompromised patients and diabetics.

Furunculosis

This is an infection of hair follicles in the auditory canal. It presents with

severe throbbing pain, exacerbated by jaw movement, with pyrexia and

often precedes rupture of an abscess.

Otitis media and glue ear

This inﬂ ammation of the middle ear usually follows an upper respiratory

tract infection.

In the early stages, the eardrum becomes retracted as the Eustachian

tube is blocked, resulting in an inﬂ ammatory middle ear exudate. If there

is infection, pus builds up, causing the middle ear pressure to rise. This is

seen on otoscopy as bulging of the eardrum. The eardrum may eventually

rupture if untreated.

Complications

These include inﬂ ammation in the mastoid air cells (mastoiditis), labyrin-

thitis, facial nerve palsy, extradural abscess, meningitis, lateral sinus throm-

bosis, and cerebellar and temporal lobe abscess.

Chronic suppurative otitis media

This is associated with a central persistent perforation of the pars tensa.

The resulting otorrhea is usually mucoid and profuse in active infection.

Glue ear

Glue ear, or otitis media with effusion, is the most common cause of

acquired conductive hearing loss in children (peaks at 3–6 years). There is

a higher incidence in patients with cleft palate and Down syndrome. The

etiology is usually Eustachian tube dysfunction with thinning of the drum.

Cholesteatoma

This is a destructive disease consisting of overgrowth of stratiﬁ ed squa-

mous epithelial tissue in the middle ear and mastoid causing erosion of

local structures and the introduction of infection.

CHAPTER 6 Ear, nose, and throat142

When infected, there may be a foul-smelling aural discharge. Bone

destruction and marked hearing loss can occur. Cholesteatoma may be

complicated by meningitis, cerebral abscesses, and facial nerve palsy.

Menière’s disease

This is also known as endolymphatic hydrops. There is distension of the

membranous labyrinthine spaces; the exact cause is not known.

Symptoms include attacks of vertigo with prostration, nausea, vomiting,

a ﬂ uctuating sensorineural hearing loss at the low frequencies, tinnitus, and

aural fullness or pressure in the ear.

Attacks tend to occur in clusters with quiescent periods between. Each

attack lasts only a few hours, and the patient usually has normal balance in

between. Over years, hearing gradually deteriorates in the affected ear.

Vestibular neuronitis

This is typically associated with sudden vertigo, vomiting, and prostration.

The symptoms are exacerbated by head movement. It often follows a viral

illness in the young or a vascular lesion in the elderly. There is no deafness

or tinnitus. The vertigo lasts for several days, but complete recovery of

balance can take months or may never be achieved.

Otosclerosis

This is a localized disease of bone that affects the capsule of the inner ear.

Vascular, spongy bone replaces normal bone around the oval window and

may ﬁ x the footplate of the stapes.

Otoscopic examination is usually normal. There may be progressive

conductive deafness manifesting after the second decade, possibly with

tinnitus and, rarely, vertigo. Pregnancy and lactation aggravate the condi-

tion. There is often a strong family history. Both ears are affected in >50%

of patients.

Benign positional vertigo

These are attacks of sudden-onset rotational vertigo provoked by lying

down ﬂ at or turning over in bed. The condition is caused by crystalline

debris in the posterior semicircular canal. It can follow an upper respira-

tory tract infection or head injury, but often there is no preceding illness.

The Dix-Hallpike maneuver (also referred to as Nylen-Barany maneu-

ver) is diagnostic (see b p. 288). If diagnosed, the person should undergo

an Epley maneuver, which is often curative. This repositions the debris in

the posterior semicircular canal into the utricle.

Labyrinthitis

This is a localized infection of the labyrinth apparatus and is difﬁ cult to

distinguish clinically from vestibular neuronitis, unless there is hearing loss

due to cochlear involvement.

Acoustic neuromas

These are benign, slowly growing tumors of the vestibular element of

cranial nerve VIII. They usually present in middle age and occur more

frequently in females. Bilateral neuromas occur in 5% of patients.

IMPORTANT PRESENTATIONS

143

The early symptoms are unilateral or markedly asymmetric, progressive

sensorineural hearing loss and tinnitus. Vertigo is rare, but patients with

large tumors may have ataxia.

Presbycusis (senile deafness)

Presbycusis is a progressive loss of hair cells in the cochlea with age,

resulting in a loss of acuity for high-frequency sounds. It becomes clinically

noticeable from the age of 60–65 years, although the degree of loss and

age of onset is variable.

Hearing is most affected in the presence of background noise.

Glomus jugulare tumor

This is a highly vascular tumor arising from glomus jugulare tissue lying in

the bulb of the internal jugular vein or the mucosa of the middle ear.

It usually presents with a hearing loss or pulsatile tinnitus. Examination

of the ear may show a deep red mass behind the ear drum. Occasionally,

they are associated with other tumors, such as pheochromocytomas or

carotid body tumors.

Allergic rhinitis

In allergic rhinitis, inhaled allergens are responsible for an antigen–anti-

body type I hypersensitivity reaction.

Common allergens in seasonal allergic rhinitis (hayfever) are pollen

(including from grass) and ﬂ owering trees. In perennial allergic rhinitis, the

principal allergens are animal dander, * dust mites, ** and feathers. Rarely,

digested allergens, such as wheat, eggs, milk, and nuts, are also involved.

The main symptoms include bouts of sneezing, a profuse rhinorrhea due

to activity of glandular elements, postnasal drip, nasal itching, and nasal

obstruction due to nasal vasodilatation and edema.

Nonallergic (vasomotor) rhinitis

This has all the clinical features of allergic rhinitis but the nose does not

respond to an antigen–antibody type 1 reaction. The reactions tend to be

to inhaled chemicals, such as deodorants, perfumes, or smoke, although

alcohol and sunlight can provoke symptoms.

Allergies can coexist, and some people seem to have instability of the

parasympathetic system in the nose, with excessive secretion of watery

mucus and congestion (vasomotor rhinitis).

Nasal polyps

Nasal polyps are pale, grayish, pedunculated, edematous mucosal tissue

that project into the nasal cavity. They most frequently arise from the

ethmoid region and prolapse into the nose via the middle meatus and are

nearly always bilateral.

In most cases, they are associated with nonallergic rhinitis and late-onset

asthma. Other causes to consider include chronic paranasal infection, neo-

plasia (usually unilateral ± bleeding), cystic ﬁ brosis, and bronchiectasis.

*

The ﬁ eld of allergy research is rather interesting. Cat allergy, for example, is actually an allergy to

one of the proteins in feline saliva—their fur is covered in it through licking.

**

Actually an allergy to dust mite feces.

CHAPTER 6 Ear, nose, and throat144

The main symptoms are watery anterior rhinorrhea, purulent postnasal

drip, progressive nasal obstruction, anosmia, change in voice quality, and

taste disturbance.

Septal perforation

Septal perforation may be idiopathic or caused by trauma (especially post-

operative nasal surgery), infection (e.g., tuberculosis, syphilis), neoplasia

(SCC, BCC, malignant granuloma), or inhaling cocaine and toxic gases.

The main clinical complaints include crusting, recurrent epistaxis, and a

whistling respiration.

Tonsillitis

Acute tonsillitis is uncommon in adults in comparison to its frequency in

children. The diagnosis is made from the appearance of the tonsils, which

are enlarged with surface exudates. The patient is usually systemically ill

with pyrexia, cervical lymphadenopathy, dysphagia, halitosis, and, in chil-

dren, abdominal pain.

Complications include peritonsillar abscess (quinsy) and retropharyn-

geal abscess.

Laryngitis

This is frequently associated with an upper respiratory tract infection and

is self-limiting. There may be associated secondary infection with Staph.

and Strep. species. The patient typically complains of hoarseness, malaise,

and fever. There may also be odynophagia, dysphagia, and throat pain.

Epiglottitis

0 This is a medical emergency. It is caused by group B Haemophilus inﬂ u-

enzae. Epiglottitis is characterized by gross swelling of the epiglottis and is

seen primarily in 3- to 7-year-olds, although adults may also be affected.

Clinical features include pyrexia, stridor, sore throat, and dysphagia.

Remember the classic radiological feature, the “thumb sign.”

Croup (laryngotracheobronchitis)

Most cases are viral (parainﬂ uenza or respiratory syncytial virus). Croup

occurs mainly between the ages of 6 months and 3 years.

Branchial cyst

These are an embryological remnant of the branchial complex during

development of the neck. They are located in the anterior triangle just in

front of the sternomastoid.

Presentation is typically at the age of 15–25 years.

145

Cardiovascular system

Applied anatomy and physiology 146

Chest pain 148

Breathlessness and edema 150

Palpitations 152

Syncope 152

Other cardiovascular symptoms 153

The rest of the history 154

General inspection and hands 155

Peripheral pulses 157

The face and neck 161

Examining the precordium 165

Auscultating the precordium 167

The rest of the body 173

Important presenting patterns 175

The elderly patient 179

Chapter 7

CHAPTER 7 Cardiovascular system146

Applied anatomy and physiology

Cardiologists consider this system to be the most important one in the

body. This system is fundamentally straightforward, and a good deal of

information about its functioning can be gleaned from physical examination.

The basic anatomy of the cardiovascular system should be familiar to read-

ers. Following is a summary of some points that have particular implications

for the clinical assessment.

The heart

The heart rotates counterclockwise during embryonic development, ﬁ nally

settling in such a way that the left ventricle lies almost entirely posteriorly

and the right anteriorly—the whole seeming to hang in the chest, held by

the aorta ( aorta comes from the Greek “aorte,” meaning “to suspend”).

The myocardium is arranged in a complex spiral such that a contraction

causes the heart to elongate and rotate slightly, hitting the anterior chest

wall as it does—this can be felt as the apex beat.

All of this movement is lubricated by a double-lined cavity ﬁ lled with a

very small amount of ﬂ uid that the heart sits in—the pericardial sac.

Heart sounds

As the ventricles contract, the tricuspid and mitral valves close, heard

as the ﬁ rst heart sound. As the ventricles relax, intraventricular pressure

drops, and blood expelled into the great vessels begins to fall back, the

aortic and pulmonary valves slam closed—this is heard as the second

heart sound. The sounds are often described as sounding like lub dub .

As each heart sound is, in fact, two valves closing, any mistiming will

cause a double, or “split,” heart sound as one valve closes shortly after the

other. A split second heart sound is normal in young adults and children.

During inspiration, intrathoracic pressure drops, drawing blood into the

chest, i delivery to the right side of the heart, and d delivery to the left as

it pools in the pulmonary veins.

Consequently, the stroke volume will be greater on the right than on

the left and the right ventricular contraction will take slightly longer. Thus,

the pulmonary valve will close very slightly later than the aortic valve,

producing the split second sound ( lub da-dub ). This is called “physiological

splitting.” Split heart sounds are considered on b p. 168.

Jugular venous pulse (JVP)

There is no valve between the right heart and the large vessels supplying it.

Thus, ﬁ lling and contraction of the right atrium will cause a pressure wave

to travel back through the vena cava. This can actually be seen in the neck

at the internal jugular vein (IJV). See b p. 161.

Arteries

As the ventricle expels blood into the arteries, it sends a pulse wave to

the periphery that can be felt. This is not the actual ﬂ ow of blood from the

ventricle at that contraction but a pressure wave. The shape and feel of

the wave can be altered by the force of expulsion, any obstacles (such as

the aortic valve), and the state of the peripheral vasculature.

APPLIED ANATOMY AND PHYSIOLOGY

147

The arteries have their own intrinsic elasticity, allowing a baseline, or

diastolic, pressure to be maintained between each pulse wave.

Veins

Blood ﬂ ows at a much lower pressure in the veins.

Above the level of the heart, gravity does most of the work in returning

the blood. Below, blood return is facilitated by contraction of muscles sur-

rounding the deep veins, helped by numerous one-way valves to prevent

backﬂ ow. Blood moves initially from the surface to the deep veins before

moving upward, again mediated by one-way valves (if these valves become

damaged, blood ﬂ ows outward to the surface veins, causing them to swell

and look tortuous—varicose veins).

Blood return is also aided by a negative pressure created by blood being

pumped out of the right ventricle, and therefore drawn in through the

right atrium at each beat.

CHAPTER 7 Cardiovascular system148

Chest pain

This is the most common—and most important—cardiovascular symp-

tom. Patients who mention it may be surprised to ﬁ nd themselves whisked

away for an ECG before they can say anything more. It is, however, usu-

ally possible to determine the probable cause of the pain with a detailed

history.

As for any other type of pain, the history must include the following:

• Nature (crushing, burning, aching, stabbing, etc.)

• Exact location

• Any radiation

• Severity (scored out of 10)

• Mode and rate of onset. What was the patient doing at the time?

• Change in the pain over time (and current score out of 10)

• Duration (if now resolved)

• Exacerbating factors (particularly, is it affected by respiration or

movement?)

• Relieving factors (including the use of nitroglycerin)

• Associated symptoms (nausea, vomiting, sweating, belching, etc.)

Patients with a history of cardiac pain can also tell you whether the pain

experienced is the same as or different from their usual angina.

Angina

Angina pectoris , or angina , is the pain caused by myocardial ischemia and

the buildup of toxic products of respiration in the muscle. This is usually

due to coronary artery disease but can also be caused by other cardiac

diseases, such as aortic stenosis or hypertrophic cardiomyopathy.

Angina comes from the Latin for “choking,” and this is often what the

patient describes. As the brain cannot interpret pain from the heart per

se, it is felt over the central part of the anterior chest and can radiate up

to the jaw or shoulder, or down the arms or even to the umbilicus. This

pattern is due to the common embryological origins of the heart and these

parts of the body. Indeed, some patients may experience angina pain only

in the arm, for example.

The “pain” of angina is usually an unfamiliar sensation; consequently,

patients may be more comfortable with the term discomfort .

In true angina, you can expect the following features:

• Retrosternal

• Descriptions such as “crushing,” “heaviness,” or “like a tight band”

• Worse with physical or emotional exertion, with cold weather, and

after eating

• Relieved by rest and nitrate spray, pill, or paste (within a couple of

minutes)

• Not affected by respiration or movement

• Sometimes associated with breathlessness

In addition, patients classically clench their right ﬁ

st and hold it to their

chest when describing the pain.

In patients with known angina, a change in the nature of the symptom

is important. Ask them how much exercise they can do before feeling the

discomfort and whether this has changed.

CHEST PAIN

149

Myocardial infarction (MI)

Patients will know this as a “heart attack.” The pain is similar to that

of angina but much more severe, persistent (despite nitroglycerin), and

associated with nausea, sweating, and vomiting. Patients may also describe

a feeling of impending doom or death—angor animi.

Pericarditis

The most common causes are viral or bacterial infection, MI, or uremia.

• Constant retrosternal soreness

• Worse on inspiration (pleuritic pain)

• Relieved slightly by sitting forward

• Not related to movement or exertion

Esophageal spasm

This is often mistaken for MI or angina.

• A severe, retrosternal burning pain

• Onset often after eating or drinking

• May be associated with dysphagia

• May have a history of dyspepsia

• May be relieved by nitroglycerin, as this is a smooth muscle relaxant (hence

the confusion with angina). But nitroglycerin will take up to 20 minutes to

relieve this pain, whereas angina is relieved within a few minutes.

Gastroesophageal reﬂ ux disease (“heartburn”)

• Retrosternal, burning pain

• Relieved by antacids, onset after eating

Dissecting aortic aneurysm

This must be differentiated from MI as thrombolysis here may prove fatal.

• Severe, “tearing” pain

• Felt posteriorly—classically between the shoulder blades

• Persistent, most severe at onset

• Patient is usually hypertensive and marfanoid (see b p. 68)

Pleuritic (respiratory) pain

This is covered in more detail in b Chapter 8. It may be caused by a wide

range of respiratory conditions, particularly pulmonary embolus (PE) and

pneumothorax.

• Sharp pain, worse on inspiration and coughing

• Not central—may be localized to one side of the chest

• No radiation

• No relief with nitroglycerin

• Associated with breathlessness, cyanosis, etc.

Musculoskeletal pain

This pain may be caused by injury, fracture, or chondritis, among other

etiologies. It is localized to a particular spot on the chest and worsens with

movement and respiration. The area may be tender to palpation.

Tietze’s syndrome is costochondritis (inﬂ ammation of the costal carti-

lages) at ribs 2, 3, and 4. It is associated with tender swelling over the

costosternal joints.

CHAPTER 7 Cardiovascular system150

Breathlessness and edema

Breathlessness and edema are presented together here, as usually they are

linked pathophysiologically in the cardiovascular patient.

Excess tissue ﬂ uid caused by a failing heart will settle wherever gravity

pulls it. In someone who is on their feet, it will settle in their ankles, caus-

ing swelling. If the patient is sitting in bed, the swelling will occur about

their sacrum, and if the patient is lying down, ﬂ uid will collect in their lungs

(pulmonary edema), causing breathlessness.

Dyspnea (breathlessness)

Dyspnea is an abnormal awareness of one’s breathing and is described in

detail in Chapter 8. Certain aspects of breathlessness should be asked of

the cardiovascular patient in particular.

As with everything in clinical medicine, you must quantify the symptom,

if you are able, in order to gauge its severity and as a baseline so that the

effects of treatment or disease progression can be monitored. The New

York Heart Association (NYHA) has devised a classiﬁ cation of breath-

lessness, shown in Box 7.1 . In practice, it makes sense to measure the

functional abilities of the patient. For example:

• How far can the patient walk on a level surface before they have to

stop (“march tolerance”)?

• What about stairs and hills—can they make it up a ﬂ ight?

• Are they sure that they stop because of breathlessness or is it some

other reason (arthritic knees, for example)?

• Has the patient had to curtail their normal activities in any way?

Orthopnea

This is shortness of breath when lying ﬂ

at. Patients will not usually volun-

teer this as a symptom, so ask them about the following:

• How many pillows does the patient sleep with and has this changed?

•

Some patients may describe having to sleep sitting upright in a chair.

• If the patient sleeps with a number of pillows, ask why. Are they

breathless when they lie down or is it for some other reason?

Paroxysmal nocturnal dyspnea (PND)

As the name suggests, PND constitutes episodes of breathlessness occur-

ring at night—usually thought to be due to pulmonary edema. Again,

patients won’t usually volunteer this information and will often react with

Box 7.1 Framework for the cardiovascular examination

• I-none at rest, some on vigorous exercise

• II-none at rest, breathless on moderate exertion

• III-mild breathlessness at rest, worse on mild exertion

• IV-signiﬁ

cant breathlessness at rest and worse on even slight

exertion (the patient is often bed-bound)

Source: The Criteria Committee of the New York Heart Association (1994). Nomenclature and

Criteria for Diagnosis of Diseases of the Heart and Great Vessels . 9th ed. Boston: Little, Brown &

Co., pp. 253-256.

BREATHLESSNESS AND EDEMA

151

surprised pleasure when you ask them about it. Sufferers will experience

waking in the night spluttering and coughing—they ﬁ nd they have to sit up

or stand and many go to the window for “fresh air” in an attempt to regain

their normal breathing.

• Do they wake up in the night coughing and trying to catch their

breath?

• If so, describe in as much detail as you can, including how often and

how badly the symptom is disturbing the patient’s sleep cycle.

Cough

Pulmonary edema may cause a cough productive of frothy white sputum.

This may be ﬂ ecked with blood (pink) due to ruptured bronchial vessels.

Ankle edema

As already mentioned, in ambulatory patients, ﬂ uid will collect at the

ankles and cause swelling. It is often surprising just how severe the swell-

ing can get before people seek medical attention. Ask the following:

• How long has this been going on for?

• Is it worse at any particular time of day? (Typically, cardiac edema is

worse toward evening and resolved somewhat overnight as the ﬂ uid

redistributes itself.)

• Exactly how extensive is the swelling? Is it conﬁ

ned to the feet and

ankles, or does it extend to the shin, knee, thigh, or even the buttocks,

genitalia, and anterior abdominal wall?

• Is there any evidence of abdominal swelling and ascites? (b p. 239)

CHAPTER 7 Cardiovascular system152

Palpitations

To have palpitations is to have an awareness of one’s own heartbeat. This

is one of the many situations in which the patient may have a very differ-

ent idea of the word’s meaning than yours. You should spend some time

understanding exactly what they mean. Patients may be unfamiliar with the

term altogether and instead describe the heart as “jumping,” “skipping,” or

“missing a beat.” Attempt to determine the following:

• When did the sensation start and stop?

• How long did it last?

• Did it come on suddenly or gradually?

• Did the patient lose consciousness? If so, for how long?

• Was the heartbeat felt as fast, slow, or some other pattern?

• Was it regular or irregular?

•

it is useful at this stage to ask the patient to tap out on their knee or

a nearby table what they felt.

• What was the patient doing when the palpitations started?

• Is there any relationship to eating or drinking (particularly tea, coffee,

wine, chocolate)?

• Could it have been precipitated or terminated by any medication?

• Has this ever happened before? If so, what were the circumstances?

• Are there any associated symptoms? (chest pain, shortness of breath,

syncope, nausea, dizziness)

• Did the patient have to stop their activities or lie down?

• Was the patient able to stop the palpitations somehow? (Often,

people discover they can terminate their palpitations with a vagal

maneuver, such as a Valsalva maneuver, a cough, or swallow.)

Syncope

This is a faint or a blackout. You must determine whether there truly was a

loss of consciousness and not simply the feeling that the patient was about

to faint (presyncope). In particular, can the patient remember hitting the

ﬂ oor? If there really was a loss of consciousness, attempt to gain a collateral

history from witnesses. Ask about the following:

• Was the onset gradual or sudden?

• How long was the loss of consciousness?

• What was the patient doing at the time? (standing, urinating, coughing)

• Were there any preceding or associated symptoms such as chest pain,

palpitations, nausea, or sweating? (see Chest Pains, b p. 148, and

Palpitations, b p. 152, this chapter)

• Was there any relationship to the use of medication?

(Antihypertensives and use of nitroglycerin spray are common

culprits.)

• When the patient came to, were there any other symptoms remaining?

• Was there any tongue-biting or urinary or fecal incontinence?

• Was there any motor activity during the unconscious episode?

• How long did it take for the patient to feel “back to normal”?

OTHER CARDIOVASCULAR SYMPTOMS

153

Other cardiovascular symptoms

Claudication

This comes from the Latin “claudicatio” meaning “to limp.” These days,

however, it is used to describe muscle pain that occurs during exercise as

a sign of peripheral ischemia.

In true claudication, the patient describes the pain thus:

• Feels like a tight cramp in the muscle

• Usually occurs in the calf, thigh, buttock, and foot

• Appears only with exercise

• Disappears at rest

• May also be associated with numbness or pins-and-needles sensation

on the skin of the foot (blood is diverted from the skin to the ischemic

muscle).

As always, you should attempt to quantify wherever possible. In this case,

determine the “claudication distance”—that is, how far the patient is able

to walk before the pain starts. This will be useful in judging the severity

of the disability and in monitoring the condition.

Rest pain

This pain, similar to claudication, comes on at rest and is usually continu-

ous, a sign of severe ischemia. The patient may describe the following:

• Continuous, severe pain in the calf, thigh, buttock, or foot

• Aching in nature

• Lasts through the day and night

• Exacerbations of the pain may wake the patient from sleep.

• The patient may ﬁ

nd slight relief by hanging the affected leg off the

side of the bed.

Fatigue

Fatigue is a difﬁ cult symptom to determine, as you will ﬁ nd that most peo-

ple claim to be more tired than normal if asked. However, this pathological

fatigue is caused by d cardiac output and d blood supply to muscles and

needs to be taken seriously. Again, quantify and determine the following:

• Is the patient able to do less than they were previously?

• Is any d in activity due to fatigue or some other symptom

(e.g., breathlessness)?

• What activities has the patient had to give up because of fatigue?

• What are they able to do before they become too tired?

CHAPTER 7 Cardiovascular system154

The rest of the history

Cardiac risk factors

These are important aspects of the history that have an impact on the risk

of cardiovascular disease. When documenting a history of a cardiovascular

case, it is worth pulling these factors out of the usual order and document-

ing them, with details where appropriate, at the end of the presenting

complaint (as below). They should not then be repeated again later in the

write-up.

• Age: i risk with age

• Gender: risk in males > females

• Obesity: How heavy is the patient? (Calculate their BMI—see b p. 56.)

• Smoking: See b p. 38 for further advice. Quantify in pack-years. Don’t

be fooled by the “ex-smoker” that gave up yesterday!

• Hypertension: Find out when it was diagnosed. How was it treated? Is

it being monitored?

• Hypercholesterolemia: Increasingly, patients will know about this;

some will even know their latest blood test results. When was it

diagnosed? How is it being treated and monitored?

• Diabetes: what type? When was it diagnosed? How is it being treated

and monitored? What are the usual glucose readings?

• FH: particularly ﬁ

rst-degree relatives who have had cardiovascular

events or diagnoses before the age of 60

Past medical history

Ask especially about the following:

• Angina—if the patient has nitroglycerin, ask how often they need to

use it and whether this use has changed signiﬁ cantly

recently.

• MI—when? How was it treated?

• Ischemic heart disease—how was the diagnosis made? Any

angiograms? Any stent placements? What other investigations has the

patient had?

• Cardiac surgery—bypass? How many arteries?

• Atrial ﬁ

brillation (AF) or other rhythm disturbance—what treatment?

On warfarin?

• Rheumatic fever

• Endocarditis

• Thyroid disease

Drug history

Take particular note of cardiac medications and attempt to assess com-

pliance and the patient’s understanding of what the medication does.

Remember, some recreational drug use can be a major cardiac stressor.

Social history

As in any other case, take note of the patient’s employment—both how

the disease has affected their ability to work and how any cardiac diagnosis

may affect the patient’s employability.

Also record the home arrangements—whether there are any caregivers

present, aids or adaptations, stairs, and so on.

GENERAL INSPECTION AND HANDS

155

General inspection and hands

The full examination framework is shown in Box 7.2 . While the order need

not be strictly adhered to, the authors feel that this is the easiest routine,

working from the hands and face to more intimate areas of the body.

Positioning

The patient should be seated, leaning back to 45*, supported by pillows,

with their chest, arms, and ankles (if appropriate) exposed. Their head

should be well supported, allowing relaxation of the muscles in the neck.

Ensure that the room is warm and that there is enough privacy. In an

exam condition, the patient should be undressed to their underwear with

appropriate drapes and gown.

If you intend to measure that patient’s blood pressure seated and stand-

ing (remember to have the patient stand for 3 minutes before measuring),

it may be wise to do this at the beginning of the examination.

General inspection

As always, take a step back and take an objective look at the patient.

• Do they look ill? If so, in which way?

• Are they short of breath at rest?

Box 7.2 Framework for the cardiovascular examination

Following is an example framework for a thorough examination of the

cardiovascular system—the information in this chapter is presented in a

slightly different order for the purpose of clarity.

This is the authors’ recommendation. Other methods exist and none

are right or wrong, so long as nothing is missed.

• General inspection

• Hands

• Radial pulse

• Brachial pulse

• Blood pressure

• Face

• Eyes

• Tongue

• Carotid pulse

• Jugular venous pressure and pulse waveform

• Inspection of the precordium

• Palpation of the precordium

• Auscultation of the precordium

• Auscultation of the neck

• Dynamic maneuvers (if appropriate)

• Lung bases

• Abdomen

• Peripheral pulses (lower limbs)

• Edema assessment

• Peripheral veins

CHAPTER 7 Cardiovascular system156

• Is there any cyanosis (see b p. 191)?

• What is their nutritional state?

•

Are they overweight?

•

Are they cachectic (underweight with muscle wasting)?

• Do they have features of any genetic syndrome such as Turner, Down,

or Marfan?

Hands

Take the patient’s right hand in yours as if to greet them, look at it care-

fully, and compare with the other side. Look especially for the following:

• Temperature (may be cold in congestive cardiac failure)

• Sweat

• State of the nails

•

Blue discoloration if peripheral blood ﬂ ow is poor

•

Splinter hemorrhages (small, streak-like bleeding in the nail bed)

seen especially in bacterial endocarditis, but may also be a sign of

rheumatoid arthritis, vasculitis, trauma, or sepsis from any source

• Finger clubbing (see b p. 191). Cardiac causes include infective

endocarditis and cyanotic congenital heart disease.

• Xanthomata—raised yellow lesions caused by a buildup of lipids

beneath the skin. This is often seen on tendons at the wrist.

• Osler’s nodes—rare manifestation of infective endocarditis (a late sign,

and the disease is usually treated before this develops). There are red,

tender nodules on the ﬁ

nger pulps or thenar eminence.

• Janeway lesions—nontender macular–papular erythematous lesions

seen on palm or ﬁ

nger pulps as a rare feature of bacterial endocarditis

PERIPHERAL PULSES

157

Peripheral pulses

All of the major pulses are described below but should be examined in the

order described on the previous page. For each, you should attempt to

detect the rate and rhythm of the pulsation. For the brachial and carotid

pulsations in particular, you should also determine the volume and charac-

ter (waveform) of the pulse.

Technique

Examination technique is described below and illustrated in Fig. 7.1 .

It is good practice not to use your thumb to feel pulses, as you may mis-

take your own pulse (which can be felt weakly in the thumb) for the weak

pulse of the patient, especially in the peripheral arteries.

Radial artery

Feeling for the waveform is not useful here as it is too far from the heart.

Use the ﬁ rst and second ﬁ ngers to feel just lateral to the tendon of the

ﬂ exor carpi radialis and medial to the radial styloid process at the wrist.

Brachial artery

Feel at the medial side of the antecubital fossa, just medial to the tende-

nous insertion of the biceps.

Carotid artery

This is the best place to assess the pulse volume and waveform.

Find the larynx, move a couple of centimeters laterally, and press back-

ward medial to the sternomastoid muscle.

0 Be sure not to compress both carotids at once, for fear of diminishing

blood ﬂ

ow to the brain, particularly in the frail and elderly.

Femoral artery

This is another useful place for assessing the waveform unless there is

disease or abnormality in the abdominal aorta.

The patient is usually stripped to their underwear by this point in the

examination and should be lying on a bed or exam table with their legs

outstretched. Ask them to lower their clothes a little more, exposing the

groin area. The femoral pulsation can be felt midway between the pubic

tubercle and the anterior superior iliac spine.

Popliteal artery

This lies deep in the popliteal fossa and is surrounded by strong tendons. It

can be difﬁ cult to feel and usually requires more pressure than you expect.

There are several techniques but we recommend the following:

With the patient lying ﬂ at and knees slightly ﬂ exed, press into the center

of the popliteal fossa with tips of the ﬁ ngers of the left hand and use the

ﬁ ngers of the right hand to add extra pressure to these.

Posterior tibial artery

Palpate at the ankle just posterior and inferior to the medial malleolus.

Dorsalis pedis

This runs lateral to the exterior hallucis longus tendon on the superior sur-

face of the foot between the bases of the ﬁ rst and second metatarsals.

CHAPTER 7 Cardiovascular system158

Pulse rate

This should be expressed in beats per minute (bpm). A rate <60 bpm is

called bradycardia whereas tachycardia is a pulse >100 bpm. A normal

healthy adult pulse rate should be 760–100 bpm.

(a) (b)

(c) (d)

(e)

(g)

(f)

Fig. 7.1 Palpation of the peripheral pulses. a) The radial pulse. b) The brachial

pulse. c) The carotid pulse. d) The femoral pulse. e) The popliteal pulse. f) The

posterior tibial pulse. g) The dorsalis pedis pulse.

PERIPHERAL PULSES

159

The most accurate method is to count the pulse for a full minute. In prac-

tice, count for a portion of this time and calculate the rate by multiplication.

Commonly, people count for 15 seconds and multiply the number by 4.

Rhythm

You should feel the pulse for as long as it takes to be sure of the rhythm. In

general, the pulse can be either regular or irregular but variations exist.

• Regular: a self-explanatory deﬁ nition. Remember that the pulse rate

may

d with inspiration and i with expiration in the normal state.

• Irregularly irregular: a completely random pattern of pulsation

synonymous with AF. The atria twitch and contract in an irregular

fashion, sending electrical impulses to the ventricles (and, therefore,

causing contraction and arterial pulsation) at random intervals.

• Regularly irregular: not quite the contradiction that it seems—a

nonregular pulse can occur in some other regular pattern. For

example, pulsus bigeminus will cause regular ectopic beats, resulting in

alternating brief gaps and long gaps between pulses. In Wenckebach’s

phenomenon, you may feel increasing time between each pulse until

one is “missed,” and then the cycle repeats.

• Regular with ectopics: a very difﬁ

cult thing to feel and be sure of

without an ECG. A normal regular heart rate may be intermittently

interrupted by a beat that is out of step, making the pulse feel almost

irregularly irregular.

Character/waveform and volume

This is best assessed at the carotid artery. Feel for the speed at which the

artery expands and collapses and for the force with which it does so. This

takes some practice to master, and it may be useful to imagine a graph

such as those shown in Fig. 7.2 . Some examples follow:

• Aortic stenosis: a “slow rising” pulse, perhaps with a palpable shudder.

This is sometimes called anacrotic or a plateau phase.

• Aortic regurgitation: a “collapsing” pulse that feels as though it

suddenly hits your ﬁ

ngers and falls away just as quickly. Try feeling at

the brachial artery and raising the arm above the patient’s heart. This is

sometimes referred to as a waterhammer

pulse.

• Pulsus bisferiens: a waveform with two peaks, found where aortic

stenosis and regurgitation coexist

• Hypertrophic cardiomyopathy: this pulse may feel normal at ﬁ rst

but

recedes quickly. It is often described as “jerky.”

• Pulsus alternans: an alternating strong and weak pulsation,

synonymous with a severely impaired left ventricle in a failing heart

• Pulsus paradoxus: pulse is weaker during inspiration (causes include

cardiac tamponade, status asthmaticus, and constrictive pericarditis)

Other tests of arterial pulsation

These are not routinely performed unless the history and the rest of the

examination have made the examiner suspicious of the speciﬁ c patholo-

gies that they represent.

CHAPTER 7 Cardiovascular system160

Radioradial delay

Feel both radial pulses simultaneously. In the normal state, the pulses will

occur together. Any delay in the pulsation reaching the radial artery on

one side may point to pathology, such as an aneurysm at the aortic arch

or subclavian artery stenosis.

Radiofemoral delay

Palpate the radial and femoral pulses on the same side simultaneously.

They should occur together. Any delay in the pulsation reaching the femo-

ral artery may point to aortic pathology, such as coarctation.

Normal

Slow rising e.g., aortic stenosis

e.g., aortic stenosis

mixed with

aortic regurgitation

e.g., aortic regurgitation

e.g., occluded artery, death

Bisferiens

Collapsing

None

Fig. 7.2 Graphical representation of different arterial pulse waveforms and their

causes.

THE FACE AND NECK

161

The face and neck

Face

Examine the patient’s face at rest. It’s a good idea to develop your own

pattern for this. The authors recommend starting with an overview, mov-

ing to the eyes, mouth, then neck. The order is not important as long as

all aspects are examined. Be sure to ask the patient to:

• Look up while you gently pull down one lower eyelid, exposing the

conjunctiva.

• Open wide. Look inside their mouth.

• Stick out their tongue.

In the cardiovascular examination, look especially for the following:

• Jaundice: seen as a yellow discoloration of the sclera

• Anemia: seen as an unusually pale conjunctiva (experience is needed here)

• Xanthelasma: yellow, raised lesions found particularly around the

eyes, indicative of high serum cholesterol

• Corneal arcus: a yellow ring seen overlying the iris. This is signiﬁ cant

in

patients <40 years but not in older persons.

• Mitral facies: rosy cheeks suggestive of mitral stenosis

• Cyanosis: seen as a bluish discoloration of the lips and tongue

• High arched palate: suggestive of diseases such as Marfan syndrome

• Dental hygiene: periodontal disease is a common source of organisms

causing endocarditis.

Carotid pulse

At this point, the carotid pulse should be examined (b p. 157).

Jugular venous pressure

Theory

The jugular veins connect to the superior vena cava (SVC) and the right

atrium without any intervening valves. Therefore, changes in pressure in

the right atrium will transmit a pressure wave up these veins that can be

seen in the neck. By measuring the height of the impulse, the pressure in

the right side of the circulation can be expressed in centimeters.

Examination

It is often said that the JVP must only be measured in the internal jugular

vein (IJV). This is not strictly the case. The external jugular vein (EJV) is

easily seen as it makes a winding course down the neck (see Fig. 7.3 ). Its

tortuous course means that impulses are not transmitted as readily or as

reliably. It is for this reason that the IJV is used.

The center of the right atrium lies 75 cm below the sternal angle, which

is used as the reference point.

The normal JVP is 78 cm of blood (therefore 3 cm above the sternal

angle). With the patient tilted back to 45*, the upper border of the pulse is

just hidden at the base of the neck. This, therefore, is used as the standard

position for JVP measurement.

2 Remember, it is the vertical distance from the sternal angle to the

upper border of the pulsation that must be measured.

CHAPTER 7 Cardiovascular system162

2 You must add 5 cm to the ﬁ gure to give the true JVP (see Fig. 7.4 ).

• With the patient lying back at 45*, expose the neck.

• Ask the patient to turn their head away from you (their left) and

ensure that the neck muscles are relaxed.

• Look for the JVP and measure the vertical distance from the top of the

pulsation to the sternal angle.

0 The result is often expressed along the lines of “3 cm above the

sternal angle.” Remember that that is a total JVP of 8 cm after adding the

extra 5 cm that are not measured.

• Try to look upward, along the line of the sternomastoid. Don’t get too

close, and use oblique lighting to make the pulsation more obvious.

2 It can sometimes be difﬁ

cult to distinguish the JVP from the carotid

pulse—see next section and

Table 7.1 for some advice.

External carotid

artery

Common carotid

artery

Point of access to

the IVJ between the

heads of the

sternomastoid

Internal

jugular vein

Sternomastoid

Fig. 7.3 The surface anatomy of the vasculature in the neck. Note that the IJV is

partly hidden by the sternocleidomastoid at the base of the neck.

45º

Max venous pulse

JVP

Sternal angle

Fig. 7.4 Measuring the JVP. Measure the vertical distance from the top of the

pulsation to the sternal angle and then add 5 cm to get the JVP.

THE FACE AND NECK

163

Differentiating jugular and carotid pulsations

The rules for differentiating the jugular and carotid pulsations ( Table 7.1 )

are guides only and not always true. For example, in severe tricuspid

regurgitation, the jugular pulse is palpable and is not easily abolished by

compression. If proving difﬁ cult, test the hepatojugular reﬂ ex.

Hepatojugular reﬂ ux

• Watch the neck pulsation.

• Exert pressure over the liver with the ﬂ

at of your right hand.

The JVP should rise by approximately 2 cm; the carotid pulse will not.

Character of jugular venous pulsation

This is rather difﬁ cult to detect without experience (see Box 7.3 ). The

jugular pulsation has two main peaks (see Fig. 7.5 ). Establish the timing of

the peaks in the cardiac cycle by palpating the carotid pulse at the same

time. The key features are as follows:

• a wave: caused by atrial contraction; seen just before the carotid pulse

• c point: slight AV-ring bulge during ventricular contraction

• x descent: atrial relaxation

• v wave: tricuspid closure and atrial ﬁ lling

• y descent: ventricular ﬁ

lling as tricuspid valve opens

Table 7.1 Characteristics of normal jugular and carotid pulsations

Jugular pulsation Carotid pulsation

2 peaks (in sinus rhythm) 1 peak

Impalpable Palpable

Obliterated by pressure Hard to obliterate

Moves with respiration Little movement with respiration

Box 7.3 A word about honesty in learning

Students often ﬁ nd the JVP hard to see while they are learning the vari-

ous examination techniques. This reminds the authors of an important

point.

In medicine, there is an almost overwhelming pressure to say “yes”

when asked, “Can you see that?” by the teacher. One may be moti-

vated by a fear of appearing stupid, taking too much of the teacher’s

time, or delaying the ward rounds further. If the real answer is “no,”

however, succumbing to this fear is useful to no one. The student fails

to learn the correct technique or the correct identiﬁ cation of the sign,

and the teacher fails to discover that their demonstration is inadequate.

Misconceptions are born and passed on from person to person.

The authors thus urge students of medicine of all ages and at all stages

to say “no, please show me again” when this is needed, and we will all

be better for it.

CHAPTER 7 Cardiovascular system164

Findings

• Raised JVP: right ventricular failure, tricuspid stenosis, tricuspid

regurgitation, SVC obstruction, pulmonary embolus, ﬂ uid overload

• Large a waves: caused usually by a hypertrophied right atrium

(pulmonary hypertension, pulmonary stenosis, tricuspid stenosis)

• Absent a wave: atrial ﬁ brillation

• “Cannon” a waves: large, irregular waves caused by contraction of the

atrium against a closed tricuspid valve; seen in complete heart block

• Large v waves: regurgitation of blood though an incompetent tricuspid

valve

• Sharp y descent: characteristic of constrictive pericarditis

• Sharp x descent: characteristic of cardiac tamponade

Kussmaul’s sign

The JVP will d during inspiration in the normal state. The JVP will rise dur-

ing inspiration (Kussmaul’s sign) in the presence of pericardial constriction,

right ventricular infarction, or, rarely, cardiac tamponade.

aa

v

c

x

y

Fig. 7.5 Representation of the normal jugular venous pulsation.

EXAMINING THE PRECORDIUM

165

Examining the precordium

The precordium refers to that part of the chest overlying the heart.

Inspection and palpation are discussed below. Auscultation is discussed in

the next section (b p. 193).

Inspection

The patient should be lying at 45* with the chest exposed. Look for the

following:

• Scars—sternal split is used to access the median structures and to

perform coronary artery bypass graft (CABG) surgery. A left lateral

thoracotomy may be evidence of previous closed mitral valvotomy,

resection of coarctation, or ligation of a patent ductus arteriosus.

• Any abnormal chest shape or movements (b p. 167)

• Pacemaker or implantable deﬁ

brillator—usually implanted over the left

pectoral region

• Any visible pulsations

Palpation

0 Before starting the exam, explain what you are going to do and how you

will do it, particularly to female patients. If possible, warm your hands.

General palpation

Place the ﬂ

at of your right hand on the chest wall—to the left, then to the

right of the sternum. Can you feel any pulsations?

• Heave —this is a sustained, thrusting pulsation usually felt at the left

sternal edge indicating right ventricular enlargement.

• Thrill —this is a palpable murmur felt as a shudder beneath your hand.

It is caused by severe valvular disease (if systolic: aortic stenosis,

ventricular septal defect, or mitral regurgitation; diastolic: mitral

stenosis)

Palpating the apex beat

This is the lowermost lateral point at which a deﬁ nite pulsation can be felt.

It is usually at the ﬁ

fth intercostal space in the mid-clavicular line (Fig. 7.6).

Findings

• Abnormal position of the apex beat: usually more lateral than expected.

This is caused by an enlarged heart or disease of the chest wall. With

chronic lung disease, the apex may be more midline.

• No apex beat felt: usually caused by heavy padding with fat or internal

padding with an overinﬂ

ated emphysematous lung. It can sometimes

be felt by asking the patient to lean forward or laterally.

Character of the apex beat

This can only be learned with experience, after having felt many normal

impulses. Some common abnormalities are as follows:

• Stronger, more forceful: hyperdynamic circulation (e.g., sepsis, anemia)

• Sustained: impulse longer than expected (left ventricular hypertrophy,

aortic stenosis, hypertrophic cardiomyopathy or hyperkinesia)

• Double impulse: (palpable atrial systole) characteristic of hyptertrophic

cardiomyopathy

CHAPTER 7 Cardiovascular system166

• Tapping: the description given to a palpable ﬁ rst heart sound in severe

mitral stenosis

• Diffuse: a poorly localized beat caused by left ventricular aneurysm

• Unpalpable: emphysema, obesity, pericardial effusion, or death

0 Beware of dextrocardia. If no beat is felt, check the right side.

Percussion

This is not useful and usually not included in the cardiovascular exam.

Right ventricle

Right atrium

Left ventricle

Ventricular

septum

Apex

Fig. 7.6 Surface anatomy of the heart and most common location of the apex

beat.

AUSCULTATING THE PRECORDIUM

167

Auscultating the precordium

Technique

The bell of the stethoscope is used to detect lower-pitched sounds; the

diaphragm, for higher-pitched sounds.

Auscultate at each of the four standard areas (Box 7.4; see Fig. 7.7).

0 These areas do not relate exactly to the anatomical position of the

valves but are areas at which the sound of each valve can be best heard.

Different methods exist for this examination. A sensible approach

would be to listen with the diaphragm at each area and then repeat, using

the bell. You can then go back and concentrate on any abnormalities. You

can then examine other areas looking for the features of certain murmurs

and extra sounds as described on the following pages.

Practice is needed here; many hearts should be listened to in order

to be familiar with the normal sounds. The physiology behind the heart

sounds and physiological splitting were described on b p. 146 and may be

worth revisiting at this point.

If you are unsure which is the ﬁ

rst and second heart sound—or where a

murmur is occurring—you can palpate one carotid pulse while listening to the

heart, enabling you to “feel” systole. The carotid pulsation occurs with S

1

.

Box 7.4 The four areas for auscultation

• Mitral : ﬁ fth intercostal space in the mid-axillary line (the apex)

• Tricuspid : ﬁ

fth intercostal space at the left sternal edge

• Pulmonary : second intercostal space at the left sternal edge

• Aortic : second intercostal space at the right sternal edge

A = Aortic

P = Pulmonary

T = Tricuspid

M = Mitral

P

A

T

M

Fig. 7.7 The four standard areas for auscultation of the precordium and the valves

that are best heard at each area.

CHAPTER 7 Cardiovascular system168

0 Remember to palpate only one carotid pulse at a time.

Findings—the heart sounds

First heart sound (S

1

)

Mitral valve closure is the main component of S

1

, and the volume depends

on the force with which it closes.

• Loud: forceful closing (mitral stenosis, tricuspid stenosis, tachycardia)

• Soft: prolonged ventricular ﬁ

lling or delayed systole (left bundle branch

block [LBBB], aortic stenosis, aortic regurgitation)

• Variable: variable ventricular ﬁ

lling (AF, complete heart block)

Second heart sound (S

2

)

• Soft: d mobility of aortic valve (aortic stenosis) or if leaﬂ ets fail to

close properly (aortic regurgitation)

• Loud: aortic component loud in hypertension or congenital aortic

stenosis (here the valve is narrowed but mobile). Pulmonary

component loud in pulmonary hypertension

Splitting of S

2

See also Applied anatomy and Physiology, this chapter (b p. 146).

• Exaggerated normal splitting: caused by a delay in right ventricular

emptying (right bundle branch block [RBBB], pulmonary stenosis,

ventricular septal defect, or mitral regurgitation)

• Fixed splitting: no difference in the extent of splitting between

inspiration and expiration. Usually due to atrial septal defect

• Reversed splitting: i.e., the pulmonary component of S

2

comes before

the aortic component. Caused by a delay in left ventricular emptying

(LBBB, aortic stenosis, aortic coarctation)

Third heart sound

This is a low-frequency (can just be heard with the bell) sound occurring

just after S

2

. It is described as a “triple” or “gallop” rhythm: da-da-dum or

ken-tuck-y . It occurs at the end of rapid ventricular ﬁ lling, early in diastole,

and is caused by a shortening of the papillary muscles or by ventricular

distension.

• Physiological: soft sound heard only at the apex, normal in children and

ﬁ

t adults up to age 30

• Pathological: indicates some impairment of left ventricular function or

rapid ventricular ﬁ

lling (dilated cardiomyopathy, aortic regurgitation,

mitral regurgitation, or constrictive pericarditis). May be associated

with a high-pitched pericardial knock

Fourth heart sound

This is a late diastolic sound (just before S

1

) caused by d compliance

or i stiffness of the ventricular myocardium. It sounds like da-lub dub or

Ten-nes-see . It coincides with abnormally forceful atrial contraction and

raised end diastolic pressure in the left ventricle.

• Never physiological

• Causes are hypertrophic cardiomyopathy and systemic hypertension.

AUSCULTATING THE PRECORDIUM

169

Findings—murmurs

These are “musical” humming sounds produced by the turbulent ﬂ ow of

blood. For each murmur heard, you should determine the following:

• Timing

• Site and radiation (where is it heard the loudest?)

• Loudness and pitch (see Box 7.5)

• Relationship to posture and respiration

The timing of the murmur is particularly essential in establishing the

sound’s origin. You must decide whether the noise occurs in systole or

diastole (feel the patient’s pulse at the carotid artery to be sure) and

then when, within that period, it occurs.

Systolic murmurs

Pansystolic

This is a murmur that lasts for the whole of systole and tends to be due

to backﬂ ow of blood from a ventricle to an atrium (tricuspid regurgita-

tion, mitral regurgitation). A ventricular septal defect will also cause a

pansystolic murmur.

Ejection systolic

These murmurs start quietly at the beginning of systole, quickly rise to

a crescendo, and then decrescendo, creating a whoosh sound. They are

caused by turbulent ﬂ ow of blood out of a ventricle (pulmonary stenosis,

aortic stenosis, hypertrophic cardiomyopathy). They are also found if ﬂ ow

is particularly fast (with fever, in healthy young adults).

Late systolic

There is an audible gap between S

1

and the start of the murmur, which

then continues until S

2

. Typically this is due to tricuspid or mitral regurgita-

tion through a prolapsing valve.

Diastolic murmurs

• Early: usually due to backﬂ ow through incompetent aortic or

pulmonary valves. It starts loudly at S

2

and decrescendos during

Box 7.5 Grading volume of a murmur

The experienced examiner should be able to give the murmur a grade

according to its loudness:

• 1—very quiet (students may only hear it if they have already been

told that it is there)

• 2—quiet but can be heard with a stethoscope wielded by an

examiner with some experience

• 3—moderate; easily heard

• 4—loud, obvious murmur

• 5—very loud; heard over the whole of the precordium and may be

accompanied by a palpable thrill

• 6—heard without the aid of a stethoscope

CHAPTER 7 Cardiovascular system170

diastole. (You can produce a similar sound by whispering the letter R

out loud).

• Mid-diastolic: begin later in diastole and may be brief or continue up to

S

1

. They are usually due to ﬂ ow through a narrowed mitral or tricuspid

valve. They are lower pitched than early diastolic murmurs.

• Austin–Flint murmur: audible vibration of the mitral valve during

diastole as it is hit by ﬂ

ow of blood due to severe aortic regurgitation

• Graham–Steele murmur: pulmonary regurgitation secondary to

pulmonary artery dilatation caused by i pulmonary artery pressure in

mitral stenosis

Continuous murmurs

These are murmurs heard throughout both systole and diastole. Common

causes include a patent ductus arteriosus or an arteriovenous ﬁ stula.

Radiation

The murmur can sometimes be heard in areas where heart sounds are not

normally auscultated—the murmur will tend to radiate in the direction of

the blood ﬂ ow that is causing the sound (see b p. 171 for summary).

For example, murmur of aortic stenosis will radiate up to the carotids,

whereas a mitral regurgitation murmur may be heard in the left axilla.

Position

Some murmurs will become louder if you position the patient in such a

way that gravity aids the ﬂ ow of blood creating the sound.

• Aortic regurgitation is heard louder if you ask the patient to sit up and

lean forward; listen at the left sternal border.

• Mitral stenosis is louder if you ask the patient to lie on their left-hand

side (listen with the bell at the apex).

Dynamic maneuvers

The following may help in identifying the origin of a murmur.

• Respiration: Right-sided murmurs (e.g., pulmonary stenosis) tend to be

louder during inspiration and quieter during expiration (because of i

venous return—see b p. 169). Ask the patient to breathe deeply while

you listen. Left-sided murmurs are louder during expiration.

• Valsalva maneuver: This is forceful expiration against a closed glottis

(consider straining over the toilet bowl). Replicate by asking the

patient to blow into the end of a syringe, attempting to expel the

plunger. This will d cardiac output and cause most murmurs to

soften. Murmurs of hypertrophic obstructive cardiomyopathy, mitral

regurgitation, and mitral prolapse will get louder on release of Valsalva.

Findings—extra sounds

These are added sounds that are often associated with a speciﬁ c mur-

mur—see Table 7.2 (b p. 171).

AUSCULTATING THE PRECORDIUM

171

Table 7.2 Selection of cardiac abnormalities and expected clinical ﬁ ndings (see also b p. 175)

Abnormality Primary site of

murmur

Radiation Timing Added sounds* Graphical Representation

of the sounds

Aortic stenosis Aortic area and

apex

To carotid arteris Ejection systolytic Ejection click

(esp.bicuspid valve)

S

1

S

2

S

1

Aortic

regurgitation

Left sternal edge Toward apex Early diastolic (Austin-Flint murmur

b p. 170)

S

1

S

2

S

1

Mitral stenosis Apex Nil Mid-diastolic Opening snap

S

1

S

2

S

1

Mitral

regurgitation

Apex Toward left axilla

or base of left lung

Pansystolytic Mid-systolytic click

(if prolapsing)

S

1

S

2

S

1

Tricuspid

regurgitation

Lower left

sternal edge

Lower right sternal

edge, lung

Pansystolytic

S

1

S

2

S

1

Pulmonary

stenosis

Upper left

sternal edge

Left clavicular

region

Ejection systolytic

S

1

S

2

S

1

Ventricular

septal defect

Left sternal edge whole of the

precordium

Pansystolytic

S

1

S

2

S

1

*Note that added sounds, such as clicks and snaps, may only be present in certain patients and should not be expected when examining someone with a certain abnormality.

CHAPTER 7 Cardiovascular system172

Opening snap

The mitral valve normally opens immediately after S

2

. In mitral stenosis,

sudden opening of the stiffened valve can cause an audible high-pitched

snap. This may be followed by the murmur of mitral stenosis. If there is no

opening snap, the valve may be rigid.

This is best heard over the left sternal border with the diaphragm of

the stethoscope.

Ejection click

Similar to the opening snap of mitral stenosis, this is a high-pitched click

heard early in systole, caused by the opening of a stiffened semilunar valve

(aortic stenosis). It is associated with bicuspid aortic valves.

Ejection click is heard at the aortic or pulmonary areas and down the

left sternal border.

Mid-systolic click

Usually caused by mitral valve prolapse, this is the sound of the valve

leaﬂ et ﬂ icking backward (prolapsing) midway through ventricular systole.

It will be followed by the murmur of mitral regurgitation.

It is best heard at the mitral area.

Tumor plop

This is a very rare ﬁ nding due to atrial myxoma. If there is a pedunculated

tumor in the atrium, it may move and block the atrial outﬂ ow during atrial

systole, causing an audible sound.

Pericardial rub

This is a scratching sound comparable to creaking leather that is heard

with each heartbeat and caused by inﬂ amed pericardial membranes rub-

bing against each other in pericarditis. It is louder as the patient is sitting

up, leaning forward, and heard best in expiration.

Metallic valves

Patients who have had metallic valve replacement surgery will have an

obviously audible mechanical “click” corresponding to the closing of that

valve. These can often be heard without the aid of a stethoscope. Some

valves have both opening and closing clicks.

If a patient’s valve click is unusually soft, this may indicate dysfunction, e.g.,

thrombus or pannus.

All patients with prosthetic valves will have a ﬂ ow murmur when the

valve is open.

THE REST OF THE BODY

173

The rest of the body

The lung bases

Examination of the lungs should form part of a thorough cardiovascular

examination (b Chapter 8). Look especially for crackles or sign of effusion.

The abdomen

See also b Chapter 9. Look especially for the following:

• Hepatomegaly. Is the liver pulsatile (severe tricuspid regurgitation)?

• Splenomegaly

• Ascites

• Abdominal aortic aneurysm

• Renal bruits (renal artery stenosis)

• Enlarged kidneys

Peripheral edema

This is an abnormal i in tissue ﬂ uid resulting in swelling—its causes are

multiple but often due to heart failure. Edema is under gravitational con-

trol so will gather at the ankles if the patient is standing or walking, at the

sacrum if sitting, and in the lungs if lying (orthopnea, b p. 150).

• Make a note of any peripheral swelling, examining both the ankles and

the sacrum.

• Note if the edema is “pitting” (are you able to make an impression in it

with your ﬁ

nger?—best tested over the anterior of the tibia).

• Note how high the edema extends (ankles, leg, thighs, etc.).

• If the edema extends beyond the thighs, it is important to examine the

external genitalia, particularly in men, where the swelling may cause

outﬂ ow

obstruction.

Varicose veins

Inspection

Varicosities appear as visible, dilated, tortuous, subcutaneous veins caused

by the backﬂ ow of blood from the deep veins (usually a branch of the long

saphenous vein).

• The patient should be examined in a standing position with the legs

fully exposed.

• Note any stasis changes, such as surrounding edema, eczema, brown

pigmentation, or ulcers.

Palpation

• Gently feel the varicose veins—hard veins may contain thrombus.

• Ask the patient to cough. If there is a palpable pulsation in the

varicosity, there may be valvular incompetence at the long saphenous

vein in the groin.

Percussion

• Apply the ﬁ

ngers of one hand to the upper part of the varicose vein.

• Gently ﬂ ick the lower part of the vein with the other hand.

•

If there is a palpable wave sent up the vein, there are incompetent

valves between those two points.

CHAPTER 7 Cardiovascular system174

Trendelenburg test

• Ask the patient to lie down and raise their leg so as to drain the veins.

• Apply a tourniquet over the saphenous vein (upper half of thigh).

• Ask the patient to stand.

•

You can then determine the site of the incompetent perforating

vein. Do the varicose veins ﬁ ll above or below the tourniquet?

• Repeat the procedure until you are able to pinpoint the exact location

of the incompetence and, by applying localized pressure, prevent the

varicose veins from ﬁ

lling at all.

IMPORTANT PRESENTING PATTERNS

175

Important presenting patterns

Valvular disease (see also b p. 171)

Mitral stenosis

• Symptoms: dyspnea, cough productive of frothy (pink?) sputum,

palpitations (often associated with AF and resultant emboli)

• Signs: palmar erythema, malar ﬂ

ush, “tapping” apex beat, left

parasternal heave, loud S

1

, mid-diastolic murmur 9 opening snap

Mitral regurgitation

• Symptoms: acute dyspnea and pulmonary congestion

• Signs: collapsing pulse, sustained apex beat displaced to the left, left

parasternal heave, soft S

1

, loud S

2

(pulmonary component), pansystolic

murmur heard at the apex radiating to left axilla ± mid-systolic click,

third heart sound

Aortic stenosis

• Symptoms: angina, syncope, dyspnea, sudden death

• Signs: Slow rising pulse, low blood pressure, narrow pulse pressure,

sustained and powerful apex beat, ejection systolic murmur radiating

to carotids, soft S

2

, 9 ejection click

Aortic regurgitation

• Symptoms: similar to aortic stenosis

• Signs: collapsing pulse, wide pulse pressure, sustained and displaced

apex beat, soft S

2

, early diastolic murmur at the left sternal edge (often

described as “blowing” or decrescendo), 9 ejection systolic murmur

(i volume). You may also hear a “pistol shot” sound over the femoral

artery with severe aortic regurgitation. See also Box 7.6 .

Tricuspid stenosis

This usually occurs along with mitral or aortic valvular disease (e.g., in

rheumatic fever) and is often the less serious of the patient’s problems.

• Signs: auscultation similar to that of mitral stenosis, hepatomegaly,

pulsatile liver, and venous congestion

Box 7.6 Some eponymous signs of aortic regurgitation

• Prominent carotid pulsation (Corrigan’s sign)

• Head-nodding in time with the heartbeat (De Musset’s sign)*

• Pulsation of the uvula in time with the heartbeat (Mueller’s sign)

• Higher blood pressure in the legs than in the arms (Hill’s sign)

• Nailbed capillary pulsation (Quincke’s sign)

*

Abraham Lincoln probably had Marfan syndrome, given his tall stature and long arms. In addi-

tion, a study of old photographs shows that he had De Musset’s sign. During his lifetime cam-

eras had longer shutter speeds, and President Lincoln’s head-nodding caused his face to appear

blurred in photographs, compared with the people sitting around him.

CHAPTER 7 Cardiovascular system176

Tricuspid regurgitation

Signs include dilated neck veins, prominent v-wave in JVP that may, rarely,

cause the earlobe to oscillate, pansystolic murmur louder on inspiration

with a loud pulmonary component of S

2

, left parasternal heave, pulsatile

liver, peripheral and sacral edema, and ascites. You may also hear a third

heart sound and evidence of AF.

Pulmonary stenosis

Signs include normal pulse with an ejection systolic murmur radiating to

lung ﬁ elds often with a palpable thrill over the pulmonary area. Other

signs of right heart strain or failure can also occur.

Pulmonary regurgitation

This is usually a coincidental ﬁ nding.

• Signs: loud S

2

that may be palpable, early diastolic murmur heard at the

pulmonary area and high at the left sternal edge

Congenital heart disease

Ventricular septal defect (VSD)

• Symptoms: Children with VSD are often asymptomatic. If there is a

large defect, the patient may suffer congestive cardiac failure with

dyspnea and fatigue.

• Signs: There may be cyanosis and clubbing of ﬁ

ngers. Heart sounds

usually appear normal, but if pulmonary hypertension develops, you may

hear a loud pulmonary component of S

2

with a right-ventricular heave.

A pansystolic murmur may also be heard at the left sternal edge, often

accompanied by a palpable thrill. The signs may settle with time; the

right heart pressure increases, causing less shunting and a softer murmur.

Atrial septal defect (ASD)

ASD is the most common congenital lesion and is often an asymptomatic

ﬁ nding discovered on investigating a murmur.

• Symptoms of secondum defect: asymptomatic if small. Symptoms include

fatigue, dyspnea, palpitations (atrial arrythmias), recurrent pulmonary

infections, and other symptoms of right heart failure. This defect is also

associated with migraine and paradoxical emboli.

• Symptoms of primum defect: These include symptoms of heart

failure in childhood with failure to thrive, chest infections, and poor

development. In adults, there may be syncope (heart block) and

symptoms suggestive of endocarditis.

• Signs: ﬁ

xed splitting of S

2

, i ﬂ ow over the normal pulmonary valve may

give an ejection systolic murmur. There is also left parasternal heave

with a normal or diffuse apical impulse. Particularly in ostium primum

defects (endocardial cushion defects), you may hear the pansystolic

murmur of mitral regurgitation or coexisting VSD (or both). Look also

for signs of pulmonary hypertension.

Patent ductus arteriosus (PDA)

PDA is a persistent embryonic connection between the pulmonary artery

and the aorta. Blood ﬂ ows from the aorta into the pulmonary artery.

IMPORTANT PRESENTING PATTERNS

177

• Symptoms: often asymptomatic. Severe cases show dyspnea on

exertion.

• Signs: collapsing pulse, heaving apex beat, “machinery” (continuous)

murmur heard all over the precordium, S

2

not heard, systolic or

diastolic thrill in the second intercostal space on the left

Coarctation of the aorta

This is a congenital narrowing of the aorta at or beyond the arch.

• Symptoms: usually asymptomatic. Symptoms may include headache,

epistaxis, dizziness, and palpitations. Claudication, leg fatigue are

also features. The coarctation may cause the heart to strain and give

symptoms of congestive cardiac failure.

• Signs: i blood pressure in the upper limbs, radiofemoral delay, ejection

systolic murmur at the left sternal edge, sometimes palpable collateral

arteries over the scapulae with interscapular bruits. Patients may also

have underdeveloped lower limbs.

• Coarctation is often associated with aortic stenosis, aortic aneurysms,

and bicuspid aortic valves. It is also seen in Turner syndrome.

Tetralogy of Fallot

This consists of pulmonary stenosis, VSD (infundibular), right ventricular

hypertrophy, and an overriding aorta. (If associated with an ASD as well,

this is Fallot’s pentalogy.)

• Symptoms: syncope, squatting relieves breathlessness, growth

retardation

• Signs: ﬁ

nger clubbing and central cyanosis with superadded paroxysms

(“spells”). Murmurs of pulmonary stenosis or the VSD may be heard

along with a systolic thrill and left parasternal heave.

Pericarditis

Causes include collagen diseases, infections such as TB, postinfarction, and

idiopathic causes.

• Symptoms of acute pericarditis: constant retrosternal soreness, worse

on inspiration (pleuritic), relieved slightly by sitting forward, not

related to movement or exertion

• If chronic, constrictive, may cause Kussmaul’s sign, impalpable apex beat,

S

3

, hepatomegaly, splenomegaly, ascities (pseudo-cirrhosis)

Pericardial effusion

• Pulsus paradoxus, i JVP, impalpable apex beat, soft heart sounds,

hepatomegaly, ascites, peripheral edema

Ischemic heart disease

See bw p. 148.

Congestive heart failure (CHF)

In simple terms, this refers to the inability of the heart to maintain an

adequate cardiac output for perfusion of vital organs with variable severity.

It is usually described in terms of “left” and “right” heart failure, but there

is usually an element of both (biventricular).

CHAPTER 7 Cardiovascular system178

Left ventricular failure

• Symptoms may include shortness of breath on exertion, orthopnea,

paroxysmal nocturnal dyspnea, cough with pink frothy sputum, fatigue,

weight loss, muscle wasting, and anorexia.

• Signs: The patient may appear tired, pale, sweaty, and clammy, and have

tachycardic, thready pulse, low blood pressure, narrow pulse pressure,

displaced apex beat (murmur of an underlying valvular abnormality?), third

and fourth heart sounds, tachypnea, and crepitations at the lung bases.

Right ventricular failure

• Symptoms: as for LV failure, with peripheral edema and facial swelling

• Signs: many of those of LV failure. Also i JVP, hepatomegaly, ascites,

peripheral (sacral?) edema, pulsatile liver (if tricuspid regurgitation)

Hypertrophic cardiomyopathy

There may be a family history, although the vast majority of cases are

sporadic, caused by new mutations.

• Symptoms: often none. If they are present, the patient may suffer from

shortness of breath, angina, and syncope.

• Signs: sharp, rising (jerky) pulse, prominent JVP a-wave, double apex

beat, late systolic murmur at left sternal border that i with Valsalva

maneuver

Peripheral vascular disease

• Symptoms: claudication, as on b p. 153.

• Signs: (see also Box 7.7 ) shiny, pale, cold limb, hair loss, absent peripheral

pulse(s). If severe, ischemic ulceration and gangrene can occur.

Deep vein thrombosis (DVT)

DVT is often confused with cellulitis and a ruptured popliteal cyst.

• Symptoms: calf pain, swelling, and loss of use

• Signs: warm, tense, swollen limb, erythema, dilated superﬁ cial

veins,

cyanosis. There may be palpable thrombus in the deep veins. Often

there is pain on palpating the calf.

Box 7.7 The acutely ischemic limb

Use the rule of Ps. The acutely ischemic limb will be

• P ainful (at ﬁ

rst, then becoming)

• P ainless (numb)

• P ale

• P aralyzed

• P ulseless

THE ELDERLY PATIENT

179

The elderly patient

Geriatricians are equally interested in cardiovascular disease—with an

aging population, the prevalence of cardiac, peripheral vascular, and stroke

disease will rise. While age is one of many risk factors for vascular disease,

older people are one of the biggest groups to beneﬁ t from primary and

secondary risk factor reduction, so be comprehensive in all assessments.

A careful history is of far more use than an inaccurate one and a list of

physical ﬁ ndings.

History

Angina

Angina presents in a multitude of ways. Avoid labeling the symptoms as

pain (which can irritate many patients); instead, listen to their complaints:

“discomfort,” “twinges,” and “aches” are equally common presentations.

Many older people have few symptoms and may present with sweating or

breathlessness. Be astute and ask if these relate to exertion.

Orthopnea

Ask why patients sleep on extra pillows. Often this is due to other symp-

toms, such as arthritis. Do they sleep upright in a chair?

Breathlessness

This relates to a low-output state and not necessarily to pulmonary edema.

Fatigue is a common presenting symptom and should not be overlooked.

Drug history

There is always a difﬁ cult balance of compliance, managing symptoms,

achieving target doses, and avoiding side effects. Avoid rushing to optimize

doses and upsetting a careful regimen. Ask about B-blocker eye drops, as

they can be absorbed systemically and exert signiﬁ cant effects.

Lifestyle

Ask about smoking and seek opportunities to explore smoking cessa-

tion—it’s never too late! Ask about alcohol use, as this may have a bearing

on decisions around anticoagulation. Advice about healthy eating is often

welcome; healthy eating is more palatable than more tablets.

Functional history

As ever, this is a key part of all histories. Targeted interventions, such

as help with bathing to avoid overexertion (and symptoms), can have a

signiﬁ cant impact.

Examination

General

Look for clues—e.g., the breathless patient returning from the bathroom,

the nitroglycerin spray close at hand.

Ausculate and think

Think especially about valve lesions. It is important to assess how much

a valvular problem could be contributing to a patient’s symptoms and

arrange for investigations to conﬁ rm this. Aortic valve replacement and

CABG are often hugely successful in older people.

CHAPTER 7 Cardiovascular system180

Edema

Be careful when palpating—contrary to popular teaching, pitting and non-

pitting edema are painful! Could it be gravitational?

Peripheral pulses

These are often overlooked but are a vital part of the examination.

Document them carefully, and look for skin changes and ulceration that

might be causing signiﬁ cant problems but are not necessarily raised in the

history.

Additional points

Alternative diagnoses

Respiratory illnesses often overlap and may mimic, e.g., pulmonary ﬁ brosis

and left ventricular failure. If things don’t add up or there is little response

to treatment, revisit your diagnosis.

181

Respiratory system

Applied anatomy and physiology 182

Dyspnea 184

Cough and expectoration 185

Other respiratory symptoms 187

The rest of the history 188

General appearance 190

Hands, face, and neck 191

Inspection of the chest 193

Palpation 194

Percussion 196

Auscultation 198

Important presenting patterns 200

The elderly patient 201

Chapter 8

CHAPTER 8 Respiratory system182

Applied anatomy and physiology

Anatomy

The respiratory tract extends from the nostrils to the alveoli and includes

the pulmonary blood supply. Clinically, it is divided into the upper respi-

ratory tract, which is the nose and pharynx, and the lower respiratory

tract, which consists of the larynx and all distal structures.

Trachea, bronchi, and bronchioles

The trachea lies in the midline deep to the sternal notch and divides into

the left and right main bronchi at the carina , level with the sternal angle.

There are about 25 further divisions before reaching the alveoli. The last

16 orders are termed bronchioles and differ from the bronchi by having no

cartilage, fewer goblet cells, and progressively less muscular walls.

Lungs

The right lung has three lobes (upper, middle, and lower) whereas the left

lung has two (upper and lower); see Fig. 8.1. Note the angle of the oblique

ﬁ ssure, dividing the upper and lower lobes such that examination of the

anterior chest is mostly that of the upper (and middle) lobes; examination

of the back is of the lower lobe.

The right middle lobe sits anterior, separated from the upper lobe by

the horizontal ﬁ ssure. The chest wall corresponding to this is between the

right fourth and sixth ribs anterior and is easily missed. The same area on

the left is the lingula , part of the left upper lobe, which reaches around the

anterior side of the heart.

The slant of the diaphragm is such that the inferior border of the lungs is

at the sixth rib anterior but extends down to the twelfth posterior.

Physiology

Lung function

Ventilation is under the inﬂ uence of the respiratory center in the brain.

This, in turn, can be inﬂ uenced by higher voluntary centers and by chem-

oreceptors that respond to changes in blood gas partial pressures. In

health, the most important ones are the brainstem chemoreceptors,

stimulating breathing in response to rising blood CO

2

.

The main muscle of breathing is the diaphragm, innervated by the

phrenic nerve. Contraction causes a ﬂ attening of the central part and

a slight elevation of the peripheral parts. This causes expansion of the

chest cavity, and as the intrathoracic pressure drops, air is sucked into the

lungs. The intercostal and scalene muscles maintain the chest wall stability.

When a larger inspiration is needed, these “accessory” muscles, including

the sternocleidomastoids, act to further expand the chest.

Expiration is largely passive, the air being expelled as the lungs recoil

under their innate elasticity.

Aside from inadequate ventilation, ineffective lung functioning can

result from inadequate perfusion of the ventilated areas. Also, impaired

gas transfer across the alveoli may be a factor—either by a thickening of

the wall (e.g., ﬁ brosis), a loss of surface area (as in COPD), or ﬂ uid in the

alveoli, such as edema, pus, or blood.

APPLIED ANATOMY AND PHYSIOLOGY

183

Defense

Mechanical defense against infection includes the narrow passages of the

nose as well as the larynx, which separates the respiratory and gastrointes-

tinal (GI) tracts. Cough receptors in the pharynx and lower airways initiate

mechanisms resulting in a deep inspiration, followed by expiration against

a closed glottis and a sudden glottal opening. This causes a rapid, forceful

expulsion of air, which we know as a cough.

Most of the respiratory tract is lined with mucous secreted from goblet

cells that catch small particles and microbes. This is continuously swept

upward toward the larynx by beating cilia on the epithelium.

In the smaller airways and alveoli, macrophages and a variety of secreted

defensive proteins act against microbes at a microscopic level.

UL UL

LL LL

UL

ML

UL

Fig. 8.1 Surface anatomy of the lungs. UL, upper lobe; ML, middle lobe;

LL, lower lobe.

CHAPTER 8 Respiratory system184

Dyspnea

Deﬁ ning dyspnea

Shortness of breath (SOB), or dyspnea , is the sensation one has when using

an abnormal amount of effort to breathe. Patients may describe “breath-

lessness,” an inability to “get their breath,” or being “short-winded.”

“Tightness” is often described and may actually be the sensation of air-

way narrowing, as in asthma, or may be chest pain, as in cardiac disease.

Tease out exactly what the patient means by this.

0 Pleuritic chest pain is worse at the height of deep inspiration; patients

may say they are “not able to get their breath.” While their complaint is of

breathlessness, their actual problem is pain on inspiration. Ask if they feel

the need to breathe faster than normal or are unable to breathe deeply. If

the latter, ask if that is due to pain or to some other sensation. If in doubt,

ask the patient to take a deep breath and watch the results.

Onset and duration

How quickly did SOB come on? Pulmonary embolus, pneumothorax, and

asthmatic attacks can come on suddenly. Pneumonia, heart failure, and

anemia cause SOB that worsens over days or weeks. Smoking-related lung

disease, by contrast, causes i breathlessness over many years.

Slower onsets are poorly reported. The patient often reports the onset

of a worsening of breathlessness. Ask when they were last able to run up

the stairs, and the real duration of breathlessness becomes apparent.

Severity

Several classiﬁ cations exist, but it is often more useful to quantify severity

in terms of functional impairment. Ask, “How far can you walk before you

have to stop? How many ﬂ ights of stairs can you manage?” Restriction of

hobbies such as gardening and dancing are also useful guides.

0 Be sure that activities are restricted by SOB and not by arthritic hips

or knees, chest pain, or some other ailment.

Exacerbating and relieving factors

What makes the breathlessness worse? Can it be reliably triggered by a

particular activity or situation? Divide symptoms into SOB at rest and SOB

on exertion and quantify as above. Remember to ask about position, e.g.,

orthopnea (b Chapter 7, p. 150).

Has the patient used inhalers? How frequently are they used? Did they

help?

Associated symptoms

See the following pages for a full breakdown. Be aware of hyperventilation,

in which the d of blood CO

2

will cause paresthesia in the lips and ﬁ ngers

along with light-headedness and, in severe cases, tetany.

COUGH AND EXPECTORATION

185

Cough and expectoration

Cough

Cough is a common but often overlooked symptom in respiratory dis-

ease usually caused by upper respiratory infection (URI) and/or smoking.

Duration of cough is important, as well as character, exacerbating factors,

and whether any sputum is produced.

Note that cough may be the only symptom of childhood asthma.

Chronic cough is that lasting >3 weeks and may be caused by asthma,

carcinoma, interstitial disease and bronchiectasis, gastroesophageal reﬂ ux

disease, and postnasal drip.

0 Smokers will have a chronic cough, particularly in the mornings, so a

history of a change in pattern is important.

The character of the cough often reveals the cause (Table 8.1).

Associated pain is common and the patient will be able to localize it

to the upper respiratory tract (e.g., laryngitis; tracheitis is particularly

painful) or the chest wall (i.e., pleurisy secondary to lobar pneumonia or

collapse).

Remember nonpulmonary causes: postnasal drip (dry, tickly), gastro-

esophageal reﬂ

ux (dry), pharyngeal pouch or tracheoesophageal ﬁ stula

(worse after eating or lying down), and angiotensin-converting enzyme

(ACE) inhibitors (dry).

Sputum

Sputum is excess respiratory secretions that are coughed up. Patients will

usually understand the term phlegm or mucous better. Features to inquire

about include the following: How often? How much? How difﬁ cult is it to

cough up? Color? Consistency? Smell?

Table 8.1 Some characteristic coughs

Cause Character

Laryngitis Cough with a hoarse voice

Tracheitis Dry and very painful

Pleurisy Sharp pain (chest wall)

Postnasal drip Tickly

Asthma Chronic, paroxysmal, worse after

exercise and at night

Esophageal reﬂ ux Dry and nauseating. Often ﬁ rst

thing in the morning.

Tracheo-esophageal ﬁ stula (rare) Nauseating and worse after eating

Epiglottitis Barking

Laryngeal nerve palsy “Bovine” hollow, brassy

Left heart failure Productive and worse on lying ﬂ at

CHAPTER 8 Respiratory system186

Attempt to quantify sputum production in terms of well-known objects,

such as teaspoons, etc. Mucoid sputum is white or clear in color but can

be turned gray in cigarette smokers. Yellow or green sputum is termed

purulent and usually indicates infection, although eosinophils in the sputum

of asthmatics can also produce a green color. See Table 8.2.

Harder “plugs” of sputum from the airways are seen in asthmatic spu-

tum. Miniature tree-like bronchial casts are produced in bronchopulmo-

nary aspergillosis.

Hemoptysis

The coughing up of blood can vary from streaks or a pink hue (e.g., CHF)

to massive, life-threatening bleeds. Establish the amount, color, frequency,

and nature of any associated sputum. (Massive hemoptysis = >500 mL

in 24 hours.) Hemoptysis is easily confused with blood originating in the

nose, mouth, and GI tract (hematemesis). Ask about, and check for, bleeds

in these areas.

Causes of hemoptysis include bronchitis, carcinoma, pulmonary embo-

lus, and infarction, TB, cystic ﬁ brosis, and lung abscesses. Infective causes

will usually produce blood-stained sputum, not pure hemoptysis.

Be alert to other potential sites of bleeding (skin, GI tract, mouth) that

could point to a coagulation disorder.

Table 8.2 Some characteristics of sputum

Nature of sputum Causes

White/gray Asthma

Smoking

Green/yellow Bronchitis

Bronchiectasis

Green and offensive Bronchiectasis

Abscesses

Sticky, rusty Lobar pneumonia

Frothy, pink Congestive cardiac failure

Separates to 3 layers

(mucoid, watery, rusty)

Severe bronchiectasis

Very sticky, often green Asthma

Sticky, with “plugs” Allergic aspergillosis

(complication of asthma)

OTHER RESPIRATORY SYMPTOMS

187

Other respiratory symptoms

Wheeze

This is a high-pitched, whistling, “musical” sound produced by narrowing

of airways, large or small. It occurs with inspiration and expiration, but is

usually louder and more prominent in the latter. If it is due to small-airway

narrowing, as in asthma, it will be accompanied by a prolonged expiratory

phase.

Causes include asthma, smoking-related lung disease, mucosal edema,

airway obstruction, airway collapse, and pulmonary edema (cardiac

asthma).

Stridor

Stridor has a harsh “crowing” inspiratory and expiratory sound with a

constant pitch. It signals large-airway narrowing, usually at the larynx or

trachea. It can precede complete airway obstruction so is treated as a

medical emergency.

Hoarseness and dysphonia

This is described in b Chapter 6 on p. 130.

Pain

Chest pain is explored fully in Chapter 7 (b p. 148). Pain arising from

respiratory disease is usually pleuritic in nature and arises from the chest

wall, parietal pleura, or mediastinum, as the lungs have no pain ﬁ bers. It

is felt as a severe, sharp pain at the height of inspiration or on coughing.

It is usually localized to a small area of chest wall. Note that patients will

avoid deep breathing and may complain of breathlessness (see Dyspnea,

this b chapter, p. 185).

Pain resulting from lung parenchymal lesions may be dull and constant

and is usually an ominous sign of spread into the chest wall.

The pain of tracheitis is a poorly localized, central soreness. Dia-

phragmatic pain may be felt at the ipsilateral shoulder tip, while pain from

the costal parts of the diaphragm may be referred to the abdomen.

In general, muscular and costal lesions will be tender to touch over

the corresponding chest wall and exacerbated by certain twisting move-

ments, whereas pleurisy is not, although this is not always the case.

Costochondritis is a common cause of pleuritic pain, of which Tietze’s

syndrome is a speciﬁ c cause associated with pain and swelling of the supe-

rior costal cartilages.

Pain in a nerve-root distribution may be due to spinal lesions or herpes

zoster virus (HZV).

CHAPTER 8 Respiratory system188

The rest of the history

Other symptoms

Fever

Fever, particularly at night, may be a sign of infection such as TB, malig-

nancy, or a connective tissue disorder.

Weight loss

This can be a symptom of carcinoma, chronic lung disease, or chronic

infection. Attempt to quantify any loss (how much in how long?).

Peripheral edema

Edema manifesting as ankle swelling at the end of the day may be a sign

of right heart failure secondary to chronic lung disease (cor pulmonale).

If severe enough, patients may exhibit signs and symptoms of left heart

failure (see b Chapter 7, p. 177).

Obstructive sleep apnea

This is caused by upper-airway obstruction by the ﬂ accid palatal muscles

during REM sleep. This causes snoring and progressive hypoxia, which

brieﬂ y wakes the patient from sleep, often accompanied by thrashing

around, disturbing those sharing the bed. The bedtime partner will

graphically tell this tale. The patient will describe early-morning head-

aches caused by CO

2

retention and daytime somnolence from sleep

deprivation.

Past medical history

• Vaccination for respiratory illnesses, particularly bacillus Calmette-

Guérin (BCG)

• Previous respiratory infections, especially TB before 1950, when

operations could result in lifelong deformity

• X-ray abnormalities previously mentioned to the patient

• Childhood (a frequently coughing child may have had undiagnosed

asthma)

• Previous intensive care unit (ICU) admissions or respirator

dependency

Drug history

• What inhalers are used and how often? Check inhaler technique.

• Previous successful use of bronchodilators and steroids

• Oral steroid therapy predisposes to infection and TB especially.

• B-blockers may exacerbate obstructive lung diseases.

• ACE inhibitors cause a dry cough.

• If O

2

therapy—cylinders or concentrator? How many hours a day?

• Illicit drug use (Cocaine is associated with respiratory disease.)

Family history

• Asthma, eczema, and allergies

• Inherited conditions (e.g., cystic ﬁ brosis [CF], A1-antitrypsin deﬁ ciency)

• Family contacts with TB

THE REST OF THE HISTORY

189

Smoking

Attempt to quantify the habit in pack-years: 1 pack-year is 20 cigarettes

per day for 1 year (e.g., 40/day for 1 year = 2 pack-years; 10/day for 2

years = 1 pack-year).

0 Beware of appearing judgmental.

Ask about previous smoking, as many patients will call themselves non-

smokers if they gave up yesterday or even on the way to the hospital!

Remember to ask about passive smoking.

Alcohol

Alcohol abusers are at greater risk of chest infections, and bingeing may

result in aspiration pneumonia.

Social history

Pets

Dogs and cats are a common source of allergens. Also ask about birds and

caged animals. Ask about exposure beyond the home, at homes of close

friends and relatives, and hobbies involving animal exposure.

Travel

Ask about travel (recent or previous) to areas where respiratory infec-

tions are endemic. Think particularly about TB. Remember that Legionella

can be caught from water systems and air-conditioning even in developed

countries.

Occupation

This factor is more important in chest medicine than in any other ﬁ eld. Be

alert to exposure to asbestos, coal, cotton, nitrogen dioxide, metals such

as tin, silver, iron oxide, and titanium, and hay, air conditioner systems,

and so on.

Trace the patient’s occupational history back, as there may be a lag of

20 or 30 years between exposure and resultant disease. Remember that

exposure may not be obvious and that the patient may have been unaware

of it at the time. Plumbers, builders, and electrical engineers may have

been exposed to asbestos in the past.

Ask also about close personal contacts—partners may be signiﬁ cantly

exposed by handling and washing clothing, for example (although this is

relatively rare).

CHAPTER 8 Respiratory system190

General appearance

Respiratory patients may be short of breath, and it may be easiest to

examine them sitting at the edge of the bed instead of in the classic posi-

tion of sitting back at 45 * . Choose a position comfortable to you both. The

patient should be undressed to the waist.

As ever, a surprising amount of information can be obtained by observ-

ing the patient before touching the patient.

Bedside clues

Look for evidence of the disease and its severity around the patient:

• Inhalers? Which ones?

• Any additional inhaler devices?

• Nebulizer?

• Is the patient receiving O

2

therapy? If so, how much and by what

method (i.e., face mask, nasal cannula, etc.)?

• Sputum container? Sputum-laden tissues?

• Remember to inspect the sputum carefully and to record the ﬁ ndings.

• Any mobility aids nearby?

• Look for cigarettes, lighter, or matches at the bedside or in a pocket.

Respiration

Watch the patient from the foot of the bed. Or watch them approach

your clinic room.

• Do they appear out of breath at rest?

• If so, do they appear in distress?

• Are they breathing through the mouth or the nose?

• Are they breathing through pursed lips? (i the expiratory

pressure—an indication of smoking-related lung disease)

• If mobile, did they have to stop on the way to the room? How quickly

did they recover?

• Count the respiratory rate. At rest, this should be <12/minute.

• Are the breaths of normal volume?

• Are they using the accessory respiratory muscles (e.g.,

sternomastoids)?

• Are they using their arms to splint their chest? (The classic position is

sitting forward, hands on knees.)

Speech

• Is their speech limited by their breathlessness? If so, can they complete

a full sentence? (an important indicator of severity in many conditions)

• Listen for hoarseness as well as the gurgling of excess secretions.

• A nasal voice may indicate neuromuscular weakness.

Cough and abnormal sounds

Watch and listen for coughing (see previous pages) as well as stridor and

wheeze.

HANDS, FACE, AND NECK

191

Hands, face, and neck

Temperature

• Cold ﬁ ngers indicate peripheral vasoconstriction or heart failure.

• Warm hands with dilated veins are seen in CO

2

retention.

Staining

Fingers stained with tar appear yellow/brown where the cigarette is held

(nicotine is colorless and does not stain). This indicates smoking but is not

an accurate indicator of the number of cigarettes smoked.

Cyanosis

This is a bluish tinge to the skin, mucous membranes, and nails (see b

Chapter 3, p. 51), evident when >2.5g/dL of reduced hemoglobin is present

(O

2

Saturation about 85%). It is easier to see in good, natural light.

Central cyanosis is seen in the tongue and oral membranes (severe

lung disease, e.g., pneumonia, PE, COPD). Peripheral cyanosis is seen only

in the ﬁ ngers and toes and is caused by peripheral vascular disease and

vasoconstriction.

Finger clubbing

There is i curvature of the nails. Early clubbing is seen as a softening of

the nail bed (nail can be rocked from side to side), but this is very difﬁ cult

to detect. Progressive clubbing leads to a loss of the nail angle at the base

and eventually to a gross longitudinal curvature and deformity.

Objectively check for clubbing by putting the patient’s nails back to back

as in Fig. 8.2. Clubbing leads to a loss of the diamond-shaped gap.

Important respiratory causes are carcinoma, asbestosis, ﬁ brosing alve-

olitis, and chronic sepsis (bronchiectasis, abscess, empyema, CF).

Pulse

Check rate, rhythm, and character. A tachycardic bounding pulse = CO

2

retention.

Tremor

• Fine tremor: caused by use of B-agonist drugs (e.g., albuterol)

• Flapping tremor (asterixis): ﬂ apping when holding hands dorsiﬂ exed

with ﬁ

ngers abducted (Fig 8.3). This is identical to the ﬂ ap of hepatic

failure (see b Chapter 9, p. 244) and is a late sign of CO

2

retention.

Blood pressure

Pulsus paradoxus (see b Chapter 7, p. 159) is caused by pericardial effu-

sion and severe asthma.

JVP

See b Chapter 7, p. 161. JVP is raised in pulmonary vasoconstriction or

pulmonary hypertension and right heart failure. It is markedly raised, with-

out a pulsation, in SVC obstruction, with distended upper chest wall veins

and facial and conjunctival edema (chemosis).

CHAPTER 8 Respiratory system192

Nose

Examine inside and out, looking for polyps (asthma), deviated septum, and

lupus pernio (red/purple nasal swelling of sarcoid granuloma).

Eyes

• Conjunctiva: evidence of anemia?

• Horner’s syndrome: (b Chapter 9, p. 274) caused by compression of

the sympathetic chain in the chest cavity (tumor, sarcoidosis, ﬁ brosis)

• Iritis: TB, sarcoidosis

• Conjunctivitis: TB, sarcoidosis

• Retina: Papilledema in CO

2

retention or cerebral metastases. Retinal

tubercles in TB. Choroiditis in TB or syphilis

Lymph nodes

See b Chapter 3, p. 58, for a full description of examination technique.

Feel especially the anterior and posterior triangles, the supraclavicular

areas. Don’t forget that the axillae receive lymph drainage from the chest

wall and breasts.

Fig. 8.3 Looking for a ﬂ apping tremor. Wrists are dorsiﬂ exed and ﬁ ngers abducted.

Fig. 8.2 Examining for clubbing. In the normal state, a diamond window will be

seen between opposed nail beds, which is lost in ﬁ nger clubbing.

INSPECTION OF THE CHEST

193

Inspection of the chest

Look at the shape and movement of the chest up close.

Surface markings

Check the whole chest for scars and lesions.

• Scars may indicate previous surgery. Look especially in the mid-axillary

lines for evidence of past chest drains.

• Radiotherapy will often cause lasting local skin thickening and

erythema.

• Veins: Look for unusually prominent surface vasculature.

Shape

• Deformity: Is there any asymmetry of shape? Remember to check the

spine for scoliosis or kyphosis.

• Surgery : TB patients from the 1940s and 1950s may have had

operations resulting in lasting and gross deformity (thoracoplasty).

• Barrel chest: a rounded thorax with i anteroposterior (AP) diameter.

Hyperinﬂ

ation is a marker of smoking-related lung disease.

• Pectus carinatum : also called “pigeon chest.” Sternum and costal carti-

lages are prominent and protrude from the chest. It is caused by i

respiratory effort when the bones are still malleable in childhood, from

asthma or rickets.

• Pectus excavatum: also called “funnel chest.” Sternum and costal

cartilages appear depressed into the chest. This is a developmental

defect, usually a normal variant with no signiﬁ

cance to pathology.

• Surgical (subcutaneous) emphysema: Air in the soft tissues will appear

as a diffuse swelling. It occurs especially in the neck; it may feel crackly

to the touch.

Breathing pattern

Again, examine rate and depth of breathing.

• Fast, deep breaths are seen in anxiety states.

• Deep, sighing breaths are Kussmaul’s respiration = systemic acidosis.

• Cheyne–Stokes breathing has an alternating pattern of deep, regular

breathing with very slow, shallow breaths. It is due to failure of the

normal respiratory regulation in response to blood CO

2

levels.

• Prolonged expiratory phase = marker of outﬂ

ow limitation, a sign of

smoking-related lung disease if coupled with pursed-lip breathing.

Movement

Observe chest wall movement during breathing at rest. Also, ask the

patient to take a couple of deep breaths in and out, and watch closely.

• Look for asymmetry. d Movement indicates lung disease on that side.

• d Movement globally is seen in COPD, along with a “pump handle”

movement of the ribs (hinged posteriorly only), compared with the

normal “bucket handle” (hinged at the front and back).

• Harrison’s sulcus is a depression of the lower ribs just above the costal

margins and indicates severe childhood asthma.

CHAPTER 8 Respiratory system194

Palpation

Mediastinal position

Trachea

The trachea should lie in the midline just beneath the sternal notch. The

trachea will shift as the mediastinum is pulled or pushed laterally. This is a

late sign and not easy to assess, unless the shift is marked.

There are several methods for checking the position, all of which are

somewhat uncomfortable for the patient. The two most popular methods

are as follows:

• Use a single ﬁ

nger to feel for the trachea; the distance between it and

the sternomastoids on each side should be the same.

• Use two ﬁ

ngers and palpate the sulci on either side of the trachea at

the same time. They should feel identical in size.

Apex beat or PMI (point of maximum impulse)

This is normally at the ﬁ fth intercostal space in the mid-clavicular line. It

will shift with the mediastinum. However, it is very difﬁ cult to palpate in

the presence of hyperexpanded lungs and may be shifted to the left if the

heart is enlarged.

Chest expansion

This is an objective measure of chest movement, using your hands as a guide.

• Put both hands on the patient’s posterior thorax, at a level just below

the nipples, anchoring your ﬁ

ngers laterally at the sides.

• Extend your thumbs so that they touch at the spinous processes; don’t

press them against the chest.

• Ask the patient to take a deep breath. As they do this, watch your

thumbs; they should move apart equally. Any d in movement on one

side should be visible.

• It is easy to move your thumbs yourself in the expected direction. Be

aware of this and allow them to follow the movement of the chest.

0 This maneuver may also be done on the anterior chest, as illustrated

in Fig. 8.4, but as one can see, personal comfort, breast size, and mod-

esty may preclude a quality exam of a female. If chest expansion must be

assessed on the anterior chest wall, it is important to explain what you are

doing, as suddenly reaching for a female chest may be misconstrued!

Tactile vocal fremitus

This is the vibration felt on the chest as the patient speaks. Each part of the

chest is tested, as for percussion.

• Place the medial edge of your hand horizontally against the chest.

• Ask the patient to say “99” or “1, 1, 1.”

• You should feel the vibration against your hand.

This test is rather crude and often neglected by clinicians. The changes are

identical to those for vocal resonance.

• i Vibration in consolidation

• d In pneumothorax, collapse, COPD and pleural effusion

PALPATION

195

Fig. 8.4 Placement of the hands for testing chest expansion. Anchor with the

ﬁ ngers and leave the thumbs free-ﬂ oating.

CHAPTER 8 Respiratory system196

Percussion

Technique

This takes some practice to master fully, thus it can serve as an excellent

indicator of how much time a student has spent performing the maneuver.

The aim is to tap the chest by the standard method and listen to and feel

for the resultant sound (see Figs. 8.5 and 8.6). For a right-handed provider:

• Place the left hand on the chest wall, ﬁ

ngers separated and lying

between the ribs.

• Press the middle ﬁ nger

ﬁ

rmly against the chest.

• Using the middle ﬁ

nger of the right hand, strike the middle phalanx of

the middle ﬁ

nger of the left hand (Fig. 8.5).

• The striking ﬁ

nger should be moved away again quickly, as keeping it

pressed on the left hand may mufﬂ

e the noise.

• The right middle ﬁ

nger should be kept in the ﬂ

exed position, the

striking movement coming from the wrist (much like playing the

piano).

0 Students quickly learn to keep the middle ﬁ

ngernail of their right hand

well trimmed!

• Students should practice on themselves and each other. Learn the

different sounds produced percussing over the lung and the more

dense liver just below.

• In clinical practice, one should percuss each area of the lung, each time

comparing right then left, as shown in Fig. 8.6.

• Don’t forget the apices, which can be assessed by percussing directly

onto the patient’s clavicle (no left hand needed).

• If an area of dullness is heard (or felt), this should be percussed in

more detail so as to map out the borders of the abnormality.

Findings

• Normal lung sounds resonant.

• Dullness = heard over areas of i density (consolidation, collapse,

alveolar ﬂ uid, pleural thickening, peripheral abscess, neoplasm)

• Stony dullness = the unique extreme dullness heard over a pleural

effusion

• Hyperresonant = areas of d density (emphysematous bullae or

pneumothorax). COPD will create a globally hyperresonant chest.

2 There should be an area of dullness over the heart that may be dimin-

ished in hyperexpansion states (e.g., COPD or severe asthma).

2The liver is manifested by an area of dullness below the level of the

sixth rib anteriorly on the right. This may also be lost with hyperinﬂ

ated

lungs.

PERCUSSION

197

Fig. 8.5 Strike the middle phalanx of the middle ﬁ nger of the left hand with the

middle ﬁ nger of the right hand.

Fig. 8.6 Areas of the chest to percuss. Test right vs. left for each area, front and

back.

CHAPTER 8 Respiratory system198

Auscultation

Technique

The diaphragm should be used, except where better surface contact is

needed in very thin or hairy patients.

• Ask the patient to take deep breaths in and out through the mouth.

• Listen to both inspiration and expiration.

• Listen over the same areas percussed, comparing left to right.

• If an abnormality is found, examine more carefully and deﬁ ne

borders.

• Listen for the breath sounds and any added sounds, and note at which

point in the respiratory cycle they occur.

0 Many patients have difﬁ

culty performing correctly here. They may take

one deep breath and hold it, may breath through the nose, or may take

only one breath. Simple prompts (“keep going, in and out”) will help. A

brief demonstration will usually solve things if all else fails.

Findings

Breath sounds

• Normal: vesicular. Produced by airﬂ ow in the large airways and larynx

and altered by passage through the small airways before reaching the

stethoscope. Often described as rustling. This is heard especially well

in inspiration and early expiration.

• Reduced sound: if local = effusion, tumor, pneumothorax, pneumonia,

or lung collapse. If global = COPD or asthma (The “silent chest” is a

sign of a life-threatening asthma attack.)

• Bronchial breathing: caused by i density of matter in the peripheral

lung, allowing sound from the larynx to the stethoscope unchanged,

has a hollow, blowing quality, heard equally in inspiration and

expiration, often with a brief pause between. (Think of a certain

black-helmeted villain in a popular space movie series.) A similar

sound can be heard by listening over the trachea in the neck.

Bronchial breathing is heard over consolidation, lung abscess at

the chest wall, and with dense ﬁ

brosis. It is also heard at the upper

border of a pleural effusion.

Added sounds

• Wheeze (rhonchi): musical whistling sounds caused by narrowed

airways. It is heard easier in expiration.

• Different-caliber airways = different-pitch note; thus asthma and

COPD can cause a chorus of notes termed polyphonic wheeze .

•

Monophonic wheeze indicates that a single airway is narrowed,

usually by a foreign body or carcinoma.

0 This is not a good marker of disease severity!

• Crackles (crepitations, rales): caused by air entering collapsed airways

and alveoli producing an opening snap. They are heard in inspiration.

•

Coarse crackles are made by larger airways opening and sound like

the snap and pop of a certain breakfast cereal. Causes include ﬂ uid

or infection.

AUSCULTATION

199

•

Fine crackles occur later in inspiration. These sound like the tear of

Velcro

®

and can also be reproduced by rolling hair at the temples

between the thumb and foreﬁ nger. Causes include ﬂ uid, infection,

or ﬁ brosis (particularly at lung bases).

0 Crackles are often a normal ﬁ

nding at the lung bases, If so, they will

clear after asking the patient to cough.

• Rub: creaking sound likened to the bending of new leather or the creak

of a footstep in fresh snow. This is heard at the height of inspiration

and is caused by inﬂ

amed pleural surfaces rubbing against each other.

•

Causes include pneumonia and pulmonary embolism with infarction.

0 Movement of the stethoscope on the chest wall sounds similar.

Vocal resonance

• Auscultatory equivalent of vocal fremitus

• Low-pitched sounds transmit well and create a vocal booming quality.

• Ask the patient to say “99” or 1, 1, 1” and listen over the same areas

as before.

• The changes are the same as those for vocal fremitus.

• A marked i resonance, such that a whisper can be clearly heard, is

termed whispered pectoriloquy .

CHAPTER 8 Respiratory system200

Important presenting patterns

Consolidation

• d Air entry locally, secondary to infection

• d Chest wall movement locally

• Dullness to percussion

• Bronchial breathing or i breath sounds

• Coarse or ﬁ

ne crackles, localized

• i Vocal resonance

Collapse

• Blockage of a major airway and collapse of the distal lung segment

• Mediastinal shift towards the abnormality

• d Chest wall movement locally

• Dullness to percussion restricted to affected lobe

• d Breath sounds

• d Vocal resonance

Pleural effusion

• Collection of ﬂ uid between the two pleural layers, creating a sound

barrier between the examiner and the patient’s lung

• Mediastinal shift away from the lesion (with a large effusion)

• d Chest wall movement locally

• Stony dull to percussion

• d Breath sounds with bronchial breathing at the upper border

• d Vocal resonance

• Sometimes a pleural rub just above

Pneumothorax

• Air in the pleural space

• Mediastinal shift away from the lesion (with a tension pneumothorax)

• d Chest wall movement locally

• Hyperresonant to percussion

• d Breath sounds

• d Vocal resonance

Interstitial ﬁ brosis

• No mediastinal shift. The trachea may move toward the ﬁ brosis in

upper-lobe disease.

• n or d chest wall movement

• n percussion note

• n breath sounds

• n vocal resonance

• Fine crackles present

THE ELDERLY PATIENT

201

The elderly patient

Up to 60% of older people may suffer respiratory symptoms but less read-

ily see their doctors about them. Lung function declines with age and

exertional breathlessness rises, often with concurrent (nonrespiratory)

illnesses. Careful, thoughtful assessment is therefore vital.

History

Clarify diagnosis

Not all disease in elders is COPD and many older people are lifelong non-

smokers. Asthma and pulmonary ﬁ brosis are often underdiagnosed.

Fatigue

Fatigue is often associated with chronic respiratory illnesses, and this may

be more disabling to individuals than respiratory symptoms themselves.

Drug history

This should be comprehensive and dovetail with other medical problems.

Anticholinergic drugs (e.g., atrovent) may precipitate glaucoma or worsen

bladder and bowel symptoms, so be thorough. Ask about vaccinations—

many people miss their annual ﬂ u vaccine because of hospitalization.

Consider vaccination as appropriate.

Nutrition and mood

Undernutrition is common with chronic diseases and those in long-term

care, affecting illnesses with higher resting metabolic rates (e.g., COPD).

Depressed mood is similarly common and should be asked about.

Social history

Functional history is paramount and may reveal key interventions. A thor-

ough occupational history is vital; many people do not know that they

have worked or lived with someone exposed to, e.g., asbestos.

Examination

General

Poorly ﬁ tting clothes or dentures may point to weight loss (undernutri-

tion, chronic disease, malignancy).

Hands

Arthritis and other deformities may make inhaler use difﬁ cult and point

to related diagnoses (e.g., rheumatoid lung disease). Clubbing may not be

present in later-onset pulmonary ﬁ brosis.

Chest

Beware of basal crepitations, which are common in older age. Pick out

discriminating signs—tachypnea, position of crackles, added sounds, etc.

Inhaler technique

This is a key examination. It may reveal why prior treatments were

unsuccessful.

CHAPTER 8 Respiratory system202

Diagnoses not to be missed

• Asthma: seen in up to 8% of individuals over 60 but underrecognized

and undertreated. Spirometry is a key investigation.

• Tuberculosis: i in the elderly, through reactivation, chronic illness, and

undernutrition. TB presents nonspeciﬁ

cally, with cough, lethargy, and

weight loss.

203

Abdomen

Applied anatomy 204

Esophageal symptoms 206

Nausea, vomiting, and vomitus 208

Abdominal pain 210

Bowel habit 212

Jaundice and pruritus 216

Abdominal swelling 217

Urinary and prostate symptoms 218

Appetite and weight 220

The rest of the history 221

Outline examination 223

Hand and upper limb 224

Face and chest 226

Inspection of abdomen 229

Auscultation 231

Palpation 232

Palpating the abdominal organs 233

Percussion 239

Rectal examination 241

Hernial oriﬁ ces 243

Important presenting patterns 246

The elderly patient 252

Chapter 9

CHAPTER 9 Abdomen 204

Applied anatomy

The abdomen includes the perineum, external and internal genitalia, and

inguinal regions. These components are discussed in Chapters 12 and 14.

Boundaries

The abdomen is deﬁ ned as the region lying between the thorax above and

the pelvic cavity below. The anterior abdominal wall is bounded by the

seventh to twelfth costal cartilages and the xiphoid process of the sternum

superiorly and the inguinal ligaments and pelvic bones inferiorly.

The abdominal cavity is separated from the thoracic cavity by the dia-

phragm. There is no such delineation, however, between the abdomen

and the pelvis; consequently, deﬁ nitions vary.

Abdominal contents

The abdomen contains structures that form part of just about every body

system.

The digestive organs of the esophagus, stomach, small intestine, large

intestine, and the associated organs (liver, gallbladder, and biliary system,

exocrine pancreas) all lie within the abdomen.

The endocrine portion of the pancreas, the adrenal glands, and gonads

represent the endocrine system.

The cardiovascular system includes the abdominal aorta with its impor-

tant branches to the liver, spleen, intestine, kidneys, and lower limbs.

The immunological system is represented by the spleen, the multi-

ple lymph nodes surrounding the aorta and intestines, and the mucosa-

associated lymphoid tissue (MALT) within the intestine itself.

The whole of the urinary system is present (kidneys, ureters, bladder,

and urethra).

Much like the thorax, the abdomen is lined by a thin layer of membra-

nous tissue: the peritoneum . This is a double lining—the parietal peritoneum

covers the internal surface of the abdominal walls while the visceral peri-

toneum covers the organs. Between the two layers (the peritoneal cavity)

is a small amount of ﬂ uid that acts as a lubricant enabling the abdominal

contents to move against each other as the body changes position or, for

example, as the gut contorts with peristalsis.

A select few organs lie behind the peritoneum on the posterior abdomi-

nal wall. They are the pancreas, a portion of the duodenum, the ascending

and descending colon, and the kidneys.

Abdominal regions

The anterior abdominal wall is artiﬁ cially divided into nine portions for

descriptive purposes. Four imaginary lines can be drawn (see Fig. 9.1 ):

• 1horizontal line between the anterior superior iliac spines

• 1horizontal line between the lower border of the ribs

• 2vertical lines at the mid-clavicular point

To make life easier, the abdomen can also be divided into four quadrants

by imagining one horizontal and one vertical line crossing at the umbilicus

(see Fig. 9.2 ). Familiarize yourself with these along with the organs lying

in each area.

205

APPLIED ANATOMY

Right upper

quadrant

Right lower

quadrant

Left upper

quadrant

Left lower

quadrant

Fig. 9.2 The four quadrants of the anterior abdominal wall.

Right

hypochondrium

Right

lumbar

Right

inguinal

Epigastrium

Left hypochondrium

Umbilical

Left lumbar

Suprapubic

Left inguinal

Fig. 9.1 The nine segments of the anterior abdominal wall.

CHAPTER 9 Abdomen 206

Esophageal symptoms

Dysphagia

This is difﬁ culty swallowing and is the principal symptom of esophageal

disease (see Box 9.1 for important causes). When a patient complains of

dysphagia, you should attempt to establish the following:

• Level of obstruction: Where does the patient feel the food or liquid

sticking? Patients can often point to a level on the chest, although the

sensation usually correlates poorly with the actual level of obstruction.

• Onset: How quickly did the symptoms emerge? Obstruction caused by

cancer, for example, may progress rapidly over a few months, whereas

those with a benign peptic stricture may describe a very long history of

GERD and progressive dysphagia.

• Course: Is it intermittent? Present for only the ﬁ

rst few swallows

(lower esophageal ring, spasm)? Progressive (cancer, stricture,

achalasia)?

• Solids/liquids: Both solids and liquids being affected equally suggests a

motor cause (achalasia, spasm). However, if solids are affected more

than liquids, some physical obstruction is more likely (e.g., cancer).

• Associated symptoms: heartburn (leads to esophageal strictures),

weight loss, wasting, fatigue (perhaps suggestive of cancer). Coughing

and choking suggest pharyngeal dysphagia due to motor dysfunction

(e.g., motor neuron disease causing bulbar or pseudobulbar palsy).

Odynophagia

This is pain on swallowing. It is usually an unpleasant substernal sensation

during the swallow and suggestive of esophageal inﬂ ammation (infective

esophagitis—candidida, herpes, cytomegalovirus; peptic ulceration; caustic

damage; esophageal perforation).

0 Remember to ask about potential causes during the drug history.

Heartburn and acid reﬂ ux

Also known as gastroesophageal reﬂ ux disease (GERD),this is caused by

regurgitation of stomach contents into the esophagus due to an incompe-

tent antireﬂ ux mechanism at the gastroesophageal junction (GEJ).

Typical features

• Site: midline, retrosternal

• Radiation: to the throat and occasionally the infrascapular regions

• Nature: burning

• Aggravating factors: worse after meals and when performing postures

that raise the intra-abdominal pressure (bending, stooping, lying

supine). Also worse during pregnancy

• Associated symptoms: often accompanied by acid or bitter taste (acid

regurgitation) or sudden ﬁ

lling of the mouth with saliva* (waterbrash)

* The salivary glands can produce 10 mL of saliva/minute—the esophag eo-salivary response.

207

ESOPHAGEAL SYMPTOMS

Acid reﬂ ux may be worsened by certain foods (alcohol, caffeine, choc-

olate, fatty meals) and some drugs (calcium channel blockers, anticholiner-

gics) that act to d the GEJ sphincter pressure.

0 Hiatal hernia is another important cause of reﬂ

ux symptoms—be sure

to inquire about this in the history.

Dyspepsia

This is commonly known as indigestion. It is very common and presents

as a variety of symptoms:

• Upper abdominal discomfort

• Bloating

• Belching

Be on the alert for features suggestive of a serious pathology (anemia,

weight loss, dysphagia, rectal blood loss, melena, and abdominal masses).

Box 9.1 Some causes of dysphagia

• Oral: painful mouth ulceration, oral, or throat infections

• Neurological: cerebrovascular event, bulbar and pseudobulbar

palsies, myasthenia gravis

• Dysmotility: achalasia, systemic sclerosis, presbyesophagus

• Mechanical: pharyngeal pouch, esophageal cancer, peptic stricture,

other benign strictures, extrinsic compression of the esophagus

(e.g., large lung or thyroid tumor)

CHAPTER 9 Abdomen 208

Nausea, vomiting, and vomitus

Nausea and vomiting

Nausea* is a feeling of sickness—the inclination to vomit. It usually occurs

in waves and may be associated with retching or heaving. It can last from

seconds to days depending on the cause.

Vomiting (emesis) usually follows nausea and autonomic symptoms, such

as salivation. It is the forceful expulsion of the gastric contents by reﬂ ex

contractions of thoracic and abdominal muscles. See Box 9.2 for causes.

The vomiting center is in the medulla and is composed of many efferent

nuclei in serial communication with each other. When the entire circuit is

activated by afferent stimuli, the complete set of actions required to cause

vomiting is triggered.

Timing

You should be clear on exactly when the vomiting tends to occur, particu-

larly its relation to meals—e.g., vomiting delayed for >1 hour after meals

suggests gastroesophageal obstruction or gastroparesis. Early-morning

vomiting is typical of pregnancy or raised intracranial pressure.

Nature of the vomitus

Although unpleasant, you should inquire about the exact nature of any

vomited material and attempt to see a sample, if possible.

Blood (hematemesis)

Presence of blood indicates bleeding in the upper gastrointestinal tract

(esophagus, stomach, duodenum). A history of bleeding must be explored

in the context of other abdominal symptoms ( Box 9.3 ). Ask especially

about the following:

• Amount of blood and exact nature of it (see Box 9.4 )

• Previous bleeding episodes, treatment and outcome (e.g., previous

surgery?)

• Cigarette smoking

• Use of drugs such as aspirin, NSAIDs, and warfarin

0 Remember to ask about weight loss, dysphagia, abdominal pain, and

melena (consider the possibility of neoplastic disease).

Bile

Assess the presence or absence of bile. Remember that bile comes largely

in two colors—the green pigment (biliverdin) often seen to color the

vomitus in the absence of undigested food. The yellow pigment (bilirubin)

appears as orange, often occurring in small lumps.**

Undigested food without bile suggests a lack of connection between the

stomach and the small intestine (e.g., pyloric obstruction).

** This is the answer to the age-old question, why are there always carrots in vomit?. The orange

globules are, in fact, dyed with bilirubin. We suggest saving that fact for your next dinner party.

* Nausea comes from the Latin, meaning “sea-sickness,” through the Greek naus, meaning “ship.”

NAUSEA, VOMITING, AND VOMITUS

209

Box 9.2 Important causes of vomiting

• Acute: GI tract infections (viral gastroenteritis, e.g., food poisoning,

Norwalk, viral hepatitis), systemic bacterial infection, mechanical

bowel obstruction, alcohol intoxication, acute upper GI bleed,

urinary tract infection

• Chronic: pregnancy, uremia, drugs (narcotics, digitalis, aminophylline,

cancer chemotherapy), gastroparesis (diabetes mellitus, scleroderma,

drugs)

• Other: peptic ulcer disease, motor disorders (post-surgery or

autonomic dysfunction), hepatobiliary disease, alcoholism, cancer

2 Don’t forget about central nervous system and vestibular problems.

Box 9.3 Causes of upper GI bleeding

• Peptic ulceration

• Erosive or ulcerative esophagitis

• Gastritis

• Varices (esophageal/gastric)

• Gastric and esophageal tumors

• Mallory–Weiss tear

• Dieulafoy’s lesion

• Vascular anomalies (e.g., angiodysplasia, AV malformation)

• Hereditary hemorrhagic telangiectasia

• Connective tissue disorders

• Vasculitis

• Bleeding disorders

Box 9.4 Nature of hematemesis

• Large volume of fresh, red blood suggests active bleeding (coincident

liver disease and/or heavy alcohol intake may suggest bleeding

esophageal varices; abdominal pain and heartburn suggest a gastric

or esophageal source such as a peptic ulceration or GERD).

• Small streaks at the end of prolonged retching may indicate minor

esophageal trauma at the GEJ (Mallory–Weiss tear).

• Coffee-grounds: This term is used for blood that has been altered by

exposure to stomach acid as the result of a bleeding site superior to

the ligament of Trietz. It appears brown and in small lumps.

CHAPTER 9 Abdomen 210

Abdominal pain

Like pain in any other region, abdominal pain may present in very different

ways and has many different causes. You should establish the site, radia-

tion, severity, character, frequency, duration, any exacerbating or relieving

factors, and associated symptoms.

Site

Like most organs, those in the abdomen cannot be felt directly—the pain

is referred to areas of the abdominal wall according to the organ’s embry-

ological origin (see Box 9.5 and Fig. 9.3 ).

• Ask the patient to point to the area affected. They often ﬁ nd

this

challenging and may indicate a wide area. In this case, ask them to

use one ﬁ

nger and point to the area of maximum intensity: “Use one

ﬁ nger and point to where the pain is worst.”

A very localized pain may originate from the parietal peritoneum. For

example, appendicitis may begin as an umbilical pain (referred from the

appendix) then move to the right iliac fossa as the inﬂ ammation spreads

to the peritoneum overlying the appendix.

Radiation

Ask the patient if the pain is felt elsewhere or if they have any other pains

(they may not associate the radiated pain with the abdominal pain).

Some examples include the following:

• Right scapula: gallbladder

• Shouldertip: diaphragmatic irritation

• Mid-back: pancreas

Character

Ask the patient what sort of pain it is. Give some examples if they have

trouble, but be careful not to lead the patient. A couple of examples

include the following:

• Colicky: This is pain that comes and goes in waves and indicates

obstruction of a hollow, muscular-walled organ (intestine, gallbladder,

bile duct, ureter).

• Burning: This usually indicates an acid cause and is related to the

stomach, duodenum, or lower end of the esophagus.

Aggravating and relieving factors

Ask the patient what appears to make the pain better or worse—or what

they do to get rid of the pain if they suffer from it often.

Box 9.5 Sites of abdominal pain and embryological origins

• Epigastric: foregut (stomach, duodenum, liver, pancreas, gallbladder)

• Periumbilical: midgut (small and large intestines including appendix)

• Suprapubic: hindgut (rectum and urogenital organs)

ABDOMINAL PAIN

211

Findings

Some characteristic pains:

• Renal colic: colicky pain at the renal angles ± loins, which are tender

to touch, radiating to the groin, testicles, or labia. Typically, the patient

writhes about, unable to ﬁ

nd a position that relieves the pain.

• Bladder pain: a diffuse severe pain in the suprapubic region

• Prostatic pain: a dull ache that may be felt in the lower abdomen,

rectum, perineum, or anterior thighs.

• Urethral pain: variable in presentation, ranging from a tickling

discomfort to a severe sharp pain felt at the end of the urethra (tip of

the penis in males) and exacerbated by micturition. It can be so severe

that patients attempt to hold urine, causing yet more problems.

• Small bowel obstruction : colicky central pain associated with vomiting,

abdominal distension ± constipation

• Colonic pain: as with small bowel obstruction but sometimes

temporarily relieved by defecation or passing ﬂ atus

• Bowel ischemia: dull, severe, constant, right upper quadrant or central

abdominal pain exacerbated by eating

• Biliary pain: severe, constant, right upper quadrant or epigastric pain

that can last hours and is often worse after eating fatty foods.

• Pancreatic pain: epigastric, radiating to the back and partly relieved by

sitting up and leaning forward

• Peptic ulcer pain: dull, burning pain in the epigastrium. Typically

episodic at night, waking the patient from sleep. It is exacerbated by

eating and sometimes relieved by consuming milk or antacids.

Foregut

Midgut

Hindgut

Fig. 9.3 Typical sites of pain according to origin.

CHAPTER 9 Abdomen 212

Bowel habit

Ask patients how often they move their bowels and if this has changed

recently. Ask also about the other symptoms on these pages.

Constipation

This disorder can mean different things to different people. Normal bowel

habit ranges from 3 times/day to once every 3 days.

Constipation is the passage of stool <3 times/week, or stools that are

hard or difﬁ cult to pass. See Box 9.6 for causes.

A thorough history should include the following:

• Duration of constipation

• Stool size and consistency

• Straining, particularly at the end of evacuation

• Associated symptoms (nausea, vomiting, weight loss)

• Pain on defecation

• Rectal bleeding

• Intercurrent diarrhea

• Fluid and ﬁ ber

intake

• Depression, lack of exercise

• Drug history (prescription and overthecounter). Particularly ask about

use of codeine, antidepressants, aluminum, and calcium antacids.

• Metabolic or endocrine diseases (thyroid disorders, hypercalcemia,

diabetes, pheochromocytoma, Hirshsprung’s disease)

• Neurological problems (autonomic neuropathy, spinal cord injury,

multiple sclerosis)

Diarrhea

This is deﬁ ned as an increase in stool volume (>200mL daily) and

frequency(3/day). There is also a change in consistency to semiformed or

liquid stool. See Box 9.7 for causes.

Establish the time course, since acute diarrhea is suggestive of infection.

Ask especially about the following:

• Color, consistency, offensive smell, ease of ﬂ ushing

• Duration

• Does the diarrhea disturb the patient’s sleep?

• Is there any blood, mucus, or pus?

• Is there associated pain or colic?

• Is there urgency?

• Nausea, vomiting, weight loss?

• Any difference if the patient fasts?

•

No change in secretory diarrhea—e.g., E. coli, Staph. aureus

•

Disappears on fasting: osmotic diarrhea

• Foreign travel

• Recent antibiotics

BOWEL HABIT

213

Rectal bleeding and melena

There are many causes of rectal blood loss ( Box 9.9 ) but, as always, a

detailed history will help. Determine the following:

• Amount

0 Small amounts can appear dramatic, coloring toilet water red.

• Nature of the blood (red, brown, black)

• Is it mixed within the stool or is it on the stool?

• Is it spattered over the bowl or with the stool, or only seen on the

paper?

• Any associated features (Mucus may indicate inﬂ ammatory

bowel

disease or colonic cancer.)

Box 9.6 Some causes of constipation

• Low-ﬁ ber diet

• Physical immobility

• Functional bowel disease

• Drugs (e.g.,opiates, antidepressants, aluminumantacids).

• Metabolic and endocrine diseases (e.g.,hypothyroidism, hypercalcemia,

hypokalemia, diabetes mellitus, porphyria, pheochromocytoma)

• Neurological disorders (e.g., autonomic neuropathy, spinal cord

injury, multiple sclerosis)

• Colonic stricture

• Anorectal disease (e.g., anal ﬁ

ssure—causes pain to the extent that

the patient may avoid defecating altogether)

• Habitual neglect

• Depression

• Dementia

Box 9.7 Some causes of diarrhea

• Malabsorption: may cause steatorrhea, a fatty, pale stool that is

extremely odorous and difﬁ cult to ﬂ ush. See Box 9.8 on b p. 214.

• iIntestinal motility: hyperthyroidism, irritable bowel syndrome (see

below).

• Exudative: inﬂ

ammation of the bowel causes small volume, frequent

stools, often with blood or mucus (e.g., colonic carcinoma, Crohn’s

disease, ulcerative colitis)

• Osmotic: large volume of stool that disappears with fasting. Causes

include lactose intolerance, gastric surgery.

• Secretory: high volume of stool that persists with fasting. No pus,

blood or excessive fat. Causes include gastrointestinal infections,

carcinoid syndrome, villous adenoma of the colon, Zollinger–Ellison

syndrome, vasoactive intestinal polypeptide (VIP)-secreting tumor.

CHAPTER 9 Abdomen 214

Melena

This is jet-black, tar-like, and pungent-smelling stool representing blood

from the upper GI tract (or right side of the large bowel) that has been

altered by passage through the gut.

The presence of melena is often asked about in hospitalized patients,

but those who have smelled true melena rarely forget the experience!

Ask about iron supplementation or bismuth-containing compounds. These

cause blackened stools but without the melena smell or consistency.

Mucus

This is a clear, viscoid secretion of the mucus membranes.* It contains

mucus, epithelial cells, leukocytes, and various salts suspended in water.

The presence of mucus in or on stools may indicate the following:

• Inﬂ

ammatory bowel disease

• Solitary rectal ulcer

• Small or large bowel ﬁ stula

• Colonic villous adenoma

• Irritable bowel syndrome

Flatus

Small amounts of gas frequently escape from the bowel via the mouth

(eructation) and anus. A notable excess of this is a common feature of

both functional and organic disorders of the gastrointestinal tract.

It is often associated with abdominal bloating and caused by the fermen-

tation of certain foods by colonic ﬂ ora.

Excessive ﬂ atus is a particular feature of the following

• Hiatal hernia

• Peptic ulceration

• Chronic gallbladder disease

• Air-swallowing (aerophagy)

• High-ﬁ ber

diet

Box 9.8 Fat malabsorption (steatorrhea)

This is a common feature of pancreatic insufﬁ ciency (e.g., due to chronic

pancreatitis, cystic ﬁ brosis). It is also caused by diseases such as celiac

disease, inﬂ ammatory bowel disease, blind bowel loops, and short

bowel syndrome.

You should be aware of these features and explore them all fully if

one is mentioned by the patient:

• Pale stool

• Offensive smelling

• Poorly formed

• Difﬁ

cult to ﬂ ush

(ﬂ oats)

* Think “slime” or even “snot.” Patients may ﬁ nd this easier to understand: “Have you noticed any

slime-like mucus in your stools?”

BOWEL HABIT

215

Box 9.9 Causes of lower GI bleeding

• Hemorrhoids

• Anal ﬁ ssure

• Diverticular disease

• Colonic carcinoma

• Colonic polyp

• Angiodysplasia

• Inﬂ

ammatory bowel disease

• Ischemic colitis

• Meckel’sdiverticulum

• Small bowel disease (e.g., tumor, diverticulae, intussusception,

Crohn’s)

• Solitary rectal ulcer

• Hemobilia (bleeding into the biliary tree)

CHAPTER 9 Abdomen 216

Jaundice and pruritus

Jaundice

Jaundice (icterus) is a yellow pigmentation of skin, sclera, and mucosa

caused by excess bilirubin in the body ﬂ uids. It is usually considered a sign,

as it is seen on examination. See also b p. 51 and Box 9.10 .

Ask about the following:

• Color of the urine (dark in cholestatic jaundice)

• Color and consistency of the stools (pale in cholestatic jaundice)

• Abdominal pain (e.g., caused by gallstones)

While the following factors should be included in any thorough history,

you should make a special point of asking about them:

• Previous blood transfusions

• Past history of jaundice

• Drugs (e.g., antibiotics, NSAIDs, oral contraceptives, phenothiazines)

• IV drug use

• Tattoos and body piercing

• Foreign travel

• Sexual history

• Family history of liver disease

• Alcohol consumption

• Any personal contacts who also have jaundice

Pruritus

This is itching of the skin and may be either localized or generalized.

It has many causes—it is particularly associated with cholestatic liver

disease (e.g., primary biliary cirrhosis, sclerosing cholangitis).

Box 9.10 Causes of jaundice

Prehepatic

• Hemolysis

• Gilbert’s disease

• Dubin–Johnson syndrome

• Rotor syndrome

Hemodialysis

• Hepatocellular

• Cirrhosis

• Acute hepatitis (viral, alcoholic, autoimmune, drug induced)

• Liver tumors

• Cholestasis from drugs (e.g., chlorpromazine)

Posthepatic

Obstruction of biliary outﬂ

ow due to the following:

•

Luminal obstruction: gallstones

• Wall pathology: congenital bile duct abnormalities, primary biliary

cirrhosis, trauma, tumor

• External compression: pancreatitis, lymphadenopathy, pancreatic

tumor, ampulla of Vater tumor

ABDOMINAL SWELLING

217

Abdominal swelling

The ﬁ ve classic causes of abdominal swelling (the 5 F’s) are shown in

Box 9.11 . To these you should also add tumor .

In decompensated cirrhosis, a combination of portal (sinusoidal) hyper-

tension and Na and H

2

O retention favors the transudation of ﬂ uid into

the peritoneal cavity (ascites). The resultant swelling may be unsightly. It

can also cause shortness of breath by putting pressure on the diaphragm

from below, particularly when supine, and may be associated with pleural

effusions.

See b p. 672 for the causes and classiﬁ cation of ascites.

Box 9.11 Five causes of abdominal swelling—the 5 F’s

• Fat

• Fluid

• Flatus

• Feces

• Fetus

CHAPTER 9 Abdomen 218

Urinary and prostate symptoms

Urinary frequency

This is the passing of urine more often than is normal for the patient.

Quantify this—how many times in a day—and also ask about the volume

of urine passed each time (you are attempting to decide whether the

patient is producing more urine than normal or simply feeling the urge to

urinate more than normal).

Urgency

This is the sudden need to urinate, a feeling that the patient may not be

able to make it to the toilet in time. Ask about the volume expelled.

Nocturia

This is urination during the night. Does the patient wake from sleep to

urinate? How many times a night? How much urine is expelled each

time?

Urinary incontinence

This is the loss of voluntary control of bladder emptying. Patients may be

hesitant to talk about this, so try to avoid the phrase “wetting yourself.”

“You could ask about it immediately after asking about urgency” “Do you

ever feel the desperate need to empty your bladder? Have you ever not

made it in time?” Or ask about a “loss of control.”

There are ﬁ ve main types of urinary incontinence:

• True: total lack of control of urinary excretion. This suggests a ﬁ stula

between the urinary tract and the exterior or a neurological condition.

• Giggle: incontinence during bouts of laughter. This is common in young

girls.

• Stress: leakage associated with a sudden i in intra-abdominal pressure

of any cause (e.g., coughing, laughing, sneezing)

• Urge: intense urge to urinate such that the patient is unable to get to

the toilet in time. Causes include overactivity of the detrusor muscle,

urinary infection, bladder stones and bladder cancer.

• Dribbling or overﬂ ow: continual loss of urine from a chronically

distended bladder. Typically this occurs in elderly males with prostate

disease.

Terminal dribbling

This is a male complaint and usually indicative of prostate disease. It is a

dripping of urine from the urethra at the end of micturition, requiring an

abnormally protracted shake of the penis and may cause embarrassing

staining of clothing.

Hesitancy

This is difﬁ culty in starting to micturate. The male patient describes stand-

ing and waiting for the urine to start ﬂ owing. Hesitancy is usually due to

bladder outﬂ ow obstruction from prostatic disease or strictures.

URINARY AND PROSTATE SYMPTOMS

219

Dysuria

Pain on micturition is usually described by the patient as “burning” or

“stinging” and is felt at the urethral meatus. Ask whether it is throughout

the passage of urine or only at the end (terminal dysuria).

Hematuria

This is the passage of blood in the urine. It is always an abnormal ﬁ nding.

0 Remember that microscopic hematuria will be undetectable to the

patient, only showing on dip-testing.

Incomplete emptying

This is the sensation that there is more urine left to expel at the end of

micturition. It suggests detrusor dysfunction or prostatic disease.

Intermittency

This is the disruption of urine ﬂ ow in a stop–start manner. Causes include

prostatic hypertrophy, bladder stones, and ureteroceles.

Oliguria and anuria

Oliguria is scanty or low-volume urination and is deﬁ ned as the excretion

of <300mL urine in 24 hours. Causes can be physiological (dehydration) or

pathological (intrinsic renal disease, shock, or obstruction).

Anuria is the absence of urine formation. You should attempt to rule

out urinary tract obstruction as a matter or urgency. Other causes include

severe intrinsic renal dysfunction and shock.

Polyuria

This is excessive excretion of large volumes of urine and must be care-

fully differentiated from urinary frequency (the frequent passage of small

amounts of urine).

Causes vary widely but include the ingestion of large volumes of water

(including hysterical polydipsia), diabetes mellitus (the osmotic effect of

glucose in the tubules results in more urine produced), failure of the action

of antidiuretic hormone (ADH) at the renal tubule (as in diabetes insip-

idus) and defective renal concentrating ability (e.g., chronic renal failure).

0 Remember also to ask the patient about the use of diuretic medication.

CHAPTER 9 Abdomen 220

Appetite and weight

Loss of appetite and changes in weight are rather non-speciﬁ c symptoms

but should raise suspicion of a serious disease if either is severe, pro-

longed, or unexpected.

2 Remember that weight loss has many causes outside of the abdomen

and a thorough systems inquiry should be conducted.

Weight loss may not be noticed by patients if they don’t regularly weigh

themselves—ask about clothes becoming loose.

0 Remember that the patient may have been intentionally losing weight,

throwing you off track. Ask if the loss is expected.

2 Ascites weighs 1kg/L and some patients with liver failure may have

10–20L of ascites, masking any dry-weight loss.

Ask the patient about their eating habit and average daily diet.

Try to determine the following:

• When the symptom was ﬁ rst

noticed

• Quantify the problem. In the case of weight loss, determine exactly

how and over what time period.

• Cause of the anorexia—does eating make the patient feel sick?

• Does eating cause pain (e.g., gastric ulcer, mesenteric angina,

pancreatitis)?

• Any accompanying symptoms (abdominal pain, nausea, vomiting, fever)

Ask also about the following:

• Color and consistency of stools (e.g., steatorrhea?)

• Urinary symptoms (see b p. 218)

• Recent change in temperature tolerance

In every case, you should calculate the patient’s BMI as on b p. 56.

The combination of weight loss with i appetite may suggest malabsorp-

tion or a hypermetabolic state (e.g., thyrotoxicosis).

THE REST OF THE HISTORY

221

The rest of the history

Past medical history

Ask especially about the following:

• Previous surgical procedures, including peri- and postoperative

complications and anesthetic complications

• Chronic bowel diseases (e.g., inﬂ

ammatory bowel disease [IBD],

including recent ﬂ

areups and treatment to date)

• Possible associated conditions (e.g., diabetes with hemachromatosis)

Drug history

Think about drugs that can precipitate abdominal diseases and remember

to ask about over-the-counter drugs. For example:

• Hepatitis: halothane, phenytoin, chlorothiazides, pyrazinamide,

isoniazid, methyl dopa, HMG CoA reductase inhibitors (statins),

sodium valproate, amiodarone, antibiotics, NSAIDs

• Cholestasis: chlorpromazine, sulfonamides, sulfonylureas, rifam-picin,

nitrofurantoin, anabolic steroids, oral contraceptive pill

• Fatty liver: tetracycline, sodium valproate, amiodar-one

• Acute liver necrosis: acetaminophen

0 Ask also about previous blood transfusions.

Smoking

Smokers are at i risk of peptic ulceration, esophageal cancer, and colo-

rectal cancer. Smoking may also have a detrimental outcome on the natu-

ral history of Crohn’s disease. There is some evidence that smoking may

protect against ulcerative colitis.

Alcohol

As always, a detailed history is required—see b p. 37. If dependence is

suspected, run through the CAGE questionnaire—see Box 9.12 .

Box 9.12 CAGE questionnaire

A positive response to any of the four questions may indicate someone

at risk of alcohol abuse. A positive answer to two or more questions

makes the presence of alcohol dependence likely.

C Have you ever felt that you should C ut down your drinking?

A Have you ever got A ngry when someone suggested that you should

cut down?

G Do you ever feel G uilty about your drinking?

E Do you ever need an E ye-opener in the morning to steady your

nerves or get rid of a hangover?

CHAPTER 9 Abdomen 222

Family history

Ask especially about a history of inﬂ ammatory bowel disease, celiac

disease, peptic ulcer disease, hereditary liver diseases (e.g., Wilson’s,

hemochromatosis) bowel cancer, jaundice, anemia, splenectomy, and

cholecystectomy.

Social history

• Risks of exposure to hepatotoxins and hepatitis through occupation

• Tattoos

• Illicit drug use (especially sharing needles)

• Social contacts with a similar disease (particularly relevant to jaundice)

• Recent foreign travel

Dietary history

• Amount of fruit, vegetables and ﬁ ber in the diet

• Evidence of lactose intolerance

• Change in symptoms related to eating certain food groups

• Sensitivities to wheat, fat, caffeine, gluten

OUTLINE EXAMINATION

223

Outline examination

As always, ensure adequate privacy. Ideally, the patient should be lying ﬂ at

with the head propped on a single pillow, arms lying at the sides.

The abdomen should be exposed at least from the bottom of the ster-

num to the symphysis pubis—preferably the whole upper torso is uncov-

ered. Do not expose the genitalia until needed.

The examination should follow an orderly routine. The authors’ sugges-

tion is shown in Box 9.13 . It is standard practice to start with the hands and

work proximally—this establishes a physical rapport before you examine

more sensitive areas.

General inspection

Looking at the patient from the end of the bed, assess their general health

and look for any obvious abnormalities described in b Chapter 3 before

moving closer. Look especially for the following:

• High or low body mass

• The state of hydration

• Fever

• Distress

• Pain

• Muscle wasting

• Peripheral edema

• Jaundice

• Anemia

Box 9.13 Framework for abdominal examination

• General inspection

• Hands

• Arms

• Axillae

• Face

• Chest

• Inspection of abdomen

• Auscultation

• Palpation of abdomen

• Light

• Deep

• Speciﬁ c

organs

• Examination of hernial oriﬁ ces

• External genitalia

• Percussion (± examination for ascites)

• Digital examination of the anus, rectum ± prostate

CHAPTER 9 Abdomen 224

Hand and upper limb

Take the patient’s right hand in yours and examine carefully for the fol-

lowing signs.

Nails

See also Chapter 4.

• Leukonychia: whitening of the nail bed due to hypoalbuminemia

(e.g., malnutrition, malabsorption, hepatic disease, nephrotic syndrome)

• Koilonychia: spooning of the nails, making a concave shape instead

of the normal convexity. Causes include congenital and chronic iron

deﬁ ciency.

• Muehrcke’s lines: transverse white lines. They are seen in

hypoalbuminemic states, including severe liver cirrhosis.

• Clubbing: described on b p. 191. abdominal causes are cirrhosis,

inﬂ

ammatory bowel disease, and celiac disease.

• Blue lunulae: a bluish discoloration of the normal lanulae seen in

Wilson’s disease

Palms

• Palmar erythema: “liver palms.” This is a blotchy reddening of the

palms of the hands, especially affecting the thenar and hypothenar

eminences. It can also affect soles of the feet. It is associated with

chronic liver disease, pregnancy, thyrotoxicosis, rheumatoid arthritis,

polycythemia, and (rarely) chronic leukemia. It can also be a normal

ﬁ nding.

• Dupuytren’s contracture: thickening and ﬁ

brous contraction of the

palmar fascia. In early stages, palpable irregular thickening of the fascia

is seen, especially that overlying the fourth and ﬁ

fth metacarpals. This

can progress to a ﬁ xed ﬂ exion deformity of the ﬁ ngers starting at the

ﬁ fth ﬁ nger and working across to the third or second. Often bilateral,

it may also affect the feet. It is seen especially with alcoholic liver

disease but may also be seen in manual workers (or may be familial).

• Anemia: Pallor in the palmar creases suggests signiﬁ cant

anemia.

• Rash: Remember syphilis in the differential.

Hepatic ﬂ ap (asterixis)

This is identical to the ﬂ ap seen in hypercapnic states (see b p. 191).

Ask the patient to stretch out their hands in front of them with the

hands dorsiﬂ exed at the wrists and ﬁ ngers out-stretched and separated

(see Fig.9.4 ).

The patient should hold that position for at least 15 seconds. If ﬂ ap is

present, the patient’s hands will move in jerky, irregular ﬂ exion and exten-

sion at the wrist and MCP joints. The ﬂ ap is nearly always bilateral. It may

be subtle and intermittent.

This is characteristic of encephalopathy due to liver failure.

If a sign of hepatic encephalopathy in a patient with previously com-

pensated liver disease, it may have been precipitated by infection, diuretic

medication, electrolyte imbalance, diarrhea or constipation, vomiting, cen-

trally acting drugs, upper GI bleeding, abdominal paracentesis, or surgery.

HAND AND UPPER LIMB

225

Upper limb

Examine the arms for any signs of the following:

• Bruising: This may be a sign of the following:

•

Hepatocellular damage and the resulting coagulation disorder

•

Thrombocytopenia due to hypersplenism

•

Marrow suppression with alcohol

• Petechiae: pin-prick bleeds that do not blanch with pressure. Possibly a

sign of thrombocytopenia

• Muscle wasting: seen as a decrease in muscle mass, possibly with

overlying skin hanging loosely. A late manifestation of malnutrition and

often seen in patients with chronic alcoholic liver disease

• Scratch marks (excoriations): suggests itch (pruritus) is present and

may be the only visible feature of early cholestasis

0 Be careful not to miss AV ﬁ

stulae or hemodialysis catheters!

Axillae

Examine carefully for the following:

• Lymphadenopathy

• Acanthosis nigricans (a thickened, blackening of the skin. Velvety in

appearance. May be associated with intra-abdominal malignancy)

Fig. 9.4 Testing for hepatic ﬂ ap. The patient should hold their arms outstretched

with wrists dorsiﬂ exed and ﬁ ngers extended and abducted for at least 15 seconds.

CHAPTER 9 Abdomen 226

Face and chest

Eyes

Ask the patient to look straight ahead while you look closely at their eyes,

orbits, and surrounding skin. Then ask the patient to look up while you

gently retract the lower lid with a ﬁ nger, looking at the underlying sclera

and conjunctiva. Look especially for the following:

• Jaundice: a yellow discoloration of the sclera. This is usually the ﬁ rst

place that jaundice can be seen. This sign is particularly useful in

patients with dark skin tones in whom jaundice would not otherwise

be obvious.

• Anemia: pallor of the conjunctivae. You will need experience to spot

this easily.

• Kayser–Fleisher rings: best seen with a slit lamp in an ophthalmology

clinic. A greenish-yellow pigmented ring is just inside the cornea-scleral

margin. It is due to copper deposition and seen in Wilson’s disease.

• Xanthelasma: raised yellow lesions caused by a buildup of lipids

beneath the skin. They are often seen encircling the eyes, especially at

the nasal side of the orbit.

Mouth

Ask the patient to show you their teeth then open wide. Look carefully at

the state of the teeth, the tongue, and the inner surface of the cheeks. You

should also subtly attempt to smell the patient’s breath.

Angular stomatitis

This is a reddening and inﬂ ammation at the corners of the mouth. It is a

sign of thiamine, vitamin B

12

, and iron deﬁ ciencies.

Circumoral pigmentation

Hyperpigmented areas surround the mouth. This is seen in Peutz–Jegher’s

syndrome.

Dentition

Note dentures or if there is evidence of tooth decay.

Telangiectasia

This is dilatation of the small vessels on the gums and buccal mucosa, seen

in Osler–Weber–Rendu syndrome.

Gums

Look especially for ulcers (causes include celiac disease, inﬂ ammatory

bowel disease, Behçet’s disease and Reiter’s syndrome) and hypertro-

phy (caused by pregnancy, phenytoin use, leukemia, scurvy [vitamin C

deﬁ ciency],or inﬂ ammation [gingivitis]).

Breath

Smell especially for the following:

• Fetor hepaticus: a sweet-smelling breath

• Ketosis: sickly sweet pear-drop smelling breath

• Uremia: ﬁ shy

smell

227

FACE AND CHEST

Tongue

Look especially for the following:

• Glossitis: smooth, erythematous swelling of the tongue. Causes include

deﬁ ciencies of iron, vitamin B

12

, and folate.

• Macroglossia: enlarged tongue. Causes include amyloidosis,

hypothroidism, acromegaly, Down syndrome, and neoplasia.

• Leukoplakia: a white-colored thickening of the tongue and oral mucus

membranes. This is a premalignant condition caused by smoking, poor

dental hygiene, alcohol, sepsis, and syphilis.

• Geographical tongue: painless red rings and lines on the surface of the

tongue looking like a map. It can be caused by vitamin B

2

(riboﬂ avin)

deﬁ ciency or may be a normal variant.

Candidiasis

Also known as thrush , this is a fungal infection of the oral membranes seen

as creamy, white curd-like patches that can be scraped off, revealing ery-

thematous mucosa below. Causes include immunosuppression, antibiotic

use, poor oral hygiene, iron deﬁ ciency, and diabetes.

Neck

Examine the cervical and supraclavicular lymph nodes as on b p. 58.

Look especially for a supraclavicular node on the left-hand side, which,

when enlarged, is called Virchow’s node (Troisier’s sign—suggestive of

gastric malignancy).

Chest

Look at the anterior chest and look especially for the signs listed below.

Spider nevi

These are telangiectatic capillary lesions.

• A central red area with engorged capillaries spreading out from it in a

spidery manner

• Caused by engorgement of capillaries from a central feeder vessel

• If the lesion is truly a spider nevus, it will be completely eliminated by

pressure at the center from a penpoint or similar instrument and will

ﬁ

ll outward when the pressure is released.

• Can range in size from those that are only just visible to up to 5 or

6mm in diameter

• Found in the distribution of the superior vena cava (see Fig. 9.5 )

• A normal adult is allowed up to 5 spider nevi.

• Causes include chronic liver disease and estrogen excess.

Gynecomastia

This is the excessive development of male mammary glands due to ductal

proliferation such that they resemble postpubertal female breasts.

• This is often embarrassing for the patient, so be sensitive in your

approach.

• It is caused by alcoholic liver disease, congenital adrenal hyperplasia,

and several commonly used drugs, including spironolactone, digoxin,

and cimetidine.

• It can also be seen during puberty in the normal male.

CHAPTER 9 Abdomen 228

Fig. 9.5 Distribution of drainage to the superior vena cava and the area where

one should look for spider nevi. The normal adult may have up to 5 such lesions.

INSPECTION OF ABDOMEN

229

Inspection of abdomen

With the abdomen exposed, you should make a careful and methodical

inspection. Squat by the side of the bed or exam table so that the patient’s

abdomen is at your eye level when looking for waves or pulsations.

Note especially the features discussed on these pages.

Scars

These may be the result of trauma or previous surgery ( Fig. 9.6 ). Recent

scars will be pink and vascular. Old scars are white and may be indurated.

Laproscopic surgery scars may be hidden in skin folds or the umbilicus.

Abdominal distension

Does the abdomen look swollen? Consider the 5 F’s ( Box 9.11 b p. 217)

and note the state of the umbilicus (everted? deep?).

Focal swellings

Treat an abdominal swelling as you would do any other lump (b p. 88) and

bear in mind the underlying anatomy and possible organ involvement.

Divarication of the recti

Particularly in the elderly and in patients who have had abdominal surgery,

the twin rectus abdominis muscles may separate laterally on contraction,

causing the underlying organs to bulge through the resultant midline gap.

Ask the patient to lift their head off the bed or to sit up slightly. Watch

for the appearance of a longitudinal midline bulge.

Prominent vasculature

If veins are seen coursing over the abdomen, note their exact location.

Attempt to map the direction of blood ﬂ ow within them:

• Place two ﬁ

ngers at one end of the vein and apply occlusive pressure.

• Move one ﬁ

nger along the vein, emptying that section of blood in a

milking action.

• Release the pressure from one ﬁ nger and watch for the ﬂ

ow of blood

back into the vein.

‘Mercedes-Benz’

scar of liver

transplantation

Upper midline

Paramedian

Lower midline

Appendix

Right

subcostal

Renal

Left inguinal

Suprapubic

Fig. 9.6 Some common abdominal surgical scars.

CHAPTER 9 Abdomen 230

• Repeat, emptying blood in the other direction.

• Given the venous valves, you should be able to determine the

direction of blood ﬂ

ow in that vein.

Inferior ﬂ ow of blood suggests superior vena cava (SVC) obstruction.

Superior ﬂ ow of blood suggests inferior vena cava (IVC) obstruction.

Flow radiating out from the umbilicus (caput medusae) indicates portal

vein hypertension (porto-systemic shunting occurs through the umbilical

veins which become engorged).

Obvious pulsations

Look across the abdomen for any pulsations. A pulsatile, expanding mass

in the epigastrium may be an abdominal aortic aneurysm.

Peristaltic waves

These are usually only seen in thin, ﬁ t, young individuals. A very obvious

bowel peristalsis is seen as rippling movements beneath the skin and may

indicate intestinal obstruction.

Striae

Stretch marks are pink or white streaky lines caused by changes in the ten-

sion of the abdominal wall. These may be normal in rapidly growing pubes-

cent teens. They are also seen in obesity, pregnancy (striae gravidarum),

and ascites and following rapid weight loss or abdominal paracentesis.

Bear in mind that these will turn pink or purple in Cushing’s syndrome,

as will other scars (see b p. 115).

Skin discoloration

There are two classical patterns of bruising or discoloration indicating the

presence of retroperitoneal blood (seen especially in pancreatitis):

Cullen’s sign: discoloration at the umbilicus and surrounding skin

Grey-Turner’s sign: discoloration at the ﬂ anks

Stomas

Look for surgical stomas or ﬁ stulae, noting their exact location, nature of

the stoma, and appearance of the exposed mucosa (if any). Remember

that a stoma may be from the large bowel, small bowel, or renal tract.

Look also at the contents of the stoma bag, noting any abnormalities such

as diarrhea, pus, mucus, or blood.

• Colostomy: usually seen in the left iliac fossa and will be ﬂ

ush to the

skin (bag may contain semisolid to formed stool)

• Ileostomy: usually in the right iliac fossa and formed as a spout of

bowel mucosa extending from the abdominal wall to prevent the

luminal contents from harming the abdominal wall (bag will contain

semi-formed and liquid stool)

• Urostomy: often formed as an ileal conduit with ureters connected to

a portion of small bowel and then to the abdominal wall. Usually in the

right iliac fossa (bag will contain urine)

• Nephrostomy: drainage of urine from the kidney pelvis to the exterior.

Usually a temporary measure following operative procedures to the

renal tract or to decompress an obstructed system. Usually at the

ﬂ

ank (bag will contain urine)

AUSCULTATION

231

Auscultation

This is an important part of the abdominal examination that is easily

missed. Listen before palpation or percussion of the abdomen.

Bowel sounds

These are low-pitched gurgling sounds produced by normal gut peristalsis.

They are intermittent but will vary in timing depending on when the last

meal was eaten. Practice listening to as many abdomens as possible to

understand the normal range of sounds.

Listen with the diaphragm of the stethoscope just below the umbilicus.

• Normal: low-pitched gurgling, intermittent

• High-pitched: often called tinkling. These sounds are suggestive of

partial or total bowel obstruction.

• Borborygmus: a loud, low-pitched gurgling that can even be heard

without a stethoscope. (The sounds are called borborygmi .) These re

typical of diarrheal states or abnormal peristalsis.

• Absent sounds: If no sounds are heard for 2 minutes, there may be a

complete lack of peristalsis—i.e., a paralytic ileus or peritonitis.

Bruits

These are sounds produced by the turbulent ﬂ ow of blood through a

vessel—similar in sound to heart murmurs. Listen with the diaphragm of

the stethoscope.

Bruits may occur in normal adults but raise the suspicion of pathological

stenosis (narrowing) when heard throughout both systole and diastole.

There are several areas you should listen at on the abdomen:

• Just above the umbilicus over the aorta (abdominal aortic aneurysm)

• Either side of midline just above the umbilicus (renal artery stenosis)

• At the epigastrium (mesenteric stenosis)

• Over the liver (AV malformations, acute alcoholic hepatitis,

hepatocellular carcinoma)

Friction rubs

These are creaking sounds like that of a pleural rub (b p. 199) heard when

inﬂ amed peritoneal surfaces move against each other with respiration.

Listen over the liver and spleen in the right and left upper quadrants,

respectively.

Causes include hepatocellular carcinoma, liver abscesses, recent per-

cutaneous liver biopsy, liver or splenic infarction, and STI-associated peri-

hepatitis (Fitz–Hugh–Curtis syndrome).

Venous hums

Rarely, it is possible to hear the hum of venous blood ﬂ ow in the upper

abdomen over a caput medusa (b p. 230) secondary to portosystemic

shunting of blood.

CHAPTER 9 Abdomen 232

Palpation

General approach

The patient should be positioned lying supine with the head supported by

a single pillow and arms at their sides.

Each of the four quadrants (see b p. 204) should be examined in turn

with light and then by deep palpation before focusing on speciﬁ c organs

(b p. 233). The order in which they are examined doesn’t matter—ﬁ nd

a routine that suits you. Ask the patient if there is any area of tenderness,

and remember to examine this part last.

Before you begin, ask the patient to let you know if you cause any dis-

comfort. You should be able to examine the abdomen without looking at

it closely. Instead, you should watch the patient’s face for signs of pain.

Light palpation

For this use the ﬁ ngertips and palmar aspects of the ﬁ ngers.

• Lay your right hand on the patient’s abdomen and gently press in by

ﬂ

exing at the metacarpophalangeal joints.

If there is pain on light palpation, attempt to determine whether the pain

is worse when you press down or when you release the pressure ( rebound

tenderness ).

If the abdominal muscles seem tense, determine whether it is localized

or generalized. Ensure that the patient is relaxed—it may be helpful for

the patient to bend their knees slightly, relaxing the abdominal muscles.

An involuntary tension in the abdominal muscles, apparently protecting

the underlying organs, is called guarding .

Deep palpation

• Once all four quadrants are lightly palpated, re-examine using more

pressure. This should enable you to feel for any masses or structural

abnormalities.

If a mass is felt, treat it as you would any other lump, describing its exact

location, size, shape, surface, consistency, mobility, movement with respi-

ration, and tenderness and whether or not it is palatial.

It is often possible to detect the putty-like consistency of stool in the

sigmoid colon. You should treat this as you would any other lump, to be

sure of its nature.

Box 9.14 Signs of peritonitis

• Pain on light palpation

• Rebound tenderness

• Involuntary guarding

• Pain recurring with slight movement of the examining hand

• Absent bowel sounds (b p.231)

PALPATING THE ABDOMINAL ORGANS

233

Palpating the abdominal organs

Liver

The normal liver extends from the ﬁ fth intercostal space on the right

of the midline to the costal margin, hiding under the ribs so is often not

normally palpable—don’t worry if you can’t feel one.

• Using the ﬂ

at of the right hand, start palpation from the right iliac fossa.

• You should angle your hand such that the index ﬁ nger is aligned with

the costal margin (see

Fig. 9.7 ).

• Exert gentle pressure and ask the patient to take a deep breath.

• With each inward breath, your ﬁ

ngers should drift slightly superiorly

as the liver moves inferiorly with the diaphragm. Relax the pressure on

your hand slightly at the height of inspiration.

• If the liver is just above the position of your hand, the lateral surface

of your index ﬁ

nger will strike the liver edge and glide over it with a

palpable step.

• If the liver is not felt, move your hand 1–2cm superiorly and feel again.

• Repeat the process, moving toward the ribs until the liver is felt.

If a liver edge is felt, you should note the following:

• How far below the costal margin it extends in ﬁ nger-breadths

or

(preferably) centimeters and record the number carefully

• Nature of the liver edge (is the surface smooth or irregular?)

• Presence of tenderness

• Whether the liver is pulsatile

Fig. 9.7 Palpation of the liver—align the lateral surface of the index ﬁ nger with the

costal margin and palpate from the right iliac fossa to the ribs in a step-wise fashion.

CHAPTER 9 Abdomen 234

Findings

• It is often possible to palpate the liver just below the costal margin at

the height of inspiration in normal, healthy, thin people.

• An enlarged liver has many causes.

• A normal liver may be palpable in patients with COPD or

asthma in whom the chest is hyperexpanded or in patients with a

subdiaphragmatic collection.

• The liver may also be palpable in the presence of Riedel’s lobe —a

normal variant in which a projection of the liver arises from the

inferior surface of the right lobe. It is more common in females and is

commonly mistaken for a right kidney or enlarged gallbladder.

Gallbladder

The gallbladder lies at the right costal margin at the tip of the ninth rib,

at the lateral border of the rectus abdominis. Normally it is only palpable

when enlarged from biliary obstruction or acute cholecystitis ( Box 9.15 ).

• Felt as a bulbous, focal, rounded mass that moves with inspiration

• Position the right hand perpendicular to the costal margin and palpate

in a medial to lateral direction (see Fig. 9.8 ).

Spleen

The spleen is the largest lymphatic organ, which varies in size and shape

between individuals—roughly the size of a clenched ﬁ st (12 × 7cm).

Normally, it is hidden beneath the left costal cartilages and is not palpable.

Enlargement of the spleen occurs in a downward direction, extending

into the left upper quadrant (and even the left lower quadrant) across

toward the right iliac fossa.

• It is palpated using a similar technique to that used to examine the

liver (b p. 233).

• Your left hand should be used to support the left of the ribcage

posterolaterally. Your right hand should be aligned with the ﬁ ngertips

parallel to the left costal margin (see Fig. 9.9 ).

• Start palpation just below the umbilicus in the midline and work

toward the left costal margin, asking the patient to take a deep breath

in and feeling for movement of the spleen under your ﬁ ngers,

much

like palpating the liver.

Box 9.15 Important gallbladder signs

Murphy’s sign

A sign of cholecystitis—pain on palpation over the gallbladder during

deep inspiration. It is positive only if there is NO pain on the left at the

same position.

Courvoisier’s law

In the presence of jaundice, a palpable gallbladder is probably NOT

caused by gallstones.

PALPATING THE ABDOMINAL ORGANS

235

• The inferior edge of the spleen may have a palpable notch centrally,

which will help you differentiate it from any other abdominal mass.

• If a spleen is felt, measure the distance to the costal border in ﬁ nger-

breadths or (preferably) centimeters.

2 A nonpalpable spleen may sometimes become palpable by reposition-

ing the patient. Ask them to roll onto their right-hand side and repeat the

examination as above.

Fig. 9.8 Palpation of the gallbladder—the examining hand should be

perpendicular to the costal margin at the tip of the ninth rib (where the lateral

border of the rectus muscle meets the costal cartilages).

Fig. 9.9 Palpation of the spleen—align the ﬁ ngertips of your right hand with the

left costal border and start palpating just below the umbilicus, working toward the

left upper quadrant.

CHAPTER 9 Abdomen 236

Kidneys

The kidneys are retroperitoneal, lying on the posterior abdominal wall

either side of the vertebral column between T12 and L3 vertebrae. They

move slightly inferiorly with inspiration. The right kidney lies a little lower

than the left (displaced by the liver).

Palpation is bimanual (both hands). You may be able to feel the lower

pole of the right kidney in normal, thin people.

• Place your left hand behind the patient at the right loin.

• Place your right hand below the right costal margin at the lateral

border of the rectus abdominis.

• Keeping the ﬁ

ngers of your right hand together, ﬂ

ex them at the

metcarpophalangeal joints, pushing deep into the abdomen.

• Ask the patient to take a deep breath—you may be able to feel the

rounded lower pole of the kidney between your hands, slipping away

when the patient exhales.

• This technique of using one hand to move the kidney toward the other

is called renal ballottement .

• Repeat the procedure for the left kidney, leaning over and placing your

left hand behind the patient’s left side (see Table 9.1 for comparison

with enlarged spleen).

Findings

• Unilateral palpable kidney: hydronephrosis, polycystic kidney disease,

renal cell carcinoma, acute renal vein thrombosis, renal abscess, acute

pyelonephritis

• Bilateral palpable kidneys: bilateral hydronephrosis, bilateral renal cell

carcinoma, polycystic kidney disease, nephrotic syndrome, amyloidosis,

lymphoma, acromegaly

Table 9.1 Differentiating an enlarged spleen and an enlarged left kidney

Enlarged spleen Enlarged kidney

Impossible to feel above Can feel above the organ

Has a central notch on the leading

edge

No notch, but you may feel the

central hilar notch medially

Moves early on inspiration Moves late on inspiration

Moves inferiomedially on inspiration Moves inferiorly on inspiration

Not ballottable Ballottable

Dullness to percussion Resonant percussion note due to

overlying bowel gas

May enlarge toward the umbilicus Enlarges inferiorly lateral to the

midline

PALPATING THE ABDOMINAL ORGANS

237

Bladder

The urinary bladder is pyramid shaped and lies within the pelvic cavity. It

is not palpable when empty.

As it ﬁ lls, it expands superiorly and may even reach as high as the umbili-

cus or just beyond if very full.

It may be difﬁ cult to differentiate it from an enlarged uterus or ovarian

cyst. The full bladder will be as follows:

• A palpable, rounded mass arising from behind the pubic symphysis

• Dull to percussion

• You will be unable to feel below it.

• Pressure on the full bladder will make the patient feel the need to

urinate.

Fig. 9.11 Palpation of the left kidney.

Fig. 9.10 Palpation of the right kidney.

CHAPTER 9 Abdomen 238

Aorta

The abdominal aorta may be palpated in the midline above the umbilicus,

felt as a longitudinal pulsatile mass. It is particularly palpable in thin people.

If it is felt:

• Position the ﬁ

ngers of each hand on either side of the outermost

palpable margins.

• Measure the distance between your ﬁ

ngers. Normal diameter

82–3cm.

• Decide whether the mass you feel is pulsatile/expansile in itself (in

which case your ﬁ

ngers will move outward) or whether the pulsation

is transmitted through other tissue (in which case your ﬁ ngers

will

move upward). See Fig. 9.12 .

Inguinal lymph nodes

The inguinal chain of lymph nodes lies along the inguinal ligament between the

pubic tubercle and the anterior superior iliac spine and should not be missed.

• Feel along this line for any lumps, treating each as you would any other

lump (b p. 88).

Small, ﬁ

rm, mobile lymph nodes are common in healthy people and are

often the result of minor sepsis or abrasions of the lower limbs.

2 By this stage of the examination, you should have examined the nodes

in the axillae, neck, supraclavicular areas, and inguinal regions.

Hernial oriﬁ ces

Described on b p. 243.

External genitalia

No thorough abdominal examination is complete without examining the

genitalia, although in clinical practice, many leave this out, considering it

inappropriate if you are not suspicious of any genitourinary pathology.

See b Chapters 12 and 14.

(a)

(b)

Fig. 9.12 Palpating a pulsatile mass. If the mass itself is expansile (a), your ﬁ ngers

will move outward. If the pulsatility is being transmitted through overlying tissues

(b), your ﬁ ngers will move upward.

PERCUSSION

239

Percussion

In the examination of the abdomen, percussion is useful for

• Determining the size and nature of enlarged organs or masses

• Detecting shifting dullness (below)

• Eliciting rebound tenderness (b p. 232)

Organs or masses will appear as dullness, whereas a bowel full of gas

will seem abnormally resonant. Good technique comes with experience.

Practice percussing your own liver. Percussion technique is described on

b p. 196.

Examining for ascites

If ﬂ uid is present in the peritoneal cavity (ascites), gravity will cause it to

collect in the ﬂ anks when the patient is lying ﬂ at—this will give dullness to

percussion laterally with central resonance as the bowel ﬂ oats.

Ascites will produce a distended abdomen, often with an everted

umbilicus. If you suspect the presence of ascites:

• Percuss centrally to laterally with the ﬁ

ngers spread and positioned

longitudinally (see

Fig. 9.13 ).

• Listen (and feel) for a deﬁ

nite change to a dull note.

There are then two speciﬁ c tests to perform.

Fig. 9.13 Testing for a ﬂ uid thrill. Ask an assistant to place their hand centrally

on the abdomen—this prevents transmission of the impulse through the abdominal

wall.

CHAPTER 9 Abdomen 240

Shifting dullness*

• Percuss centrally l laterally until dullness is detected. This marks the

air-ﬂ uid level in the abdomen.

• Keep your ﬁ

nger pressed there as you do the following:

• Ask the patient to roll onto the opposite side (i.e., if dullness is

detected on the right, roll the patient to their left-hand side).

• Ask the patient to hold the new position for about half a minute.

• Repeat percussion, moving laterally to central over your mark.

• If the dullness truly was an air-ﬂ

uid level, the ﬂ

uid will now be moved

by gravity away from the marked spot and the previously dull area will

be resonant.

Fluid thrill

In this test, you are attempting to detect a wave transmitted across the

peritoneal ﬂ uid. This is only really possible with massive ascites.

0 You need an assistant for this test (you can ask the patient to help).

• Ask your assistant to place the ulnar edge of one of their hands in the

midline of the abdomen (see Fig. 9.13 ).

• Place your left hand on one side of the abdomen, about level with the

mid-clavicular line.

• With your right hand, ﬂ

ick the opposite side of the patient’s abdomen.

• If a ﬂ uid thrill can be detected, you will feel the ripple from the ﬂ ick

transmitted as a tap to your left hand.

The assistant’s hand is important—it prevents transmission of the impulse

across the surface of the abdominal wall.

Liver

Percuss to map the upper and lower borders of the liver—note the length,

in centimeters, at the mid-clavicular line.

Spleen

Percussion from the left costal margin toward the midaxillary line and the

lower left ribs may reveal dullness suggestive of splenic enlargement that

could not normally be palpated.

Kidneys

Percussion is useful in differentiating an enlarged kidney from an enlarged

spleen or liver. The kidneys lie deep in the abdomen and are surrounded by

perinephric fat, which makes them resonant to percussion. Splenomegaly

or hepatomegaly will be dull.

Bladder

Dullness to percussion in the suprapubic region may be helpful in deter-

mining whether an ill-deﬁ ned mass is an enlarged bladder (dull) or dis-

tended bowel (resonant).

* This is also the punchline to the medical student joke: “What’s the deﬁ nition of ward rounds?”

RECTAL EXAMINATION

241

Rectal examination

This is an important part of the examination and should not be avoided

simply because it is considered unpleasant. It is particularly important in

patients with symptoms of rectal bleeding, tenesmus, change in bowel

habit, and pruritus ani.

2 Remember: If you don’t put your ﬁ

nger in it, you may put your foot

in it.

Before you begin

Explain to the patient what is involved and obtain verbal consent. Choose

your words carefully, adjusting your wording to suit the patient. Favorite

phrases include “hindend,” “backside,” and “bottom.” Tell the patient that

you need to examine their bottom with a ﬁ nger. Warn that it ‘probably

won’t hurt’ but may feel cold and a little unusual.

Ask for another staff member to chaperone, to protect yourself against

future claims of inappropriate treatment and to reassure the patient.*

As you proceed, explain each stage to the patient.

Equipment

• Chaperone

• Nonsterile gloves

• Tissues

• Lubricating jelly

Technique

• With informed verbal consent obtained, ensure adequate privacy.

• Uncover the patient from the waist to the knees.

• Ask the patient to lie in the left lateral position with their legs bent

such that their knees are drawn up to their chest and their buttocks

facing toward you—preferably projecting slightly over the edge of the

bed or exam table.

• Ensure that there is a good light source, preferably a mobile lamp.

• Put on a pair of gloves.

• Separate the buttocks carefully by lifting the right buttock with your

left hand.

• Inspect the perianal area and anus.

•

Look for rashes, excoriations, skin tags, ulcers, anal warts, ﬁ stulous

openings, ﬁ ssures, external hemorrhoids, abscesses, fecal soiling,

blood, and mucus.

• Ask the patient to strain or bear down and watch for the projection of

pink mucosa of a rectal prolapse.

• Lubricate the tip of your right index ﬁ

nger with the jelly.

* Accepted practice is that all providers have a chaperone when performing an intimate examina-

tion. In practice, male providers performing an examination on a female always have a chaperone

present, while the need for a chaperone in other situations is judged individually at the time.

CHAPTER 9 Abdomen 242

• Begin by placing the pulp of your right index ﬁ nger against the anus in

the midline and press in ﬁ rmly but slowly.

•

Most anal sphincters will reﬂ exively tighten when touched but will

quickly relax with continued pressure.

• When the sphincter relaxes, gently advance the ﬁ

nger into the anal

canal.

• Assess anal sphincter tone by asking the patient to tighten around your

ﬁ nger.

• Rotate the ﬁ

nger backward and forward, covering the full 360

*, feeling

for any thickening or irregularities.

• Push the ﬁ

nger further into the rectum.

• Examine all 360˚ by moving the ﬁ nger in sweeping motions. Note:

•

Presence of thickening or irregularities of the rectal wall

•

Presence of palpable feces, and its consistency

•

Any points of tenderness

• Next, in the male, identify the prostate gland, which can be felt

through the anterior rectal wall.

•

The normal prostate is smooth-surfaced, ﬁ rm with a slightly rubbery

texture, measuring 2–3cm diameter. It has two lobes with a palpable

central sulcus.

• Gently withdraw your ﬁ

nger and inspect the glove for feces, blood, or

mucus and note the color of the stool, if present. Test the stool for

occult blood if a testing card is available.

• Tell the patient that the examination is over and wipe any feces or jelly

from the gluteal cleft with the tissues. Some patients may prefer to do

this themselves.

• Thank the patient and ask them to get dressed. You may need to help.

Findings

If any mass or abnormality is identiﬁ ed on the exterior or interior of the

areas examined, its exact location should be noted. It is conventional to

record as the position on a clock face, with 12 o’clock indicating the anter-

ior side of the rectum at the perineum. Other features of the mass should

be recorded as described on b p. 88.

• Benign prostatic hyperplasai (BPH): The prostate is enlarged but the

central sulcus is preserved, often exaggerated.

• Prostate cancer: The gland loses its rubbery consistency and may

become hard. The lateral lobes may be irregular and nodular. There is

often distortion or loss of the central sulcus. If the tumor is large and

has spread locally, there may be thickening of the rectal mucosa either

side of the gland, creating winging of the prostate.

• Prostatitis: The gland will be enlarged, boggy, and very tender.

2 Hints

• If the patient experiences severe pain, with gentle pressure on the

anal opening, consider anal ﬁ ssure, ischiorectal abscess, anal ulcer,

thrombosed hemorrhoid, or prostatitis.

• In this situation, you may have to apply local anesthetic gel to the

anal margin before proceeding. If in doubt, ask a senior resident or

attending physician.

HERNIAL ORIFICES

243

Hernial oriﬁ ces

A hernia is an abnormal protrusion of a structure, organ, or part of

an organ out of the cavity in which it belongs. A hernia can usually be

reduced—i.e., its contents returned to the original cavity either spontane-

ously or by manipulation.

Abdominal hernias are usually caused by portions of bowel protrud-

ing through weakened areas of the abdominal wall. In the abdomen, her-

nias usually occur at natural openings of the abdominal wall (e.g., inguinal

canals, femoral canals, umbilicus, esophageal hiatus) or acquired weak

spots such as surgical scars.

Most abdominal hernias have an expansile cough impulse—asking the

patient to cough will increase the intra-abdominal pressure, causing a vis-

ible or palpable impulse.

Strangulation

Hernias that cannot be reduced (irreducible) may become ﬁ xed and swol-

len as their blood supply is occluded, causing ischemia and necrosis of

the herniated organ. The hernias are painfully swollen with overlying ery-

thema and may cause disruption of normal gut function (e.g., intestinal

obstruction).

An approach to hernias

• Determine the characteristics as you would for any lump (b p. 88),

including position, temperature, tenderness, shape, size, tension, and

composition.

• Make note of the characteristics of the overlying skin.

• Palpate the hernia and feel for a cough impulse.

• Attempt reduction of the hernia.

• Percuss and auscultate the hernia (listening for bowel sounds or bruits).

• Always remember to examine the same site on the opposite side.

Inguinal hernias

Anatomy

The inguinal canal extends from the pubic tubercle to the anterior supe-

rior iliac spine. In the male, it carries the spermatic cord (vas deferens,

blood vessels and nerves). In the female, it is much smaller and carries the

round ligament of the uterus.

After testicular descent, the canal closes but the site is weakened.

The internal ring is an opening in the transversalis fascia lying at the mid-

inguinal point, halfway between the anterior superior iliac spine and the

pubic symphysis (about 1.5cm above the femoral pulse).

The external ring is an opening of the external oblique aponeurosis and

is immediately above and medial to the pubic tubercle (see Fig. 9.14 ).

• Direct inguinal hernia: This is herniation at the site of the external ring.

• Indirect inguinal hernia: This is the most common site (85% of

all hernias). Herniation is through the internal ring with bowel or

omentum traveling down the inguinal canal and may protrude through

the external ring into the scrotum. It is more likely to strangulate than

direct inguinal hernias.

CHAPTER 9 Abdomen 244

Examination

• The patient should be examined standing up and undressed from the

waist down (some hernias may spontaneously reduce when supine).

• Palpate especially for tenderness and consistency of the lump.

•

Herniated omentum will appear rubbery, nonﬂ uctuant, and dull to

percussion.

•

Herniated gut will be ﬂ uctuant and resonant. You may be able to

hear bowel sounds within the hernia.

• With two ﬁ

ngers on the mass, ask the patient to cough, and feel for an

expansile cough impulse.

• Attempt to reduce the hernia by massaging it back toward its

suspected site of origin.

•

For indirect hernias, you should use the ﬂ at of your hand, directing

the hernia from below and guide it through the external ring, up the

inguinal canal laterally toward the internal ring.

• Once reduced, the hernia should not reappear until you release the

pressure.

• With the hernia reduced, try pressing over the site of the internal ring

and asking the patient to cough. An indirect hernia will remain reduced,

whereas a direct hernia will protrude once more (see Table 9.2 ).

Femoral hernias

Anatomy

The femoral canal is the small component of the femoral sheath medial

to the femoral vessels and contains loose connective tissue, lymphatic

vessels, and lymph nodes. It is bordered anteriorly by the inguinal liga-

ment, the pectineal ligament posteriorly, the femoral vein laterally, and the

lacunar ligament medially.

Femoral vein

iliac spine

Inguinal

ligament

Femoral canal

External

inguinal ring

Internal

inguinal ring

Femoral artery

Symphysis pubis

Fig. 9.14 Sites of the internal and external inguinal rings.

HERNIAL ORIFICES

245

Femoral hernias are protrusions of bowel or omentum through this

space (see Box 9.16 for differential). They are more common in middle-

aged and elderly women and can easily strangulate given the small, rigid

opening they pass through.

Examination

• Examine with patient standing up and undressed from the waist down.

• Examine as you would any other hernia and attempt reduction.

• If present, a femoral hernia will appear as a lump just lateral and

inferior to the pubic tubercle, about 2cm medial to the femoral pulse.

Other abdominal wall hernias

• Umbilical/paraumbilical: herniation through a defect near the

umbilicus (considered congenital if identiﬁ ed in children)

• Epigastric: herniation through the linea alba above the umbilicus

• Spigalean: herniation through the linea semilunaris (lateral to the

rectus sheath), usually below and lateral to the umbilicus; rare

• Obturator: herniation through the obturator canal, associated with

increasing age and multiparity

• Perineal: herniation through the pelvic ﬂ

oor diaphragm; rare

• Incisional: herniation through the site of previous surgery. The bulge

is usually seen underlying a surface surgical scar. There is increasing

incidence with advanced age, but it can be caused by wound infection

and associated fasciitis or muscle necrosis.

Table 9.2 Differentiation of inguinal hernias

Indirect inguinal hernia Direct inguinal hernia

Can descend into the scrotum Very rarely descends to the

scrotum

Reduces upward, laterally, backward Reduces upward and backward

Remains reduced with pressure at

the internal ring

Not controlled by pressure over

the internal ring

The causative defect is not palpable Defect in the abdominal wall is

palpable

Reappears at the internal ring and

ﬂ ows medially

Reappears in the same position as

before reduction

Box 9.16 Differential diagnosis of femoral hernia

• Inguinal hernia

• Very large lymph node

• Ectopic testicle

• Psoas bursa or abscess

• Lipoma

CHAPTER 9 Abdomen 246

Important presenting patterns

Chronic liver disease

Any of the following features may be seen. With severe disease and

decompensation, more will become apparent:

Portal hypertension

Raised pressure in the hepatic portal vein is often secondary to liver dis-

ease or noncirrhotic causes such as portal vein thrombosis. Causes are

portosystemic shunting and esophageal varices. Signs include

• Fetor hepaticus

• Splenomegaly

• Risk of gastrointestinal blood loss from varices (anemia, hematemesis,

melena)

• Ascites

• Caput medusae

Alcoholic liver disease

This may cause all the features of chronic liver disease as described

above. In addition, alcohol dependency or addiction is associated with

the following:

• Tolerance

• Withdrawal symptoms

• Alcohol taken in larger amounts and for longer than intended

• Persistent desire to cut down

Men Women

• Gynecomastia • Breast atrophy

• Testicular atrophy • Irregular menses

• Impotence

•

Amenorrhea

• Jaundice • Purpura

• Palmar erythema • Easy bruising

• Leuconychia • Epistaxis

• Clubbing • Menorrhagia

• Spider nevi • Loss of libido

• Telangiectasia • Hair loss

• Hepatomegaly • Bilateral parotid swelling

• Ascites • Encephalopathy

• Variceal bleeding—manifesting as hematemesis and/or melena.

IMPORTANT PRESENTING PATTERNS

247

• Excessive time spent in activities related to alcohol intake

• Abandoning social, occupational or recreational activities

• Continued use despite an awareness of the adverse physiological and

psychological effects of continued use

Fatty liver

Hepatic steatosis has many other causes, including drugs, pregnancy, and

diabetes mellitus. Deposition of fat occurs as a result of preferential alco-

hol oxidation. It is reversible with abstinence but may proceed to cirrhosis

with continued use. There are no speciﬁ

c clinical features.

Alcoholic hepatitis

This is hepatocellular inﬂ ammation with lymphocyte inﬁ ltration, steatosis,

cholestasis, ﬁ brosis, and necrosis. Clinical features include the following:

• Fever

• Jaundice

• Tender hepatomegaly

• May hear a bruit over the liver

Cirrhosis

This is severe hepatic ﬁ

brosis with micronodules. There is loss of hepato-

cytes, impaired synthetic function, and portal hypertension. Other causes

of cirrhosis include chronic viral hepatitis (B or C), sclerosingcholangitis,

Wilson’s disease, hemachromotosis, A

1

-antitrypsin deﬁ ciency, primary

biliary cirrhosis, Budd–Chiari syndrome, and several drugs (e.g., amiodar-

one, methyldopa, and methotrexate). Clinical features can be any of those

listed under Chronic Liver Disease, above.

Extrahepatic manifestations of alcoholic liver disease or alcoholism

• Obesity or malnutrition • Osteoporosis

• Diarrhea • Falls

• Gastric erosions • Seizures

• Peptic ulcer disease • Cognitive impairment (b p. 262)

• Pancreatitis • Metabolic encephalopathy

• Varices • Peripheral neuropathy

• Ascites • Ataxic gait (b p. 321)

• Splenomegaly • Wernicke’s encephalopathy

• Hypertension • Korsakoff’s syndrome

• Loss of secondary sexual

characteristics

• Cardiomyopathy

• Osteomalacia • Arrhythmias (especially atrial

ﬁ brillation)

CHAPTER 9 Abdomen 248

Hepatic encephalopathy

Shunting of blood away from the portal circulation, seen in chronic liver

disease, allows potentially neurotoxic substances absorbed in the gut to

bypass the liver where they would normally be removed.

Hepatic encephalopathy is graded as follows:

Grade 0 Normal mental state

Grade I Altered mood or behavior (d attention span, difﬁ culty with

numbers, and lack or awareness)

Grade II i Drowsiness, slurred speech, mild to moderate confusion

Grade III Stupor but responsive to stimuli, signiﬁ cant confusion,

restlessness

Grade IV Coma

Malabsorption

Numerous disorders can cause malabsorption states. They can be grouped

as pancreatic insufﬁ ciency, bile salt malabsorption, small bowel mucosa

defects (celiac disease, tropical sprue, giardiasis, disaccharidase deﬁ ciency,

Whipple’s disease, short bowel syndrome), bacterial overgrowth, and spe-

ciﬁ c delivery defects.

General symptoms and signs of malabsorption include the following:

• Muscle wasting

• Weight loss

• Pallor

• Diarrhea (watery)

• Steatorrhea: pale, fatty stools; offensive smelling and difﬁ

cult to ﬂ ush

• Glossitis

• Angular stomatitis (vitamin B

2

, B

12

, and folic acid deﬁ ciencies)

• Intraoral purpura and easy bruising (vitamin K deﬁ ciency)

• Follicular keratitis: hyperkeratotic white patches (vitamin A deﬁ ciency)

Acute pancreatitis

Symptoms

• Pain—central abdominal or epigastric, radiating through to the back.

Sometimes relieved slightly by sitting forward.

• Vomiting

Signs

• Tachycardia

• Fever

• Jaundice (rarely)

• Peritonitis (bowel ileus, very tender abdomen, guarding)

• Retroperitoneal bleed: Cullen’s or Grey–Turner’s signs (b p. 230)

Chronic pancreatitis

In developed countries, the most common cause is chronic heavy alcohol

intake. A small group of patients can inherit chronic pancreatitis through

an autosomal dominant gene with incomplete penetrance.

Clinical features are usually due to pancreatic enzyme deﬁ ciencies and

malabsorption and chronic pain. There may be acute exacerbations, pre-

senting as acute pancreatitis. Loss of pancreatic endocrine function may

cause diabetes.

IMPORTANT PRESENTING PATTERNS

249

Cholangitis

This is biliary sepsis. It is suggested by Charcot’s triad:

• Right upper quadrant pain

• Fever

• Jaundice

You may also be able to elicit Murphy’s sign (b p. 234).

Celiac disease

This a common cause of malabsorption. It affects 1 in 133 (2 million) peo-

ple in the United States. Incidence is much higher (up to 1/22) if a ﬁ rst-

degree relative has the disease.

1

T-cell-mediated autoimmune disease of

the small bowel mucosa is characterized by villous atrophy and i intraepi-

thelial lymphocytosis in response to ingestion of gluten.

Gluten is a high-molecular weight compound containing gliadins and

peptides. It is found in a huge number of foods containing wheat, barley,

and rye. Controversy exists over eating oats.

Clinical features are listed below.

Symptoms

• Tiredness

• Malaise

• Diarrhea or steatorrhea

• Abdominal discomfort and bloating

• Weight loss

• Anxiety

• Depression

• Peripheral paresthesia

Signs

• Muscle wasting

• Mouth ulceration

• Angular stomatitis

• Ankle edema (low serum albumin)

• Polyneuropathy

• Muscle weakness

• Tetany

Associated with

• Autoimmune thyroid disorders, chronic liver disease, ﬁ brosing

alveolitis, ulcerative colitis, insulin-dependent diabetes mellitus

Possible complications to be aware of

• Small bowel lymphoma (rare)

• Small bowel adenocarcinoma (rarer)

• Ulcerative jejunitis

• Splenic atrophy

• Anemia

• Osteomalacia

• Osteoporosis

• Secondary lactose intolerance

1

http://digestive.niddk.nih.gov/ddiseases/pubs/celiac.

CHAPTER 9 Abdomen 250

Inﬂ ammatory bowel disease: ulcerative colitis (UC)

This is a chronic relapsing disease of unknown etiology involving superﬁ cial

inﬂ ammation of the colonic mucosa, starting from the rectum and work-

ing proximally without any breaks. The terminal ileum may be affected by

backwash ileitis. Periods of remission may give no symptoms at all.

Symptoms

• Diarrhea (often with blood or mucus)

• Weight loss

• Fever

• Abdominal pain

• Proctitis may cause rectal bleeding, mucus, tenesmus, and constipation.

Complications to be aware of

• Toxic megacolon

• Iron deﬁ ciency

anemia

• Increased risk of colorectal carcinoma

• Fistula formation (rare)

Inﬂ ammatory bowel disease: Crohn’s disease

Like ulcerative colitis, this is a chronic inﬂ ammatory disease of the gas-

trointestinal tract but differs from UC in that lesions occur anywhere from

the mouth to anus but especially at the terminal ileum and anorectum.

Pathology involves deep ulceration, cobblestoning of the mucosa, ﬁ ssuring

and abscess formation with skip lesions, and non-caseating granulomas.

Symptoms

If disease is limited to the colon, symptoms may be identical to UC.

• Loose stools or diarrhea (usually not bloody)

• Anorexia

• Malaise

• Weight loss

• Abdominal pain (insidious, often in the right lower quadrant)

• Perianal pain

• Joint pains

Note on examination (these can occur in UC also)

• Aphthous mouth ulcers

• Uveitis

• Anemia

• Arthropathy

Active Crohn’s disease

• Colicky pain often in the right iliac fossa

• May have diarrhea with blood and mucus

• Weight loss

• Borborygmus (b p. 231)

• May be a palpable inﬂ

ammatory mass in the right iliac fossa

• Abdominal distension

• ± Bowel obstruction

IMPORTANT PRESENTING PATTERNS

251

Active Crohn’s colitis

• Similar presentation to ulcerative colitis

• Perianal disease more likely to produce ﬁ ssuring and ﬁ stula

formation

Complications to be aware of

• Fistula formation (from the bowel to any other abdominal organ or

the exterior)

• Small increased risk of colorectal carcinoma (especially in long-standing

disease limited to the colon)

• Vitamin B

12

deﬁ ciency

• Iron deﬁ ciency

• Abscess formation

• Stricture formation

• Systemic infection

Extraintestinal features of inﬂ ammatory bowel disease

• Seronegative arthropathy of large or small joints (peripheral, non-

deforming, particularly at the knees, ankles, and wrists)

• Sacroiliitis

• Anterior uvetitis

• Erythema nodosum

• Pyoderma gangrenosum

• Ureteric calculi

• Gallstones

• Sclerosing cholangitis

• Cholangiocarcinoma

• Nutritional deﬁ

ciencies (Osteoporosis? Osteomalacia?)

• Bile salt malabsorption

• Osteoporosis secondary to longterm steroid use or malabsorption

• Systemic amyloidosis

Irritable bowel syndrome (IBS)—Rome III

diagnostic criteria

Symptoms of abdominal discomfort or pain need to meet a frequency

criterion (3 or more days a month for at least 3 months) in the preceding

6 months and has two out of three features:

• Relief or improvement with defecation

• Onset associated with a change in frequency of stool

• Onset associated with a change in form/appearance of stool

Other symptoms that support the diagnosis of IBS:

• Abnormal stool frequency (>3/day or <3/week)

• Abnormal stool form (lumpy/hard, loose/watery)

• Abnormal stool passage (straining, urgency, feeling of incomplete

evacuation)

• Passage of mucus

• Bloating or feeling of abdominal distension

CHAPTER 9 Abdomen 252

The elderly patient

Gastrointestinal disease presents as a huge spectrum in older patients,

encompassing nutrition, oral care, and continence in addition to the range

of presentations described in this chapter. While many older people suf-

fer gastrointestinal symptoms, often due to underlying illnesses or the

effect of medication, they may be embarrassed about discussing them.

Thoughtful and holistic assessment is paramount, and simple interventions

can pay dividends.

History

Oral care

This is an often overlooked but key part of any assessment. Dentures

may be ill-ﬁ tting or lost, and dietary intake can suffer as a consequence.

Hospitalized patients are particularly prone to losing their dentures.

Clarify symptoms and diagnoses

Does the patient really have an irritable bowel? (See below.) Many patients

may describe themselves as having such diagnoses, but take the time to

clarify what this means. Recent changes of bowel habit must always be

viewed with a degree of alarm and causes considered.

Constipation

This can often lead to serious decline in patients. It is often easily

remediable.

Weight and nutrition

Ask yourself why has the patient lost weight. The range of diagnoses

is broad, but contemplate mood, dietary habits, and functional abilities

in your assessments—it may be a matter of dislike of delivered frozen

meals.

Drug history

Always consider the side effects of medication—analgesics and constipa-

tion, recent antibiotics, and diarrhea. Ask about over-the-counter drugs

including NSAIDs (and topical drugs) and laxatives.

Continence

This is another key part of the assessment; try to discuss it sensitively

and determine if there factors additional to any GI disturbance, includ-

ing mobility, cognition and visual problems. This dovetails with the ever-

important functional history.

Examination

General

Look out for signs of weight loss—wasting, poorly ﬁ tting clothes, etc. For

inpatients, a completed weight chart and careful consideration may allevi-

ate some of the problems of poor nutrition and acute illness.

Look in the mouth

A range of diagnoses is often apparent. Denture care should be assessed

(poor cleaning associated with recurrent stomatitis), and other problems

such as oral candida are obvious.

THE ELDERLY PATIENT

253

Observe

Look for other signs of systemic disease that might point to the cause of

the gastrointestinal symptoms (e.g., multiple telangiectasia, valvular heart

disease in GI bleeding).

Examine

Examine thoroughly for lymphadenopathy. Remember to examine her-

nial oriﬁ ces—the cause of abdominal pain may be instantly obvious and

correctable.

Rectal examination

This is vital—changes in bowel habit, continence, iron deﬁ ciency anemia,

and bladder symptomatology all indicate that this should be performed.

Diagnoses not to be missed

Functional bowel disorders

These tend to be less common in older people, so always consider under-

lying organic problems. Endoscopic examinations are often well tolerated

and have a good diagnostic yield.

Biliary sepsis

This is the third most common source of infection in older people (after

chest and urine sepsis) and may lack many of the salient presenting fea-

tures described previously in this chapter. Be alert to this possibility when

considering differential diagnoses and choosing antibiotics.

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255

Nervous system

Presenting symptoms in neurology 256

The rest of the history 258

The outline examination 259

General inspection and mental state 259

Speech and language 260

Cognitive function 262

Cranial nerve I: olfactory 263

Cranial nerve II: optic 264

Cranial nerve II: ophthalmoscopy 268

Pupils 273

Cranial nerves III, IV, and VI 276

Palsies of cranial nerves III, IV, and VI 280

Cranial nerve V: trigeminal 283

Cranial nerve VII: facial 285

Cranial nerve VIII: vestibulocochlear 287

Cranial nerves IX and X 289

Cranial nerve XI: accessory 291

Cranial nerve XII: hypoglossal 293

Motor: applied anatomy 294

Motor: inspection and tone 296

Motor: upper limb power 298

Motor: lower limb power 300

Tendon reﬂ exes

302

Other reﬂ exes 305

Primitive reﬂ exes

307

Sensory: applied anatomy 308

Sensory examination 312

Coordination 315

Some peripheral nerves 317

Gait 321

Important presenting patterns 323

The unconscious patient 331

The elderly patient 334

Chapter 10

CHAPTER 10 Nervous system256

Presenting symptoms in neurology

The history is key in the examination of many neurological cases. If the

patient cannot give a complete story (e.g., when describing a loss of con-

sciousness or seizure), collateral histories should be gained from any wit-

nesses to the event(s)—relatives, friends, the primary care provider, or

even passers-by.

Approach to neurological symptoms

Symptoms can vary widely in neurology; the intricacies of a few are

discussed below. For all symptoms, you should try to understand the

following:

• Exact nature of the symptom

• Onset (Sudden? Slow—hours? Days? Weeks? Months?)

• Change over time (Progressive? Intermittent? Episodes of recovery?)

• Precipitating factors

• Exacerbating and relieving factors

• Previous episodes of the same symptom

• Previous investigations and treatment

• Associated symptoms

• Any other neurological symptoms

Dizziness

Narrow the exact meaning down without appearing aggressive or disbe-

lieving. Dizziness is used by different people to describe rather different

things:

• A sense of rotation = vertigo

• Swimminess or light-headedness —a nonspeciﬁ

c symptom that can be

related to pathology in many different systems

• Presyncope —the unique feeling one gets just prior to fainting

• Incoordination —many will say they are dizzy when, in fact, they can’t

walk straight because of either ataxia or weakness.

Headache

This should be treated as any other type of pain. Establish character,

severity, site, duration, time course, frequency, radiation, aggravating and

relieving factors, and associated symptoms.

• Ask about facial and visual symptoms. (Some different types of

headaches are described on b p. 329.)

Numbness and weakness

These two words are often confused by patients, describing a leg as

“numb” when it is weak with normal sensation. Also, patients may report

numbness when, in fact, they are experiencing pins and needles (paresthe-

sia)or pain.

Tremor

Here you should establish if the tremor occurs only at rest, only when

attempting an action, or both. Is it worse at any particular time of the day?

The severity can be established in terms of its functional consequence (can

the patient hold a cup or bring food to their mouth?).

PRESENTING SYMPTOMS IN NEUROLOGY

257

Again, establish exactly what is being described. A tremor is a shaking,

regular or jerky involuntary movement.

Syncope

This is discussed in b Chapter 7.

Falls and loss of consciousness (LOC)

An eyewitness account is vital. Establish also whether the patient actually

lost consciousness. People often describe “blacking out” when in fact they

simply fell to the ground (drop attacks have no LOC). An important ques-

tion here is, “Can you remember hitting the ground?”.

Ask about preceding symptoms and warning signs—they may point

toward a different organ system (sweating or weakness could be a marker

of hypoglycemia; palpitations may indicate a cardiac dysrhythmia).

Seizures

These are very difﬁ cult to assess, even for experienced history-takers!

Establish early on if there was any impairment of consciousness, and seek

collateral histories. Laypersons usually consider seizure = “ﬁ t” = tonic–

clonic seizure. Doctors’ understanding of seizure may be quite different. A

surprising number of people also suffer pseudoseizures , which are nonor-

ganic and have a psychological cause.

A few points to consider are as follows:

• Syncopal attacks can often cause a few tonic–clonic or myoclonic jerks,

which may be mistaken for epilepsy.

• True tonic–clinic seizures may cause tongue-biting, urinary and fecal

incontinence, or all of the above.

• People presenting with pseudoseizure can have true epilepsy as well,

and vice versa.

Visual symptoms

Commonly, there is visual loss, double vision, or photophobia (pain when

looking at bright lights). Here, establish exactly what is being experi-

enced—“double vision” (diplopia) is often complained of when, in fact,

the vision is blurred or sight is generally poor (amblyopia) or clouded.

CHAPTER 10 Nervous system258

The rest of the history

Ask if the patient is right- or left-handed (consider disability from loss of

function; this may also be useful when thinking about cerebral lesions).

Direct questioning

In every patient, inquire about neurological symptoms other than the pre-

senting complaint (headaches, ﬁ ts, faints, blackouts, visual symptoms, pins

and needles, tingling, numbness, weakness, incontinence, constipation, or

urinary retention).

Past medical history

A birth history is important here, particularly in patients with epilepsy.

Additional forms of neurological injury are often present at birth, for

instance, in the case of brachial plexus injury during dystotic deliveries.

Brain injury at birth has neurological consequences.

While a thorough history is required, inquire especially about the

following:

• Hypertension—if so, what treatment?

• Diabetes mellitus—what type? What treatment?

• Thyroid disease

• Mental illness (e.g., depression)

• Meningitis or encephalitis

• Head or spinal injuries

• Epilepsy, convulsions, or seizures

• Cancer

• HIV/AIDS

Drug history

Ask especially about the following:

• Anticonvulsant therapy (current or previous)

• Oral contraceptive or other estrogen-based contraceptive preparation

• Corticosteroids

• Anticoagulants or antiplatelet agents

Family history

A thorough history, as always, is important. Ask about neurological diag-

noses and evidence of missed diagnoses (seizures, blackouts, etc.).

Tobacco and alcohol

These are as important to ask about here as for any other system.

Social history

• Occupation: Neurological disease can have a signiﬁ

cant impact on

occupation, so ask about this at an early stage—some suggest right at

the beginning of the history. Also ask about exposure to heavy metals

or other neurotoxins.

• Is patient driving? Many neurological conditions have implications here.

• Ask about the home environment in detail (this will be very useful

when considering handicaps and consequences of the diagnosis).

• Ask about support systems—family, friends, home help, day visits.

GENERAL INSPECTION AND MENTAL STATE

259

The outline examination

It is easy to get bogged down in some of the complexities of the neurologi-

cal examination, but it is not something to be afraid of. Students should

embrace it; practice often, as a competent neurological examination is a

sure sign of someone who has spent plenty of time on honing their clinical

skills. The following is a brief outline of how it should be approached:

• Inspection, mood, conscious level

• Speech and higher mental functions

• Cranial nerves (CN) II–XII

• Motor system

• Sensation

• Coordination

• Gait

• Any extra tests

• Other relevant examinations

•

Skull, spine, neck stiffness, eardrums, blood pressure, anterior chest,

carotid arteries, breasts, abdomen, lymph nodes

General inspection and mental state

The neurological exam should start with any clues that can be gleaned

from simply looking at and engaging with the patient.

• Is the patient accompanied by caregivers, and how does the patient

interact with those people?

• Does the patient use any walking aids or other forms of support?

• Are there any abnormal movements? (b p. 315)

• Observe the gait as they approach the clinic room, if able (b p. 321).

• Is there any speech disturbance? (b p. 260)

• What is their mood like?

•

A detailed mood assessment (b p. 458) is not necessary here.

•

Ask the patient how they feel.

•

What is the state or their clothing, hair, skin, and nails?

•

Is there any restlessness, inappropriately high spirits, or

pressure of speech?

•

Are they obviously depressed with disinterest?

•

Are they denying any disability?

CHAPTER 10 Nervous system260

Speech and language

Speech and language difﬁ culties, especially expressive dysphasia, may be

extremely distressing for the patient and their family. This topic must be

approached with care, reassurance, and a calm seriousness in the face of

possible bizarre and amusing answers to questions.

Examination

Speech and language problems may be evident from the start of the his-

tory and require no formal testing. You should brieﬂ y test the patient’s

language function by asking them to read or obey a simple written com-

mand (e.g., “close your eyes”) and write a short sentence.

If apparently problematic, speech can be tested formally by asking the

patient to respond to progressively harder questions, with answers rang-

ing from yes/no, simple statements, to more complicated sentences, and

ﬁ nally by asking them to repeat complex phrases or tongue-twisters (see

Dysarthria section).

Before jumping to conclusions, ensure that the patient is not deaf or

that their hearing aid is working, and that they can understand English.

Dysarthria

This is a defect of articulation with language function intact (writing will

be unaffected). There may be a cerebellar lesion, a lower motor neuron

(LMN) lesion of the cranial nerves, an extrapyramidal lesion, or a problem

with muscles in the mouth and jaws or their nerve supply.

• Listen for slurring and the rhythm of speech.

• Test function of different structures by asking the patient to repeat

•

“Yellow lion” or words with D , L , and T (tests tongue function).

•

“Peter Piper picked a pickle,” or words with P and B (tests lip function).

• Cerebellar lesions: slow, slurred, low volume with equal emphasis on all

syllables (scanning)

• Facial weakness: speech is slurred.

• Extrapyramidal lesions: monotonous, low volume, lacks normal rhythm

Dysphonia

This constitutes defective volume—huskiness. Dysphonia is usually from

laryngeal disease, laryngeal nerve palsy, or, rarely, muscular disease, such

as myasthenia gravis. It may also be “functional” (psychological).

Dysphasia

This is a defect of language, not just speech, so reading and writing may

also be affected (some patients attempt to overcome speaking difﬁ culties

with a notepad and pen, only to be bitterly disappointed).

In very simple terms, the main language areas of the brain are illustrated

in Fig. 10.1 . Deﬁ cits can be understood in terms of lesions in one or more

of these areas. There are four main types of dysphasia.

Global dysphasia

Both Broca’s and Wernicke’s areas are affected. The patient is unable to

speak or understand speech at all.

Expressive dysphasia

This is also called anterior , motor , or Broca’s dysphasia.

SPEECH AND LANGUAGE

261

• Lesion in Broca’s area (frontal lobe), involved in language production

• Understanding remains intact

• Unable to answer questions appropriately

• Speech is nonﬂ

uent, broken with abnormal word ordering

• Unable to repeat sentences

• Can be very distressing for patients. Ask, “Do you know what you

want to say, but can’t get it out?” and you’ll be met with a grateful

smile, nod, and handshake.

Receptive dysphasia

Also called posterior , sensory , or Wernicke’s dysphasia.

• Lesion in Wernicke’s area creates problems with understanding

spoken or written language (dyslexia) and problems with word-ﬁ nding

• Unable to understand commands or questions

• Speech is ﬂ

uent with lots of meaningless grammatical elements.

• May contain meaningless words

• Unable to repeat sentences

• Patients are often unaware of their speech difﬁ

culty and will speak in a

nonsensical way, often becoming frustrated with other people’s lack of

understanding.

• Jargon dysphasia describes a severe form of receptive dysphasia

containing only meaningless words (neologisms) and sounds.

• Paraphasia is the supplementation of one word with another.

Conductive dysphasia

There is a lesion in the arcuate fasciculus and/or other connections

between the two primary language areas.

• Patient can comprehend and respond appropriately

• Unable to repeat a sentence

Nominal dysphasia

• All language function is intact except for naming of objects.

• Caused by lesion in angular gyrus

• Patient may function with circumlocution (e.g., says “that thing that I

write with” if unable to say “pen”)

Broca’s

area

Arcuate

fasciculus

Wernicke’s

area

Fig. 10.1 Simple representation of the main language areas of the brain.

CHAPTER 10 Nervous system262

Cognitive function

Neurological diseases may affect function such that patients’ appearance or

communication skills are at odds with their social standing or educational

level. Formal assessment of a person’s mental state is thus important. This

also allows for any future change to be noted and monitored.

Abbreviated mental test score (10 points)

This serves as a brief screening tool with a maximum score of 10 points. A

more detailed, 30-point, score is shown in Box 15.11 (b p. 464).

Approach this gently—patients often dislike being tested without warning.

Always explain the purpose of the questions, and ask permission to proceed.

Hints

When testing 5-minute recall:

• If thinking of an address for the patient to remember, be careful not to

give out your own!

• Beware of repeating the test too often. Patients may well remember

“42 West Street” from the last time it was asked.

Table 10.1 Abbreviated mental test score

1. Date of birth “What is your date of birth?”

2. Age “How old are you?”

3. Time “What time is it?”

•

Correct to the nearest hour

4. Year “What year is it now?”

•

Note that hospital patients often lose track of the day

or month, not the year.

5. Place “Where are we?” or “What is this place?”

•

Name of the hospital, clinic, or surgery ward

6. Head of

state

“Who is the current president?”

•

A name is required. Such descriptions as “that man in all

the trouble” won’t do—even if it is potentially correct!

7. Current

event

In recognition of the patient’s age, culture, and education, it

may be appropriate to ask the year of a noteworthy event,

such as, “When was President Kennedy shot?” “When

were aircraft crashed into the World Trade Center?”

8. 5-minute

recall

Tell the patient an address (often “42 West Street” is

used) and ask them to repeat it back to you to ensure

they’ve heard it correctly. Ask them to remember it. Five

minutes later, ask them to recall the address.

•

They must remember the address in full to score the point.

9. 20–1 “Count backward from 20 down to 1”

•

Patients sometimes need a prompt here: “Like this: 20,

19, 18, and so on.”

10. Recognition “What job do I do?” (doctor) and “What job does this

man or woman do?” (nurse)

•

Both must be correct to score a point.

CRANIAL NERVE I: OLFACTORY

263

Cranial nerve I: olfactory

Applied anatomy

• Sensory: smell

• Motor: none

Fibers arise in the mucous membrane of the nose. Axons pass across the

cribiform plate to the olfactory bulb. The olfactory tract runs backward

below the frontal lobe and projects mainly in the uncus of the ipsilateral

temporal lobe.

Note: Olfactory epithelium also contains free nerve endings of the ﬁ rst

division of cranial nerve V.

Examination

This nerve is not routinely tested unless the patient complains of loss of

sense of smell (anosmia) and exhibits other signs suggestive of a frontal or

temporal lobe cause (e.g., tumor).

• Casual: Take a nearby odorous object (e.g., coffee or chocolate) and

ask the patient if it smells normal.

• Formal: A series of identical bottles containing recognizable smells are

used. The patient is asked to identify them. Commonly used agents

include coffee, vanilla, camphor, and vinegar.

Test each nostril separately and determine if any loss of smell is uni- or

bilateral.

Findings

• Bilateral anosmia: usually nasal, not neurological

Causes include upper respiratory tract infection, trauma, smoking, old age,

and Parkinson’s disease. Less commonly, there are tumors of the ethmoid

bones or congenital ciliary dysmotility syndromes.

• Unilateral anosmia: mucous-blocked nostril, head trauma, subfrontal

meningioma

Hints

Peppermint, ammonia, and menthol stimulate the free trigeminal endings

so are not a good test of cranial nerve I.

CHAPTER 10 Nervous system264

Cranial nerve II: optic

Applied anatomy

With an understanding of anatomy of the optic nerves, defects in the visual

ﬁ eld enable localization of a lesion within the brain.

The optic nerve begins at the retina (and is the only part of the central

nervous system [CNS] that can be directly visualized). The nerve passes

through the optic foramen and joins its fellow nerve from the other eye

at the optic chiasm just above the pituitary fossa. Here, the ﬁ bers from the

nasal half of the retina cross over. They continue in the optic tract to the

lateral geniculate body. From there, they splay out such that those from

the upper retina pass through the parietal lobe and the others through

the temporal lobe.

0 Students easily get confused here and should focus on gaining full

understanding of these processes at an early stage. Because of the refrac-

tion at the lens, images are represented on the retina upside down and

back to front. Therefore, the nasal half of the retinal receives input from

the temporal part of the visual ﬁ eld in each eye, while the temporal half of

the retinal receives input from the nasal half of the eye.

Further back in the optic system, ﬁ bers from the nasal halves of the ret-

inas cross, so, for example, the left side of the brain receives input from

the right side of vision (the left temporal retina and the right nasal retina)

and vice versa (see Fig. 10.2 , b p. 267).

Visual acuity

Sharpness or clarity of vision is formally tested using a Snellen’s chart.

• In good light, the patient should stand 20 feet away from the chart.

• Each eye is tested in turn, and the patient is asked to read the chart.

• The number above each line indicates the distance at which a person

with normal sight should be able to read it.

• Record the line reached—allow a maximum of two errors per line.

•

Indicate results as distance from chart/distance it should be read,

e.g., 20/20.

If the patient can’t see any of the letters, record whether they can

• Count ﬁ

ngers held in front of their face (CF)

• See hand movements (wave your hand)

• Perceive light

•

Record as CF, HM, PL, or NPL (not perceive light).

Color vision

• Not tested routinely and not considered in this book

• Tested using Ishihara plates

Visual ﬁ elds

The area that each eye can see without moving can be mapped out. They

are not circular—eyebrows and the nose obstruct superiorly and nasally,

whereas there is no obstruction laterally.

Sitting opposite the patient, the examiner’s left visual ﬁ eld (for example)

should be an exact mirror image of the patient’s right visual ﬁ eld. In this

way, the patient’s ﬁ elds can be tested against the examiner’s.

CRANIAL NERVE II: OPTIC

265

Gross defects and visual neglect (inattention)

Sit opposite the patient, 71 m apart, at eye level Test ﬁ rst for gross defects

and visual neglect, with both eyes open.

• Raise your arms up and out to the sides so that one hand is in the

upper right quadrant of your vision and one in the upper left.

• Ask the patient to look directly at you (“look at my nose”).

• Move one index ﬁ

nger and ask the patient, while looking straight at

you, to point to the hand that is moving.

• Test with the right, left, and then both hands.

• Test the lower quadrants in the same way.

• If visual neglect is present, the patient will be able to see each hand

moving individually but report seeing only one hand when both are

moving (compare with sensory inattention, b p. 312).

Testing each eye

In the same position as above, ask the patient to cover their right eye while

you cover your left, and look directly at one another.

• If you were now to trace the outer borders of your vision in the air

half-way between yourself and the patient, it should be almost identical

to the area seen by the patient.

Test each quadrant individually:

• Stretch your arm out and up so that your hand is just outside your

ﬁ

eld of vision, an equal distance between you and the patient.

• Slowly bring your hand into the center (perhaps wiggling one ﬁ nger)

and ask the patient to say “yes” as soon as they can see it.

• You should both be able to see your hand at the same time.

• Test upper right and left, lower right and left individually, bringing your

hand in from each corner of vision at a time.

• Ensure that the patient remains looking directly at you (many will

attempt to turn and look at the hand if not prompted correctly).

• Map out any areas of visual loss in detail, ﬁ

nding borders. Test if any

visual loss extends across the midline horizontally or vertically.

• Test each eye in turn (you both may require a short break between

eyes, as this requires considerable concentration).

Repeat the above procedure with a red-headed pin or similar small red

object to map out areas of visual loss in more detail.

• Ask the patient to say “yes” when they see the pin as red .

• Start by mapping out the blind spot, which should be 715° lateral

from the center at the midline (this tests both your technique and the

patient’s reliability as a witness before proceeding).

Decide if any defect is of a quadrant, half the visual ﬁ

eld or another shape

and in which eye, or both. Record by drawing the defect in two circles

representing the patient’s visual ﬁ elds, as shown in Fig. 10.2 b p. 267.

If the patient is unable to cooperate

Like much of the neurological examination, gross defects can be seen with-

out the patient’s cooperation (confused or drowsy). Test for response to

“menace” by bringing your hand in sharply from the side, stopping just

short of hitting the patient in the eye. If your hand can be seen, the patient

will blink. Test vision on the left and the right.

CHAPTER 10 Nervous system266

Some common visual ﬁ eld defects

Compare the defects below with the corresponding number on Fig. 10.2

showing the position of the lesion and a representation of the ﬁ elds, as it

should be recorded in the patient’s notes.

• Tunnel vision: a confusing term. A constricted visual ﬁ eld,

giving

the impression of looking down a pipe or tunnel, may be caused

by glaucoma, retinal damage or papilledema. Tubular vision is often

functional.

• Enlarged blind spot: caused by papilledema

• Unilateral ﬁ eld

loss:

(1) blindness in one eye caused by devastating

damage to the eye, its blood supply, or optic nerve.

• Central scotoma: a hole in the visual ﬁ

eld (macular degeneration,

vascular lesion or, if bilateral, toxins). If bilateral, this may indicate a

very small defect in the corresponding area of the occipital cortex

(multiple sclerosis).

• Bitemporal hemianopia: (2) the nasal half of both retinas and,

therefore, the temporal half of each visual ﬁ

eld is lost (damage

to the center of the optic chiasm, such as a pituitary tumor,

craniopharyngioma, suprasellar meningioma).

• Binasal hemianopia: the nasal half of each visual ﬁ

eld is lost (very rare)

• Homonymous hemianopia: (3) may be left or right. Commonly seen in

stroke patients. The right or left side of vision in both eyes is lost (e.g.,

the nasal ﬁ

eld in the right eye and the temporal ﬁ

eld in the left eye).

If the central part of vision (corresponding to the macula) is spared,

the lesion is likely in the optic radiation; without macula sparring, the

lesion is in the optic tract.

• Homonymous quadrantanopia: corresponding quarters of the vision

are lost in each eye (e.g., the upper temporal ﬁ

eld in the right and the

upper nasal ﬁ

eld in the left)

•

Upper quadrantanopias (4) suggest a lesion in the temporal lobe.

•

Lower quadrantanopias (5) suggest a lesion in the parietal lobe.

CRANIAL NERVE II: OPTIC

267

1

1.

2.

3.

4.

5.

6.

Retina

Optic nerve

3

4

5

6

2

Optic chiasm

Optic tract

Lateral

geniculate body

Optic

radiation

Occipital

cortex

Fig. 10.2 Representation of the visual tracts from the retina to the occipital

cortex showing main structures and expected visual ﬁ eld loss according to the

site of the lesion.

CHAPTER 10 Nervous system268

Cranial nerve II: ophthalmoscopy

Direct ophthalmoscopic examination of the fundus is a vital part of any

neurological examination but is often avoided, as it is considered difﬁ cult.

It can provide the observer with vital information about the condition

of the optic nerve head. The exam takes practice, but the experienced

observer can gain views of the fundus, macular region, and retinal vascular

arcades. It is worth practicing at every opportunity. The direct ophthalmo-

scope gives a greatly magniﬁ ed view of the fundus; gaining a view of the

peripheral retina beyond the equator requires examination with a slit lamp

or indirect ophthalmoscope, not covered in this book.

For a complete ophthalmoscopic examination, it is often worth dilating

the pupil by instilling a few drops of a mydriatic medication (1% cyclopen-

tolate) into the inferior conjunctival sac. With a little practice, one often

ﬁ nds that this is not necessary for a routine examination.

0 If you plan to dilate the pupil, ask the patient if they have any history

of angle-closure glaucoma or episodes of seeing haloes around lights at

nighttime. If you suspect this, or the anterior chamber of the eye appears

shallow, it is best to err on the side of caution—dilating the pupil could

occlude the drainage angle and precipitate an acute attack.

Examination

• Performed in a dimly lit room with the patient sitting or lying down

• Ask the patient to focus on a distant object and keep their eyes still

(this relaxes accommodation as much as possible).

• Look through the ophthalmoscope 30 cm away from the patient and

bring light in nasally from the temporal ﬁ

eld to land on the pupil.

•

The pupil will appear red, and opacities in the visual axis will appear

as black dots or lines.

•

By cycling through the different lenses of the ophthalmoscope, you

should be able to gain an impression of where these opacities lie.

Possible locations are the cornea, aqueous, lens (and its anterior and

posterior capsules), and vitreous.

• Dial up a hypermetropic (plus) lens on the ophthalmoscope to focus

on the corneal surface and move in as close as possible to the patient’s

eye—by gradually d the power of the lens, you can examine the

cornea, iris, and lens. (Formal examination of these structures is best

done with the slit lamp, although a great deal of information can be

gained with the direct ophthalmoscope.)

• Continue to d the power of the lens until you can sharply focus on the

retinal vessels. It is often best to pick up one of the vascular arcades

in the periphery and track them in toward the optic disc. This allows

the peripheral quadrants to be examined before viewing the optic

disc. Take time to look at the vessels carefully, particularly where the

arteries cross the veins.

• Ask the patient to look directly into the light of the ophthalmoscope

so you can gain a view of the macular region.

CRANIAL NERVE II: OPHTHALMOSCOPY

269

The normal fundus

Optic disc

• The healthy disc is a pale pink/yellow color and round or slightly oval

( Fig. 10.3 ).

• The margins between the disc and the surrounding retina should be

crisp and well deﬁ

ned. Occasionally, a surrounding ring is present,

which may be slightly lighter or darker in color.

• At the center of the disc is the physiological cup. It appears paler in

color than the rest of the disc.

Macular region

• Located temporally from the optic disc

• This is the region with the maximum concentration of cones.

• At the center of the macula is the fovea —a tiny pit devoid of blood

vessels and responsible for ﬁ ne

resolution.

• Disease involving the macula and fovea can cause devastating

visual loss.

Retinal vessels

• The central retinal artery and vein enter and leave the globe in the

center of the optic disc.

• Veins appear larger and darker in color than the arteries.

• Spontaneous venous pulsations are seen in many normal eyes.

• Arterial pulsations should not be visible in normal eyes.

Hint

View the macula by directing light on the most sensitive part of the eye.

This can often be unpleasant for the patient and will lead to more marked

miosis and a restricted view.

Optic cup

Optic disc

Vein

Artery

Macula

Fig. 10.3 The normal appearance of the fundus of the right eye.

CHAPTER 10 Nervous system270

Abnormal ﬁ ndings on fundoscopy

Optic disc swelling

Appearance

• The optic disc is raised, swollen, and enlarged.

• The disc often appears darker in color.

• The margins of the disc are blurred and become indistinct from the

adjacent retina.

• Retinal vessels can be seen arching down from the raised disc toward

the peripheral retina.

• In severe cases, retinal hemorrhage may be seen around the disc.

The term papilledema is often incorrectly used to describe optic disc

swelling. Papilledema is swelling of the optic disc due to raised intracranial

pressure (ICP) ( Fig. 10.4 ).

Causes

• Space-occupying lesions, including intracranial malignancy, subdural

hematoma, and cerebral abscess

• Subarachnoid hemorrhage (often associated with vitreous

hemorrhage)

• Chronic meningitis

• Idiopathic intracranial hypertension (IIH)

• Malignant hypertension

• Ischemic optic neuropathy

Optic disc cupping

Appearance

• The physiological cup is indented with respect to the rest of the disc.

• Retinal vessels kink sharply as they emerge over the rim of the cup

( Fig. 10.5 ).

• Hemorrhages may be present.

Causes

• Most commonly one of the various types of glaucoma

Optic atrophy

Appearance

• Pale optic disc due to loss of nerve ﬁ

bers in the optic nerve head

(

Fig. 10.6 )

Causes

• Ischemic optic neuropathy

• Optic neuritis

• Trauma

• Optic nerve compression

Retinal hemorrhages

Appearance

The appearance of a hemorrhage depends on its location within the vari-

ous layers of the retina. Deep hemorrhages appear as dots from the close

packing of cells in this region. More superﬁ

cial hemorrhages in the nerve

ﬁ

ber layer appear as more widespread blotches.

CRANIAL NERVE II: OPHTHALMOSCOPY

271

Fig. 10.4 Severe papilledema. Note how the disc margins are blurred and that

there is a lack of normal cupping at the disc.

Fig. 10.5 Optic disc cupping, in this case secondary to glaucoma. Note how the

vessels seem to disappear over the edge of the disc as if falling down a hole.

Fig. 10.6 Optic atrophy. The optic disc is pale and well demarcated.

CHAPTER 10 Nervous system272

Causes

Many pathological processes:

• Diabetes mellitus

• Hypertension

• Subarachnoid hemorrhage

• Blood dyscrasias

• Systemic vasculitis

• Valsalva related

• Trauma

• Bacterial endocarditis (known speciﬁ

cally as Roth spots)

Central or branch retinal artery occlusion

Appearance

• Large areas of ischemic white retina associated with sudden

catastrophic visual loss

• Calciﬁ

c, cholesterol, or ﬁ brin-platelet emboli can often be seen

occluding the retinal artery or branch.

Causes

• Either embolic or thrombotic (remember giant cell arteritis)

Central or branch retinal vein occlusion

Appearance

• Large, widespread ﬂ ame-shaped hemorrhages classically giving the

fundus a stormy-sunset appearance. It is associated with gradual-onset

painless, blurred vision and visual loss.

• Optic disc swelling may be present.

Causes

• Blood dyscrasias

• Diabetes mellitus

• Glaucoma

Foster–Kennedy syndrome

Appearance

• Unilateral optic atrophy

• Contralateral papilledema

• Central scotoma

• Anosmia (variable)

• Systemic symptoms such as headache, dizziness, vertigo, and vomiting

Causes

• Meningioma of optic nerve, olfactory groove or sphenoid wing

• Frontal lobe tumor

PUPILS

273

Pupils

Applied anatomy

The pupil is the aperture at the center of the iris. Variation in pupil size is

brought about by two muscles in the iris under the control of the auto-

nomic nervous system:

• Sphincter pupillae muscle: found in the iris at margin of the pupil and

innervated by parasympathetic ﬁ

bers. It constricts the pupil (miosis).

• Dilator pupillae muscle: radially arranged smooth muscle. Innervated by

sympathetic nervous system. It dilates the pupil (mydriasis).

The pupillary light response

The pupillary light response has afferent and efferent limbs that can be

affected separately in a number of pathologies. The afferent ﬁ bers

leave

the eye in the optic nerve and separate in the midbrain to synapse with

the third nerve nuclei. Efferent pathway ﬁ

bers then travel to synapse in the

ciliary ganglion before innervating the sphincter pupillae.

Examination

Inspect both pupils in good light—is there a discrepancy in size (anisoco-

ria) or shape? (This is present in 25% of the normal population and does

not necessarily indicate pathology. It may be secondary to previous ocular

inﬂ ammatory disease, trauma, or surgery.) If anisocoria is present, one

must determine which of the pupils is the correct size.

• A pathologically constricted pupil is more obvious in dim light as the

normal pupil dilates.

• A pathologically large pupil will be more apparent in bright illumination

when the normal pupil will constrict.

Test pupil responses to direct and consensual light. This is best done in a

dimly lit room. Ask the patient to look into the distance to ensure the eye

is relaxed and dis-accommodated. Shine a light upward from just inferior

to the lower lid to avoid dazzling the patient.

• Constriction of the pupils should be seen almost instantaneously

in response to illumination in both the illuminated eye (direct) and

nonilluminated eye (consensual). Repeat for both eyes.

The afferent limb of the pupillary light pathway is assessed using the

Marcus–Gunn swinging light test, to look for a relative afferent pupil defect

(RAPD). If present, do the following:

• Shine light in the normal eye and both pupils constrict. (The

consensual response in the affected eye is intact.)

• Swing light to the affected eye and both pupils dilate. (Afferent drive

to cause constriction of the pupils from the affected eye is reduced

compared to that of the unaffected eye.)

• Swing light back to the normal eye and both pupils constrict.

• Finally, check the near reﬂ

ex (the efferent limb of the pupil reﬂ ex).

Ask the patient to focus on a distant object and then look immediately

to your index ﬁ nger

held 730 cm in front of their face.

The normal response will be for the pupils to constrict in response to

convergence and accommodation.

CHAPTER 10 Nervous system274

Findings: some pupil abnormalities

Argyll–Robertson pupil

Midbrain lesions caused by neurosyphilis target the more dorsally located

ﬁ bers that subserve the light response. The ventrally located ﬁ bers

responsible for accommodation are spared.

• Appearance: a small, irregular pupil that accommodates but does not

react to light

• Causes: neurosyphilis and diabetes mellitus

Holmes–Adie pupil

There is denervation of the iris and ciliary body due to ciliary ganglionitis

(although some would dispute this). Associated loss of tendon reﬂ exes

is

seen in some patients and is termed Holmes–Adie syndrome

.

Appearance

• Unilateral dilated pupil—accommodates (and relaxes) very slowly and

shows absent or depressed light reﬂ

ex. It is supersensitive to 0.1%

pilocarpine (muscarinic agonist causing constriction).

Causes

• Usually idiopathic and predominates in young adult females

(5:4 8 2:1). It may also follow iridoplegia or ocular trauma.

Horner’s syndrome

This involves interruption of the sympathetic nerve supply to the iris.

Appearance

• Unilateral miotic pupil with partial ptosis (due to paralysis of Muller’s

muscle—a small smooth muscle in the upper lid). Movement of the

upper lid should be intact as the levator muscle is supplied by the

oculomotor nerve. There is also a variable interruption of sudomotor

innervation to the ipsilateral side of the face.

• Sweating is absent if the lesion occurs proximal to the carotid plexus,

after which the sudomotor ﬁ bers

separate.

Causes

The protracted course of the sympathetic pathway makes it vulnerable to

disruption at many different points.

• Congenital—often associated with an alteration in iris pigment

(heterochromia); injury or surgery to the neck (avulsion of C8 and

T1 nerve roots results in Klumpke’s paralysis); multiple sclerosis;

caver nous sinus disease; neoplasia involving the mediastinum, cervical

cord or apex of the lung; infarction—secondary to occlusion of the

basilar or posterior inferior cerebellar artery; thoracic aortic aneurysm;

syringomyelia or syringobulbia

PUPILS

275

Box 10.1 More on the RAPD

At rest, the patient’s pupils are equal and of normal size. RAPD

is relative because the response seen when light is shone on the

affected pupil is less than that seen when light is shone in the normal

pupil, and afferent because it demonstrates a problem in the afferent

limb of the light response in the affected eye. The response indicates

unilateral or asymmetrical optic nerve disease or extensive retinal

pathology. An RAPD will not be seen in patients with corneal or

lens opacities.

CHAPTER 10 Nervous system276

Cranial nerves III, IV, and VI

The third (oculomotor), fourth (trochlear), and sixth (abducens) nerves are

considered together, as their primary function is to provide motor innerva-

tion to the extrinsic muscles of the eye. Connections exist with the horizon-

tal gaze center in the pons and the vertical gaze center in the midbrain.

Applied anatomy: CN III

• Motor: levator palpebrae superioris, superior rectus, medial rectus,

inferior rectus, inferior oblique (all the extrinsic muscles of the eye

except the lateral rectus and superior oblique)

• Autonomic: parasympathetic supply to the constrictor (sphincter)

pupillae of the iris and ciliary muscles

The main oculomotor nucleus lies anterior to the aqueduct of the

midbrain. The Edinger–Westphal nucleus (accessory parasympathetic

nucleus) lies posterior to the oculomotor nucleus. Fibers pass anteriorly,

through the cavernous sinus and enter the orbit through the superior

orbital ﬁ

ssure.

Applied anatomy: CN IV

• Motor: superior oblique

The nucleus lies just inferior to that of the oculomotor nerve and has

connections with the cerebral hemispheres, visual cortex, and nerves III,

VI, and VIII. Its ﬁ

bers pass posteriorly and immediately cross one another.

They then travel through the cavernous sinus, entering the orbit through

the superior orbital ﬁ ssure.

Applied anatomy: CN VI

• Motor: lateral rectus

The nucleus lies beneath the fourth ventricle. It connects with the nuclei

of the III and IV cranial nerves through the medial longitudinal fasciculus

(MLF). It emerges from the pons and travels through the cavernous sinus

to enter the orbit through the superior orbital ﬁ ssure.

Examination

The patient should be sitting facing you with their eyes straight ahead.

Ensure that visual acuity has already been assessed and recorded.

• Inspect the position of the lids.

•

Is there ptosis (drooping of the lid)?

•

Are the epicanthic folds prominent? (This may cause pseudosquint.)

• Look at the position of the eyes in neutral gaze.

•

An asymmetrical position suggests strabismus (squint); this should be

assessed with the cover test (see Box 10.2 , b p. 277).

• Ask the patient to follow your index ﬁ

nger in vertical, horizontal, and

oblique planes, avoiding extremes of gaze. Draw a large imaginary H

directly in front of the patient.

•

Is nystagmus present (rapid to-and-fro movements of the eyes)?

•

Ask the patient if they see double at any stage (diplopia).

• The patient’s eyes should be able to follow the moving target

smoothly. This is termed pursuit . (It is often slowed or interrupted with

saccades in Huntington’s chorea and Parkinson’s disease.)

CRANIAL NERVES III, IV, AND VI

277

• Now hold up your index ﬁ nger on one side of their head and your

thumb on the other—in their temporal visual ﬁ elds. Ask the patient

to look quickly between the ﬁ nger and thumb. This tests saccadic eye

movements—they should be accurate, smooth, and rapid.

• Ask the patient to look from a distant object to a near object—the

eyes should converge smoothly and equally in association with

accommodation and pupil constriction. This is called convergence .

Hints

Patients will often attempt to turn their head to look at your moving

ﬁ nger. This can be overcome in two ways:

• Fully explain the examination before beginning. Often, an instruction,

such as, “Please follow the tip of my ﬁ

nger with your eyes but keep

your head still,” works wonders.

• If the patient continues to turn their head, you can stabilize it by gently

placing your free hand on their forehead.

Abnormal ﬁ ndings

Ptosis (drooping of the lid)

Causes include the following:

• Weakness of the levator muscle in myasthenia gravis

• Third-nerve palsy

• Disruption of insertion of the levator muscle into the tarsal plate of

the lid, through either surgery or trauma

Strabismus or squint

This is an abnormality of coordinated eye movements. In divergent squint,

one eye is directed toward the target, the other is turned laterally. In

convergent squint, the other eye is turned medially.

Squint is broadly categorized into two forms:

• Nonparalytic: seen in childhood. Both eyes have full range of movement

but only one eye is directed toward the target of ﬁ xation.

• Paralytic: Movement of one or more of the extraocular muscles

is decreased because of disease of the muscle, a nerve palsy, or a

physical obstruction to movement in a particular direction (e.g.,

tethering, trauma, or neoplasm).

Box 10.2 Cover–uncover test

This test is used for further analysis of nonparalytic squint.

• The patient should be sitting in front of you.

• Present a ﬁ

xation target in front of them (the top of your pen, for

example).

• Ask them to cover their right eye.

• Closely observe the uncovered left eye—one of three responses is

possible:

•

The eye doesn’t move—normal

•

The eye moves nasally to ﬁ xate—divergent squint present

•

The eye moves temporally to ﬁ xate—convergent squint present

• Now repeat the test, covering the left eye.

CHAPTER 10 Nervous system278

Pick up a subtle squint by holding a pen light about 10 inches away from

the center of the patient’s face. The reﬂ ection of light should be from the

same position on the cornea in both eyes. If this is not the case, the ﬁ xating

eye will have the central reﬂ ection.

0 A more sophisticated assessment of squint is made in eye clinics, using

a syntophore.

Further assessment of a squint should always involve a detailed exami-

nation of the cornea, lens, vitreous, and retina, to exclude opacities and

abnormalities.

Nystagmus

For oscillating movements of the eyes, there are several subclassiﬁ

cations

based on clinical appearance and lesion location. Watch the movements

carefully. Are the to-and-fro phases of the movements the same speed in

both directions, or is one more rapid than the other?

Vestibular

This is a type of jerk nystagmus (to-and-fro movements are of different

velocities). It is caused by disease in the labyrinth or its central connec-

tions. The fast phase is away from the side of the lesion. There are often

horizontal and rotary components. It is usually only present in the acute

phase of labyrinthine disease.

Pendular nystagmus

The velocity of the movements is the same in both directions. This is often

a congenital condition associated with d visual acuity. It is also seen in

cerebrovascular disease and multiple sclerosis.

Patients with acquired nystagmus will often complain of continual move-

ment of their visual environment (oscillopsia), which is not the case with

congenital nystagmus.

Optokinetic nystagmus

This is a normal response of the eye when trying to follow a moving object

(e.g., when looking from the window of a train). It is formally assessed

using a rotating drum painted with vertical black and white lines.

Movements are controlled by the cerebral hemisphere, toward which

the drum is rotating, causing pursuit movement in the direction of rotation

followed by saccadic movement back in the opposite direction. Defective

optokinetic nystagmus is seen in lesions of the deep parietal lobe, when

drum rotation is toward the affected cerebral hemisphere.

Upbeat nystagmus

The fast phase is upward. Causes include brainstem disease, intoxication

with alcohol, and a number of other drugs, including phenytoin.

Downbeat nystagmus

The fast phase is downward. This is seen in toxic states and demyelinating

disease. There is also herniation of cerebellar tissue through the foramen

magnum, as seen in Chiari malformation.

CRANIAL NERVES III, IV, AND VI

279

Gaze-evoked nystagmus

The fast phase is toward the direction of action of the affected muscle.

This is usually seen in dysfunction of extraocular muscles secondary to

intrinsic weakness or nerve palsy.

Hint

When assessing nystagmus, try to avoid the extremes of lateral gaze (i.e.,

not >30*). This will elicit end-point nystagmus —a physiological response

not to be confused with a pathological process.

CHAPTER 10 Nervous system280

Palsies of cranial nerves III, IV, and VI

CN III: oculomotor

Appearance

The pupil is dilated and responds to neither light nor accommodation.

All of the extraocular muscles are paralyzed except for the lateral rectus

and the superior oblique. The unopposed action of these causes the eye

to look down and out. Paralysis of the levator muscle causes complete

ptosis.

Causes

These include diabetes mellitus (pupil sparing), lesions involving the supe-

rior orbital ﬁ ssure, cavernous sinus disease, aneurysm of the posterior

communicating artery, and Weber’s syndrome (associated contralateral

hemiplegia).

CN IV: trochlear

Appearance

Paralysis of the superior oblique causes the eye to elevate when adducting.

The patient will complain of diplopia and have difﬁ culty looking down-

ward and inward on the affected side. The patient may try to compen-

sate for this by tilting their head away from the side of the lesion (ocular

torticollis).

Causes

Trauma, surgery, diabetes mellitus, atherosclerosis, or neoplasia may be

involved.

CN VI: abducens

Appearance

Paralysis of the lateral rectus muscle means the eye cannot be abducted

from the midline and the unopposed action of the medial rectus leaves

the eye deviated nasally at rest. The patient will complain of diplopia in

horizontal gaze. Lesions in the sixth nerve nucleus also involve the lateral

gaze center and lead to a gaze paresis.

Causes

These include diabetes mellitus, atherosclerosis, multiple sclerosis, neo-

plastic lesions, raised ICP leading to compression of the nerve on the

edge of the petrous temporal bone (a false localizing sign), trauma, and

surgery.

Combined nerve palsies

Given the close proximity of nerves III, IV, and VI at points along their

courses, lesions at speciﬁ c anatomical locations can lead to combined

nerve palsies.

Cavernous sinus

All three nerves involved in oculomotor control, along with sympathetic

ﬁ bers to the iris and the ophthalmic and maxillary divisions of the trigemi-

nal nerve, pass through here.

PALSIES OF CRANIAL NERVES III, IV, AND VI

281

Common lesions include caroticocavernous ﬁ stula; expanding pituitary

tumor; cavernous sinus thrombosis, associated with proptosis and injec-

tion of conjunctival vessels (chemosis); and an aneurysm.

Orbit

A complex range of ophthalmoplegias can result from any compres-

sive lesion located within the orbit. Proptosis may be present with vari-

able optic nerve involvement. Many lesions may directly impinge on the

extraocular muscles as well as the innervating nerves.

Superior orbital ﬁ ssure

The superior orbital ﬁ ssure transmits all the nerves supplying the extraoc-

ular muscles along with the ophthalmic division of the trigeminal nerve.

Inﬂ ammation or a lesion at the superior orbital ﬁ ssure leads to Tolosa–

Hunt syndrome , a complex unilateral ophthalmoplegia associated with

anesthesia over the forehead and ocular pain.

Some other eye movement disorders

Internuclear ophthalmoplegia

This is interruption of the MLF, connecting the nuclei of cranial nerves III

and VI on opposite sides.

Voluntary gaze toward one side is initiated by the opposite cerebral

hemisphere. Descending ﬁ bers then decussate to the horizontal gaze

center in the pons and parapontine reticular formation where further

impulses are transmitted directly to the sixth nerve nucleus, causing

abduction of the ipsilateral eye.

Conjugate adduction of the contralateral eye is brought about by

impulses transmitted via the medial longitudinal fasciculus to the third

nerve nucleus, thus maintaining binocular single vision.

Appearance

• Impaired adduction in the ipsilateral eye in unilateral lesions.

Nystagmus is often seen in the abducting eye.

• Bilateral lesions often cause vertical nystagmus and impaired vertical

pursuit.

• Convergence remains intact.

• The patient will complain of horizontal diplopia due to impaired

adduction on the affected side, not to nystagmus in the abducting eye.

Common causes

• Cerebrovascular disease, multiple sclerosis

Lesions of the parapontine reticular formation (PPRF)

The PPRF is responsible for conjugate eye movements in horizontal gaze.

Appearance

• Failure of horizontal eye movements toward the side of the lesion—a

horizontal gaze paresis

• An ipsilateral internuclear ophthalmoplegia if the lesion extends to

involve the MLF

• Preservation of vertical gaze

• Contralateral deviation of the eyes in the acute phase

CHAPTER 10 Nervous system282

Causes

• Vascular disease, demyelinating disease, neoplasia

Parinaud’s syndrome

Lesions occurring in the dorsal midbrain involve the vertical gaze center,

hence this syndrome is also known as dorsal midbrain syndrome.

Appearance

• Impaired upward gaze in both eyes, resulting in convergence,

retraction of the globe into the orbit, and nystagmus

• Light-near dissociation of the pupils—the near reﬂ

ex is intact but

response to light is poor.

Causes

• Demyelinating disease, vascular disease affecting the dorsal midbrain,

enlarged third ventricle

CRANIAL NERVE V: TRIGEMINAL

283

Cranial nerve V: trigeminal

Applied anatomy

Sensory

• Facial sensation in three branches—ophthalmic (V1), maxillary (V2),

and mandibular (V3). Distribution is shown in Fig. 10.7 .

Motor

• Muscles of mastication

Nerve originates in the pons, travels to trigeminal ganglion at the petrous

temporal bone, and splits. V

1

passes through the cavernous sinus with

CN III and exits via the superior orbital ﬁ ssure; V

2

leaves via the infraor-

bital foramen (also supplies the palate and nasopharynx); V

3

exits via the

foramen ovale with the motor portion.

Examination

Inspection

Inspect the patient’s face—wasting of the temporalis will show as hollow-

ing above the zygomatic arch.

Testing motor function

• Ask the patient to clench their teeth. Feel both sides for the bulge of

the masseter and temporalis.

• Ask the patient to open their mouth wide—the jaw will deviate

toward the side of a V lesion.

• Again ask them to open their mouth, but provide resistance by holding

their jaw closed with one of your hands.

V

1

V

2

V

3

Fig. 10.7 Distribution of the sensory branches of the trigeminal nerve.

V

1

= ophthalmic, V

2

= maxillary, V

3

= mandibular. Note that V

1

extends to the

vertex and includes the cornea and V

3

does not include the angle of the jaw.

CHAPTER 10 Nervous system284

Testing sensory function

• Assess light touch for each branch and ask patient to say “yes” if felt.

•

Choose three spots to test on each side to make the examination

easy to remember—forehead, cheek, and mid-way along jaw.

• For each branch, compare left to right. Ignore minor differences (it’s

difﬁ

cult to press with exactly the same force each time).

• Test pin-prick sensation at the same spots, using a sterile pin.

• Temperature sensation is not routinely tested—consider this only if

abnormalities in light touch or pin-prick are found. Use specimen tubes

or other small containers full of hot or cold water.

Findings

• Wasting of muscles: long-term V palsy, motor neuron disease (MND),

myotonic dystrophy

• Loss of all sensory modalities: V ganglion lesion (e.g., herpes zoster)

• Loss of light touch only—with loss of sensation on ipsilateral side of

the body: contralateral parietal lobe (sensory cortex) lesion.

• Loss of light touch in V only: lesion at sensory root pons

• Loss of pin-prick only—along with contralateral side of body: ipsilateral

brainstem lesion

• Loss of sensation in muzzle distribution (nose, lips, anterior cheeks):

damage to the lower part of the spinal sensory nucleus (syringomyelia,

demyelination)

Reﬂ exes

Jaw jerk

0Explain to the patient what you will do; this could appear threatening!

• Ask the patient to let their mouth hang loosely open.

• Place your ﬁ

nger horizontally across their chin and tap your ﬁ nger

with

a patella hammer.

• Feel and watch jaw movement.

•

There should be a slight closure of the jaw, but this varies widely in

normal people. A brisk and deﬁ nite closure may indicate an upper

motor neuron (UMN) lesion above the level of the pons (e.g.,

pseudobulbar palsy).

Corneal reﬂ ex

Afferent = V

1

, efferent = VII.

• Ask the patient to look up and away from you.

• Gently touch the cornea with a wisp of cotton wool. Bring this in from

the side so it cannot be seen approaching.

• Watch both eyes. A blink is a normal response.

•

No response = ipsilateral V

1

palsy

•

Lack of blink on one side only = VII palsy

• Watch out for contact lenses, as they will give a reduced sensation.

Ask the patient to remove them ﬁ rst.

Hints

• Note the sensory distribution. The angle of the jaw is not supplied by

V

3

but by the great auricular nerve (C2, C3).

• When testing the corneal reﬂ ex, touch the cornea (overlies the iris),

not the conjunctiva (overlies the sclera).

CRANIAL NERVE VII: FACIAL

285

Cranial nerve VII: facial

Applied anatomy

• Sensory: external auditory meatus, tympanic membrane, small portion

of skin behind the ear. Special sensation: taste anterior 2/3 of tongue

• Motor: muscles of facial expression, stapedius

• Autonomic: parasympathetic supply to lacrimal glands

The nucleus lies in the pons, the nerve leaves at the cerebellopontine

angle with CN VIII. The nerve gives off a branch to the stapedius at the

geniculate ganglion, while most of the nerve leaves the skull via the stylo-

mastoid foramen and travels through the parotid gland.

Examination

Muscles of facial expression

Test both the left and right sides at the same time. Some patients have

difﬁ cultly understanding the instructions—the authors recommend a quick

demonstration following each command, allowing the patient to mirror

you (e.g., “puff out your cheeks like this”). This exam can be quite embar-

rassing; the examiner making equally strange faces can lighten the mood

and aid in the patient’s cooperation and enthusiasm.

• Look at the patient’s face at rest. Look for asymmetry in the nasolabial

folds, angles of the mouth, and forehead wrinkles.

• Ask the patient to raise their eyebrows (“look up!”). Watch the

forehead wrinkle.

• Attempt to press their eyebrows down and note any weakness.

• Ask patient to close their eyes tightly. Watch, then test against

resistance with your ﬁ

nger and thumb, saying, “Don’t let me pull

them apart.”

• Ask the patient to blow out their cheeks. Watch for air escaping on

one side.

• Ask the patient to bare their teeth (e.g., “show me your teeth!”). Look

for asymmetry.

• Ask the patient to purse their lips and to whistle for you. Look for

asymmetry. The patient will always smile after whistling (see below).

Whistle-smile sign

Failure to smile when asked to whistle (whistle-smile negative) is usually

due to emotional paresis of the facial muscles and is synonymous with

Parkinsonism.

External auditory meatus

This should be examined brieﬂ

y if only CN VII is examined—it can be

done as part of CN VIII if examining all the cranial nerves.

Taste

This is rarely tested outside specialist clinics.

• Each side is tested separately, using cotton buds dipped in the solution

of choice applied to each side of the tongue. Be sure to swill the

mouth with distilled water between each taste sensation.

• Test sweet, salty, bitter (quinine), and sour (vinegar).

CHAPTER 10 Nervous system286

Findings

• Upper motor nerve lesion will cause loss of facial movement on the

ipsilateral side but with preservation of forehead wrinkling—both

sides of the forehead receive bilateral nervous supply (unilateral =

cerebrovascular accident [CVA], etc.; bilateral = pseudobulbar palsy,

motor neuron disease).

• Lower motor nerve lesion will cause loss of all movement on the

ipsilateral side of the face (unilateral = demyelination, tumors, Bell’s

palsy, pontine lesions, cerebellopontine angle lesions; bilateral =

sarcoid, Guillain–Barré syndrome [GBS], myesthenia gravis).

• Bell’s palsy: idiopathic unilateral LMN VII paresis

• Ramsay–Hunt syndrome: unilateral paresis caused by herpes at the

geniculate ganglion (look for herpes rash on the external ear)

Hints

• Bell’s phenomenon is the upward movement of the eyeballs when the

eye closes. This occurs in the normal state but can be clearly seen if

the eyelids fail to close because of VII palsy.

• VII palsy does not cause eyelid ptosis.

• Long-standing VII palsy can cause ﬁ

brous contraction of the muscles

on the affected side, resulting in a more pronounced nasolabial fold

(the reverse of the expected ﬁ ndings).

• Bilateral VII palsy will cause a sagging, expressionless face and is often

missed.

(a)

(d) (e)

(b) (c)

Fig. 10.8 Testing the muscles of facial expression as described on b p. 285.

(a) Eyebrows; (b) eyelids; (c) pufﬁ ng out the cheeks; (d) baring teeth; (e) whistle.

CRANIAL NERVE VIII: VESTIBULOCOCHLEAR

287

Cranial nerve VIII: vestibulocochlear

Applied anatomy

• Sensory: hearing (cochlear), balance and equilibrium (vestibular)

• Motor: none

The eighth nerve comprises two parts.

The cochlear branch originates in the organ of Corti in the ear and passes

through the internal auditory meatus to its nucleus in the pons. Fibers pass

to the superior gyrus of the temporal lobes.

The vestibular branch arises in the utricle and semicircular canals, joins

the auditory ﬁ

bers in the facial canal, enters the brainstem at the cerebel-

lopontine angle, and ends in the pons and cerebellum.

Examination

Inquire ﬁ rst about symptoms—hearing loss or changes, or balance prob-

lems. Peripheral vestibular lesions cause ataxia during paroxysms of ver-

tigo but not at other times.

Begin by inspecting each ear as described in b Chapter 6 (p. 132).

Hearing

Test each ear separately. Cover one by pressing on the tragus or cre-

ate white noise by rubbing your ﬁ ngers together at the external auditory

meatus.

Simple test of hearing

• Whisper a number into one ear and ask the patient to repeat it.

• Repeat with the other ear.

• Be careful to whisper at the same volume in each ear (the end of

expiration is best) and at the same distance (about 24 inches).

Rinne’s test

• Tap a 512 Hz* tuning fork and hold adjacent to the ear (air

conduction, Fig. 10.9a ).

• Then apply the base of the tuning fork to the mastoid process (bone

conduction)—see Fig. 10.9b .

• Ask the patient which position sounds louder.

•

Normal = air conduction > bone conduction = “Rinne’s positive”

•

In neural (or perceptive) deafness, Rinne’s test will remain positive.

•

In conductive deafness, the ﬁ ndings are reversed (bone > air).

Weber’s test

• Tap a 512 Hz tuning fork and hold the base against the vertex or

forehead at the midline (see Fig. 10.9c ).

• Ask the patient if it sounds louder on one side.

•

In neural deafness, the tone is heard better in the intact ear.

•

In conductive deafness, the tone is heard better in the

affected ear.

* This is the C above middle C for those musically inclined.

CHAPTER 10 Nervous system288

Vestibular function

Turning test

• Ask the patient to stand facing you, with arms outstretched.

• Ask them to march on the spot, then close their eyes (continue

marching).

• Watch!

•

The patient will gradually turn toward the side of the lesion;

sometimes they will turn right round 180*.

Hallpike’s maneuver

This is a test for benign positional vertigo (BPV). Do not test those with

known neck problems or possible posterior circulation impairment.

• Explain to the patient what will happen.

• Sit the patient facing away from the edge of the bed such that when

they lie back, their head will not be supported (over the edge).

• Turn their head to one side and ask them to look in that direction.

• Lay them back quickly, supporting their head so that it lies about 30*

below the horizontal.

• Watch for nystagmus (the affected ear will be lowermost).

• Repeat with the head turned in the other direction.

•

No nystagmus = normal

•

Nystagmus, with a slight delay (10 seconds) and fatigable (can’t be

repeated successfully for 10–15 minutes) = BPV

•

Nystagmus, no delay and no fatiguing = central vestibular syndrome

(a)

(b)

(c)

Fig. 10.9 (a) Testing air conduction. (b) Testing bone conduction. (c) Position

of the tuning fork for Weber’s test.

CRANIAL NERVES IX AND X

289

Cranial nerves IX and X

The ninth (glossopharyngeal) and tenth (vagus) nerves are considered

together as they have similar functions and work together to control the

pharynx, larynx, and swallowing.

Applied anatomy: IX

• Sensory: pharynx, middle ear. Special sensation: taste on posterior 1/3

of tongue

• Motor: stylopharyngeous

• Autonomic: parotid gland

This nerve originates in the medulla, passes through the jugular foramen.

Applied anatomy: X

• Sensory: tympanic membrane, external auditory canal, and external

ear. Also proprioception from thorax and abdomen

• Motor: palate, pharynx, and larynx

• Autonomic: carotid baroreceptors

This nerve originates in the medulla and pons, leaves the skull via the

jugular foramen.

Examination

Pharynx

• Ask the patient to open their mouth. Inspect the uvula (use a tongue

depressor if necessary). Is it central or deviated to one side? If to one

side, which side?

• Ask the patient to say “aah.” Watch the uvula. It should move upward

centrally. Does it deviate to one side?

Gag reﬂ ex

This is unpleasant for the patient and should only be tested if a IX or X

nerve lesion is suspected (afferent signal = IX, efferent = X).

• With the patient’s mouth open wide, gently touch the posterior

pharyngeal wall on one side with a tongue depressor or other sterile

stick.

• Watch the uvula (it should lift up).

• Repeat on the opposite side.

• Ask the patient if they felt the two touches and if there was any

difference in sensation.

Larynx

• Ask the patient to cough. Normal character? Gradual onset or sudden?

• Listen to the patient’s speech. Note volume and quality and whether it

appears to fatigue (gets quieter as time goes on).

Test swallow

• At each stage, watch the swallow action. Are there two phases or

one smooth movement? Delay between ﬂ

uid leaving the mouth (oral

phase) and pharynx and larynx reacting (pharyngeal phase)? Is there

any coughing or choking? Any “wet” voice?

• Terminate the test at the ﬁ

rst sign of the patient aspirating.

CHAPTER 10 Nervous system290

• Offer the patient a teaspoon of water to swallow. Repeat x 3.

• Offer the patient a sip of water. Repeat x 3.

• Offer the patient the glass for a mouthful of water. Repeat x 3.

Findings

Uvula

• Moves to one side = X lesion on the opposite side

• No movement = muscle paresis

• Moves with “aah” but not gag and d pharyngeal sensation = IX palsy

Cough

• Gradual onset of a deliberate cough = vocal cord palsy

• “Wet,” bubbly voice and cough (before the swallow test) = pharyngeal

and vocal cord palsy (X palsy)

• Poor swallow and aspiration = combined IX and X or lone X lesion

CRANIAL NERVE XI: ACCESSORY

291

Cranial nerve XI: accessory

Applied anatomy

• Sensory: none

• Motor: sternocleidomastoids and upper part of trapezii

The accessory nerve is composed of cranial and spinal parts. The cra-

nial accessory nerve arises from the nucleus ambiguous in the medulla.

The spinal accessory nerve extends from the lateral part of the spinal

cord down to C5 as a series of rootlets. These join together and ascend

adjacent to the spinal cord, passing through the foramen magnum to join

with the cranial portion of the accessory nerve. It leaves the skull via the

jugular foramen.

The cranial portion joins with the vagus nerve (X). The spinal portion

innervates the sternocleidomastoids and the upper ﬁ

bers of the trapezii.

2 Note that each cerebral hemisphere controls the ipsilateral sternoclei-

domastoid and the contralateral trapezius.

Examination

The cranial portion of the accessory nerve cannot be tested separately.

• Inspect the sternocleidomastoids. Look for wasting, fasciculation,

hypertrophy, and any abnormal head position.

• Ask the patient to shrug their shoulders, and observe.

• Ask the patient to shrug again, using your hands on their shoulders to

provide resistance.

• Ask the patient to turn their head to each side, ﬁ

rst without and then

with resistance (use your hand on their cheek).

Findings

Isolated accessory nerve lesions are very rare. CN XI lesions usually

present as part of a wider weakness or neurological syndrome.

• Bilateral weakness: with wasting caused by muscular problems or

motor neuron disease

• Unilateral weakness (trapezius and sternomastoid same side) suggests a

peripheral neurological lesion.

• Unilateral weakness (trapezius and sternomastoid of opposite sides),

usually with hemiplegia, suggests a UMN lesion ipsilateral to the weak

sternomastoid.

Hints

• Remember that the action of the sternocleidomastoid is to turn the

head to the opposite side (e.g., poor head turning to the left indicates a

weak right sternocleidomastoid).

• When providing resistance to head turning, be sure to press against

the patient’s cheek (see Fig. 10.10 ). Lateral pressure to the jaw can

cause pain and injury, particularly in older and frail patients.

CHAPTER 10 Nervous system292

(a)

(b)

Fig. 10.10 (a) Using resistance against lateral head-turning. Be careful not to apply

pressure to the patient’s jaw. (b) Testing the trapezius against resistance.

CRANIAL NERVE XII: HYPOGLOSSAL

293

Cranial nerve XII: hypoglossal

Applied anatomy

• Sensory: none

• Motor: muscles of the tongue

The nucleus lies on the ﬂ oor of CN IV ventricle. Fibers pass ventrally,

leaving the brainstem lateral to the pyramidal tracts. The nerve leaves the

skull via the hypoglossal foramen.

Examination

• Ask the patient to open wide and inspect the tongue on the ﬂ oor

of the mouth. Look for size and evidence of fasciculation.

• Ask the patient to protrude the tongue. Look for deviation or

abnormal movements.

• Ask the patient to move the tongue in and out repeatedly, then from

side to side.

• To test for subtle weakness, place your ﬁ

nger on the patient’s cheek

and ask them to push against it from the inside, using their tongue.

Findings

• A LMN neuron lesion will cause fasciculation on the affected side and

a deviation toward the affected side on protrusion. There will also be

a weakness on pressing the tongue away from the affected side.

• A unilateral UMN lesion will rarely cause any clinically obvious signs.

• A bilateral UMN lesion will give a small, globally weak tongue with

reduced movements.

• A bilateral LMN lesion (e.g., motor neuron disease) will also produce a

small, weak tongue.

• Rapid in-and-out movement on protrusion (trombone tremor) can be

caused by cerebellar disease, extrapyramidal syndromes, and essential

tremor.

Hint

Rippling movements may be seen if the tongue is held protruded for long

periods. This is normal and should not be mistaken for fasciculations.

CHAPTER 10 Nervous system294

Motor: applied anatomy

The motor system is complex. A detailed description is beyond the scope

of this book; what follows is a brief overview.

Cortex

The primary motor area is the precentral gyrus of the cerebrum. It is here,

along with adjacent cerebral areas, that initiation of voluntary movement

occurs. Muscle groups are represented by areas of the cortex from medial

to lateral, as shown in Fig. 10.11 . The size of the area dedicated to muscle

corresponds to the precision of movement (= the number of motor units

that are involved).

Pyramidal (direct) pathways

These are concerned with precise, voluntary movements of the face, vocal

cords, hands, and feet. The simplest pathways consist of two neurons. The

upper motor neuron (UMN) originates in the cerebral cortex then passes

down through the internal capsule, brainstem, and spinal cord where it

synapses with a lower motor neuron (LMN). This, in turn, leaves the cord

to synapse with the skeletal muscle ﬁ bers.

There are three pyramidal tracts:

• Lateral corticospinal: control of precise movement in the hands and feet

and represents 90% of the UMN axons. These cross over (decussate)

in the medulla oblongata before continuing to descend so that nerves

from the right side of the brain control muscles on the left of the body

and vice versa.

Swallowing

Tongue

Jaw

Lips

Face

Eye

Brow

Neck

Thumb

Index

Middle

Little

Hand

Wrist

Elbow

Shoulde

r

Trunk

Hip

Knee

Ankle

Toes

Ring

Fig. 10.11 Coronal section through the motor cortex showing the representation

of different muscle groups. Note the larger areas given to those muscles performing

precise movements—hands, face, and lips.

MOTOR: APPLIED ANATOMY

295

• Anterior corticospinal: control of the neck and trunk and holds 10% of

the UMN axons. These do not cross in the medulla but descend in the

anterior white columns of the spinal cord. They decussate at several

spinal levels and exit at the cervical and upper thoracic segments.

• Corticobulbar: voluntary muscles of the eyes, face, tongue, neck, and

speech. They terminate at nuclei in the pons and medulla, some

crossed, others not. They control cranial nerves III, IV, V, VI, VII, IX, X,

XI, and XII.

Extrapyramidal (indirect) pathways

These constitue all of the other descending pathways. They are complex

circuits involving the cortex, limbic system, basal ganglia, cerebellum, and

cranial nerve nuclei. There are ﬁ ve major tracts controlling precise move-

ments of the hands and feet, movement of the head and eyes in response

to visual stimuli, muscle tone, and truncal stability and balance.

Basal ganglia and nuclei are complex circuits concerned with the pro-

duction of automatic movement and planning movement sequences. They

also appear to inhibit intrinsically excitable circuits.

Cerebellum

This is involved in learning and performing skilled, automatic movements

(e.g., running, playing the piano) and in posture and balance. It monitors

intention, receives signals for actual movements, compares the difference,

and makes corrective adjustments.

Box 10.3 A word about functional weakness

Large parts of the neurological examination rely on cooperation of the

patient. Occasionally, patients can give the appearance of neurological

disability that does not exist, for any number of psychiatric or psychoso-

cial reasons. The examination here is very difﬁ

cult even for very expe-

rienced practitioners. Consider a functional component to the problem

if you see the following:

• Abnormal distribution of weakness

• Normal reﬂ

exes and tone despite weakness

• Movements are variable and power erratic.

• Variation is seen on repeat testing.

Be careful! Don’t jump to conclusions. Do not assume symptoms are

functional if they are unusual. All patients should be given the beneﬁ t

of

the doubt. Functional weakness is a diagnosis largely of exclusion.

CHAPTER 10 Nervous system296

Motor: inspection and tone

Inspection

As for any other system, the examination begins when you ﬁ rst set eyes

on the patient and continues through the history-taking.

• Any walking aids or abnormal gait (see b p. 321)?

• Shake hands—abnormalities of movement? Strength? Relaxation?

• Any abnormal movements when sitting?

• Any obvious weaknesses (e.g., hemiplegia)?

• Does the patient have good sitting balance?

Inspection can be formalized at the examination stage of the encounter.

The patient should be seated or lying comfortably with as much of their

body exposed as possible. Look at all muscle groups for the following:

• Abnormal positioning, due to weakness or contractures

• Wasting

• Fasciculation (irregular contractions of small areas of muscle)

Make a point of inspecting the shoulder girdle, small muscles of the hand,

quadriceps, anterior compartment of the lower leg, and ankle. Look at the

foot for contractures or abnormalities of shape.

Tone

The aim is to test resting tone in the limbs. This takes practice; the feel of

normal, d or i tone can be taught only through experience.

0The assessment can be difﬁ

cult, as it relies on the patient being relaxed;

telling the patient to relax usually has the opposite effect! They can be

distracted by a counting task or told to relax the limb “as if you’re asleep.”

Distracting the patient with light conversation is a generally successful

ploy. You should also repeat the following maneuvers at different speeds

and intervals to catch the patient at an unguarded moment.

Arms

• Take the patient’s hand in yours (as if shaking it) and hold their elbow

with your other hand (see Fig. 10.12a ). From this position, you can

•

Pronate and supinate the patient’s forearm.

•

Roll the patient’s wrist through 360*.

•

Flex and extend the patient’s elbow.

Legs

• Hip: With the patient lying ﬂ at, legs straight, hold onto the patient’s

knee and roll it from side to side (see

Fig. 10.12b ).

• Knee: With the patient in the same position, put your hand behind

the patient’s knee and raise it quickly ( Fig. 10.12c ). Watch the heel—it

should lift from the bed or exam table slightly if tone is normal.

• Ankle: Holding the foot and the lower leg, ﬂ

ex and dorsiﬂ

ex the ankle

( Fig. 10.12d ).

MOTOR: INSPECTION AND TONE

297

Findings

Normal tone

• Slight resistance in movement (feel through experience)

d Tone

• Flaccid due to LMN or cerebellar lesions or myopathies

i Tone

• Spasticity (clasp-knife rigidity): The limb appears stiff. With increased

pressure, there is a sudden give and the limb moves. This is seen in

UMN lesions.

• Rigidity (lead pipe): The limb is equally stiff through all movements.

• Rigidity (cogwheel): an extrapyramidal sign, caused by tremor super-

imposed on a rigid limb. The limb moves in a stop–go halting fashion.

• Gegenhalten: (paratonia) seen in bilateral frontal lobe damage and

catatonic states. Tone i with i pressure from the examiner—the

patient appears to be resisting movement.

• Myotonia: a slow relaxation after action. When asked to make a ﬁ st,

the patient is unable the release it quickly and will be slow to let go of

a handshake (e.g., myotonic dystrophy).

• Dystonia: The limb or head has an abnormal posture that looks

uncomfortable.

(a) (b)

(c) (d)

Fig. 10.12 Testing tone. (a) Testing the upper limb. (b) Testing tone at the hip.

(c) Testing tone at the knee. (d) Testing tone at the ankle.

CHAPTER 10 Nervous system298

Motor: upper limb power

As for the muscles of the face, the examiner should demonstrate each

movement, mirroring the patient (see Fig. 10.13 ).

This also allows each action that the patient makes to be opposed by

the same (or similar) muscle groups in the examiner—test their ﬁ ngers

against your ﬁ ngers, and so on. Each muscle group should be graded from

0 to 5 according to the system shown in Box 10.4 .

Examination of the upper limbs also allows both sides to be tested at

once, providing direct comparison between left and right (see Fig.10.13 ).

0Be careful not to hurt frail, elderly patients or those with osteoarthritis

(OA), rheumatoid arthritis (RA), or other rheumatological disease.

Shoulder

• Abduction (C5): Ask the patient to abduct their arms with elbows

bent. Ask them to hold still as you attempt to push their arms down.

• Adduction (C6, C7): The patient should hold their arms tightly to their

sides with elbows bent. You attempt to push their arms out.

Elbow

• Flexion (C5, C6): The patient holds their elbows bent and supinated in

front of them. Hold the patient at the elbow and wrist and attempt to

extend their arm: “Don’t let me straighten your arm!”

• Extension (C7): Patient holds position above as you resist extension at

the elbow by pushing on their distal forearm or wrist: “Push me away!”

Wrist

• Flexion (C6, C7): With arms supinated, the patient should ﬂ ex their

wrist and hold as you try to extend it by pulling from your own wrists.

• Extension (C6, C7): The opposite of ﬂ

exion. The patient holds their

hand out straight and resists your attempts to bend it.

Fingers

• Flexion (C8): Ask the patient to squeeze your ﬁ ngers or

(better) ask

the patient to grip your ﬁ ngers palm to palm (see Fig. 10.13c ) and

resist your attempts to pull their hand open.

• Extension (C7, C8): Ask the patient to hold their ﬁ

ngers out straight.

You support their wrist with one hand and try to push their ﬁ ngers

down with the side of your hand over their ﬁ

rst interphalangeal joints.

• Abduction (T1): Ask the patient to splay their ﬁ

ngers out and resist

your attempts to push them together.

• Adduction (T1): Holding the patient’s middle, ring, and little ﬁ nger

with one hand and their index ﬁ

nger with the other, ask the patient

to pull their ﬁ

ngers together or place a piece of paper between their

outstretched ﬁ ngers and ask them to resist your attempts to pull it

away.

Pronator drift

This is a useful test of subtle weakness. The patient is asked to hold their

arms outstretched in front, palms upward and eyes closed. If one side is

weak, the arm will pronate and slowly drift downward.

MOTOR: UPPER LIMB POWER

299

Box 10.4 Muscle strength testing classiﬁ cations

• 5 = Normal power

• 4 = Movement against resistance but not normal

• 3 = Movement against gravity, but not against resistance

• 2 = Movement with gravity eliminated (e.g., can move leg from side

to side on bed but not lift it)

• 1 = Contractions but no movement seen

• 0 = No movement

(a) (b)

(c) (d)

(e) (f)

Fig. 10.13 Testing power in the upper limbs. (a) Shoulder movements. (b) Elbow

movements. (c) Finger ﬂ exion. (d) Finger extension. (e) Finger abduction. (f) Finger

adduction.

CHAPTER 10 Nervous system300

Motor: lower limb power

The patient should be seated on an exam table or bed with legs out-

stretched in front of them. The limbs should be exposed as much as pos-

sible so that contractions of the muscles can be seen .

Again, power is tested for each muscle group on one side and then the

other ( Fig. 10.14 ). Comparing left with right and score results according to

the scale in Box 10.4 (b p. 299).

(a) (b)

(c) (d)

(e)

Fig. 10.14 Testing power in the lower limb against resistance. (a) Flexing the hip.

(b) Extending the hip. (c) Flexing and extending the knee. (d) Plantar ﬂ exion at the

ankle. (e) Dorsiﬂ exion at the ankle.

MOTOR: LOWER LIMB POWER

301

Hip

• Flexion (L1, L2, L3): With the lower limbs lying on the bed or couch,

the patient raises each leg, keeping the knee straight. Oppose the

movement by pushing down on the thigh just above the knee: “Stop

me from pushing down!”

• Extension (L5, S1): Ask the patient to keep their leg pressed against

the bed as you attempt to lift it, either with a hand beneath the calf or

the ankle: “Stop me from lifting your leg up!”

• Abduction (L4, L5, S1): Ask the patient to move their leg out to the

side as you oppose the movement with a hand on the lateral thigh:

“Stop me pushing your legs together!”

• Adduction (L2, L3, L4): With the legs central, put your hand on

the medial thigh and attempt to pull the leg out to the side against

resistance: “Don’t let me pull your legs apart!”

Knee

• Flexion (L5, S1): Take hold of the patient’s knee with one hand and

their ankle with the other and ﬂ ex the leg to about 60

*. (The patient

may think you want them to resist this, so often a quick instruction

of “bend at the knee” is required.) Ask the patient to bend their

leg further (“stop me straightening your leg out”) and oppose the

movement at their ankle.

• Extension (L3, L4): With the patient’s leg in the ﬂ

exion position, have

the patient extend their leg (“push me away,” “straighten your leg

out”) as you oppose it. Alternatively, attempt to bend the patient’s leg

from a straightened starting position.

Ankle

• Plantar ﬂ exion (S1, S2): With the patient’s leg out straight and ankle

relaxed, put your hand on the ball of the foot and ask the patient to

push you away: “Push down and stop me pushing back!”

• Dorsiﬂ exion (L4, L5): From the starting position for plantar ﬂ exion,

hold the patient’s foot just above the toes and ask them to pull their

foot backward. Patients often attempt to move their entire leg here, so

tell them, “Pull your foot back and stop me pushing your foot down,”

along with an accompanying hand gesture.

CHAPTER 10 Nervous system302

Tendon reﬂ exes

Theory

The sudden stretch of a muscle is detected by the muscle spindle, which

initiates a simple two-neuron reﬂ ex arc, causing that muscle to contract.

Tendons are struck with a reﬂ ex hammer (causing a sudden stretch of

the muscle) and the resultant contraction is observed. In LMN lesions or

myopathies, the reﬂ ex is diminished or absent, but is hyperactive or brisk

in UMN lesions.

Technique

The tendons are tapped with a reﬂ ex hammer ( Fig. 10.15 ). For each reﬂ ex,

test the right, then left, and compare. The hammer should be held at the

far end of the handle and swung in a loose movement from the wrist. The

patient should be relaxed (see b p. 303).

Record deep tendon results according to the scale in Box 10.5 .

Examination

Biceps(C5, C6)

With the patient seated, lay their arms across their abdomen. Place your

thumb across the biceps tendon and strike it with the reﬂ ex hammer as

above. Watch the biceps for contraction.

Supinator (C5, C6)

The muscle tested is actually the brachioradialis. With the patient’s arms

lying loosely across their abdomen, put your ﬁ ngers on the radial tuberos-

ity and tap with the hammer. The arm will ﬂ ex at the elbow. If brisk, the

ﬁ ngers may also ﬂ ex.

Triceps (C7)

Taking hold of the patient’s wrist, ﬂ ex their arm to 790*. Tap the triceps

tendon about 5 cm superior to the olecranon process of the ulna. Watch

the triceps.

Fingers (C8)

This is only present if tone is pathologically i. With your palm up and the

patient’s arm pronated, lay their ﬁ ngers on yours. Strike the back of your

ﬁ ngers. The patient’s ﬁ ngers will ﬂ ex.

Knee (L3, L4)

With the patient’s leg extended, use one hand behind their knee to lift

their leg to 760*. Tap the patella tendon and watch the quadriceps. If brisk,

proceed to testing for clonus here.

Knee clonus

With the patient’s leg extended, place your thumb and index ﬁ nger over

the superior edge of the patella. Create a sudden downward (toward the

feet) movement and hold . Watch the quadriceps. Any beat of clonus here

is abnormal.

TENDON REFLEXES

303

(a) (b)

(c) (d)

(e) (f)

(g)

Fig. 10.15 Testing tendon reﬂ exes. (a) Biceps. (b) Triceps. (c) Supinator.

(d) Fingers. (e) Knee. (f) Ankle. (g) Alternative method for ankle.

CHAPTER 10 Nervous system304

Ankle (S1, S2)

With the hip ﬂ exed and externally rotated and the knee ﬂ exed to 790*,

hold the foot and tap the Achilles tendon. Watch the calf muscles for

contraction and ankle ﬂ exion.

Alternatively, with the leg extended and relaxed, place your hand on the

ball of the foot and strike your hand with the hammer.

Augmentation

If the reﬂ ex is absent, it can sometimes be elicited by asking the patient to

perform an augmenting action, which acts to increase the activity of neu-

rons in the spinal cord. This effect is short-lived, however, so you should

aim to test the reﬂ ex in the ﬁ rst 10 seconds of the augmentation.

• For upper limb reﬂ

exes, ask the patient to clench their teeth.

• For lower limb reﬂ

exes, ask the patient to lock their ﬁ ngers

together,

pulling in opposite directions.

Box 10.5 Recording deep tendon reﬂ exes

These are usually recorded as a list, or often by applying the numbers

below to the appropriate area of a stick-man sketch.

• 0 = absent

• ± = present only with reinforcement

• 1+ = less than normal

• 2+ = normal

• 3+ = hyperactive without clonus.

• 4+ = hyperactive with clonus.

OTHER REFLEXES

305

Other reﬂ exes

In normal practice, the plantar response is the only one of the following

routinely tested.

Abdominal reﬂ ex

This test relies on observing the abdominal muscles. It is therefore not

easy in those with a covering of fat. It is also less obvious in children,

the elderly, multiparous patients, or those who have had abdominal

surgery.

• The patient should lie on their back, relaxed, with abdomen exposed.

• Using a tongue depressor or something similar, stroke each of the

4 segments of the abdomen in a brief movement toward the umbilicus.

• As each segment is stroked, the abdominal muscles will reﬂ exively

contract.

• Summarize the ﬁ

ndings diagrammatically using a simple 2 x 2 grid and

indicating the presence or absence of a response by marking “+” and

“–”, respectively (“9” for an intermediate response).

The upper segments are supplied by T8–T9; the lower, by T10–T11.

Cremasteric reﬂ ex (L1, L2)

Given its nature, this reﬂ ex is very rarely tested and requires a full expla-

nation and consent from the patient ﬁ rst.

• With the male patient standing and naked from the waist down, lightly

stroke the upper aspect of their inner thigh.

• The ipsilateral cremaster muscle contracts and the testicle will brieﬂ y rise.

Plantar response (L5, S1, S2)

This is sometimes, inappropriately, called the Babinski reﬂ ex .

• The patient should be lying comfortably, legs outstretched.

• Warn the patient that you are about to touch the sole of their foot

(this may prevent a startled withdrawal response).

• Stroke the patient’s sole with a tongue depressor or similar

disposable item (many people use their ﬁ

ngernail, but this has obvious

implications for sterility).

• Stroke from the heel, up the lateral aspect of the sole to the base of

the ﬁ

fth toe (

Fig. 10.16 ). If there is no response, the stroke can be

continued along the ball of the foot to the base of the big toe.

• Watch the big toe for its initial movement.

•

Normal response is plantar ﬂ exion of the big toe.

•

UMN lesions will cause the big toe to dorsiﬂ ex. This is the Babinski

response.

• Document your ﬁ

ndings using arrows:

•

d for plantar ﬂ exion

•

i for dorsiﬂ exion

•

– for an absent response

• If the leg is withdrawn and the heel moves in a ticklish reaction, this is

called a withdrawal response and the test should be repeated.

CHAPTER 10 Nervous system306

Ankle clonus

A rhythmical contraction of a muscle when suddenly stretched is a sign

of hyperreﬂ exia due to a UMN lesion. With the patient lying on the

bed, knee straight, and thigh slightly externally rotated, suddenly dorsiﬂ ex

the foot. More than three beats of clonus—as long as the foot is held

dorsiﬂ exed—is abnormal.

Fig. 10.16 Testing the plantar response. The arrow shows the direction that the

stroke should take.

PRIMITIVE REFLEXES

307

Primitive reﬂ exes

These are reﬂ exes seen in the newborn, but they may still be present in

a few normal adults. They return somewhat in the elderly but are seen

mainly in frontal lobe disease and encephalopathy.

The primitive reﬂ exes are not routinely tested unless the examiner is

looking speciﬁ cally for frontal lobe signs or Parkinson’s disease.

Glabellar tap

• Using your index ﬁ nger, repeatedly tap (gently) the patient’s forehead

between the eyebrows.

• If normal, the patient will blink only with the ﬁ

rst three or four taps.

Palmomental reﬂ ex

• Stroke the patient’s palm, using sharp, ﬁ rm pressure from the radial

side to the ulnar side.

• Watch the patient’s chin.

• If the reﬂ

ex is present, there will be a contraction of the ipsilateral

mentalis seen in the neck and chin.

Grasp reﬂ ex

• Gently stroke your ﬁ ngers over the patient’s palm in a radial–ulnar

direction, telling the patient not

to grip your hand.

• If present, the patient will involuntarily grasp your hand and seemingly

refuse to let go.

Snout (or pout) reﬂ ex

• With the patient’s eyes closed, gently tap their lips with your ﬁ ngers or

(very cautiously) with a patellar hammer.

• An involuntary puckering of the lips is a positive reﬂ ex.

Suckling reﬂ ex

With the patient’s eyes closed, gentle stimulation at the corner of their

mouth will result in a suckling action at the mouth. The patient’s head may

also turn toward the stimulus.

CHAPTER 10 Nervous system308

Sensory: applied anatomy

The sensory system, like the rest of the nervous system, is vastly complex.

The following is a simpliﬁ ed explanation that should provide enough back-

ground to make sense of the examination technique and ﬁ ndings.

Spinal roots and dermatomes

At each spinal level, a spinal nerve arises that contains sensory and motor

neurons serving a speciﬁ c segment of the body. The area of skin supplied

by the sensory neurons corresponding to each spinal level can be mapped

out—each segment is called a dermatome . See Figs. 10.18 and 10.19 on

b p. 310, 311.

There is considerable overlap such that loss of sensation in just one der-

matome is usually not testable (and textbooks show a marked variation in

dermatome maps). Health sciences students should become familiar with

the dermatomal distribution at an early stage.

Somatic sensory pathways

There are two main spinal pathways for sensory impulses. The clinical

importance of these can be seen in spinal cord damage and is summarized

on b p. 326.

Posterior columns

These convey light touch, proprioception, and vibration sense, as well as

stereognosis (the ability to recognize an object by touch), weight discrimi-

nation, and kinesthesia (the perception of movement).

Nerves from receptors extend up the ipsilateral side of the spinal cord

to the medulla, their axons forming the posterior columns (fasciculus gra-

cilis and fasciculus cuneatus). The second-order neurons decussate (cross

over) at the medulla and travel in the medial lemniscus to the thalamus.

From there, the impulse is conveyed to the sensory cortex.

Spinothalamic tract

This carries pain and temperature sensation. From a clinical point of view,

the important difference here is that the ﬁ rst-order neurons synapse in the

posterior gray horn on joining the spinal cord. The second-order neurons

then cross over and ascend the contralateral side of the cord in the spi-

nothalamic tract to the thalamus.

Sensory cortex

This is located at the postcentral gyrus, just posterior to the motor cortex.

Much like the motor strip, the areas receiving stimuli from various parts of

the body can be mapped out (see Fig. 10.17 ). A lesion affecting one area

will cause sensory loss in the corresponding body area on the contralat-

eral side (see Somatic Sensory Pathways, above).

SENSORY: APPLIED ANATOMY

309

Pharynx

Tongue

Gums, jaw

Lower lip

Lips

Upper lip

Face

Nose

Eye

Thumb

Index

Middle

Ring

Little

Hand

Wrist

Forearm

Elbow

Arm

Shoulder

Head

Neck

Trunk

Hip

Leg

Genitals

Toes

Foot

Fig. 10.17 Sensory cortex map showing areas corresponding to the different

parts of the body. Note the large areas given over to the ﬁ ngers and lips.

CHAPTER 10 Nervous system310

C4 C4

C5

C8

C6

C7

C3 C3

C7

C8

C6

C5

T1

L1 L1

L2 L2

L3 L3

T1

L4

L5

S1 S1

L5

T2

T3

T4

T5

T6

T7

T8

T9

T10

T11

Fig. 10.18 The dermatomes (anterior view). Students should be familiar with

these diagrams, particularly the limbs. Note important landmarks to aid recall

(C7 covers the middle ﬁ nger, T4 lies at the level of the nipples, T10 is over the

umbilicus).

SENSORY: APPLIED ANATOMY

311

C4

C3

C4

C5

C6

C8

S2

L5

L4

L5

S1

L3

L2

C8

C6

C5

S4

S3

T1

S5

C7

T1

L1

L2

T2

T3

T4

T5

T6

T7

T8

T9

T10

T11

T12

Fig. 10.19 The dermatomes (posterior view).

CHAPTER 10 Nervous system312

Sensory examination

This examination can be difﬁ cult, as it requires concentration and co-

operation on the part of both the patient and the examiner. The results

depend on the patient’s response and are thus partly subjective. Many

patients prove unreliable witnesses from a lack of understanding or

attempts to please the examiner. Education, explanation, and reassur-

ance are important at all times.

Often, sensory loss (particularly vibration and temperature) is not

noticed by the patient, and revealing them during the course of an exami-

nation may be upsetting. Keep this in mind as you proceed.

Technique

The examination should be inﬂ uenced by the history. In practice, only light

touch is tested as a quick screening exam if no deﬁ cit is expected.

If you are testing vibration sense and proprioception, it may be best to

test these ﬁ rst, as they require the least concentration and can be used

to assess the patients’ reliability as a witness, before testing the other

sensory modalities.

For each modality, begin at any area of supposed deﬁ cit and work out-

ward, mapping the affected area, then move to a systematic examination

from head to toe. Always test one side, then the other for each limb and

body area. Aim to test one spot in each dermatome.

Light touch

With the patient’s eyes closed, touch their skin with a wisp of cotton wool

and ask them to say “yes” when it is felt. The interval between each touch

should be irregular and unpredictable.

• In practice, a gentle touch with a ﬁ

nger is often used. However, this

risks testing pressure, not light-touch sensation—it is also harder to

ensure that equal force is applied in all areas.

0Do not make tiny stroking movements on the skin—this stimulates hair

ﬁ

bers and is not a test of light touch.

0Be aware of areas where decreased sensation is expected (foot cal-

luses, etc.).

• After testing each limb and body area, double check with the patient:

“Did that feel the same all over?” Explore any areas of abnormal

sensation more thoroughly before moving on.

Sensory inattention

• This is a subtle but often clinically important sign of parietal lobe

dysfunction. The patient feels a stimulus on the affected part, but not

when there is competition from a stimulus on the opposite side.

• Ask the patient to close their eyes and tell you if they feel a touch on

their left or right—use any body part—commonly hands and feet as a

quick screen.

• Touch the right hand, then the left hand, then both.

• The touches should be repeated randomly to conﬁ

rm the result.

SENSORY EXAMINATION

313

•

For example, with a right-sided parietal lesion, the patient will feel

both left and right stimuli, but when both sides are touched, they

will not be able to feel the stimulus on the left.

Vibration sense

A 128 Hz tuning fork (compare with CN VIII) is used.

• Ask the patient to close their eyes, tap the tuning fork, and place the

base on a bony prominence. Ask if the patient can feel the vibration .

• If yes, then conﬁ

rm by taking hold of the tuning fork with your other

hand to stop the vibration after asking the patient to tell you when the

vibration ceases.

• As always, compare left to right and work in a systematic fashion,

testing bony prominences:

•

Fingertip, wrist, elbow, shoulder, anterior superior iliac spine, tibial

tuberosity, matatarsophalangeal joint, and toes

Proprioception

Testing of proprioception in the manner described below provides a

rough gauge, thus results must be interpreted with the rest of the history

and examination.

Loss of position sense is usually distal. Start by testing the patient’s big

toe as follows. This technique can be used at any joint.

• With the patient’s eyes closed and leg relaxed, grasp the distal

phalanyx of the big toe from the sides.

• While stabilizing the rest of the foot, move toe up and down at joint.

• Ask the patient if they can feel any movement and in which direction.

• Flex and extend the joint, stopping at intervals to ask the patient

whether the toe is up or down.

• If proprioception is absent, test other joints, working proximally.

• The toe is gripped from the sides —if held incorrectly, pressure on the

nail may suggest that the toe is pressed down.

• Normal proprioception should allow the patient to identify very subtle

movements that are barely visible.

Box 10.6 Romberg’s sign

This is a further test of joint position sense. When proprioception is lost

in the limbs, patients can often stand and move normally as long as they

can see the limb in question.

0Perform with care, only if you are able to safely catch the patient in

the event of a fall!

• Ask the patient to stand, and you stand facing them.

• Ask the patient to close their eyes.

• If there is loss of proprioception, the patient will lose their balance

and fall. If so, catch them with care, asking them to open their eyes

again immediately if they haven’t already done so.

CHAPTER 10 Nervous system314

Pin-prick

Use a disposable pin or safety pin—not a hypodermic needle, as these

break the skin (a line of tiny wounds up a patient’s arm or weeping edema

up a shin is an infection risk and very embarrassing).

• Test as you would for light touch, gently pressing the pin on the skin.

• Test each dermatome in a systematic way, mapping out abnormalities.

• On each touch, ask the patient to say whether it feels sharp or dull .

• Occasionally, test the patient’s reliability as a witness with a negative

control by using the opposite (blunt) end of the pin.

Temperature

• This is not routinely tested outside of specialist clinics. Loss of

temperature sensation may be evident from the history (accidental

burns?).

• When tested, test tubes or similar vessels containing hot and ice-cold

water are used, and each dermatome is tested as with pin-prick.

• Remember to ensure the exterior of the tube is dry.

COORDINATION

315

Coordination

Coordination should be tested in conjunction with gait (b p. 321).

Cerebellar lesions cause incoordination on the ipsilateral side (b p. 327).

For each of the following, compare performance on the left and right.

Upper limbs

Finger–nose test

• Ask the patient to touch the end of their nose with their index ﬁ nger.

• Hold your own ﬁ

nger out in front of them—at arm’s reach from

the patient—and ask them to then touch the tip of your ﬁ nger with

theirs.

• Ask them to move between their nose and your ﬁ nger

(

Fig. 10.20 ).

• Look for intention tremor (worse as it approaches the target) and

past-pointing (missing the target entirely).

• The test can be made more difﬁ

cult by moving the position of your

ﬁ

nger each time the patient touches their nose.

Rapid alternating movements

• This is hard to describe and should be demonstrated to the patient.

Ask the patient to repeatedly supinate and pronate their forearm,

keeping the other arm still such that they clap their hands palm to

palm, then back to palm, and so on (see Fig. 10.21 ).

• Alternatively, ask them to mimic screwing in a lightbulb.

•

Slow and clumsy = dysdiadokokinesis

•

0 Dysdiadokokinesis is the inability to perform rapidly alternating

movements (diadoke = Greek for “succession”). It is not, as many

students think, the actual test.

Fig. 10.20 Finger–nose testing.

CHAPTER 10 Nervous system316

Rebound

• From a resting (arms at their side) position, ask the patient to quickly

abduct their arms and stop suddenly at the horizontal level.

•

In cerebellar disease, there will be a delay in stopping and the arm

will oscillate about the intended ﬁ nal position.

• Alternatively, pull on the patient’s ﬂ

exed arms (as if testing elbow

ﬂ

exion power) and suddenly let go. If lacking coordination, the patient

will hit his- or herself in the face. This test does little for provider–

patient trust and is rarely performed for obvious reasons.

Lower limbs

Heel–shin test

• With the patient sitting, legs outstretched, ask them to slide the heel

of one foot up and down the shin of the other leg at a moderate pace.

•

A lack of coordination will manifest as the heel moving side to side

about the intended path.

•

In sensory, in contrast to cerebellar, ataxia (lack of proprioception),

patients will perform worse with their eyes closed.

Foot tapping

• The patient taps your hand with their foot as fast as possible.

•

The nondominant side performs poorly in normal individuals.

Fig. 10.21 Testing rapidly alternating movements. This can be hard to describe to

a patient—a brief demonstration is usually required.

SOME PERIPHERAL NERVES

317

Some peripheral nerves

Peripheral nerve lesions may occur in isolation (e.g., trauma, compression,

neoplasia) or as part of a wider pathology (e.g., mononeuritis multiplex).

The following pages describe the signs associated with lesions of a selec-

tion of peripheral nerves.

Upper limb

Median nerve (C6–T1)

• Motor: muscles of the anterior forearm, except ﬂ exor carpi ulnaris, and

LOAF (lateral 2 lumbricals, opponens pollicis, abductor pollicis brevis

and ﬂ

exor pollicis brevis)

• Sensory: thumb, anterior index and middle ﬁ

ngers, as well as some of

the radial side of the palm (see

Fig. 10.22 )

Examining a lesion

• Weakness and wasting of the thenar eminence

• With the hand lying ﬂ

at, palm up, hold your pen above the thumb

and ask the patient to move their thumb vertically to touch it (pen-

touching test)—they will not be able to.

• Often power is good here despite symptoms and obvious carpel

tunnel syndrome.

• For lesions of the nerve at the cubital fossa, perform Ochsner’s

clasping test for weakness of ﬂ

exor digitorum superﬁ

cialis. Ask the

patient to clasp their hands together. If a lesion is present, the index

ﬁ nger will fail to ﬂ ex.

Ulnar nerve (C8–T1)

• Motor: all of the small muscles of the hand except LOAF and ﬂ exor

carpi ulnaris

• Sensory: ulnar side of the hand, little ﬁ

nger, and half of ring ﬁ nger

(see

Fig. 10.22 ).

Examining a lesion

• This is hard to test. There may be visible wasting of the small

muscles of the hand, with clawing of the ﬁ

ngers (extension at the

phalangeometacarpal joints and ﬂ

exion at the interphalangeal joints).

• Froment’s sign: ask the patient to grasp a piece of paper between

their thumb and foreﬁ

nger. Alternatively, ask them to make a ﬁ st.

The

thumb is unable to adduct and so will ﬂ ex instead (see Fig. 10.23 ).

Radial nerve (C5–C8)

• Motor: triceps, brachioradialis, and extensors of the hand

• Sensory: a small area over the anatomical snuffbox—hard to test

Examining a lesion

• Look for wrist drop. If not obvious, ask the patient to ﬂ

ex at the

elbow, pronate the forearm, and extend the wrist (you may need to

demonstrate). Wrist weakness will become clear. See also

Box 10.7

for testing nerve compression.

CHAPTER 10 Nervous system318

Radial

Ulnar

Median

Fig. 10.22 Sensory distribution of the major peripheral nerves in the hand. There

is considerable overlap and the small area supplied by the radial nerve may not be

detectable clinically.

(a) (b)

Fig. 10.23 Froment’s sign. (a) Normal. (b) Froment’s positive.

Box 10.7 Tinel’s sign

This is a test for nerve compression. It is commonly used at the wrist to

test for median nerve compression in carpal tunnel syndrome.

• Percuss the nerve over the site of possible compression (at the

wrist, gently tap centrally near the ﬂ

exor palmaris tendon).

• If the nerve is compressed, the patient will experience tingling in the

distribution of the nerve on each tap.

SOME PERIPHERAL NERVES

319

Lower limb

Lateral cutaneous nerve of the thigh (L2–L3)

• Motor: none

• Sensory: lateral aspect of the thigh (see Fig. 10.24a )

Examining a lesion

There may be some sensory loss as indicated, but in practice this is very

hard to test. Although sensory loss to this nerve is rare, conditions such as

meralgia paresthetica can result in a complete or partial loss of sensation

in this nerve distribution.

Common peroneal nerve (L4–S2)

• Motor: anterior and lateral compartments of the leg

• Sensory: dorsum of the foot and anterior aspect of the leg

Examining a lesion

• Foot drop with corresponding gait (b p. 321). Weakness of foot

dorsiﬂ exion

(

b p. 297) and eversion. Preserved inversion ( Fig. 10.24b )

• In an L5 lesion there will be a similar deﬁ

cit but will also display a

weakness of inversion, hip abduction, and knee ﬂ exion.

Femoral nerve (L2–L4)

• Motor: quadriceps

• Sensory: medial aspect of the thigh and leg (see Fig. 10.24d )

Examining a lesion

• Weakness of knee extension is only slightly affected—hip adduction is

preserved (b p. 356).

• Stretch: With the patient lying prone, abduct the hip, ﬂ

ex the knee and

plantar-ﬂ

ex the foot. The stretch test is positive if pain is felt in the

thigh/inguinal region.

Sciatic nerve (L4–S3)

• Motor: all the muscles below the knee and some hamstrings.

• Sensory: posterior thigh, ankle and foot (see Fig. 10.24c ).

Examining a lesion

• Foot drop and weak knee ﬂ exion

(

b p. 321).

• Knee jerk reﬂ ex

(

b p. 302) is preserved but ankle jerk and plantar

response (b p. 302) are absent.

• Stretch test: with the patient lying supine, hold the ankle and lift the

leg, straight, to 90*. Once there, dorsiﬂ

ex the foot. If positive, pain will

be felt at the back of the thigh.

CHAPTER 10 Nervous system320

(a) (b)

(c) (d)

Fig. 10.24 Distribution of the sensory component of some lower limb nerves.

(a) Lateral cutaneous nerve of the thigh. (b) Common peroneal nerve. (c) Sciatic

nerve. (d) Femoral nerve.

GAIT

321

Gait

This is easily missed from the neurological examination. Gait is often dif-

ﬁ cult to test in a crowded ward or cramped exam room. However, you

should try to incorporate it into your assessment.

Gait can be observed informally as the patient makes their way to the

clinic room or returns to their chair on the ward. Watch the patient stand,

and use the same opportunity for Romberg’s test ( Box 10.6 , b p. 313).

The patient may be simply lacking in conﬁ dence, and this will be evident

later. Do not test if you suspect a severe problem with balance.

Examination

• Ask the patient to walk a few yards, turn, and walk back to you.

• Note especially the following:

•

Use of walking aids

•

Symmetry

•

Length of paces

•

Lateral distance between the feet

•

How high the feet and knees are lifted

•

Bony deformities

•

Disturbance of normal gait by abnormal movements

• You may want to consider asking the patient to

•

Walk on tiptoes (inability = S1 or gastrocnemius lesion)

•

Walk on their heels (inability = L4/L5 lesion—foot drop)

Findings

• Hemiplegia: One side will be obviously weaker than the other with

the patient tilting the pelvis to lift the weak leg, which may swing out

to the side. Gait may be unsafe without the use of walking aid.

• Scissoring: If both legs are spastic (cerebral palsy, MS), toes drag on

ﬂ

oor, trunk sways from side to side, and legs cross over on each step.

• Parkinsonism: ﬂ

exed posture with small, shufﬂ

ing steps. No or little

arm swing. Difﬁ culty starting, stopping, and turning. Gait seems hurried

(festinant) as legs attempt to prevent the body from falling forward.

• Cerebellar ataxia: broad-based (legs wide) gait with lumbering body

movements and variable distance between steps. The patient has

difﬁ

culty turning (be there to catch them).

• Sensory ataxia (loss of proprioception): The patient requires more

sensory input to be sure of leg position so lifts legs high (high-stepping)

and stamps the feet down with a wide-based gait. They may also watch

their legs as they walk. Romberg’s is positive (see Box 10.6 , b p. 313).

• Waddling (weakness of proximal lower limb muscles): The patient fails

to tilt the pelvis as normal and then rotates to compensate, also at the

shoulders. You may also see i lumbar lordosis.

• Foot drop (L4/L5 lesion, sciatic, or common peroneal nerves): Failure

to dorsiﬂ

ex the foot leads to a high-stepping gait with i

ﬂ exion at the

hip and knee. If bilateral, this may indicate peripheral neuropathy.

• Apraxic (usually frontal lobe pathology such as normal pressure

hydrocephalus or cerebrovascular disease): Problems with gait occur

even if all other movements are normal. The patient may appear

CHAPTER 10 Nervous system322

frozen to the spot and be unable to initiate waking. Movements are

disjointed once walking.

• Marche à petits pas (diffuse cortical dysfunction): There is upright

posture and small steps with a normal arm swing.

• Painful gait: The cause will normally be obvious from the history. The

patient limps with an asymmetrical gait due to painful movement.

• Functional (also known as hysterical): Gait problems will be variable

and inconsistent, often with bizarre and elaborate consequences.

The patient may fall without causing injury. Gait is often worse when

watched.

IMPORTANT PRESENTING PATTERNS

323

Important presenting patterns

Neck stiffness

This is caused by a number of conditions provoking painful extensor mus-

cle spasm, including bacterial and viral meningitis, subarachnoid hemor-

rhage, parkinsonism, raised intracranial pressure, cervical spondylosis,

cervical lymphadenopathy, and pharyngitis.

None of the following tests should be conducted if there is suspicion of

cervical injury or instability.

Testing stiffness

• Lay the patient ﬂ at.

• Taking their head in your hands, gently rotate it to the sides in a “no”

movement, feeling for stiffness.

• Lift the head off the bed and watch the hips and knees—the chin

should easily touch the chest.

Brudzinski’s sign

When the head is ﬂ exed by the examiner, the patient brieﬂ y ﬂ exes at the

hips and knees. This is a test for meningeal inﬂ ammation.

Kernig’s sign

• A further test of meningeal inﬂ ammation

• With the patient lying ﬂ at,

ﬂ

ex their hip and knee, holding the weight

of the leg yourself ( Fig. 10.25 ).

• With the hip ﬂ

exed to 90

*, extend the knee joint so as to point the leg

at the ceiling.

• If positive, there will be resistance to leg-straightening (caused by

hamstring spasm as a result of inﬂ

ammation around the lumbar spinal

roots) and pain felt at the back of the neck.

Lhermitte’s phenomenon

• A test for intrinsic lesion in the cervical cord (not meningeal irritation)

• When the neck is ﬂ

exed as for testing stiffness, the patient feels an

electric shock–like sensation down the center of their back.

Upper motor and lower motor nerve lesions

Upper motor neuron (UMN) lesions

These are deﬁ ned as damage above the level of the anterior horn cell—

anywhere from the spinal cord to the primary motor cortex.

• No muscle wasting (although patients will have disuse atrophy in long-

term weakness)

• iTone. Spasticity (clasp-knife) due to stretch reﬂ ex

hypersensitivity

• The typical pattern of weakness ( Box 10.8 ) is termed pyramidal:

•

Upper limbs: weak abductors and extensors

•

Lower limbs: weak adductors and ﬂ exors

• iTendon reﬂ

exes and clonus. Up-going plantar response

CHAPTER 10 Nervous system324

(a)

(b)

Fig. 10.25 Testing for Kernig’s sign. The patient’s leg is ﬂ exed at the hip and

knee, then extended at the knee as above. If positive, there is resistance to knee

extension in this position and pain is felt at the back of the neck.

IMPORTANT PRESENTING PATTERNS

325

Lower motor neuron (LMN) lesions

• Muscle wasting. Fasciculation

• Diminished tone

• Flaccid weakness

• Diminished deep tendon reﬂ

exes. Plantar response may be down-going

or absent.

Motor neuron disease (MND)

There is damage to anterior horn cells, medulla, and spinal tracts.

• UMN and LMN pattern of weakness

• Fasciculations almost always present

• Reﬂ

exes normal or i until later in the disease

• Plantar response is up-going

• External ocular muscles almost never involved

• No sensory disturbance (distinguishing presentation from a

polyneuropathy)

Parkinsonism

This is a pattern of symptoms comprising an akinetic-rigid syndrome.

Parkinsonism has a number of causes, including drug-induced and other

intracranial pathologies. Diagnosis of Parkinson’s disease (loss of dopaminer-

gic neurons in the subtantia nigra) is often inaccurate; there is no single test.

• Triad of resting tremor, bradykinesia, and rigidity

• Face: mask-like and expressionless facies, little blinking, positive

glabellar tap reﬂ ex

(

b p. 307)

• Gait: ﬂ

exed posture with d arm swing. Gait is festinant

, meaning

hurried, often in small, shufﬂ ing steps, with feet barely lifted off the

ground. The patient is slow to start and has difﬁ culty stopping.

• Tone: i tone with cogwheel or lead-pipe rigidity (b p. 297).

• Tremor: pill-rolling ﬂ

exion at the thumb and foreﬁ

nger at 4–8 Hz

• Speech: extrapyramidal dysarthria; soft, quiet, and hesitant speech. You

may have to wait some time for the answer to a question.

• Writing: writing is small and neat—micrographia.

Abnormal movements deﬁ ned

• Akathisia: motor restlessness with a feeling of muscle quivering and an

inability to remain in a sitting position

• Athetosis: slow, writhing involuntary movements, often with ﬂ exion,

extension, pronation, and supination of the ﬁ

ngers and wrists

• Blepharospasm: intermittent spasm of muscles around the eyes

• Chorea: nonrhythmical, dance-like, spasmodic movements of the limbs

or face. Movements appear pseudopurposeful (the patient often hides

Box 10.8 Some deﬁ nitions of weakness

• Monoplegia: one limb affected

• Hemiplegia: one side of the body (left or right).

• Paraplegia: both lower limbs affected.

• Quadriplegia: all 4 limbs

CHAPTER 10 Nervous system326

the condition by turning a spasm into a voluntary movement—e.g.,

the arm suddenly lifts up and the patient pretends they were adjusting

their hair).

• Dyskinesia: repetitive, automatic movements that stop only during

sleep

• Tardive dyskinesia: dyskinetic movements, often of the face (lip-

smacking, twisting of the mouth). This is often a permanent side effect

of neuroleptic therapy.

• Dystonia: markedly i tone, often with spasms causing uncomfortable-

looking postures

• Hemiballismus: violent involuntary ﬂ

inging movements of the limbs on

one side, like severe chorea

• Myoclonus: brief, shock-like movement of a muscle or muscle group

• Pseudoathetosis: writhing limb movements (often ﬁ

nger or arm) much

like athetosis but caused by a loss of proprioception. The arm returns

to the normal position when the patient notices it straying.

• Myokymia: continuous quivering and rippling movements of muscles at

rest, like a bag of worms. Facial myokymia occurs especially near the

eyes.

• Tic: repetitive, active, habitual, purposeful contractions causing

stereotyped actions. It can be suppressed for brief periods, with effort.

• Titubation: rhythmical contraction of the head. There may be either

yes–yes or no–no movements.

• Tremor: repetitive, alternating movements, usually involuntary

Spinal cord lesions

As neurons in some spinal cord tracts relate to the contralateral side of

the body, others the ipsilateral side, certain types of spinal cord damage

will give predictable patterns of motor and sensory loss.

Complete section of the cord

There is loss of all modalities below the level of the lesion.

Hemisection of the cord

This is also known as Brown-Sequard syndrome.*

• Motor: below the level of the lesion, UMN pattern of weakness on

ipsilateral side

• Sensory: below the level of the lesion:

•

Contralateral loss of pain and temperature sensation

•

Ipsilateral loss of light touch, vibration sense, and proprioception

•

Light touch may remain intact, as some ﬁ bers travel in the

spinothalamic tract.

Posterior column loss

There is loss of vibration sense and proprioception on both sides below

the level of the lesion.

* Charles Edward Brown-Sequard discovered this while studying victims of failed murder attempts

among traditional cane cutters in Mauritius.

IMPORTANT PRESENTING PATTERNS

327

Subacute combined degeneration of the cord

Posterolateral column syndrome is often due to vitamin B

12

deﬁ ciency.

• Loss of vibration sense and proprioception on both sides below the

level of the lesion

• UMN weakness in lower limbs, absent ankle reﬂ exes

• Also peripheral sensory neuropathy, optic atrophy, and dementia

Anterior spinal artery occlusion

• Loss of pin-prick and temperature sensation below the lesion

• Intact light-touch, vibration sense, and proprioception

Central lesions

These include syringomyelia—longitudinal cavities in the central part of

the spinal cord and brainstem.

• Loss of pain and temperature sensation over the neck, shoulders, and

arms in a ‘cape’ distribution.

• Intact vibration sense, proprioception, and light touch.

• Atrophy and areﬂ

exia in the arms.

• UMN weakness in the lower limbs.

• Look also for scoliosis due to weakness of paravertebral muscles.

Cerebellar lesions

Signs are ipsilateral to the lesion and may include the following:

• Nystagmus (b p. 276)

• Speech is staccato, scanning (b p. 260).

• Diminished tone, drift and tremor in limbs (upper especially, p. 256)

• Finger–nose testing (b p. 315) may reveal intention tremor and past-

pointing.

• Dysdiadokokinesis (b p. 315)

• Rebound (b p. 316)

• Pendular jerks—best seen in knee. Test tendon reﬂ

ex at knee

as normal. If pendular, the extensor response will continue to

several beats.

• Poor sitting balance

• Ataxic gait

Disturbance of higher functions

This includes a selection of testable consequences of cortical lesions.

Parietal lobe

• Sensory and visual inattention (b p. 312 and b p. 265).

• Visual ﬁ eld defects (b p. 264).

• Gerstmann’s syndrome: right–left dissociation, ﬁ

nger agnosia, dysgraphia

(writing defect), dyscalculia (test with serial 7s; instruct the patient to count

backwards from 100 in increments of seven. For instance 100, 93, 86 ect.).

Agnosias (lack of sensory perceptual abilities)

• Hemi-neglect —patient ignores one side of their body

• Asomatagnosia —patient fails to recognize own body part

• Anosagnosia —patient is unaware of neurological deﬁ cits

• Finger agnosia —patient is unable to show you different ﬁ ngers

when

requested (e.g., “show me your index ﬁ nger”)

CHAPTER 10 Nervous system328

• Astereognosis —inability to recognize an object by touch alone

• Agraphaesthesia —inability to recognize letters or numbers when

traced on the back of the hand

• Prosopagnosia —inability to recognize faces (test with faces of family

members or famous faces from a nearby magazine)

Apraxias (inability to perform movements or use objects correctly)

• Ideational apraxia —unable to perform task but understands what is

required

• Ideomotor apraxia —performs task but makes mistakes (e.g., puts tea

into kettle and pours milk into cup)

• Dressing apraxia —inability to dress correctly (test with a dressing

gown). This is one of a number of apraxias named after the action

tested.

Temporal lobe

• Memory loss—confabulation (invented stories and details)

Frontal lobe

• Primitive reﬂ exes

• Concrete thinking (unable to explain proverbs—e.g., ask to explain

what “a bird in the hand is worth two in the bush” means)

• Loss of smell sensation

• Gait apraxia (b p. 321)

Myopathies

Muscle disease causes a weakness similar to that of LMN lesions with

no sensory loss. Tendon reﬂ exes are reduced or absent. The causes and

types are numerous.

Myotonias

These are characterized by continued, involuntary muscle contraction

after voluntary effort has ceased.

Myotonic dystrophy

This is a defect of skeletal muscle Cl

–

channels caused by a trinucleotide

repeat, usually. It becomes evident at age 20–50.

• Distal limb weakness

• Weak sternomastoids (evident by weakness of neck ﬂ exion

with

normal power on neck extension)

• Weak facial muscles (expressionless face)

• Test by shaking the patient’s hand—they may be unable to let go.

• It is also associated with frontal baldness, cataracts (look for thick

glasses), mild intellectual impairment, cardiomyopathy, hypogonadism,

and glucose intolerance.

Percussion myotonia

• Tap the patient’s thenar eminence. This will cause contraction and very

slow relaxation of abductor pollicis brevis.

Myaesthenia gravis

This is an autoimmune disease with antibodies against acetylcholine

receptors.

IMPORTANT PRESENTING PATTERNS

329

• Complex palsies, including extraocular muscles. Weakness is proximal

and often includes the eyelids (ptosis) and muscles of mastication.

• Weakness increases with use. Patients report i severity of symptoms

at the end of the day.

• In the early stages, patients will feel tired as they expend extra energy

in performing routine tasks. Friends may notice ptosis (see Fig. 10.25 ).

Test for fatiguability:

• Ask the patient to look to the ceiling and hold the position. Watch for

ptosis.

• Ask the patient to hold their arms above their head, or out to the

sides—watch for i weakness.

Some characteristic headaches summarized

Tension headache

• Bilateral—frontal, temporal

• Sensation of tightness radiating to neck and shoulders

• Can last for days

• No associated symptoms

Subarachnoid hemorrhage

• Sudden, dramatic onset like being hit with a brick

• Occipital initially—may become generalized

• Associated with neck stiffness and sometimes photophobia

Sinusitis

• Frontal, felt behind the eyes or over the cheeks

• Ethmoid sinusitis is felt deep behind the nose.

• Overlying skin may be tender.

• Worse on bending forward

• Lasts 1–2 weeks. Associated with coryza

Temporal (giant cell) arteritis

• Diffuse, spreading from the temple—unilateral

• Tender overlying temporal artery (painful brushing hair)

• Jaw claudication while eating

• Blurred vision—can lead to loss of vision if severe and untreated

Meningitis

• Generalized

• Associated with neck stiffness and signs of meningism (b p. 323)

• Nausea, vomiting, photophobia

• Purpuric rash is caused by septicemia, not meningitis per se.

Cluster headache

• Rapid onset, usually felt over one eye

• Associated with a bloodshot, watering eye and facial ﬂ ushing

• May also have rhinorrhea (runny nose)

• Last for a few weeks at a time

Raised intracranial pressure

• Generalized headache, worse when lying down, straining, coughing, on

exertion or in the morning

CHAPTER 10 Nervous system330

* Hence the name. Migraine is a shortened version of hemicranium (say the second and third

syllables out loud), meaning “half the head.”

• Headache may wake the patient in the early hours.

• It may be associated with drowsiness, vomiting, and focal neurology.

Migraine

• Unilateral—rarely crosses the midline*

• Throbbing and pounding headache

• Associated with photophobia, nausea, vomiting, and neck stiffness

• May have preceding aura

THE UNCONSCIOUS PATIENT

331

The unconscious patient

History

• Is there an eyewitness account? State of clothing—loss of continence?

• Look for alert necklace or bracelet. Look in patient’s wallet or purse.

Examination

ABC (Airway, Breathing, Circulation)

• Is the airway patent? Should the patient be in the recovery position?

• Measure the respiratory rate, note pattern of breathing. Is O

2

needed?

• Is there cyanosis? Feel the pulse. Listen to the chest. Measure heart

rate and blood pressure (BP).

Skin

• Look for injury, petechial hemorrhage, and evidence of intravenous

(IV) drug use.

Movements and posture

• Watch! Is the patient still or moving? Are all four limbs moving equally?

• Are there any abnormal movements—ﬁ

tting, myoclonic jerks?

• Test tone and compare both sides.

• Squeeze the nail bed to test the response to pain (all four limbs).

• Test tendon reﬂ

exes and plantar response.

• Decorticate posture (lesion above the brainstem): ﬂ

exion and internal

rotation of the arms, extension of the lower limbs

• Decerebrate posture (lesion in the midbrain): extension at the elbow,

pronation of the forearm, and extension at the wrist. Lower limbs are

extended.

Consciousness

• Attempt to wake the patient by sound. Ask them their name. If

responsive, are they able to articulate appropriately? Note the best

response. Be aware of possible dysphasia or aphasia that may cause an

inappropriate response in an otherwise alert individual.

•

Score level of consciousness according to GCS ( Box 10.9 ).

Neck

• Do not examine the neck if there may have been trauma. Test for

meningeal irritation (b p. 323)—these signs d as coma deepens.

Head

• Inspect for signs of trauma and facial weakness. Test pain sense.

•

Battle’s sign: bruising behind the ear = a base of skull fracture.

Ears and nose

• Look for CSF leakage or bleeding. Test any clear ﬂ uid for glucose

(positive result = CSF). Inspect eardrums.

Tongue and mouth

• Look for cuts on the tongue (seizures) and corrosive material around

the mouth. Smell breath for alcohol or ketosis. Test the gag reﬂ

ex; it is

absent in brainstem disease or deep coma.

CHAPTER 10 Nervous system332

Eyes

• Pupils: measure size in mm. Are they equal (b p. 273)? Test direct

and consensual light responses. Pupils

i with atropine, tricyclic

antidepressants, and amphetamine; d with morphine and metabolic coma.

• Test corneal reﬂ ex.

• Fundi: look especially for papilledema and retinopathy.

• Doll’s head maneuver: take the patient’s head in your hands and turn

it from side to side. The eyes should move to stay ﬁ

xed on an object;

this indicates an intact brainstem.

Box 10.9 Glasgow Coma Scale (GCS)

This is an objective score of consciousness. Repeated testing is useful for

judging whether coma is deepening or lifting. There are three categories.

Note that the lowest score in each category is 1, meaning that the low-

est possible GCS = 3 (even if the patient is dead).

Eye opening (max 4 points)

Spontaneously open 4

Open to (any) verbal stimulus 3

Open in response to painful stimulus 2

No eye opening at all 1

Best verbal response (max 5 points)

Conversing and orientated (normal) 5

Conversing but disorientated and confused 4

Inappropriate words (random words, no conversation) 3

Incomprehensible sounds (moaning, etc.) 2

No speech at all 1

Best motor response (max 6 points)

Obeying commands (e.g., “raise your hand”) 6

Localizing to pain (moves hand toward site of stimulus) 5

Withdraws to pain (pulls hand away from stimulus) 4

Abnormal ﬂ exion to pain (decorticate posturing) 3

Abnormal extension to pain (decerebrate posturing) 2

No response at all 1

Box 10.10 AVPU

This is a more simpliﬁ ed score used in rapid assessment of conscious-

ness and by nonspecialist nurses in monitoring consciousness level.

A = Alert

V = responds to Voice

P = responds to Pain

U = Unresponsive

THE UNCONSCIOUS PATIENT

333

Rest of the body

• Brief but thorough exam. Look especially for trauma, fractures, signs of

liver disease (b p. 246), and added heart sounds.

Other bedside tests

• Test urine, capillary glucose, and temperature.

CHAPTER 10 Nervous system334

The elderly patient

Diagnosing and managing neurological illness can be complex; the combi-

nation of cognitive failure and the effects of an aging neurological system

can present additional signiﬁ cant challenges for clinicians.

Presentations of neurological disease are varied, and the range of diag-

noses diverse. Epilepsy, Parkinsonism, and dementia are all common prob-

lems in older age, so resist the temptation to restrict your diagnoses to

stroke or TIA.

History

Witness histories

These are vital. Many patients may attend with vague symptoms that may

be underplayed. Partial complex seizures may be very difﬁ cult to diagnose,

so pursue witness histories from families, neighbors, and home care staff,

etc. Inquire not just about the present incident but also prior function and

any decline.

Drug history

Falls are a common presentation and often multifactorial. Always remem-

ber to ask about any drugs that may lower blood pressure, even if the

primary cause of the fall is due to neurological disease.

Intercurrent illness

This may precipitate further seizures or make pre-existing neurological

signs seem worse. Don’t rush to diagnose a worsening of the original

problem—careful assessment pays dividends.

Cognition and mood disorders

These often complicate presentations. Look for clues in the history, and

ask witnesses.

Functional history

This is a key part of the neurological history. The disease itself may be

incurable—functional problems often are not.

Examination

Observe

Nonverbal clues may point to mood or cognitive disorders. Handshakes

and facial expressions are an important part of the examination

Think

Think about patterns of illness and attempt to identify if there are single

or multiple lesions. There may often be more than one diagnosis—e.g.,

cerebrovascular disease and peripheral neuropathy due to diabetes.

Assess cognition

Use a scale that you are comfortable with, such as the Abbreviated Mental

Test Score (AMTS, b p. 262; Mini-Mental State Examination [MMSE], but

remember, no half marks!

THE ELDERLY PATIENT

335

Gait

Even simple observation of a patient’s walking can reap rewards. Always

include it in your examination where practicable and note why, if unable.

Therapy colleagues

Sharing observations is a useful practice. Therapists are a huge source of

knowledge and experience, so seek them out to learn from them.

Additional points

Communicating diagnoses

Many diagnoses—e.g., dementia and motor neuron disease—can be dev-

astating, so be thoughtful in your approach. Clarify what the patient knows

and what has already been said. Learn ﬁ rst from your senior colleagues

how to explain the diagnosis and, more importantly, talk about its impact.

It is also vital to reassure patients—many with benign essential tremors

are terriﬁ ed that they may have Parkinson’s disease

Managing uncertainty

Many diagnoses are not clear, especially in the early stages of diseases. Try

to resist labeling your patients when a diagnosis is unclear; be open about

uncertainty—patients often cope with it better than their doctors.

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337

Musculoskeletal system

Applied anatomy and physiology 338

Important locomotor musculoskeletal symptoms 340

The rest of the history 344

The outline examination 346

GALS screen 347

Elbow 349

Shoulder 351

Spine 354

Hip 356

Knee 358

Ankle and foot 363

Important presenting patterns 365

The elderly patient 373

Chapter 11

The hand examination is described in Chapter 3, b p. 62

CHAPTER 11 Musculoskeletal system338

Applied anatomy and physiology

The joint

A joint (articulation) is a connection or point of contact between bones or

between bone and cartilage.

Joints are classiﬁ ed according to the type of material uniting the articu-

lating bones as well as the degree of movement they allow. There are

three types:

• Fibrous joints: held together by ﬁ

brous (collagenous) connective

tissue and are ﬁ

xed or immoveable. They do not have a joint cavity.

Examples include the connections of the skull bones.

• Cartilagenous joints: held together by cartilage, are slightly moveable

and have no cavity. An example is the vertebral joints.

• Synovial joints: covered by cartilage with a synovial membrane

enclosing a joint cavity. These joints are freely moveable and the most

common type of joint functionally, being typical of nearly all joints of

the limbs.

Synovial joints

Articular cartilage covers the surface of the bones and d friction at the

joint and facilitates shock absorption. A sleeve-like bag (ﬁ brous capsule

lined with a synovial membrane) surrounds the synovial joint ( Fig. 11.1 ).

The inner synovial membrane secretes synovial ﬂ uid, which has a

number of functions, including lubrication and supply of nutrients to the

cartilage. The ﬂ uid contains phagocytic cells that remove microbes and

debris within the joint cavity.

Synovial joints are usually supported by accessory ligaments and muscle.

There are different types of synovial joints. Some of the more important

types are as follows:

Bone

Capsule

Synovium

Joint space

(synovial fluid)

Bone

Hyaline

articular

cartilage

Fig. 11.1 Diagram of cross-section through a typical synovial joint.

APPLIED ANATOMY AND PHYSIOLOGY

339

• Hinge: movement occurs primarily in a single plane (e.g., elbow, knee,

and interphalangeal joints) (see Box 11.1 ).

• Ball and socket: allows movement around three axes (ﬂ exion/extension,

abduction/adduction, and rotation). Examples are the shoulder and hip.

• Pivot: a ring of bone and ligament surrounds the surface of the other

bone, allowing rotation only (e.g., atlantoaxial joint at C1 and C2

vertebrae and the connection between the radius and ulna).

• Gliding: ﬂ

at bone surfaces allow side-to-side and backward and

forward movements (e.g., between carpals, tarsals, sternum and

clavicle and the scapula and clavicle).

• Saddle: similar to a hinge joint but with a degree of movement in a

second plane (e.g., base of thumb).

Box 11.1 Some movements at synovial joints

Angular movements

• Flexion: a decrease in angle between the articulating bones

(e.g., bending the elbow = elbow ﬂ exion)

• Extension: an increase in angle between the articulating bones

(e.g., straightening the elbow = elbow extension)

• Abduction: movement of a bone away from the midline (e.g., moving

the arm out to the side = shoulder abduction)

• Adduction: movement of a bone toward the midline (e.g., bringing the

arm in to the side of the body = shoulder adduction)

Rotation

This involves movement of a bone about its longitudinal axis.

• Internal or medial rotation: rotating a bone toward the

midline (e.g., turning the lower limb such that the toes point

inward = internal rotation at the hip)

• External or lateral rotation: rotating a bone away from the

midline (e.g., turning the lower limb such that the toes point

outward = external rotation at the hip)

Special movements

These occur at speciﬁ

c joints only.

• Pronation: moving the forearm as if turning a doorknob

counterclockwise (internal rotation of the forearm in anatomical

position)

• Supination: moving the forearm as if turning a doorknob clockwise

(external rotation of the forearm in anatomical position)

• Dorsiﬂ

exion: moving the ankle to bring the dorsum of the foot

toward the tibia

• Plantar ﬂ

exion: moving the ankle to bring the plantar surface in line

with the tibia (e.g., pointing toes or depressing a pedal)

• Inversion: tilting soles of the feet inward to face each other

• Eversion: tilting soles of the feet outward away from each other

• Protraction: moving the mandible forward

• Retraction: moving the mandible backward.

CHAPTER 11 Musculoskeletal system340

Important locomotor musculoskeletal

symptoms

As with any system, but especially the musculoskeletal system, a carefully

and accurately compiled history can be very informative and may point to

a diagnosis even before examination or laboratory tests.

Pain

Pain is the most common symptom with problems of the musculoskeletal

system and should be approached in the same way as any other type of

pain (b p. 33). Determine its character, nature of onset, site, radiation,

severity, periodicity, exacerbating and relieving factors (particularly how it

is inﬂ uenced by rest and activity), and diurnal variation.

• Pain in a joint is called arthralgia .

• Pain in a muscle is called myalgia .

Character

• Bone pain is typically experienced as boring and penetrating and

is often worse at night. Causes include tumor, chronic infection,

avascular necrosis, and osteoid osteoma.

• Pain associated with a fracture is usually sharp and stabbing and is

often exacerbated by movement.

• Shooting pain is suggestive of nerve entrapment (e.g., disc protrusion).

Onset

• Acute onset of pain is often a manifestation of infection, such as septic

arthritis or crystal arthropathies (e.g., gout).

• Osteoarthritis and rheumatoid arthritis (RA) can cause chronic pain.

Site

Determine the exact site of maximal pain, if possible, and any associated

lesser pains. Remember that the site of pain is not necessarily the site of

pathology; often pain is referred. Referred pain is due to the inability of the

cerebral cortex to distinguish between sensory messages from embryo-

logically related sites. See Boxes 11.2 and 11.3.

Box 11.2 Some causes of knee arthralgia

Chondromalacia patellae

This is from softening of the patellar articular cartilage and is felt as a

patellar ache after prolonged sitting. It is usually seen in young people.

Osteochondritis dissecans

This is usually associated with trauma resulting in osteochondral fracture

that forms a loose body in the joint, with underlying necrosis.

Osgood–Schlatter’s disease

This arises as a result of a traction injury of the tibial epiphysis, which is

classically associated with a lump over the tibia.

IMPORTANT LOCOMOTOR MUSCULOSKELETAL SYMPTOMS

341

Box 11.3 Some causes of arthralgia in adults

Knee

• Osteoarthritis

• Referred from the hip

• Chondromalacia patellae

• Trauma

• Osteochondritis dissecans

• Bursitis

• Tendonitis

• Osgood–Schlatter’s disease

• Rheumatoid arthritis

• Infection

• Malignancy

Hip

• Osteoarthritis

• Referred pain—e.g., from a lumber spine abnormality

• Trauma

• Rheumatoid arthritis

• Infection

• Hernia

• Tendonitis

• Bursitis

Shoulder

• Rotator cuff disorders (e.g., tendonitis, rupture,

adhesivecapsulitis or frozen shoulder)

• Referred pain—e.g., cervical, mediastinal, cardiac

• Arthritis—glenohumeral, acromioclavicular

Elbow

• Lateral epicondylitis (tennis elbow)

• Medial epicondylitis (golfer’s elbow)

• Olecranon bursitis

• Referred pain from neck or shoulder (e.g., cervical spondylosis)

• Osteoarthritis

• Rheumatoid arthritis

Mechanical or degenerative back pain

• Arthritis

• Trauma

• Disc prolapse

• Osteoporosis

• Infection

• Ankylosing spondylitis

• Spondylolisthesis

• Lumbar spinal or lateral recess stenosis

• Spinal tumors—especially metastases from the lung,

breast, prostate, thyroid, and kidney

• Metabolic bone disease

CHAPTER 11 Musculoskeletal system342

Stiffness

This is a subjective symptom that must be explored in detail to establish

exactly what the patient means.

Stiffness is the inability to move the joints after a period of rest. It may

be due to mechanical dysfunction, local inﬂ ammation of a joint, or a com-

bination of both.

2 If stiffness predominates over pain, consider spasticity or tetany. Look

for hypertonia and other upper motor neuron signs (b p. 297).

Ask the patient the following:

• When is the stiffness worst?

•

Early-morning stiffness is seen in inﬂ ammatory conditions (e.g.,

rheumatoid arthritis), whereas mechanical joint disease will become

worse as the day progresses.

• Which joints are involved? Or is the stiffness generalized?

•

A generalized stiffness may be seen in rheumatoid arthritis and

ankylosing spondylitis.

• How long does it take the patient to get going in the morning?

• How is the stiffness related to rest and activity?

•

Mechanical joint diseases will be exacerbated by prolonged activity.

Locking

This is the sudden inability to complete a certain movement and suggests

a mechanical block or obstruction, usually caused by a loose body or torn

cartilage within the joint (often secondary to trauma).

Swelling

Joint swelling can be due to a variety of factors, including inﬂ ammation of

the synovial lining, an increase in volume of synovial ﬂ uid, hypertrophy of

bone, or swelling of structures surrounding the joint.

This symptom is particularly signiﬁ cant in the presence of joint pain and

stiffness. Establish the following:

• Which joints are affected (small or large)?

• Is the distribution symmetrical or not?

• What was the nature of onset of the swelling?

•

Rapid onset: hematoma or hemarthrosis (exacerbated by

anticoagulants or any underlying bleeding disorder)

•

Slow onset is suggestive of a joint effusion.

• Are the joints always swollen or does it come and go (and when)?

• Is there any associated pain?

• Do the joints feel hot to touch?

• Is there erythema? (This is common in infective, traumatic, and crystal

arthropathies.)

• Have the joints in question sustained any injuries?

Deformity

Establish the following:

• Time frame over which the deformity has developed

• Any associated symptoms, such as pain and swelling

• Any resultant loss of function? (What is the patient now unable to do

with the joint in question?)

IMPORTANT LOCOMOTOR MUSCULOSKELETAL SYMPTOMS

343

Acute deformity may arise with a fracture or dislocation. Chronic deformi ty

is more typical of bone malalignment and may be partial/ subluxed or

complete/dislocated. Some common deformities are discussed later in

this chapter (see also Box 11.4 ).

Weakness

Always inquire about the presence of localized or generalized weakness,

which suggests a peripheral nerve lesion or systemic cause, respectively.

Consider that the weakness may be neurogenic or myopathic in origin.

Sensory disturbance

Ask about the exact distribution of any numbness or paraesthesia and

document any exacerbating and relieving factors.

Loss of function

Loss of function is the inability to perform an action (disability) and is distin-

guished from the term handicap , which is the social and functional result

or impact that disability has on the individual’s life.

Loss of function can be caused by a combination of muscle weakness,

pain, mechanical factors, and damage to the nerve supply.

The questions you ask will depend partly on the patient’s occupation. It

is also essential to gain some insight into the patient’s mobility: Can they

use stairs? How do they cope with personal care such as feeding, washing

and dressing? Can they manage shopping and cooking?

Extra-articular features

Several musculoskeletal disorders (e.g., rheumatoid arthritis) cause extra-

articular or multisystem features, some of which are outlined below:

• Systemic symptoms: fever, weight loss, fatigue, lethargy

• Skin rash

• Raynaud’s phenomenon

• Gastrointestinal (e.g., diarrhea and resultant reactive arthritis or

enteropathic arthritis secondary to inﬂ

ammatory bowel disease)

• Urethritis (Reiter’s syndrome)

• Eye symptoms

• Cardiorespiratory: breathlessness (pulmonary ﬁ

brosis?), pericardial and

pleuritic chest pain, aortic regurgitation, and spondyloarthropathies.

• Neurological: nerve entrapment, migraine, depression, stroke

Box 11.4 Some terminology of joint deformity

Valgus

The bone or part of limb distal to the joint is deviated laterally. For

example, a valgus deformity at the knees would give “knock knees” that

tend to meet in the middle, despite the feet being apart.

Varus

Here, the bone or part of limb distal to the joint is deviated medially.

For example, a varus deformity at the knees would give “bow legs” with

a gap between the knees, even if the feet are together.

CHAPTER 11 Musculoskeletal system344

The rest of the history

Past medical history

Ask about all previous medical and surgical disorders and inquire speciﬁ -

cally about any previous history of trauma or musculoskeletal disease.

Family history

It is important to note any FH of illness, especially those musculoskeletal

conditions with a heritable element:

• Osteoarthritis

• Rheumatoid arthritis

• Osteoporosis

Note that the seronegative spondyloarthropathies (e.g., ankylosing spond-

ylosis) are more prevalent in patients with the HLA B27 haplotype.

Drug history

Take a full drug history, including all prescribed and over-the-counter

medications. Assess the efﬁ cacy of each treatment, past and present.

Ask about side effects of any drugs taken for musculoskeletal disease:

• Gastric upset associated with nonsteroidal anti-inﬂ ammatory

drugs

(NSAIDs)

• Long-term side effects of steroid therapy, such as osteoporosis,

myopathy, infections, and avascular necrosis

Ask also about medication with known adverse musculoskeletal effects:

• Statins: myalgia, myosistis, and myopathy

• ACE inhibitors: myalgia

• Anticonvulsants: osteomalacia

• Quinolone: tendinopathy

• Diuretics, aspirin, alcohol: gout

• Procainamide, hydralazine, isoniazid: systemic lupus erythematosus

(SLE)

2 Bear in mind that illicit drugs may increase the risk of developing infec-

tious diseases, such as TB, HIV, and hepatitis, all of which can cause mus-

culoskeletal complaints.

Smoking and alcohol

As always, full smoking and alcohol histories should be taken (b p. 37

and 38).

Social history

This should form a natural extension of the functional inquiry and include a

record of the patient’s occupation if not already noted and ethnicity.

• Certain occupations predispose to speciﬁ c

musculoskeletal

problems—e.g., repetitive strain injury, hand-vibration syndrome, and

fatigue fractures seen sometimes in dancers and athletes.

• Ethnicity is relevant, as there is an overrepresentation of lupus and TB

in Asian populations. Both of these disorders are linked to a variety of

musculoskeletal complaints.

THE REST OF THE HISTORY

345

• If the patient is an older person, make a note about the activities of

daily living (ADL), how mobile the patient is, and if there are any home

adaptations, such as a chair lift or railings.

• Remember to ask about home care or other supports.

• Where appropriate, take a sexual history. This is important because

reactive arthritis or Reiter’s syndrome may be caused by sexually

transmitted diseases, such as chlamydia and gonorrhea.

CHAPTER 11 Musculoskeletal system346

The outline examination

A full examination of the entire musculoskeletal system can be long and

complicated (but see Box 11.5 for framework). In this chapter, we have

broken down the examination into the following joints and regions: elbow,

shoulder, spine, hip, knee, ankle, and foot.

2 The hand examination is discussed in Chapter 3, b p. 62.

Box 11.5 Examination framework

Examination of each joint should follow the standard format:

• Look

• Feel

• Move*

•

Passive

•

Active

• Measure

• Special tests

• Function

2 In a thorough locomotor examination, examine the joints above and

below the symptomatic one. For example, for an elbow complaint, also

examine the shoulder and wrist.

* Limitation of active movement reﬂ ects underlying pathology of the tendons and muscle sur-

rounding the joint, but limitation of both active and passive movement suggests an intrinsic

joint problem.

GALS SCREEN

347

GALS screen

The overall integrity of the musculoskeletal system can be screened very

quickly by using the GALS method of assessment.

You may use this method to make a quick, screening examination of the

whole musculoskeletal system in order to identify the joints or regions

that need to be examined in more detail (see also Box 11.6 ).

The GALS screen consists of four components:

• G = gait

• A = arms

• L = legs

• S = spine

Box 11.6 Modiﬁ ed GALS screen

The GALS screen was originally devised as a quick screen for abnormal-

ity without symptoms. Our slightly modiﬁ ed version follows:

Gait

• Watch the patient walk.

•

There should be symmetry and smoothness of movement and arm

swing with no pelvic tilt and with normal stride length. The patient

should be able to start, stop, and turn quickly.

Arms (sitting on couch)

• Inspection: Look for muscle wasting and joint deformity at the

shoulders, elbows, wrists, and ﬁ

ngers. Squeeze across the second to

ﬁ

fth metacarpals—there should be no tenderness.

• Shoulder abduction: Ask the patient to raise their arms out sideways,

above their head. Normal range is 170–180°.

• Shoulder external rotation: Ask the patient to touch their back

between their shoulder blades.

• Shoulder internal rotation: Ask the patient to touch the small of their

back. They should touch above T10.

• Elbow extension: Ask patient to straighten out arms. Normal is 0*.

• Wrist and ﬁ

nger extension: the prayer sign (b p. 65).

• Wrist ﬂ exion and ﬁ nger extension: reverse prayer sign (b p. 65).

• Power grip: Ask patient to make a tight ﬁ

st, hiding ﬁ ngernails.

• Precision grip: Ask patient to put their ﬁ ngertips on their thumb.

Legs (lying on couch)

• Inspection: Look for swelling or deformity at the knee, ankle, and

foot, as well as quadriceps muscle wasting. Squeeze across the

metatarsals—there should be no tenderness.

• Hip and knee ﬂ

exion: Test passively and actively. Normal hipﬂ exion is

120*, normal knee ﬂ exion is 135*.

• Hip internal rotation: Normal is 90* at 45* ﬂ exion.

See b

p. 356.

• Knee: bulge test (b p. 358) and patellar tap (b p. 358)

• Ankle: Test dorsiﬂ

exion (normal 15

*) and planarﬂ exion (normal 55*).

CHAPTER 11 Musculoskeletal system348

Spine (standing)

• Inspection from behind: Look for scoliosis, muscle bulk at the

paraspinals, shoulders, and gluteals, and level iliac crests.

• Inspection from the side: Look for normal thoracic kyphosis and

lumbar and cervical lordosis.

• Tenderness: Feel over the mid-supraspinatus—there should be no

tenderness.

• Lumbar ﬂ

exion: Ask patient to touch their toes. Normal is ﬁ nger-

ﬂ

oor distance <15 cm. Lumbar expansion (Schober’s test b p. 355)

• Cervical lateral ﬂ

exion: Ask the patient to put their ear on their

shoulder.

Republished with permission from Doherty et al. (1992). Ann Rheum Dis 51:1165–1169.

Box 11.6 (Contd.)

ELBOW

349

Elbow

Look

Look around the bed for any mobility aids or other clues. Ask the patient

to stand. Make sure both upper limbs are exposed and look at the patient

from top to toe.

Inspect the elbow joint from the front, side, and behind, noting:

• Malalignment of the bones

• Scars

• Skin change (e.g., psoriatic plaques)

• Skin or subcutaneous nodules

• Deformities

•

Varus (cubitus varus) can be caused by a supracondylar fracture.

•

Valgus (cubitus valgus) can be caused by nonunion of a lateral

condylar fracture.

• Muscle wasting

• Swelling

Feel

2 Always ask about pain before getting started.

Palpate the joint posteriorly and feel for the following:

• Temperature

• Subcutaneous nodules

• Swelling

•

Soft swelling may be due to olecranon bursitis.

•

Hard swelling suggests a bony deformity.

•

Boggy swelling suggests synovial thickening (e.g., secondary to RA).

• If ﬂ uid is present, attempt to displace it on either side of the

olecranon.

• Carefully palpate the joint margin for tenderness and note if it is

localized to the medial epicondyle (golfer’s elbow) or the lateral

epicondyle (tennis elbow).

Move

0 Check that there is good shoulder function before attempting to assess

elbow movements.

2 Remember to test passive movements (you do the moving) and active

movements (the patient does the moving) at each stage.

• Ask the patient to place their arms on the back of their head.

• Next assess elbow ﬂ

exion and extension with the upper arm ﬁ xed.

•

Remember to compare with the opposite side.

• With the elbows tucked into the sides and ﬂ exed to a right angle, test

the radioulnar joints for pronation (palms toward ﬂ

oor) and supination

(palms toward the sky) ( Fig. 11.2 ).

Measure

Measure elbow ﬂ exion and extension in degrees from the neutral position

(i.e., consider a straight elbow joint to be 0*).

CHAPTER 11 Musculoskeletal system350

Function

Observe the patient pouring a glass of water and then putting on a

jacket.

Flexion

Extension

Supination Pronation

Fig. 11.2 Movements at the elbow joint. (a) Flexion and extension. (b) Pronation

and supination (remember that pronation and supination require movement at the

elbow as well as at the wrist).

SHOULDER

351

Shoulder

Look

Look for any aids or adaptations. Ask the patient to remove any covering

clothing and have them expose the upper limbs, neck, and chest. Scan the

patient from top to toe. Inspect from the front, side, and behind.

Look especially for the following:

• Contours

•

Make note of any obvious asymmetry or deformity, such as winging

of the scapula, prominence of the acromioclavicular joint, and

wasting of the deltoid or short rotators that overlie the upper and

lower segments of the scapula.

• Joint swelling

•

This is more obvious from the front and may be a clue to acute

bleeds, rheumatoid effusions, pseudogout, or sepsis.

• Scars

• Bruising or other skin or subcutaneous tissue changes

• Position of both shoulders, looking for evidence of dislocation

•

Posterior dislocation can be seen when the arm is held in

aninternally rotated position.

•

Anterior dislocation can be seen easily when the arm is displaced in

a forward and downward position.

2 Remember to inspect the axillary regions.

Feel

2 Always ask about pain before getting started.

Make note of any temperature changes, tenderness, or crepitus. Standing

in front of the patient:

• Palpate the soft tissues and bony points in the following

order:sternoclavicular joint, clavicle, acromioclavicular joint, acromial

process, head of humerus, coracoid process, spine of scapula, greater

tuberosity of humerus.

• Check the interscapular area for pain.

• Palpate the supraclavicular area for lymphadenopathy.

Move

2 Remember to test passive movements (you do the moving) and active

movements (the patient does the moving) at each stage. Quantify any

movement in degrees (measure) .

0 To test true glenohumeral movement, anchor the scapula by pressing

ﬁ rmly down on the top of the shoulder. After about 70* of abduction, the

scapula rotates on the thorax—movement is scapulothoracic.

• Flexion: Ask the patient to raise their arms forward above their head.

• Extension: Straighten the arms backward as far as possible.

• Abduction: Move the arm away from the side of the body until the

ﬁ

ngertips are pointing to the ceiling.

• Adduction: Ask the patient to move the arm inward toward the

opposite side, across the trunk.

CHAPTER 11 Musculoskeletal system352

• External rotation: With the elbows held close to the body and ﬂ exed

to 90*, ask the patient to move the forearms apart in an arc-like

motion, to separate the hands as widely as possible.

• Internal rotation: Ask the patient to bring the hands together again

across the body. (Loss of rotation suggests a capsulitis.)

• Compound movements: These types of movements may be employed

as screening tests to assess shoulder dysfunction, taking the place of a

fuller examination if no abnormalities are detected. See Fig. 11.3.

•

Ask the patient to put both hands behind their head

(externalrotation in abduction).

•

Ask the patient to reach up their back with the ﬁ ngers to touch a

spot between their shoulder blades (internal rotation in adduction).

Special tests

Testing for a rotator cuff lesion or tendonitis: the painful arc

Ask the patient to abduct the shoulder against light resistance.

Pain in early abduction suggests a rotator cuff lesion and usually occurs

between 40* and 120*. This is due to a damaged and inﬂ amed supraspina-

tus tendon being compressed against the acromial arch.

Testing for acromioclavicular arthritis

If there is pain during a high arc of movement (starting around 90*) and the

patient is unable to raise their arm straight up above their head to 180*,

even passively, this suggests acromioclavicular arthritis.

Function

Ask the patient to scratch the center of their back or to put on a jacket.

(a) (b)

Fig. 11.3 Compound movements. (a) External rotation and abduction.

(b) Internal rotation and adduction

SHOULDER

353

Box 11.7 A word about winging of the scapula

This is due to weakness of the serratus anterior, from damage to the

long thoracic nerve, injury to the brachial plexus, injury or viral infec-

tions of C5–7 nerve roots, and muscular dystrophy.

Winging only becomes obvious when the serratus anterior contracts

against resistance, such as pushing outstretched hands against a wall.

CHAPTER 11 Musculoskeletal system354

Spine

Look

Scan around the room for any clues, such as a wheelchair or walking aids.

Watch how the patient walks into the room or moves around the bed

area. Study their posture, paying particular attention to the neck.

Ask the patient to strip down to their underwear. Inspect from in front,

the side, and behind, in both the standing and sitting positions.

Look especially for the following:

• Scars

• Pigmentation

• Abnormal hair growth

• Unusual skin creases

• Asymmetry, including abnormal spinal curvature

•

Kyphosis: convex curvature—normal in the thoracic (T) spine

•

Lordosis: concave curvature—normal in the lumbar (L) and cervical

(C) spines

•

Scoliosis: side-to-side curvature away from the midline

2 A question-mark spine with exaggerated thoracic kyphosis and a loss of

lumbar lordosis is a classic sign of ankylosing spondylitis.

Feel

Palpate each spinous process, noting any prominence or step, and feel the

paraspinal muscles for tenderness.

You should also make a point of palpating the sacroiliac joints.

Move

C-spine

Assess active movements of the C-spine ﬁ rst. These include ﬂ exion,

extension, lateral ﬂ exion, and rotation. It is often helpful to demonstrate

these movements yourself.

• Flexion: Ask the patient to put their chin on their chest.

• Extension: Ask the patient to look up to the ceiling.

• Lateral ﬂ

exion: Ask the patient to lean their head sideways, placing an

ear on their shoulder.

• Rotation: Ask the patient to look over each shoulder.

T- and L-spine

Movements at the thoracic and lumbar spine include ﬂ exion,

extension,

lateral ﬂ

exion, and rotation.

• Flexion: Ask the patient to touch their toes.

• Extension: Ask the patient to lean backward.

• Lateral ﬂ

exion: Ask the patient to bend sideways, sliding each hand

down their leg as far as possible.

• Rotation: Anchor the pelvis (put a hand on either side) and ask the

patient to twist at the waist to each side in turn.

Measure

Schober’s test

This is a useful measurement of lumbar ﬂ exion.

SPINE

355

• Ask the patient to stand erect with normal posture. Identify the level

of the posterior superior iliac spines on the vertebral column.

• These are located at 7 L5.

• Make a small pen mark at the midline 5 cm below and 10 cm above

this point.

• Now instruct the patient to bend at the waist to full forward ﬂ exion.

• Measure the distance between the two marks, using a tape measure.

• The distance should have increased to >20 cm (an increase of >5 cm).

If not, there is a limitation in lumbar ﬂ

exion (e.g., found in ankylosing

spondylitis).

Special tests

Sciatic nerve stretch test

• This test is used to look for evidence of nerve root irritation (see also

Box 11.8 ).

• With the patient lying supine, hold the ankle and lift the leg, straight,

to 90*. Once there, dorsiﬂ

ex the foot (Bragard test). If positive, pain is

felt at the back of the thigh. The pain may be relieved by knee ﬂ exion.

• A positive stretch test suggests tension of the nerve roots supplying the

sciatic nerve (L5–S2), commonly over a prolapsed disc (L4/5 or L5/S1).

0 This test is partially age dependent. Most elderly people will struggle to

ﬂ

ex their hip beyond 70

*.

Femoral nerve stretch test

With the patient lying prone, abduct and extend the hip, ﬂ ex the knee, and

plantarﬂ ex the foot. The stretch test is positive if pain is felt in the thigh or

inguinal region. See b p. 319.

Box 11.8 Neurological examination

Don’t forget the neurological aspects of the examination. The femoral

and sciatic stretch tests may uncover root irritation, but you should

also examine for the neurological and functional consequences as in

b Chapter 10.

CHAPTER 11 Musculoskeletal system356

Hip

Look

Expose the whole lower limb. Look around the room for any aids or

devices such as orthopedic shoes or walking aids. If they have not done so

already, ask the patient to walk, and note the gait. Note if there is evidence

of a limp or obvious pain.

With the patient in standing position, inspect from the front, side, and

behind. Look for the following:

• Scars

• Sinuses

• Asymmetry of skin creases

• Swelling

• Muscle wasting

• Deformities

Pay attention to the position of limbs (e.g., external rotation, pelvic tilting,

standing with one knee bent or foot held plantarﬂ

exed or in equinus).

Feel

Feel for bony prominences, such as the anterior superior iliac spines and

greater trochanters. Check that they are in the expected position.

Palpate the soft tissue contours and feel for any tenderness in and

around the joint.

Move

Ask the patient if they have any pain before you examine them.

2 Fix the pelvis by using your left hand to stabilize the contralateral

anterior superior iliac spine, since any limitation of hip movement can eas-

ily be hidden by movement of the pelvis.With the patient supine :

• Flexion: Ask the patient to ﬂ

ex the hip until the knee meets the

abdomen. Normal is around

7120*.

• Abduction: With the patient’s leg held straight, ask them to move it

away from the midline. Normal is 30–40*.

• Adduction: With the patient’s leg held straight, ask them to move it

across the midline. Normal is 730*.

With the patient prone:

• Extension: Ask the patient to raise each leg off the bed. Normal is only

a few degrees.

• Internal rotation: Ask the patient to keep the knees tight together and

spread the ankles as far as possible.

• External rotation: Ask the patient to cross the legs over.

Passive movements

Most of these movements should be assessed by the examiner as for

active movements while the patient is in a relaxed state.

• Passive external and internal rotation: With the patient supine, ﬂ ex

the

knee, stabilizing it with one hand while the other hand moves the heel

laterally or medially so that the heel either moves away or toward the

midline (internal and external rotation respectively).

HIP

357

Measure (limb length)

0 True shortening, in which there is loss of bone length, must not becon-

fused with apparent shortening due to a deformity at the hip, in which

there is no loss of bone length.

Technique

• With the patient supine, place the pelvis square and the lower limbs in

comparable positions in relation to the pelvis.

• Measure the distance from the anterior superior iliac spine to the

medial malleolus on each side (true length) .

•

Apparent length is measured from a midline structure, such as the

xiphisternum or umbilicus, to the medial malleolus.

Special tests

Trendelenberg test

This is useful as an overall assessment of the function of the hip and will

expose dislocations or subluxations, weakness of the abductors, shorten-

ing of the femoral neck, or any painful disorder of the hip.

• Ask the patient to stand up straight without any support.

• Ask them to raise their left leg by bending the knee.

• Watch the pelvis (normally it should rise on the side of the lifted leg).

• Repeat the test with the patient standing on the left leg.

• A positive test is when the pelvis falls on the side of the lifted leg,

indicating hip instability on the supporting side (i.e., the pelvis falls to

the left = right hip weakness).

Thomas test

A ﬁ xed

ﬂ

exion deformity of the hip (often seen in osteoarthritis) can be

hidden when the patient lies supine by tilting the pelvis and arching the

back. The Thomas test will expose any ﬂ exion deformity.

• With the patient lying supine, feel for lumbar lordosis (palm upward).

• With the other hand, ﬂ

ex the opposite hip and knee fully to ensure

that the lumbar spine becomes ﬂ attened.

• If a ﬁ xed-ﬂ

exion deformity is present, the opposite leg ﬂ exes

too

(measure the angle relative to the bed).

• Remember to repeat the test on the other hip.

Function

Assess gait. See Chapter 10, b p. 321.

CHAPTER 11 Musculoskeletal system358

Knee

Look

Scan the room for any walking aids or other clues and inspect the patient

standing. The lower limbs should be completely exposed except for

underwear so that comparisons can be made.

Compare one side to the other and look for the following:

• Deformity (valgus, varus, or ﬂ exion)

• Scars or wounds to suggest infection past or present

• Muscle wasting (quadriceps)

• Swelling (including posteriorly)

• Erythema

• Look for loss of the medial and lateral dimples around the knees,

which suggests the presence of an effusion.

Feel

2 Always ask about pain before getting started. Always compare sides.

With the patient lying supine:

• Palpate for temperature using the back of the hand.

• Ask if the knee is tender on palpation.

• Feel around the joint line while asking the patient to bend the

knee slightly.

• Palpate the collateral ligaments (either side of the joint).

• Feel the patellofemoral joint (by tilting the patella).

Examining for a small effusion—the bulge sign

• Holding the patella still, empty the medial joint recess using a wiping

motion of your index ﬁ nger

(

Fig. 11.4a ).

•

This will milk any ﬂ uid into the lateral joint recess.

• Now apply a similar wiping motion to the lateral recess and

• Watch the medial recess ( Fig. 11.4b ).

•

If there is ﬂ uid present, a distinct bulge should appear on the

ﬂ attened, medial surface and it is milked out of the lateral side.

Examining for a large effusion—the patellar tap

If the effusion is large, the bulge sign is absent, as you will be unable to

empty either recess of ﬂ uid—use the patellar tap instead.

• Move any ﬂ

uid from the medial and lateral compartments into the

retropatellar space.

•

Apply ﬁ rm pressure over the suprapatellar pouch with the ﬂ at of

the hand and use your thumb and index ﬁ nger placed on either side

of the patella to push any ﬂ uid centrally (see Fig. 11.5a ).

• With the ﬁ

rst one or two ﬁ ngers of the other hand, push the patella

down ﬁ

rmly (see Fig. 11.5b ).

• If ﬂ

uid is present, the patella will bounce off the lateral femoral

condyle behind. You will feel it being pushed down and then “tap”

against the femur.

KNEE

359

Move

2 Remember to test passive movements (you do the moving) and active

movements (the patient does the moving) at each stage. Quantify any

movement in degrees (measure) .

• Begin by moving the joint passively and feel over the knee with one

hand for any crepitus.

• Flexion: Ask the patient to maximally ﬂ

ex the knee. Normal

8135*.

• Extension: Ask the patient to straighten the leg at the knee.

• Hyperextension: Assess by watching the patient lift the leg off the bed

and then holding the feet stable in both hands above the bed or couch,

and ask the patient to relax. Ensure that you are not causing the

patient any discomfort.

Measure

The visual impression of wasting of the quadriceps can be conﬁ rmed by

measuring the circumference of the thighs at the same level using a ﬁ xed

bony point of reference e.g., 2.5 cm above the tibial tubercle.

(a) (b)

Fig. 11.4 Examining for the bulge sign. (a) Wipe any ﬂ uid from the medial joint

recess. (b) Wipe the ﬂ uid back out of the lateral joint recess and watch themedial

side.

(a) (b)

Fig. 11.5 Testing for patellar tap. (a) Use the palmar surface, thumb, and index

ﬁ nger of one hand to move any ﬂ uid into the retropatellar space. (b) Attempt to

tap the patella on the femur using the other hand.

CHAPTER 11 Musculoskeletal system360

Special tests

Testing for medial and lateral collateral ligament instability

• Take the patient’s foot with your right hand.

• Hold the patient’s extended knee ﬁ rmly with your left hand (

Fig. 11.6 ).

• Attempt to bend the distal leg medially (varus)

•

This tests the lateral collateral ligament.

• Attempt to bend the distal leg laterally (valgus).

•

This tests the medial collateral ligament.

• Repeat the above with the knee at 30* of ﬂ exion.

•

Normally, the joint should move no more than a few degrees.

Excessive movement suggests torn or stretched collateral ligament.

Anterior and posterior drawer tests

These test the anterior and posterior cruciate ligaments, which prevent

the distal part of the knee from moving anteriorly and posteriorly.

• Ensure that the patient is lying in a relaxed supine position.

• Ask the patient to ﬂ

ex the knee to 90

*.

• You may wish to position yourself perched on the patient’s foot to

stabilize the leg. Warn the patient about this ﬁ rst!

• Wrap your ﬁ

ngers around the back of the knee, using both hands,

positioning the thumbs over the patella pointing toward the ceiling

(

Fig. 11.7 ).

• Push up with your index ﬁ

ngers to ensure the hamstrings are relaxed.

• The upper end of the tibia is then pulled forward and pushed

backward in a rocking motion.

•

Normally, there should be very little or no movement seen.

•

Excessive anterior movement reﬂ ects anterior cruciate laxity.

•

Excessive posterior movement denotes posterior cruciate laxity.

McMurray test

This is a test for detecting meniscal tears ( Fig. 11.8a ).

• With the patient lying supine, bend the hip and knee to 90*.

• Grip the heel with your right hand and press on the medial and lateral

cartilage with your left hand.

• Internally rotate the tibia on the femur and slowly extend the knee.

• Repeat, but externally rotate the distal leg while extending the knee.

• Repeat with varying degrees of knee ﬂ exion.

•

If there is a torn meniscus, a tag of cartilage may become trapped

between the articular surfaces, causing pain and an audible click. You

may also be able to feel the click with your left hand.

Apley test

This is another test for meniscal tears ( Fig. 11.8b ).

• Position the patient prone with the knee ﬂ

exed to 90

*.

• Stabilize the thigh with your left hand.

• With your right hand, grip the patient’s foot.

• Rotate or twist the foot and press downward in a grinding motion.

•

This test should produce symptoms if a meniscus is torn.

KNEE

361

Fig. 11.6 Testing collateral ligament stability.

Fig. 11.7 Performing the anterior drawer test.

CHAPTER 11 Musculoskeletal system362

(a)

(b)

Fig. 11.8 Testing for meniscal tears. (a) McMurray test. (b) Apley grinding test.

ANKLE AND FOOT

363

Ankle and foot

Look

Expose the lower limbs and make note of any walking or other aids

present. Take a moment to also examine the shoes carefully for any

abnormal wear or stretching.

Examine feet and ankles when the patient is standing and, more care-

fully, with the patient lying on a couch or bed. Look for the following:

• Skin or soft tissue lesions, including calluses, swellings, ulcers, and scars

• Muscle wasting at the calf and lower leg

• Deformities, especially those involving the arch

•

Pes planus (ﬂ at foot)

•

Pes cavus (high-arched foot)

• Look for a bunion (bony deformity) at the ﬁ rst

metatarsophalangeal

(MTP) joint.

• Look for a bunionette at the ﬁ

fth MTP joint.

• Examine nails carefully for any abnormalities, such as fungal infections

or in-growing toenails.

2 Don’t forget to look between the toes. You may also wish to inspect

for evidence of other abnormalities, such as hammertoes, claw toes, or

clubbing of the feet (talipes equinovarus).

Feel

2 Always ask about pain before getting started.

• Assess the skin temperature and compare over both the feet.

• Look for areas of tenderness, particularly over bony prominences

(lateral and medial malleoli, MTP joints, interphalangeal joints, and

heel) as well as the metatarsal heads.

• Squeeze across the MTP joints and assess pain and movement.

• Remember to palpate any swelling, edema, or lumps.

Move

The ankle and foot constitute a series of joints that function as a unit.

2 Remember to test passive movements (you do the moving) and active

movements (the patient does the moving) at each stage.

Active movements should be performed with the patient’s legs hanging

over the edge of the bed.

• Ankle dorsiﬂ exion: Ask the patient to point their toes at their head.

• Ankle plantarﬂ exion: Ask the patient to push their toes down toward

the ﬂ

oor, like pushing on a pedal.

• Inversion: (subtalar joint between the talus and calcaneus): Grasp the

ankle with one hand and, with the other, grasp the heel, thereby ﬁ xing

the calcaneus, and turn the sole inward toward the midline ( Box 11.9 ).

• Eversion: as inversion but turn sole outward, away from the midline.

• Midtarsal joints: Grasp the heel with one hand and attempt to move

the tarsus up and down and from side to side with the other.

• Toe ﬂ exion: Ask the patient to curl their toes.

• Toe extension: Ask the patient to straighten their toes.

• Toe abduction: Ask the patient to fan out their toes as far as possible.

• Toe adduction: Ask patient to hold a piece of paper between the toes.

CHAPTER 11 Musculoskeletal system364

Measure

Calf circumference can be measured bilaterally to check for any discrepan-

cies that may highlight muscle wasting or hypertrophy (e.g., 10 cm below

the tibial tuberosities).

Special tests

Thompson or Simmond test

This test is used to assess for a ruptured Achilles tendon.

• Ask the patient to kneel on a chair with their feet hanging over the

edge. Squeezes both calves

• Normally the feet should plantarﬂ

ex. If the Achilles tendon is ruptured,

there will be no movement on the affected side.

Function

It is also helpful to observe the patient’s gait with and without shoes. Be

sure to ask the patient if they are able to do this.

Box 11.9 A word on inversion and eversion

Orthopedic purists will say that the ankle cannot invert or evert as it

is mainly a simple hinge—the eversion and inversion tests are, there-

fore, “failure only” tests. You should note that some eversion and inver-

sion is possible in the normal state at the tarsal joints, as tested by

neurologists.

Orthopedic practitioners test pathological inversion and eversion by

watching the heels from behind as the patient stands on tiptoes.

IMPORTANT PRESENTING PATTERNS

365

Important presenting patterns

Rheumatoid arthritis (RA)

RA is a chronic inﬂ ammatory, multisystem, autoimmune disease medi-

ated by proinﬂ ammatory cytokines, such as tumor necrosis factor alpha

(TNF-A), and in some cases is characterized by the presence of rheuma-

toid factor (RF).

There is a strong association with HLA-DR4, and patients with DR4

tend to have more severe disease. It affects around 1–3% of the population

in all racial groups, with peak age of onset in the fourth and ﬁ fth decades

and a female–male ratio of 3:1.

The usual pattern of disease is insidious but can also be episodic with

complete resolution between attacks (palindromic) or acute. The clinical

features of RA can be divided into articular and extra-articular features

and are summarized below.

Articular features

RA usually presents as a symmetrical polyarthritis affecting the wrists and

small joints of the hands and feet. Occasionally, a patient presents with a

monoarthritis of a larger joint, such as the knee or shoulder. Common

presenting symptoms are joint pain, stiffness, and swelling that are typically

worse in the mornings and improve as the day progresses. The disease

eventually leads to varying degrees of functional loss.

Signs of RA in the hands and wrist

There is synovitis involving the wrists and metacarpophalangeal (MCP)

and proximal interphalangeal (PIP) joints, with sparing of the distal inter-

phalangeal (DIP) joints.

• Ulnar deviation of ﬁ

ngers (subluxation or dislocation at MCP joints)

• Swan neck deformity: hyperextension of PIP joints with ﬂ

exion of MCP

and DIP joints.

• Boutonniere’s deformity: ﬂ

exion deformity of PIP joints with extension

of DIP and MCP joints

• Z-deformity of thumb: ﬂ

exed MCP joint with extended interphalangeal

joint of thumb

• Triggering of ﬁ nger

• Generalized wasting of small muscles of hand

• Cutaneous vasculitis

Signs of RA in the feet

• Forefoot synovitis with proximal phalangeal subluxation dorsally

• Metatarsal head erosion and displacement toward the ﬂ oor.

The

patient experiences this as like walking on marbles.

• Valgus deformities

• Collapse of longitudinal arch

Signs of RA in the spine

• Atlantoaxial subluxation 9 spinal cord compression

CHAPTER 11 Musculoskeletal system366

Extra-articular features of RA

• Rheumatoid nodules: common at sites of pressure (elbows and wrists).

They are associated with more severe disease and always RF positive.

• Tenosynovitis and bursitis

• Carpal tunnel syndrome

• Amyloidosis (proteinuria, hepatosplenomegaly)

• Systemic features (fever, malaise, weight loss, and lymphadenopathy)

Anemia

Causes include the following:

• Anemia of chronic disease

• GI bleeding associated with NSAID use

• Bone marrow suppression secondary to disease-modifying

antirheumatic drugs, such as gold and penicillamine

• Megaloblastic anemia from folic acid deﬁ

ciency (also secondary to

methotrexate) or pernicious anemia

• Felty’s syndrome (RA, splenomegaly, and leucopenia)

Lung features

• Pleuritic pain

• Pleural effusions

• Pulmonary ﬁ brosis

• Pulmonary nodules

• Obliterative bronchiolitis

• Caplan syndrome (massive lung ﬁ

brosis in patients with pneumoniosis)

Neurological features

• Peripheral nerve entrapment

• Mononeuritis multiplex

• Peripheral neuropathy

• Cervical myelopathy due to atlantoaxial subluxation

Cardiac features

• Pericarditis

• Pericardial effusions

Eye features

• Painless episcleritis

• Painful scleritis

• Scleromalacia perforans

• Keratoconjunctivitis sicca

• Sjögren’s syndrome

• Cataracts (chloroquine, steroids)

Vasculitis

• Nail fold infarcts

• Cutaneous ulceration

• Digital gangrene

• Cerebral and mesenteric infarction

• Coronary and renal vasculitis (rare)

Skin lesions

• Palmar erythema

• Pyoderma gangrenosum

IMPORTANT PRESENTING PATTERNS

367

Osteoarthritis

Osteoarthritis is a chronic disorder of synovial joints that is characterized

by focal cartilage loss and an accompanying reparative bone response.

It represents the single-most important cause of musculoskeletal

disability with a prevalence that increases with age and has a female

preponderance.

The joints commonly affected include the hips, knees, spine, and ﬁ rst

carpometacarpal, ﬁ rst

metatarsal, and DIP joints.

Secondary causes include trauma, RA, infection, neuropathic (Charcot’s)

joints, and metabolic disorders (e.g., Paget’s disease, acromegaly,

hemachromatosis, avascular necrosis, and hypoparathyroidism).

Clinical features

Common symptoms include swelling, deformity, stiffness, weakness, and

pain that is normally worse after activity and relieved by rest.

Common signs include the following:

• Hard, bony swellings of the DIP joints (Heberden’s nodes)

• Bony nodules at the PIP joints (Bouchard’s nodes)

•

These are bony outgrowths at the joint margins (osteophytes).

• “Square hand” deformity due to subluxation of the base of the thumb

• Valgus and varus deformities

• Crepitus

• Wasting and weakness (especially of the quadriceps and glutei)

• Tilting of the pelvis

Crystal arthropathies

Gout

Gout is a disorder of purine metabolism. It is characterized by hyper-

uricemia due to either overproduction or underexcretion of uric acid

( Box 11.10 ). Prolonged hyperuricemia leads to the formation of urate

crystals in the synovium, other connective tissues, and the kidney.

Clinical features of acute gout

• Severe pain and swelling classically in the great toe MTP joint, worse at

night and associated with redness ( Box 11.11 )

• Occasionally multiple joints are involved.

• 9 Systemic symptoms

Clinical features of chronic (tophaceous) gout

• Tophus formation (soft tissue deposits of urate found especially in

digits, helix of the ear, bursae, and tendon sheaths)

•

9 Overlying necrotic skin with chalky exudate of urate crystals

Pseudogout

This is caused by deposition of calcium pyrophosphate crystals in the syn-

ovium, joint capsule, and tendons. It is the most common cause of an acute

monoarthritis in older adults and may present as either an acute synovitis

or a chronic arthritis.

It is linked to chondrocalcinosis (calciﬁ cation of articular cartilage).

On examination, you may ﬁ nd a swollen, erythematous, and tender joint

(often knees, wrist, elbow, ankle, or shoulder, and MCP joints, especially

the index and middle) associated with systemic upset.

CHAPTER 11 Musculoskeletal system368

Spondyloarthropathies

These include ankylosing spondylitis, psoriatic arthritis, reactive arthritis,

and enteropathic arthritis. This is a group of related and overlapping forms

of inﬂ ammatory arthritis that characteristically lack rheumatoid factor

and are associated with HLA-B27. They present at any age, though young

males are primarily affected.

They also share a number of key features:

• Enthesitis (An enthesis is the insertion of a tendon, ligament, or capsule

into a bone.)

• Synovitis

• Sacroiliitis

• Dactylitis

• Peripheral arthritis affecting predominantly the large joints

Ankylosing spondylitis

Ankylosing spondylitis usually develops in early adulthood with a peak age

of onset in the mid-20s and is three times more common in males.

Common symptoms

• Lower back pain and stiffness that is typically worse in the morning and

after long periods of rest

• Chest pain as a result of T-spine involvement as well as enthesitis at

the costochondral joints

• Tender sacroiliac joints

Box 11.10 Causes of hyperuricemia

• Drugs: diuretics, ethanol, low-dose salicylates, pyrazinamide,

ethambutol, nicotinic acid, and cyclosporine

• Chronic renal failure

• Myeloproliferative and lymphoproliferative disorders (i purine

metabolism)

• Obesity

• Hypertension

• Hypothyroidism

• Hyperthyroidism

• Familial

• Excessive dietary purines

2 It is more common in the summer months because of reduced ﬂ uid

intake and increased ﬂ uid

loss.

Box 11.11 Conditions associated with gout

• Obesity

• Type IV hyperlipidemia

• Hypertension

• Impaired glucose tolerance or diabetes

• Ischemic heart disease

IMPORTANT PRESENTING PATTERNS

369

• Pain in peripheral joints, such as the shoulders and knees

Musculoskeletal features and signs

• Question-mark posture (loss of lumbar lordosis, ﬁ xed kyphoscoliosis

of the T-spine, compensatory extension of the C-spine)

• Protuberant abdomen

• Schober’s test is positive (see b p. 354)

• Achilles tendonitis

• Plantar fasciitis

Some extraskeletal features

• Anterior uveitis

• Aortic regurgitation

• Apical lung ﬁ brosis

• AV block

• Amyloidosis (secondary)

• Atlantoaxial dislocation

• Traumatic fracture of a rigid spine

• Hypoxia

• Fever

• Weight loss

Psoriatic arthritis

Psoriatic arthropathy affects up to 10% of patients with psoriasis and may

precede or follow the skin disease.

2 The arthropathy does not correlate with the severity of skin lesions.

There are ﬁ

ve main subtypes of psoriatic arthropathy:

• Asymmetrical distal interphalangeal joint arthropathy

• Asymmetrical large joint mono- or oligoarthropathy

• Spondyloarthropathy and sacroiliitis

• Rheumatoid-like hands (clinically identical to RA but seronegative)

• Arthritis mutilans (a severely destructive form with telescoping of the

ﬁ ngers)

Associated clinical features

• Psoriatic plaques (classically found on the extensor surfaces and scalp,

behind the ears, and in the navel and natal cleft)

• Nail involvement (pitting, onycholysis, discoloration, and thickening)

• Dactylitis (sausage-shaped swelling of the digits due to tenosynovitis)

Reactive arthritis

• An aseptic arthritis, strongly linked to a recognized episode of

infection. Common causes are gut and genitourinary pathogens.

• It mainly affects young adults and usually presents with asymmetric

and oligoarticular arthritis with symptoms starting a few days to a few

weeks after the infection.

• Enthesitis and dactylitis are other common features. Patients may

experience pain in the articular joints.

Associated extraskeletal features

• Urethritis

• Conjunctivitis

• Skin and mucosal lesions

CHAPTER 11 Musculoskeletal system370

Reiter’s syndrome

This is a form of reactive arthritis associated with the classic triad of

• Arthritis

• Urethritis

• Conjunctivitis

It often follows dysenteric infections such as Shigella , Salmonella ,

Campylobacteria , and Yersinia or infections of the genital tract. Other ﬁ nd-

ings that may be encountered are mouth ulceration, circinate balanitis,

keratoderma blennorrhagica (pustular-like lesions found on the palms or

soles), and persistent plantar fasciitis.

Enteropathic arthritis

Enteropathic arthritis is a peripheral or axial arthritis occurring in associa-

tion with inﬂ

ammatory bowel disease (IBD) and does not typically corre-

late with the severity of bowel disease. However, the peripheral arthritis

has been shown to improve if the affected bowel is resected.

Osteoporosis

Osteoporosis is a systemic skeletal disorder involving d bone mass (osteo-

penia) and microarchitectural deterioration, resulting in an i risk of frac-

ture. Classiﬁ cation (and treatment) is based on measurement of bone

mineral density (BMD), with comparison to that of a young healthy adult.

The underlying pathology is related to an imbalance between osteoblast

cells producing bone and osteoclast cells removing bone, which ultimately

produces a net loss of bone. See Box 11.12 for risk factors.

• Type I: accelerated (mainly trabecular) bone loss secondary to estrogen

deﬁ

ciency and leads to fracture of vertebral bodies as well as the distal

forearm in women in their late 60s and 70s

• Type II: age-related cortical and trabecular bone loss occurring in both

sexes and leads to fractures of the proximal femur in the elderly

Clinical features

The process leading to established osteoporosis is asymptomatic and the

condition usually presents only after bone fractures.

Features differ according to the fracture site. The most common clinical

features include the following:

• Marked kyphosis

• Loss of height

• Protuberant abdomen

• Spinal tenderness

Paget’s disease

This disorder of bone remodeling is characterized by i osteoclastic and

osteoblastic cell activity, leading to accelerated but disorganized bone

resorption and formation.

Paget’s disease is the second most common disease of bone after oste-

oporosis, is more common in males, and affects around 3% of the popula-

tion >40 years of age. It occurs more commonly in Britain than anywhere

else in the world; there are thought to be up to one million sufferers in

the UK.

IMPORTANT PRESENTING PATTERNS

371

While the exact etiology remains unknown, a number of factors have

been implicated, including a slow viral infection. Some 30% of Paget’s

patients have an affected ﬁ rst-degree relative.

Important clinical features and complications

• Enlargement of the skull

• Hearing loss (ossicles are involved and VIII nerve compression)

• Optic atrophy and angioid streaks

• Cardiac failure

• Kyphosis, anterior bowing of the tibia, lateral bowing of the femur

• i Bone warmth

• d Mobility

• Fractures

• Sarcomatous change (rare)

• Cord compression

• Cerebellar signs

• Hypercalcemia

Box 11.12 Risk factors for osteoporosis

• Smoking

• High alcohol consumption

• BMI <19

• Family history

• Premature menopause

• Prolonged immobilization

• Prolonged secondary amenorrhea

• Primary hypogonadism

• Low dietary calcium and vitamins

• Older age

• Female gender

• Sedentary lifestyle

• Caucasian or Asian origin

Chronic disorders, such as the following:

• Anorexia nervosa

• Malabsorption syndromes

• Primary hyperthyroidism

• Post-transplantation

• Cushing’s syndrome

• Chronic renal failure

CHAPTER 11 Musculoskeletal system372

Box 11.13 Some important causes of a swollen knee

• RA

• Ruptured Baker’s cyst

• Pseudogout

• Gout

• Edematous states (e.g., CHF,

nephrotic syndrome)

• Trauma

• Charcot’s knee

• Septic arthritis

• Hemarthrosis

THE ELDERLY PATIENT

373

The elderly patient

Rheumatological diseases represent a huge spectrum of illness in older

people, often complicating and concurrent with other diseases—e.g., the

impact of severe arthritis on COPD or heart failure or the effect of hip or

knee arthritis on recovery after acute stroke.

Arthritis and osteoporosis are two major factors in the geriatric giants

of immobility and instability—pertinent reminders of the widespread

effect of musculoskeletal illness with advancing age.

History

Method of presentation

This can vary, ranging from the fall that leads to a femoral neck fracture

or a referral “off legs” or with declining mobility. Older people will often

have an existing diagnosis of some form of arthritis—the difﬁ culty is not in

the diagnosis but in understanding the impact on everyday life.

Musculoskeletal illnesses are a key part of such presentations, and atten-

tion to these illnesses is vital. However, it is important to remember that

presentations such as falls are multifactorial—try to work out how muscu-

loskeletal illness contributes to mobility or risk of falls.

Intercurrent illness

This may often precipitate gout or particularly pseudogout. Equally impor-

tant are those illnesses that disturb carefully balanced homeostasis, leading

to a fall and fracture. Your task is to not just treat the consequence of the

fall but look at why it happened in the ﬁ rst place

Septic joints

They can be notoriously difﬁ cult to diagnose at times. Unilateral large joint

swelling and acute arthritis should ring alarm bells, especially if the patient

is unwell. A myriad of causes contribute to back pain, but never forget

deep-seated infection, such as discitis or osteomyelitis, which may be a

consequence of something as innocuous as a urinary infection.

Drug history

This is a keystone of any assessment. Consider the side-effect proﬁ le of

NSAIDs or whether gout has been precipitated by the effects of diuretics

or low-dose aspirin. If the patient has sustained a fragility fracture due to

osteoporosis, are they on appropriate treatment?

Never forget the i number of older people whose arthritis is success-

fully treated with disease-modifying drugs, and understand the effects

of such drugs (and the need to prescribe concurrent folic acid with

methotrexate).

Activities, occupation, and interests

These overlap with the functional history. Multidisciplinary assessment

is vital for tailoring rehabilitation, physical aids, and future care, where

appropriate. Ask about hobbies and interests—improving balance, mini-

mizing pain, and maximizing function may allow patients to carry on with

activities that are a key part of their lives (and might represent an oppor-

tunity for continued exercise or rehabilitation).

CHAPTER 11 Musculoskeletal system374

Examination

General

The signs are often very clear but despite this, easily overlooked. The need

here is for a careful and thoughtful assessment of function as well as dis-

ease activity. Always ask about your patient’s comfort, and examine care-

fully, explaining what you wish to do, to avoid misunderstanding and pain.

Pattern of disease

Look for typical patterns of disease and single-joint pathology. Look at

the ankles, feet, and back. It takes only a little more time to undertake

a good examination, but is depressingly common to see patients with

poor balance and a history of falls whose ﬁ les detail no musculoskeletal

assessment.

Disease activity

Be careful when palpating, but look to see if an acute exacerbation of joint

disease may well have contributed to the current presentation.

Gait and balance

These are often overlooked but are a vital part of the examination. Learn

(e.g., from the ward physiotherapist) how to undertake the get up and go

test, a well-validated test of gait and balance (see Box 11.14 ). This assess-

ment should overlap with neurological assessment when appropriate.

Box 11.14 Get up and go

This is an easy test to do and one that gives a wealth of information. In

essence, ask the patient to rise to standing from a chair, walk 10 feet,

then turn and return to the chair. The clinician’s role is not that of a pure

observer—you must make an assessment of safety and be on hand to

support the patient, if needed.

375

Male reproductive system

Applied anatomy and physiology 376

Sexual history 378

Symptoms 379

Examining male genitalia 381

Important presenting patterns 386

The elderly patient 388

Chapter 12

CHAPTER 12 Male reproductive system376

Applied anatomy and physiology

Anatomy

The male reproductive system consists of a pair of testes, a network of

excretory ducts (epididymis, ductus deferens, and ejaculatory tracts), sem-

inal vesicles, prostate, bulbourethral glands, and the penis.

Penis

The penis consists of erectile tissue contained within two dorsally placed

corpora cavernosa and the corpus spongiosum, which lies on their ventral

surface. The corpora are attached proximally to the inferior pubic rami.

The corpus spongiosum expands distally to form the glans penis and sur-

rounds the urethra.

The three corpora are contained within a ﬁ brous tubular sheath of fas-

cia and covered by freely mobile (and elastic) skin. A loose fold of skin, the

prepuce or foreskin, extends distally to cover the glans penis.

Scrotum

This is a muscular out-pouching of the lower part of the anterior abdomi-

nal wall. It contains the testes, epididymis, and lower ends of the sper-

matic cords. The scrotum acts as a climate-control system for the testes.

Muscles in the wall of the scrotum, in conjunction with muscle ﬁ bers in the

spermatic cord, allow it to contract and relax, moving the testicles closer

or further away from the body.

Testes

These are paired, ovoid organs measuring 74 x 3 x 2 cm, found within the

scrotal sac. The testes are made up of masses of seminiferous tubules that

are responsible for producing spermatozoa. Interstitial or Leydig cells lying

between these tubules produce the male sex hormones.

In the fetus, the testes develop close to the kidneys in the abdomen,

then descend caudally through the inguinal canal to reach the scrotum at

738 weeks gestation.

Each testis is covered by an outer ﬁ brous capsule (tunica albuginea).

Laterally and medially lies the visceral layer of the tunica vaginalis (a

closed serous sac—an embryonic derivative of the processus vaginalis,

which normally closes before birth). The posterior surface of the testis

is devoid of tunica vaginalis and is pierced by numerous small veins

that form the pampiniform plexus. The seminiferous tubules converge

here to form the efferent tubules, which eventually give rise to the

epididymis.

Spermatic cord

This suspends the testis in the scrotum and contains structures running

between the testis and the deep inguinal ring (the ductus deferens, arter-

ies, veins, testicular nerves, and epididymis).

The cord is surrounded by the layers of the spermatic fascia (internal

spermatic fascia) formed from the transversalis fascia, the cremasteric

fascia formed from fascia covering the internal oblique, and the external

spermatic fascia formed from the external oblique aponeurosis.

APPLIED ANATOMY AND PHYSIOLOGY

377

The cremasteric fascia is partly muscular. Contraction of the cremaster

muscle draws the testis superiorly. The raising and lowering of the testis

acts to keep it at a near-constant temperature.

Epididymis

This is a convoluted duct 76 cm in length lying on the posterior surface of

the testis. It is a specialized part of the collecting apparatus where sperma-

tozoa are matured before traveling up the vas deferens to join the ducts

draining the seminal vesicles, known as the ejaculatory ducts.

The seminal vesicles are paired organs that lie on the posterior surface

of the bladder and contribute most of the ﬂ uid that makes up semen,

along with fructose, ascorbic acid, amino acids, and prostaglandins.

Prostate gland

This is a ﬁ rm, walnut-sized structure that lies inferior to the bladder, encir-

cling the urethra. Many short ducts produce ﬂ uid that is emptied into the

urethra and makes up a proportion of semen.

Bulbourethral glands

These are small, pea-sized glands located near the base of the penis.

In response to sexual stimulation, the bulbourethral glands secrete an

alkaline mucus-like ﬂ uid that neutralizes the acidity of the urine in the

urethra and provides a small amount of lubrication for the tip of the penis

during intercourse.

Sex hormones

Three hormones are the regulators of the male reproductive system:

• Follicle-stimulating hormone (FSH) is produced in the anterior pituitary

gland and stimulates spermatogenesis by its action on Sertoli cells.

• Luteinizing hormone (LH) is produced in the anterior pituitary gland

and stimulates the production of testosterone from Leydig cells.

• Testosterone is produced in the testis and adrenal gland and

aids in development of male secondary sexual characteristics and

spermatogenesis.

Male sexual response

There are four stages of the sexual response:

• Excitement or arousal is under control of the parasympathetic nervous

system. During this stage, the penis becomes engorged with blood and

stands out from the body. Other changes include an i in heart rate,

blood pressure, respiratory rate, and skeletal muscle tone.

• Plateau: Continued sexual stimulation maintains the changes made in

the arousal phase. This can last from a few seconds to many minutes.

• Orgasm: In males, this is the briefest stage and mediated by the

sympathetic nervous system. Rhythmic contractions of the perineal

muscles and accessory glands and peristaltic contraction of the seminal

ducts result in ejaculation. This is usually followed by a refractory period

during which another erection cannot be achieved. This varies between

individuals, from minutes to hours, and lengthens with advancing age.

• Resolution: Blood pressure, heart rate, respiratory rate, and muscle

tone return to the unaroused state. This is accompanied by a sense of

relaxation.

CHAPTER 12 Male reproductive system378

Sexual history

This can be awkward for both the patient and the history-taker. It should

be undertaken in a sensitive, conﬁ dent, and conﬁ dential manner. Before

the discussion takes place, the patient should be reassured about the lev-

els of privacy and conﬁ dentiality and that they are free to openly discuss

their sexual life and habits.

Make no assumptions, remain professional, and try to use the patient’s

own words and language. Be aware of cultural and religious differences

surrounding sex and talking about it. See b p. 48 for further guidance.

You should approach a sexual history in a structured way, as below.

Sexual activity

This should include an assessment of the risk of acquiring a sexually trans-

mitted infection (STI).

Determine the number and gender of the patient’s sexual partners, their

risk of having an STI, and the precautions (if any) that were taken. Try ask-

ing the following questions:

• Do you have sex with men, women, or both?

• In the past 2 months, how many people have you had sex with?

• When did you last have sexual intercourse?

• Was it with a man or a woman?

• Were they a casual or regular partner?

• Where were they from?

• Do they use injected drugs?

• Do they have any history of sexually transmitted infections?

• How many other partners do you think they’ve had recently?

• In what country did you have sex?

• What kind of sex did you take part in? (e.g., vaginal, anal, oral)

• For each type of sex, did you use a condom?

• Does your partner have any symptoms?

• Have you had any other partners in the last 6 weeks?

•

If so, repeat the questions above for each partner.

Previous history

You also need to establish the history of STIs for the patient:

• Have you had any other STIs?

• Have you ever had a sexual check-up?

• Have you ever been tested for HIV, hepatitis, or syphilis?

• Have you ever been vaccinated against hepatitis A or B?

Psychological factors

Concerns over loss of libido and sexual function may point to a complex

psychological cause for symptoms. Explore this delicately and ask about

• History of sexual abuse

• Problems with the relationship

• Sexual partners outside the relationship

• Any other cause for anxiety

• History of depression or anxiety

SYMPTOMS

379

Symptoms

Urethral discharge

If the patient complains of discharge or “mucus” from the end of their

penis, establish the following:

• Amount

• Color

• Presence of blood?

• Relation between the discharge and urination or ejaculation

• Is there any pain?

• Are there any other symptoms, such as conjunctivitis or arthralgia?

• Has the patient recently had symptoms of gastroenteritis?

You should also determine when this symptom was ﬁ

rst noticed and

how that relates to any sexual contacts that the patient has had and the

possibility of exposure to STIs (see previous pages).

Rashes, warts, ulcers

Treat a genital skin lesion as you would any other rash (b p. 80). Also

ask about the following:

• Similar lesions elsewhere (mouth, anus)

• Foreign travel

Determine the risk of recent exposure to STIs as previously.

Testicular pain

This is often felt as deep, burning pain and accompanied by nausea. Treat

as pain in any other location, as on b p. 33. Also ask about associated

genital symptoms, such as testicular swelling, dysuria, or hematuria (see

Box 12.1 ).

Common causes include testicular torsion, mumps, orchitis, andepidi-

dymitis. Remember the possibility of cancer.

Erectile dysfunction

The term impotence should be avoided by health-care providers because

of its negative social implications. Patients may use the term impotence

Box 12.1 The rest of the history

A full history needs to be taken in all cases, as described in Chapter 2.

The following may have particular relevance here.

PMH

Ask especially about the following:

• Sexually transmitted infections (as previously)

• Orchitis or a history of mumps

• Inguinal, scrotal, and testicular injury or surgery

• Urethral injury

Smoking and alcohol

Detailed histories should be taken as described in b Chapter 2 (p. 41).

CHAPTER 12 Male reproductive system380

for a number of different sexual problems. Ask speciﬁ cally if the patient

means the following:

• Difﬁ

culty in achieving or maintaining an erection (erectile dysfunction)

• Difﬁ

culty with premature ejaculation (ejaculatory dysfunction)

• Difﬁ culty in reaching orgasm (orgasmic dysfunction)

Remember that an erection is not necessary for men to reach orgasm

or to ejaculate . Erectile dysfunction

is the inability to gain and maintain an

erection for satisfactory completion of sexual activities.

If a patient complains of impotence, this needs to be explored in more

detail. Establish particularly if the lack of function is related to a particular

partner or situation or is constant. Ask the following questions:

• Are you able to get an erection at all?

• Do you wake with an erection in the morning?

• Are you able to get an erection to masturbate?

If the cause is psychological, the patient will often still wake with an erec-

tion (the so-called morning glory) but not be able to perform in a sexual

situation. This can be tested with a sleep study, if necessary. Psychological

factors should be explored with sensitivity.

Organic causes for erectile dysfunction include atherosclerosis, diabe-

tes mellitus, multiple sclerosis, pelvic fractures, urethral injury, or other

endocrine dysfunction.

Drug history is important. Drugs associated with erectile dysfunction

include barbiturates, benzodiazepines, phenothiazines, lithium, antihyper-

tensives (e.g., B-blockers), alcohol, estrogens, methadone, and heroin.

Loss of sexual desire (libido)

This can be an early sign of a pituitary tumor, but the cause is more often

deeply rooted in the patient’s psychology. Ask the following questions:

• How often do you shave your face?

• Has this changed recently?

• Do you have any muscle wasting or pain?

• Explore any issues about the sexual partner and the patient’s

relationship with them.

Infertility

Around 10% of couples have difﬁ culty with conception. Male infertility

accounts for 1/3 of childless relationships. This is a complex topic and not

within the scope of this book.

Relevant information to ascertain includes the following:

• Age of both partners

• Length of time they have been trying to conceive

• Presence of existing children belonging to both partners, and children

of each partner from prior relationships

• Frequency and timing of intercourse

• Any erectile, ejaculatory, or orgasmic dysfunction

• Drug history of both partners

• Factors suggestive of endocrine malfunction, as under Loss of Sexual

Desire

• Smoking and alcohol consumption

• Menstrual history from partner

EXAMINING MALE GENITALIA

381

Examining male genitalia

Explain to the patient that you would like to examine the penis and testes

and reassure them that the procedure will be quick and gentle.

You should have a chaperone present, particularly if you are female. A

chaperone, however, is often desirable even in circumstances where the

examiner is male.

Ensure that the examination room is warm and that you are unlikely to

be disturbed. With the patient on a bed or couch, raised to a comfortable

height, ask them to pull their clothing down. You should be able to see the

genitalia and lower part of the patient’s abdomen at the very least.

Penis

Inspection

Make a careful inspection of the organ, noting the following:

• Size

• Shape

• Presence or absence of a foreskin

• Color of the skin

• The position and caliber of the urethral meatus (see Box 12.2 )

• Any discharge

• Any abnormal curvature

• Any lesion, scaling, scabbing or other superﬁ

cial abnormality such as

erythema or ulceration, particularly at the distal end (glans)

Palpation

Palpate the whole length of the penis to the perineum and note the state

of the dorsal vein, which is usually easily seen stretching the length of the

penis at the dorsal midline. Note also any abnormalities of the underlying

tissues (e.g., ﬁ rm areas) that may not be visible—this may represent the

plaques of Peyrone’s disease.

Retract the foreskin to expose the glans penis and urethral meatus.

The foreskin should be supple, allowing smooth and painless retraction.

Look especially for any secretion or discharge and collect a specimen, if

possible. The patient may be able to milk the shaft of the penis to express

the secretion.

Box 12.2 Hypospadias

Hypospadias is the abnormal, ventral, positioning of the urethralmeatus.

It is seen in 1 in 250 males. In the vast majority, the hypospadias is

slight.

Patients may have a hooded foreskin with the meatus at the very edge

of the glans or a very slightly ventral meatus that iscompletely covered

by a normal foreskin.

Slight hypospadias has no effect on sexual function but may be a cause

of anxiety and embarrassment resulting in psychosexual problems once

the patient is aware that his penis is “different.”

CHAPTER 12 Male reproductive system382

There is often a trace of smegma underlying the foreskin. This is a nor-

mal ﬁ nding.

0 Remember to replace the foreskin at the end of the examination.

Note that in the presence of phimosis, the foreskin will be nonretractile

and attempts may cause considerable pain.

Scrotum and contents

Reminder

Before touching the genitalia, consider assessing the patient for the pres-

ence of the cremasteric reﬂ ex when evaluating complaints of testicular

pain. Please note, however, that the assessment of the cremasteric reﬂ ex

can be unreliable in a patient who is tense or anxious.

Examining the scrotum and scrotal contents is best done with the

patient standing up.

Inspection

Make a careful examination of the scrotal skin. It is usually wrinkled and slightly

more pigmented than the rest of the patient’s body and should be freely

mobile of the testis. One testis usually hangs lower than the other. Remember

to lift the scrotum, inspecting the inferior and posterior aspects.

Look especially for the following:

• Edema

• Sebaceous cysts

• Ulcers

• Scabies

• Scars

Palpation

The scrotal contents should be gently supported with your left hand and

palpated with the ﬁ ngers and thumb of your right hand. It may help to ask

the patient to hold their penis to one side (see Fig. 12.1 ).

• Check that the scrotum contains two testes.

•

Absence of one or both testes may be due to previous excision,

failure of the testis to descend, or a retractile testis.

•

If there appears to be a single testis, carefully examine theinguinal

canal for evidence of a discrete swelling that could be an

undescended testis.

• Make careful note of any discrete lumps or swellings in the body of the

testis.

•

Any swelling in the body of the testis must be considered to be

suggestive of a malignancy.

• Compare the left and right testes, noting the size and consistency.

•

The testes are normally equal in size, and smooth, with a ﬁ rm,

rubbery consistency. If there is a signiﬁ cant discrepancy, ask the

patient if he has ever noticed this.

• Feel for the epididymis, which lies at the posterolateral aspect of each

testis.

• The vas can be distinguished from the rest of the cord structures, lying

along the posterior aspect of the bundle, and feels ﬁ

rm and wire-like.

It runs from the epididymis to the external inguinal ring.

383

EXAMINING MALE GENITALIA

Scrotal swellings

If a lump is palpated:

• Decide if the lump is conﬁ ned to the scrotum. Are you able to feel

above it? Does it have a cough impulse? Is it ﬂ

uctuant? (You will be

unable to get above swellings that descend from the inguinal canal.)

• Deﬁ

ne the lump as any other mass, as described on b p. 88.

• Transillumination is often important here. Darken the room and shine

a small torch through the posterior part of the swelling (see Fig. 12.2 ).

•

A solid mass remains dark, whereas a cystic mass or ﬂ uid will

transilluminate.

(a)

(b)

Fig. 12.1 (a) Examine the scrotum with the patient standing and use both hands.

It is sometimes preferable to ask the patient to hold their penis aside (b).

CHAPTER 12 Male reproductive system384

Perineum and rectum

Don’t overlook the perineum, anal canal, and rectum. In particular, a digital

rectal examination should be performed as described on b p. 241, with

particular attention to feeling the prostate and seminal vesicles.

Local lymphatics

• Lymph from the skin of the penis and scrotum drains to the inguinal

lymph nodes.

• Lymph from the covering of the testes and spermatic cord drains

initially to the internal, then common, iliac nodes.

• Lymph from the body of the testes drains to the para-aortic lymph

nodes—these are impalpable.

• Your examination is not complete without a careful palpation of the

inguinal lymph nodes ( Fig. 12.3 ). This is best done with the patient lying

comfortably on a bed or couch.

• If any swelling is found, it should be described in the same way as any

lump (b p. 88).

Fig. 12.2 Attempt to transilluminate any swelling by shining a small penlight

through it. Unlike the ﬁ gure above, the room should be darkened.

385

EXAMINING MALE GENITALIA

Horizontal

group

Vertical

group

Fig. 12.3 Diagrammatic representation of the inguinal lymph nodes.

CHAPTER 12 Male reproductive system386

Important presenting patterns

Phimosis

This is a narrowing of the end of the foreskin that prevents its retrac-

tion over the glans penis. It can cause difﬁ culty with micturition and lead

to recurrent balanitis. It may cause interference with erections and sexual

intercourse.

• Causes : congenital, infection, trauma, inﬂ ammation

(balanitis)

Paraphimosis

In this case, the foreskin can be retracted but then cannot be replaced

over the glans. This results in edema, which limits its movement still fur-

ther. If left in this condition, it can become necrotic or gangrenous.

This condition commonly occurs in men 15–30 years old. It is a frequent

complication of urinary catheterization if the practitioner fails to replace

the foreskin after the procedure is performed.

Hypospadias

See also Box 12.2 , b p. 384. Hypospadias is a congenital abnormality

in which the urethra opens on the ventral surface of the penis. Minor

degrees result in a hooded or dorsal foreskin and spraying of the urine

during micturition.

Openings on the ventral surface of the shaft of the penis (secondary

hypospadias) or openings at the scrotum or perineum (tertiary hypospa-

dias) may cause serious difﬁ culties with micturition and sexual function.

Balanitis and balanoposthitis

Balanitis is inﬂ ammation of the glans penis. Balanoposthitis is inﬂ amma-

tion of the glans and the foreskin. Such inﬂ ammation presents as redness,

swelling, and pain of the affected parts, often with difﬁ culty retracting the

foreskin.

• Causes: Candida albicans (especially in patients with diabetes), herpes

infection, carcinoma, drug eruptions, poor hygiene

Priapism

This is a painful, persistent erection and a serious feature of sickle crisis.

Other causes include leukemia, drugs (e.g., erectile dysfunction treat-

ments or psychotropics), and neurogenic (e.g., diseases of spinal cord).

Penile ulcers

Conditions causing ulceration of genitalia include herpes simplex (vesicles

followed by ulceration), syphilis (nontender ulceration), malignancy (e.g.,

squamous cell carcinoma—nontender), and Behçet’s syndrome.

Hydrocele

This is ﬂ uid entrapment in the tunica vaginalis, causing usually painless

swelling of the scrotum, the size of which can be considerable. Hydroceles

will surround the testis, making it impalpable. It will transilluminate.

As well as congenital abnormalities in the inguinal canal, hydrocele can

be caused by trauma, infection, and neoplastic disease.

IMPORTANT PRESENTING PATTERNS

387

Epididymal cysts

These are harmless, painless swellings arising behind and separate from

the testis itself. The examiner may be unable to feel the rest of the epidi-

dymis. The testicle (anteriorly) should be normal. Epididymal cysts will

transilluminate.

Varicocele

This involves abnormal dilatation of the veins in the spermatic cord caused

by incompetent valves in the testicular vein. They only become apparent

when the patient is standing and almost disappear when the patient is

supine. These are much more common on the left.

Varicoceles are usually painless (although they can cause a deep ache in

some men) and, in themselves, harmless. Varicocele is, however, associ-

ated with a reduction in fertility (it makes the testis abnormally warm).

They are classically described as feeling like a bag of worms on palpation.

Orchitis

This is inﬂ ammation of the testis. The affected organ will hang higher in

the scrotum and may be swollen and warm with redness of the overlying

skin. It will be very tender to palpation. The patient may be systemically

unwell with fever.

Testicular torsion

This presents in a very similar way to orchitis and is often difﬁ cult to distin-

guish, although the onset is much more sudden in torsion. Twisting of the

testis on the spermatic cord (torsion) will cause ischemia and severe pain.

Frequently, this pain is referred to the abdomen, often mimicking acute

abdominal conditions such as appendicitis.

It usually occurs in young adults and teenagers, with a peak age of 14.

Torsion is usually inward, toward the midline.

This is a urological emergency, and its presence must initially be con-

ﬁ rmed through vascular ultrasonography to conﬁ rm the presence of

diminished blood ﬂ ow. If the testicle is left in this condition without being

untwisted (with appropriate analgesia), surgical removal of the testis may

be necessary. Immediate surgical referral is advised if this is suspected.

Testicular carcinoma

This should be at the top of your list of differential diagnoses in the case of

an intrascrotal mass. Teratomas commonly occur between the ages of 20

and 30 years, whereas seminomas are more common at age 30–40 years.

There may be associated pain and tenderness or a dull aching, dragging

sensation in the scrotum and groin. Look for constitutional symptoms sug-

gestive of neoplastic disease, such as malaise, wasting, and anorexia, as

well as leg swelling (venous or lymphatic obstruction), lymphadenopathy,

or an associated abdominal mass.

CHAPTER 12 Male reproductive system388

The elderly patient

Much of the information on this page overlaps with that on the female

reproductive system in Chapter 14. We would encourage the reader to

regard both sections as a whole.

It is important to recognize that bladder carcinoma and diseases of the

prostate are some of the most common urogenital problems faced by

older men; remember to screen for such problems in any assessment. For

prostate diseases, it is also important to know that patient awareness is

high, so you should expect questions and a wish to be involved in treat-

ment decisions. Equally so, many of these problems are faced by patients

with cognitive impairment, in whom history may be limited and thorough

assessment is vital.

Retain a holistic outlook on male urogenital problems, and you will be

less likely to miss delirium because of acute epididymo-orchitis—a not

uncommon presentation!

Studies report that half of U.S. adults ages 65–74 and more than 25% of

those age 75 or older maintain active sexual lives. Avoiding sexual issues

in this population can cause major problems to be overlooked. Many men

over the age of 70 experience erectile dysfunction, so try not to make

assumptions when seeing older people with sexual health problems.

History

Explore

Explore the history. Even for patients with prostate disease, how will the

effects of treatment (e.g., TURP or conventional surgical prostate resec-

tion) affect relationships or sexual activity? Keep your thought processes

open when assessing continence problems—there may symptoms of both

obstruction and incontinence in many men. See also Box 12.3.

Box 12.3 A note on (recurrent) urinary tract infections

Most readers will have already seen many older patients with this com-

mon (and often over diagnosed) problem.

While many diagnoses are made on clinical suspicion, it is vital to

undertake urinalysis and obtain urine for microscopy and culture to

conﬁ rm the presence of urinary tract infections (UTIs). The reasoning

is twofold: avoiding rushing to a label of UTI as the cause of delirium or

mobility decline will reduce the chance of missing the correct diagnosis.

Similarly, a proven culture diagnosis of UTI aids in prescribing and helps

identify recurrent infections. Recognizing the latter may reveal underly-

ing diagnoses and reduce discomfort or even hospitalization for some

patients.

So, when faced with recurrent infections, be assiduous and request

urine cytology (to look for bladder cancers) and ultrasound (for struc-

tural abnormalities), and discuss the value of cystoscopy and rotating or

long-term antibiotics with urology colleagues.

THE ELDERLY PATIENT

389

PMH

Vascular diseases, metabolic, and neurological illnesses may all be under-

pinning diagnoses when faced with impotence. Could the new presenta-

tion of balanitis indicate diabetes?

Drug history

Aside from obvious culprits (e.g., diuretics), consider the effects of anti-

depressants, digoxin, and antihypertensives on both bladder and sexual

function.

SH and sexual history

Always take an appropriate functional history, particularly if there are con-

tinence problems. Consider alcohol and tobacco in relation to impotence,

and undertake a detailed occupational history if the patient presents with

hematuria (bladder cancer?).

Have the conﬁ dence to take a sexual history if there are problems with

erectile or ejaculatory dysfunction. As indicated earlier, many older people

have active sex lives and you’re more likely to be embarrassed about tak-

ing the history than they are recounting it.

Examination

General

In addition to the detailed examination considered earlier in this chapter,

keep in mind the need for a general examination, focusing on mood and

neurological assessment in particular.

Cognition

This is a key part of this assessment, particularly for continence and erec-

tile dysfunction problems.

Urogenital

Think subtly: in older men, orchitis may present with declining mobility,

delirium, or falls, so don’t forget to undertake a thorough examination in

older adults, even when there is apparently little to indicate a urogenital

problem. For patients with urinary catheters, whether short or long term,

examination is a mandatory part of assessment.

391

Female breast

Applied anatomy and physiology 392

Important symptoms 394

Inspection of the breast 397

Palpation of the breast 399

Examining beyond the breast 402

Important presentations 404

Chapter 13

392 CHAPTER 13 Female breast

Applied anatomy and physiology

Anatomy of the breast

The two mammary glands are highly developed apocrine sweat glands.

They develop embryologically along two lines extending from the axillae

to the groin—the milk lines (see Fig. 13.1 ). In humans, only one gland

develops on each side of the thorax, although extra nipples with breast

tissue may sometimes occur.

The breasts extend from the second to the sixth ribs and transversely

from the lateral border of the sternum to the mid-axillary line.

For the purposes of examination, each breast may be divided into four

quadrants by horizontal and vertical lines intersecting at the nipple. An

additional lateral extension of breast tissue (the axillary tail) stretches

from the upper outer quadrant toward the axilla (see Fig. 13.2 ).

Each mammary gland consists of 15–20 lobes separated by loose adi-

pose tissue and subdivided by collagenous septa. Strands of connective

tissue called the suspensory ligaments of the breast (Cooper’s ligaments)

run between the skin and deep fascia to support the breast. Each lobe is

further divided into a variable number of lobules composed of grape-like

clusters of milk-secreting glands termed alveoli and is drained by a lactif-

erous duct that opens onto the nipple. Myoepithelial cells surround the

alveoli, which contract and help propel the milk toward the nipples.

The nipple is surrounded by a circular pigmented area called the areola

and is abundantly supplied with sensory nerve endings. The surface of this

area also contains the glands of Montgomery, which act to lubricate the

nipple during lactation.

Lymphatic drainage

Lymphatic drainage from the medial portion of the breast is to the internal

mammary nodes. The central and lateral portions drain to the axillary

lymph nodes, which are arranged into ﬁ ve groups (see Fig. 13.7 , p. 403).

Physiology—normal breast changes in women

• Puberty: During adolescence, estrogen promotes the development of

the mammary ducts and distribution of fatty tissue, while progesterone

induces alveolar growth.

• The menstrual cycle: Toward the second half of the menstrual cycle,

after ovulation, the breasts can become tender and swollen. They

return to their resting state after menstruation.

• Pregnancy: High levels of placental estrogen, progesterone, and

prolactin promote mammary growth in preparation for milk

production.

• Postnatal: The sharply declining levels of estrogen and progesterone

permit prolactin to stimulate the alveoli and produce milk. Suckling

stimuli increases the secretion of prolactin as well as releases oxytocin,

which stimulates myoepithelial cells to contract.

• Menopause: The breasts become softer and more homogenous

and undergo involutional changes, including d size, atrophy of the

secretory portions, and some atrophy of the ducts.

APPLIED ANATOMY AND PHYSIOLOGY

393

Fig. 13.1 Illustration of the two milk lines along which the nipples form—

occasionally extra nipples can be found.

Upper

inner

Upper

outer

Lower

inner

Lower

outer

Tail of

Spence

Fig. 13.2 Illustrations showing the four quadrants of the breast with the axillary

tail.

CHAPTER 13 Female breast394

Important symptoms

First steps

Begin by establishing a menstrual history (see Box 13.1 and b Chapter 14).

You should also determine the date of the last period of menstruation.

Pre-existing disease in the breast is likely to become more noticeable dur-

ing the second half of the menstrual cycle—lumps often get bigger or

become more easily palpable.

2 Bear in mind that seeking medical attention for a breast lump or tender-

ness can produce extreme anxiety and embarrassment in patients. Men

with gynecomastia are also likely to feel anxious about their breast devel-

opment ( Box 13.2 ). Be sure that you adopt an appropriately sensitive,

sympathetic, and professional approach.

Breast pain (mastalgia)

As for pain at any other site, you should establish the site, radiation, char-

acter, duration, severity, exacerbating factors, relieving factors, and associ-

ated symptoms. Also ask the following:

• Is the pain unilateral or bilateral?

• Is there any heat or redness at the site?

• Are there any other visible skin changes?

• Is the pain cyclical or constant—and is it related to menstruation?

• Is there a history of any previous similar episodes?

• Is the patient breastfeeding?

• Is the patient on any hormonal therapy (especially perimenopausal)?

The most common cause of mastalgia in premenopausal women is

hormone-dependent change. Other benign causes include mastitis and

abscesses. One in 100 breast cancers presents with mastalgia as the sole

symptom.

Box 13.1 Menstrual history

It is important to take a clear and accurate menstrual history, as outlined

in b Chapter 14. Establish the following:

• Age of ﬁ rst

menses

• Usual time between menstruation

• Usual duration of menstruation

• Usual quantity of menstruation

• Age of menopause (if applicable)

• Number of pregnancies

• Previous history of breast-feeding

• The date of the beginning of the last menstrual period.

IMPORTANT SYMPTOMS

395

Nipple discharge

Important causes of nipple discharge include ductal pathology, such as

ductal ectasia, papilloma, and carcinoma.

Ask about the following:

• Is the discharge true milk or some other substance?

• What color is the discharge (e.g., clear, white, yellow, blood-stained)?

• Is it spontaneous or nonspontaneous?

• Is the discharge unilateral or bilateral?

• Are there any changes in the appearance of the nipple or areola?

• Mastalgia?

• Are there any breast lumps?

• Periareolar abscesses or ﬁ

stulae indicating periductal mastitis?

•

This is closely linked to smoking in young women. Periductal mastitis

is also associated with hidradenitis suppuritiva. Ask about abscess

elsewhere, e.g., axilla and groin. The symptoms are often recurrent.

0 Remember that after childbearing, some women continue to discharge

a small secretion of milk (galactorrhea). However, in rare instances this

can be the ﬁ

rst presenting symptom of a prolactin-secreting pituitary

adenoma. In the case of true bilateral galactorrhea, you should also ask

about

• Headaches

• Visual disturbances, especially visual ﬁ eld

deﬁ

cits

Box 13.2 Male breast

Gynecomastia

This is enlargement of male breast tissue, which should not normally

be palpable. There is an i in ductal and connective tissue.

Gynecomastia is a common occurrence in adolescents and the eld-

erly. It is seen in obese men due to increased adipose tissue.

In many patients, gynecomastia is drug related and the full causative

list is long. Important drug causes include estrogen receptor binders,

such as estrogen, digoxin, and marijuana, as well as anti-androgens, such

as spironolactone and cimetidine.

2 In the history, ask about drug and hormone treatment (e.g., for

prostate cancer).

2 You should also make a full examination of the patient, looking for

signs of hypopituitarism, chronic liver disease, and thyrotoxicosis.

Remember to carefully examine the genitalia.

Breast cancer in males

The female–male ratio for breast cancer is 100:1.

The appearance and pathology of breast cancer in males is similar to

that in females.

The most common presentation in males is a hard, painless lump ﬁ xed

to the skin or chest wall, followed by nipple discharge.

CHAPTER 13 Female breast396

Box 13.4 Risk factors for breast cancer in females

• Advancing age

• Breast cancer in a ﬁ rst-degree relative

• BRCA genes

• Previous cancer in the other breast

• Early menarche (<12 years)

• Late menopause (>55 years)

• Nulliparity (no pregnancies)

• No previous breast-feeding

• Previous radiotherapy—e.g., mantle radiotherapy for Hodgkin’s disease

• Oral contraceptive pill or hormone therapy

Box 13.3 Some causes of breast lumps

• Cyst

• Fibroadenoma

• Carcinoma

• Fat necrosis

• Hamartoma

• Lipoma

• Epidermoid cyst

• Cystosarcoma

Breast lumps

These are a very important presenting complaint with a number of causes

( Box 13.3 ), the most important one being cancer (see Box 13.4 for risk

factors). Establish the following:

• When the lump was ﬁ rst

noticed

• Whether the lump has remained the same size or enlarged

• Whether the size of the lump changes according to menstrual cycle

• Is there any pain?

• Are there any local skin changes?

• Is there a history of breast lumps (ask about previous biopsies,

diagnoses, and operations)?

• A full systems inquiry should include any other symptoms that might

suggest a neoplastic disease (weight loss, loss of appetite, fatigue, etc.)

and metastatic spread to other organ systems (shortness of breath,

bony pain, etc.).

Age

A good clue as to the likely diagnosis of a lump is the age of the patient:

• Fibroadenomas are common between 20 and 30 years.

• Cysts are common between 30 and 50 years.

• Cancer is very rare <30 years of age but more likely in the >50 age-

group.

INSPECTION OF THE BREAST

397

Inspection of the breast

Before you start

• When examining the female breast, you should have a chaperone

present. Ideally, the chaperone should be female.*

• The patient should be fully undressed to the waist and sitting on the

edge of the exam table with her arms by her side.

• You should be able to see the neck, breasts, chest wall, and arms.

General inspection

Stand in front of the patient and observe both breasts, noting:

• Size

• Tanner stage

• Symmetry

• Contour

• Color

• Scars

• Venous pattern on the skin

• Any dimpling or tethering of the skin

• Ulceration (describe fully as on b p. 90)

• Skin texture, e.g., any visible nodularity

•

An unusual ﬁ nding but one that should not be missed is the orange-

peel appearance of peau d’orange caused by local edema. This is

seen in breast carcinoma and following breast radiotherapy.

Nipples

Note whether the nipples are

• Symmetrical

• Everted, ﬂ

at, or inverted

• Scaling (may indicate eczema or Paget’s disease of the breast)

• Associated with any discharge

•

Single-duct discharge can indicate a papilloma or cancer.

•

Multiple-duct discharge at the nipple suggests ductal ectasia.

If abnormalities are present, ask if these are a recent or long-standing

appearance. Make note of any additional nipples, which can occur any-

where along the mammary line.

Axillae

Ask the patient to place her hands on her head, and repeat the inspection

process. Pay particular attention to any asymmetry or dimpling that is now

evident. Examine the axillae for masses or color change.

Maneuvers

Finally, dimpling or ﬁ xation can be further accentuated by having the

patient perform the following maneuvers (see Fig. 13.3 ):

• Lean forward while sitting

• Rest her hands on her hips

• Press her hands against her hips (pectoral contraction maneuver)

* Prudent advice is that all providers should have a chaperone present when performing an inti-

mate examination and the chaperone should be the same sex as the patient.

CHAPTER 13 Female breast398

(a) (b)

(c)

Fig. 13.3 Maneuvers for breast inspection. (a) Anatomical position. (b) Hands on

hips. (c) Arms crossed above the head.

PALPATION OF THE BREAST

399

Palpation of the breast

Before you start

Palpation of the breast should be performed with the patient lying supine

on the exam table. Examination of the breast is best performed with the

hand on the side to be examined placed behind her head ( Fig. 13.4 ). A

maneuver for ﬂ attening a large breast is to have the patient roll onto her

contralateral hip, keeping the shoulders ﬂ at against the table.

1

Inform the patient that an adequate breast exam will take approximately

3 minutes per breast; taking this time will help in detecting breast masses.

Palpation

Ask the patient if there is any pain or tenderness, and examine that area

last. Also ask her to tell you if you cause any pain during the examination.

Begin the examination on the asymptomatic side; this allows you to

determine the texture of the normal breast ﬁ rst.

Ask the patient to point out any areas of tenderness; come to these last.

Breast

Palpation is performed by keeping the hand ﬂ at, using the ﬁ nger pads and

applying three levels of pressure as the breast tissue is palpated in a circu-

lar pattern against the underlying chest wall.

0 Most breasts will feel lumpy if pinched.

You should proceed in a systematic way to ensure that the whole breast

is examined. There are two regularly used methods (see Fig. 13.5 ); the

authors favor the vertical strip method:

• Start below the areola and work outward in a circumferential pattern,

ensuring that all quadrants have been examined.

• Examine breast systematically from the mid-axillary line, palpating up

and down between the clavicle and the bra line toward the sternum.

2 Do not forget to examine the axillary tail of Spence stretching from the

upper-outer quadrant to the axilla.

Lumps

• If you feel a lump, describe it according to the method on b p. 88,

noting especially the position, color, shape, size, surface, nature of the

surrounding skin, tenderness, consistency, temperature, and mobility.

• Next ascertain its relation to the overlying skin and underlying muscle.

• You must decide whether you are feeling a lump or a lumpy area.

Skin tethering

A lump may be described as tethered to the skin if it can be moved

independently of the skin for a limited distance but pulls on the skin if

moved further.

Tethering implies that an underlying lesion has inﬁ

ltrated Cooper’s liga-

ments, which pass from the skin through the subcutaneous fat.

Tethering may involve the skin itself with cancers or abscesses .

1

Barton MB, Russell H, Fletcher SW (1999). Does this patient have breast cancer? The screening

clinical breast examination: should it be done? How?, JAMA 282(13):1270–1280.

CHAPTER 13 Female breast400

On inspection at rest, there may be puckering of the skin surface (as if

being pulled from within) or there may be no visible abnormality.

To demonstrate tethering:

• Move the lump from side to side and look for skin dimpling at the

extremes of movement.

• Ask the patient to lean forward while sitting.

• Ask the patient to raise her arms above her head as in Fig. 13.3 .

Skin ﬁ

xation

This is caused by direct, continuous inﬁ ltration of the skin by the under-

lying disease. The lump and the skin overlying it cannot be moved inde-

pendently. It is on a continuum with skin tethering. This may be associated

with some changes of skin texture.

Relation of a lump to muscle

The lump may be tethered or ﬁ xed to the underlying muscle (e.g., pec-

toralis major).

2 Lumps attached to the underlying muscle can be moved to some degree

if the muscle is relaxed but are less mobile if the muscle is tensed.

• Ask the patient to rest her hand on her hip with the arm relaxed.

• Hold the lump between your thumb and foreﬁ

ngers and estimate its

mobility by moving it in two planes at right angles to each other (e.g.,

up/down and left/right).

• Ask the patient to press her hand against her hip, causing contraction

of pectoralis major. Repeat the mobility exercise.

Immobile lumps

If a lump is immobile in all situations, it may have spread to involve the

bony chest wall (e.g., in the upper half of the breast or axilla).

Nipple

If the patient complains of nipple discharge, ask her to gently squeeze and

express any discharge. Note the color, presence of blood, and odor.

Milky, serous or green-brown discharges are almost always benign. A

bloody discharge may indicate neoplasia (e.g., papilloma or cancer).

Although the time typically spent palpating the breast is considered an

excellent time to instruct the patient in self-examination, recent recom-

mendations have not supported the usefulness of teaching it. In any case,

women should be counseled on breast awareness. Providers should con-

tinue to look for further information on this.

PALPATION OF THE BREAST

401

Fig. 13.4 Correct position of the patient for examination of the breast.

(a) (b)

Fig. 13.5 Two methods for systematic palpation of the breast. (a) Work

circumferentially from the areola. (b) Examine each half at a time, working from

bottom to top.

CHAPTER 13 Female breast402

Examining beyond the breast

Lymph nodes

The technique is described in detail on b p. 58.

Support the patient’s arm. For example, when examining the right axilla,

abduct the patient’s right arm gently and support it at the wrist with your

right hand while examining the axilla with your left hand.

Examine the main sets of axillary nodes ( Fig. 13.6 ):

• Central

• Lateral

• Medial (pectoral)

• Infraclavicular

• Supraclavicular ( Fig. 13.7 )

• Apical

If you feel any lymph nodes, consider site, size, number, consistency,

tenderness, ﬁ

xation, and overlying skin changes.

Remember to also palpate for lymph nodes in the lower deep cervical

lymph chain at the same time as the supraclavicular nodes.

The rest of the body

If cancer is suspected, perform a full general examination, keeping in mind

the common sites of metastasis of breast cancer. Examine especially the

lungs, liver, skin, skeleton, and central nervous system.

B

E

D

C

A

A = Lateral

B = Pectoral

C = Central

D = Subscapular

E = Infraclavicula

r

Fig. 13.6 Axillary lymph nodes.

EXAMINING BEYOND THE BREAST

403

E

H

C

G

F

D

A

B

A = Supraclavicular

B = Posterior triangle

C = Jugular chain

D = Preauricular

E = Postauricular

F = Submandibular

G = Submental

H = Occipital

Fig. 13.7 Cervical and supraclavicular lymph nodes.

CHAPTER 13 Female breast404

Important presentations

Fibroadenoma

This is a benign neoplasm of the breast that is composed of both ﬁ brous

and glandular tissue. It is usually found in young women <30 years old.

It presents as a painless, solid, mobile, well-circumscribed, rounded

breast mass with a smooth surface and rubbery consistency.

They may be multiple and bilateral with no axillary lymphadenopathy.

Large ﬁ broadenomas may be found in teenagers.

Fibrocystic disease

This is another common benign breast condition consisting of ﬁ brous

(rubbery) and cystic changes in the breast.

It usually presents with pain or tenderness that varies with the menstrual

cycle. Cysts and ﬁ brous nodular fullness can be found on examination. A

solitary cyst is usually smooth, spherical, and tense. It is rarely possible to

elicit ﬂ uctuation or to transilluminate. The axillary lymph nodes should

not be palpable.

Fat necrosis

This can occur after trauma. The physical signs can mimic cancer (e.g., a

ﬁ rm, hard lump with skin tethering).

Abscesses

These occur mainly during childbearing years and are often associated

with trauma to the nipple during breast-feeding.

They present with a painful, spherical lump with surrounding edema.

Breast often shows additional signs of inﬂ ammation (hot, red). The patient

may have constitutional symptoms, including malaise, night sweats, hot

ﬂ ushes, and rigors.

Most recurrent or chronic breast abscesses occur in association with

duct ectasia or periductal mastitis. The associated periductal ﬁ brosis can

often lead to nipple retraction.

Abnormal nipple and areola

Diseases of the nipple are important because they must be differentiated

from malignancy and they cause concern to patients.

Unilateral retraction or distortion of a nipple is a common sign of breast

carcinoma, as is blood-stained nipple discharge. The latter suggests an

intraductal carcinoma or benign papilloma.

A unilateral red, crusted, and scaling areola suggests an underlying carci-

noma (Paget’s disease of the breast) or, more commonly, eczema. Ask the

patient if she has eczema at other sites and examine appropriately.

Breast cancer

After non-melanoma skin cancers, breast cancer is the most common

form of cancer affecting women in the United States. It is second to lung

IMPORTANT PRESENTATIONS

405

cancer as a cause of cancer mortality.* It is rare under the age of 35, with

the incidence steadily increasing per decade.

There are a number of risk factors (see b Box 13.4 , p. 396). Several

on-line risk calculators are available for use by patients and clinicians to

estimate breast cancer risk (www.nci.nih.gov; Gail model).

There are two main types, which may be invasive or in situ:

• Ductal

• Lobular

In situ cancer is usually not palpable and diagnosed on mammography or

biopsy. Clinicians should remember that mammography does not detect

all breast cancers. It is estimated that 4–10% of cancers will be detected

on clinician exam alone.

There are a number of prognostic factors in breast cancer, mostly

related to the histological presentation of the tumor.

Presenting symptoms

The presenting symptoms may be related to the primary lesion. For

example:

• Palpable mass

• Pain (1/100 cancers present with mastalgia only)

• Nipple discharge, retraction, or rash

• Dimpling of the breast tissue

• Local edema

The presenting symptom may be related to the effects of secondary

spread. For example:

• Arm swelling (lymphatic or venous obstruction)

• Backache (skeletal inﬁ ltration)

• Malaise

• Loss of weight

• Dyspnea

• Cough

• Nodules in skin

• Jaundice

• Mental changes

• Seizures

• Symptoms of hypercalcemia (e.g., thirst)

*

http://www.cdc.gov/cancer/breast/statistics/

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407

Female reproductive

system

Applied anatomy 408

Applied physiology 411

History-taking in gynecology 413

Abnormal bleeding in gynecology 415

Other symptoms in gynecology 419

Outline gynecological examination 423

Pelvic examination 424

Taking a cervical smear 430

History-taking in obstetrics 433

Presenting symptoms in obstetrics 437

Outline obstetric examination 441

Abdominal examination 442

The elderly patient 447

Chapter 14

CHAPTER 14 Female reproductive system408

Applied anatomy

Pelvis

The bony pelvis is composed of the two pelvic bones with the sacrum and

coccyx posteriorly. The pelvic brim divides the “false pelvis” above (part

of the abdominal cavity) and the “true pelvis” below.

• Pelvic inlet: also known as the pelvic brim. It is formed by the sacral

promontory posteriorly, the iliopectineal lines laterally, and the

symphysis pubis anteriorly.

• Pelvic outlet: formed by the coccyx posteriorly, ischial tuberosities

laterally, and pubic arch anteriorly. The pelvic outlet has three wide

notches. The sciatic notches are divided into the greater and lesser

sciatic foramina by the sacrotuberous and sacrospinous ligaments,

which can be considered part of the perimeter of the outlet clinically.

• The pelvic cavity: lies between the inlet and the outlet. It has a deep

posterior wall and a shallow anterior wall giving a curved shape.

The contents of the pelvic cavity

The pelvic cavity contains the rectum, sigmoid colon, coils of the ileum,

ureters, bladder, female reproductive organs, fascia, and peritoneum.

Female internal genital organs

Vagina

The vagina is a thin-walled distensible, ﬁ bromuscular tube that extends up

and backward from the vestibule of the vulva to the cervix. It is ~8 cm long

and lies posterior to the bladder and anterior to the rectum.

The vagina serves as an eliminatory passage for menstrual ﬂ ow, forms

part of the birth canal, and receives the penis during sexual intercourse.

Fornix

This is the vaginal recess around the cervix and is divided into anterior,

posterior, and lateral regions, which, clinically, provide access points for

examining the pelvic organs.

Uterus

The uterus is a thick-walled, hollow, pear-shaped muscular organ consist-

ing of the cervix, body, and fundus. In the nulliparous female, it is 7–8 cm

long, ~5 cm wide, and ~2.5 cm deep. The uterus is covered with perito-

neum that forms an anterior uterovesical fold, a fold between the uterus

and rectum termed the pouch of Douglas , and broad ligaments laterally.

The uterus receives, retains, and nourishes the fertilized ovum.

Uterine orientation

In most females, the uterus lies in an anteverted and anteﬂ exed position.

• Anteversion: the long axis of the uterus is angled forward.

• Retroversion: The fundus and body are angled backward and therefore

lie in the pouch of Douglas. This occurs in about 15% of the female

population. A full bladder may result in retroversion clinically.

APPLIED ANATOMY

409

• Anteﬂ exion: The long axis of the body of the uterus is angled forward

on the long axis of the cervix.

• Retroﬂ

exion:

The body of the uterus is angled backward on the cervix.

Fallopian tubes

The fallopian, or uterine, tubes are paired tubular structures 710 cm long.

The fallopian tubes extend laterally from the cornua of the uterine body,

in the upper border of the broad ligament, and open into the peritoneal

cavity near the ovaries. The fallopian tube is divided into four parts:

• Infundibulum: distal, funnel-shaped portion with ﬁ nger-like

ﬁ

mbriae

• Ampulla: widest and longest part of tube outside the uterus

• Isthmus: thick-walled with a narrow lumen and, therefore, least

distensible part. The isthmus enters the horns of the uterine body.

• Intramural: that part which pierces the uterine wall

The main functions of the uterine tube are to receive the ovum from

the ovary, provide a site where fertilization can take place (usually in the

ampulla), and transport the ovum from the ampulla to the uterus. The

tube also provides nourishment for the fertilized ovum.

Ovaries

The ovaries are whitish-gray, almond-shaped organs measuring 74 cm x 2 cm

that are responsible for production of the female germ cells, ova, and female

sex hormones, estrogen and progesterone.

They are suspended on the posterior layer of the broad ligament by

a peritoneal extension (mesovarium) and supported by the suspensory

ligament of the ovary (a lateral extension of the broad ligament and meso-

varium) and the round ligament, which stretches from the lateral wall of

the uterus to the medial aspect of the ovary.

Perineum

The perineum lies inferior to the pelvic inlet and is separated from the

pelvic cavity by the pelvic diaphragm.

Seen from below with the thighs abducted, it is a diamond-shaped area

bounded anteriorly by the pubic symphysis, posteriorly by the tip of the

coccyx, and laterally by the ischial tuberosities.

The perineum is artiﬁ cially divided into the anterior urogenital triangle,

containing the external genitalia in females, and an anal triangle, containing

the anus and ischiorectal fossae.

Female external genital organs

These are collectively known as the vulva . It consists of the following:

• Labia majora: a pair of fat-ﬁ lled folds of skin extending on either side

of the vaginal vestibule from the mons towards the anus.

• Labia minora: a pair of ﬂ

at folds containing a core of spongy

connective tissue with a rich vascular supply. Lie medial to the labia

majora.

• Vestibule of the vagina: between the labia minora, contains the

urethral meatus and vaginal oriﬁ

ce. Outlet for mucous secretions from

the greater and lesser vestibular glands.

CHAPTER 14 Female reproductive system410

• Clitoris: short, erectile organ; the female homologue of the male penis.

Like the penis, a crus arises from each ischiopubic ramus and join in

the midline forming the ‘body’ capped by the sensitive ‘glans’.

• Bulbs of vestibule: 2 masses of elongated erectile tissue, ~3 cm long,

lying along the sides of the vaginal oriﬁ ce.

• Bulbs of vestibule: Greater and lesser vestibular glands.

APPLIED PHYSIOLOGY

411

Applied physiology

Menstrual cycle

Menstruation is the shedding of the functional superﬁ cial 2/3 of the

endometrium after sex hormone withdrawal. This process, consisting

of three phases, is typically repeated ~300–400 times during a woman’s

life. Coordination of the menstrual cycle depends on a complex inter-

play between the hypothalamus, pituitary gland, ovaries, and uterine

endometrium.

Cyclical changes in the endometrium prepare it for implantation in the

event of fertilization and menstruation in the absence of fertilization. It

should be noted that several other tissues are sensitive to these hormones

and undergo cyclical change (e.g., the breasts and the lower part of the

urinary tract).

The endometrial cycle can de divided into three phases.

Phases of the menstrual cycle

The ﬁ rst day of the menses is considered day 1 of the menstrual cycle.

Proliferative or follicular phase

This begins at the end of the menstrual phase (usually day 4) and ends at

ovulation (days 13–14). During this phase, the endometrium thickens and

ovarian follicles mature.

The hypothalamus is the initiator of the follicular phase. Gonadotrophin-

releasing hormone (GnRH) is released from the hypothalamus in a pulsa-

tile fashion to the pituitary portal system surrounding the anterior pituitary

gland. GnRH causes release of follicle-stimulating hormone (FSH). FSH is

secreted into the general circulation and interacts with the granulosa cells

surrounding the dividing oocytes.

FSH enhances the development of 15–20 follicles each month and

interacts with granulosa cells to enhance aromatization of androgens into

estrogen and estradiol.

Only one follicle with the largest reservoir of estrogen can withstand

the declining FSH environment, while the remaining follicles undergo

atresia at the end of this phase.

Follicular estrogen synthesis is essential for uterine priming but is also

part of the positive feedback that induces a dramatic preovulatory lutein-

izing hormone (LH) surge and subsequent ovulation.

Luteal or secretory phase

The luteal phase starts at ovulation and lasts through day 28 of the men-

strual cycle.

The major effects of the LH surge are the conversion of granulosa

cells from predominantly androgen-converting cells to predominantly

progesterone-synthesizing cells. High progesterone levels exert negative

feedback on GnRH, which in turn d FSH/LH secretion.

At the beginning of the luteal phase, progesterone induces the endome-

trial glands to secrete glycogens, mucus, and other substances. These

glands become tortuous and have large lumina due to i secretory activity.

Spiral arterioles extend into the superﬁ cial layer of the endometrium.

CHAPTER 14 Female reproductive system412

In the absence of fertilization by day 23 of the menstrual cycle, the

superﬁ cial endometrium begins to degenerate, and consequently ovar-

ian hormone levels d. As estrogen and progesterone levels fall, the

endometrium undergoes involution.

If the corpus luteum is not sustained by human chorionic gonado-

trophin (hCG) hormone from the developing placenta, menstruation

occurs 14 days after ovulation. If conception occurs, placental hCG main-

tains luteal function until placental production of progesterone is well

established.

Menstrual phase

In this phase, there is a gradual withdrawal of ovarian sex steroids, which

causes slight shrinking of the endometrium, thus the blood ﬂ ow of spi-

ral vessels is reduced. This, together with spiral arteriolar spasms, leads

to distal endometrial ischemia and stasis. Extravasation of blood and

endometrial tissue breakdown lead to the onset of menstruation.

The menstrual phase begins as the spiral arteries rupture, releasing

blood into the uterus and the apoptosing endometrium is sloughed off.

During this period, the functionalis layer of the endometrium is

complete ly shed. Arteriolar and venous blood, remnants of endometrial

stroma and glands, leukocytes, and red blood cells are all present in the

menstrual ﬂ ow. Shedding usually lasts ~4–7 days.

HISTORY-TAKING IN GYNECOLOGY

413

History-taking in gynecology

It is important to remember that many females can be embarrassed by

having to discuss their gynecological problems, so it is vital to appear con-

ﬁ dent, remaining open to questions or concerns, and be nonjudgmental.

Although there are parts particular to this history, most of it is the same

as the basic outline described in b Chapter 2. We suggest that readers

review that chapter before going on.

Patient proﬁ le

This includes the patient’s name, age, date of birth, and occupation.

Chief complaint

Ask the patient to tell you in her own words what she perceives as being

the main symptoms. Document each in order of severity.

History of presenting illness

More detailed questioning will depend on the presenting complaint (see

following pages). As described on b p. 33, ascertain the following:

• Exact nature of the symptom

• Onset

•

When and how it began (e.g., suddenly, gradually—over how long?)

•

If long-standing, why is the patient seeking help now?

• Periodicity and frequency

•

Is the symptom constant or intermittent?

•

If intermittent, how long does it last each time?

•

What is the exact manner in which it comes and goes?

•

2 How does it relate to the menstrual cycle?

• Change over time

• Exacerbating and relieving factors

• Associated symptoms

• Degree of functional disability caused

Menstrual history

• Age of menarche (ﬁ rst menstrual period)

•

Normally at about 12 years, but can be as early as 9 or as late as 16

• Date of last menstrual period (LMP)

• Duration and regularity of periods (cycle)

•

Normal menstruation lasts 4–7 days.

•

The average length of the menstrual cycle is 28 days (i.e., the time

between ﬁ rst day of one period and the ﬁ rst day of the following

period), but it can vary between 21 and 42 days in normal women.

• Menstrual ﬂ

ow: whether light, normal, or heavy (see

b p. 415)

• Menstrual pain: whether it occurs prior to or at the start of bleeding

• Irregular bleeding

•

E.g., intermenstrual blood loss, postcoital bleeding

• Associated symptoms

•

Bowel or bladder dysfunction, pain

• Hormonal contraception or hormone therapy (HT)

• Age at menopause (if this has occurred)

CHAPTER 14 Female reproductive system414

Past gynecological history

Record all details of the following:

• Previous cervical smears, including date of last Pap smear, any

abnormal smear results, and treatments received

• Previous history and results of human papillomavirus (HPV) testing

• Previous history of HPV vaccination

• Previous gynecological problems and treatments, including surgery and

pelvic inﬂ

ammatory disease (PID)

Contraception

It is essential to ask women of reproductive age who are sexually active

with men about contraception, including the methods used, duration of

use and acceptance, current method, and future plans.

Past obstetric history

• Gravidity and parity: see b p. 434 for a full explanation.

Document the speciﬁ cs of each pregnancy:

• Current age of the child and age of the mother when pregnant

• Birth weight

• Complications of pregnancy, labor, and puerperium

• Miscarriages and terminations. Note gestation time and complications.

Ask if Rhogam was given if Rh negative.

Past medical history

This is as described in b Chapter 2. Pay particular attention to any history

of chronic lung or heart disease, and note all previous surgical procedures.

Drug history

This is as described in b Chapter 2. Ask about all medication and drugs

taken (prescribed, over the counter, herbs, vitamins, and illicit drugs).

Record dosage and frequency, as well as any known drug allergies.

2 Make particular note to ask about use of the oral contraceptive pill

(OCP), patch, implant, vaginal ring, or hormone-releasing intrauterine

device (IUD) and of HT if not done so already.

Family history

Note especially any history of genital tract cancer, breast cancer, or

diabetes.

Smoking and alcohol

As always, document this fully, as described on b p. 37.

Social history

Take a standard SH, including living conditions and marital status.

This is also an extra chance to explore the impact of the presenting

problem on the patient’s life, in terms of her social life, employment, home

life, and sexual activity (see Sexual History, b p. 378). This discussion may

lead to issues far beyond the presenting complaint.

It is important to obtain a history regarding sexual abuse (rape, incest,

childhood molestation). Women who have a history of sexual abuse may

have ﬂ ashbacks during an exam or may be unable to tolerate a full exam.

ABNORMAL BLEEDING IN GYNECOLOGY

415

Abnormal bleeding in gynecology

Menorrhagia

This is deﬁ ned as >80 mL of menstrual blood loss per period (nor-

mal = 20–60 mL) and may be caused by a variety of local, systemic, or

iatrogenic factors. Menorrhagia is hard to measure, but periods are consid-

ered heavy if they lead to frequent changes (every 1–2 hours) of sanitary

products and there are clots >1 inch in diameter. Causes are listed in

Box 14.1

In the absence of structural uterine disease or other pathology, menor-

rhagia can also be described as dysfunctional uterine bleeding (DUB). This is

often found in adolescence or in the perimenopausal period.

In addition to the standard questions for any symptom, ask about the

following:

• Number of sanitary pads or tampons used per day and the strength

(absorbency) of those products

• Bleeding through to clothes or onto the bedding at night (ﬂ ooding)

• The need to use two pads at once

• The need to wear double protection (i.e., pad and tampon together)

• Any clots in the menstrual ﬂ

ow (compare to the size of coins)

• Interference with normal activities

2 Remember to ask about symptoms of iron-deﬁ ciency anemia, such as

lethargy, breathlessness, and dizziness.

Dysmenorrhea

This is pain associated with menstruation and is thought to be caused

by i levels of endometrial prostaglandins during the luteal and menstrual

phases of the cycle, resulting in uterine contractions ( Box 14.2 ). The pain

is typically cramping, localized to the lower abdomen and pelvic regions

and radiating to the thighs and back.

Dysmenorrhea may be primary or secondary:

• Primary: occurring from menarche

Box 14.1 Some causes of menorrhagia

• Hypothyroidism

• IUD

• Fibroids

• Endometriosis

• Polyps—cervix, uterus

• Uterine cancer

• Infection (STIs)

• Previous sterilization

• Warfarin therapy

• Aspirin

• NSAIDs

• Clotting disorders (e.g., von-Willebrand’s disease)

CHAPTER 14 Female reproductive system416

• Secondary: occurring in females who previously had normal periods

(often caused by pelvic pathology)

When taking a history of dysmenorrhea, take a full pain history as on

b p. 33 and detailed menstrual history (b p. 413), and ask about the rela-

tionship of the pain to the menstrual cycle. Remember to ask about the

functional consequences of the pain—how does it interfere with normal

activities?

Intermenstrual bleeding (IMB)

Intermenstrual bleeding is uterine bleeding that occurs between the men-

strual periods. Causes are listed in Box 14.3

As for all of these symptoms, a full standard battery of questions should

be asked (b p. 413), as full menstrual history (b p. 413), past medical

and gynecological histories (b p. 414), and sexual history (b p. 414).

Ask also about association of the bleeding with hormonal therapy, con-

traceptive use, and previous cervical smears.

Postcoital bleeding

This is vaginal bleeding precipitated by sexual intercourse. It can be caused

by similar conditions to those for intermenstrual bleeding ( Box 14.4 ). Take

a full and detailed history, as for IMB.

Amenorrhea

This is the absence of periods and may be primary or secondary.

• Primary: failure to menstruate by 16 years of age in the presence of

normal secondary sexual development or failure to menstruate by

14 years in the absence of secondary sexual characteristics.

Box 14.2 Some causes of secondary dysmenorrhea

• Pelvic inﬂ ammatory disease

• Endometriosis

• Uterine adenomyosis

• Fibroids

• Endometrial polyps

• Premenstrual syndrome

• Cessation of OCP

Box 14.3 Some causes of intermenstrual bleeding

• Obstetric: pregnancy, ectopic pregnancy, gestational trophoblastic

disease

• Gynecological: vaginal malignancy, vaginitis, cervical cancer,

adenomyosis, ﬁ

broids, ovarian cancer

• Iatrogenic: anticoagulants, corticosteroids, antipsychotics,tamoxifen,

selective serotinin reuptake inhibitors (SSRIs), rifampicin, antiepileptic

drugs (AEDs)

ABNORMAL BLEEDING IN GYNECOLOGY

417

• Secondary: normal menarche, then cessation of menstruation with no

periods for at least 6 months.

2 Amenorrhea is a normal feature in prepubertal girls, pregnancy, during

lactation, postmenopausal females, and in some women using hormonal

contraception (see Box 14.5 ).

History-taking

A full and detailed history should be taken as described on b p. 33 and in

b Chapter 2. Ask especially about the following:

• Childhood growth and development

• If secondary amenorrhea:

•

Age of menarche

•

Cycle days

•

Day and date of LMP

•

Presence or absence of breast soreness

•

Mood change immediately before menses

• Chronic illnesses

• Previous surgery (including cervical surgery, which can cause stenosis,

and, more obviously, oophorectomy and hysterectomy)

• Prescribed medications known to cause amenorrhea, such

as phenothiazines and metoclopramide (they produce either

hyperprolactinemia or ovarian failure)

• Illicit or recreational drugs

• Sexual history

• Social history, including any emotional stress at school, work, or home,

and exercise and diet—include here any weight gain or weight loss.

Box 14.4 Some causes of postcoital bleeding

These are similar to those for intermenstrual bleeding, as well as vaginal

infection with Chlamydia , gonorrhea, trichomoniasis, or yeast. Cervicitis

can also result in bleeding.

Box 14.5 Some causes of amenorrhea

• Hypothalamic: idiopathic, weight loss, intense exercise

• Hypogonadism from hypothalamic or pituitary damage: tumors,

craniopharyngiomas, cranial irradiation, head injuries

• Pituitary: hyperprolactinemia, hypopituitarism

• Delayed puberty: constitutional delay

• Systemic: chronic illness, weight loss, endocrine disorders (e.g.,

Cushing’s syndrome, thyroid disorders)

• Uterine: mullerian agenesis

• Ovarian: PCOS, premature ovarian failure (e.g., Turner’s syndrome,

autoimmune disease, surgery, chemotherapy, pelvic irradiation,

infection)

• Psychological: emotional stress at school, home, or work

CHAPTER 14 Female reproductive system418

• Systems review: include vasomotor symptoms, hot ﬂ ashes, virilizing

changes (e.g., i body hair, greasy skin), galactorrhea, headaches, visual

ﬁ eld disturbance, palpitations, nervousness, hearing loss

Postmenopausal bleeding

This is vaginal bleeding occurring >6 months after menopause. It requires

reassurance and prompt investigation, as it could indicate the presence of

malignancy (see Box 14.6 ). In addition to the points outlined for amenor-

rhea, ask about the following:

• Local symptoms of estrogen deﬁ

ciency, such as vaginal dryness,

soreness, and superﬁ

cial dyspareunia (b p. 419)

• Itching (pruritus vulvae—more likely in non-neoplastic disorders)

• Presence of lumps or swellings at the vulva

Cervical or endometrial malignancy

This is often present with profuse or continuous vaginal bleeding or with

a bloodstained, malodorous discharge.

Box 14.6 Some causes of postmenopausal bleeding

• Cervical carcinoma

• Uterine sarcoma

• Vaginal carcinoma

• Endometrial hyperplasia, carcinoma, or polyps

• Cervical polyps

• Trauma

• Hormone therapy (HT)

• Bleeding disorder

• Vaginal atrophy

• Sexually transmitted infections

OTHER SYMPTOMS IN GYNECOLOGY

419

Other symptoms in gynecology

Pelvic pain and dyspareunia

As with any type of pain, pelvic pain may be acute or chronic (see also

Box 14.7 ). Chronic pelvic pain is often associated with dyspareunia.

Dyspareunia

This is painful sexual intercourse and may be experienced superﬁ cially at

the area of the vulva and introitus on penetration or deep within the pelvis

(see Box 14.8 for causes). Dyspareunia can lead to failure to reach orgasm,

avoidance of sexual activity, and relationship problems.

When taking a history of pelvic pain or dyspareunia, you should obtain a

detailed history as for any type of pain (b p. 34) including site, radiation,

character, severity, mode and rate of onset, duration, frequency, exacer-

bating factors, relieving factors, and associated symptoms.

You also need to establish the relationship of the pain to the menstrual

cycle. Ask about the following:

• Date of LMP

• Cervical (Pap) smears

• Intermenstrual or postcoital bleeding

• Previous gynecological procedures (e.g., IUD, hysteroscopy)

• Previous PID or genitourinary infections

• Previous gynecological surgery (adhesion formation?)

• Vulvovaginal discharge

Box 14.7 Gynecological vs. gastrointestinal pain

Distinguishing between pain of gynecological and gastrointestinal origin

is often difﬁ cult. This is because the uterus, cervix, and adnexae share

the same visceral innervation as the lower ileum, sigmoid colon, and

rectum. Be careful in your history to rule out a gastrointestinal problem,

and keep an open mind.

Box 14.8 Some causes of dyspareunia

• Scars from episiotomy

• Vaginal atrophy

• Vulvitis

• Vulvar vestibulitis

• PID

• Ovarian cysts

• Endometriosis

• Varicose veins in pelvis

• Ectopic pregnancy

• Infections (STIs)

• Bladder or urinary tract disorder

• Cancer in the reproductive organs or pelvic region

CHAPTER 14 Female reproductive system420

• Bowel habit, nausea, and vomiting (b p. 208)

• A detailed sexual history (b p. 378) should include contraceptive use

and the degree of impact the symptoms have on the patient’s normal

life and psychological health.

Vaginal discharge

Vaginal discharge is a common complaint during the childbearing years. In

addition to the standard questions (b p. 413), ask about the following:

• Color, volume, odor, and presence of blood

• Irritation

• Hygiene habits including douching

• Which OTC remedies have been tried

2 Don’t forget to ask about diabetes and obtain a full drug history,

including recent antibiotic use; both may precipitate candidal infection.

• Obtain a full sexual history (b p. 378). A full gynecological history

should include history of cervical (Pap) smear testing, use of ring

pessaries, and recent history of surgery (i risk of vesicovaginal

ﬁ stulae).

2 Lower abdominal pain, backache, and dyspareunia suggest PID.

2 Weight loss and anorexia may indicate underlying malignancy.

Physiological vaginal discharge

Physiological discharge is usually scanty, mucoid, and odorless. It occurs

with the changing estrogen and progesterone levels during the menstrual

cycle (clear discharge i in quantity mid-cycle, with subsequent thickening

as a physiological sign of ovulation) and pregnancy.

It may arise from vestibular gland secretions, vaginal transudate, cervical

mucus, and residual menstrual ﬂ uid.

Pathological vaginal discharge

This usually represents infection (trichomonal or candidal vaginitis) and

may be associated with pruritus or burning of the vulval area.

• Candida albicans: discharge is typically thick and causes itching

• Bacterial vaginitis: discharge is gray and watery with a ﬁ

shy smell. It is

seen especially after intercourse.

• Trichomonas vaginalis: discharge is typically profuse, opaque, cream-

colored, and frothy. It also has a characteristic ﬁ

shy smell. This may also

be accompanied by urinary symptoms, such as dysuria and frequency.

Vulval symptoms

The main symptom to be aware of is itching or irritation of the vulva (pruri-

tis vulvae). It can be debilitating and socially embarrassing. Embarrassment

often delays the seeking of advice.

Causes include infection, vulval dystrophy, neoplasia, and other derma-

tological conditions. Ask especially about the following:

• Nature of onset, exacerbating and relieving factors

• Abnormal vaginal discharge

• History of cervical intraepithelial neoplasia ([CIN] thought to share a

common etiology with vulval intraepithelial neoplasia [VIN])

• Sexual history

OTHER SYMPTOMS IN GYNECOLOGY

421

• Dermatological conditions such as psoriasis and eczema

• Symptoms suggestive of renal or liver problems (b p. 210)

• Diabetes

• Use of douching and feminine hygiene products

Urinary incontinence

This is an objectively demonstrable involuntary loss of urine that can be

both a social and hygienic problem.

The two most common causes of urinary incontinence in females are

stress incontinence (SI) and detrusor overactivity (DO). Other less commonly

encountered causes include mixed SI and DO, sensory urgency, chronic

voiding problems, and ﬁ stulae.

When taking a history of urinary incontinence, ascertain under what cir-

cumstances the patient experiences symptom. See also b p. 435. Remember

to ask about the functional consequences on the patient’s daily life.

Stress incontinence

Patients notice small amounts of urinary leakage with a cough, sneeze, or

exercise. One-third may also admit to symptoms of DO.

Ask about the following:

• Number of children (i risk with i parity)

• Genital prolapse

• Previous pelvic ﬂ oor

surgery

Detruser overactivity

With DO there is urge incontinence, urgency, frequency, and nocturia

(see b p. 447). Ask about the following:

• History of nocturnal enuresis

• Previous neurological problems

• Previous incontinence surgery

• Incontinence during sexual intercourse

• Drug history (see note under The Elderly Patient, b p. 447)

Overﬂ ow

incontinence

Voiding disorders can result in chronic retention, leading to overﬂ ow

incontinence and i predisposition to infection. The patient may complain

of hesitancy, straining, poor ﬂ ow, and incomplete emptying in addition to

urgency and frequency.

Fistulae

Suspect these if incontinence is continuous during the day and night.

Genital prolapse

Genital prolapse is descent of the pelvic organs through the pelvic ﬂ oor

into the vaginal canal (possible causes are listed in Box 14.9 ). In the female

genital tract, the type of prolapse is named according to the pelvic organ

involved. Some examples include the following:

• Uterine: uterus

• Cystocele: bladder

• Vaginal vault prolapse: apex of vagina after hysterectomy

• Enterocele: small bowel

• Rectocele: rectum

CHAPTER 14 Female reproductive system422

Mild degrees of genital prolapse are often asymptomatic. More exten-

sive prolapse may cause vaginal pressure or pain, introital bulging, a feeling

of something coming down, and impaired sexual function.

Uterine descent often gives symptoms of backache, especially in older

patients.

There might be associated symptoms of incomplete bowel emptying

(rectocele) or urinary symptoms such as frequency or incomplete empty-

ing (cystocele or cystourethrocele).

Box 14.9 Some causes of genital prolapse

• Estrogen-deﬁ ciency states: advancing age and menopause (atrophy

and weakness of the pelvic support structures)

• Childbirth: prolonged labor, instrumental delivery, fetal macrosomia,

i parity

• Genetic or congenital factors: e.g., spina biﬁ da

• Chronic raised intra-abdominal pressure: e.g., chronic cough,

constipation

Box 14.10 Some other common vulval conditions

• Dermatitis: atopic, seborrheic, irritant, allergic, steroid induced (itch,

burning, erythema, scale, ﬁ ssures, licheniﬁ cation)

• Vulvovaginal candidiasis: itch, burning, erythema, vaginal discharge

• Lichen sclerosus: itch, burning, dyspareunia, white plaques, atrophic

wrinkled surface

• Psoriasis: remember to look for other areas of psoriasis; scalp, natal

cleft, nails

• Vulval intraepithelial neoplasia: itch, burning, multifocal plaques

• Erosive vulvovaginitis: erosive lichen planus, pemphigoid, pemphigus

vulgaris, ﬁ

xed drug eruption (chronic painful erosion and ulcers with

superﬁ cial

bleeding)

• Atrophic vaginitis: secondary to estrogen deﬁ

ciency (thin, pale, dry

vaginal epithelium; superﬁ

cial dyspareunia, minor vaginal bleeding,

pain)

OUTLINE GYNECOLOGICAL EXAMINATION

423

Outline gynecological examination

The gynecological examination should include a full abdominal examina-

tion before proceeding to pelvic, speculum, and bimanual examinations.

Explain to the patient that you would like to examine their genitalia and

reproductive organs, and reassure them that the procedure will be quick and

gentle. You should have a chaperone present, particularly if you are male.*

As always, ensure that the room is warm and well lit, preferably with a

moveable light source, and that you will not be disturbed.

The examination should follow an orderly routine. The authors’ sug-

gestion is shown in Box 14.11. It is standard practice to start with the

cardiovascular and respiratory systems—this not only gives a measure of

the general health of the patient but also establishes a physical rapport

before you examine more sensitive areas.

General inspection and other systems

Always begin with a general examination of the patient (as described in b

Chapter 3), including temperature, hydration, coloration, nutritional sta-

tus, lymph nodes, and blood pressure. Note especially the following:

• Distribution of facial and body hair, as hirsutism may be a presenting

symptom of various endocrine disorders

• Height and weight

• Examine the cardiovascular and respiratory systems in turn(see b

Chapters 7 and 8).

• Examine breasts in a systematic approach. Although the value of

teaching and performing breast self-exam is debated, patient education

on breast awareness during the exam is a good use of time and should

be done (see b Chapter 13).

Abdominal examination

A full abdominal examination should be performed (see b Chapter 9).

Look especially in the periumbilical region for scars from previous lapar-

oscopies and in the suprapubic region, where transverse incisions from

caesarean sections and most gynecological operations are found.

Box 14.11 Framework for gynecological examination

• General inspection

• Cardiorespiratory examination

• Breast examination

• Abdominal examination

• Pelvic examination

•

External genitalia—inspection

•

External genitalia—palpation

•

Speculum examination

•

Bimanual examination

* Attitudes regarding chaperones vary. Ofﬁ cial advice is that all providers should have a chaper-

one when performing an intimate examination and the chaperone should be the same sex as the

patient. In practice, male providers performing an examination on a female and females performing

an examination on a male should always have a chaperone present; the need for a chaperone in

other situations is judged at the time.

CHAPTER 14 Female reproductive system424

Pelvic examination

The patient should be allowed to undress in privacy and, if necessary, to

empty her bladder ﬁ rst.

Setup and positioning

Before starting the examination, explain to the patient what will be

involved. Keep the abdomen covered. Ensure good lighting, and always

wear disposable, latex-free gloves.

Ask the patient to lie on her back on an examination table with both

knees bent up; the head of the table can be raised for comfort. The but-

tocks should be at the edge of the main table surface, with the heels

placed in stirrups or the feet on the table extension. Her knees should fall

to the side when the exam starts. In many clinical settings, it is standard

to use stirrups to support the heels; however, keeping the feet on the

table extension during the exam has been found to increase comfort and

decrease the patient’s sense of vulnerability during the exam.

1

Examination of the external genitalia

• Uncover the mons to expose the external genitalia, making note of the

pattern of hair distribution.

• Separate the labia from above with the foreﬁ

nger and thumb of your

gloved left hand.

• Inspect the clitoris, urethral meatus, and vaginal opening.

• Look especially for any of the following:

•

Discharge

•

Redness

•

Ulceration

•

Atrophy

•

Old scars

• Ask the patient to cough or strain down and look at the vaginal walls

for any prolapse.

Palpation

• Palpate length of the labia majora between the index ﬁ

nger and thumb.

•

The tissue should feel pliant and ﬂ eshy.

• Palpate for Bartholin’s gland with the index ﬁ

nger of the right hand just

inside the introitus and thumb on the outer aspect of labium majora.

•

Bartholin’s glands are only palpable if the duct becomes obstructed,

resulting in a painless cystic mass or an acute Bartholin’s abscess.

The latter is seen as a hot, red, tender swelling in the posterolateral

labia majora.

Speculum examination

Speculum examination is carried out to see further inside the vagina and

to visualize the cervix. It also allows the examiner to take a cervical smear

or swabs.

1

Seehusen DA, Johnson DR, Earwood JS, et al. (2006). Improving women’s experience during

speculum examinations at routine gynaecological visits: randomized clinical trial. BMJ 333:171.

PELVIC EXAMINATION

425

There are different types of vaginal specula (see Fig. 14.1 ), but the most

common is the bivalve speculum (Peders on or Graves). Plastic, dispos-

able speculum are in use in many clinics. It is important that you familiarize

yourself with the operation of the speculum before examining a patient so

that you can concentrate on the ﬁ ndings (see Box 14.12 ).

Inserting the speculum

• Explain to the patient that you are about to insert the speculum into

the vagina, and provide reassurance that this should not be painful.

• Warm the speculum under running water.

• Test the temperature of the speculum on the inner thigh (warning the

patient before this is done).

• Using the left hand, open the lips of the labia minora to obtain a good

view of the introitus.

• Hold the speculum in the right hand with the main body of the

speculum in the palm (see Fig. 14.2 ) and the closed blades projecting

between index and middle ﬁ ngers.

• Gently insert the speculum into the vagina, held with your wrist turned

such that the blades are in line with the opening between the labia.

• The speculum should be angled down and backward due to the angle

of the vagina.

• Maintain a posterior angulation and rotate the speculum through 90*

to position handles downward.

Handle

Thumb screw

Upper blade

Lower blade

(a) (b)

Fig. 14.1 (a) Sim’s speculum—used mainly in examination of women with vaginal

prolapse. (b) Cusco’s speculum.

Box 14.12 A word about specula

Many departments and clinical areas now used plastic or disposable

specula. These do not have a thumb-screw but have a ratchet to open

and close the blades.

Take care to familiarize yourself with the operation of the speculum -

before starting the examination. The clicking noise can startle a patient,

so it is best to comment on this prior to insertion.

Plastic specula with a light source are very convenient and much easier

to use than struggling to properly position a large lamp.

CHAPTER 14 Female reproductive system426

• When it cannot be advanced further, maintain a downward pressure

and press on the thumb piece to hinge the blades open, exposing the

cervix and vaginal walls.

• Once the optimum position is achieved, tighten the thumbscrew or

engage the locking mechanism (plastic speculum).

Findings

Inspect the cervix, which is usually pink, smooth, and regular.

• Look for the external os (central opening), which is round in

nulliparous women and slit-shaped after childbirth.

• Look for cervical ectopy (eversions), which appear as strawberry-

red areas spreading circumferentially around the os and represent

extension of the endocervical epithelium onto the surface of the

cervix.

• Note the presence of an IUD string if you obtained that history.

• Identify any ulceration or growths that may suggest cancer.

• Cervicitis may give a mucopurulent discharge associated with a red,

inﬂ

amed cervix that bleeds on contact. Take swabs for culture.

Removing the speculum

2 This should be conducted with as much care as insertion. You should

still be examining the vaginal walls as the speculum is withdrawn.

• Undo the thumbscrew or lock and withdraw the speculum.

0 The blades should be held open until their ends are visible distal to

the cervix to avoid causing pain.

• Rotate the open blades in a counterclockwise direction to ensure that

the anterior and posterior walls of the vagina can be inspected.

Fig. 14.2 Hold speculum in the right hand such that the handles lie in the palm

and the blades project between the index and middle ﬁ ngers.

PELVIC EXAMINATION

427

• Near the introitus, allow the blades to close, taking care not to pinch

the labia or pubic hairs.

Bimanual examination

Digital examination helps identify the pelvic organs. Ideally, the bladder

should be emptied, if not already done so by this stage. In some cases,

and with patients over age 50, a rectal exam is done as the last step of the

bimanual exam.

Getting started

• Explain to the patient that you are about to perform an internal

examination of the vagina, uterus, tubes, and ovaries, and obtain verbal

consent.

• The patient should be positioned as described on b p. 424.

• Expose the introitus by separating the labia with the thumb and

foreﬁ

nger of the gloved left hand.

• Gently introduce the lubricated index and middle ﬁ

ngers of the gloved

right hand into the vagina.

•

Insert your ﬁ ngers with the palm facing laterally and then rotate 90*

so that the palm faces up.

•

The thumb should be abducted and the ring and little ﬁ nger ﬂ exed

into the palm (see Fig. 14.3 ).

Vagina, cervix, and fornices

• Feel walls of the vagina, which are slightly rugated, supple, and moist.

• Locate the cervix—usually pointing down in the upper vagina.

•

The normal cervix has a similar consistency to that of cartilage in the

tip of the nose.

• Assess the mobility of the cervix by moving it from side to side and

note any tenderness suggesting infection.

• Gently palpate the fornices on either side of the cervix.

Uterus

• Place your left hand on the lower anterior abdominal wall about 4 cm

above the symphysis pubis.

Fig. 14.3 Correct position of ﬁ ngers of the right hand for vaginal examination.

CHAPTER 14 Female reproductive system428

• Move the ﬁ ngers of your right internal hand to push the cervix upward

and simultaneously press the ﬁ ngertips of your left external hand

toward the internal ﬁ ngers ( Fig. 14.4 ).

•

You should be able to capture the uterus between your two hands.

Note the following features of the uterine body:

• Size: A uniformly enlarged uterus may represent a pregnancy, ﬁ broid,

or endometrial tumor.

• Shape: Multiple ﬁ

broids tend to give the uterus a lobulated feel.

• Position

• Surface characteristics

• Any tenderness

2 Remember that an anteverted uterus is easily palpable bimanually, but

a retroverted uterus may not be.

• Assess a retroverted uterus with the internal ﬁ

ngers positioned in the

posterior fornix or during the rectovaginal exam.

Ovaries and fallopian tubes

• Position the internal ﬁ

ngers in each lateral fornix (ﬁ

nger pulps facing

the anterior abdominal wall) and place your external ﬁ ngers over each

iliac fossa in turn.

• Press the external hand inward and down, and the internal ﬁ ngers

upward and laterally.

• Feel the adnexal structures (ovaries and fallopian tubes), assessing size,

shape, mobility, and tenderness.

•

Ovaries are ﬁ rm, ovoid and often palpable. If there is unilateral or

bilateral ovarian enlargement, consider benign cysts (smooth and

compressible) and malignant ovarian tumors.

•

Normal fallopian tubes are not palpable.

•

There may be marked tenderness of the lateral fornices and cervix

in acute infection of the fallopian tubes (salpingitis).

Rectal

• If a rectal exam is done and you want to test any fecal material for

blood, change gloves prior to the exam.

Fig. 14.4 Bimanual examination of the uterus.

PELVIC EXAMINATION

429

• The third ﬁ nger of the examining hand is inserted into the rectum,

with the second ﬁ nger in the vagina (rectovaginal).

• Palpate the uterus and adnexal structures as described under Uterus,

and Ovaries and Fallopian Tubes. Palpate the rectal wall for any masses

or abnormalities.

Masses

It is often not possible to differentiate between adnexal and uterine

masses. However, there are some general rules:

• Uterine masses may be felt to move with the cervix when the uterus is

shifted upward, whereas adnexal masses will not.

• If you suspect an adnexal mass, there should be a line of separation

between the uterus and the mass, and the mass should be felt

distinctly from the uterus.

• While the consistency of the mass may help distinguish its origin in

certain cases, an ultrasound is necessary to further evaluate the mass.

Finishing the examination

• Withdraw your ﬁ

ngers from the vagina.

•

Inspect the glove for blood or discharge.

• Redrape the genital area and allow the patient to get dressed in

privacy—offer them tissues to wipe and assistance, if needed.

CHAPTER 14 Female reproductive system430

Taking a cervical smear

Theory

The purpose of the cervical smear is to detect premalignant conditions

of the cervix. The U.S. Preventive Services Task Force recommends

screening sexually active women with a cervix starting 3 years after ini-

tial sexual activity or at age 21. Cervical samples should be taken regu-

larly (at least every 3 years). See Box 14.13 for taking samples during

pregnancy.

Routine sampling after age 65 is not recommended for women with

adequate, recent negative screening and who are not at high risk for cer-

vical cancer. There is no indication for routine screeing in women who

have had a hysterectomy for benign disease. Current recommendations

indicate that there is insufﬁ cient evidence to recommend routine screen-

ing for human papillomavirus (HPV) as a primary cancer screen. (http://

www.ahrq.gov/clinic/USpstf/uspscerv.htm).

A sample of cells from the squamocolumnar junction are obtained

and a cytological examination performed to look for evidence of cervical

intraepithelial neoplasia (CIN). Early stages of cervical cellular abnormality

are easily and successfully treated.

Most clinical settings now use liquid-based cytology (LBC), to minimize

the number of inadequate samples.

Equipment

• Specula of different sizes

• Disposable latex-free gloves

• Request form

• Sampling device—plastic broom, spatula or cytobrush ( Fig. 14.5)

• LBC vial—preservative for sample

Before you start

• Ensure that the woman understands the purpose of the examination.

• Discuss how and when she will receive the results.

• Document the date of the last menstrual period.

• Document the use of hormonal treatment (e.g., contraception, HT).

• Record the details of the last smear and previous abnormal results.

• Ask about irregular bleeding (e.g., postcoital or postmenopausal).

• Ask about unusual discharge.

• Where appropriate, offer screening for Chlamydia infection (under age

25 years, symptomatic).

Box 14.13 Cervical smears in pregnancy

Cervical smears may be performed during pregnancy. However, the

broom or brush type sampling devices may cause excessive (and con-

cerning) bleeding, so the more traditional wooden or plastic spatula is

often used instead.

TAKING A CERVICAL SMEAR

431

Procedure

• Prepare the woman as for a vaginal examination, remembering to

make her comfortable and allow privacy—see b p. 424.

• Write the patient’s identiﬁ

cation details on the LBC vial.

• Insert the speculum to identify and visualize cervix as on b p. 425.

Record any abnormal features of the cervix.

• Insert the plastic broom so that the central bristles of the brush are

in the endocervical canal and the outer bristles in contact with the

ectocervix (see Fig. 14.6 ).

• Using pencil pressure, rotate the brush 5 times in a clockwise

direction.

•

The bristles are beveled to scrape cells only on clockwise rotation.

Fig. 14.5 The end of a typical Cervex-Brush

®

.

Fig. 14.6 Representation of how to use a Cervex-Brush

®

. Note that the longer,

central bristles are within the cervical canal, while the outer bristles are in contact

with the ectocervix.

CHAPTER 14 Female reproductive system432

• Rinse the brush thoroughly in the preservative (ThinPrep

®

) or break

off brush into the preservative (SurePath

®

).

• If using a cytobrush, spatula, and slide, obtain adequate endocervical

(cytobrush) and ectocervical (spatula) samples and apply the specimen

to the slide (roll the brush across the slide; apply a thin smear of

material from the spatula to the slide) and apply ﬁ xative.

• Place the slide in transport packaging with a completed request form.

• Remove the speculum as on b p. 426.

• Perform the bimanual exam.

• Allow the patient to get dressed in privacy.

Current practice recommendations and consensus guidelines are

available from the American Society of Colposcopy and Cervical

Pathology Web site at: http://www.asccp.org/

HISTORY-TAKING IN OBSTETRICS

433

History-taking in obstetrics

Although some parts are particular to this history, most of this process is

the same as the basic outline described in b Chapter 2. We suggest that

readers review that chapter before going on.

Demographic details

• Name, age, and date of birth

• Gravidity and parity—see Box 14.15

Estimated date of delivery (EDD)

The EDD can be calculated from the last menstrual period (LMP) by

Naegele’s rule,* which assumes a 28-day menstrual cycle ( Box 14.4 ).

It is important to consider at this point any details that may inﬂ uence the

validity of the EDD as calculated from the LMP, such as the following:

• Was the last period normal?

• What is the usual cycle length?

• Are the patient’s periods usually regular or irregular?

• Was the patient using the oral contraceptive pill in the 3 months prior

to conception? If so, calculations based on her LMP are unreliable.

Current pregnancy

Ask about the patient’s general health and that of her fetus. If there is a pre-

senting complaint, the details should be documented in full as on b p. 33.

Also ask about the following:

• Fetal movements

•

These are not usually noticed until 20 weeks’ gestation in the ﬁ rst

pregnancy and 18 weeks’ in the second or subsequent pregnancies.

• Any important laboratory tests or ultrasound scans

•

This include dates and details of all the scans, especially the ﬁ rst scan

(dating or nuchal translucency scan).

Box 14.14 Calculating the EDD

• Subtract 3 months from the ﬁ rst day of the LMP.

• Add on 7 days and 1 year.

If the normal menstrual cycle is <28 days or >28 days, then an appropri-

ate number of days should be subtracted from or added to the EDD,

respectively. For example, if the normal cycle is 35 days, 7 days should

be added to the EDD.

* Named after the German obstetrician Franz Naegele, following the rule’s description in his

Lehrbuch der Geburtshuelfe, published for midwives in 1830. The formula was actually developed by

Harmanni Boerhaave. See Boerhaave H. (1744) Praelectiones Academicae in Propias Institutiones Rei

Medicae . Von Haller A (ed). Göttingen: Vandehoeck. Vol. 5 (part 2), p. 437.

The parts of the history detailed below are only those that differ from

those described in b Chapter 2 and earlier in this chapter (b p. 413).

CHAPTER 14 Female reproductive system434

Past obstetric history

Ask about all of her previous pregnancies, including miscarriages, termina-

tions, and ectopic pregnancies.

For each pregnancy, note the following:

• Age of the mother when pregnant

• Antenatal complications

• Duration of pregnancy

• Details of induction of labor

• Duration of labor

• Presentation and method of delivery

• Birth weight and sex of infant

2 Also ask about any complications of the puerperal period, which is

the period from the end of the third stage of labor until involution of the

uterus is complete (about 6 weeks).

Possible complications include the following:

• Postpartum hemorrhage

• Infections of the genital and urinary tracts

• Deep vein thrombosis (DVT)

Box 14.15 Gravidity and parity

These terms can be confusing. Although it is worth knowing the deﬁ ni-

tions and how to use them, they should be supplemented with a detailed

history and not relied on alone, as you may miss subtleties that alter

your outlook on the case.

Gravidity (G)

• The number of pregnancies (including the present one) to any stage

Parity (P)

• The outcomes of the pregnancies. The notations after the P refer to

full-term (F), premature (P), abortions (spontaneous or terminations)

(A), and living children (L).

Examples

• A woman who is currently 20 weeks pregnant and has had two

normal deliveries:

•

G 3 P 2002

• A woman who is not pregnant and has had a single live birth and one

miscarriage at 17 weeks:

•

G 2 P 1011

• A woman who is currently 25 weeks pregnant, has had three normal

deliveries, one miscarriage at 9 weeks, and a termination at 7 weeks:

•

G 6 P 3023

Twins

• A woman who is not pregnant and had a delivery of twins at 34

weeks:

•

G 1 P 0202

HISTORY-TAKING IN OBSTETRICS

435

• Perineal complications, such as breakdown of the episiotomy site or

perineal wounds

• Psychological complications (e.g., postpartum depression)

Past gynecological history

• Record all previous gynecological problems with full details of how the

diagnosis was made, treatments received, and the success or otherwise

of that treatment.

• Record date of the last cervical smear and any previous abnormal

results.

• Take a full contraceptive history.

Past medical history

Take a full PMH as on b p. 35. Note especially those conditions that may

have an impact on the pregnancy:

• Diabetes

• Thyroid disorders

• Addison’s disease

• Asthma

• Epilepsy

• Hypertension

• Heart disease

• Renal disease

• Infectious diseases, such as TB, HIV, syphilis, and hepatitis

•

Identiﬁ cation of such conditions allows early referral to a specialist

for shared care as needed.

• All previous operative procedures

• Blood transfusions and receipt of other blood products

• Psychiatric history

Drug history

• Take a full drug history (b p. 36), which should include all prescribed

medications, OTC medicines, herbal treatments, vitamins, and illicit drugs.

• Record any drug allergies and their nature.

• If currently the patient is pregnant, ensure that she is taking 400 mcg

of folic acid daily until 12 weeks’ gestation to reduce the incidence of

spina biﬁ da.

Smoking and alcohol

A full history should be taken (b p. 37).

Family history

Family history is an important aspect of the obstetric history and should

not be overlooked.

• Ask about any pregnancy-related conditions, such as congenital

abnormalities, problems following delivery ( Box 14.16 ), etc.

• Ask also about a FH of diabetes.

2 Ask especially if there are any known hereditary illnesses.

Appropriate counseling and investigations such as chorionic villus

sampling or amniocentesis may need to be offered.

CHAPTER 14 Female reproductive system436

Social history

A full standard SH (b p. 41) should be taken. Ask about the following:

• Her partner—age, occupation, health

• How stable the relationship is

• If she is not in a relationship, who will give her support during and

after the pregnancy?

• Ask if the pregnancy was planned or not.

• If she works, ask about her job and if she has any plans to return to

work.

0 You may also use this opportunity to give advice on regular exercises

and avoidance of certain foods, e.g., seafood (high mercury content), soft

cheeses (risk of Listeria ), and calf liver (high vitamin A content).

Box 14.16 A word about deliveries

The verb to deliver is often misused by students of obstetrics, as it is

often misused by the public at large.

Babies are not delivered; the mothers are delivered of the child, as in

being relieved of a burden.

Check your nearest dictionary!

437

PRESENTING SYMPTOMS IN OBSTETRICS

Presenting symptoms in obstetrics

Bleeding—during pregnancy

Treat as any symptom. In addition, you should build a clear picture of how

much blood is being lost, and when and how it is affecting the current

pregnancy (see also Box 14.17 ).

After establishing an exact timeline and other details about the symp-

tom, ask about the following:

• Exact nature of the bleeding (fresh or old)

• Amount of blood lost

• Number of sanitary pads or tampons used daily

• Presence of clots (and, if present, size of those clots)

• Presence of pieces of tissue in the blood

• Presence of mucoid discharge

• Fetal movement

Box 14.17 Some causes of vaginal bleeding in early

pregnancy

Ectopic pregnancy

• Symptoms: light bleeding, abdominal pain, fainting if pain and blood

loss is severe

• Signs: closed cervix, uterus slightly larger and softer than normal,

tender adnexal mass, cervical motion tenderness

Threatened miscarriage

• Symptoms: light bleeding; sometimes cramping, lower abdominal pain

• Signs: closed cervix, uterus corresponds to dates; sometimes uterus

is softer than normal

Complete miscarriage

• Symptoms: light bleeding; sometimes light cramping, lower abdominal

pain and history of expulsion of products of conception

• Signs: uterus smaller than dates and softer than normal; closed

cervix

Incomplete miscarriage

• Symptoms: heavy bleeding; sometimes cramping lower abdominal

pain, partial expulsion of products of conception

• Signs: uterus smaller than dates and cervix dilated

Molar pregnancy

• Symptoms: heavy bleeding, partial expulsion of products of

conception that resemble grapes; sometimes nausea and vomiting,

cramping lower abdominal pain, history of ovarian cysts

• Signs: dilated cervix, uterus larger than dates and softer than normal

Information adapted from World Health Organization, Department of

Reproductive Health Research (2007). Vaginal bleeding in early preg-

nancy. In Managing Complications in Pregnancy and Childbirth: A Guide for

Midwives and Doctor s . Geneva: WHO.

CHAPTER 14 Female reproductive system438

• Associated symptoms, such as abdominal pain (associated with

placental abruption; placenta previa is painless).

• Possible trigger factors—recent intercourse, injuries (see Box 14.18 )

• Any history of cervical abnormalities and the result of the last smear

Abdominal pain

A full pain history should be taken as on b p. 33, including site, radiation,

character, severity, mode and rate of onset, duration, frequency, exacer-

bating factors, relieving factors, and associated symptoms.

Take a full obstetric history and systems review. Ask especially about

a past history of preeclampsia, preterm labor, peptic ulcer disease, gall-

stones, appendectomy, and cholecystectomy.

0 Remember that the pain may be unrelated to pregnancy, so keep an

open mind! Causes of abdominal pain in pregnancy include the following:

• Obstetric: preterm or term labor, placental abruption, ligament pain,

symphysis pubis dysfunction, preeclampsia or HELLP (Hemolysis,

Elevated Liver enzyme levels, Low Platelet count) syndrome, acute

fatty liver of pregnancy

• Gynecological: ovarian cyst rupture, torsion, hemorrhage, uterine

ﬁ broid

degeneration

• Gastrointestinal: constipation, appendicitis, gallstones, cholecystitis,

pancreatitis, peptic ulceration

• Genitourinary: cystitis, pyelonephritis, renal stones, renal colic

Labor pain

This is usually intermittent and regular in frequency and associated with

tightening of the abdominal wall.

Bleeding—after pregnancy

This is called postpartum hemorrhage , or PPH.

• Primary PPH: >500 mL blood loss within 24 hours following delivery

• Secondary PPH: any excess bleeding between 24 hours and 6 weeks

post-delivery (No amount of blood is speciﬁ

ed in the deﬁ nition.)

2 Take a full history as for bleeding during pregnancy, on b p. 437. Ask

Box 14.18 Some causes of bleeding in second and third

trimesters (>24 weeks)

This is known as antepartum hemorrhage (APH).

Placenta previa

The placenta is positioned over the lower pole of the uterus, obscuring

the cervix. Bleeding is usually after 28 weeks and often precipitated by

intercourse. Findings may include a relaxed uterus, fetal presentation

not in the pelvis, and normal fetal condition.

Placental abruption

This is detachment of a normally located placenta from the uterus before

the fetus is delivered. Bleeding can occur at any stage of the pregnancy.

Possible ﬁ ndings include a tense, tender uterus, d or absent fetal move-

ments, fetal distress, or absent fetal heart sounds.

439

PRESENTING SYMPTOMS IN OBSTETRICS

also about symptoms of infection, an important cause of secondary PPH

(see Boxes 14.18 and 14.19 ).

Hypertension

Hypertension is a common and important problem in pregnancy. You

should be alert to the possible symptoms that can result from it, such

as headache, blurred vision, vomiting, and epigastric pain after 24 weeks,

convulsions, or loss of consciousness.

Pregnancy-induced hypertension

• Two readings of diastolic blood pressure 90–110, systolic BP >140,

4 hours apart after 20 weeks gestation; no proteinuria

Mild proteinuric pregnancy-induced hypertension/preeclampsia

• Two readings of diastolic blood pressure 90–110, systolic BP >140,

4 hours apart after 20 weeks gestation, and proteinuria 1–2+

Severe proteinuric pregnancy-induced hypertension/preeclampsia

• Diastolic blood pressure 110 or greater after 20 weeks’ gestation and

proteinuria 3+.

• Other symptoms may include hyperreﬂ

exia, headache, clouding of

vision, oligura, abdominal pain, pulmonary edema. There may be

evidence of HELLP syndrome.

Eclampsia

• Convulsions associated with raised blood pressure and/or proteinuria

beyond 20 weeks gestation. The patient may be unconscious.

Box 14.19 Some causes of postpartum hemorrhage

Primary

• Uterine atony (most frequent cause)

• Genital tract trauma

• Coagulation disorders

• Retained placenta

• Uterine inversion

• Uterine rupture

Secondary

• Retained products of conception

• Endometritis

• Infection

CHAPTER 14 Female reproductive system440

Box 14.21 Minor symptoms of pregnancy

These so-called minor symptoms of pregnancy are often experienced by

many women as normal, physiological changes occur. This is not to say

that they should be ignored, as they may point to pathology.

• Nausea and vomiting: severity varies greatly and is more common in

multiple pregnancies and molar pregnancies. Persistence of vomiting

may suggest pathology such as infections, gastritis, biliary tract

disease, or hepatitis.

• Frequent urination: An expected ﬁ

nding in pregnancy, it does not

exclude the possibility of urinary tract infection.

• Heartburn/gastroesophageal reﬂ ux: Heartburn is a frequent

complaint during pregnancy due partially to compression of the

stomach by the gravid uterus. See b p. 206.

• Constipation: often secondary to i progesterone. It improves with

gestation (b p. 212).

• Shortness of breath: due to dilatation of the bronchial tree

secondary to i progesterone. Peaks at 20–24 weeks. The growing

uterus also has an impact. Other possible causes (such as PE) need

to be considered. See b p. 184.

• Fatigue: very common in early pregnancy, peaking at the end of the

ﬁ

rst trimester. Fatigue in late pregnancy may be due to anemia.

• Insomnia: due to anxiety, hormonal changes, and physical discomfort

• Pruritus: Generalized itching in the third trimester may resolve after

delivery. Biliary problems should be excluded (b p. 216).

• Hemorrhoids: may resolve after delivery

• Varicose veins: especially at the feet and ankles

• Vaginal discharge: Exclude infection and spontaneous rupture of the

membranes.

• Pelvic pain: Stretching of pelvic structures can cause ligament pain

that resolves in the second half of the pregnancy. Symphysis-pubis

dysfunction causes pain on abduction and rotation at the hips and on

mobilization.

• Backache: often ﬁ

rst develops during the ﬁ

fth to seventh months of

pregnancy

• Peripheral paresthesias : Fluid retention can lead to compression of

peripheral nerves, such as carpal tunnel syndrome. Other nerves can

be affected, e.g., lateral cutaneous nerve of the thigh.

Box 14.20 Risk factors for postpartum hemorrhage

These include placental abnormalities, polyhydramnios, prolonged labor,

very rapid labor, multiple gestation, previous PPH or APH, preeclampsia,

coagulation abnormalities, genital tract lacerations, and small maternal

stature.

OUTLINE OBSTETRIC EXAMINATION

441

Outline obstetric examination

Explain to the patient that you would like to examine her uterus and baby,

and reassure her that the procedure will be quick and gentle. You should

have a chaperone present, particularly if you are male.

As always, ensure that the room is warm and well lit, preferably with a

moveable light source, and that you will not be disturbed.

As with the gynecological examination, you should follow an orderly

routine. The authors’ suggestion is shown in Box 14.22. It is standard prac-

tice to start with the cardiovascular and respiratory systems—this not

only gives a measure of the general health of the patient but also estab-

lishes a physical rapport before you examine more sensitive areas.

General inspection

Always begin with a general examination of the patient (as in Chapter 3),

including temperature, hydration, coloration, nutritional status, lymph

nodes, and blood pressure. Note especially the following:

• Any brownish pigmentation over the forehead and cheeks, known

as chloasma

• Distribution of facial and body hair, as hirsutism may be a presenting

symptom of various endocrine disorders

• Height and weight, and calculate BMI (b p. 56)

2 Blood pressure should be measured in the left lateral position at 45*

to avoid compression of the IVC by the gravid uterus.

0 Anemia is a common complication of pregnancy, so examine the

mucosal surfaces and conjunctivae carefully (b p. 51).

• Examine the cardiovascular and respiratory systems in turn(see

Chapters 7 and 8).

•

Flow murmurs are common in pregnancy and, although usually of no

clinical signiﬁ cance, must be recorded in detail.

• A routine breast examination is usually performed. Take note of

inverted nipples, which may interfere with breast-feeding.

Box 14.22 Framework for obstetric examination

• General inspection

• Cardiorespiratory examination

• Breast examination

• Abdominal inspection

• Abdominal palpation

•

Uterine size

•

Fetal lie

•

Fetal presentation

•

Engagement

•

Amniotic ﬂ uid estimation

• Auscultation of the fetal heart

• Vaginal examination

2 Perform urinalysis (particularly urine dipstick)

CHAPTER 14 Female reproductive system442

Abdominal examination

Inspection

Look for abdominal distension caused by the gravid uterus rising from the

pelvis. Look also for the following:

• Asymmetry

• Fetal movements

• Surgical scars

•

Pubic hairline (transverse suprapubic Pfannenstiel incision)

•

Paraumbilical region (laparoscopic scars)

• Cutaneous signs of pregnancy

•

Linea nigra (black line), which stretches from the pubic symphysis

upward in the midline

•

Red stretch marks of current pregnancy (striae gravidarum)

•

White stretch marks (striae albicans) from a previous pregnancy

•

Other areas that can undergo pigmentation in pregnancy include the

nipples, vulva, umbilicus, and recent abdominal scars.

• Umbilical changes

•

Flattening as pregnancy advances

•

Eversion secondary to i intra-abdominal pressure (e.g., caused by

multiple pregnancies or polyhydraminios)

Palpation

Before palpating the abdomen, always ask about any areas of tenderness

and examine those areas last. Palpation should start as for any standard

abdominal examination (Chapter 9) before proceeding to more speciﬁ c

maneuvers in an obstetric examination.

Uterine size

This provides an estimation of gestational age in weeks ( Fig. 14.7 ) and

is objectively measured and expressed in centimeters as the symphysial–

fundal height (distance from the symphysis pubis to the upper edge of the

uterus) ( Boxes 14.23 and 14.24 ).

0 You need a tape measure for this—don’t start without it!

• Use the ulnar border of the left hand to press ﬁ

rmly into the abdomen

just below the sternum.

• Move your hand down the abdomen in small steps until you can feel

the fundus of the uterus.

• Locate the upper border of the bony pubic symphysis by palpating

downward in the midline, starting from a few centimeters above the

pubic hair margin.

• Measure the distance between the two points that you have found in

centimeters, using a ﬂ

exible tape measure.

Fetal lie

This describes the relationship between the long axis of the fetus and the

long axis of the uterus ( Fig. 14.8 ). In general, it can be the following:

• Longitudinal: The long axis of the fetus matches the long axis of the

uterus. Either the head or breech will be palpable over the pelvic inlet.

• Transverse: The fetus lies at right angles to the uterus and the fetal

poles are palpable in the ﬂ anks.

443

ABDOMINAL EXAMINATION

• Oblique: The long axis of the fetus lies at an angle of 45* to the long axis

of the uterus; the presenting part will be palpable in one of the iliac fossae.

Examination technique

The best position is to stand at the mother’s right side, facing her feet.

• Put your left hand along the left side of the uterus.

• Put your right hand on the right side of the uterus.

• Palpate systematically toward the midline with one hand and then the

other hand—use dipping movements with ﬂ

exion of the MCP joints to

feel the fetus within the amniotic ﬂ uid.

• You should feel the fetal back as ﬁ

rm resistance or the irregular shape

of the limbs.

36 weeks

20 weeks

12 weeks

Fig. 14.7 The distance between the fundus (upper border of the uterus) and the

pubic symphysis can be used as a guide to the number of weeks’ gestation. You can

also, therefore, judge whether the uterus is smaller or larger than expected, which

may point to problems with the pregnancy.

Box 14.23 Symphysial–fundal height (cm) 8 weeks

gestation

At 16–36 weeks, there is a margin of error of 92 cm, 93 cm at 36–40

weeks, and 94 cm at 40 weeks on.

Box 14.24 Uterine size—milestones

• The uterus ﬁ rst becomes palpable at 12 weeks’ gestation.

• 20 weeks’ gestation = at the level of the umbilicus

• 36 weeks’ gestation = at the level of the xiphisternum

CHAPTER 14 Female reproductive system444

• Now palpate more widely, using the two-handed technique above to

stabilize the uterus, and attempt to locate the head and the breech.

•

The head can be felt as a smooth, round object that is ballotable—

that is, it can be bounced (gently) between your hands.

•

The breech is softer, less discrete, and not ballotable.

Fetal presentation

This is the part of the fetus that presents to the mother’s pelvis. Possible

presenting parts include the following:

• Head: cepahalic presentation. One option in a longitudinal lie

• Breech: podalic presentation. The other option in a longitudinal lie

• Shoulder: seen in a transverse lie

Examination technique

• Stand at the mother’s right side, facing her feet.

• Place both hands on either side of the lower part of the uterus.

• Bring the hands together ﬁ

rmly but gently.

•

You should be able to feel either the head, breech, or other part as

described under Fetal Lie.

It is also possible to use a one-handed technique (Paulik’s grip) to feel for

the presenting part—this is best left to obstetricians. In this technique,

you use a cupped right hand to hold the lower pole of the uterus. This is

possible in 795% of pregnancies at about 40 weeks.

Engagement

When the widest part of the fetal skull is within the pelvic inlet, the fetal

head is said to be engaged .

In a cephalic presentation, palpation of the head is assessed and expressed

as the number of ﬁ fths of the skull palpable above the pelvic brim. A ﬁ fth of

a fetal skull is roughly equal to a ﬁ nger breath on an adult hand.

Longitudinal Transverse Oblique

Fig. 14.8 Some examples of fetal lie.

445

ABDOMINAL EXAMINATION

• The head is engaged when three or more ﬁ fths are within the pelvic

inlet—that is when two or fewer ﬁ fths are palpable.

• When three or more ﬁ

fths are palpable, the head is not engaged.

Number of fetuses

The number of fetuses present can be calculated by assessing the number

of fetal poles (head or breech) present.

• If there is one fetus present, two poles should be palpable (unless the

presenting part is deeply engaged).

• In a multiple pregnancy, you should be able to feel all the poles except

one, as one is usually tucked away out of reach.

Amniotic ﬂ uid volume estimation

The ease with which fetal parts are palpable can give an indication of the

possibility of d or i amniotic ﬂ uid volume.

• i Volume will give a large-for-dates uterus that is smooth and

rounded. The fetal parts may be almost impossible to palpate.

• d Volume may give a small-for-dates uterus. The fetus will be easily

palpable, giving an irregular, ﬁ

rm outline to the uterus.

Percussion

This is usually unhelpful in an obstetric examination, unless you suspect

polyhydramnios (increased amniotic ﬂ uid volume). In this case, you may

wish to attempt to elicit a ﬂ uid thrill (b p. 239).

Auscultation

Auscultation is used to listen to the fetal heart rate (FHR). This is usually

performed using an electronic hand-held Doppler fetal heart rate monitor

and can be used as early as 14 weeks.

Using Pinard’s fetal stethoscope

With the prevalance and low cost of the modern fetal Doppler, a Pinard’s

fetal stethoscope is no longer likely to be seen or used. Fetascopes are not

generally useful until 28 weeks’ gestation. It is a simple-looking device that

looks like an old-fashioned ear-trumpet ( Fig. 14.9 ).

• Place the bell of the instrument over the anterior fetal shoulder,

where the fetal heart sounds are best heard.

• Press your left ear against the stethoscope to hold it between your

head and the mother’s abdomen in a hands-free position, or hold the

instrument lightly with one hand.

• Press against the opposite side of the mother’s abdomen with your

other hand to stabilize the uterus.

• It should sound like a distant ticking noise. The rate varies between

110 and 150/minute at term and should be regular.

2 Record the rate and rhythm of the fetal heart.

Vaginal examination

Vaginal examination enables you to assess cervical status before induction

of labor. You should attempt this only under adequate supervision if you

are unsure of the procedure.

CHAPTER 14 Female reproductive system446

This examination allows you to assess the degree of cervical dilatation

(in centimeters) using the examining ﬁ ngers.

0 Examination of the vagina and cervix should be performed under

aseptic conditions in the presence of ruptured membranes or in patients

with abnormal vaginal discharge.

Technique

The examination should be performed as described on b p. 427. It takes

experience to reliably determine the ﬁ ndings.

Findings

Assess the following:

• Degree of dilation

•

Full dilation of the cervix is equivalent to 10 cm.

•

Most obstetric departments will have plastic models of cervices in

various stages of dilatation with which you can practice.

• Length of the cervix

•

Normal length is 73 cm but shortens as the cervix effaces secondary

to uterine contraction.

• Consistency of the cervix, which can be described as follows:

•

Firm

•

Mid-consistency

•

Soft (this consistency facilitates effacement and dilatation)

• Position

•

As the cervix undergoes effacement and dilatation it tends to be

pulled from a posterior to an anterior position.

• Station of the presenting part

•

The level of the head above or below the ischial spines may be

estimated in centimeters.

Fig. 14.9 A Pinard’s stethoscope.

THE ELDERLY PATIENT

447

The elderly patient

It is easy to be seduced into thinking that the principal focus should be on

very medical diagnoses, such as urinary tract infections, which contribute

to signiﬁ cant morbidity (and mortality) in older people.

Continence issues are frequently overlooked in most clinical assess-

ments. Large-scale surveys of prevalence have shown up to 20% of women

over 40 reporting difﬁ culties with continence. So while this is more com-

mon in older people, you should always be mindful of problems in younger

adults as well.

Although continence issues are one of the geriatric giants of disease

presentation, it is important to recall the physiology of postmenopausal

changes, such as vaginal atrophy and loss of secretions, which can com-

plicate urinary tract infections, continence, and uterovaginal prolapse in

older patients.

Assessment

Tact and understanding

Although problems are common, patients may be reluctant to discuss them

or have them discussed in front of others. Engaging in a discussion about

bladder and/or sexual function can seem daunting, but if done empathet-

ically, remembering not to appear judgmental or be embarrassed, you may

reveal problems that have seriously affected your patient’s quality of life.

Treating problems such as these, even with very simple interventions,

can be of immeasurable value to the patient. Remember to consider STIs

in your differential. “Elderly” does not mean sexual inactivity.

Holistic assessment of urinary problems

Learn to think when asking about bladder function, and work out a pattern

of dysfunction—e.g., bladder instability or stress incontinence. Remember

that bladder function may be disrupted by drugs, pain, or lack of privacy.

Continence issues may reﬂ ect poor mobility or visual and cognitive

decline.

Genital symptoms

Don’t forget to consider vaginal or uterine pathology—view postmeno-

pausal bleeding with suspicion. Discharges may represent active infection

(if Candida , consider diabetes) or atrophic vaginitis (see Box 14.25 ).

Past medical history

Pregnancies and previous surgery in particular may help point to a diag-

nosis of stress incontinence. Are urinary tract infections recurrent—has

bladder pathology been excluded?

Drugs

Many are obvious—diuretics and anticholinergics; some are more sub-

tle—sedatives may provoke nocturnal loss of continence. Does your

patient drink tea or coffee?

Tailored functional history

This is the cornerstone of these pages and of any assessment you perform.

It largely relates to bladder function—is the bathroom located upstairs or

CHAPTER 14 Female reproductive system448

down? How are the stairs? Does your patient already have continence aids,

such as bottles, commodes, or pads, and do they manage well with them?

Box 14.25 A word on atrophic vaginitis

Up to 40% of postmenopausal women will have symptoms and signs of

atrophic vaginitis. The vast majority will be elderly and may be reluctant

to discuss this with their doctors. A result of estrogen decline, the sub-

sequent i vaginal pH and thinned endometrium lead to both genital and

urinary symptoms and signs.

An decrease in vaginal lubrication presents with dryness, pruritus, and

discharges, accompanied by an i rate of prolapse. Urinary complications

can result in frequency, stress incontinence, and infections.

Careful physical examination often makes the diagnosis clear with

labial dryness, loss of skin turgidity, and smooth, shiny vaginal epithe-

lium. A range of treatment options, including topical estrogens, simple

lubricants, and continued sexual activity when appropriate, are all key

interventions to manage this common condition.

449

Psychiatric assessment

Approach to psychiatric assessment 450

History 452

Mental status examination 458

Physical examination 466

Important presenting patterns 467

Medical conditions with psychiatric symp-toms and signs 476

Chapter 15

CHAPTER 15 Psychiatric assessment450

Approach to psychiatric assessment

In taking a psychiatric history and assessing mental state, it is crucial to

communicate to the patient with empathy, respect, competence, and

interest, in a nonjudgmental fashion. This approach will create an atmo-

sphere of trust that encourages the patient to talk honestly about their

thoughts and feelings.

Central to the psychiatric interview process is the art of active listen-

ing to what is said and an awareness of any nonverbal communication

between patient and assessor.

Be prepared to spend anywhere from 30 minutes to an hour, depending

on the circumstances, conducting an interview. This might seem a daunt-

ing task in the early stages, particularly as patients rarely ﬁ nd a narrative.

However, staying on track is often made easier by remembering to write

out the headings for parts of the assessment in advance.

Preparation and preliminary considerations

The room

Before proceeding to questioning, adequate preparations should be made

regarding the place where the assessment is to be carried out. An inter-

view room should be a safe environment, especially when seeing a patient

who is potentially violent. Your facility will normally have rooms speciﬁ -

cally conﬁ gured for the performance of psychiatric examinations.

• Inform your colleagues and departmental staff of your location.

• You should know where to locate, and how to use, the panic button.

• You should be accompanied by a colleague if you are seeing a patient

with a history of violent behavior.

• Remove any objects that might pose a danger (i.e., those that can be

used as a weapon).

• Know your nearest exit point and ensure that it is open or unblocked.

• Never allow the patient to come between you and the door.

• Ensure adequate privacy and lighting.

• Ideally, the patient should be sitting off-center, so that all of their body

may be seen but without the situation appearing too threatening.

• The height of your seats should be equal or similar.

Conduct of interview

Begin by introducing yourself, explaining who you are and the purpose of

your assessment. Use a handshake—a widespread sign of introduction and

welcome. Establish whether or not the patient wishes a friend or relative

to be present (and whether you feel it is appropriate).

The interview should generally start in an informal way to establish a

friendly and concerned rapport. This might involve a short period of neu-

tral conversation.

Try to avoid leading or direct questions. Use relatively broad, open, gen-

eral questions and leave speciﬁ

c closed questions for further clariﬁ cation

later. Allow breaks and digressions within reason, especially with sensitive

individuals. At appropriate intervals, clarify what the patient has said by

repeating sentences and asking them to conﬁ rm

this.

APPROACH TO PSYCHIATRIC ASSESSMENT

451

Examination

In psychiatry, you should be examining the patient’s mental state; this is

described later. However, don’t overlook physical examination, as this is

often an important part of the assessment. Conduct the physical examina-

tion is described in Chapters 2 and 3. A useful framework for psychiatric

assessment is given in Box 15.1

Box 15.1 Framework for psychiatric assessment

History

• Name, age, marital status, occupation, ethnic origin, and religion

• Source, mode, and reason for referral

• Chief complaint

• History of present illness

• Risk assessment

• Past psychiatric history

• Past medical history

• Drug history

• Family history

• Personal history

•

Birth and early development

•

School

•

Occupational history

•

Psychosexual history

•

Marital history

•

Children

•

Forensic history

• Premorbid personality

• Social history

Mental state examination

• Appearance and behavior

• Speech

• Mood

• Thought content

• Perception

• Cognitive functioning

• Insight

Physical examination

• As appropriate

CHAPTER 15 Psychiatric assessment452

History

The psychiatric history is very similar in structure to the standard medical

history described in Chapter 2. Symptoms and issues should be dealt with

in the same way (see Box 15.2 ).

Patient proﬁ le

Start by making a note of the patient’s name, age, marital status, occupa-

tion, ethnic origin, and religion.

Source, mode, and reason for referral

Record here all the information you have about the patient from other

sources—relatives, caregivers, social workers, counselors, primary care

team, and police, if relevant.

• Who has asked for the individual to be seen and why?

• What was the mode of referral—voluntary, or involuntary as a referral

from other clinicians or law enforcement (as under the Baker Act)?

Chief complaint

Obtain a brief description of the principal complaint(s) and the time frame

of the problem in the individual’s own words.

This can be difﬁ cult if the patient is in a psychotic state and does not

believe a problem exists. In these cases, try to comment on the presenting

complaint as described by an informant.

Box 15.2 Factors asked about for a physical or mental

symptom

The following is repeated from Chapter 2. Treat psychiatric symptoms in

a similar way, but remember that the patient may not regard their issue

as a symptom, so tailor your language carefully.

• Exact nature of the symptom

• Onset

•

Date it began

•

How it began (e.g., suddenly, gradually–over how long?)

•

If long-standing, why is the patient seeking help now?

• Periodicity and frequency

•

Is the symptom constant or intermittent?

•

How long does it last each time?

•

What is the exact manner in which it comes and goes?

• Change over time

•

Is it improving or deteriorating?

• Exacerbating factors

•

What makes the symptom worse?

• Relieving factors

•

What makes the symptom better?

• Associated symptoms

HISTORY

453

History of present illness

This is a detailed account of the presenting problems in chronological

order (as for any other kind of symptom as in Chapter 2):

• Onset of illness (when was the patient last well?)

• How did the condition develop?

• Severity of the patient’s symptoms

• Precipitating factors (including any signiﬁ

cant life events preceding

onset of the symptoms)

• Exacerbating factors (what makes the symptoms worse?)

• Relieving factors (what makes the symptoms better?)

• How has it affected the patient’s daily life, pattern, or routine (effect

on interpersonal relationships, working capacity, etc.)?

• Treatment history. Include treatment tried during the course of the

present illness, previous drug treatments, electroconvulsive therapy,

and psychosocial interventions.

• Associated symptoms

• Systematic inquiry. Similar to the standard medical history, run

through other psychiatric symptoms and ask the patient if they have

experienced them (see Box 15.3 ). Explore related symptoms; if

the patient admits to a few depressive symptoms, ask about other

symptoms of depression.

Risk assessment

This includes an assessment of not only self-harm but also the possibility

of harm to others. This should be broached in a serious and sensitive way.

Some useful questions in assessing suicide risk ( Box 15.4 ) are as follows:

• How do you feel about the future?

• Does life seem worth living?

• Do you have thoughts of hurting or harming yourself?

• Have you had thoughts of harming others?

• Have you ever thought of ending it all?

If suicidal thoughts are present, ask how often they occur and if the patient

has made a speciﬁ

c plan and what the plan is.

• Ask about the means, e.g., prescribed and over-the-counter drugs,

guns, or knives.

• Explore for feelings of excessive guilt and loss of self-esteem.

Box 15.3 Tailoring the history

In the taking of a history in any specialty, you should formulate your

questions according to what is said. Also, information may not be pro-

vided by the patient in the order you would like.

This is particularly true of psychiatry—if the patient is talking freely,

you may ﬁ nd them providing information that comes under a number of

different subheadings in your history. Be ﬂ exible, note the information in

the appropriate places, and then ﬁ ll in the gaps with direct questions.

CHAPTER 15 Psychiatric assessment454

If thoughts involving harming others are present, ask about the speciﬁ c

persons and circumstances surrounding these thoughts.

• Ask about the means, e.g., presence of weapons such as guns or

knives.

Previous history of self-harm

Ask about previous attempts—when, where, how, and why. Ask in detail

about the most recent attempt:

• What events led up to the attempt (see Box 15.5 )?

• Were there any speciﬁ

c precipitating factors?

• Was there concurrent use of drugs and alcohol?

• What were the methods used?

• Was it planned?

• Was there a suicide note?

• Were there any active attempts made to avoid being discovered?

Box 15.4 Risk factors for suicide

Biological

• Age >40 years

• Male gender

Medical and psychiatric history

• Previous suicide attempts

• Previous deliberate self-harm

• Psychiatric disorder (depression, substance misuse, schizophrenia,

personality disorder, obsessive-compulsive disorder, panic disorder)

• Chronic physical illness

• History of trauma or abuse

• Substance misuse (including alcohol)

Personality

• Impulsivity, poor problem-solving skills, aggression, perfectionism,

low self-esteem

Family history

• Family history of mental health, substance abuse, family violence, or

suicide attempts among family members

Social

• Lack of social support, isolation

•

Unemployment or retired

•

Single, unmarried, divorced, or widowed

• Presence of ﬁ rearms in the home

•

History of previous incarceration

• Previous exposure to suicidal behaviors in others to whom they have

had close exposure

Access to means

• Weapons in the home or through occupational or social activities

HISTORY

455

• What is the meaning of the action (wanted to die, share distress)?

• Also ask about the circumstances surrounding discovery and how they

were brought to medical attention (if at all).

• Was this what the patient expected?

Protective factors for suicide

These are factors that would stop a person from attempting suicide ( Box

15.6 ). Record what social supports are available to the person (friends,

church, doctor, counselor).

Assessing homicidal intent

If faced with a patient expressing homicidal intent, you should inform a

senior colleague and law enforcement authorities immediately. Legal

instruments such as the Baker Act should be used to prevent the patient’s

release in order to protect those individuals against whom they state this

intent.

Some questions to assess a homicidal or violent patient are as follows:

• Are you upset with anyone?

• Do you have thoughts of hurting anyone?

• Have you made plans to harm someone?

• How would you harm them? (It is important to establish whether the

patient has actually made plans for carrying out the action.)

Past psychiatric history

Explore in detail previous contact with psychiatry and other services for

mental health problems. Include as far as possible:

• Dates of illness, symptoms, diagnoses, treatments, hospitalizations,

previous outpatient treatment, and compulsory treatment under the

Baker Act.

Box 15.5 Factors that may precipitate suicide

The overriding theme here is loss—loss of occupation, independence,

family member, friend, social supports, or freedom.

• Death, separation, or divorce

• Imprisonment, or threat thereof

• Humiliating event

• Job loss

• Reminder of a past loss

• Unwanted pregnancy

Box 15.6 Protective factors for suicide

• Strong family and social connections

• Hopefulness, good skills in problem solving

• Cultural or religious beliefs discouraging suicide

• Responsibility for children

CHAPTER 15 Psychiatric assessment456

Past medical history

This should be evaluated in the same way as in the general medical history,

but remember to ask in particular about obstetric complications, epilepsy,

head injuries, and thyroid disorders.

Drug and alcohol history

• Ask about all current drug intake, including prescribed and over-the-

counter medicines.

• Take a detailed history of substance abuse, if relevant, recording the

type, quality, source, route of administration, and cost.

• Ask about alcohol, tobacco, and any allergic reactions. If necessary, use

the CAGE questionnaire (b p. 221).

Family history

Explore family relationships in detail (parents, siblings, spouse, children).

It is useful to draw a family tree and record age, health, occupation, per-

sonality, quality of relationship, family history of mental illness, including

alcoholism, suicide, and deliberate self-harm, as well as any other serious

family illnesses.

Also record the details and times of certain important family events,

such as death, separation, or divorce, and their impact on the patient.

Personal history

The personal history is a chronological account of the individual’s life from

birth up to the present. This section, which is often lengthy, should be

tackled under the following subheadings.

Birth and early development

• Begin with recording the place and date of birth, gestation at delivery,

and any obstetric complications or birth injuries.

• Inquire about developmental milestones.

• Ask about neurotic traits in childhood (night terrors, sleep walking,

bedwetting, temper tantrums, stammer, feeding difﬁ culties).

• Ask about relationships with peers, siblings, parents, and relatives,

particularly in adolescence.

• Record any adverse experiences (physical or emotional abuse).

• Note any signiﬁ

cant life events, such as separations and bereavement.

School

• Explore how they did at school socially, academically, and athletically.

• Record the start and end of their education and qualiﬁ cations.

• Ask about the type of school, relationships with peers, teachers, and

extracurricular interests and whether there was a history of academic

difﬁ

culty or truancy.

Occupational history

• Inquire about all previous jobs held, dates, and reason for change, level

of satisfaction with employment, and ambitions.

• Include present job and economic circumstances.

HISTORY

457

Psychosexual history

This can be a difﬁ cult section of the history to elicit and is often dependent

on how willing the patient is to volunteer such intimate details. However,

try not to avoid it. It may have to be excluded if judged inappropriate or

likely to cause distress.

• Record the onset of puberty (and menarche, if female).

• Sexual orientation (heterosexual, bisexual, gay, or lesbian)

• Gender identity (transsexual)

• First sexual encounter

• Current sexual practices (practice of safer sex?)

• Any of sexual abuse

• Record any history of sexual dysfunction.

Marital history

This includes a detailed account of number of marriages, duration, qual-

ity of relationships and personality, age and occupations of spouses, and

reasons for breakup of relationship(s).

Children

• Ask about the sex, age, and mental and physical health of all children.

Forensic history

This may or may not be volunteered by the patient. Begin by asking non-

threatening questions: “Have you ever been in trouble with the law?”

• Ask about criminal record and any previous episodes of violence or

other acts of aggression.

Premorbid personality

This is the patient’s personality before the onset of mental illness. An inde-

pendent account is especially important for this part of the history.

• It may help to ask the patient how they would describe themselves

and how they think others would describe them.

• Ask about social relationships and supports.

• Include interests and recreational activities.

• Inquire speciﬁ

cally about temperament—what’s their mood like on

most occasions?

• Ask the patient to describe the nature of their emotional reactions,

coping mechanisms, and character (e.g., shy, suspicious, irritable,

impulsive, lacking in conﬁ

dence, history of obsession).

• What are their moral and religious beliefs?

Social history

Ask especially about ﬁ nances, legal problems, occupation, dependants,

and housing. If elderly, ask about social support, such as home care or

attendance at a day center, and how they cope with activities of daily living

(hygiene, mobility, domestic activity).

CHAPTER 15 Psychiatric assessment458

Mental status examination

The mental status examination is a vital part of the psychiatric assessment.

It is your assessment of the patient’s mental state based on your observa-

tions and interaction. It begins as soon as you see the patient. Mental state

features prior to the interview, whether described by the patient or by

other informants, are considered part of the history.

Appearance and behavior

This involves a brief descriptive note of your observations, both at ﬁ rst

contact and through the interview process. It should include a description

of the following:

• Dress and grooming

•

Patients with depression, dementia, and drug abuse may show

evidence of self-neglect.

•

Flamboyant clothes with clashing colors may be worn by a manic

patient.

•

Loose-ﬁ tting clothes may indicate an underlying anorexia or other

eating disorder.*

• Facial appearance

• Eye contact

• Degree of cooperation

• Posture

• Mannerisms

• Motor activity

•

Excessive movement indicating agitation?

•

Very little movement (retardation) suggesting depression?

• Abnormal movements

•

E.g., tics, chorea, tremor, stereotypy—repetitive movements, such as

rocking or rubbing hands

• Gait

• Any other physical characteristics worth noting

Speech

Describe in terms of the following:

• Rate

• Quantity (i = pressure of speech and is often associated with ﬂ ight

of

ideas,

d = known as poverty of speech)

• Fluency

• Articulation (including stammering, stuttering, and dysarthria)

• Form: this is the way in which a person speaks, rather than actual

content (see Box 15.7 ).

Mood and affect

Mood is a pervasive and sustained emotion that can color the patient’s per-

ception of the world over long periods. Affect is the patient’s immediate

emotional state, including the external expression of feeling.

* Loose-ﬁ tting clothing is usually not a sign of weight loss, contrary to popular belief. In fact,

patients with anorexia tend to deliberately wear baggy clothes to hide their underlying skeletal

appearance.

MENTAL STATUS EXAMINATION

459

Examining mood and affect involves consideration of the patient’s sub-

jective emotional state and your objective evaluation.

Abnormalities of mood include depression, elation, euphoria, anxiety,

and anger. You should note whether mood is consistent with thought and

action or is incongruous.

Abnormalities of affect include the following:

• Blunting: the coarsening of emotions and insensitivity to social context.

This is commonly used synonymously with affective “ﬂ attening.”

• Flattening of affect: a reduction in range and depth of outward emotion

• Lability: superﬁ cially

ﬂ

uctuating and poorly controlled emotions.

This may be found in delirium, dementias, frontal lobe damage, and

intoxication.

Thought content

Preoccupations

These include phenomena such as obsessive thoughts , or ruminations

characterized by an intrusive preoccupation with a topic. The patient

cannot stop thinking about it even though they may realize that it is

irrational.

Box 15.7 Some examples of abnormal speech or thought

form

The following are examples of abnormal speech; however, the speech is

a manifestation of the underlying thought processes. One could argue,

therefore, that the following are abnormalities of thought form.

• Flight of ideas: associated with mania. Ideas ﬂ

ow rapidly but remain

connected although sometimes by unusual associations. The

patient’s train of thought tends to veer off on wild tangents.

•

Derailment: loosening of association seen in formal thought

disorders (e.g., schizophrenia) in which train of thought slips of the

track. Things may be said in juxtaposition that lack a meaningful

association or the patient may shift from one frame of reference to

another.

• Perseveration: mainly seen in dementia and frontal lobe damage.

The patient ﬁ

nds moving to the next topic difﬁ

cult, resulting in an

inappropriate repetition of a response.

• Incoherence: pattern of speech that is essentially incomprehensible

at times

• Echolalia: feature of dementia. This is a repetitive pattern of speech

in which a patient echoes words or phrases said by the interviewer.

• Neologisms: found mainly in schizophrenia and structural brain

disease (see b p. 261). New words are invented that have no

meaning.

• Circumstantiality: a long-winded pattern of speech loaded down

with unnecessary detail and digression before ﬁ

nally getting to

the point. The patient is, however, able to maintain their train of

thought.

CHAPTER 15 Psychiatric assessment460

Phobias represent a fear or anxiety that is out of proportion to the

situation, cannot be reasoned or explained away, and leads to avoidance

behavior.

Other types of ruminations particularly important to establish here

include suicidal or homicidal thoughts, in addition to morbid ideation (e.g.,

ideas of guilt, unworthiness, burden, and blame).

Abnormal beliefs

Overvalued ideas

These are isolated beliefs that are not obsessive in nature and preoccupy

an individual to the extent of dominating their life. That is, the patient is

able to stop thinking about them, but they choose not to.

The core belief of anorexia nervosa—the belief that one is fat—is an

example of an overvalued idea. Other examples include unusual sect or

cult beliefs, forms of morbid jealousy, and hypochondriasis.

Delusions

These are ﬁ xed false beliefs based on an incorrect inference about reality,

not consistent with a patient’s intelligence and cultural background (see

Box 15.8 ). Importantly, these cannot be corrected by reasoning. They can

sometimes be difﬁ cult to differentiate from overvalued ideas. The differ-

ence is that the patient ﬁ rmly believes the delusion to be true.

Box 15.8 Some examples of delusions and associated

terminology

• Mood-congruent delusion: a delusion with content that has an

association to mood. For example, a depressed person may believe

that the world is ending.

• Mood-incongruent delusion: a delusion with content that has no

association to mood. This is seen in schizophrenia.

• Nihilistic delusion: a false feeling that self, others, or the world is

nonexistent or coming to an end

• Paranoid delusion: any delusion that is self-referential. In psychiatry,

paranoid does not carry the lay meaning of fearful or suspicious.

• Delusions of reference: a false belief that others are talking about

you or that events are somehow connected with you. For example,

the patient may believe that people on TV or the radio are actually

talking directly to them. The feelings and delusional messages

received are usually negative in some way, but the fact that the

patient alone is being spoken to has a grandiose quality.

• Delusion of grandeur: an exaggerated perception of one’s importance,

power, or identity. Usually, patients believe they have made an

important achievement that has not been suitably recognized.

• Delusions of control: a false belief that a person’s will, thoughts,

or feeling are being controlled by external forces. These include

disorders of the possession of thought.

MENTAL STATUS EXAMINATION

461

Delusions may be primary with no discernable connection with any pre-

vious experience or mood (characteristic of schizophrenia) or secondary

to an abnormal mood state or perception. In this way, the content of the

delusions can give a clue to the nature of the mental illness.

Perception

Alteration in normal perception consists of changes to our normal, famil-

iar awareness or ordinary experiences. These include sensory distortions

(heightened or dulled perception), sensory deceptions (illusions and halluci-

nations), and disorder of self-awareness (depersonalization, derealization).

Disorders of self-awareness

• Depersonalization is the feeling that the body is strange and unreal.

• Derealization is the perception of objects in the external world as

being strange end unreal.

Both of these phenomena commonly occur in stressful situations, with

drug intoxication, anxiety, depressive disorders, and in schizophrenia.

Many psychologically normal people can experience an element of dereal-

ization or depersonalization if sleep deprived.

Box 15.8 (Con’d.)

•

Thought broadcasting: the false belief that the patient’s thoughts

can be heard by others

•

Thought insertion: the belief that an outside force, person, or

persons are putting thoughts in the patient’s mind. Thought

withdrawal is the belief that thoughts are being removed.

•

Thought echo: thoughts being heard spoken aloud

•

Thought blocking: the experience of having one’s train of thought

halted

• Passivity feelings: examples of delusions of control. They may include

made acts and impulses, where the individual feels they are being

made to do something by another, made movements, where patients

believe their limbs are controlled by someone else, made emotions,

where they are experiencing someone else’s emotions.

• Erotomania: a belief that another person is in love with the patient.

Patients often believe that innocent glances from another person

have a deeper, sexual meaning.

• Capgras delusion

1

: belief that those around you (often loved ones)

have been removed and replaced with exact replicas. Patients exist

in a world of impersonators. The delusion may extend to animals

and objects. Patients may believe that they are their own double.

• Religious delusions: any delusions with a religious or spiritual content.

0 Be careful here! Beliefs considered normal for a person’s religious

or cultural background (e.g., a Christian believing that God has cured

their illness) are not classed as delusions.

1

Capgras JMJ, Reboul-Lachaux J (1923). L’illusion des ‘sosies’ dans un délire systématisé

chronique. Bulletin de la Société clinique de médecine mentale 11:6–16.

CHAPTER 15 Psychiatric assessment462

Illusions

An illusion is a misperception or misinterpretation of real sensory stimuli. It

may affect any sensory modality. Inquire as to when they occur and what

signiﬁ cance they have.

Illusions frequently arise from a sensory impairment, such as partial

sightedness or deafness, and represent an understandable attempt at ﬁ lling

in the gap. Most people have experienced some form of visual illusions—

for example, mistaking a distant object for a person, particularly in poor

lighting (e.g., at night).

Hallucinations

Hallucination is a false perception that is not based on a real external

stimulus. It is experienced as true and coming from the outside world.

They may occur in any sensory modality, although visual and auditory

hallucinations are most common ( Box 15.9 ).

Importantly, not all hallucinations point to psychiatric disease. For

example, some hallucinations occur in normal people when falling asleep

(hypnagogic) or on waking (hypnopompic), and although the nature of

dreams is heavily debated, it could be said that they are hallucinations.

Note also the Charles Bonnet syndrome ( Box 15.10 ).

Sensory distortions

This includes heightened perception with especially vivid sensations (e.g.,

hyperacusis), dulled perception, and changed perception. For example,

patients may experience objects as having a changed shape, size, or color.

Box 15.9 Some examples of hallucinations

• Auditory hallucinations: false perception of sounds, usually voices,

but also other noises such as music. The hallucination of voices

may be classed as second person, where the voice is speaking to the

patient (“you should do this”) or third person, where the voice or

voices are talking about the patient (“he should do this”).

• Visual hallucinations: false perceptions involving both formed (e.g.,

faces, people) and unformed (e.g., lights, shadows) images

• Scenic or panoramic hallucinations: a form of visual hallucination

involving whole scenes, such as battles

• Olfactory hallucinations: the false perception of odors

• Gustatory hallucinations: the false perception of taste

• Tactile hallucinations: the false perception of touch or surface

sensation (e.g., phantom limb; crawling sensation in or under skin in

delirium tremens—formication)

• Somatic hallucination: the false sensation of things occurring in or to

the body, most often visceral in origin. Somatic hallucinations include

haptic (touch, tickling, pricking), thermic (heat/cold), and kinathetic

(movement and joint position).

• Pseudohallucinations: These are recognized as not being real by the

patient, acquiring an as-if quality, and have some degree of voluntary

control.

MENTAL STATUS EXAMINATION

463

Cognitive function

Cognition can be described as the mental processes of appraisal, judgment,

memory, and reasoning. Evaluation of cognitive functioning is important

for detecting impairment, following the course of an illness, and monitor-

ing improvement or response to treatment.

The Mini-Mental State Examination (MMSE)

The MMSE provides a brief quantitative measure of cognitive func-

tioning and can be used in both a psychiatric or general medical set-

ting. It tests attention, orientation, immediate and short-term recall,

language, and the ability to follow verbal and written commands (see

Box 15.11 ).

Notes on conducting the MMSE

It is important to remember that there are no half marks in this test—be

strict and rigorous. The maximum total score is 30.

• Orientation: Rather than asking for each part of the date in turn, ask

the patient for today’s date and then ask speciﬁ

cally for those parts

omitted. Do the same for place (“where are we now?”).

• Registration: Say the name of the objects clearly and slowly, allowing

about 1 second to say each. The ﬁ

rst repetition determines the

patient’s score, but keep repeating the names of the object until the

patient has got all three, to enable testing of recall later.

• Attention and calculation: If the patient can’t perform this

mathematical task, ask them to spell the word WORLD

backward.

The score is the number of letters in the correct order

(e.g., dlrow = 5, dlorw = 3).

Box 15.10 Charles Bonnet syndrome

This is a good example of hallucinations in a psychiatrically normal

patient. In this syndrome, patients with some kind of visual impair-

ment (usually older people) see visual hallucinations within the area of

impaired vision. The hallucinations are often cartoon-like characters or

faces. For example, the authors once came across a patient with a visual

scotoma due to retinal injury. The voice of our Irish consultant would

trigger the hallucination of a leprechaun dancing and cavorting within

their blind spot.

The syndrome is also an example of pseudohallucination, as often the

patient realizes that the visions are not real.

It was ﬁ rst described by the Swiss philosopher Charles Bonnet in

1760, whose 87-year-old grandfather admitted seeing visions of buildings

and people after developing severe cataracts in both eyes.

Charles Bonnet syndrome is likely much more common than most

medical people realize. Older sufferers are often afraid to admit to it,

for fear of being diagnosed with a psychiatric disorder or being labeled

“Insane.”

CHAPTER 15 Psychiatric assessment464

• Repetition: Allow one trial. Score 1 only if the repetition is completely

correct. Make sure you say it slowly and clearly so that the patient can

hear!

• Three-stage command: Say all three stages of the command before

giving the piece of paper to the patient. Do not prompt the patient as

you go. Score 1 point for each part conducted correctly.

• Reading: Say “read this sentence and do what it says.” Score 1 point if

the patient closes their eyes, no points if they simply read the sentence

out loud.

• Writing: Be sure not to dictate a sentence or give any examples. The

sentence must make sense and contain a subject and a verb. Correct

grammar, punctuation, and spelling are not necessary.

• Copying: All 10 angles must be present, and 2 must intersect. Ignore

mistakes from tremor and ignore rotation of the diagram.

Interpreting the ﬁ nal

score

The MMSE score will vary within the normal population by age and number

of years in education (decreasing with advancing age and increasing with

advanced schooling). The median score is 29 for people with 9 years of

education, 26 for 5–8 years of education, and 22 for 0–4 years.

1

Box 15.11 Mini-Mental State Examination (MMSE) Sample

Items

Orientation to time

“What is the date?”

Registration

“Listen carefully. I am going to say three words. You say them back after

I stop. Ready? Here they are…

APPLE (pause), PENNY (pause), TABLE (pause). Now repeat those

words back to me.” [Repeat up to 5 times, but score only the ﬁ rst

trial.]

Naming

“What is this?” [Point to a pencil or pen.]

Reading

“Please read this and do what it says.” [Show examinee the words on

the stimulus form.]

CLOSE YOUR EYES

Reproduced by special permission of the Publisher, Psychological Assessment Resources, Inc.,

16204 North Florida Avenue, Lutz, FL 33549, from the Mini Mental State Examination, by Marshal

by Psychological Assessment Resources, Inc. Further reproduction is prohibited without permis-

sion of PAR, Inc. The MMSE can be purchased from PAR, Inc. by calling (813) 968-3003.

MENTAL STATUS EXAMINATION

465

As a rule of thumb, scores of <23 are taken to indicate mild, <17 mod-

erate, and <10 severe cognitive impairment. This is a nonlinear scale, how-

ever. For more information, see Crum et al. (1993).

1

Insight

This is how well the patient is able to understand or explain their condi-

tion. When assessing insight, ask the following questions:

• Do they recognize and accept that they are suffering from a mental or

physical illness?

• Are they willing to accept treatment and agree to a management plan?

Note also whether an individual’s attitudes are constructive or uncon-

structive, realistic or unrealistic.

If not accepting of a psychiatric diagnosis, to what does the patient

attribute their difﬁ

culties or abnormal experiences?

Summary

At the end of the assessment, a summary should be made of history and

mental state examination, which should encompass a statement of diagno-

sis or differential diagnosis, etiolgical factors, and a plan for further inves-

tigations and management.

1

Crum RM, Anthony JC, Bassett SS, Folstein MF (1993). Population-based norms for the Mini-

Mental State Examination by age and educational level, JAMA 18:2386–2391.

CHAPTER 15 Psychiatric assessment466

Physical examination

A full physical examination, particularly that of the neurological system

should be seen as an integral part of the assessment of a psychiatric

patient.

You may want to tailor an examination to look for, or exclude, physical

conditions that give rise to the psychiatric symptoms and signs that you

have discovered. See the end of this chapter for details.

IMPORTANT PRESENTING PATTERNS

467

Important presenting patterns

Schizophrenia

The term schizophrenia * is often described as a single disease, but the

diagnostic category includes a group of disorders, probably with hetero-

geneous causes, but with somewhat similar behavioral symptoms and

signs ( Box 15.12 ). It is a psychosis, characterized by splitting of normal

links between perception, mood, thinking, behavior, and contact with

reality.

The prevalence of schizophrenia is 70.5% worldwide, with equal

incidence in both sexes. The onset is usually in adolescence or early

adulthood. Symptoms tend to remit, although a return to baseline is

unusual.

Clinical features

Schizophrenia is characterized by delusions and hallucinations with no

insight. These symptoms are often followed by a decline in social func-

tioning. Historically, several different diagnostic classiﬁ cations have been

developed. For the latest diagnostic criteria, see the ICD-10 or DSM-IV or

DSM-V (due in 2012).

Bleuler’s four A’s

In 1910, Bleuler coined the term schizophrenia . He went on to characterize

the key features, summarized as the four A’s.

• Associative loosening (disconnected, incoherent thought process)

• Ambivalence (the ability to experience two opposing emotions at the

same time—e.g., loving and hating a person)

• Affective incongruity (affect disassociated with thought)

• Autism (self-absorption and withdrawal into a fantasy world)

Box 15.12 Subtypes of schizophrenia

• Simple: Negative symptoms tend to predominate.

• Paranoid: Delusions and hallucinations are prominent and tend to

include religious, grandiose, and persecutory ideas.

• Hebephrenic: Affective incongruity predominates, with shallow range

of mood. Delusions and hallucinations tend to lack an organized

theme.

• Catatonic: Anhedonia, avolition, alogia, and poverty of movement

are the key features. This may lead to a “waxy ﬂ

exibility,” where the

patient’s limbs can be moved into, and stay in, certain positions.

* Schizophrenia comes through Latin from the Greek skhizein, “to split” and phren, “mind.” The

term phrenic refers also to the diaphragm. This is because in ancient Greece, the mind was thought

to lie in the diaphragm.

CHAPTER 15 Psychiatric assessment468

Crow’s positive and negative symptoms

In 1980, Crow

1

suggested that the symptoms of schizophrenia could be

divided into two distinct groups—those that are positive and those that

are negative. This remains a useful way to think of the symptoms.

Crow went on to suggest that schizophrenia could be split into two syn-

dromes, comprising mostly positive or negative symptoms, respectively.

Positive symptoms

• Delusions (including ideas of reference)

• Hallucinations

• Thought disorder

Negative symptoms

• Blunted affect

• Anhedonia (lack of enjoyment)

• Avolition (lack of motivation)

• Alogia (poverty of speech)

• Social withdrawal

• Self-neglect

Schneider’s ﬁ rst-rank

symptoms

Kurt Schneider listed his ﬁ rst-rank symptoms of schizophrenia in 1959

2

.

One of these, Schneider said, is diagnostic of schizophrenia in the absence

of organic brain disease or drug intoxication.

• Third-person auditory hallucinations (running commentary, arguments,

or discussions about the patient)

• Thought echo, or “echo de la pensée”

• Disorders of thought control (withdrawal, insertion, broadcast)

• Passivity phenomena

• Delusional perception

• Somatic passivity

Schneider’s criteria have been criticized for being too narrow, providing a

snapshot of a patient at only one time, and for not taking into account the

long-term negative symptoms.

For information on etiology, treatment, and prognosis, see appropriate

other Handbooks in this series.

Delirium

Delirium , or acute confusional state, is a transient global disorder of cog-

nition that is characterized by an acute onset and a ﬂ uctuating course.

It represents one of the most important and misdiagnosed problems in

medicine and surgery (see Box 15.13 for assessment).

Delirium may occur in as many as 10–20% of hospital inpatients, with

elderly patients being the most vulnerable. Approximately 60% of patients

suffer delirium following hip fracture.

1

Crow TJ (1980). Molecular pathology of schizophrenia: more than one disease process? BMJ

280:66–68.

2

Schneider K (1959). Clinical Psychopathology. New York: Grune and Stratton.

IMPORTANT PRESENTING PATTERNS

469

Following is a brief summary of the main features and causes. You should

bear all the possible causes in mind and tailor your physical examination

and investigations accordingly (see Chapter 10).

Predisposing factors (risk factors)

• Increasing age

• Pre-existing cognitive defect

• Psychiatric illness

• Severe physical comorbidity

• Previous episode of delirium

• Deﬁ

cits in hearing or vision

• Anticholinergic drug use

• New environment or stress

Causes (precipitants)

Delirium is usually multifactorial, with a single cause being difﬁ cult

or

impossible to identify. Some factors include the following:

Intracranial factors

• Trauma

• Vascular disease (e.g., stroke)

• Epilepsy and postictal states

• Tumor

• Infection (meningitis, encephalitis, tuberculosis, neurosyphilis)

Extracranial factors

• Drugs—both prescribed and recreational, intoxication, and withdrawal

• Electrolyte imbalances

• Infection (e.g., urinary tract, chest, septicemia)

• Endocrine (e.g., thyroid dysfunction, hypo- and hyperglycemia)

• Organ failure (heart, lung, liver, kidney)

• Hypoxia

• Acid–base disturbance

Box 15.13 Confusion assessment method (CAM)

This is method is commonly used to assess delirium in the clinical set-

ting.

1

The patient must display both features 1 and 2 plus either 3 or 4.

• 1 Acute onset and ﬂ uctuating course:

often best obtained from a

relative or member of the ward staff. Onset is hours to days, lucid

periods are often in the morning.

• 2 Inattention: easily distracted, attention wanders in conversation

• 3 Disorganized thinking: rambling or irrelevant conversation, illogical

ﬂ

ow of ideas, unable to maintain a coherent stream of thought

•

4 Altered level of consciousness: drowsy or over active, may

ﬂ uctuate. May experience nightmares and hallucinations.

1

Inouye S, van Dyck C, Alessi C, et al. (1990). Clarifying confusion: the confusion assessment

method. Ann Intern Med 113(12):941–948

CHAPTER 15 Psychiatric assessment470

• Nutritional deﬁ ciencies

• Postoperative or postanesthetic states

• Miscellaneous

•

Sensory deprivation

•

Sleep deprivation

•

Fecal impaction

•

Change of environment

Symptoms

• Fluctuating level of consciousness

• Difﬁ culty maintaining, or frequently shifting, attention

• Disorientation (often worse at night)

• Illusions

• Hallucinations (often simple, visual)

• Apathy

• Emotional lability

• Depression

• Disturbance of the normal sleep–wake cycle

Differential diagnosis

• Dementia (often coexists with delirium and i risk of delirium 2- to

3-fold), depression, psychosis, AIDS-related complex

Anxiety disorders*

Generalized anxiety disorder (GAD)

The main feature is excessive anxiety and worry about events or activities

that the patient ﬁ nds difﬁ cult to control, such as work or school perfor-

mance. The symptoms must be present for more than 6 months and

include three or more of the following:

• Restlessness or feeling on edge

• Easily fatigued

• Difﬁ

culty concentrating or mind goes blank

• Irritability

• Muscle tension

• Sleep disturbance (insomnia and fatigue on waking)

Panic disorder

This involves spontaneous occurrence of severe panic attacks (periods of

fear that peak within

10 minutes).

These should be accompanied by four or more of the following: tachy-

cardia, sweating, trembling or shaking, shortness of breath, a feeling of

choking, chest pain, dizziness, lightheadedness or presyncope, paresthesia,

depersonalization or derealization, nausea, abdominal pain, fear of dying,

fear of losing control, and hot ﬂ ushes.

Phobic disorders

A phobia is an irrational fear that produces an avoidance of the subject of

the fear (an object, person, activity, or situation). A phobia is perceived by

the patient as excessive (i.e., they have insight).

* Based on DSM-IV criteria.

IMPORTANT PRESENTING PATTERNS

471

Agoraphobia

†

is not fear of wide open spaces per se, as is commonly

thought, but is anxiety caused by being in places or situations from which

escape may be difﬁ cult or in which help might not be available in the event

of a panic attack. These situations may include being outside, being home

alone, being in a crowded place, or traveling on a bus or train.

Social phobia

This is a fear of social situations in which the person is exposed to unfa-

miliar people or to possible scrutiny by others. The fear is of the resulting

humiliation caused by a poor performance.

Avoidance behavior, anticipation, or distress at the time of the social

encounter leads to impairment in functioning at work or in school and can

have a signiﬁ cant impact on the patient’s life.

Other speciﬁ c phobias

These are marked and persistent fears cued by the presence or anticipa-

tion of speciﬁ c objects or situations. The list is manifold. Our favorites,

from which no medic can suffer, include bromidrosiphobia (the fear of

body odor), spermophobia (the fear of germs), belonephobia (the fear

of needles), phronemophobia (the fear of thinking), iatrophobia (the fear

of doctors), and, of course, pinaciphobia (the fear of lists).

Obsessive-compulsive disorder (OCD)

This is characterized by time-consuming obsessions or compulsions that

cause social impairment or mental distress.

Obsessions are intrusive thoughts, feelings, ideas, or sensations. They are

recognized by the patient as their own (compare with thought insertion)—

the patient usually tries to ignore or suppress them.

Compulsions are conscious, purposeful behaviors through which the

person attempts to neutralize or prevent a discomfort or dreaded event.

Examples include repeated hand-washing, checking, and counting.

The key here is that the obsessions and compulsions are recognized as

coming from within the patient, and the patient feels powerless to stop

and is distressed by their presence. Severe obsessions and compulsions

can occur in depression, schizophrenia, generalized anxiety disorder, panic

disorder, and other disorders.

Dementia

Dementia is usually a disease of older people and refers to a global dete-

rioration of higher mental functioning, without impairment in conscious-

ness, that is progressive and usually irreversible.

Dementia usually presents with a history of chronic, steady decline in

short- and long-term memory and is associated with difﬁ culties in social

relationships, work, and activities of daily living. Important manifestations

include disruption of language and intelligence as well as changes in per-

sonality and behavior. Apathy, depression, and anxiety are frequently

found, and psychotic phenomena may be seen in a third of patients.

†

Agoraphobia comes from the Greek agora, meaning “the marketplace.”

CHAPTER 15 Psychiatric assessment472

A diagnosis of dementia is based on MMSE results and information from

other sources, such as the patient’s family, friends, and employers.

Dementia may be primary or secondary to diseases:

• Chronic CNS infection: HIV, syphilis, meningitis, encephalitis

• CNS trauma: anoxia, diffuse axonal injury, dementia pugilistica

(repeated head injury—seen in boxers), chronic subdural hematoma

• i Intracranial pressure: neoplasia, hydrocephalus

• Toxins: heavy metals, organic chemicals, chronic substance abuse

• Vitamin deﬁ

ciencies: B

12

, folate

• Autoimmune disease: SLE, temporal arteritis, sarcoidosis

Other possible causes include endocrinopathies, Wilson’s disease, and

lipid storage diseases.

Alzheimer’s disease

The key pathological changes in Alzheimer’s disease (AD) are decreased

brain mass and increased size of the ventricles. There is neuronal loss and

occurrence of amyloid plaques and neuroﬁ

brillary tangles. AD makes up

7

50% of all cases of dementia and 790% of all primary dementias. The main

features are memory impairment and at least one of the following:

• Aphasia (b p. 260)

• Apraxia (b p. 328)

• Agnosia (b p. 327)

• Abnormal executive functioning (planning, organizing, abstracting,

sequencing)

Vascular dementia/multi-infarct dementia

This makes up about 20–30% of all cases of dementia. Onset may be abrupt

and/or with a stepwise decline. Vascular dementia is associated with more

patchy cognitive impairment then AD, often with focal neurological signs

and symptoms such as hyperreﬂ

exia, extensor plantar responses, pseu-

dobulbar, bulbar, or other cranial nerve palsies, gait abnormalities, and

focal weakness.

The primary pathology is multiple small areas of infarction (cortex and

underlying white matter). It is important to note vascular risk factors such

as previous stroke, hypertension, heart disease, diabetes, and smoking.

Lewy body dementia

Lewy body dementia accounts for up to 20% of all cases. Patients with this

disorder show features similar to AD but also often have recurrent visual

hallucinations, ﬂ uctuating cognitive impairment, parkinsonian features, and

extrapyramidal signs.

Frontotemporal dementia

This accounts for 5% of all dementia. Pick’s disease is a form of frontotem-

poral dementia characterized by the presence of neuronal Pick’s bodies

(masses of cytoskeletal elements).

The predominance of frontal lobe involvement is evidenced by pro-

found personality changes, social impairment, and stereotyped behavior.

However, visuospacial skills are usually preserved. The patient may also

show primitive reﬂ exes (b p. 307).

IMPORTANT PRESENTING PATTERNS

473

Huntington’s disease

Huntington’s is an autosomal dominant disease presenting as early as the

third decade and is associated with a subcortical type of dementia. Apart

from the movement disorder showing involuntary choreiform movements

of the face, shoulders, upper limbs, and gait, the symptoms of the demen-

tia include psychomotor slowing and personality alteration with apathy

or depression.

Parkinson’s disease

Patients with Parkinson’s disease have cognitive slowing along with the

signs described earlier (b p. 325). Dementia is seen in later stages of

disease.

Creutzfeldt–Jakob disease (CJD)

Contrary to common perception, this is not a new disease or one that

affects young people. The most frequently seen of this family of diseases

is sporadic CJD, which has no known cause. Onset is usually between the

forth and sixth decades of life and is associated with a very rapid progres-

sion of dementia, in addition to signs such as myoclonus, seizures, and

ataxia—the time to death is typically a few months.

Variant CJD (vCJD) is a disease mainly conﬁ ned to the UK, ﬁ rst reported

in 1996, and is thought to have resulted from transmission of infection

from cattle suffering from bovine spongeiform encephalopathy (BSE). The

average age of onset is 27 years, presenting initially with behavioral symp-

toms. The duration is of a year or more.

Affective disorders

Bipolar disorder

Bipolar disorder, previously known as manic-depression, is usually charac-

terized by periods of deep, prolonged depression with periods of exces-

sively elevated and irritable mood, known as mania .

It is important to note that patients presenting only with mania, and

no evident depression, are said to have bipolar disorder. There are three

main patterns of disease:

• Bipolar I disorder : one or more episodes of major depression with

episodes of mania

• Bipolar II disorder: milder bipolar disorder consisting of recurrent

periods of depression and hypomania but no manic episodes

• Cyclothymic disorder: characterized by frequently occurring hypomanic

and depressive symptoms that do not meet the diagnostic criteria of

manic episodes or major depression

Mania

Manic episodes are characterized by profound mood disturbance, consist-

ing of an elevated, expansive, or irritable mood that causes impairment at

work or danger to others ( Box 15.14 ). These patients may suffer delusions

and hallucinations, the former usually involving power, prestige, position,

self-worth, and glory. The key feature is disinhibition.

CHAPTER 15 Psychiatric assessment474

There may be several of the following:

• Inﬂ

ated self-esteem or grandiosity

• Reduced need for sleep

• Racing thought, ﬂ

ight of ideas, and distractibility

• Excessive talking or pressured speech

• i Level of goal-focused activity at home, at work, or sexually

• Psychomotor agitation

• Excessive involvement in pleasurable activities, often with unfortunate

consequences (especially sexual indiscretions, unrestrained spending)

Box 15.14 Typical mental state examination in affective

disorders

Mania

• Appearance: bright, colorful, or garish clothing, hyperactivity,

hypervigilance, restlessness

• Speech: fast, pressured, ﬂ ight of ideas

•

Mood and affect: joy, elation, jubilance, euphoria, annoyance,

irritability

• Thought content: expansive and optimistic thinking, excessively self-

conﬁ

dent or grandiose, distractible, rapid production of ideas and

thoughts

•

Perception: mood-congruent and mood-incongruent delusions.

Fleeting auditory or, more rarely, visual hallucinations. Delusions of

wealth, power, inﬂ

uence, or religious signiﬁ cance

•

Cognitive functioning: usually unaffected

• Insight: seriously impaired judgment and no insight

Depression

• Appearance: reduced eye contact, poor grooming and hygiene,

change in weight, psychomotor agitation, or retardation

• Speech: slow, monotonous, or lacking in spontaneity

• Mood and affect: sadness, numbness, irritability, anhedonia, reduced

concentration, loss of energy, and motivation

• Thought content: preoccupied with negative ideas and nihilistic

concerns, overwhelmed or inadequate, helpless, worthless, hopeless,

suicidal

• Perception: delusions and hallucinations (usually mood congruent),

especially second-person auditory hallucinations. For example,

auditory hallucinations of voices call the patient worthless.

• Cognitive functioning: poor memory and concentration but level of

consciousness is normal. Depressed patients may score falsely low

on an MMSE if they are not willing to answer the questions (“I don’t

know”)—pseudodementia.

• Insight: diminished judgment and insight

IMPORTANT PRESENTING PATTERNS

475

Depression

Depressive disorders can be classiﬁ ed as bipolar or unipolar and as mild,

moderate, or severe. They may include somatic symptoms and psychotic

symptoms (delusions and hallucinations that are usually mood-congruent)

in the case of severe depression.

The diagnostic criteria, treatment, and prognosis can be found in the

Oxford Handbook of Psychiatry . Depression can cause signiﬁ cant social

impairment and distress.

In general terms, features of major depression include the following:

• Depressed mood with feelings of worthlessness

• Diminished interest or pleasure (anhedonia)

• Signiﬁ

cant weight loss or gain

• Insomnia or hypersomnia

• Psychomotor agitation or retardation

• Fatigue or loss of energy

• Diminished ability to think or concentrate; indecisiveness

• Recurrent thoughts of death, suicide, suicide attempts, or speciﬁ c

plans

for suicide

Hypomania

Hypomanic episodes are characterized by a persistently elevated, expan-

sive, or irritable mood with features similar to mania. However, the

episode is not severe enough to cause marked impairment in social or

occupational functioning, and delusions and hallucinations do not occur.

CHAPTER 15 Psychiatric assessment476

Medical conditions with psychiatric

symptoms and signs

There are many medical conditions that can produce psychiatric clinical

features. This can sometimes lead to failure of the underlying medical

condition to be recognized and treated appropriately. It is important in

psychiatry to consider possible organic causes for the symptoms and signs

before starting psychiatric treatment. Further, many medical disorders are

associated with psychiatric diagnoses.

The following is a sample of such situations, aimed at illustrating the

above points, rather than providing an exhaustive list.

Neurological disorders

Seizure disorder

• Ictal events, including status epilepticus, may mimic psychosis.

• Automatisms are seen in some temporal lobe seizures.

• The preictal prodrome can involve changes in mood, particularly

irritability, and auras (including auditory and olfactory hallucinations)

can be seen in temporal lobe epilepsy. These may also include

epigastric sensations, déja vu or jamais vu .

• The postictal state often involves confusion and disorientation.

Parkinson’s disease

• Patients may suffer from major depression, anxiety syndromes,

hallucinations, and delusions.

Brain tumors and cerebrovascular events (depend on location)

• Frontal: personality change, cognitive impairment, motor and language

disturbance

• Dominant temporal lobe: memory and speech impairment, Korsakoff

psychosis in bilateral lesions

• Occipital lesions: visual agnosis, visual hallucinations

• Limbic and hypothalamic: affective symptoms, rage, mania

Multiple sclerosis (MS)

• Cognitive deﬁ

cits, dementia, bipolar disorder, major depression

Infectious diseases

• Neurosyphilis: primarily affects the frontal lobe (irritability, poor self-

care, mania, progressive dementia)

• Meningitis: especially with indwelling shunts, can cause acute

confusion, memory impairment

• Herpes simplex encephalitis: bizarre and inconsistent behavior,

seizures, anosmia, hallucinations (olfactory and gustatory), psychosis

• HIV encephalitis: progressive subcortical dementia, major depression,

suicidal behavior, anxiety disorders, abnormal psychological reactions

Endocrine disorders

• Hyperparathyroidism: delirium, sudden stupor and coma. Visual

hallucinations with associated hypomagnesaemia

477

MEDICAL CONDITIONS WITH PSYCHIATRIC SYMPTOMS: SIGNS

• Hypoparathyroidism: psychosis, depression, anxiety

• Hyperthyroidism: depression, anxiety, hypomania, psychosis

• Hypothyroidism: depression, apathy, psychomotor retardation, poor

memory, delirium and psychosis myxoedema madness

Rheumatological disorders

• Systemic lupus erythematosus (SLE): delirium, psychosis, severe

depression

Metabolic disorders

• Hyponatraemia: confusion, depression, delusions, hallucinations,

seizures, stupor, coma

• Hypernatremia: acute changes of mental state

• Encephalopathy

• Uremia encephalopathy: memory impairment, depression, apathy,

social withdrawal

Vitamin deﬁ ciencies

• B

1

(thiamine): asthenia, fatigue, weakness, depression

• B

12

(cyanocobalamin): impaired cognitive function

This page intentionally left blank

479

Pediatric assessment

History-taking 480

Examination: an approach 482

Respiratory system 484

Ear, nose, and throat 488

Cardiovascular system 490

Abdomen and gastrointestinal system 493

Palpation 495

Nervous system 497

Developmental assessment 500

The newborn 502

Chapter 16

CHAPTER 16 Pediatric assessment480

History-taking

Children and providers

The specialty of pediatrics is very different from adult medicine. Children

grow, change, and mature. Your style and approach to history-taking and

examination will depend greatly on the child’s age, independence, and

understanding, so ﬂ exibility is essential. The most important thing to

remember during your time as a provider is that pediatrics should be

pleasurable.

An approach to the child patient

The child needs to be put at ease and made to feel welcome.

• Make a complimentary remark, or show them an interesting toy. The

fascination of how to turn on a tuning fork can amaze many children.

• Tell the child your name, and ask theirs.

• Make friends with them by asking what their favorite class is at school

or what they had for breakfast.

• Shake hands with children—even toddlers may enjoy this formality.

History

A structured approach to history-taking is important to keep from for-

getting things, but avoid excessive rigidity, as it is sometimes necessary

to pursue a different line of questioning to gain essential information.

Box 16.1 is a list of useful headings in pediatric history-taking that should

be memorized to avoid missing essential information.

Talking to the child

Ask the child to give their account of events with parental corrobora-

tion. Children under 5 years old may lack the vocabulary to describe their

symptoms but will be able to point to parts that hurt. Sometimes it is

important to quiet the eager parent to hear from the patient!

Talking to parents

Most of the history is likely to be gained from the parents or guardians.

First conﬁ rm the relationship of the history provider.

• Ask if they have an infant medical record book—this contains

information about height and weight percentiles, immunizations,

development, and illnesses in the ﬁ

rst few years of life.

• Ask if they have any views on what the cause of the child’s trouble is.

Listen carefully to the parents; they are the observer of their child.

• Ensure that all terms used are appropriately deﬁ ned—you

should

be gleaning information from the parents’ observations and not

their

interpretation of the symptoms.

For example, the word wheeze is often used incorrectly; sometimes a

demonstration can be helpful. Further, the parent may interpret a baby’s

cries as pain, when, in fact, it is your task to establish the circumstances of

the cries and thus the cause.

As children get older, parents may have a hazy memory for early events.

Establishing symptoms in relation to easily remembered events (e.g. ﬁ rst

walked) may clarify the timeline.

HISTORY-TAKING

481

“You can do anything with children if you only play with them.”

—Otto von Bismarck, 19th century

Box 16.1 Outline of pediatric history

• Presenting complaint and history of presenting complaint

• Birth history

•

Place of birth

•

Gestation and pregnancy

•

Birth weight

•

Delivery

•

Perinatal events and subsequent hospital course

• Feeding methods and weaning

•

If the child is bottle fed, note how the formula is mixed (how

many scoops or number of ounces).

• PMH, including hospital admissions, infections, injuries

• Developmental history

• School progress

• Immunizations

• Drugs

• Allergies

• Family tree with sibling’s ages, including deaths, miscarriages, and

stillbirths

• Parental age and occupation

• Family illnesses and allergies

• Housing

•

Include a discussion about the child’s bedroom, with furnishings, as

they may spend 12 hours of each day there.

• Travel

• Systems review

“You can do anything with children if you only play with them.”

—O

tto von Bismarck, 19th century

CHAPTER 16 Pediatric assessment482

Examination: an approach

Examination of children varies depending on the age and cooperation

of the child (see also Box 16.2 ). School-age children and babies may be

examined on an exam table with a parent nearby, whereas toddlers may

be best examined on the parent’s lap ( Box 16.3 ). If the child is asleep on

the parent’s lap, much of the examination should be completed before

waking them.

Undressing

Let the parent undress the child, and only expose the part of the body

you will be examining.

Positioning

Some children may prefer to be examined standing up. Only lay the child

down when you have to, as this can be very threatening.

Putting the child at ease

Slowly introduce yourself to the child’s space during the examination by

exchanging toys, for example.

Explain what you are going to do and be repeatedly reassuring, children

can be embarrassed by silence after a provider’s question but will be com-

forted by endless rambling. And remember—don’t ask permission, as this

will often be refused!

Examination

First, use a hands-off approach. Allow the child to look at you, and let

them play in your presence. Watch the child. How do they interact with

their parents? Do they look well or ill? Do they look clean, well nourished,

and well cared for?

Kneel on the ﬂ oor so that you are at the child’s level. Use a style and

language appropriate to the age of the child—a toddler will understand

the word tummy better than the word abdomen .

Box 16.2 Some distraction techniques to help examination

• Playing peek-a-boo

• Letting toddlers play with your reﬂ ex hammer or tuning fork

• Giving infants something to hold

• Asking mom or dad to wave a bright toy in front of the child

Box 16.3 The mother’s lap

1. Be cautious about taking any baby or young child to an exam table.

It is often better to leave them on their mother’s knee for most of

the examination.

2. Avoid taking a baby off their mother’s knee if they are beyond 7–8

months of age—this will invariably result in screaming.

EXAMINATION: AN APPROACH

483

Be opportunistic

Do not adhere to a rigid examination protocol—e.g., you may have to

listen to the heart ﬁ rst while the child is quiet, then look at the hands later.

Never examine the presenting part only. Be thorough and train yourself to

be a generalist ( Box 16.4 ).

Sometimes, demonstrating with a cooperative older sibling, parent, or a

stuffed toy may put a child more at ease about what is to be done.

Leave unpleasant procedures, such as examination of the ears and

throat, for last.

Presenting your ﬁ ndings

When presenting your ﬁ ndings, translate what you see into appropriate

terminology. Informing a colleague that a child “looks funny” is not very

helpful, but the saying that the child is dysmorphic, followed by a detailed

description is acceptable. Describe in simple terms the relevant features

that make the child look unusual, e.g., low-set ears, wide-set eyes.

2 There is no substitute for examining lots of normal children.

“Pediatrics is a specialty bound by age and not by system.”

—Apley

“Pediatrics is a s

p

ecialt

y

bound b

y

a

g

e and not b

y

s

y

stem.

”

—

Apley

Box 16.4 Using this chapter

The examination routines in this chapter describe the techniques

to employ and the signs to look for in each body system. For more

detailed information about how to perform certain aspects, the reader

should refer to the relevant organ system chapter elsewhere in this

book (e.g., how to perform accurate percussion, where to listen to

heart sounds, and so on).

CHAPTER 16 Pediatric assessment484

Respiratory system

Key points from the history

• Is the child short of breath or wheezy (remember to deﬁ ne terms)?

• Is there stridor or croup?

• Is there a cough? Does it disturb sleep?

• Does anything trigger the symptoms—sports, cold weather, pets?

• Has the child expectorated or vomited any sputum?

• Is the infant short of breath during breast or bottle feeding?

• Is there a possibility the child could have inhaled a foreign body?

• Is there a FH of respiratory problems, such as asthma or cystic ﬁ brosis?

• Does the child have a fever—suggestive of infection?

• Has anyone else been ill? Any contacts with tuberculosis?

• What’s happening at the child-care facility?

• Has the child traveled abroad recently?

• How does the respiratory problem limit the child’s life—how much

school is missed, can they participate in sports, how far can they run, is

sleep disturbed?

Examination

Inspection

Look around for any clues—is the patient on oxygen? Are there inhalers

or nebulizers at the bedside? Remember if mom or dad’s clothing smells

of tobacco, the child is breathing smoke too.

General inspection

• Is the child comfortable or in respiratory distress ( Box 16.5 )? Look for

the following:

•

Nasal ﬂ aring

•

Use of accessory muscles of respiration

•

Intercostal retractions (sucking in of the muscles between the ribs)

and subcostal retractions (drawing in of the abdomen)

•

Grunting (a noise at the end of expiration, which is the infant’s

attempt to maintain a positive end expiratory pressure)

• Is the child running around or just sitting on the parent’s knee?

• Are they restless or drowsy?

• Count the respiratory rate (see Table 16.1 ).

• Listen for wheeze or stridor (a harsh inspiratory sound caused by

upper airways obstruction).

• What type of cough does the child have ( Box 16.6 )?

Box 16.5 Pain

Children may complain of pain when they wish to indicate distress or

discomfort that their vocabulary will not allow. Remember also that

diseases may present differently in children than in adults. For example,

children may describe chest pain with chest tightness and asthma.

Pneumonia often produces abdominal pain in children.

RESPIRATORY SYSTEM

485

• Has the child coughed up any sputum? (Children under 5 years will

swallow sputum, which is often vomited after a bout of coughing.)

Hands

• Clubbing (cystic ﬁ brosis, bronchiectasis)

• Measure the radial pulse—pulsus paradoxus (Chapter 7, b p. 159) is

an important feature of acute, severe asthma in children.

Face

• Check the conjunctiva for anemia.

• Look for central cyanosis in the tongue.

• Look for petechiae (nonblanching spots from small burst blood

vessels) around the eyes from a prolonged bout of coughing.

Chest

• Look for chest movement. Is it symmetrical? Is the child splinting

(failing to move) one side of the chest?

•

Children who splint their chest as a consequence of pneumonia

often also have a slight spinal scoliosis.

• Look at the chest shape. Is there any chest wall deformity?

•

Harrison’s sulcus: permanent groove in the chest wall at the insertion

of the diaphragm in long-standing asthma

•

Barrel chest: air trapping in asthma

•

Pectus carinatum: “pigeon chest” seen in long-standing asthma Pectus

excavatum: normal variant

Table 16.1 Normal respiratory and heart rates, by age

Age (years) Heart rate (bpm) Respiratory rate

<1 120–160 30–60

1–3 90–140 24–40

3–5 75–110 18–30

5–12 75–100 18–30

12–16 60–90 12–16

Box 16.6 Some childhood coughs

The following factors may give important clues to origin of the cough:

• Productive: cystic ﬁ brosis, bronchiectasis, pneumonia

• Nocturnal: asthma, cystic ﬁ brosis

• Worse on wakening: cystic ﬁ brosis

• Brassy: tracheitis

• Barking: croup (laryngotracheobronchitis)

• Paroxysmal: pertussis, foreign body

• Worse during exercise: asthma

• Disappears when sleeping: habitual cough

• During or after feeding: aspiration

CHAPTER 16 Pediatric assessment486

Palpation

• Feel the neck for enlarged cervical lymph nodes.

• Palpate the trachea to ensure that it is midline.

• Then move onto the chest.

•

Feel for the apex beat. This may be displaced in effusion, collapse, or

tension pneumothorax.

•

Assess expansion (see b Chapter 8, p. 194), commenting on extent

and symmetry.

•

In young children, you may be able to feel crackles.

Percussion

Percussion is rarely useful in infants and toddlers. Remember to also per-

cuss for the normal cardiac dullness as well as the upper and lower bor-

ders of the liver.

• Dull = consolidation

• Hyperresonant = air-trapping or pneumothorax

• Stony dull = pleural effusion

Auscultation

0 Before using a stethoscope on the child, pretend to auscultate the

parent’s or an older sibling’s chest or a less vulnerable part of the child’s

body (e.g., their leg).

2 Remember to listen under the axillae as well as the anterior and

posterior chest wall.

2 Especially in young children, upper airway noises may be transmitted to

the chest, so if they are old enough, ask them to cough to clear them.

Listen for the following:

• Breath sounds

•

Are they vesicular (normal), absent, or bronchial?

• Added sounds (e.g., wheeze or crackles—see b Chapter 8, p. 198, for

more details) (see Table 16.2 for some associated conditions)

• Absent breath sounds in one area suggests a pleural effusion,

pneumothorax, or dense consolidation.

2 i Respiratory rate and work of breathing are the most important signs

of a lower respiratory tract infection in infancy, as sometimes palpation,

percussion, and auscultation will be normal.

RESPIRATORY SYSTEM

487

Table 16.2 Some common respiratory conditions and signs

Condition Age Inspection Auscultation

Bronchiolitis <1 year Pale, coryza,

cough, retractions,

tachypnea

Wheezes and

crackles throughout

chest

Croup (laryngo-

tracheobronchitis)

1–2 years Stridor, hoarse voice,

barking cough

Clear

Asthma >1 year Tachypnea,

retractions ± audible

wheeze and use of

accessory muscles

Wheeze, variable

air entry throughout

chest. Crackles in

young children

Pneumonia Infant Tachypnea,

retractions, ﬂ ushing

due to fever, grunting

May be clear,

reduced breath

sounds over affected

area, crackles

Pneumonia Child Tachypnea,

retractions, ﬂ ushed,

generally ill

Abdominal pain

(may be the only

symptom), crackles

and bronchial

breathing over

affected area

CHAPTER 16 Pediatric assessment488

Ear, nose, and throat

Ear, nose, and throat (ENT) conditions are a common reason for children

to present to the provider.

0 Examination of this system should be left until last, as many children

ﬁ

nd it unpleasant.

Key points from the history

• Does the child pull at their ears (suggests infection)?

• Does the child complain of an earache or a sore throat?

• Is there coryza (runny nose)?

• Does the child have a fever?

• Does the infant drool more than normal (suggests sore throat)?

Examination

Ears

• Sit the child on the parent’s lap, facing to the side.

• Ask the parent to hold the child’s head against their chest with one

hand, and to ﬁ

rmly hold the child’s arms and upper body with the

other hand (see

Box 16.7 ).

• With an infant, gently pull the pinna back before inserting the

otoscope. When examining an older child, pull the pinna up.

• Use the otoscope as in adults—see Chapter 6, b p. 132.

See Table 16.3 for common conditions of the eardrum.

Table 16.3 Some common ﬁ ndings when examining the eardrum

Appearance of drum Condition

Translucent, clear light reﬂ ex Normal

Red, bulging, loss of light reﬂ ex Acute otitis media

Retracted, loss of light reﬂ ex, dull Glue ear (chronic otitis media with effusion)

Box 16.7 More on ear examination

While asking the parent to hold the child’s head during the ear examina-

tion is the usually taught method, this often leads to a struggle.

It is equally appropriate to allow the child free movement of the head,

providing you splint the hand holding the otoscope against the child’s

face so that your hand (and otoscope) will move as the child’s head

moves. This can lead to a less distressing examination.

0 In infancy, the pinna should be pulled forward (not back) to straighten

the auditory canal.

EAR, NOSE, AND THROAT

489

Nose

• Examine the nose externally for discharge.

• The nose may be examined very gently, using an otoscope.

•

Polyps are a common ﬁ nding in asthma and cystic ﬁ brosis.

•

Pale, boggy nasal mucosa suggests allergic rhinitis.

Throat

• Sit the child upright on the parents lap facing toward you.

• Ask the parent to hold the child’s forehead with one hand, with the

back of the child’s head against their chest.

•

The parent should ﬁ rmly hold the child’s arms with the other hand.

• The difﬁ culty now is encouraging the child to open their mouth!

•

Ask the child to open their mouth “as wide as a lion’s.”

•

Tempt an infant to open their mouth with the paciﬁ er.

•

Sometimes children will be more inclined to open their mouth if you

promise not to use a tongue depressor.

• When the child’s mouth is open, gently depress the tongue with the

tongue depressor if it is obstructing view of the tonsils.

• Decide whether the tonsils are

•

Normal: pink and small

•

Acutely inﬂ amed: red, enlarged, with purulent areas

•

Chronically hypertrophied: enlarged and pitted, but not inﬂ amed

Lymph nodes

• Always feel for cervical and supraclavicular lymphadenopathy.

CHAPTER 16 Pediatric assessment490

Cardiovascular system

Key points from the history

• Does the child ever have blue spells (cyanosis)?

• Does the child become tired, pale, or sweaty (indicating heart failure)?

• If the patient is an infant, ask how long the child takes to feed from a

bottle. Breathlessness may inhibit feeding.

• Is the child growing normally? Plot on a percentile chart.

• Does the child suffer from recurrent chest infections?

• Does the child suffer from abdominal pain (caused by organomegaly)?

• Is there a history of fainting or collapse?

• Has the child ever complained of their heart racing (would imply an

arrhythmia such as supraventricular tachycardia)?

• Is there a FH of congenital heart disease?

Examination

Inspection

Search for evidence of heart failure: pallor, cyanosis, sweating, respiratory

distress, and tachypnea.

Hands

• Clubbing is seen in cyanotic congenital heart disease.

• Search for signs of endocarditis, including splinter hemorrhages,

Janeway lesions, and Osler’s nodes.

Face

• Anemia in the conjunctiva

• Central cyanosis (“stick your tongue out!”)

Neck

The jugular venous pulse and pressure are difﬁ

cult to appreciate in young

children, given the relative shortness of the neck.

Peripheral pulses

Palpate the radial, brachial, and femoral pulses.

0 The femoral pulse, although sometimes awkward to feel, must always

be sought to ensure coarctation of the aorta is not missed. Assess:

• Volume: Is it full or thready? (You need to practice feeling many pulses

to appreciate the difference.) A thready, weak, or small volume pulse

indicates hypovolemia. Look for pulsus paradoxus (b Chapter 7,

p. 159).

• Rate: Heart rate varies with age, activity, distress, excitement, and fever

(pulse rate will i by 10 bpm with every temperature rise of 1ºC).

• Rhythm

•

Sinus arrhythmia: an i in pulse rate on inspiration, with slowing on

expiration. This is very common in children.

•

Occasional ventricular ectopic beats are normal in children.

• Character

•

Collapsing pulse in children is most commonly due to a patent

ductus arteriosus.

•

Slow rising pulse suggests ventricular outﬂ ow obstruction.

CARDIOVASCULAR SYSTEM

491

Blood pressure

Blood pressure readings in children are not easy, but they are important,

so remember to perform this test. The use of the correct cuff size is vital

to prevent inaccurate readings.

Anxiety and poor technique are the most common causes for raised

blood pressure in children, so it should be measured several times.

Chest

Note the presence of the following:

• Precordial bulge: causes the sternum and ribs to bow forward

• Visible ventricular impulse: right ventricular (RV) impulse may be

visible under xiphoid process. The left ventricular (LV) impulse (PMI) is

often visible in thin children and in children with true LV hypertrophy.

• Scars: indicative of previous heart surgery

Palpation

• Feel the PMI to determine its location and character. It is usually

situated in the fourth intercostal space in the mid-clavicular line in

infants or toddlers (often difﬁ

cult to localize if they are plump), and in

the fourth or ﬁ

fth intercostal space in older children.

•

LV hypertrophy results in a diffuse, forceful, and displaced apex beat,

felt as a heave.

•

If the apex is impalpable, consider dextrocardia (inverted heart with

apex pointing to the right) or pericardial effusion. Levocardia is the

normal orientation of the heart to the left.

• Right ventricular heave: Place your ﬁ

ngertips along the left sternal

border (LSB). If the child has RV hypertrophy, you will feel your ﬁ ngers

lift up with each impulse.

• Palpate in the four valve areas (aortic, pulmonary, tricuspid, and mitral)

for thrills.

• Palpate the abdomen for hepatomegaly, which suggests heart failure

(percuss the upper border of the liver—a normal-sized liver may be

displaced downward by lung disease such as bronchiolitis.) Raised JVP,

pulmonary, and peripheral edema are rarely seen in children.

Auscultation

Listen to the heart sounds in the four valve areas with the diaphragm and

bell of the stethoscope (preferably pediatric size).

First heart sound (S1) is best heard at the apex with the bell.

• Loud S

1

is heard with high cardiac output states (e.g., anxiety, exercise,

fever).

• Soft S

1

is heard with emphysema and impaired LV function.

Second heart sound (aortic = A2 and pulmonary = P2) is best heard at the

base with the diaphragm. It is normally split in children.

• Soft P

2

is heard with stenotic pulmonary valve (e.g., tetralogy of Fallot).

• Loud P

2

is heard with pulmonary hypertension.

• Wide ﬁ

xed splitting is caused by atrial septal defect.

CHAPTER 16 Pediatric assessment492

Third heart sound is due to rapid ventricular ﬁ lling.

• Causes include i LV stroke volume (aortic or mitral regurgitation)

and restricted ventricular ﬁ lling (constrictive pericarditis, restrictive

cardiomyopathy). It may be normal in children.

Fourth heart sound is due to forceful atrial contraction.

• Causes include hypertrophic cardiomyopathy and severe hypertension.

Murmurs

Auscultate for murmurs ( Table 16.4 ) over the four valve areas and at the

back. About 30% of children have innocent murmurs.

Innocent murmurs

The patient is asymptomatic. These are systolic (except venous hum), with

no radiation or thrill. Change occurs with altering patient posture.

• Venous hum: due to turbulent ﬂ

ow in the head and neck veins. A

continuous murmur in diastole and systole is heard below the clavicles,

which disappears when the child lies ﬂ at.

• Ejection murmur: due to turbulent ﬂ

ow in the outﬂ

ow tracts of the

heart. It is heard in the second to fourth left intercostals spaces.

Pathological murmurs

These are systolic or diastolic and may radiate. The patient may have a

thrill and may be symptomatic.

• Atrial septal defect: soft ejection systolic murmur at the upper LSE due

to i RV outﬂ

ow. Fixed wide splitting of the second heart sound may

ﬁ

rst be detected at school entry.

• Ventricular septal defect: parasternal thrill . Loud pansystolic murmur

occurs at the lower left sternal border (LSB) . It radiates throughout

the precordium . Signs of heart failure may be present.

• Coarctation of the aorta: ejection systolic murmur is heard between the

shoulder blades. Femoral pulses are weak or absent.

• Patent ductus arteriosus: collapsing pulse. A continuous “machinery

murmur” is heard below the left clavicle.

• Also see b Chapter 7, p. 171.

Table 16.4 Quick guide to common pediatric murmurs

Symptom Cause

Cyanosis + murmur Usually tetralogy of Fallot

Cyanosis + murmur + operation Possibly tetralogy of Fallot or

transposition of the great arteries

Pink + loud systolic murmur Probable ventricular septal defect

(most common form of CHD)

Pink + murmur + impalpable femorals Coarctation of the aorta

Continuous low-pitched murmur Probable patent ductus arteriosus

ABDOMEN AND GASTROINTESTINAL SYSTEM

493

Abdomen and gastrointestinal system

Key points from the history

Determine whether the child takes in sufﬁ cient calories for growth and

has a well-balanced diet. Ask about height and weight gain.

2 This may be an appropriate time for dietary teaching.

When taking a history, start at the head and work down to avoid miss-

ing things.

• Does the child have a good appetite?

• Does the child vomit?

•

How much?

•

Are they hungry afterward?

•

Is it forceful (projectile) or effortless (regurgitation)?

•

Is it related to eating?

•

What does it contain? Ask about coffee grounds or other

appearances of the vomit. (Bile-stained vomiting in an infant always

indicates obstruction and must be considered pathological.)

• Does the child suffer from abdominal pain?

• Does the child ever have a bloated abdomen?

• Are there any urinary symptoms?

• Ask about bowel habit—is the child constipated?

• Have there been any frequent or loose stools? Are the stools

particularly offensive (suggests malabsorption)?

• Is there a relevant FH (e.g., celiac or inﬂ

ammatory bowel disease)?

Examination

Inspection

Start with a general inspection of the patient, looking especially for the

following:

• Visible liver edge or spleen

• Peristalsis (important in diagnosing pyloric stenosis during a test feed)

• Jaundice

• Observe for signs of liver disease (see b Chapter 9, p. 246), including

spider nevi, xanthomata, and purpura.

• Edema over the tibia and sacrum

• Whether the child is under- or overweight

• Wasted buttocks (suggesting weight loss—typical of celiac disease)

Hands

• Clubbing, palmar erythema

Face

• Check the conjunctiva for anemia.

• Periorbital edema (e.g., in nephrotic syndrome)

Abdomen

• Abdominal distension (see Boxes 16.8 and 16.9 )

• Gross ascites may be evident—the abdomen will be distended and the

umbilicus everted.

• Caput medusae (cutaneous collateral veins with blood ﬂ owing away from

the umbilicus due to

i portal venous pressure; see Chapter 9, b p. 229).

CHAPTER 16 Pediatric assessment494

Box 16.9 Detecting peritoneal inﬂ ammation

A further useful technique is to ask the patient to make their belly “as fat

as possible” and “as thin as possible.” Also ask them to cough. If perito-

nitis is present, any of these maneuvers may result in pain.

Box 16.8 Causes of abdominal distension in a child

• Fat

• Fluid

• Flatus

• Feces

• Organomegaly

• Muscle hypotonia

• Exaggerated lordosis (normal in young children)

PALPATION

495

Palpation

0 Young children may resist abdominal examination. First try distraction

techniques. If these fail, use the child’s hand to guide yours around the

abdomen. If there is doubt as to the signiﬁ

cance of tenderness in a child’s

abdomen, listen with your stethoscope and gently apply more pressure.

Often, quite ﬁ rm pressure can be tolerated in this way where there was

previously tenderness.

The aims of palpation are to

• Determine the presence of normal abdominal organs.

• Detect enlargement of the abdominal organs.

• Detect the presence of abnormal masses or ﬂ uid.

Procedure

• Ensure the child is relaxed and that your hands are warm.

• Inquire about pain before you begin.

• Palpate for tenderness (light palpation ﬁ

rst, then deep palpation).

•

Feel for guarding (tensing of the abdominal muscles, which may

indicate underlying tenderness).

• Palpate the spleen. This is normally felt 1–2 cm below the costal

margin in infancy. It is soft and can be tipped on inspiration. Begin

palpation in the right iliac fossa and move toward the left upper

quadrant, to avoid missing a very large spleen. It may help to turn the

child onto their right side.

• To palpate the liver, start in the right iliac fossa and move upward in

time with the child’s respiratory movements until the liver edge meets

your ﬁ

ngers. A liver edge 1–2 cm below the costal margin is normal up

to the age of 2 or 3 years. See

Box 16.10 regarding hepatomegaly.

• Kidneys are not easy to palpate in children (they are easier to palpate

in newborns), so if you can feel them, they are probably enlarged.

They are best palpated bimanually. The kidneys move with respiration

and have a smooth outline, and one can get above them (unlike the

liver and spleen).

• Palpate for other masses and check for constipation (usually felt as a

hard, indentable, nontender mass in the left iliac fossa).

Box 16.10 Conﬁ rming hepatomegaly

If in doubt, conﬁ rmation of liver enlargement can be made by

• Placing the stethoscope over the xiphoid process.

• Gently rubbing the abdomen, progressing up from the right iliac

fossa.

•

When the rubbing hand is over the liver, the sound will be heard

through the stethoscope.

CHAPTER 16 Pediatric assessment496

Percussion

• Ascites. Test for shifting dullness (described in b Chapter 9, p. 240)

as a sign of ascites.

• Gaseous distension

• Percuss to determine the size of the liver and spleen

Auscultation

• Bowel sounds

Rectal examination

This is rarely indicated in children. However, it is often useful to inspect

the perianal region for ﬁ ssures, tags, soiling, and pinworms.

Male genitalia

Penis

• Note the state of hygiene.

• True micropenis is rare. If the penis looks small, it is probably because

it is buried in suprapubic fat.

• Check the urethral oriﬁ

ce is at the tip of the glans. If not, is there

epispadius (dorsal opening, very rare) or hypospadias (ventral

opening)?

Scrotum

The child should be standing up.

• Inspect for normal rugosity of the scrotum.

• Palpate for the testes.

•

If they are not present in the scrotum, feel at the inguinal canal and,

if found, try to milk the testis down.

•

Many undescended testes are subsequently found on re-examination

as retractile testes, so be gentle in your approach to avoid provoking

a cremasteric reﬂ ex!

Female genitalia

Inspect the female external genitalia if there are urinary symptoms.

NERVOUS SYSTEM

497

Nervous system

Key points from the history

• Detailed birth and perinatal history, including maternal drugs or illness

• Careful history of developmental milestones

• Hearing or visual concerns. Did the child pass the newborn hearing

screen?

• Any change in school performance, personality or behavior

(e.g., aggression)?

• Ask about symptoms of raised intracranial pressure (e.g., headache,

vomiting).

• Any change in gait or frank ataxia?

• Does the child have limited function—what can they do? What do

they need help with?

• Obtain relevant FH of learning difﬁ

culties or genetic conditions.

Examination

Examination of the nervous system in school-age children should be

performed as in adults. Young children cannot cooperate with a formal

neurological examination, so assessment is opportunistic—observation

becomes important. The assessment of a young child is described below.

Young children—where to start

Palpate the anterior fontanel when the child is quiet to

• Determine the presence of raised intracranial pressure (felt as fullness

or bulging).

• Determine the degree of dehydration (felt as a sunken fontanel).

2 It is impossible to assess fontanel tension in crying babies.

2 Pulsation of the fontanel is normal.

• Measure the maximum occipitofrontal head circumference and plot

this on a percentile chart.

Cranial nerves

It is not possible to systematically examine cranial nerves in infants or

young children; below is a rough guide (see b Chapter 10).

• I (olfactory): very difﬁ cult

• II (optic): Ask the parents—can the child see?

• III, IV, VI (eye movements): Gain the infant’s visual attention with an

object and move it back and forth. Watch for the range of ocular

movements as the child tracks the object. Pendular nystagmus may

indicate a visual defect. See Box 16.11 for assessment of strabismus.

• V (trigeminal): rooting reﬂ ex

• VII (facial): Facial palsy will become apparent when the child cries.

Asymmetry will be more obvious. Does the child close both eyes?

• VIII (vestibulocochlear): Formal hearing tests are performed at birth.

• IX, X: swallowing

• XI (accessory): neck and shoulder movements

• XII (hypoglossal): tongue movement

CHAPTER 16 Pediatric assessment498

• Pupils: Check for size, shape, and reaction to light.

• Fundi should be examined but should be left to the end of the

examination, as it is unpleasant (and sometimes impossible).

Tone

• Observe the child’s response to gravity.

•

Hypotonic infant: slips through in ventral suspension (holding them

up with a hand in each axilla), droops over your hand during ventral

suspension, head lags when pulled to sit, frog legs posture.

•

Hypertonic infant: scissoring of lower limbs when the baby is picked

up. Resistance to movement of limbs. The baby will seem to move

in one piece.

Move limbs through their range of movements. Important areas to exam-

ine include the following:

• Arm ﬂ

exors and extensors

• Arm supinators and pronators (most sensitive for i tone)

• Hip adductors

• Leg extensors

• Leg ﬂ exors

• Ankle extension

Power

Observe for the following:

• Symmetry

• Spontaneous movements (Reduced movement is indicative of muscle

weakness.)

Sensation

This is difﬁ

cult to assess. Only response to pain can be conﬁ dently

elicited

in young children, but please don’t try this!

Box 16.11 Assessment of strabismus

Any strabismus persisting beyond the age of 6 weeks needs specialist

assessment, as strabismus may lead to amblyopia (cortical blindness).

• Ask when the strabismus is most apparent—latent strabismus may

only be present when the child is tired.

Examination

• Corneal light reﬂ

ection test: shine a penlight at a spot directly

between the patient’s eyes to produce a reﬂ ection in the cornea.

The reﬂ ected light that you see should be at the same spot on each

eye. If the reﬂ ection from the corneas is asymmetrical, strabismus is

probably present.

• Eye movements: to detect a paralytic strabismus (rare)

• Cover test: encourage the child to ﬁ

x on a toy, and cover the normal

eye with a card or occluder. If the ﬁ

xing eye is covered, the affected

eye moves to take up ﬁ xation.

•

Manifest (constant) strabismus: on removal of the cover, the eyes

move again as the ﬁ xing eye takes up ﬁ xation.

NERVOUS SYSTEM

499

Reﬂ exes

• Tendon reﬂ exes can be elicited by tapping the tendon with a ﬁ nger

for

babies, and using a reﬂ ex hammer for children.

•

The examiner should know the nerve roots responsible for the

reﬂ exes (see b Chapter 10, p. 330).

2 Remember that the plantar response is upward until age 8 months.

• Primitive reﬂ

exes: The presence of primitive reﬂ exes beyond 6 months

of age is abnormal and will inhibit normal development.

•

Persistence is indicative of a UMN lesion (e.g., cerebral palsy). See

Table 16.5 .

Coordination (assess in older children)

Ask the child to do the following:

• Stand on one leg and then hop.

• Walk on tiptoes.

• Walk on heels. This is a good test for coordination and overall

neurological integrity. Patients with any kind of spasticity, for example,

will be unable to do this.

• Do the ﬁ

nger-to-nose test and heel-to-shin test if child is old enough.

Gait (assess in older children)

• Spastic gait: Spasticity of extensor muscles causes a stiff gait on a

narrow base. Toes catch the ground ﬁ rst (e.g., cerebral palsy).

• Hemiplegic gait: If the spasticity is unilateral, the affected leg drags

stifﬂ

y and is circumducted as it is brought forward.

• Ataxic gait: broad based, unsteady, with frequent falls

• Lower limb weakness (distal): The affected leg is lifted over obstacles,

then the foot returns to the ground with a slap.

• Lower limb weakness (proximal): There is a waddling gait as the

pelvis is thrown side to side, being poorly supported by lower limbs

(e.g., muscular dystrophy)

• Limp has several causes, but always rule out dislocation of the hip.

Table 16.5 Some primitive reﬂ exes and age of extinction

Reﬂ ex Age of extinction

Stepping reﬂ ex 2 months

Palmar grasp 3–4 months

Moro reﬂ ex 4–5 months

Asymmetric tonic neck reﬂ ex 6 months

CHAPTER 16 Pediatric assessment500

Developmental assessment

Development is a continuous process, the rate of which varies consider-

ably among normal children.

Development is divided into four areas:

• Gross motor

• Fine motor and vision

• Speech and hearing

• Social

Delay in all four areas is usually abnormal, but delay in one area may not

be ( Table 16.6 ). For example, some children become expert at bottom

shufﬂ

ing or scooting. Thus having learned an effective means of traveling,

the need to walk becomes less important.

Performing a developmental assessment

• Observation is key. Young children will often not cooperate. Take

a history from the parents about milestones the child has achieved

( Table 16.7 ) .

• Be systematic and evaluate each of the four developmental areas.

• Learn a few essential milestones, as it is difﬁ

cult to remember them all.

2 If an infant was born prematurely, allow for this by calculating their

corrected age from their expected due date.

• Limit distractions and present one task at a time.

Equipment for developmental assessment

• Wooden blocks: for assessing palmar grasp and building towers

• Coins or Cheerios: for testing pincer grip

• Pencil and paper: for assessing ﬁ

ne motor skills

• Different-colored cards or colorful book

Table 16.6 Developmental warning signs

Age Warning sign

Any Regression in previously acquired skills or a halt in

developmental progress

8 weeks No smiling

6 months Persistent primitive reﬂ exes. Hand preference (this should not

appear until 18 months)

12 months No sitting. No pincer grip. No double babble

18 months Not walking. No words

4 years No words

DEVELOPMENTAL ASSESSMENT

501

Table 16.7 Developmental milestones

Age Gross motor Fine motor Language Social

3 months Head control, pushes up

with arms

Opens hand Laughs Smiles (6 weeks)

6 months Sits Palmar grasp, reaches, transfers Babbles

(monosyllabic: ba, ka, da)

Eats solid food

9 months Crawls, pulls to stand Pincer grip begins to develop Double babble

(dada, mama, baba)

Stranger awareness,

waves bye-bye

12 months Walks Developed pincer grip Mommy, daddy, speciﬁ cally Peek-a-boo

18 months Walks upstairs, jumps Scribbles, 3-block tower 2-word phrases Mimics

2 years Kicks, runs Draws straight line,

6–8 block tower

Begins to use clauses

(including verbs)

Uses spoon skillfully,

undresses, symbolic play

3 years Hops, walks upstairs

adult-style

Draws a circle, builds a bridge

with blocks

Says name, knows colors Dresses, has a friend,

dry diapers by day

4 years Stands on one leg, hops Draws a cross, makes 3 steps

with blocks

Sentences of 5+ words Does up buttons

5 years Can ride a bicycle Draws a triangle Ties shoelaces, dry all night

CHAPTER 16 Pediatric assessment502

The newborn

The vast majority of newborns have a normal intrauterine life and normal

birth and are physically normal. However, because there is wide variation

in the spectrum of normal, it is important to stress the value of examining

a large number of neonates to appreciate the normal spectrum.

In the delivery room

All newborns should have a brief examination at birth to determine

whether resuscitation is needed and to rule out any major abnormalities.

The APGAR score is used to gauge the need for resuscitation

( Table 16.8 ) .

In the nursery

A more thorough examination is carried out prior to discharge. At this

stage, the baby is unrecognizable from the one you met in the delivery

room—they will be pink, vigorous, and feeding well.

Ask brieﬂ y about whether the baby has passed urine and meconium

(the ﬁ rst, black sticky stool), and inquire about the progress of feeding as

well as a FH of congenital anomalies. Of particular importance is a FH of

dislocated hips, renal abnormalities, and deafness.

• Examination should start at the top and work down, to ensure nothing

is missed.

• Undress the baby yourself as the examination proceeds, to get a feel

for how the baby handles.

General observation

First observe the baby without disturbing him or her.

• Color: pink, pale, cyanosed, or jaundiced? Acrocyanosis (cyanosis of the

hands and feet) is normal, provided the lips and tongue are pink.

• Rash: a blotchy erythematous rash occurs in about half of all neonates;

this is usually harmless and is called erythema toxicum .

• Peeling of skin is common, especially in post-dates babies.

Table 16.8 APGAR score

Sign 0 1 2

Appearance White/blue Blue extremities,

pink trunk

Pink

Pulse Absent <100bpm >100 bpm

Grimace on

stimulation of foot

None Frown/grimace Cry

Activity, tone Floppy Some limb ﬂ exion Active movement

Respiratory effort Absent Irregular, slow Loud cry

THE NEWBORN

503

Hand and face

• Shape of the head can vary widely in the ﬁ rst week.

• Fontanels should be soft and ﬂ

at. The size of the anterior fontanel also

varies widely, from 1 to 4 cm in diameter. The posterior fontanel may

accept a little ﬁ ngertip.

• Cranial sutures: Are they fused?

• Look for trauma from the birth, such as caput succedaneum (edema

caused by pressure over the presenting part) and molding (head

changing shape as it passes through the birth canal), forceps marks, and

subconjunctival hemorrhages. In general, these conditions will resolve

within the ﬁ rst

week.

•

A cephalhematoma is a localized, ﬂ uctuant swelling, usually over the

parietal bone, caused by subperiosteal bleeding. This will resolve

over a few months.

• Ears can be of different shape and size. Look for preauricular sinuses

and ear tags, and observe their position.

Mouth

• Palate: Look at it when the infant cries, then palpate it for a cleft with a

clean ﬁ nger.

•

Epstein’s pearls are small, white cysts in the midline of the hard

palate. They are normal and resolve spontaneously.

• Jaw: A small jaw (micrognathia) may be part of the Pierre Robin

sequence (midline cleft, small jaw, posterior displacement of the

tongue, which can cause upper airway obstruction).

• Tongue: Note the size. If it is large and protruding, this may indicate a

number of syndromes (e.g., Down syndrome).

Eyes

• Note the position and size.

• Look for the red reﬂ

ex with an ophthalmoscope to exclude a cataract,

which would be seen as a white reﬂ ection.

•

To encourage the baby to open their eyes, wrap them in a blanket

(a crying baby will not open their eyes) and sit them upright.

•

If this fails, give the baby something to suck on, or startle with the

Moro reﬂ ex.

• Sticky eyes can be the result of ophthalmia neonatorum (purulent

conjunctivitis in the ﬁ

rst 3 weeks of life), usually due to accumulation

of lacrimal ﬂ

uid due to incomplete drainage of the nasolacrimal duct.

Respiratory system and chest

• Observe: This is best done with a quiet baby (either sleeping or with

the aid of a paciﬁ er).

• Chest: Comment on size, symmetry, and shape.

• Respiratory rate should be <60/minute. Note the work of breathing. Are

there any subcostal or intercostal retractions? Is the baby grunting?

•

Normal newborn respiration should be quiet, effortless, and

predominantly diaphragmatic (abdomen moves more than the chest).

• Auscultate the lung ﬁ

elds to ensure symmetrical air entry. Crepitations

may be normal in the ﬁ

rst few hours of life.

• Breasts: Engorgement is common in male and female infants.

CHAPTER 16 Pediatric assessment504

Cardiovascular system

• Observe: Note color, respiratory effort, and precordial heave.

• Apex beat: Palpate and feel for any thrills (common in neonates).

• Femoral pulse: This is extremely important; its absence may imply

coarctation of the aorta. This requires a relaxed, still baby and lots of

patience.

0 Remember that too much pressure may obliterate it. A collapsing pulse

(water hammer) suggests patent ductus arteriosus.

• Heart rate should be between 100 and 160 bpm.

• Auscultate for the heart sounds and murmurs. Systolic murmurs are

common and usually best heard along the left sternal edge.

Abdomen

• Observe: Distension could be bowel obstruction or abdominal mass.

• Umbilical stump: Count the three vessels. Note any signs of infection,

such as an unpleasant smell, discharge, or periumbilical erythema.

•

The cord will spontaneously separate around the fourth or ﬁ fth day.

• Palpate: Gently feel the abdomen for intra-abdominal organs and

exclude organomegaly. Use warm hands and a paciﬁ er, if necessary.

0 The liver edge is soft and easily missed.

• Kidneys: Determine presence and size by balloting.

•

It is possible to palpate the lower poles of the kidneys in normal

neonates.

• Bladder: Palpate suprapubically. If felt, this suggests outlet obstruction.

• Anus: Infants with an imperforate anus may still pass meconium via a

ﬁ

stula, so check that the anus is patent and in the correct position.

Male genitalia

• Urethra: Identify the urethral oriﬁ

ce and exclude hypospadias.

• Testes: Palpate gently. If they cannot be found in the scrotum,

commence in the inguinal area and palpate downward.

•

If a testis appears larger than normal, transilluminate the scrotum

(b Chapter 12, p. 384) to check for the common condition

hydrocele.

• Inguinal hernia: These are more common in preterm infants.

0 Put the diaper back on quickly, for obvious reasons. In the event of

failure to quickly cover the genitalia, note the urinary stream, as a weak

stream may indicate posterior urethral valves.

Female genitalia

• Labia minora may not be fully covered, especially in preterm infants.

• Vaginal tags are common and resolve spontaneously in the ﬁ rst

week.

• Vaginal discharge and occasionally bleeding can occur, and is normal.

• Note i pigmentation and clitoromegaly.

Limbs

• Ensure that all joints have full range of movement, to exclude any

congenital contractures.

• Examine ﬁ

ngers and toes for syndactyly (fused digits) or polydactyly

(extra digits).

THE NEWBORN

505

Examination of the hips

This is to detect congenital dislocation and instability of the hips, and

should be left until last, as it will make the baby cry.

• Observe for unequal leg length and asymmetry of skin creases.

Hip examination is in two parts:

• Lay the infant supine on a ﬂ

at surface with hips and knees at 90*.

• Stabilize pelvis with one hand and with the other, grasp the knee

between thumb and palm, with the ﬁ

ngertips over the greater

trochanter.

•

Barlow test assesses whether the hip can be dislocated. Pull the hip

up and then push down and laterally.

•

Ortolani test assesses whether the hip is dislocated. Pull the hip

up into the acetabulum (producing a “clunk”); then the hip can be

abducted (Ortolani = out).

Feet

• Talipes equino varus: primary clubfoot. This is usually a ﬁ xed

structural

deformity requiring early manipulation and ﬁ xation.

• Calcaneo valgus: common. Dorsum of the foot is in a position close to

the shin. It resolves after about 2 months with i calf muscle tone.

• Positional talipes is extremely common and involves no bony deformity.

It is easily corrected by movement and treated with physiotherapy.

Spine

Lay the infant prone in one hand and with the other, palpate the spine,

checking for spina biﬁ

da occulta or a dermal sinus.

Neurological examination

Because infants with little or no cerebral cortex can show normal reﬂ exes

and tone, you should observe the baby’s state of consciousness through-

out the examination. This should vary from quiet sleep to semi-wakeful-

ness to an alert state.

A normal infant will be consolable when they cry, whereas it is very

difﬁ cult to settle a neurologically abnormal infant.

Inspection of the spine

Any midline lesion over the spine needs immediate investigation. A single

hair might indicate communication with the spinal column (spina biﬁ da).

Posture

Posture is generally ﬂ exor, although abnormal intrauterine positions can

distort this, such as extended breech position.

Movements

Watch spontaneous limb movements, noting the presence of jitteriness.

Tone

Assess and compare the ﬂ exor recoil of the limbs.

Evaluate tone in response to gravity:

• Pull-to-sit test. Let the baby grasp your ﬁ

ngers and pull the baby up to

sit. The head should ﬂ

ex and follow the traction to an upright position

and hold momentarily. Also observe the tone in the baby’s arms.

CHAPTER 16 Pediatric assessment506

• Ventral suspension is assessed by grasping the infant under each axilla.

A normal infant will support themselves in this position by extending

their back and hips, lifting their head, and ﬂ

exing their arms and legs.

Primitive reﬂ exes (see Box 16.12 )

These are used to assess asymmetry of function, gestational age, and neu-

rological function.

Vision

Assessment of vision should be carried out with the infant in an alert state.

The baby will ﬁ x on an interesting object 8 inches away and will follow

the target.

Hearing

This can be assessed by sounding a loud rattle outside of the infant’s vision.

The baby should look toward the noise.

Head circumference and weight

Finally, measurement and plotting of head circumference and birthweight

on a growth chart is of utmost importance.

Box 16.12 Primitive reﬂ exes

• Palmar grasp: Fingers close to hold an object placed in the palm.

• Rooting: When pressure is applied to the cheek, the head turns

toward the pressure and the mouth opens.

• Sucking: When a ﬁ

nger is placed in the mouth, the infant will suck

vigorously.

• Stepping: Hold the infant with both hands and lower the feet onto a

surface. The legs will move in a stepping fashion.

• Moro reﬂ ex: Lay the infant supine on your hand and forearm. When

the head is dropped a couple inches, the upper limbs abduct, extend,

and ﬂ

ex in a symmetrical ﬂ

owing movement. A unilateral response

indicates damage (usually transient) to the ﬁ fth and sixth cervical

roots, producing Erb’s palsy.

507

Examination under

special circumstances

Overview 508

Disasters, terrorism, and public health emergencies 509

Sexual assault 510

Other thoughts 510

Chapter 17

CHAPTER 17 Examination under special circumstances 508

Overview

This chapter provides an overview and Web URLs for some special con-

siderations that medical personnel should address within the topics of

natural disasters, terrorism events, public health emergencies, and sexual

assault. Detailed information is beyond the scope of this text.

In many communities, there are speciﬁ c laws that address and deﬁ ne the

working relationship among health and law enforcement ofﬁ cials. Health-

care providers should be aware of these laws and incorporate a working

knowledge of all appropriate regulations (or at least where to locate the

information) before it is needed.

Often in these situations, support personnel, such as social workers,

may have left for the day, and providing timely and appropriate care can

be challenging without basic knowledge and skills.

DISASTERS, TERRORISM, AND PUBLIC HEALTH EMERGENCIES

509

Disasters, terrorism, and public

health emergencies

The need for increased opportunities for health-profession students and

providers to learn about emergency preparedness is a direct outcome

of horriﬁ c natural disasters (Hurricane Katrina, the Haiti earthquake),

terrorism events (Oklahoma City, New York City), and concerns about

pandemic inﬂ uenza.

The U.S. Centers for Disease Control and Prevention (CDC) has exten-

sive training opportunities and information on its Web site ( www.bt.cdc.

gov ). A readiness assessment survey for health-care facilities can be found

at http://www.ahrq.gov/prep/cbrne . Personal readiness information can be

found at http://www.fema.gov/areyouready

Skills such as good communication and teamwork are essential in deal-

ing with emergencies. An understanding of the role of primary providers

in the Public Health Surveillance systems is critical, as they may be the ﬁ rst

to see the effects of widespread biological or radiation exposures. Early

identiﬁ cation will lead to appropriate treatment and has the potential of

saving lives.

Beyond participating in surveillance activities and having a high index of

suspicion, providers should acquire competencies in patient care that pre-

pares them to assist in disasters, terrorism events, or public health emer-

gencies. They should be knowledgeable about reporting sentinel events to

the appropriate public health authorities.

Providers should be able to determine the absence or presence of

symptoms characteristic of exposure to chemical, biological, radiological,

nuclear, or explosive agents (CBRNE). They should also know to assess

for evidence of psychological trauma. This could be a result of the event or

triggered by experiences of previous events. Providers should watch for

delayed stress reactions in responders or community members.

Physical assessment and evaluation need to be appropriate to the expo-

sure or trauma. It is essential to know how to access information in the

event of a local emergency. The Internet may not always be accessible in

an emergency, so a reliable backup plan should be in place.

Care will be both acute (trauma, antibiotics, vaccines, antidotes) and

chronic (burn and wound long-term care, physical therapy) and should

address physical and emotional aspects of healing. There may be a need to

collect and preserve evidence for forensic purposes; this should be done

once life-threatening injuries are attended to.

Appropriate precautions must be taken to avoid exposures spreading to

other patients, care providers, and the wider population. As such, provid-

ers should be familiar with and have access to personal protective equip-

ment, isolation levels, isolation rooms, and decontamination areas.

1

Markenson D, DiMaggio C, Redlener I (2005). Preparing health professions students for terror-

ism, disaster, and public health emergencies: core competencies, Acad Med 80(6):517–526.

CHAPTER 17 Examination under special circumstances 510

Sexual assault

Sexual assault victims have suffered an extreme trauma and need to be

treated with respect and understanding. Many localities will have a victim

advocacy program, through which advocates can come to the clinic or

emergency room to support the victim and help arrange for aftercare

counseling.

Providers should be aware of state laws and the proper procedure for

collecting forensic evidence (often there are evidence collection kits with

all the materials needed for collecting evidence and maintaining the integ-

rity of the evidence chain).

In addition to the physical trauma, providers should also address the

psychological effects of the assault. It is essential that the necessary exam

and specimen/culture collection not retraumatize the patient. Allowing

patients to control the pace of the exam and ensuring that they know

what is going to happen to them each step of the way is paramount.

If the victim was assaulted by an intimate partner, the provider may have

to notify law enforcement authorities, regardless of whether the victim

wants to do this. If the victim is a minor, child protective services may

need to be called in.

Appropriate cultures and monitoring for STIs and pregnancy should be

initiated. Patients will need long-term follow-up, which should be arranged

at the initial visit. Providers should remember that victims can be of either

gender; providers need to make an extra effort to remain nonjudgmental

in their approach.

Since the 1970s, programs to educate sexual assault nurse examiners

(SANE) have been developed. A comprehensive development and opera-

tion guide is available online from the U.S. Department of Justice, Ofﬁ ce of

Justice Programs, Ofﬁ ce for Victims of Crime, at: www.ojp.usdoj.gov/ovc/

publications/infores/sane/saneguide.pdf .

These programs have allowed specialized services for assault victims to

become available nationwide.

Other thoughts

Hints

Consider keeping an inexpensive disposable or digital camera in the

patient care area for photodocumentation.

511

Practical procedures

Using this chapter 512

Inﬁ ltrating anesthetic agents 512

Sterility and preparation 513

Hand-washing 514

Injections 516

Venipuncture 518

Peripheral IV catheterization 522

Setting up an infusion 524

External jugular vein catheterization 526

Central venous catheterization 527

Blood pressure measurement 531

Recording a 12-lead ECG 533

A rterial blood gas sampling 535

Peak ﬂ

ow measurement

537

Inhaler technique 538

Oxygen administration 544

Basic airway management 547

Tracheostomy management 555

Endotracheal (ET) intubation 557

Noninvasive ventilation (NIV) 559

Pleural ﬂ

uid sampling (thoracentesis)

561

Chest tube insertion 563

Nasogastric (NG) tube insertion 567

Ascitic tap 569

Abdominal paracentesis (drainage) 571

Male urethral catheterization 573

Female urethral catheterization 575

Suprapubic catheterization 577

Basic suturing 579

Lumbar puncture 581

Pericardial aspiration 583

Deﬁ brillation

584

Knee joint aspiration 588

Chapter 18

CHAPTER 18 Practical procedures512

Using this chapter

This chapter describes those practical procedures that the primary care

provider may be expected to perform.

Obviously, some of these are more complicated than others, and some

should only be performed once you have been trained speciﬁ cally in the

correct technique.

Each procedure has a difﬁ culty icon as follows:

1 Requires no speciﬁ

c further training and primary care

providers should be competent to perform.

2

Requires some skill. Experienced providers should be able to

perform with ease.

22 More complex procedures that you may only come across

in specialty jobs and will not be required to perform without

speciﬁ

c guidance from specialists or highly experienced

clinicians.

Rules are made to be broken

Many procedures and practical skills do not have a “correct” method but

have an accepted method. These methods should, therefore, be abided

by, although deviation from the routine by a competent practitioner, when

circumstances demand, is acceptable.

Many procedures have local variations—if in doubt, check the standard

method used in your hospital or facility.

Inﬁ ltrating anesthetic agents

A large number of procedures involve the inﬁ ltration of local anesthetic

agents. The importance of this procedure cannot be overlooked. Injection

of a large amount of anesthetic into a vein could lead to potentially fatal

cardiac arrhythmias. It is also important, of course, to ensure that you do

not damage any vessels.

Advance and withdraw

Whenever you inject anything, you should advance the needle and attempt

to withdraw the plunger at each step. If you do not aspirate blood, you

may then go ahead and inﬁ ltrate the anesthetic.

Making a surface bleb

• Take the syringe of anesthetic (e.g., 1% lidocaine) and a small needle.

• Pinch a portion of skin, insert the needle horizontally into the surface.

• Withdraw the plunger to ensure no blood is aspirated then inject a

small amount of the anesthetic—you should see a wheal of ﬂ uid

rise.

• The area of skin will now be sufﬁ

ciently anesthetized to allow you to

inﬁ ltrate

deeper.

• Remember —no epinephrine-containing anesthetic agents for

inﬁ

ltration into the digits!

STERILITY AND PREPARATION

513

Sterility and preparation

Most equipment will come in prepacked sterile wrapping. When perform-

ing a procedure in which sterility is important, all packaging should be

opened using a no-touch technique.

Large packs of equipment

Some equipment is available in pre-prepared sterile packs. For example,

a catheterization pack may contain gauze, cotton balls, a cleansing agent,

lubricant, and a sterile vessel. These come wrapped in plastic and then

internally wrapped with material for the placement of a sterile ﬁ eld while

opening the pack.

Any such packs should be placed on a stand that has ﬁ rst been appro-

priately cleaned. You should then carefully open the pack, touching the

corners only, and using sterile gloved hands.

The opened pack can then be used as a sterile surface on which to place

additional sterile equipment.

Smaller pieces of equipment

Most equipment (e.g., needles, syringes) comes sterilized and wrapped in

paper or plastic. These should also be opened using a no-touch technique

if absolute sterility is needed.

For example, unwrap a needle by peeling back the packaging as if peel-

ing a banana and allow the needle to drop onto the pre-prepared sterile

ﬁ eld.

CHAPTER 18 Practical procedures514

1 Hand-washing

Theory

Hand-washing is the single-most important procedure for preventing the

spread of infections. It is underperformed in frequency and quality.

Hands should be washed before every episode of care that involves

direct contact with a patient’s skin, their food, invasive devices, or dress-

ings, and after any activity or contact that could result in hands becoming

contaminated, such as using community computers to enter data.

Alcohol sanitizers can also be regularly used when entering or leaving a

patient care area and before and after examining patients.

Equipment

• Soap and alcohol gel

• Disposable paper towels

• Moisturizer (if required)

Procedure

If hands are not visibly soiled, hand-sanitizing with alcohol-cleansing agents

may be as if not more effective than hand-washing.

When required to wash our hands, we should use soap and warm water.

Those parts often missed are the tips of ﬁ ngers, thumbs, and between the

ﬁ ngers.

The following routine is advised ( Fig. 18.1 ):

• First, rub hands palm to palm ( Fig. 18.1 a).

• Rub right palm over the left dorsum.

• Rub left palm over the right dorsum.

• Wash palm to palm with the ﬁ

ngers interlaced (

Fig. 18.1 b).

• Wash the backs of the ﬁ ngers with opposing palms, with ﬁ ngers

interlocked (

Fig. 18.1 c).

• Perform rotational rubbing of the right thumb clasped with the left ﬁ st

( Fig. 18.1 d).

• Perform rotational rubbing of the left thumb clasped with the right ﬁ st.

• Wash the right palm with rotational rubbing using ﬁ

ngers of left hand.

• Wash the left palm with rotational rubbing using the ﬁ

nger of the right

hand (

Fig. 18.1 e).

• Wash the space between the thumbs and ﬁ rst

ﬁ

ngers by interlocking

them and rubbing together ( Fig. 18.1 f).

• Rinse away all soap and pat dry using disposable paper towels.

• Apply moisturizer to protect the skin from the drying effects of regular

washing.

2 Hints

• Keep nails short, clean, and polish free.

• Avoid wearing wristwatches and jewelry, especially rings with ridges or

stones.

• Any cuts or abrasions should be covered with waterproof dressing.

515

HAND-WASHING

(a) (b)

(c) (d)

(e) (f)

Fig. 18.1 The correct stages of hand-washing as described on previous page.

CHAPTER 18 Practical procedures516

1 Injections

Theory

This is an important and routine procedure that is often carried out by

nursing staff, although providers may be asked to administer medication at

times. Good injection technique can make the experience for the patient

relatively painless. Three commonly used routes of administration are sub-

cutaneous (SC), intramuscular (IM), and intradermal (ID).

2 Before gloving for any procedure, conﬁ

rm the absence of latex allergy.

2 Before attempting an injection, familiarize yourself with the operation of

any syringe cover or guard device.

Equipment

• Syringe (size depends on injection)

• Needles: 25-gauge (G) for SC route; 21–23G for IM route

• Extra 21G needle for drawing up dose

• Alcohol swab

• Gloves

• Cotton

• Sharps container

• Medication for injecting

• Band-aid for covering injection site

Procedures

Subcutaneous injections

The SC route is used for a slow absorption of medication and is ideal for

drugs such as insulin.

• Introduce yourself, conﬁ

rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Wash your hands and put on a pair of gloves.

2 Always check that you have the correct drug and correct dose and

that it is within the expiration date before injecting it.

• Draw up the medication using a 21G needle and double check the

medication, dose, and expiration date.

• Expel any air in the syringe and replace with a 25G needle or other

needle appropriate for the medication being injected.

• Clean the injection site with the alcohol swab.

• Pinch a fold of skin so as to lift the adipose tissue away from the

underlying muscle.

• Insert the needle horizontally into the fold and draw back to ensure

you are not in a vein.

• Inject the medication.

• Withdraw needle and apply cotton to the site to absorb any bleeding.

Suitable SC sites include the forearm, triceps area, and abdomen.

Intramuscular injections

IM injections are administered through the epidermis, dermis, and SC tis-

sue into the muscle. They provide rapid systemic action and allow rela-

tively large doses to be absorbed.

517

INJECTIONS

Suitable IM sites typically include the deltoid muscle, dorsogluteal site,

ventrogluteal site, and lateral thigh or vastus lateralis muscle, depending

on available muscle mass. A related method of IM injection, the Z-track

method, is used for “sealing” the injection site to prevent staining from

medications such is iron.

0 Remember to avoid sites of inﬂ

ammation, swelling, infection, or skin

lesions.

• Introduce yourself, conﬁ

rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Wash your hands and put on a pair of gloves.

2 Always check that you have the correct drug and correct dose and

that it is within the expiration date before injecting it.

• Draw up the medication using a 21G needle and have a colleague

double check the medication, dose, and expiration date.

• Expel any air in the syringe and replace with a 25G needle or other

needle appropriate for the medication being injected.

• Inspect the proposed site for adequate muscle mass.

• Clean the injection site with the alcohol swab.

• IM injections should be given at a 90

0

angle to ensure the needle

reaches the muscle and to reduce pain.

• A good way to ensure accuracy and avoid a needle-stick injury is to

rest the heel of the palm on the thumb of the nondominant hand.

• Pull the skin down or to one side at the intended site.

• Hold the syringe between the thumb and foreﬁ

nger and insert the

needle at full depth.

• Draw back on the syringe to ensure the needle is not in a vein.

• Slowly inject the medication.

• After needle insertion and injection, allow 10 seconds before removing

the needle, to facilitate diffusion of the medication into the muscle.

• Withdraw the needle and wipe the area clean with cotton.

Intradermal injections

The ID route provides a local, rather than systemic, effect and is used

primarily for diagnostic purposes, such as allergy or tuberculin testing.

This involves the same preliminary procedures as for IM injection

except a 25G needle is inserted at a 10–15

0

angle, bevel up, just under

the epidermis.

Up to 0.5 mL is injected until a wheal appears on the skin surface—just

as when creating a bleb of local anesthetic.

CHAPTER 18 Practical procedures518

*

There is no solid evidence for beneﬁ t in using alcohol wipes unless there is visible dirt at the veni-

puncture site. However, their use is policy in most facilities and should be used accordingly.

1 Venipuncture

Two methods exist: the common method of collecting blood directly into

the tubes by Vacutainer

®

, and the traditional needle-and-syringe method.

Equipment

• Gloves • Sticky tape

• Alcohol swabs • Gauze or cotton ball

• Tourniquet

• Needle (try 21G ﬁ rst), a syringe, and blood collection bottle or:

• Vacutainer

®

tube, holder, and blood collection needle

• Don’t forget a band-aid!

Procedure

Using a needle and syringe

• Introduce yourself, conﬁ rm the patient’s identity, explain the

procedure, and obtain verbal consent.

• The patient should be lying or sitting comfortably with the arm from

which blood is to be taken resting on a pillow.

• Select a vein site—usually the antecubital fossa (see Fig. 18.2 ).

• Apply tourniquet proximal to the puncture site and recheck vein.

• Put on gloves and ask the patient to clench their ﬁ

st a few times.

• Cleanse the area with an alcohol swab in spirals, inside to out.*

• Attach the needle to a syringe and unsheathe it.

• Use the thumb of your nondominant hand to gently anchor the skin

just below the puncture site.

0Warn patient to expect a sharp scratch and to not move their arm.

• Insert the needle ﬁ

rmly through the skin, bevel up, at an angle of

20–40

0

over the vein.

• With experience, you will feel a slight give as the vein is entered.

Blood will visibly enter the hub (plastic portion) of the needle

(ﬂ ashback).

• Carefully holding the needle in position, pull back on the plunger.

•

There are several ways of doing this. The authors favor holding the

needle and syringe in the nondominant hand, once in place, and

pulling back with the dominant hand.

• When enough blood is taken, release the tourniquet before removing

the needle from the vein.

• Apply a clean cotton ball or folded gauze to the puncture site as the

needle is withdrawn. Pressure should be applied for >1 minute. (Ask

the patient to do this for you, if they are able.)

• Apply a band-aid to the site, and thank the patient.

• Vacuum blood tubes are ﬁ

lled by puncturing the rubber top with the

needle and allowing the blood to enter the tube.

• Remember to label the tubes correctly, ideally at the patient’s bedside,

and dispose of sharps in a sharps bin.

519

VENIPUNCTURE

Cephalic vein

Anterior median

vein of the forearm

Basilic vein

Median cubital vein

Fig. 18.2 Representation of peripheral veins of the upper limb.

Using a Vacutainer

®

system

Much of the procedure is the same as for using a needle and syringe.

• Vacutainer

®

needles are double-ended, one standard needle and one

needle covered by a rubber sleeve.

• Attach a Vacutainer

®

holder over the covered needle (see Fig. 18.3 ).

• The needle is inserted into the vein as with a syringe, but no ﬂ ashback

will be visible.

• Once in place, the Vacutainer

®

tubes are attached to the needle directly

by pushing them onto the covered needle using the tube holder.

• Allow enough blood to enter the tube (some tubes must be ﬁ lled—

check local laboratory guidance).

• Multiple tubes may be ﬁ

lled by removing and replacing tubes while

carefully holding the needle in position.

Inappropriate sites for venipuncture

• Edematous areas

• Cellulitic areas

• Hematomas

• Phlebitis or thrombophlebitis

• Scarred areas

• Arm in which there is a transfusion or infusion

• Arm on the side of previous mastectomy

• Arms with AV ﬁ

stulae or vascular grafts

CHAPTER 18 Practical procedures520

Fig. 18.3 Vacutainer

®

blood collection system, ready for use.

Hints

• If extraction of blood with the Vacutainer

®

proves difﬁ cult, it may be

easier to switch to the needle-and-syringe technique, as this gives you

more control over the ﬂ ow of blood.

• Venipuncture can be performed at any peripheral vein. Inpatients from

whom it is difﬁ

cult to draw blood often have the blood taken from the

back of their hands, feet, or legs.

• In difﬁ

cult to reach places, it is often easier to use a butterﬂ y

needle.

This is a smaller needle attached to a length of tubing that can be

used with either technique. It allows for greater control of the

needle.

521

VENIPUNCTURE

Box 18.1 Taking blood from a central venous catheter

Theory

Central lines should only be used for taking blood if it is not possible to

obtain a sample via the peripheral route. Do not risk catheter sepsis or

a clotted line unless there are no alternatives!

Practicality

Central lines are frequently used for taking blood for assorted reasons.

Avoidance of additional needle-sticks for patient comfort is a primary

concern.

Blood culture requirements may preclude use of the central line for

obtaining a sample. However, blood may need to be obtained from the

central line and a peripheral site simultaneously to assist in differentia-

tion of a source of sepsis.

In any case, caution must be observed to appropriately obtain a

specimen from a port that may have been salinized or heparinized, and

proper care of the port must be exercised after use of the port. Proper

caution will decrease risk of catheter sepsis or a clotted line.

Facility policy will dictate what is done.

Equipment

• 3 x 10 mL syringes

• 0.9% isotonic or heparinized saline

• Chlorhexidine, povidone-iodine, or other recommended agent

• Gauze

• Sterile gloves

• Drape

Procedure

• Introduce yourself, conﬁ

rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Stop any infusions for at least 1 minute before sampling.

• Place the patient in a supine position.

• Ask the patient to turn their head away from the line site during the

procedure.

• Drape the site in case of splash, and put on a pair of sterile gloves.

• Spray or paint the line with the chosen sanitizing agent.

• Clamp the line before removing the cap.

• Connect a 10 mL syringe to the line before unclamping.

• Withdraw 5–10 mL of blood, clamp the line, and remove syringe.

• Discard the blood.

• Connect a new 10 mL syringe to the line, unclamp it, and withdraw

another 10 mL of blood.

• Clamp the line and remove the syringe (keep this sample).

• Fill a further syringe with saline and attach to the line.

• Unclamp the line, instill the saline, and clamp the line again.

• Remove the syringe and replace the cap.

CHAPTER 18 Practical procedures522

1 Peripheral IV catheterization

Theory

Peripheral IV catheterization is a generic skill that most students should

have learned early in their education. A thin tube line is inserted into a

vein, allowing easy venous access that is used in many situations, including

the administration of ﬂ uids and IV medication.

Equipment

• Gloves • Sticky tape

• Alcohol swabs • Gauze or cotton ball

• Tourniquet • Catheter of appropriate size (see Box 18.2, Fig. 18.4)

• Saline for injection • 5 mL syringe

Procedure

• Introduce yourself, conﬁ rm the patient’s identity, explain the

procedure, and obtain verbal consent.

• The patient should be lying or sitting comfortably with the arm in

which the catheter is to be inserted resting on a pillow.

• Apply the tourniquet to the arm and identify a suitable vein.

0 Often those veins that can be felt are more reliable than those that are seen .

The vein should be superﬁ cial and have a straight course for a few centimeters.

• Put on gloves and clean the overlying skin with the alcohol swab.

• Remove the catheter from its packaging.

• Ensure that the catheter is functioning properly by slightly withdrawing

the needle and replacing it. Fold down the wings and open and close

the port on the top.

0 Warn patient to expect a sharp scratch and to not move their arm.

• Insert the catheter ﬁ

rmly through the skin, bevel up, at an angle of

20–40

0

over the vein.

• With experience, you will feel a slight give as the vein is entered. Blood

will visibly enter the hub (plastic portion) of the catheter (ﬂ ashback).

• Once the ﬂ

ashback is seen, hold the needle in place with one hand and

slide the catheter off the needle—into the vein—with the other. Once

the catheter is fully inserted, the needle should be sitting just within it,

preventing blood from spilling.

• Release the tourniquet.

• Press over the vein at the tip of the catheter, remove the needle, and

dispose of it safely in a sharps bin.

• Put the cap on the catheter and ﬁ

x it in place with tape and the

appropriate dressing.

• Draw up saline into the syringe and ﬂ

ush it through the catheter using

the port on the top. Watch the vein—if the catheter is misplaced, the

saline will enter the subcutaneous tissues, causing swelling.

2 Don’t forget to do this—it conﬁ

rms that the catheter is working and

clears it of blood that would form a clot.

Hints

• Try to avoid the antecubital fossa. Although this is often the easiest

place to see and feel a vein, catheters at that site can become

523

PERIPHERAL IV CATHETERIZATION

kinked and blocked as well as cause pain for the patient on bending

the arm.

• Avoid an arm with a ﬁ

stula or AV shunt.

• Bring a selection of different-sized catheters to the bedside, allowing

you to choose a smaller gauge if you experience problems.

• Don’t be afraid to ask for assistance from nursing or auxiliary staff if

the patient is likely to move their arm during the procedure.

Fig. 18.4 A selection of standard IV catheters.

Box 18.2 Sizing catheters

Like needles, catheters are color-coded according to size. Each is given

a gauge (G), which has an inverse correlation to the external diameter.

Color-coding is standardized across manufacturers.

The standard-size catheter is green, or 18G, but for most hospital

patients, a pink, or 20G, cannula will sufﬁ ce. Even blue catheters are ade-

quate in most circumstances unless fast ﬂ ows of ﬂ uid are required.

Gauge

External

diameter

(mm)

Length (mm)

Approximate

maximum ﬂ ow

rate (mL/min)

Color

14G 2.1 45 290 Orange

16G 1.7 45 172 Gray

18G 1.3 45 76 Green

20G 1.0 33 54 Pink

22G 0.8 25 25 Blue

CHAPTER 18 Practical procedures524

Port with cap

for attaching tubing set

Rubber port for

injection ingredients

Fig. 18.5 Diagrammatic representation of the base of a ﬂ uid bag and the port in

which the tubing set should be inserted.

1 Setting up an infusion

Theory

Fluid therapy is one of the core skills for nurses. While it is usually the

nursing staff that sets up an IV infusion, providers should nevertheless be

competent at this technique.

Equipment

• Gloves

• An appropriate ﬂ uid

bag

• Tubing (infusion) set

• IV (standard) pole

• Infusion pump, if required

Procedure

0 IV infusions require IV access—see b p. 522. Check the ﬂ uid in the bag

and ﬂ uid prescription chart.

• Ask a colleague to double-check the prescription and the ﬂ

uid and sign

their name on the chart.

• Open the ﬂ

uid bag and tubing set, which come in sterile packaging.

• Unwind the tubing set and close the adjustable valve.

• Remove the sterile cover from the bag outlet and from the sharp end

of the tubing set (see Fig. 18.5 ).

• Using a lot of force, push the tubing set end into the bag outlet.

• Invert the bag and hang it on a stand.

• Squeeze the drip chamber to half ﬁ

ll it with ﬂ uid.

• Partially open the valve to allow the drip to run, and watch ﬂ uid run

through to the end (it might be best to hold the free end over a sink in

case of spills).

• If bubbles appear, try tapping or ﬂ

icking the tube.

• Once the tubing is ﬁ lled with liquid, connect it to the catheter.

• Adjust the valve and watch the drips in the chamber.

• Adjust the drip rate according to the prescription (see Box 18.3 ).

525

SETTING UP AN INFUSION

Box 18.3 Drip rate

Most infusions tend to be given with electronic devices that pump the

ﬂ uid in at the prescribed rate. However, it is still important that health-

care professionals be able to set up a drip at the correct ﬂ ow rate

manually.

Using a standard tubing set, clear ﬂ uids will form drips of about 0.05

mL—that is, there will be approximately 20 drips/mL. You can then cal-

culate the number of drips per minute for a given infusion rate.

Infusion and drip rates

Prescription

number of hours

per liter of ﬂ uid

Infusion

rate (mL/hr)

Infusion

rate (mL/min)

Drip rate

(drips/min)

1 1000 16 320

2 500 8 160

4 250 4 80

6 166 3 60

8 125 2 40

10 100 1.6 32

12 83 1.4 28

24 42 0.7 14

CHAPTER 18 Practical procedures526

2 External jugular vein catheterization

Theory

The external jugular vein lies superﬁ cially in the neck, running down from

the angle of the jaw and across the sternocleidomastoid muscle before

passing deep to drain into the subclavian vein. It is sometimes used to

provide essential venous access in cardiac arrest and other emergency

situations in which no peripheral access is obtainable.

See Fig. 18.6 for the surface anatomy of the external jugular vein.

Equipment

• Antiseptic solution or antiseptic wipe

• 2 x 5 mL syringes

• 1 25G orange needle

• 1 21G green needle

• 1% lidocaine

• 14G or 16G catheter

• 0.9% saline ﬂ ush

• Dressing

• Gloves

• Sharps bin

Procedure

• Introduce yourself, conﬁ rm the identity of the patient, explain the

procedure, and obtain verbal consent, if possible.

• Wash your hands and put on a pair of gloves.

• Tilt the patient to 10–15

0

head-down to facilitate venous ﬁ lling.

• Once the external jugular vein is visible, clean the area with antiseptic

solution.

• Reconﬁ

rm the patient’s identity, the procedure, and the site.

• Attach a 25G (orange) needle to a 5 mL syringe and make a SC bleb of

1–2 mL of 1% lidocaine and inﬁ ltrate around the insertion site.

0 Be careful not to insert any anesthetic into the vein.

• Position yourself at the head of the bed.

• Remove the cap from the catheter and attach a clean 5 mL syringe.

• Turn the patient’s head away from the side of insertion.

• Catheterize using the same technique as for peripheral venous access.

2 Remember to aspirate as you advance the catheter. Correct placement

will be conﬁ

rmed once you are able to aspirate venous blood.

• Fix the catheter in place, using a suitable dressing.

• Flush the catheter with 5 mL of 0.9% saline solution.

• Dispose of all sharps in a sharps bin, wash your hands, and help the

patient to a comfortable position.

• Document details of the procedure in patient record.

Hints

In an emergency situation, you may forgo the anesthetic, as venous access

may be needed swiftly.

527

CENTRAL VENOUS CATHETERIZATION

3 Central venous catheterization

Theory

Central venous access is the placement of a catheter in a vein that leads

directly to the heart. There are a number of central veins, including the

internal jugular, external jugular, subclavian, femoral, and antecubital.

For each of these, the basic equipment and preparation are the same.

Central venous catheterization is performed for vascular access, total

parenteral nutrition (TPN), infusion of irritant, vasoactive, and inotropic

drugs, measurement of central venous pressure (CVP), cardiac catheteri-

zation, pulmonary artery catheterization, transvenous cardiac pacing, and

hemodialysis or plasmaphoresis.

Single- and multi-lumen catheters are available; the type to be used

should be decided on prior to insertion according to the anticipated use

(e.g., concurrent CVP monitoring and multiple-drug infusion). Frequently,

quad-lumen catheters are used because of their versatility. Decisions on

catheter selection are also contingent on length of the catheter needed

relative to the size of the patient.

For the inexperienced, a CVP kit it can be overwhelming, given the

variety of materials included for performing the procedure.

Equipment

• Appropriate instrument stand

• Sterile pack including sterile drapes

• Sterile gown and gloves

• Suture material e.g., 2/0 silk on a curved needle

• Antiseptic solution

• Local anesthetic—approximately 5 mL of 1% lidocaine

• Central venous line kit

• 21G green and 25G orange needles

• Saline or heparinized saline to prime and ﬂ

ush the line prior to and

after insertion

• Sterile dressing

• Ultrasound machine

Procedure—internal jugular vein

• Introduce yourself, conﬁ rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Remember, this can be a potentially frightening procedure. Explanations

and reassurance must be given before and during the procedure.

• Put on a sterile gown and gloves.

• Unwrap all equipment.

• Check that the wire passes through the needle freely. Attach 3-way

taps to all catheter ports. Flush all lumens with heparinized saline.

• Place the patient in a supine position, at least 15

0

head-down.

•

This is usually quite easy on a tilting bed and is performed to distend

the neck veins and reduce the risk of air embolism.

• Turn the head away from the venipuncture site.

• Cleanse the skin with antiseptic solution and drape the area.

• Stand at the head of the bed.

CHAPTER 18 Practical procedures528

• Locate the cricoid cartilage and palpate the carotid artery lateral to it.

• The site for insertion is approximately 1/3 of the way up the

sternocleidomastoid, just between its two heads.

• Reconﬁ

rm the patient’s identity, the procedure, and the site.

• Use local anesthetic to numb the venipuncture site once located.

• Inﬁ

ltrate the skin and deeper tissues with a smaller orange needle and

then replace with a green needle.

• Introduce the large-caliber introducer needle, attached to an empty

syringe, into the center of a triangle formed by the two lower heads of

the sternocleidomastoid muscle and clavicle.

• Keep your ﬁ

nger on the carotid artery and ensure that the needle

enters the skin lateral

to the artery.

• Direct the needle caudally at an angle of 30–40

0

to the skin, toward

the ipsilateral nipple. The vein is usually within 2–3 cm of the skin.

• Aspirate as the needle is advanced. Once you see blood, catheterize

the vein using the Seldinger technique.

• Remove the syringe and occlude the needle lumen with a thumb.

• Straighten the J tip of the spring guide wire and advance into the vessel

through the needle.

• Holding the spring-wire in place, remove the needle while maintaining

a ﬁ

rm grip on the wire at all times.

• Enlarge the cutaneous puncture site with the cutting edge of the

scalpel positioned away from the spring-wire guide.

• Use the dilator provided to enlarge the site and thread the tip of the

catheter into the vessel using the spring-wire guide.

• Grasp the catheter near the skin and, using a slight twisting motion,

advance into the vein.

• Make sure before you push the catheter forward that the wire is

visible at the proximal end. Hold the wire at all times to prevent it from

getting lost inside the patient.

• Hold the catheter and remove the spring-wire guide.

• Check lumen placement by aspirating through the pigtails and ﬂ ush

with saline.

• Lock off the 3-way taps. The patient can now be leveled.

• Secure the catheter in place with a suture and cover with an adhesive

sterile dressing. (Do not forget to anesthetize suture sites as well.)

• Request a chest X-ray to verify correct catheter position and to

exclude a pneumothorax.

• Catheters have a radio-opaque strip for this purpose.

• The catheter tip should lie in the SVC at the level of the carina.

• Dispose of your sharps and clear the instrument stand.

• Document the details of the procedure in the patient record.

Complications of internal jugular vein catheterization

• Pneumothorax • Infection

• Hemothorax • Thrombosis of vessel

• Chylothorax • Neural injury

• Air embolism • Cardiac tamponade

• Arrhythmais • AV ﬁ stula

• Carotid artery puncture • Patient discomfort

529

CENTRAL VENOUS CATHETERIZATION

Procedure: femoral vein

The femoral vein lies medial to the femoral artery immediately beneath

the inguinal ligament. It is commonly used in an ICU setting for place-

ment of a double-lumen hemoﬁ ltration line and when central access is not

feasible by other routes. This is impractical for mobile patients and raises

concerns regarding the sterility of the groin area.

• Introduce yourself, conﬁ

rm the identity of the patient, explain the

procedure, and obtain consent.

• Extend the patient’s leg and abduct slightly at the hip.

• Use full aseptic technique.

• Before initiating the procedure, reconﬁ

rm the patient’s identity, the

procedure, and the site.

• Locate the femoral artery, keep a ﬁ

nger on the artery, and introduce

a needle attached to a 10 mL syringe at 45

0

, 1.5 cm medial to the

femoral artery pulsation, 2 cm below the inguinal ligament.

• Slowly advance the needle cephalad and posteriorly while gently

withdrawing the plunger.

• When a free ﬂ

ow of blood appears, follow the Seldinger approach as

detailed for the internal jugular vein.

• Ultrasound can be used to identify the vessels and ensure that the vein

is punctured near the inguinal ligament where the artery and vein lie

side by side.

*

Procedure: subclavian vein

The subclavian vein is preferred for central venous access if the patient has

a cervical spine injury and is best for long-term parenteral nutrition, pacing

wires, or Hickman lines. It is, however, associated with a higher incidence

of incorrect line placement than internal jugular catheterization. Given the

local anatomy, pressure cannot be exerted on the subclavian artery if it is

accidentally punctured.

The subclavian vein is a continuation of the axillary vein and runs from

the apex of the axilla, behind the posterior border of the clavicle and

across the ﬁ rst rib to join the internal jugular vein, forming the brachio-

cephalic vein behind the sternoclavicular joint ( Fig. 18.6 ).

• Introduce yourself, conﬁ

rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Place the patient in a supine position, head-down.

• Turn the head to the contralateral side.

• Reconﬁ

rm the patient’s identity, procedure, and site prior to starting.

• Using full sterile technique, introduce a needle attached to a 10 mL syringe,

1 cm below the junction of the medial 1/3 and outer 2/3 of the clavicle.

*

U.K. Guidelines produced by the National Institute for Clinical Excellence (NICE) in September

2002 encourage the routine use of 2-D (B-mode) ultrasound guidance for CVC insertion into the

internal jugular vein in adults and children in elective and emergency situations. There is, however,

limited evidence supporting ultrasound use for subclavian and femoral vein catheterization based

on anatomy. Ultrasonography enables direct visualization of the anatomy before and during cath-

eterization. Portable ultrasound machines can be used at the bedside. An additional review of this

issue can be viewed in McGee DC, Gould MK (2003). Preventing complications of central venous

catheterization. N Engl J Med 348;1123–1133.

Assorted U.S. procedural guidelines can be seen at http://www.guidelines.gov

CHAPTER 18 Practical procedures530

• Direct the needle medially, slightly cephalad, and posteriorly behind

the clavicle toward the suprasternal notch.

• Slowly advance the needle while gently withdrawing the plunger.

• When a free ﬂ

ow of blood appears, follow the Seldinger approach as

detailed for internal jugular vein catheterization.

• The catheter tip should lie in the SVC above the pericardial reﬂ ection.

• Perform a chest X-ray to conﬁ

rm position and exclude pneumothorax.

• As before, ultrasound can be used to guide puncture of the vein, using

a more lateral approach.

Removing internal jugular venous catheters

• Remove any dressing and suture material.

• Ensure that all drugs and infusions have been stopped.

• Lay the patient down to reduce the risk of air embolism.

• Ask the patient to take a deep breath and fully exhale.

• Remove the line smoothly with a steady pull, while the patient is

breath-holding, and apply ﬁ

rm pressure to the puncture site for at

least 5 minutes to stop bleeding.

• Sit the patient up.

• If infection is suspected, send the tip of the line in a sterile dry

specimen container for culture.

External carotid

artery

Common carotid

artery

Right internal

subclavian vein

Right branchiocephalic

vein

Superior vena cava

Point of access to

the IVJ between the

heads of the

sternomastoid

Internal

jugular vein

Sternomastoid

Right subclavian

Point of

insertion for

central access

(a)

(b)

vein

Fig. 18.6 Surface anatomy of the internal jugular vein (a) and subclavian vein (b).

531

BLOOD PRESSURE MEASUREMENT

1 Blood pressure measurement

Theory

BP is measured with a sphygmomanometer, usually at the brachial artery.

Machines, operated by nurses or health-care assistants usually measure

BP, but these are not fool-proof and a good working knowledge of the

“old-fashioned,” manual method of BP measuring is still essential.

A cuff is applied to the upper arm and inﬂ ated to cut off the arterial

supply. The pressure is released slowly and a stethoscope used to listen

for the blood ﬂ ow.

When the pressure in the cuff equals the systolic blood pressure, blood

will audibly pulse through the artery. When the cuff pressure falls below

the diastolic blood pressure, the blood will ﬂ ow continuously and the

sound of intermittent blood ﬂ ow will disappear.

Equipment

• A (functioning) sphygmomanometer with:

• An appropriately sized cuff (see Table 18.1 )

• Stethoscope

Procedure

• Introduce yourself, explain the procedure, and obtain verbal consent.

2 Check that the sphygmomanometer is working and is within the calibra-

tion box or that the dial reads “0.”

• The patient should be sitting, relaxed for 5 minutes beforehand.

• Apply the cuff to the upper arm with the air bladder anteriorly

(indicator over the brachial artery).

• Using your left arm, support the patient’s arm so that it is held

horizontally at the level of mid-sternum (avoid hyperextension of

elbow).

• Close the valve (may be a screw or lever), monitor the patient’s radial

artery, and inﬂ

ate the cuff until the radial pulse is no longer palpable.

• Listen over the brachial artery at the antecubital fossa, using the

diaphragm or the bell of the stethoscope, while deﬂ

ating the cuff at a

rate of 2–3 mmHg/second.

• Note the point at which the pulsation is audible (Korotkoff* phase

I—the systolic BP)

Table 18.1 National Guideline Clearinghouse guidelines for choice of BP

cuff *

Arm circumference (cm) Cuff size Bladder dimensions (cm)

22–26 Small adult/child 12 × 22

27–34 Adult 16 × 30

35–44 Large adult 16 × 36

45–52 Adult thigh cuff 16 × 42

* Available at: www.guideline.gov

CHAPTER 18 Practical procedures532

• And the point at which the sounds disappear (Korotkoff phase V—the

diastolic BP).

• Record the BP as “systolic/diastolic” to the nearest 2 mmHg.

2 Hints

• In some people with normal blood pressure, the sounds may not

disappear completely. In this case, a distinct mufﬂ ing of the noise

(Korotkoff phase IV) should be used to indicate the diastolic BP.

• BP recording may be particularly difﬁ

cult in a noisy environment or

at the time of an emergency (which is when providers are most often

asked to record the BP) or when the BP is very low. In this case, a

rough estimation of the systolic BP may be made by feeling for the

return of the radial pulse as the cuff is deﬂ ated.

533

RECORDING A 12-LEAD ECG

1 Recording a 12-lead ECG

Theory

The ECG is a recording of the electrical activity of the heart. Electrodes are

placed on the limbs and chest for a 12-lead recording. The term 12-lead

relates to the number of directions that the electrical activity is recorded

from and is not the number of electrical wires attached to the patient!

Equipment

• ECG machine capable of recording 12 leads

• 10 ECG leads (4 limb leads, 6 chest leads)—should be attached to

machine

• Conducting sticky pads (ECG electrodes)

Procedure

• Introduce yourself, conﬁ rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Position the patient so that they are sitting or lying comfortably with

their upper body, wrists, and ankles exposed.

• Each electrode is attached by clipping it to the sticky pads and sticking

them to the patient’s skin.

• The leads are usually labeled. The limb leads are often color-coded:

•

Right arm—red

•

Left arm—yellow

•

Right leg—green

•

Left leg—black

• The arm leads are of medium length and should be attached to a

hairless part of the patient’s wrists.

• The leg leads are the longest and should be attached to the patient’s

ankles (the hairless part just superior to the lateral malleolus is ideal).

• Position the chest leads as follows (see Fig. 18.7 ):

•

V1—fourth intercostal space at the right sternal border

•

V2—fourth intercostal space at the left sternal border

•

V3—midway between V2 and V4

•

V4—ﬁ fth intercostal space in the mid-clavicular line on the left

•

V5—left anterior axillary line, level with V4

•

V6—left mid-axillary line, level with V4

• Turn on the ECG machine. These are usually self-explanatory and

require just one button to be pressed—marked analyze or record .

• Check the calibration and paper speed:

•

1 mV should cause a vertical deﬂ ection of 10mm.

•

Paper speed should be 25 mm/sec (5 large squares per second).

• Ensure that the patient’s name, DOB, as well as date and time of the

recording are clearly recorded on the trace.

• Remove the leads and discard the sticky electrode pads.

CHAPTER 18 Practical procedures534

2 Hints

• Encourage patient to relax, as muscle contraction causes interference.

• Ensure that you cleanse the area gently with an alcohol swab before

attaching an electrode, to ensure a good connection.

• AC electrical lines and ﬂ

uorescent lights may cause 60-cycle

interference. If this is the case, try turning off the ﬂ uorescent

lights.

V

1

V

2

V

3

V

4

V

5

V

6

Fig. 18.7 Correct positioning of electrodes for a standard 12-lead ECG.

535

ARTERIAL BLOOD GAS SAMPLING

1 Arterial blood gas sampling

Theory

An arterial sample is obtained to assess pH, PO

2

, PCO

2

, HCO

3

–

, and

base excess or deﬁ cit. It is also sometimes used for rapid assessment of

electrolytes.

Equipment

• ABG kit (usually contains heparin-ﬁ lled syringe, needle and vented cap)

• Gauze or cotton ball

• Tape

• Sterile gloves

Procedure

• Wash your hands and put on gloves.

• Verify patient identity, explain the procedure, and obtain verbal

consent. Be sure to warn the patient of potential pain, and ask them to

keep as still as possible.

• Note the patient’s temperature and oxygen support.

• Chose a site for arterial puncture.

Radial

Because there are no adjacent nerves or vessels, this is the most com-

monly used site.

• Assess for adequate ulnar arterial circulation by performing the Allen’s

Test.

• Obstruct the radial artery with ﬁ ngertip

pressure.

• Ask the patient to make a tight ﬁ st to expel blood from the hand and

maintain pressure on the radial artery.

• Ask them to open their hand and watch for ﬂ

ushing of the palm; this

indicates adequate perfusion.

• Take the blood gas syringe, ensuring that the heparin has coated the

inside by withdrawing and advancing plunger.

• Attach the needle and expel the excess heparin.

• Position the wrist in extension.

• Palpate the radial arterial pulse along its length using your middle and

index ﬁ ngers.

• Clean the skin.

• Having chosen a suitable spot, insert the needle with the bevel facing

toward the direction of blood ﬂ

ow, using an appropriate angle.

• Advance the needle until arterial pressure ﬁ

lls the syringe.

• Obtain a sample of 1–3 mL and withdraw the needle.

• Apply pressure to the puncture site with gauze or a cotton ball until

bleeding has stopped (minimum 2 minutes).

• Remove and discard the needle with care and place a vented cap on

the syringe. Holding vertically, expel any air through the vent.

• Mix sample gently and take it to a blood gas analyzer.

CHAPTER 18 Practical procedures536

Femoral

• Position patient with the hip extended and slightly internally rotated.

• Note that the femoral nerve is just lateral to the artery, so maintain a

medial approach.

• Use the same procedure as above but use a 21G needle, aiming at the

pulsation positioned between your index and middle ﬁ nger.

Brachial

• Position the elbow in extension.

• Watch for adjacent nerves (see Fig. 18.8 ).

Appropriate angles for needle insertion

• Radial artery—45

0

• Brachial artery—60

0

• Femoral artery—90

0

Hints

• The key to success is carefully lining up the needle over a palpable

pulsation—take your time!

• If there is no ﬂ

ashback, withdraw the needle slightly, change the angle,

and advance. Note that most pain is from puncturing the skin, so do

not remove the needle fully when repositioning.

• If there will be some delay in analyzing the sample, store the blood-

ﬁ

lled syringe on ice.

• Sources of blood gas result errors are as follows:

•

Air in the sample

•

Delay in analyzing sample or delay in icing

•

Excess heparin in the syringe

•

Accidentally obtaining a venous or mixed AV sample

•

Alterations in temperature

Cephalic vein

Median cubital vein

Radial artery

Brachial artery

Basilic vein

Ulnar artery

Fig. 18.8 Position of the brachial artery and surrounding structures at the

antecubital fossa. The right arm is pictured.

537

PEAK FLOW MEASUREMENT

1 Peak ﬂ ow measurement

Theory

Peak expiratory ﬂ ow rate (PEFR) is a measure of the maximum speed of

expiration. Expressed in liters/minute, this simple and easy-to-administer test

is a useful indicator of airway caliber and may be performed before and after

administration of a bronchodilator to assess reversible airway obstruction.

Normal values are based on gender, age, and height.

Equipment

• Peak ﬂ ow meter (see Fig. 18.9 )

• Clean disposable mouthpiece

Procedure

• Introduce yourself, explain the procedure, and obtain verbal consent.

• The patient should be standing or sitting upright.

• Ensure that the meter is set to 0.

• Ask the patient to take a deep breath in, hold the mouthpiece in their

mouth, and seal their lips tightly around it.

• The patient should blow out as hard and as fast as possible.

2The PEFR needs a hard and short maximal blow-out. The patient does

not have to blow out completely.

• Make note of the reading achieved.

• The procedure should be repeated and the best of 3 efforts recorded.

• The result should be compared to the normal value on the Nunn-

Greggs nomogram.

• If the patient is to keep a record, be sure to explain how to record

the readings appropriately. (Sometimes a 2-week diary is kept by the

patient to assess for diurnal variation.)

2 Hints

• If the patient is having difﬁ culty performing the test correctly, a brief

demonstration often proves useful.

• If a patient has very variable ﬂ

ow measurements, repeat your

demonstration and go on asking for ﬂ

ows until three consistent

readings have been recorded.

Fig. 18.9 Electronic and mechanical peak ﬂ ow meters.

CHAPTER 18 Practical procedures538

1 Inhaler technique

A person new to respiratory medicine may be surprised by the sheer

number of different inhaler devices on the market. Each has its advantages

and disadvantages and a different set of drugs that it can deliver.

Here we outline the inhaler devices currently available and the instruc-

tions for use, written as you would explain them to a patient. We suggest

that providers become familiar with the different devices by asking your

pharmacist if you can see placebo versions.

Instructions for use of devices are typically available from the manufac-

turer’s Web site. Full video demonstrations illustrating appropriate use

of devices are often available at manufacturer’s Web sites, so these sites

should not be overlooked.

Devices are constantly changing. Many devices are currently used, some

of which have gone out of production. Some common devices include

Clickhaler, Spinhaler, Aerohaler, Diskhaler, Rotahaler, Foradil inhaler, and

Pulvinal. Included here is Handihaler, which is in current use.

Metered-dose inhaler (MDI)

This is the ﬁ rst device developed and the one people think of as a typical

inhaler ( Fig. 18.10 ). It is small and cheap and has many different drugs and

doses. However, there is no dose counter and it requires much coordin-

ation to use correctly, making it unsuitable for the very young or elderly

or those with arthritis or other ailments affecting the hands.

Instructions for use

• Take one dose at a time.

• Remove the cap and shake the inhaler several times.

• Sit upright, hold the head up, and breathe out.

• Place the inhaler in the mouth and seal lips around the mouthpiece.

Fig. 18.10 A metered-dose inhaler (MDI).

539

INHALER TECHNIQUE

• Breathe in, press the canister down to release drug, and continue to

take a deep breath in. (The canister should be pressed just after the

start of inhalation, not before.)

• Remove inhaler and hold breath for as long as possible, up to 10 sec.

• Recover before taking the next dose, and replace the cap.

Autohaler

This is one of the breath-actuated inhalers, releasing a dose of the drug

when a breath is taken ( Fig. 18.11 ). This eliminates the need for hand

coordination and can reassure patients that a dose has been successfully

administered.

Some people, however, may still ﬁ nd the priming lever hard to use or

may have difﬁ cultly remembering to prime the device for each dose. Also,

the puff and click during inhalation can be distracting.

Instructions for use

• Remove the cap and shake the inhaler several times.

• Prime the device—push the lever right up, keeping the inhaler upright.

• Sit upright, hold the head up and breathe out.

• Seal lips around the mouthpiece.

• Inhale slowly and deeply —don’t stop when the inhaler clicks, and

continue taking a really deep breath.

• Remove the inhaler and hold breath for as long as possible, up to

10 seconds.

• Push lever down and replace the cap.

• Recover before taking the next dose.

• Advise the patient that they won’t feel the spray hitting the back of the

throat, although there may be a slight taste disturbance.

Fig. 18.11 Autohaler. Note the lever on the top. The inhaler must be primed for

each dose.

CHAPTER 18 Practical procedures540

2 Hints

• Patients unable to push the lever up by hand can sometimes use the

edge of a table to push it against.

• Patients should breathe in steadily, not as fast as possible.

Diskus

This is one of the dry-powder devices ( Fig. 18.12 ) and has superseded

the Diskhaler. Like most of the other inhalers, it is preloaded and has an

integral cap. It also has a dose counter. However, it is more expensive than

some of the other devices and has a several-step priming mechanism that

some patients may not be able to cope with.

Instructions for use

• Hold the outer casing and push the thumb grip away from you,

exposing the mouthpiece, until you hear a click.

• Holding the mouthpiece toward you, slide the lever back until it clicks

(the device is now primed and the dose counter moves on 1).

• Sit upright, hold the head up, and breathe out.

• Holding the Diskus lever, seal lips around the mouthpiece.

• Inhale deeply and steadily.

• Remove the inhaler and hold breath for as long as possible, up to 10

seconds.

• To close, slide the thumbgrip toward you, so that the cover moves

over the mouthpiece, until you hear a “click.”

• Recover before taking the next dose.

• Advise the patient that they won’t feel the spray hitting the back of the

throat, although there may be a slight taste disturbance.

Turbohaler

This is another dry-powder device with preloaded drug ( Fig. 18.13 ). There

is no dose counter, but a window that turns red after 20 doses—the

device is empty when there is red at the bottom of the window. Some

Fig. 18.12 Accuhaler (Diskus) closed and open. Note the thumbgrip, lever, and

mouthpiece.

541

INHALER TECHNIQUE

people ﬁ nd the lack of taste disadvantageous (they like to be sure the dose

has been given). Again, those with hand problems or deformities may ﬁ nd

it difﬁ cult to use.

Instructions for use

• Unscrew and remove the white cover.

• Hold the inhaler upright.

• Twist the grip clockwise then counterclockwise as far as it will go until

a “click” is heard.

• Sit upright, hold the head up, and breathe out.

• Seal lips around the mouthpiece.

• Inhale slowly and as deeply as possible.

• Remove the inhaler and hold breath for 10 seconds.

• Replace cover.

• Recover before taking the next dose.

• Advise the patient that they won’t feel the spray hitting the back of the

throat, although there may be a slight taste disturbance.

There are devices available that can calculate whether a person has a suf-

ﬁ

cient inspiratory ﬂ

ow rate to deliver the drug into the airways.

Handihaler

At the time of this writing, this is relatively new to the market and only

available for tiotropium. It is a dry-powder device with an integrated cap

and requires a lower inspiratory ﬂ ow rate than other devices ( Fig. 18.14 ).

Fig. 18.13 Turbohaler. Note the tiny dose-indicating window.

CHAPTER 18 Practical procedures542

However, it is not preloaded, thus a dose needs to be inserted via cap-

sule at each use. This task requires some dexterity. Some people also ﬁ nd

the cap hard to open, as a moderate amount of strength is needed to get

it right.

Instructions for use

• Open cap by pulling upward, exposing the mouthpiece.

• Open the mouthpiece by pulling upwards exposing the chamber.

• Take a capsule from the blister-pack and insert it into the chamber.

• Replace the mouthpiece (make sure it clicks) and leave the cap open.

• Press the side button in a few times to pierce the capsule (you can

watch through the small window).

• Sit upright, hold the head up, and breathe out.

• Seal lips around the mouthpiece.

• Breathe in deeply to a full breath (you should hear the capsule

vibrate).

• Remove inhaler and hold breath for as long as is comfortable.

• Breathe out slowly.

• Remove the use capsule and replace the cap.

Spacer devices

These are used with a standard MDI and allow the drug to be puffed

into a chamber before it is inhaled. This reduces deposition of the drug

in the upper airways (and the local side effects) and increases peripheral

lung deposition. This also means that no coordination is required and the

Fig. 18.14 Handihaler. Note the button at the side for piercing the capsule and

the small window at the front.

543

INHALER TECHNIQUE

patient has more time to inhale the drug. These are particularly useful for

the very young or elderly, or those with severe breathlessness.

These devices are, however, bulky, which patients may ﬁ nd embarrass-

ing. They also require a certain amount of dexterity to put together.

There are a number of spacer devices available, but only the

Aerochamber ( Fig. 18.15 )is discussed here.

Instructions for use (Aerochamber)

• Remove cap of the MDI, shake the inhaler, and insert into the back of

the Aerochamber.

• Breathe out.

• Seal lips around the mouthpiece.

• Press down the canister once to release the drug.

• Breathe in slowly and deeply—the Aerochamber will whistle if you

breathe too quickly.

• Hold breath for 10 seconds.

• Breathe out through mouthpiece and breathe in again (do not press

the canister a second time). This may be repeated up to 4 or 5

breaths.

• If a second dose is required, relax for a minute and repeat steps 3–5.

• Remover the inhaler and replace the cap.

Cleaning the Aerochamber

• The device must be rinsed daily in soapy water.

• Allow to air-dry on a drainer—do not rub (creates static electricity).

• Aerochambers should be replaced by a new model every 6 months.

Fig. 18.15 Aerochamber with MDI inserted in the end.

CHAPTER 18 Practical procedures544

1 Oxygen administration

Theory

This is the administration of supplementary oxygen when tissue oxygena-

tion is impaired.

The aim is to achieve adequate tissue oxygenation (without causing a

signiﬁ cant d in ventilation and consequent hypercapnia or oxygen toxicity)

while minimizing cardiopulmonary workload.

2 Oxygen is a drug with a correct dosage and side effects, which, when

administered correctly, may be life saving.

The primary responsibility for oxygen prescription lies with the hospital

medical staff. It is good practice to record the following:

• Whether delivery is continuous or intermittent

• Flow rate/percentage used

• What SaO

2

should be

When to treat

• Tissue hypoxia is difﬁ cult to recognize, as clinical features are

nonspeciﬁ c. They include altered mental state, dyspnea, cyanosis,

tachypnea, arrhythmias, and coma.

• Treatment of tissue hypoxia should correct any arterial hypoxemia

(cardiopulmonary defect or shunt, e.g., PE, pneumonia, asthma), any

transport deﬁ cit (anemia, low cardiac output), and the underlying causes.

2 Remember, SaO

2

/PaO

2

can be normal when tissue hypoxia is caused by

low cardiac-output states.

Equipment

See b p. 546.

Procedure

• Explain what is happening to the patient and ask their permission.

• Choose an appropriate oxygen delivery device (see next page).

• Choose an initial dose:

•

Cardiac or respiratory arrest: 100%

•

Hypoxemia with PaCO

2

<40 mmHg: 40–60%

•

Hypoxemia with PaCO

2

>40 mmHg: 24% initially

• Decide on the acceptable level of SaO

2

or PaO

2

and titrate oxygen

accordingly.

• If possible, try to measure a PaO

2

in room air prior to giving

supplementary oxygen. (This is not absolutely necessary, especially if

the patient is in severe respiratory distress or is hypoxic.)

• Work with nursing staff, respiratory therapist, or outreach services for

support in setting up equipment.

• Apply the oxygen and monitor via oximetry (SaO

2

) and/or repeat

ABGs (PaO

2

) in 30 minutes.

• If hypoxemia continues, the patient may require respiratory support

either invasively or noninvasively—consult with a respiratory specialist.

• Stop supplementary oxygen when tissue hypoxia or arterial hypoxemia

has resolved.

545

OXYGEN ADMINISTRATION

Hints

• Only 10% of patients with COPD are susceptible to CO

2

retention

with oxygen therapy. Use Venturi-style masks and monitor closely.

• Think about what is normal for the individual.

Oxygen administration equipment

The method of delivery will depend on the type and severity of respi-

ratory failure, breathing pattern, respiratory rate, risk of CO

2

retention,

need for humidiﬁ cation, and patient compliance.

Each oxygen delivery device ( Fig. 18.16 ) comprises an oxygen supply, ﬂ ow

rate, tubing, interface 9 humidiﬁ cation. (Humidiﬁ cation should be used for

patient comfort, presence of thick tenacious secretions, or ﬂ ows >4 L/min.)

Nasal cannulas

These direct oxygen via two short prongs up the nasal passage They

• Can be used for long periods of time.

• Prevent rebreathing.

• Can be used during eating and talking.

Local irritation, dermatitis, and nose bleeding may occur, and rates of

above 4 L/min should not be used routinely.

Low-ﬂ

ow oxygen masks

These deliver oxygen concentrations that vary depending on the patient’s

minute volume. At these low ﬂ ow rates there may be some rebreathing of

exhaled gases (they are not sufﬁ ciently expelled from the mask).

Fixed performance masks

These achieve a constant concentration of oxygen independent of the

patient’s minute volume.

The masks contain Venturi barrels where relatively low rates of oxygen

are forced through a narrow oriﬁ ce, producing a greater ﬂ ow rate that

draws in a constant proportion of room air through several gaps.

Partial and non-rebreather masks

Masks such as these have a reservoir bag that is ﬁ lled with pure oxygen

and depend on a system of one-way valves that prevent mixing of exhaled

gases with the incoming oxygen.

The concentration of oxygen delivered is set by the oxygen ﬂ ow rate.

High-ﬂ ow oxygen masks

Masks or nasal prongs generate ﬂ ows of 50–120 L/min using a high-ﬂ ow

regulator to mix air and oxygen at speciﬁ c concentrations.

These masks are highly accurate, as delivered ﬂ ow rates will match a

high respiratory rate in patients with respiratory distress. It should always

be used with humidiﬁ cation.

CHAPTER 18 Practical procedures546

(a)

(b)

(e)

(d) (f)

(c)

Fig. 18.16 (a) Nasal cannula. (b) Low-ﬂ ow/variable-concentration mask. (c) Non-

rebreather mask. (d) Mask with Venturi valve attached. (e) Selection of Venturi

valves. (f ) Humidiﬁ cation circuit.

547

BASIC AIRWAY MANAGEMENT

2 Basic airway management

Theory

An inadequate airway ( Box 18.4 ) leads rapidly to hypoxemia and, if uncor-

rected, brain damage and death. Endotracheal intubation remains the gold

standard for securing an airway and protecting the patient from aspiration

( Box 18.5 ).

Airway management without intubation is an important skill to master

and consists of the use of one or more of the following: triple maneuver,

face masks, oropharyngeal and nasopharyngeal airways, laryngeal masks,

and other supraglottic devices, e.g., Combitube. It may be carried out

when intubation equipment or skills are unavailable, if intubation is difﬁ -

cult, or on a patient with a partially obstructed airway.

Urgency is an important factor in planning and securing an airway in the

most appropriate manner. This will depend on risk of vocal cord injury,

degree of patient cooperation, anatomy of airway, equipment at hand, and

your own experience.

Before you start

2 Think about simple positioning and the recovery position of the patient,

especially for airway protection alone.

Assess for airway obstruction:

• LOOK (into mouth and for chest or abdominal movement)

• LISTEN (snoring, gurgling, wheezing)

• FEEL (expired air)

2 Complete airway obstruction is silent.

Make sure that you have the following:

• Oxygen tubing

• Suction equipment

• Ambu-bag

• Rebreather bag

Hints

• A fully conscious, talking patient is able to maintain his or her own

airway and needs no further assessment.

0 Do not use a head tilt or chin lift in suspected cervical spine injury,

except as a last resort.

Airway maneuvers

The following techniques are performed with the patient lying supine, and

all aim to open the airway with simple physical maneuvers. These are

Box 18.4 Common causes of airway obstruction

• Tongue (due to unconciousness)

• Soft tissue swelling (trauma, tumor)

• Foreign material (blood, vomit)

• Direct injury

•

Secretions

•

Bronchospasm

CHAPTER 18 Practical procedures548

Box 18.5 Secure airways

A secure airway may be necessary in patients with the following:

• Apnea

• Glasgow Coma Scale <9/15

• High aspiration risk

• Respiratory failure

• Unstable mid-face trauma

• Airway injuries

Fig. 18.17 Performing a head tilt.

useful as a ﬁ rst step in managing a patient with a compromised airway and

are used in conjunction with an oxygen mask. They are also useful in situ-

ations where no airway devices are available.

If unsuccessful, you should go on to use additional equipment.

Head tilt

Place your hands around the patient’s forehead and tilt backward to

achieve upper cervical extension ( Fig. 18.17 ).

Chin lift

• This is usually used with the head tilt.

• Place the tips of the index and middle ﬁ

ngers of your right hand under

the front of the patient’s mandible.

• Lift up, pulling the mandible anteriorly ( Fig. 18.18 ).

Jaw thrust

• Use this maneuver if there is suspicion of an injury to the cervical

spine. This is a two-handed technique.

• Holding the patient from behind, place the ﬁ

ngers of both hands

behind the angle of the mandible.

• Lift the mandible with these ﬁ

ngers while using your thumbs to

displace the chin downward, opening the mouth (

Fig. 18.19 ).

2 Hint

0 Do not use a head tilt or chin lift in a patient with (or suspected to

have) cervical spine injuries.

549

BASIC AIRWAY MANAGEMENT

Fig. 18.18 Performing a chin lift.

Fig. 18.19 Performing a jaw thrust.

Airway devices

Face masks

2 Use the smallest-ﬁ tting mask to ﬁ t over the mouth and nose.

This is a simple mask that is ﬁ tted over the nose and mouth. You may

use an airway to aid ventilation or to clear any obstruction.

One-hand technique

• Place your thumb and index ﬁ

nger on the mask in a C

shape (see

Fig. 18.20 ).

• Grasp the jaw with the remaining ﬁ

ngers, pulling face into the mask.

CHAPTER 18 Practical procedures550

Fig. 18.20 Use of a face mask, one-handed technique.

Fig. 18.21 Use of a face mask, two-handed technique.

Two-hand technique

• Place your thumbs on either side of the nasal portion of the mask.

• Use your index ﬁ ngers to support the body of the mask.

• Use your other ﬁ ngers to lift the jaw and extend the neck (

Fig. 18.21 ).

Oropharyngeal airway

2 Use this when the patient is semiconscious.

This device consists of a ﬂ ange (limits depth of insertion), bite portion

(teeth of patient rest against this), and curved body (follows curvature of

the tongue), which has a lumen allowing passage of air and suction.

Different sizes are available and are color coded. The correct size is

determined by measuring the airway against the distance between the cor-

ner of the mouth and the angle of the jaw (Figs. 18.22 and 18.23).

551

BASIC AIRWAY MANAGEMENT

Technique

• Lubricate and insert the airway upside down.

• Once it is well into the mouth rotate 180˚ and advance to full position.

•

Alternatively, hold the tongue down and forward with a tongue

depressor until the airway is in place.

Fig. 18.22 Oropharyngeal airways.

Fig. 18.23 Chose size of the oropharyngeal airway by measuring from the

patient’s teeth to the angle of the mandible.

CHAPTER 18 Practical procedures552

•

Check for no gagging, snoring, or vomiting and that air is moving in

and out.

• Use a size 10/12/14 catheter for suction, if required.

Nasopharyngeal airway

2 This is tolerated better than the oropharyngeal airway in alert patients.

This device consists of a ﬂ

ange (limits depth of insertion). The pharyn-

geal end has a bevel to facilitate nontraumatic insertion and a curved body

with lumen allowing passage of air and suction. Some airways come with-

out an adequate ﬂ

ange, so a safety pin is used at the nasal end to prevent

the airway from falling back into the nose (see Fig. 18.24 ).

Different sizes are available. Determine the correct size by comparing

with the distance between the nostril and the tragus (see Fig. 18.25 ).

Technique

• The wider nostril is traditionally chosen, but most airways are beveled

for introduction into the left nostril.

• Lubricate airway and pass directly into the nasal passage, passing along

the ﬂ

oor of the nose or aiming for the back of the opposite eyeball.

• Use a size 10/12 catheter for suction, if required.

Fig. 18.24 Nasopharyngeal airways.

553

BASIC AIRWAY MANAGEMENT

Laryngeal mask airway (LMA)

This consists of a tube with an inﬂ atable cuff designed to seal around the

laryngeal opening ( Fig. 18.26 ). The patient must be deeply unconscious.

Technique

• Maintain oxygenation by bag and mask.

• Deﬂ

ate the cuff of the LMA using a 20 mL syringe.

• Lubricate the outer cuff with aqueous gel. This part will not be in

contact with the larynx.

• The patient should be in a supine position with head and neck in

alignment.

• Stand behind the patient or, if this is not possible, from the front.

• Hold the tube like a pen and pass it into the mouth with the distal

aperture facing the feet of the patient.

• Push back over the tongue while applying the tip to the surface of the

palate until it reaches the posterior pharyngeal wall.

• The mask is then pressed backward and down until it reaches the back

of the hypopharynx and resistance is felt.

• The black line on the tube should be aligned with the nasal septum.

• Inﬂ

ate the cuff with usually 20–30 mL of air.

• The tube should lift out of the mouth slightly; the larynx is pushed

forward if it is in the correct position.

• Attach breathing circuit and gently ventilate patient with 100% oxygen.

• Conﬁ

rm correct placement by auscultating the chest in the axillary

regions and observe for bilateral chest movement.

• Insert a bite block or oropharyngeal airway alongside the tube and

secure the airway with the tape or tie provided.

Fig. 18.25 Chose size of the nasopharyngeal airway by measuring from the

patient’s nostril to the tragus.

CHAPTER 18 Practical procedures554

Fig. 18.26 A laryngeal mask airway.

555

TRACHEOSTOMY MANAGEMENT

3 Tracheostomy management

Theory

A tracheostomy is an opening in the anterior wall of the trachea below the

larynx that can facilitate ventilation and respiration.

A mini-tracheostomy is a narrow-diameter, cufﬂ ess tube inserted into the

trachea, through which a catheter can be passed to stimulate a cough and/

or suction. This is not a method for protecting the airway or delivering any

kind of ventilatory support except emergency oxygen therapy.

Tracheostomy may be performed if the need for an endotracheal tube

is prolonged, to facilitate weaning, to identify an inability to maintain or

protect an airway, and to secure and clear an airway.

Patients may have a permanent tracheostomy in place or even a stoma.

These often do not need humidiﬁ cation or suction unless the patient is

acutely ill.

Equipment

Tracheostomy tube

The tracheostomy tube may be stitched in or secured around the neck and

is either single or double lumen (has an inner tube that can be removed

for cleaning). The tubes are either fenestrated or nonfenestrated.

Fenestrated tubes allow the passage of air and secretions into the

mouth. These are good for weaning.

Humidiﬁ cation

Heated humidiﬁ cation is used for the short term and is the gold standard.

A heat moisture exchanger is used for patients with minimal secretions or

who are mobile.

Procedures

Open suction

The aim is to remove secretions and prevent blockages in the tracheos-

tomy tube, bronchial obstruction, and alveolar collapse.

• Use a catheter with diameter no more than one 1/2 the internal

tracheotomy diameter. [(Size of outer diameter) – 2 x 2 = x; e.g., 8.0

mm – 2 x2 = 12].

• Negative pressure should be 100–150 mmHg.

• Wear gown, gloves, and protective eyewear.

• Attach a sterile catheter to suction equipment, ensuring a good seal,

and leave most of the packaging in place.

• Place under the nondominant arm.

• Put a clean, disposable glove on the dominant hand and do not

touch anything other than the catheter tip.

• Pull the packaging away with the nondominant hand.

• Open the suction port.

• Introduce the tip of the catheter into the tracheostomy tube with

the dominant hand gently but quickly.

• Depth of insertion should be 0.5–1.0 cm beyond the end of the

tracheostomy tube (about 1/3 the length of catheter).

CHAPTER 18 Practical procedures556

• Insert until the patient coughs.

• Withdraw the tip 0.5 cm and apply suction.

• Continue to withdraw slowly and continuously.

• Close the suction port and discard the glove and catheter.

2 Suction should last no more than 10 seconds.

2 Allow sufﬁ

cient time between passes for recovery.

• Repeat until secretions are cleared.

• After suction, ensure that the patient is reconnected to respiratory

support and oxygen and that oxygen levels are returned to normal.

Tube occlusion

• Call for help.

• Reassure the patient.

• Ask the patient to cough, or attempt to clear secretions via suction.

• Remove the inner cannula and replace it with a new one.

• If there is no inner cannula, deﬂ

ate the cuff and administer oxygen

facially, instill 2–5 mL 0.9% saline, and suction to try to clear blockage.

• If you are unable to clear the blockage, a total tube change may be

required (try using a smaller size, if necessary).

• If tube insertion fails, then consider mask-to-stoma ventilation

(consider suction via stoma).

2 If respiration stops all together, initiate the proper code, call for anes-

thesia service, inﬂ

ate the cuff, and manually ventilate using a catheter

mount and rebreather or Ambu-bag.

Swallowing assessment

This should be performed by the appropriate practitioner (e.g., radiologist

or speech and language therapist).

• Sit the patient up.

• Suction via tracheotomy prior to cuff deﬂ ation.

• Deﬂ

ate cuff fully, if possible, or to maximum degree that the patient

can tolerate.

• Ensure that there is an appropriate inner cannula in place.

• Give the patient sips of water from a teaspoon and follow the

procedure explained on b p. 289.

• Intermittently check for voice quality (ask the patient to say “ah” or

count out loud).

• Stop if the patient deteriorates, fatigues, shows signs of persistent

coughing or aspiration on suction, or has a persistently “wet” voice.

Hints

• Practice techniques before needing them in an emergency.

• Stridor is a good indication that an airway is partially blocked.

• Always remember to humidify oxygen in tracheostomy patients.

557

ENDOTRACHEAL (ET) INTUBATION

3 Endotracheal (ET) intubation

Theory

There are three main indications for tracheal intubation: relieving airway

obstruction, protecting the airway from aspiration, and facilitating artiﬁ cial

ventilation of the lungs.

2 Remember, if you are inexperienced in this technique, never perform

tracheal intubation unsupervized.

2 In an emergency situation, it is safer to bag and mask the patient or use

a laryngeal mask airway if one is available and await assistance.

Equipment

• Laryngoscope (check bulb)—usually size 3 is adequate

• Selection of ET tubes (size 7 in most women and size 8 in most men)

• Sterile lubricant

• 20 mL syringe for cuff inﬂ ation

• Tape to tie tube in place

• Rigid stilette or gum-elastic bougie

• Self-inﬂ

ating bag and oxygen supply

• Stethoscope for conﬁ

rming correct position of tube

• Suction apparatus with a wide-bore, rigid suction end (Yankauer)

Procedure

• In the awake patient, introduce yourself, conﬁ rm the patient’s identity,

explain the procedure, and obtain verbal consent.

• Wash your hands and put on a pair of gloves.

• Pre-oxygenate the patient with a high concentration of oxygen for a

minimum of 15 seconds.

2 Remember, intubation must take no longer than 30 seconds.

• Position the neck such that it is distally extended and proximally

slightly ﬂ

exed, with a small pillow underneath the head—an

exaggeration of the normal cervical lordosis.

2 If a cervical injury is suspected, the head and neck should be maintained

in neutral alignment.

• Stand at the head of the bed and open the mouth.

• Inspect for loose dentures or foreign material—remove any if present.

• Hold the laryngoscope in the left hand and look down its length as you

insert.

• Slide the scope into the right side of the mouth until the tonsillar fossa

comes into view.

• Now move the blade to the left so that the tongue is pushed into a

midline position.

• Advance blade, following the posterior edge of the soft palate until the

uvula comes into view.

• Advance blade over the base of the tongue, and the epiglottis should

pop into sight.

• With blade positioned between the epiglottis and base of the tongue

(vallecula), apply traction in the line of the handle of the laryngoscope.

CHAPTER 18 Practical procedures558

•

This movement should lift the epiglottis and expose the V-shaped

glottis behind.

• Once the triangular-shaped laryngeal inlet is in view, position the ET

tube between the vocal cords so that the tube is just distal to them.

•

Use mark on the tube above the cuff to indicate correct position.

•

This is around 21 cm in a female and 22 cm in a male.

• If difﬁ culty is experienced passing ET tube into the larynx, pass a gum-

elastic bougie ﬁ

rst and then try passing a lubricated ET tube over this.

• Once the ET tube is in position, inﬂ

ate the cuff while ventilating

through the ET tube with a self-inﬂ

ating bag ( Fig. 18.27 ).

• Verify correct positioning of the tube by observing chest movement

and auscultate at the sides of the chest in the mid-axillary line (both

sides of the chest should move equally, and you should hear breath

sounds at both lung bases).

• Secure the ET tube with a tie.

• Obtain a chest X-ray to conﬁ

rm the tube position. The ET tube has a

radio-opaque line within it.

• Document the details of the procedure in the patient notes.

Important note

2 The insertion of the ET tube should take no more than 30 seconds from

start to ﬁ nish. If 30 seconds pass and the tube is not in the correct pos-

ition, remove all the equipment and bag/mask ventilate the patient until

you are ready to try again.

Some complications of ET intubation

• Trauma to teeth, airway, larynx, or trachea

• Aspiration

• Airway obstruction

• Tube misplacement

• Hypoxia from prolonged attempts

• Tracheal stenosis (late complication)

Fig. 18.27 ET tube with attached syringe. The cuff has been inﬂ ated to

demonstrate.

559

NONINVASIVE VENTILATION (NIV)

3 Noninvasive ventilation (NIV)

Theory

NIV is the application of positive pressure ventilatory support via a facial

or nasal interface and not via an airway (ET tube, tracheostomy) (see Box

18.6 for setup). NIV should be operated only by trained staff in an appro-

priate area. It may be used in acute conditions in the hospital or in chronic

conditions at home.

Patients need to be spontaneously breathing, maintaining their airway

(i.e., conscious), and compliant. It is not a substitute for mechanical venti-

lation unless this has been decided as the ceiling of treatment.

Pressures are usually documented in cmH

2

O (rather than mmHg), and

it is good practice that the decision of maximal pressure to be used is

documented in the medical notes so that if a patient continues to deterio-

rate, the intensivist, pulmonologist, or anesthesiologist has an appropriate

management strategy in place.

Contraindications

These include undrained pneumothorax and pulmonary hemorrhage. It

is good practice to review a recent chest X-ray to rule these out before

beginning.

Cautions

These comprise bullae, unstable cardiovascular system, abscess, facial

trauma, basal skull fracture, recent bronchial or esophageal surgery, per-

sistent vomiting, and high bronchial tumor.

CPAP

Continuous Positive Airways Pressure (CPAP) maintains a single pres-

sure continuously throughout both inspiratory and expiratory phases.

It is used in the treatment of type I respiratory failure (obstructive

sleep apnea and cardiopulmonary edema, and occasionally in pulmonary

embolus, pneumonia, and weaning from ventilation).

BiPAP

Bilevel Positive Airways Pressure (BiPAP) ventilation uses different

pressures on expiration (EPAP) and on inspiration (IPAP). Higher EPAP

increases functional residual capacity (FRC), while higher IPAP augments

tidal volume. The system is normally pressure driven but can be volume

driven.

It is used in the treatment of type II respiratory failure (i.e., hypoventila-

tion, chronic neuromuscular conditions, and exacerbations of COPD).

CHAPTER 18 Practical procedures560

Box 18.6 Setting up NIV

This is not something that the inexperienced provider will be expected

to do. The following is a brief guide that should allow you to understand

what is involved.

CPAP

Equipment

• Mask, head strap, positive end-expiratory pressure (PEEP) valves

(5–7.5–10 cmH

2

O)

• Circuit, safety pop-off/blow-off valve

• High-ﬂ

ow generator for oxygen and air

• Heated humidiﬁ cation

Procedure

• Explain the procedure to the patient and obtain verbal consent.

• Use measuring templates to assess appropriate-size interface and

minimize air leaks.

• Set oxygen and ﬂ

ow rate and ensure that the PEEP valve opens a

small distance only and never fully closes.

• Start with a low pressure and slowly increase for patient comfort

and to gain compliance.

• Aim to reduce the work of breathing.

• Continuously monitor ABG/SaO

2

, heart rate, and BP. Watch for

abdominal distension.

BiPAP

Equipment

• Mask (facial/nasal), prongs, full face mask, head strap

• Circuit, exhalation port

• Entrained oxygen, if required

• Heated humidiﬁ cation

• Ventilator (NIPPV1/2/3, Breas, BiPAP vision)

Procedure

• Explain the procedure to the patient and obtain verbal consent.

• Use measuring templates to assess appropriate-size interface and

minimize air leaks.

• Start with low pressures and slowly increase for patient comfort and to

gain compliance. (Trial data in COPD is based on pressures of 20/5.)

• Setting inspiratory and expiratory times will need to be continuously

reassessed, as respiratory rate will change over time.

• Initially aim to match the patient’s own ventilatory pattern, but

eventually aim to d respiratory rate and i tidal volume/ﬂ ow

using

the minimal pressures possible.

• Monitor ABG/SaO

2

, heart rate, and BP at 1 and 4 hours. Watch for

abdominal distension.

561

PLEURAL FLUID SAMPLING (THORACENTESIS)

2 Pleural ﬂ uid sampling

(thoracentesis)

Theory

After identifying a pleural effusion, a small volume of ﬂ uid may be aspirated

and sent for biochemical, cytological, and microbiological analysis.

A neurovascular bundle runs on the inferior/inner aspect of each rib; to

avoid this, needles for aspiration are inserted immediately above a rib.

Equipment

• Instrument stand

• Sterile/wound care pack

• Sterile gloves

• Antiseptic solution

• 5 mL syringe

• 20 mL syringe

• 1 vial of local anesthetic (usually

1% lidocaine)

• Selection of needles

(2 green, 1 orange/blue)

• 2 sterile sample containers

• 1 pair of culture bottles

• Biochemistry tube for glucose

sample

Procedure

• Introduce yourself, check the patient’s identity, explain the procedure,

obtain verbal consent, and unwrap the equipment.

• Position the patient to sit upright on the edge of the bed, leaning

forward with arms raised—use a pillow on a raised bedside. table for

the patient to lean on (see Fig. 18.29 ).

• Percuss upper border of the effusion posteriorly, and choose a site

one or two intercostal spaces below that.

• Mark the chosen spot at the upper edge of a rib with a pen.

• Wash your hands and put on sterile gloves.

• Clean the marked area with the antiseptic solution on a cotton ball.

Work outward in a spiraling fashion.

• Pause to reconﬁ

rm patient identity, the procedure, and site.

• Draw up 5 mL of the lidocaine with the green needle.

• Swap the needle for an orange one and inﬁ

ltrate the skin, creating a

surface bleb.

• Swap for a green (18G) needle and inﬁ

ltrate anesthetic deeper.

Advance needle in a step-wise manner, drawing back the syringe each

time it is advanced to ensure vasculature is avoided (

Fig. 18.30 ) and

inﬁ ltrating anesthetic before advancing again.

• Once you reach the pleural cavity, a ﬂ

ashback of pleural ﬂ

uid may be

obtained.

• Take the 20 mL syringe, attach a green (18G) needle and aspirate

20 mL of pleural ﬂ

uid, being careful to use the anesthetized tract.

• Withdraw the needle and cover the wound with a suitable dressing

(dry gauze and medical sticky tape will sufﬁ ce).

• Put 4 mL of ﬂ

uid in each bottle and send to the laboratories for

•

Biochemistry (pH, protein, LDH, amylase, glucose)

•

Cytology

•

Microbiology (MC&S plus TB stain and culture, if indicated)

CHAPTER 18 Practical procedures562

• Request a chest X-ray post-procedure to check for pneumothorax

only if the procedure was difﬁ cult or high risk.

Hints

2 If pH needs to be measured, the sample must be sent to the laboratory

immediately.

0 Some laboratories will not measure pH—check before you begin. An

alternative is to save a small amount of ﬂ uid, draw it up in a primed blood

gas syringe, and run it through a blood gas analyzer to gain an instant pH

measurement.

• In larger individuals, the pleural cavity may be at some depth from the

skin. If this is the case, use a longer needle—needles of IV catheters

are often signiﬁ

cantly longer despite being the same gauge.

Pillow

Bedside

table

Bed or chai

r

Arms crossed,

head on arms

Fig. 18.28 Position patient comfortably leaning forward—use a bedside table and

pillow for them to lean on with their arms crossed.

Fig. 18.29 Insert needle just above a rib, at the lower border of the intercostal

space, to avoid the neurovascular bundle.

563

CHEST TUBE INSERTION

Equipment

• Instrument stand

• 10 mL 1% lidocaine

• 10 mL syringe

• 1 orange (14 gauge) needle

• 1 green (18 gauge) needle

• Sterile gloves

• Sterile pack (containing cotton

balls, container, drape)

• Barrier pad (Blue pad/Chux)

• Suitable dressing

• Seldinger chest tube kit

(containing chest tube,

in-troducer, chest drain needle,

syringe, scalpel, 3-way tap, guide

wire)

• Suture (no. 15)

• Povidone-iodine solution

• Chest drain tubing

• Chest drainage bottle

• 500 mL sterile water

Procedure

• Introduce yourself, conﬁ rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Double-check the history and chest X-ray to be sure of which side

needs the drain.

• Position the patient sitting on a chair or the edge of their bed, arms

raised. Instead of asking the patient to hold their arm over their head,

it is often easier to ask them to cross their arms and lean on a bedside

table with a pillow, raised level with their shoulders (see Fig. 18.28 ).

• Triple-check the side by brieﬂ

y examining the patient (tap out dullness

of an effusion or listen for the

d breath sounds of a pneumothorax).

• The usual site for insertion is in the mid-axillary line, within a triangle

formed by the diaphragm, the latissimus dorsi, and the pectoralis major

( Fig. 18.30 ). For apical pneumothoraces, you may wish to choose the

second intercostal space in the mid-clavicular line.

• Place the barrier pad on the bed to absorb any spillage.

• Mark your chosen spot (just above a rib to avoid hitting the

neurovascular bundle; see Fig. 18.29 ) with a pen.

22Chest tube insertion

Theory

Tubes are inserted to drain either ﬂ uid (pleural effusion/empyema) or air

(pneumothorax) from the pleural cavity. In both cases, the insertion of the

tube is almost entirely identical.

The tube is connected to a container with a small amount of water (cre-

ating an airtight seal), so there is no direct connection between the pleural

cavity and air. On inspiration, the negative intrathoracic pressure draws

water up the tube (about 4 cm); on expiration, the water level falls and

(if draining a pneumothorax) air bubbles through the water. This one-way

valve allows air or ﬂ uid to drain from the chest but not re-enter.

The method described below is the Seldinger technique . While other

techniques exist for wide-bore tubes, these are now only used in the set-

ting of blunt trauma and cardiothoracic surgery, or for other problems

such as extensive surgical emphysema overlying a pneumothorax.

CHAPTER 18 Practical procedures564

• Sterilize the area with antiseptic solution or povidone-iodine on cotton

balls, working in a spiral pattern outward from the insertion point.

• Pause to reconﬁ

rm the patient identity, procedure, and site.

• Using the syringe and the orange needle, anesthetize the skin (see b

p. 512), forming a subcutaneous bleb.

• Swap the orange needle for the green (18G) one and anesthetize

deeper, remembering to aspirate before injecting, to ensure that you

have not hit a vessel. Anesthetize right down to the pleural cavity and

only stop when you aspirate air or pleural ﬂ uid.

• Use the scalpel to make a small cut in the skin.

• Now use the drain-kit needle with the curved tip and syringe (in some

kits, this has a central stylet that needs to be removed ﬁ

rst). With the

curved tip facing down (up for a pneumothorax), advance through the

anesthetized route until you are aspirating either air or ﬂ uid

again.

• Remove the syringe and hold the needle steady.

• Thread the guide wire through the needle into the pleural cavity (this

usually comes precoiled but often needs to be retracted slightly ﬁ rst

to straighten the curve on the tip). See Fig. 18.31 .

• Once the wire is half-way in the chest, discard the covering.

• Now withdraw the needle from the chest but be sure to not

remove the guide wire—KEEP HOLD OF IT AT ALL TIMES.

• Thread the needle right off the end of the guide wire. You should now

have the wire in the chest, but nothing else.

• Thread the introducer over the guide wire and into the chest, twisting

back and forth as you go to open up a tract for the drain’s passage.

You can then slide the introducer back off the wire—but be careful

not to pull the wire out of the chest.

• The chest drain has a central stiffener in place; leave this in situ. Now

thread the drain over the wire and into the chest, curving downward.

Always HOLD ON TO THE WIRE with one hand—you may need to

pull the wire out of the chest slightly so that it protrudes from the end

of the drain before you push the drain into the chest. You don’t want

to push it right into the chest and lose it!

• Once the drain is in place, withdraw the wire and the central stiffener.

• Quickly attach the 3-way tap and make sure all the ports are closed.

• You can now stitch the drain in place ( Fig. 18.32 ). This needn’t be

complicated—a simple stitch just above the drain will sufﬁ

ce with the

ends then wrapped tightly around the drain, knotted several times.

• Fix the drain in place with a suitable dressing.

• Attach the drain to the tubing and the tubing to the drain collection

bottle, which you have preﬁ

lled with 500 mL of sterile water.

• Open the 3-way tap. You should either see the ﬂ

uid start to ﬂ ow

or

air start to bubble in the collection bottle. Ask the patient to take a

few deep breaths and watch the water level in the tubing to ensure it

is rising and falling.

• Warn the patient not to knock the bottle over and to keep it below

the level of their umbilicus.

• Request a post-insertion chest X-ray.

565

CHEST TUBE INSERTION

Fig. 18.30 Correct positioning of the patient for chest drain insertion and ideal

site of drain insertion.

Fig. 18.31 Prepare the guide wire before starting the procedure by retracting

slightly so as to straighten the curved tip.

CHAPTER 18 Practical procedures566

Fig. 18.32 Diagrammatic representation of a suitable stitch to hold the drain in

place.

567

NASOGASTRIC (NG) TUBE INSERTION

1 Nasogastric (NG) tube insertion

Theory

In this procedure, a plastic tube is inserted through the nose, down the

back of the throat and esophagus, and into the stomach.

The bore of the tube (large = 16, medium = 12, small = 10) is dictated

by the tube’s intended purpose. For short- or medium-term nutritional

support in patients with a defective swallow, a ﬁ ne-bore tube is used.

Larger bores are used to drain the stomach contents and decompress

intestinal obstruction.

• Contraindications: severe facial trauma and basal skull fractures

• Complications: aspiration, tissue trauma, electrolyte loss, tracheal or

duodenal intubation, perforation of esophagus or stomach

Equipment

• Disposable gloves • 50 mL syringe

• Protective gown • Drainage bag (if necessary)

• Drape • Adhesive tape or steristrips

• Lubricant gel • Emesis basin

• NG tube • Paper towel

• Cup of water and straw

• Suction pump (if indicated)

Procedure

• Introduce yourself, conﬁ rm the patient’s identity, explain the

procedure, and obtain verbal consent.

• Wash your hands thoroughly, and put on gloves and gown.

• Ideally, the patient should be seated upright (often, the head tilted

slightly forward can aid insertion).

• Examine the patient’s nose for deformity or obstructions and decide

which nostril to use.

• Use the tube to measure the distance xiphoid process l earlobe l tip

of nose and note the distance.

• Lubricate the ﬁ

rst 4–8 cm of tube. You may also wish to use local

anesthetic spray on the patient’s throat, if available.

• Pass the tube into the nostril and then posteriorly, a short distance at

a time. You will feel it turn the corner at the nasopharynx and another

slight obstruction as it passes into the esophagus.

• If the patient is able, ask them to swallow as the tube passes the

pharynx—a brief sip of water may help here.

• Advance the tube as far as the premeasured distance.

• To check for correct placement, you may wish to aspirate some stomach

contents with the syringe and test the ﬂ uid’s pH (it should be <6).

• Secure the tube to the patient’s nose with some tape. You may also

wish to curl it back over their ear and secure it to their cheek.

• Request a chest X-ray and conﬁ

rm the tube’s position ( below

the

diaphragm in the region of the gastric bubble) before using for feeding.

• Record the procedure in the patient’s notes.

CHAPTER 18 Practical procedures568

2 Hints

• If resistance is felt, try rotating the tube while advancing it. Never force

it.

• Partially cooling the tube can stiffen the tube, making it easier to pass.

2 No longer considered appropriate, an alternate test for correct place-

ment was to insert a small bolus of air (20–30 mL) via the tube with

the syringe while listening to the epigastrium with the stethoscope. One

would thus hear the air entering the stomach.

569

ASCITIC TAP

22 Ascitic tap

Theory

In this procedure, a needle is inserted through the abdominal wall, allow-

ing withdrawal of a small amount of ﬂ uid for diagnostic purposes.

Equipment

• 1 green (18 gauge) needle

• 1 orange (14 gauge) needle

• 10 mL syringe

• 20 mL syringe

• 5–10 mL 1% lidocaine solution

• Povidone-iodine or antiseptic

solution

• Microbiology culture bottles

(anaerobic and aerobic)

• Sterile pack (including gloves,

cotton balls, and container)

• 2 sterile collection bottles

• Biochemistry tube (glucose)

• Hematology tube

Procedure

• Introduce yourself, conﬁ rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Ensure that the patient has emptied their bladder.

• Position the patient lying supine or in the lateral decubitus position,

leaving the right side available. Undress this side, exposing abdomen.

• Percuss the extent of the ascitic dullness (b p. 239).

• Mark your chosen spot in the region of the right iliac fossa (preferably)

within the area of dullness ( Fig. 18.33 ).

• Clean the area thoroughly with antiseptic, and put on sterile gloves.

• Pause to reconﬁ

rm patient identity and the procedure and site.

• Inﬁ ltrate the skin and subcutaneous tissues with lidocaine via the orange

needle and 10 mL syringe and wait a minute for it to take effect.

• Attach the green needle to the 20 mL syringe and insert it into the

abdomen, perpendicular to the skin. Advance the needle as you

aspirate until ﬂ

uid is withdrawn.

• Aspirate as much ﬂ

uid as possible (up to the 20 mL).

• Remove the needle and apply a suitable sterile dressing.

• Put >4 mL of ﬂ

uid in each bottle and send to the lab for the following:

•

Biochemistry—standard collection bottle (albumin, LDH, amylase)

•

Biochemistry—accurate glucose collection tube (glucose)

•

Cytology

•

Hematology (total and differential white cell count)

•

Microbiology (C&S)

CHAPTER 18 Practical procedures570

Site in IF (iliac fossa) for aspiration

L

Fig. 18.33 Performing a diagnostic ascitic tap.

571

ABDOMINAL PARACENTESIS (DRAINAGE)

22 Abdominal paracentesis (drainage)

Theory

In this procedure, a drain is inserted into the abdominal cavity, allowing

drainage of large amounts of ascitic ﬂ uid for therapeutic purposes.

The procedure below relates to a Bonanno drainage kit—the essence is

the same as for other catheter kits ( Fig. 18.34 ), although minor details may

differ. Refer to the manufacturer’s instructions.

Equipment

• 1 orange (14 gauge) needle

• 1 green (18 gauge) needle

• 2 x 10 mL syringes

• 5–10 mL 1% lidocaine solution

• Povidone-iodine or antiseptic

solution

• Sterile pack (including gloves,

cotton balls, and container)

• Bonanno abdominal catheter

pack (catheter, sleeve, puncture

needle, and adaptor clamp)

• Catheter bag

• Catheter bag stand

• Scalpel

Procedure

• Introduce yourself, conﬁ rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Ensure that the patient has emptied their bladder.

• Position the patient lying supine or in the lateral decubitus position,

leaving the right side available. Undress this side, exposing abdomen.

• Percuss the extent of the ascitic dullness (b p. 239).

• Mark your chosen spot in the region of the right iliac fossa (preferably)

within the area of dullness.

• Clean the area thoroughly with antiseptic and put on sterile gloves.

• Pause to reconﬁ

rm patient identity and the procedure and site.

• Inﬁ ltrate the skin and subcutaneous tissues with lidocaine via the orange

needle and 10 mL syringe and wait a minute for it to take effect.

• Attach the green needle to the other 10 mL syringe and insert into

the abdomen, perpendicular to the skin. Advance the needle as you

aspirate until ﬂ

uid is withdrawn.

• Prepare the catheter kit—straighten the catheter (which is curled in

the pack) using the plastic covering sheath provided.

• Take the needle provided in the pack and pass through the sheath such

that the needle bevel is directed along inside the curve of the catheter

( Fig. 18.35 ). Continue until the needle protrudes from the catheter tip.

• Close off the rubber at the end of the catheter.

• Make a small incision in the skin with the scalpel.

• Grasp catheter needle 710 cm above the distal end and, with a ﬁ rm

thrust, push needle through the abdominal wall to 73 cm deep.

• Disengage needle from the catheter hub and advance catheter until

the suture disc is ﬂ

at against the skin.

• Withdraw needle.

• Connect adaptor-clamp to the catheter hub and securely attach the

rubber portion of the clamp into a standard drainage catheter bag.

CHAPTER 18 Practical procedures572

Fig. 18.34 The assembled catheter components.

Fig. 18.35 Inserting the needle into the curved catheter.

• Carefully suture the catheter into the abdominal wall—you may also

need to apply further tape to ensure the catheter won’t fall out.

• Ensure that the clamp is open to allow ﬂ

uid to drain.

Hints

• In cirrhotic patients, protein loss should be replaced (and

hemodynamic stability maintained) by infusing human albumin solution

(HAS) IV at a rate of 100 mL of 20% HAS for every 3 L of ascitic ﬂ uid

drained—check local protocols with the gastroenterology department.

• Usually catheters are not left in place for >24 hours.

• During drainage, the ﬂ

ow may stop, which suggests that the drain is

blocked. This may be positional, and simply moving the patient may

solve the problem.

573

MALE URETHRAL CATHETERIZATION

1 Male urethral catheterization

Theory

A urinary catheter has a balloon near the tip that is inﬂ ated via a side-arm

near the other end. Once inside the bladder, the inﬂ ated balloon prevents

it from falling, or being pulled, out.

Equipment

• Catheter pack (containing a basin, a small bowl with cotton balls, a

sterile towel, sterile gauze, and sterile gloves)

• Antiseptic solution or vial of saline

• Appropriate urological anesthetic gel

• 10 mL water-ﬁ lled

syringe

• Catheter bag (leg bag if situation is not acute)

• Male catheter (12F or 14F)

Procedure

• Wash your hands thoroughly. Conﬁ rm the patient’s identity, explain

the procedure, and obtain verbal consent.

• Unwrap all the equipment onto an instrument stand in an aseptic

fashion and pour saline solution over the cotton balls.

• Position the patient supine with genitalia exposed. Raise the bed to a

comfortable height.

• Wash your hands again and put on gloves. Create a hole in the center

of the towel, or use a fenestrated drape, and drape over the patient so

the penis can be reached through the hole.

• From here on, use your nondominant hand to hold the penis with

some gauze.

• Clean the penis with the wet cotton balls, working away from the

meatus. Remember to retract the foreskin and clean beneath.

• Lift penis to a vertical position, carefully position the nozzle of the

lubricant gel inside the meatus, and instill the full 10 mL slowly. (If

proving problematic, this can be aided by gentle milking action.)

• Position kidney bowl between patient’s thighs to catch spillages later.

• The catheter will be in a plastic wrapper with a tear-away portion near

the tip. Remove this portion, being careful not to touch the catheter.

• Insert the tip of the catheter into the urethral meatus and advance

slowly but ﬁ

rmly by feeding it out of the remaining wrapper.

• On passing through the prostate, some resistance may be felt, which,

if excessive, may be countered by adjusting the angle of the penis by

pulling it to a horizontal position between the patient’s legs.

• On entering the bladder, urine should start to drain. Advance the

catheter far enough to ensure the balloon is beyond the urethra.

• Inﬂ

ate the balloon with the 10 mL of water via the secondary catheter

lumen.

0 Warn the patient to alert you to any pain, and watch his face.

• Remove the syringe and withdraw the catheter until resistance is felt.

• Attach draining tube and catheter bag.

• Replace the foreskin, and clean and re-dress the patient as necessary.

CHAPTER 18 Practical procedures574

Hints

• You may wish to verify the presence of a full bladder with a bladder

ultrasound before starting.

• Lack of urine drainage may be caused by blockage by anesthetic gel, an

empty bladder, or catheter misplacement.

• Attempt to aspirate urine with a catheter-tipped syringe. Feel for a full

bladder. If there is any doubt about position of the catheter, remove it

immediately (deﬂ

ating balloon ﬁ

rst) and seek appropriate consultation.

• Always record the residual volume—this is essential in cases of urinary

retention.

• Consider the use of prophylactic antibiotics before the procedure.

• Complications include pain, infection, misplacement, and trauma.

• Patients with prostate disease can often experience some mild

hematuria following catheterization. Don’t worry about this, but watch

carefully and be sure the bleeding doesn’t continue or form into clots.

2 Be aware of latex allergy!

575

FEMALE URETHRAL CATHETERIZATION

1 Female urethral catheterization

Theory

A urinary catheter has a balloon near the tip that is inﬂ ated via a side-arm

near the other end. Once inside the bladder, the inﬂ ated balloon prevents

it from falling, or being pulled, out.

Female staff will usually catheterize females.

0 Consider antibiotic prophylaxis.

Equipment

• Catheter pack (containing a basin, a small vessel with cotton balls, a

sterile towel, and sterile gauze)

• Sterile gloves

• Saline solution

• 5 mL 1% lidocaine/lubricant gel in preﬁ lled

syringe

• 10 mL water-ﬁ lled

syringe

• Catheter bag

• Female catheter (12F or 14F)

Procedure

• Wash your hands thoroughly. Conﬁ rm the patient’s identity, explain

the procedure, and obtain verbal consent.

• Unwrap all the equipment onto a cleaned (antiseptic) instrument stand

in an aseptic fashion and pour saline over the cotton balls.

• Position the patient supine with knees ﬂ

exed and hips abducted with

the heels together. Raise the bed to a comfortable height.

• Wash your hands again and put on gloves. Lay the towel and drape it

over the patient so the genitalia are exposed.

• From here on, use your nondominant hand to hold the labia apart,

approaching the patient from the right-hand side, leaning over her

ankles in order to reach the genitalia from below.

• Clean genitalia with the wet cotton balls (using each once only),

working in a pubis–anus direction (see Fig. 18.36 ).

• Carefully position the nozzle of the lubricant gel inside the meatus and

instill most of the 5 mL.

• Position the bowl between the patient’s thighs to catch spillages.

• The catheter will be in a plastic wrapper with a tear-away portion near

the tip. Remove this portion, being careful not to touch the catheter,

and apply a little lidocaine gel to the catheter tip.

• Insert the tip of the catheter into the urethral meatus and advance

slowly but ﬁ

rmly by feeding it out of the remaining wrapper.

• On entering the bladder, urine should start to drain. Advance the

catheter fully to ensure the balloon is beyond the urethra.

• Inﬂ

ate the balloon with 10 mL of water via the catheter side-arm.

0 Warn the patient to alert you to any pain and watch her face.

• Remove the syringe and withdraw the catheter until resistance is felt.

• Attach draining tube and catheter bag.

• Clean and re-dress the patient as necessary.

• Record the residual urinary volume.

CHAPTER 18 Practical procedures576

Hints

• Some female patients are easier to catheterize in a different position—

lying on their side with knees raised.

• Lack of urine drainage may be caused by blockage by lubricant gel, an

empty bladder, or catheter misplacement.

• Attempt to aspirate urine with a catheter-tipped syringe. Feel for a

full bladder. If there is any doubt about the position of the catheter,

remove it immediately (deﬂ

ating balloon ﬁ

rst) and seek advice.

• Complications

•

Pain

•

Infection

•

Misplacement and trauma

2 Be aware of latex allergy!

Mons pubis

Glans clitoris

Urethral meatus

Labium majus

Vaginal orifice

Anus

Fig. 18.36 Diagrammatic representation of the female external genitalia showing

position of the urethral meatus.

577

SUPRAPUBLIC CATHETERIZATION

22 Suprapubic catheterization

Theory

Suprapubic catheterization is sometimes seen as a safer and more efﬁ cient

means of controlling bladder drainage than urethral catheterization, par-

ticularly if the patient has had treatment or surgery involving the vagina,

urethra, ureter, or prostate. Patients may in fact ﬁ nd this more accept-

able than urethral catheterization. Also, it allows assessment of when the

patient is able to void spontaneously, without having to remove (and pos-

sibly replace) a urethral catheter.

The catheter is inserted directly into the bladder, through the abdom-

inal wall just superior to the pubic symphysis. Safe placement under local

anesthesia requires a very full bladder.

The procedure below relates to the Bonanno Suprapubic tray. The

essentials of the technique remain the same for other catheterization sys-

tems, although small details may differ—refer to the pack instructions.

Many urologists currently favor the Bard Addacath system.

• Instrument (Mayo) stand

• 1 Bonanno Suprapubic catheter

tray (contains puncture needle,

catheter with sleeve, and

adaptor clamp)

• 1 drainage bag

• Povidone-iodine or antiseptic

solution

• 2 x 10 mL syringes

• 5–10 mL 1% lidocaine

• 1 green needle

• 1 orange needle

• Sterile pack (containing

gloves, swab, and container)

• Fine, nonabsorbable suture

Equipment

Procedure

• Introduce yourself, conﬁ rm identity of the patient, explain the

procedure, and obtain verbal consent.

• Position the patient supine with genitalia exposed. Raise the bed to a

comfortable height.

• Unwrap all the equipment onto an instrument stand in an aseptic

fashion and pour antiseptic solution over the cotton balls.

• Before commencing, make sure that the patient has a palpable bladder.

If not, distend the bladder with 500–700 mL of saline solution instilled

via a urethral catheter (if urethral route is available and feasible).

2 If the bladder is not full, proceed no further.

• Put on sterile gloves, and prep the suprapubic area with antiseptic

solution.

• Pause to reconﬁ

rm patient identity and the procedure and site.

• The point of insertion is in the midline, two ﬁ

nger-breadths above the

pubic symphysis and well below the upper edge of palpable bladder.

• Assemble the Bonanno catheter components (see Fig. 18.34 ).

• Advance the catheter sleeve along the course of the radio-opaque

catheter from a proximal position adjacent to the suture disc to the

distal end of the catheter to allow straightening of the coiled catheter.

• Inﬁ

ltrate the insertion area with the lidocaine.

CHAPTER 18 Practical procedures578

• Carefully insert the 18-gauge puncture needle into the catheter so that

the heel of the needle bevel is directed along inside the curve of the

catheter and move in a clockwise direction, until the bevel extends

beyond the catheter tip ( Fig. 18.35 ).

• Slide the straightener sleeve off the distal end of the catheter.

• Grasp the catheter needle ~9 cm above the distal end and, with a

ﬁ

rm thrust, push the needle through the abdominal wall, heading in a

slightly caudal direction, until you feel resistance disappear.

• Check position of the catheter in the bladder by removing the black

vent plug, and aspirate urine with a 10 mL syringe.

• Disengage needle from the catheter hub and advance catheter until

the suture disc is ﬂ

at against the skin.

• Withdraw needle.

• Connect adaptor-clamp to the catheter hub and securely attach the

rubber portion of the clamp into a standard drainage catheter bag.

• Carefully suture the catheter into the abdominal wall—you may also

need to apply further tape to ensure the catheter won’t fall out.

• Ensure that the clamp is open to allow urine to drain.

Hints

• It may be easier to use a scalpel to make a small stab incision before

inserting the needle.

579

BASIC SUTURING

1 Basic suturing

Theory

Basic suturing, or stitching, has many practical applications outside the ﬁ eld

of surgery.

Whether you are called upon to suture a central line in place or are stitch-

ing up a laceration, it’s a skill you should practice before you need to use it.

There are many useful texts and articles that describe in more detail the ﬁ ne

art of suturing, and we refer you to these. Undoubtedly, the best way to learn

is by watching a surgeon and then doing it yourself. In most clinical skills labs

you should ﬁ nd the necessary equipment to practice these skills.

Equipment

• Instrument (Mayo) stand • Tape

• Dressing pack • Sterile gloves

• 21-gauge green needle • Sharps bin

• 25-gauge orange needle • Toothed forceps

• 10 mL and 20 mL syringes • Needle holder

• Gauze • Scissors

• Antiseptic solution • Scalpel

• Sutures

(selection depending on site and nature of wound)

Procedure

• Introduce yourself, conﬁ rm identity of the patient, explain the

procedure, and obtain verbal consent.

• First assess the wound and decide on the size of the suture material.

•

Remember that there are alternative ways to achieve wound closure,

such as glue, staples, and steri-strips. Always consider the most

appropriate means of closing a wound.

• Before suturing, irrigate the wound and remove any foreign bodies and

any nonviable or infected tissue.

• Use a needle holder such as toothed forceps, where possible, to

minimize the risk of needle-stick injury.

• Hold the needle 2/3 of the way from the needle tip.

• Lift the skin edge farthest away without pinching or damaging it.

• Pierce the skin with the needle at 90˚.

• Rotate your wrist to pass the needle into the middle of the wound.

• Release the forceps and clasp the needle again as it protrudes into the

wound, rotating it out of the wound.

• Next press the near side with the closed forceps to evert the skin

edge, and pass the needle through, taking a smooth semicircular

course to exit at 90˚ to the wound edge. See Fig. 18.37 .

• This method ensures a square bite and good eversion of the wound.

• Now perform a surgeon’s knot.

•

Wrap the long end of the thread around the forceps, which is used

to transfer the coil around the short end (grab the short tail and pull

in toward you, pulling the long end away).

•

Repeat the cycle.

CHAPTER 18 Practical procedures580

• Remember to cut the ends of the thread off, leaving a few mm so that

they can be easily removed later.

2 When removing sutures, clean the wound with antiseptic solution, use

forceps or a blade, and pull the suture out across rather than away from

the wound.

The time taken to remove nonabsorbable sutures depends on location:

• Face: 5–7 days or less

• Scalp: 7–10 days

• Limbs and trunk: 12–14 days

Fig. 18.37 Diagrammatic representation of the stages involved in a basic suture.

581

LUMBAR PUNCTURE

2 Lumbar puncture

Theory

A needle is introduced between the lumbar vertebrae at a level below

termination of the spinal cord. It then passes through the dura into the

subarachnoid space and a sample of cerebrospinal ﬂ uid (CSF) is obtained.

Lumbar puncture (LP) is used for diagnostic and therapeutic purposes,

which are too numerous to list.

Equipment

Level of iliac

crests

Fig. 18.38 Correct position of the patient for a lumbar puncture.

• Sterile gloves

• Sterile pack (containing drape,

cotton balls, and container)

• Antiseptic solution

• Sterile gauze dressing

• 5–10 mL 1% lidocaine

• 2 x10 mL syringe

• Biochemistry tube for glucose

• Orange needle (14 gauge)

• Green needle (18 gauge)

• LP needle

• LP manometer

• 3-way tap (may be included in

LP kit)

• Sterile collection tubes

Procedure

• Introduce yourself, conﬁ rm identity of the patient, explain the

procedure, and obtain verbal consent.

• Position patient lying on their left-hand side with the neck, knees, and

hips ﬂ

exed as much as possible (ask the patient to clasp their hands

around their knees, if they are able). Put a pillow between the patient’s

knees to prevent the pelvis from tilting (see

Fig. 18.38 ).

• Ensure that the patient can hold this position comfortably.

• Identify the iliac crest—the disc space vertically below this (as you are

looking) will be 7L3–L4.

• Mark the space between the vertebral spines with a pen.

• Wash your hands and put on sterile gloves.

CHAPTER 18 Practical procedures582

• Unwrap all equipment and ensure that it ﬁ ts together correctly.

• Apply the drapes around the area and sterilize with the antiseptic

solution and cotton balls in outward-spiral motions.

• Pause to reconﬁ

rm patient identity and the procedure and site.

• Inject the lidocaine (using a 10 mL syringe and the orange needle) at

the marked site to raise a small wheal.

• Swap out the orange needle for the green one and inﬁ ltrate

the

lidocaine deeper. Take care to aspirate before injecting to ensure that

blood vessels are avoided.

• Wait for 71 minute for the anesthetic to take effect.

• Introduce the spinal needle (22G usually) through the marked site at

about 90˚ to the skin, heading slightly toward the umbilicus. Keep the

bevel facing up the patient’s spine.

• Gently advance the needle through the ligaments (to 75 cm depth).

• At this point, a further push of the needle should produce a give as the

needle enters the subarachnoid space (this takes a little practice to feel

with conﬁ dence).

• If at any point the needle strikes bone and cannot be advanced,

withdraw slightly, re-aim it, and advance in a stepwise fashion until the

gap is found.

• Withdraw the stylet from the needle. CSF should begin to drip out.

• Measure the CSF pressure—connect the manometer to the end of the

needle via the 3-way tap (the CSF will rise up the manometer, allowing

you to read off the number).

• Open the tap and allow the CSF to drip into the three collection

tubes, about 5 or 6 drips per tube. The tubes should be labeled “1,”

“2,” and “3,” in order of collection. Collect a few more drips into the

biochemistry tube for glucose measurement.

• Replace the stylet and remove the needle. Apply a sterile dressing.

• Send the ﬂ

uid for analysis.

•

Cell count (bottles 1 and 3)

•

Microscopy, culture, and sensitivities (M,C&S) (bottles 1 and 3)

•

Biochemistry: glucose, protein (bottle 2)

• Advise the patient to lie ﬂ

at for 1 hour, and ask nursing staff to check

CNS observations regularly during that time.

Hints

• Always use the smallest-gauge spinal needle available.

• Treatment of mild post–lumbar puncture headache (PLPH) is

supportive with NSAIDs and ﬂ uids.

• If the patient suffers a severe or prolonged headache after the

procedure, it may be possible to inject 720 mL of venous blood

into the LP site to produce an epidural blood patch (EBP), a “blood

patch”—ask for anesthesiology advice!

583

PERICARDIAL ASPIRATION

22 Pericardial aspiration

Theory

Emergency pericardial aspiration (drainage of ﬂ uid from the pericardial

cavity) may be performed in cardiac tamponade or large pericardial effu-

sions where there is hemodynamic compromise. This procedure can also

be used to obtain diagnostic pericardial ﬂ uid.

Equipment

• Sterile gown and gloves

• Antiseptic solution

• Sterile towels

• 10 mL syringe

• 50 mL syringe

• Three-way tap

• ECG monitoring, deﬁ

brillator and resuscitation equipment

• Local anesthetic

• Needles

• 18-gauge catheter

Procedure

• If the patient is conscious, introduce yourself, conﬁ rm the identity of

the patient, explain the procedure, and obtain verbal consent.

• Establish IV access and connect the ECG monitor with full

resuscitation equipment at hand.

• Provide adequate sedation, if necessary.

• Put on sterile gloves and gown.

• Pause to reconﬁ

rm patient identity and the procedure and site.

• If time permits, use local anesthesia to inﬁ ltrate the insertion site.

• Attach the 18-gauge catheter to the 50 mL syringe.

• Introduce needle at 45

0

to the skin immediately below and to the left

of the xiphoid process to a depth of 6–8 cm, in a direction aiming for

the tip of the scapula.

• Aspirate continuously and watch the ECG.

•

If the needle touches the ventricle, an injury pattern (depressed ST

segment) or arrhythmia may be seen—withdraw the needle slightly.

• Aspirate pericardial ﬂ

uid through the syringe and 3-way tap.

• Aspiration should produce immediate hemodynamic improvement.

• You can check if the ﬂ

uid you are aspirating is pure blood if it clots

quickly. Heavily bloodstained pericardial ﬂ

uid does not clot.

• Perform a chest X-ray and echocardiogram after the procedure.

• You may wish to insert a pericardial drain (seek consultation).

• Document the details of the procedure in the notes.

Possible complications

• Pneumothorax

• Arrhythmia

• Myocardial puncture

• Damage to the coronary arteries

CHAPTER 18 Practical procedures584

1 Deﬁ brillation

Theory

Electrical deﬁ brillation is the only effective therapy for cardiac arrest

caused by ventricular ﬁ brillation (VF) or pulseless ventricular tachycardia

(VT). The American Heart Association (AHA) has long supported early

attempted deﬁ brillation, because the chances of successful deﬁ brillation

decline at a rate of 7–10% with each minute of delay.

In the hospital setting, two types of deﬁ brillator may be encountered:

the traditional manual deﬁ brillator and the newer automated external

deﬁ brillators (AED).

There are two types of AED: most are semiautomatic and advise the

need for a shock, but this has to be delivered by the operator, when

prompted. Some also have the facility to enable the operator to override

the device and deliver a shock manually, without any prompts. A few fully

automatic AEDs are also available.

In recognition of changing guidelines, the reader is directed to the AHA

Web site: www.americanheart.org for the most current resuscitation

guidelines.

Equipment

• Deﬁ brillator

• Gel pads

Procedure for manual deﬁ brillation

• Switch on the deﬁ brillator and ensure that the skin is dry and free of

excess hair.

• Attach the ECG electrodes accordingly:

•

Red under right clavicle

•

Yellow under left clavicle

•

Green at the umbilicus

• Ascertain that the ECG rhythm is shockable (VF/pulseless VT).

• Place the deﬁ

brillation gel pads on the patient’s chest (

Fig. 18.39 ):

•

One just to the right of the sternum, below the clavicle

•

The other just lateral to the cardiac apex

• Shave chest hair only if it is excessive and will interfere with electrical

contact.

• Select 360J on the deﬁ brillator.

• Place the paddles ﬁ

rmly on the gel pads.

• Press the charge button on the paddles to charge the deﬁ brillator and

shout, “

stand clear—charging.”

• Check that all staff have stepped back (including yourself) and that no

one is touching the patient or their bed.

2 Ensure that high-ﬂ

ow oxygen has also been removed.

2 Check the monitor again to ensure a shockable rhythm.

• Shout “stand clear—shocking” and press both discharge buttons

simultaneously to discharge the shock.

• Follow protocol overleaf ( Fig. 18.40 ). Return paddles to deﬁ brillator

before continuing with cardiopulmonary resuscitation (CPR).

585

DEFIBRILLATION

Fig. 18.39 Correct position of gel pads or AED electrodes on patient. Ensure

that they are not touching or overlying any wires, oxygen tubing, or any other

conducting material. Ensure that the patient’s chest is dry and shaved if particularly

hairy.

Procedure for AEDs ( Fig. 18.41 )

• Switch on the deﬁ brillator, ensure the skin is dry and free of excess

hair, and attach the electrode pads (same position as the gel pads in

manual deﬁ brillation; see Fig. 18.39 ).

• Continue CPR while this is done if more than one assistant is present.

• Make sure no one is touching the patient during ECG analysis by AED.

• Follow the voice prompts.

•

These are usually programmable, and the American Heart

Association recommends that they be set as follows:

• A single shock only when a shockable rhythm is detected

• No rhythm, breathing, or pulse check after the shock

• A voice prompt for immediate resumption of CPR after the

shock.

• Two minutes allowed for CPR using a ratio of 30 compressions

to 2 rescue breaths before a voice prompt to assess the rhythm,

breathing, or a pulse is given.

2 If a shock is indicated, shout “stand clear” and perform visual checks

to ensure no personnel are in contact with the patient or their bed and

that any oxygen has been removed.

• Push the shock button and continue as directed.

CHAPTER 18 Practical procedures586

Hypoxia

Hypovolaemia

Hypo/hyperkalaemia/metabolic

Hypothermia

Tension pneumothorax

Tamponade, cardiac

Toxins

Thrombosis (coronary or pulmonary)

* Reversible causes

Unresponsive?

Open airway

Look for signs of life

Call

Resuscitation Team

CPR 30:2

Until defibrillator/monitor

attached

Assess

rhythm

Immediately resume

CPR 30:2

for 2 min

Immediately resume

CPR 30:2

for 2 min

1 Shock

150–360J biphasic

or 360J monophasic

Shockable

(VF/pulseless VT)

Non-shockable

(PEA/asystole)

During CPR:

- Correct reversible causes*

- Check electrode position

and contact

- Attempt/verify:

IV access airway and oxygen

- Give uninterrupted

compressions when

airway secure

- Give adrenaline

every 3–5 min

- Consider: amiodarone,

atropine, magnesium

Fig. 18.40 Algorithm for advanced life support using a manual deﬁ brillator.

Reproduced with permission from the Resuscitation Council (UK) guidelines. It is

recommended to consult the latest AHA guidelines when available.

587

DEFIBRILLATION

Unresponsive

Call for help

Open airway

Not breathing normally

CPR 30:2

Until AED is attached

Send or go for AED

Call 999

AED

assesses

rhythm

Immediately resume

CPR 30:2

for 2min

Continue until the victim starts to

breathe normally

1 Shock

150–360 J biphasic

or 360J monophasic

Shock

advised

No shock

advised

Immediately resume

CPR 30:2

for 2min

Fig. 18.41 AED algorithm. Reproduced with permission from the Resuscitation

Council (UK) guidelines..

CHAPTER 18 Practical procedures588

22 Knee joint aspiration

Theory

In the context of a swollen joint, a joint aspiration is performed for both

diagnostic (to identify infectious and crystal arthropathies) and therapeutic

(to relieve tense effusions and hemarthroses) purposes.

A sample of ﬂ uid may be removed and sent for microscopy, culture and

sensitivity and to be examined for crystals under polarized light.

This same procedural approach may be used for joint injections (e.g.,

steroids and local anesthetic to suppress inﬂ ammation).

Equipment

Procedure

• Introduce yourself, conﬁ rm the identity of the patient, explain the

procedure, and obtain verbal consent.

• Ensure that the patient is relaxed and lying comfortably on the couch

or bed with the knee exposed and slightly ﬂ exed.

• Palpate the outline of the patella and the medial joint line (aspiration is

easier on the medial side).

• Wash your hands and put on a pair of sterile gloves.

• Clean the site with the cotton balls and antiseptic solution.

• Pause to reconﬁ

rm patient identity and the procedure and site.

• Inﬁ

ltrate the insertion site with local anesthetic. Use 1–2 mL of

1% lidocaine using the 25-gauge orange needle and a 5 mL syringe.

Remember to aspirate before injecting.

• Take a 20 mL syringe and attach a 21-gauge green needle.

• Insert the needle at an angle of about 45

0

in the gap between the

lower border of the patella and the medial joint line ( Fig. 18.42 ).

• If the needle is in the joint space (about 2 cm in), you should be able

to freely aspirate synovial ﬂ

uid. Aspiration can be aided by pressing on

the opposite side of the joint with your free hand.

• Once the syringe is full, remove it from the joint and transfer the ﬂ uid

into sterile specimen bottles.

• Send to microbiology for microscopy, culture, and sensitivity and a

further sample to the biochemistry department to look for crystals.

• Following aspiration, ask the patient to rest the knee for 24–48 hours.

• Record in the notes the procedural details, including the color of the

synovial ﬂ

uid and the investigations requested.

• 5–10 mL 1% lidocaine

• 1 x 20 mL syringe

• 1 x 5 mL syringe

• 1 x 21-gauge (green) needle

• 1 x 25-gauge (orange) needle

• Sterile gloves

• Antiseptic solution

• Sterile bottles

• Dressing pack with cotton balls

589

KNEE JOINT ASPIRATION

Fig. 18.42 Aspiration of the knee joint—insert the needle at about 45

0

heading

distally below the patella.

This page intentionally left blank

591

Data interpretation

ECG: introduction 592

Chest X-rays: introduction 616

Abdominal X-rays: introduction 641

Radiology: pelvis 646

Radiology: hips and femurs 648

Radiology: knees 650

Radiology: shoulder 652

Radiology: cervical spine 654

Radiology: thoracic and lumbar spine 656

Lung function tests 658

Arterial blood gas analysis 663

Cerebrospinal ﬂ

uid (CSF)

667

Urinalysis 669

Pleural and ascitic ﬂ uid

671

Chapter 19

CHAPTER 19 Data interpretation592

ECG: an introduction

The ﬁ rst step in making sense of an electrocardiogram (ECG) printout is

to understand the electrical conduction process in the normal heart.

Electrophysiology of the heart

Cardiac myocytes

In their resting state, the surface of cardiac myocytes (muscle cells) is

polarized with a potential difference of 790 mV across the cell membrane

(negatively charged intracellularly and positively charged extracellularly).

Depolarization (reversal of this charge) results in movement of calcium

ions across the cell membranes and subsequent cardiac muscle contrac-

tion. It is this change in potential difference that can be detected by the

ECG electrodes and represented as deﬂ ections on a tracing.

Basics of the tracing

It is easiest to imagine an electrode ‘looking’ at the heart from where it is

attached to the body.

Depolarization of the myoctes that spreads toward the electrode is

seen as an upward deﬂ ection, electrical activity moving away from the

electrode is seen as downward deﬂ ection, and activity moving to one

side but neither toward nor away from the electrode is not seen at all

( Fig. 19.1 ).

Electrical conduction pathway

In the normal heart, pacemaker cells in the sinoatrial (SA) node initiate

depolarization. The depolarization ﬁ rst spreads through the atria, and this

is seen as a small upward deﬂ ection (the P wave) on the ECG.

The atria and the ventricles are electrically isolated from each other.

The only way in which the impulse can progress from the atria to the

ventricles normally is through the atrioventricular (AV) node. Passage

Direction of

depolarization

Deflection on

ECG trace

Toward electrode

Away from electrode

Downward deflection

Upward deflection

Neither toward nor

away from electrode

No deflection

or

Fig. 19.1 Diagrammatic representation of how the electrodes monitor waves of

depolarization.

ECG: AN INTRODUCTION

593

through the AV node slows its progress slightly. This can be seen on an

ECG as the isoelectric interval between the P wave and QRS complex,

the PR interval.

Depolarization then continues rapidly down the rapidly conducting

Purkinje ﬁ bers—bundle of His, then down left and right bundle

branches—to depolarize both ventricles ( Fig. 19.2 ). The left bundle has

two divisions (fascicles). The narrow QRS complex on ECG shows this

rapid ventricular depolarization.

Repolarization of the ventricles is seen as the T wave. Atrial repolari-

zation causes only a very slight deﬂ ection, which is hidden in the QRS

complex and not seen.

2 The P wave and QRS complex show the electrical depolarization of

atrial and ventricular myocardium, respectively, but the resultant mechani-

cal muscle contraction, which usually follows, cannot be inferred from the

ECG trace (e.g., in pulseless electrical activity [PEA]).

12-lead ECG

Leads

Electrodes are placed on the limbs and chest for a 12-lead recording.

The term 12-lead refers to the number of directions that the electrical

activity is recorded from, not number of electrical wires attached to

the patient.

The six chest leads (V

1–6

) and six limb leads (I, II, III, aVR, aVL, aVF) com-

prise the 12-lead ECG. These reﬂ ect the electrical activity of the heart

from various directions. The chest leads correspond directly to the six

electrodes placed at various points on the anterior and lateral chest wall

(see Fig. 19.3 ). The six limb leads represent the electrical activity through a

combination of the four electrodes placed on the patient’s limbs, e.g., lead

I is generated from the right and left arm electrodes.

2 Remember there are 12 ECG leads—12 different views of the

electrical activity of the heart—but only 10 actual electrodes placed on

the patient’s body.

1. Impulse begins at SA node

2. Spreads through atria

3. Conducted through

the AV node

4. Down the bundle

of His

5. Spreads through

the ventricles

from the apex

Fig. 19.2 Electrical conduction pathway in the normal heart.

CHAPTER 19 Data interpretation594

0 Additional leads can be used (e.g., V7–9 extending laterally around the

chest wall) to look at the heart from further angles, such as in suspected

posterior myocardial infarction (MI).

ECG orientation

When a wave of myocardial depolarization ﬂ

ows toward a particular lead,

the ECG tracing shows an upward deﬂ ection. A downward deﬂ ection

represents depolarization moving away from that lead. The key to inter-

preting the 12-lead ECG is thus to remember the directions at which the

different leads view the heart.

The six limb leads look at the heart in the coronal plane (see Fig. 19.4 ).

• aVR views the right atrium.*

• aVF, II, and III view the inferior or diaphragmatic surface of the heart.

• I and aVL examine the left lateral aspect.

The six chest leads examine the heart in a transverse plane.

• V

1

and V

2

look at the right ventricle.

• V

3

and V

4

look at the septum and anterior aspect of the left ventricle.

• V

5

and V

6

look at the anterior and lateral aspects of the left ventricle.

Although each of the 12 leads gives a different view of electrical activity

of the heart, for simplicity’s sake when considering the standard ECG

trace we can describe the basic shape common to all leads ( Fig. 19.5 ).

V

1

V

2

V

3

V

4

V

5

V

6

Fig. 19.3 V

1–6

electrode placement on the chest wall.

* All the vectors in lead aVR will be negative in the normal ECG.

ECG: AN INTRODUCTION

595

60º 60º

30º30º

30º 30º

aVR

aVF

aVL

II

I

III

Fig. 19.4 The respective views of the heart of the six limb leads. Note the

angles between the directions of the limb leads—these become important when

calculating the cardiac axis.

P

R

T

Q

S

ST segment

QRS

Com

p

lex

Fig. 19.5 Basic shape of the ECG tracing.

CHAPTER 19 Data interpretation596

ECG tracing

Waves

• P wave represents atrial depolarization and is a positive (upward)

deﬂ ection, except in aVR.

• QRS complex represents ventricular depolarization and comprises

•

Q wave —so called if the ﬁ rst QRS deﬂ ection is negative (downward).

Pathological Q waves are seen in infarction (b p. 612).

•

R wave —the ﬁ rst positive (upward) deﬂ ection. It may or may not

follow a Q wave.

•

S wave —a negative (downward) deﬂ ection following the R wave

• T wave represents ventricular repolarization and is normally a positive

(upward) deﬂ ection, concordant with the QRS complex.

0 Remember, Q waves appear following an MI, so they should be

absent from the normal ECG trace.

Rate

The heart rate can be calculated by dividing 300 by the number of large

squares between each R wave (with machine trace running at the standard

speed of 25 mm/sec and deﬂ

ection of 1 cm/10 mV).

• 3 large squares between R waves = rate 100

• 5 large squares = rate 60

Normal rate is 60–100 beats per minute (bpm).

• Rate <60 = bradycardia

• Rate >100 = tachycardia

Intervals and timing

• PR interval: from start of the P wave to start of the QRS complex. This

represents the built-in delay in electrical conduction at the AV node.

Normally <0.20 seconds (5 small squares at standard recording speed)

• QRS complex: width of the QRS complex. Normally <0.12 seconds (3

small squares at standard rate)

• R–R interval: from the peak of one R wave to the next. This is used in

calculation of the heart rate (see above).

• QT interval: from start of the QRS complex to end of the T wave. It

varies with heart rate. Corrected QT = QT/square root of the R–R

interval. Corrected QT interval should be 0.38–0.42 seconds.

Rhythm

• Is rhythm (and time between successive R waves) regular or irregular?

•

If irregular but in a clear pattern, then it is ‘regularly irregular’ (e.g., types

of heart block—see b p. 599).

•

If irregular but with no pattern, then it is ‘irregularly irregular’ (e.g., atrial

ﬁ brillation).

ECG axis

Cardiac axis

The cardiac axis, or QRS axis , refers to the overall direction of depolarization

through the ventricular myocardium in the coronal plane.

0

Remember, Q waves appear following an MI, so they should be

a

bsent

f

rom the normal E

CG

trace.

ECG: AN INTRODUCTION

597

Zero degrees is taken as the horizontal line to the left of the heart

(the right of your diagram).

The normal cardiac axis lies between –30° and +90° ( Fig. 19.6 ). An axis

outside of this range may suggest pathology, either congenital or acquired.

Cardiac axis deviation may be seen in healthy individuals with distinctive

body shapes—right-axis deviation if tall and thin, left-axis deviation if

short and stocky.

Calculating the axis

Look at Fig. 19.4. Leads I, II, and III all lie in the coronal plane (along with

aVR, aVL, and aVF). By calculating the relative depolarization in each of these

directions, one can calculate the cardiac axis. To accurately determine the

cardiac axis, use leads I, II, and III, as described below.

• Draw a diagram like the one in Fig. 19.7 showing the three leads—be

careful to use the correct angles.

• Look at ECG lead I. Count the number of millimeters (mm) above the

baseline that the QRS complex reaches.

• Subtract from this the number of mm below the baseline that the QRS

complex reaches.

• Now measure this number of centimeters along line I on your diagram

and make a mark (measure backward for negative numbers).

• Repeat this for leads II and III.

• Extend lines from your marks, perpendicular to the leads ( Fig. 19.6 ).

• The direction from the center of the diagram to the point at which all

these lines meet is the cardiac axis.

Calculating the axis—short cuts

There are many shorter ways of roughly calculating the cardiac axis. These

are less accurate, however.

C

ardiac axis deviation ma

y

be seen in health

y

individuals with distinctive

body shapes—right-axis deviation if tall and thin, left-axis deviation i

f

s

h

ort an

d

stoc

k

y.

–30º

+90º

0º

Range of

normal ECG

axis

Fig. 19.6 The normal ECG axis.

CHAPTER 19 Data interpretation598

An easy method is to look at only leads I and aVF. These are perpendicular

to each other and make a simpler diagram than the one described above.

(AV) conduction abnormalities

In the normal ECG, each P wave is followed by a QRS complex. The

isoelectric gap between is the PR interval and represents slowing of the

impulse at the AV junction. Disturbance of the normal conduction here,

leads to heart block.

Causes of heart block include ischemic heart disease, idiopathic ﬁ brosis

of conduction system, cardiomyopathies, inferior and anterior MI, drugs,

such as digoxin, B-blockers, and verapamil, and physiological factors (ﬁ rst

degree) in athletes.

III

Axis

II

60°

30°30°

I

30

°

Fig. 19.7 Calculating the ECG axis using leads I, II, and III. See text on previous page.

Box 19.1 Causes of axis deviation

Left axis deviation (<–30°)

• Left ventricular hypertrophy

• Left bundle branch block (LBBB)

• Left anterior hemiblock (anterior fascicle of the left bundle)

• Inferior MI

• Cardiomyopathies

• Tricuspid atresia

Right axis deviation (>+90°)

• Right ventricular hypertrophy

• Right bundle branch block (RBBB)

• Anterolateral MI

• Right ventricular strain (e.g., pulmonary embolism)

• Cor pulmonale

• Fallot’s tetralogy (pulmonary stenosis)

ECG: AN INTRODUCTION

599

First-degree heart block

The PR interval is ﬁ xed but prolonged at >0.20 seconds (5 small squares

at standard rate). See rhythm strip 1 ( Fig. 19.8 ).

Second-degree heart block

Not every P wave is followed by a QRS complex.

• Möbitz type I: PR interval becomes progressively longer after each P

wave until an impulse fails to be conducted at all. The interval then

returns to the normal length and the cycle is repeated (rhythm strip 2;

Fig. 19.8 ). This is also known as the Wenckebach phenomenon .

• Möbitz type II: PR interval is ﬁ

xed but not every P wave is followed by

a QRS complex. The relationship between P waves and QRS complex

Rhythm strip 1—first-degree heart block.

Rhythm strip 2—second-degree heart block Möbitz type I.

Rhythm strip 3—second-degree heart block Möbitz type II.

Rh

y

thm stri

p

4—third-de

g

ree

(

com

p

lete

)

heart block.

Fig. 19.8 Rhythm strips showing AV conduction abnormalities.

CHAPTER 19 Data interpretation600

may be 2:1 (two P waves for every QRS), 3:1 (three P waves per

QRS), or random. See rhythm strip 3 ( Fig. 19.8 ).

Third-degree heart block

This is also called complete heart block ; see rhythm strip 4 ( Fig. 19.8 ). There

is no conduction of impulse through the AV junction. Atrial and ventricular

depolarization occur independent of one another. Each has a separate

pacemaker triggering electrical activity at different rates (rhythm strip 4).

The QRS complex is an abnormal shape, as the electrical impulse does

not travel through ventricles via normal routes (see Ventricular Escape

Rhythm, b p. 609).

0 In third-degree heart block, P waves may be seen merging with QRS

complexes if they coincide.

0 If in doubt about the pattern of P waves and QRS complexes, mark out

the P-wave intervals and the R–R intervals separately, then compare.

2 P waves are best seen in leads II and V

1

.

Ventricular conduction abnormalities

Depolarization of both ventricles usually occurs rapidly through left and

right bundle branches of the His–Purkinje system (see Fig. 19.9 ). If this

process is disrupted as a result of damage to the conducting system,

depolarization will occur more slowly through nonspecialized ventricular

myocardium. The QRS complex, usually <0.12 seconds’ duration, will

become prolonged and is described as a broad .

Right bundle branch block (RBBB)

Conduction through the AV node, bundle of His, and left bundle branch

will be normal but depolarization of the right ventricle occurs by the slow

spread of electrical current through myocardial cells ( Fig. 19.10 ). The

result is delayed right ventricular depolarization, giving a second R wave

known as R’ (R prime).

RBBB suggests pathology in the right side of the heart but can be a

normal variant.

ECG changes

• RSR pattern seen in V

1

• Cardiac axis usually remains normal unless left anterior fascicle is also

blocked (bifascicular block), which results in left axis deviation.

• T wave d in anterior chest leads (V

1

–V

3

)

SA node

AV node

Right bundle

branch

Posterior facicle

Anterior facicle

Bundle of His

Left bundle branch

Fig. 19.9 Diagrammatic representation of the conducting system of the heart.

ECG: AN INTRODUCTION

601

Some causes of RBBB

• Hyperkalemia

• Congenital heart disease (e.g., Fallot’s tetralogy)

• Pulmonary embolus

• Cor pulmonale

• Fibrosis of conduction system

Left bundle branch block (LBBB)

Conduction through the AV node, bundle of His, and right bundle branch

will be normal but depolarization of the left ventricle occurs by the slow

spread of electrical current through myocardial cells ( Fig. 19.11 ). The

result is delayed left ventricular depolarization.

LBBB should always be considered pathological.

I II III V

1

V

2

V

3

aVF aVL aVR V

4

V

5

V

6

Fig. 19.10 Typical 12-lead ECG showing RBBB.

I II III V

1

V

2

V

3

aVF aVL aVR V

4

V

5

V

6

Fig. 19.11 Typical 12-lead ECG showing LBBB.

CHAPTER 19 Data interpretation602

ECG changes

• M pattern seen in V

6

• T wave d in lateral chest leads (V

5

–V

6

)

Some causes of LBBB

• Hypertension

• Ischemic heart disease

• Acute MI

• Aortic stenosis

• Cardiomyopathies

• Fibrosis of conduction system

0 LBBB on the ECG causes abnormalities of the ST segment and T wave.

You should not comment any further on these parts of the tracing.

Box 19.2 Bundle branch block mnemonic

• In LBBB, the QRS complex in V

1

looks like a W and like an M in V

6

.

This can be remembered as WiLLiaM . There is a W at the start, an

M at the end, and an L in the middle, for ‘left.’

• Conversely, in RBBB, the QRS complex in V

1

looks like an M and in

V

6

, like a W . Combined with an R , for ‘right,’ you have MaRRoW .

Sinus rhythms

Supraventricular rhythms arise in the atria. They may be physiological in

some causes of sinus brady and tachycardia or be caused by pathology

within the SA node, the atria, or the ﬁ rst parts of the conducting system.

Normal conduction through the bundle of His into the ventricles will

usually give narrow QRS complexes.

Sinus bradycardia

This is a bradycardia (rate <60 bpm) at the level of the SA node. The

heart beats slowly, but conduction of the impulse is normal (rhythm strip

1, Fig. 19.12 ).

Some causes of sinus bradycardia

• Drugs (B-blockers, verapamil, amiodarone, digoxin)

• Sick sinus syndrome

• Hypothyroidism

• Inferior MI

• Hypothermia

• i Intracranial pressure (ICP)

• Physiological (athletes)

Sinus tachycardia

This is a tachycardia at the level of the SA node—the heart is beating too

quickly but conduction of impulse is normal (rhythm strip 2, Fig 19.12).

ECG: AN INTRODUCTION

603

ECG features

• Ventricular rate >100 (usually 100–150 bpm)

• Normal P wave before each QRS

Some causes of sinus tachycardia

• Drugs (epinephrine/adrenaline, caffeine, nicotine)

• Pain

• Exertion

• Anxiety

• Anemia

• Thyrotoxicosis

• Pulmonary embolus

• Hepatic failure

• Cardiac failure

• Hypercapnia

• Pregnancy

• Constrictive pericarditis

Supraventricular tachycardias

These are tachycardias (rate >100 bpm) arising in the atria or the AV

node. As conduction through the bundle of His and ventricles will be

normal (unless there is other pathology in the heart), the QRS complexes

appear normal.

There are four main causes of a supraventricular tachycardia that you

should be aware of: atrial ﬁ brillation, atrial ﬂ utter, junctional tachycardia,

and re-entry tachycardia.

Atrial ﬁ brillation (AF)

This is disorganized contraction of the atria in the form of rapid, irregular

twitching. There will thus be no P waves on the ECG.

Electrical impulses from the twitches of the atria arrive at the AV node

randomly. They are then conducted via the normal pathways to cause

Rhythm strip 1—sinus bradycardia.

Rhythm strip 2—sinus tachycardia.

Fig. 19.12 Rhythm strips from lead II showing a sinus bradycardia (rhythm strip 1)

and sinus tachycardia (rhythm strip 2).

CHAPTER 19 Data interpretation604

ventricular contraction. The result is a characteristic ventricular rhythm

that is irregularly irregular with no discernable pattern ( Fig. 19.13 , rhythm

strip 1).

ECG features

• No P waves. Rhythm is described as irregularly irregular.

• Irregular QRS complexes

• Normal appearance of QRS

• Ventricular rate may be i (fast AF)—typically 120–160 per minute.

Some causes of atrial ﬁ

brillation

• Idiopathic

• Ischemic heart disease

• Thyroid disease

• Hypertension

• MI

• Pulmonary embolus

• Rheumatic mitral or tricuspid valve disease

Rhythm strip 1—atrial fibrillation.

Rhythm strip 2—atrial flutter with 2:1 block.

Rhythm strip 3—atrial flutter with 4:1 block.

Fig. 19.13 Rhythm strips from lead II showing some supraventricular tachycardias.

ECG: AN INTRODUCTION

605

Atrial ﬂ utter

This is abnormally rapid contraction of the atria. The contractions are

not disorganized or random, as in AF, but are fast and inadequate for the

normal movement of blood. Instead of P waves, the baseline will have a

typical saw-tooth appearance (sometimes known as F waves ).

The AV node is unable to conduct impulses faster than 7200/min. Atrial

contraction faster than that leads to impulses failing to be conducted. For

example, an atrial rate of 7300/min will lead to every other impulse being

conducted, giving a ventricular rate (and pulse) of 7150/min. In this case,

it is called 2:1 block ( Fig. 19.13 , rhythm strip 2). Other ratios of atrial to

ventricular contractions may occur.

A variable block at the AV node may lead to an irregularly irregular

pulse indistinguishable from that of AF on clinical examination.

ECG features

• Saw-tooth appearance of baseline

• Normal appearance of QRS complexes

Causes of atrial ﬂ

utter

Similar to those of AF (see previous page)

Junctional (nodal) tachycardia

Here the area in or around the AV node depolarizes spontaneously;

the impulse will be immediately conducted to the ventricles. The QRS

complex will be of a normal shape but no P waves will be seen.

ECG features

• No P waves

• QRS complexes are regular and normal shape

• Rate may be fast or may be of a normal rate

Some causes of junctional tachycardia

• Sick sinus syndrome (including drug-induced)

• Digoxin toxicity

• Ischemia of the AV node, especially with acute inferior MI

• Acutely after cardiac surgery

• Acute inﬂ

ammatory processes (e.g., acute rheumatic fever) that may

involve the conduction system

• Diphtheria

• Other drugs (e.g., most antiarrhythmic agents)

Wolff–Parkinson–White syndrome

In Wolff–Parkinson–White (WPW) syndrome, there is an extra conduct-

ing pathway between the atria and the ventricles (the bundle of Kent)—a

break in the normal electrical insulation. This accessory pathway is not spe-

cialized for conducting electrical impulses so does not delay the impulse

as the AV node does. However, it is not linked to the normal conduction

pathways of the bundle of His.

Depolarization of the ventricles will occur partly via the AV node and

partly by the bundle of Kent. During normal atrial contraction, electrical

activity reaches the AV node and the accessory pathway at roughly the

same time. While it is held up temporarily at the AV node, the impulse

CHAPTER 19 Data interpretation606

passes through the accessory pathway and starts to depolarize the ventri-

cles via nonspecialized cells (pre-excitation), distorting the ﬁ rst part of the

R wave and giving a short PR interval. Normal conduction via the bundle of

His then supervenes. The result is a slurred upstroke of the QRS complex

called a delta wave (see Fig. 19.14 ).

This is an example of a fusion beat , in which normal and abnormal ventricular

depolarization combine to give a distortion of the QRS complex.

2 Re-entry tachycardia

The accessory pathway may allow electrical activity to be conducted from

the ventricles back up to the atria.

For example, in a re-entry tachycardia, electrical activity may be

conducted down the bundle of His, across the ventricles, and up the

accessory pathway into the atria ( Fig. 19.15 ), causing them to contract

again, and the cycle is repeated ( Fig. 19.16 ). This is called a re-entry circuit .

Fig. 19.14 Rhythm strip showing WPW syndrome.

Conduction

at the AV

node

Accessory

conduction

pathway

Fig. 19.15 Diagrammatic representation of re-entry tachycardia.

Fig. 19.16 Rhythm strip showing a re-entry tachycardia.

ECG: AN INTRODUCTION

607

Ventricular rhythms

Most ventricular rhythms originate outside the usual conduction path-

ways, meaning that excitation spreads by an abnormal path through the

ventricular muscle to give broad or unusually shaped QRS complexes.

Ventricular tachycardia (VT)

There is a focus of ventricular tissue depolarizing rapidly within the

ventricular myocardium. VT is deﬁ ned as three or more successive

ventricular extrasystoles at a rate of >120/min. Sustained VTs last >30

seconds.

VT may be stable , showing a repetitive QRS shape (monomorphic;

Fig.19.17, rhythm strip 1) or unstable , with varying patterns of the QRS

complex (polymorphic).

It may be impossible to distinguish VT from an SVT with bundle branch

block on a 12-lead ECG.

ECG features

• Wide QRS complexes that are irregular in rhythm and shape

• AV dissociation—independent atrial and ventricular contraction

• May see fusion and capture beats on ECG as signs of atrial activity

independent of ventricular activity. This is said to be pathognomonic.

•

Fusion beats: depolarization from AV node meets depolarization

from ventricular focus, causing hybrid QRS complex

•

Capture beats: atrial beat conducted to ventricles causing a normal

QRS complex in among the VT tracing

• Rate can be up to 130–300/min.

• QRS concordance: all QRS complexes in chest leads are either mainly

positive or mainly negative—suggests ventricular origin of tachycardia.

• Extreme axis deviation (far negative or far positive)

Some causes of ventricular tachycardia

• Ischemia (acute including MI or chronic)

• Electrolyte abnormalities (d K, d Mg)

• Aggressive adrenergic stimulation (e.g., cocaine use)

• Drugs, especially antiarrhythmics

Box 19.3 Classiﬁ cation of Wolff–Parkinson–White

syndrome

The bundle of Kent may connect the atria with either the right or the left

ventricle. Thus, WPW is classically divided into two groups according to

the resulting appearance of the QRS complex in the anterior chest leads.

In practice, this classiﬁ cation is simplistic, as 11% of patients may have

more than one accessory pathway.

• Type A: upright delta wave and QRS in V

1

•

May be mistaken for RBBB or posterior MI

• Type B: downward delta wave and QRS in V

1

, positive elsewhere

•

May be mistaken for LBBB or anterior MI

CHAPTER 19 Data interpretation608

Ventricular ﬁ brillation (VF)

This is disorganized, uncoordinated depolarization from multiple foci in

the ventricular myocardium ( Fig. 19.17 , rhythm strip 2).

ECG features

• No discernible QRS complexes

• A completely disorganized ECG

Some causes of ventricular ﬁ

brillation

• Coronary heart disease

• Cardiac inﬂ ammatory diseases

• Abnormal metabolic states

• Proarrhythmic toxic exposures

• Electrocution

• Tension pneumothorax, trauma, and drowning

• Large pulmonary embolism

• Hypoxia or acidosis

Box 19.4 Fine VF

This is VF with a small-amplitude waveform ( Fig. 19.17 , rhythm strip 3). It

may resemble asystole on the ECG monitor (see Fig. 19.18 , rhythm strip

5, b p. 609), particularly in an emergency situation.

In a clinical situation, you should remember to increase the gain on the

monitor to ensure that what you think is asystole is not really ﬁ ne VF, as

the management for each is very different.

Rhythm strip 1—monomorphic ventricular tachycardia (VT).

Rhythm strip 2—ventricular fibrillation (VF).

Rhythm strip 3—“fine” ventricular fibrillation.

Fig. 19.17 Rhythm strips showing ventricular rhythms.

ECG: AN INTRODUCTION

609

Rhythm strip 1—a single ventricular extrasystole.

Rhythm strip 2—multiple, unifocal, ventricular extrasystole.

Rhythm strip 3—ventricular escape in the case of complete heart block.

Rhythm strip 4—agonal rhythm.

Rhythm strip 5—asystole.

Fig. 19.18 Rhythm strips showing some ventricular rhythms.

CHAPTER 19 Data interpretation610

Box 19.5 Torsades de pointes

Torsades de pointes , literally meaning ‘twisting of points,’ is a form of

polymorphic VT characterized by a gradual change in the amplitude and

twisting of the QRS axis ( Fig. 19.19 ). In the United States, it is known as

cardiac ballet .

Torsades usually terminates spontaneously but frequently recurs and

may degenerate into sustained VT and VF.

Torsades results from a prolonged QT interval. Causes include con-

genital long-QT syndromes and drugs (e.g., antiarrhythmics). Patients

may also have d K and d Mg.

Fig. 19.19 Torsades de pointes. The axis of the QRS complex rotates—seen

from a ﬁ xed position, there is a repeated change of amplitude.

Other ventricular rhythms

Ventricular extrasystoles (ectopics)

These are ventricular contractions originating from a focus of depolariza-

tion within the ventricle. As conduction is via abnormal pathways, the QRS

complex will be unusually shaped ( Fig. 19.18 , rhythm strips 1 and 2).

Ventricular extrasystoles are common and harmless if there is no

structural heart disease. If they occur at the same time as a T wave, the

R-on-T phenomenon , they can lead to VF.

Ventricular escape rhythm

This occurs as a backup when conduction between the atria and the

ventricles is interrupted (as in complete heart block).

The intrinsic pacemaker in ventricular myocardium depolarizes at a slow

rate (30–40/min) (see Fig. 19.18 , rhythm strip 3).

The ventricular beats will be abnormal and wide with abnormal T waves

following them. This rhythm can be stable but may suddenly fail.

Asystole

This is a complete absence of electrical activity and is not compatible with

life (see Fig. 19.18 , rhythm strip 5).

There may be a slight wavering of the baseline, which can be easily

confused with ﬁ ne VF in emergency situations (see Box 19.5 ).

Agonal rhythm

This is a slow, irregular rhythm with wide ventricular complexes that vary

in shape ( Fig. 19.18 , rhythm strip 4). This is often seen in later stages of

unsuccessful resuscitation attempts as the heart dies. Complexes become

progressively broader before all recognizable activity is lost (asystole).

ECG: AN INTRODUCTION

611

P- and T- wave abnormalities

P wave

This represents depolarization of the small muscle mass of the atria. The

P wave is thus much smaller in amplitude than the QRS complex.

Normal

• In sinus rhythm, each P wave is closely associated with a QRS complex.

• P waves are usually upright in most leads, except aVR.

• P waves are <3 small squares wide and <3 small squares high.

Abnormal

• Right atrial hypertrophy will cause tall, peaked P waves ( Fig. 19.20 ,

rhythm strip 1). Causes include pulmonary hypertension (in which case

the wave is known as P pulmonale and tricuspid valve stenosis ).

• Left atrial hypertrophy will cause the P wave to become wider and

twin-peaked, or biﬁ

d

( Fig. 19.20 , rhythm strip 2). This is usually caused

by mitral valve disease, in which case the wave is known as P mitrale .

T wave

This represents repolarization of the ventricles. The T wave is most

commonly affected by ischemic changes. The most common abnormality

is inversion, which has a number of causes.

Normal

• Commonly inverted in V

1

and aVR

• May be inverted in V

1

–V

3

as normal variant

Abnormal

• Myocardial ischemia or MI (e.g., non-Q-wave MI) can cause T-wave

inversion ( Fig. 19.20 , rhythm strip 3). Changes need to be interpreted

in light of clinical picture.

• Ventricular hypertrophy causes T inversion in those leads focused on

the ventricle in question. For example, left ventricular hypertrophy will

give T changes in leads V

5

, V

6

, II, and aVL.

• Bundle branch block causes abnormal QRS complexes due to

abnormal pathways of ventricular depolarization. The corresponding

abnormal repolarization gives unusually shaped T waves, which have

no signiﬁ

cance in themselves.

• Digoxin causes a characteristic T-wave inversion with a down-sloping

of the ST segment known as the reverse tick sign. This occurs at

therapeutic doses and is not a sign of digoxin toxicity (see Fig. 19.20 ,

rhythm strip 4).

• Electrolyte imbalances cause a number of T-wave changes.

•

i K can cause tall tented T waves.

•

d K can cause small T waves and U waves (broad, ﬂ at waves

occurring after the T waves; Fig. 19.20 , rhythm strip 5).

•

i Ca can cause small T waves with a prolongation of the QT

interval (d Ca has the reverse effect).

•

Other causes of T-wave inversion include subarachnoid hemorrhage

and lithium use.

CHAPTER 19 Data interpretation612

Rhythm strip 1—peaked P waves.

Rhythm strip 2—bifid P waves.

Rhythm strip 3—T wave inversion after myocardial infarction.

Rhythm strip 4—Hyperkalemia with peaked T waves.

Rhythm strip 5—Hyperkalemia with small T waves and U waves.

Fig. 19.20 Rhythm strips showing some P-and T-wave abnormalities.

ECG: AN INTRODUCTION

613

ST segment

This is the portion of the ECG from the end of the QRS complex to the

start of the T wave and is an isoelectric line in the normal ECG (see Fig. 19.5 ,

b p. 595.). Changes in the ST segment can represent myocardial ischemia

and, most importantly, acute MI ( Fig. 19.21 , rhythm strip 1).

ST elevation

The degree and extent of ST elevation is of crucial importance in ECG

interpretation, as it determines whether reperfusion therapy ( thrombolysis

or primary PCI) is considered in an acute MI.

Rhythm strip—Lead V

2

showing acute myocardial infarction.

Rhythm strip—Pericarditis. The ST elevation is usually described as

‘saddle-shaped’.

Rhythm strip—Ischemia.

Rhythm strip—Digoxin use showing the ‘reverse-tick’.

Fig. 19.21 Rhythm strips showing some ST segment abnormalities.

CHAPTER 19 Data interpretation614

Causes of ST elevation

• Acute MI—convex ST elevation in affected leads (the tombstone

appearance), often with reciprocal ST depression in opposite leads

• Pericarditis—widespread concave ST elevation (saddle-shaped; Fig. 19.21 ,

rhythm strip 2)

• Left ventricular aneurysm—ST elevation may persist over time.

ST depression

ST depression can be horizontal, upward sloping, or downward sloping.

Causes of ST depression

• Myocardial ischemia—horizontal ST depression and an upright T

wave ( Fig. 19.21 , rhythm strip 3). May be the result of coronary artery

disease or other causes (e.g., anemia, aortic stenosis)

• Digoxin toxicity—downward sloping (reverse tick; Fig. 19.21 , rhythm

strip 4)

• Nonspeciﬁ

c changes—ST segment depression that is often upward

sloping may be a normal variant and is not thought to be associated

with any underlying signiﬁ cant

pathology.

2 In exercise ECG testing, which looks to induce ischemic changes, the

extent, timing, and nature of ST changes can help quantify the probability

of ischemic heart disease.

Myocardial infarction

In the ﬁ rst hour following an MI, the ECG can remain normal. However,

when changes occur, they usually develop in the following order:

• ST segment becomes elevated and T waves become peaked.

• Pathological Q waves develop.

• ST segment returns to baseline and T waves invert.

The leads in which these changes take place can help you identify which

part of the heart has been affected and, therefore, which coronary artery

is likely to be occluded.

• Anterior: V

2

–V

5

• Anterolateral: I, aVL, V

5

, V

6

• Inferior: III, aVF (sometimes II also)

• Posterior: The usual depolarization of the posterior of the left ventricle

is lost, giving a dominant R wave in V

1

. Imagine it as a mirror image of

the Q wave you would expect with an anterior infarction.

• Right ventricular: often no changes on the 12-lead ECG. If suspected

clinically, leads are placed on the right of the chest, mirroring the

normal pattern and are labeled V

1

R, V

2

R, V

3

R, and so on.

Hypertrophy

If the heart is faced with having to overcome pressure overload (e.g., left

ventricular hypertrophy in hypertension or aortic stenosis) or higher systemic

pressures (e.g., essential hypertension), it will i its muscle mass in response.

This muscle mass can result in changes in the ECG.

Atrial hypertrophy

This can lead to changes in the P wave.

ECG: AN INTRODUCTION

615

Ventricular hypertrophy

This can lead to changes in the cardiac axis, QRS complex height and

depth, and the T wave.

Left ventricular hypertrophy (LVH)

• Tall R wave in V

6

and deep S wave in V

1

• May also see left axis deviation

• T-wave inversion in V

5

, V

6

, I, aVL

• Voltage criteria for LVH includes the following:

•

R wave >25 mm (5 large squares) in V

6

•

R wave in V

6

+ S wave in V

1

>35 mm (7 large squares)

Right ventricular hypertrophy

• Dominant R wave in V

1

(i.e., R wave bigger than S wave)

• Deep S wave in V

6

• May also see right axis deviation

• T-wave inversion in V

1

–V

3

Paced rhythms

Temporary or permanent cardiac pacing may be indicated for a number

of conditions, such as complete heart block or symptomatic bradycardia.

These devices deliver a tiny electrical pulse to an area of the heart, initiating

contraction. This can be seen on the ECG as a sharp spike.

Many different types of pacemakers exist, and can be categorized

according to the following:

• The chamber paced (atria or ventricles or both)

• The chamber used to detect the heart’s electrical activity (atria or

ventricles or both)

• How the pacemaker responds—most are inhibited by the normal

electrical activity of the heart

On the ECG, look for the pacing spikes (see Fig. 19.22 ), which may

appear before P waves if the atria are paced, before the QRS complexes

if the ventricles are paced, or both.

0 Be careful not to mistake the vertical lines that separate the different

leads on some ECG printouts as pacing spikes!

2 Paced complexes do not show the expected changes described else-

where in this section. Thus you are unable to diagnose ischemia in the

presence of pacing.

Fig. 19.22 Rhythm strip showing dual-chamber pacing.

CHAPTER 19 Data interpretation616

Chest X-rays: introduction

Experienced clinicians and radiologists who look at a chest ﬁ lm and

immediately give a diagnosis are able to do so through years of practice

and the development of pattern recognition. For the nonspecialist, careful

review of chest radiographs requires systematic examination of the ﬁ lm,

including all systems and body parts in it.

While there is no ‘correct’ method, you should ensure that all is examined.

You can do this by region; we do it by organ system. See Box 19.6 for a

framework for reporting chest X-ray (CXR) results.

Technical considerations

2 It should be remembered that the CXR is not a slice of the chest. It

is a two-dimensional representation of all the internal structures, created

by X-rays passing through them. Features can overlie each other, hiding

abnormalities or creating unusual features with compound images. As

such, the image can be inﬂ

uenced by a whole host of external factors.

Projection

This refers to the direction at which the X-ray beam passes.

• PA (posterior–anterior): The cassette is placed in front of the patient

and X-rays pass from the back. This is a standard CXR.

• AP (anterior–posterior): The cassette is placed at the back of the patient

and X-rays are ﬁ

red from in front. An AP ﬁ

lm may be taken in the ill

or injured patient who is unable to stand in front of the X-ray machine.

• Lateral: These views are from either the left or the right of the patient.

The direction of the beam has consequences for the appearance of the

intrathoracic structures. As the X-rays leave the machine, they diverge.

Thus objects near the cassette will appear their true size, but objects

further from the cassette (i.e., nearer the source of radiation) will appear

enlarged (see Fig. 19.23 ).

Box 19.6 Framework for reporting a chest ﬁ lm

• Name

• DOB

• Exam date

• Technical considerations

•

Stationary vs. portable

•

Type of ﬁ lm

•

Position of patient

•

Projection

•

Orientation

•

Rotation

•

Exposure

•

Inspiration

•

Inclusion

• Clinical review

CHEST X-RAYS: INTRODUCTION

617

This is particularly important for viewing the heart—it is not possible to

accurately judge heart size on an AP ﬁ lm, as the heart lies much further

from the cassette.

Position

Standard X-rays are taken with the patient standing. Any deviation from

this will usually be marked on the ﬁ lm, allowing you to learn more about

the patient and adjust your assessment of the image.

• Sitting: suggests a severe illness as the patient is unable to stand

•

The diaphragm will be artiﬁ cially raised, inﬂ ation of the lungs will be

reduced, soft tissues at the front of the patient may be folded.

• Supine or prone: suggests a very severe illness (patient is unable to sit).

•

Structures will be displaced within the chest, with abnormal

distribution of blood supply to the lungs; ﬂ uid levels will not be seen.

Orientation

• Films should have position markers. Often only one side is labeled

(e.g., R , for the right of the patient).

• The image should be presented as if you are looking at the patient—that

is, the patient’s right on your left, and vice versa.

• Ensure that the marker is on the correct side—watch for the relatively

rare cases of dextrocardia.

Rotation

Films should be taken with the patient facing directly away from the source

(for PA ﬁ lms).

You should ensure that this is the case, as rotation can cause abnormal

appearances of the mediastinum and other structures.

• Look at the spinous processes of the thoracic vertebrae—these should

appear at the center of each bone.

• Look also at the distance between the medial ends of the clavicles and

the spinous process of the nearest vertebra—these should be equal.

Exposure

The appropriate exposure depends largely on patient size. Too little will

cause the lungs to appear too white, too much will make structures appear

too dark ( Fig. 19.24 ) and subtle signs may be lost.

• As a rule of thumb, you should just be able to make out the thoracic

vertebral bodies through the image of the heart.

PA AP

Fig. 19.23 An exaggeration of X-ray beam divergence. Note that when the heart

is closer to the origin of the beam, it appears larger on the resultant image.

CHAPTER 19 Data interpretation618

Inﬂ ation

A chest X-ray should be taken with fully inﬂ ated lungs. A poor inspiration

can make the lungs appear denser, draw the trachea to the right, and make

the heart appear abnormally large.

• There should be t 9 ribs visible posteriorly.

•

Count from the top down, but be careful, as it is often easy to

confuse the ﬁ rst couple of ribs and the clavicles.

•

To be sure, ﬁ nd the anterior end of the ﬁ rst rib and trace it

posteriorly; the second rib often appears quite close below.

2 See Fig. 19.25 for a comparison of adequate and inadequate lung

inspiration.

Inclusion

Does the ﬁ

lm show all the structures that you wish it to? You should be

able to see the apices of both lungs and both costophrenic angles.

Fig. 19.24 Radiograph showing an inadequate image quality. The lung ﬁ elds

appear too black and the apices of the lungs are not included in the image.

Box 19.7 Densities

2 Be aware that there are ﬁ ve basic densities on X-rays:

• Black: gas

• Dark gray: fat

• Light gray: soft tissues and ﬂ uid

• White: bone and calciﬁ cation

• Intense white: metal

CHEST X-RAYS: INTRODUCTION

619

Fig. 19.25 Radiographs of the same patient showing the effect of inspiration. The

upper image has a good inspiration, the lower is inadequate. Note how the lungs

appear denser in the lower image and the heart is enlarged.

CHAPTER 19 Data interpretation620

Right

brachiocephalic

vessels

Left

brachiocephalic

vessels

Aortic arch

Pulmonary

trunk

Left atrial

appendage

Left

ventricle

SVC

IVC

Right

atrium

Fig. 19.26 Diagram illustrating the normal outline of the mediastinum and the

structures giving rise to the shape.

Clinical interpretation

Heart and mediastinum

The key to understanding the mediastinum is knowledge of the normal

anatomy. All the structures, apart from the trachea, appear as ﬂ uid or soft-

tissue density and are hard to distinguish separately. Much can be learned

by looking at the shape of the mediastinum ( Fig. 19.26 ).

Examine the following:

• Mediastinal border, looking for abnormality

• Trachea and bronchi

• Heart, looking for visible valves (metal heart valves will appear opaque

on the CXR—see Fig. 19.52 , b p. 638)

• Cardiac size: should be <1/2 of the thoracic width on a PA ﬁ lm.

Measure carefully (with a ruler).

• Look for masses, calciﬁ

cation, or free air (pneumomediastinum).

Abnormalities

• Venous engorgement: look at the lung ﬁ elds.

• Hiatal hernia: may be seen as a rounded object sitting behind the heart

or causing distortion of the normal mediastinal outline. There may be a

visible ﬂ

uid level within it (

Fig. 19.27 ).

• Enlarged heart: enlargement of one or more chamber may be seen

on the mediastinal outline or simply by enlargement of the heart size

(Fig.19.28).

• Pericardial effusion: massive enlargement of the heart with a classical

boot shape ( Fig. 19.29 )

• LV aneurysm: seen as an enlarged left side of the heart—look for

calciﬁ

cation, which will appear white.

• Pericardial calciﬁ

cation: seen as a patchy white outline of the heart

CHEST X-RAYS: INTRODUCTION

621

Fig. 19.27 Radiograph showing a large hiatal hernia. A ﬂ uid level can be seen

within the herniated stomach behind the heart.

Fig. 19.28 Radiograph showing a mass in the upper portion of the mediastinum

on the left.

CHAPTER 19 Data interpretation622

Hila

The hila are the regions at which the lungs connect to the central

circulation. They appear as opaque regions on the right and the left side of

the mediastinum. Most of the image is created by the pulmonary arteries

and veins coming to and from the heart.

The hila should be rounded and symmetrical. As the left pulmonary

artery is slightly superior to the right, the left hilum appears 71 cm higher

than the right. On each side, the bronchi appear as lucent structures.

Look for the following:

• Difference in density

• Asymmetry

• Loss of the normal concavity

• 2 Check for rotation of the ﬁ lm.

Causes of hilar enlargement

• Vascular: smoothly enlarged and irregularly shaped. Arterial

enlargement is due to congestion or aneurysm or pulmonary

hypertension (usually bilateral).

0 Pulmonary hypertension will also cause d peripheral vasculature in the

lung ﬁ eld

( Fig.

19.30 ).

• Lymph nodes: smoothly enlarged, regular masses within the hila. Causes

include neoplastic (bronchial carcinoma, lymphoma, metastatic),

infective (especially TB—look also for peripheral abscesses or miliary

shadowing), and inﬁ

ltrative (sarcoid—look also for pulmonary nodules)

(

Fig. 19.31 ).

• Other masses: irregular masses, sometimes with poorly deﬁ ned

edges

Fig. 19.29 Radiograph showing a large pericardial effusion. The heart appears

grossly enlarged with a typical boot shape.

CHEST X-RAYS: INTRODUCTION

623

Fig. 19.30 Radiograph showing pulmonary hypertension. The engorged

pulmonary arteries are clearly visible at both hila.

Fig. 19.31 Radiograph showing bilateral hilar lymphadenopathy, in this case, due

to sarcoidosis.

CHAPTER 19 Data interpretation624

Look at each bone in detail, including the shoulder girdles, ribs, clavicles,

and thoracic vertebrae. Look at the density and trabecular pattern. Look

for the following:

• Lytic lesions

• Sclerosis

• Erosions

• Fractures

• Dislocation

Vertebrae

Ensure that the size and density are uniform and the spaces equal.

Remember to look for paraspinous soft tissue masses.

Ribs

• Trace each from the back to the front, note width of space between.

• New fractures appear as sharp lines—look for associated

complications, such as surgical emphysema and pneumothorax.

• Old fractures appear as widened areas of rib, often with a slight

distortion of the line of the bone.

Lytic lesions

Bone looks as if it is smudged. This may be the only sign of metastatic

disease.

Soft tissues

Remember that chest cavities are surrounded on all sides by soft tissue,

including the front and the back. Look at all the regions visible. Look for

calciﬁ

cation and free air.

Surgical emphysema

Air pockets exist in the soft tissues ( Fig. 19.32 ). Anterior or posteriorly,

this can be difﬁ cult to see, and may only be seen indirectly by distortion of

the image of the other structures. Laterally, side-on views of the pockets

of air can be seen as radiolucent, lozenge-shaped or tapering structures.

Breasts

Female and male breast tissue overlying the inferior part of the lung may

give the appearance of an increase in lung density. Look for missing breasts

as a clue to underlying disease ( Fig. 19.33 ).

Nipples

Nipples often appear as rounded opacities that could be mistaken for

lesions within the lung.

Abdomen

One should be able to see air in the stomach as a bubble below the left

hemidiaphragm. Often, there is an air-ﬂ uid level within it creating a shape

with a rounded top and a horizontal lower edge.

A gastric bubble on the right may indicate either situs inversus or mis-

labeling of the ﬁ lm.

Look below the diaphragm for free air (pneumoperitoneum), often seen

as a wisp of radiolucency between the liver and the right hemidiaphragm

or above the gastric bubble ( Fig. 19.34 ).

CHEST X-RAYS: INTRODUCTION

625

Fig. 19.32 Radiograph showing extensive surgical emphysema on the left of the

chest. Insert shows a close-up. Also visible is the chest tube causing the problem.

Fig. 19.33 Radiograph showing a patient with disseminated breast cancer. Aside

from the multiple pulmonary lesions, there is a lack of breast shadow on the left,

indicating that this patient has had a left mastectomy.

CHAPTER 19 Data interpretation626

Lungs

Readers should review normal lung anatomy. The points pertinent to the

physical examination are also relevant to the radiographic examination.

Normal

Seen head on, the oblique ﬁ ssures are not visible. As the upper lobes lie

anterior to the lower lobes, the lung ﬁ eld on the CXR is both the upper

and lower lobes (on the left). Normal features include the following:

• Lung ﬁ

elds are of equal density.

• The right hemidiaphragm is slightly higher than the left.

• Sharp costophrenic angles and cardiophrenic angles

• The horizontal ﬁ

ssure in the right lung passes horizontally from the

midpoint of the right hilum to about the sixth rib in the axillary line.

• The pleura should be thin and symmetrical.

Examining the ﬁ lm

Scan the entire lung, looking for areas that are too black, too white, or

abnormally placed. Look for abnormal calciﬁ cation.

2 Look especially at the ﬁ

rst ribs, behind the heart, and behind the

diaphragms, where lesions can often be missed.

2 Ensure that the lung markings extend to the periphery.

Collapse

On ﬁ

lm, loss of air in a lobe or lung region appears dense. Look for the

following:

• Changes to the normal anatomy and asymmetrical density

• Mediastinal and tracheal shift (The volume loss in the affected lung will

pull the mediastinum toward the lesion.)

• Loss of clarity of the borders of the heart and the diaphragms

(Collapse nearby will cause a blurred outline.)

Right upper lobe

Collapses are upward and to the midline ( Fig. 19.35 ). The horizontal

ﬁ

ssure may be elevated and mediastinum shifted to the right. There is a

white mass to the right of the upper part of the mediastinum.

Fig. 19.34 Close-up showing free air below the left hemidiaphragm.

CHEST X-RAYS: INTRODUCTION

627

Fig. 19.35 Radiograph showing right upper lobe collapse.

Right middle lobe

This is difﬁ cult to see on PA ﬁ lm. It may be seen as a slight blurring of the

right heart border and elevation of the right hemidiaphragm ( Fig. 19.36 ).

On lateral ﬁ lm, collapse here is seen as a triangle of white with its apex

at the hilum and base anteriorly.

Right lower lobe

A triangular area of white is between the right heart border and diaphragm,

causing both to be indistinct.

Left upper lobe

Collapse is hard to see; the left hemithorax is hazy with loss of clarity at

the left heart border ( Fig. 19.37 ). Collapse is easier to see on lateral ﬁ lm.

Left lower lobe

There is a sail-like shape of white ( Fig. 19.38 ), but hidden behind the heart

border so it is difﬁ cult to spot. Look for a double edge to the heart.

CHAPTER 19 Data interpretation628

Fig. 19.36 Radiographs showing right middle lobe collapse. This is seen only as

a slight increase in density to the right of the heart on the PA ﬁ lm. The collapse is

much easier to see here than on the lateral ﬁ lm.

Fig. 19.37 PA radiograph showing left upper lobe collapse.

CHEST X-RAYS: INTRODUCTION

629

Fig. 19.38 Radiograph showing left lower lobe collapse—note the sail-like shape

of white behind the heart.

Consolidation

Consolidation is usually a sign of infection—ﬂ uid within the alveolar

spaces, making an area of the lung appear denser ( Fig. 19.39 ). Look for

the following:

• Focal area of i density with indistinct margins

• Heterogeneous alveolar shadowing

• Not present on previous X-rays (Focal ﬁ

brosis may appear similar but

is usually long-standing with a chronic course.)

• There may be a sharp demarcation at lobar margins (right upper

lobe consolidation may be seen with a sharp horizontal lower border

where it meets the right middle lobe) (see Box 19.8 ).

• Air bronchograms: as the airways remain patent, an air-ﬁ lled

bronchus

passing through an area of consolidation may be seen as a radiolucent

(black) tube.

Fibrosis

Increased density of the lung tissue in ﬁ brosis causes a reticulonodular

(net-like with nodules) pattern of opacity. As it progresses, it may cause

a honeycomb appearance of the lung. Be careful to differentiate ﬁ brosis

from edema or consolidation.

Features of ﬁ brosis ( Figs. 19.40 and 19.41 ) are as follows:

• Often bilateral, although not necessarily symmetrical

• Causes d lung volumes

CHAPTER 19 Data interpretation630

• If focal, draws the mediastinum toward the affected side

• Causes blurring of the heart and diaphragm borders

• Has a distinctive reticulonodular pattern

Pulmonary edema

This causes an alveolar pattern of shadowing. If due to congestive cardiac

failure, there will also be changes in the appearance of the heart.

Features of pulmonary edema secondary to heart failure ( Fig. 19.42 ):

• Enlarged heart

• Bilateral, although not necessarily symmetrical, lung shadowing

• Classically, in middle and upper zones, causing a bat’s wing appearance

Box 19.8 Differentiating right lower zone consolidation

Consolidation at the base of the right lung may either be in the right

middle lobe and/or right lower lobe. Look for blurring of the structures

nearby.

• The right middle lobe does not touch the diaphragm—consolidation

here will cause blurring of the right heart border, whereas the

diaphragm remains distinct.

• The right lower lobe lies against the diaphragm but very little of it

touches the heart—consolidation here will cause blurring of the right

hemidiaphragm but leave the right heart border relativelydistinct.

Fig. 19.39 Radiograph showing right lower lobe consolidation.

CHEST X-RAYS: INTRODUCTION

631

Fig. 19.40 Radiograph showing a patient post–lung transplant. The right lung is

the patient’s native lung and is severely ﬁ brosed—note the reticular shadowing and

the d volume. The left lung is the healthy donated lung.

Fig. 19.41 Close-up of a radiograph showing pulmonary ﬁ brosis.

• Pulmonary venous engorgement

•

The vessels appear to extend further than normal into the lung ﬁ eld.

•

Vessels in the upper zone appear larger than normal (often >5 mm

diameter)—upper lobe blood diversion.

• Kerley’s B lines: short, horizontal white lines close to the lung

periphery, usually extending horizontally into the lung ﬁ

eld. They are

found particularly at the bases and caused by edema of the interlobular

septa.

CHAPTER 19 Data interpretation632

Fig. 19.42 Radiograph showing severe pulmonary edema. There is extensive

alveolar shadowing in both lung ﬁ elds, and the heart is enlarged. Note also the ECG

lead attached to the patient’s chest—a sign of the clinical severity.

Fig. 19.43 Radiograph showing a right upper zone mass.

CHEST X-RAYS: INTRODUCTION

633

Coin lesions

The lung masses often have well-demarcated borders. They could also

represent a focal area of consolidation or a pleural lesion ( Fig. 19.43 ). Look

for the following:

• Calciﬁ

cation within the lesion (rare if malignant)

• Air bronchogram within lesion (indicating consolidation, not a mass)

• Cavitation

• Changes in the bones and soft tissues nearby

• Lymph node enlargement in the hila

• Other lesions

Cavitating lesions

These lung lesions have a central cavity, creating a circular radiographic

appearance. If there is ﬂ

uid within the lesion, an air-ﬂ

uid level may be seen

( Fig. 19.44 ). Look at the rest of the ﬁ lm for clues to the nature of the lesion

(i.e., lymphadenopathy, other lesions, signs of infection). Possible causes

include lung abscess, neoplasm, or focal area of infarction.

Bronchiectasis

This can be difﬁ cult to diagnose on a plain X-ray. The combination of

airway enlargement, airway wall thickening, and alveolar shadowing can,

however, give a distinct appearance.

• Ring shadows: affected bronchi are seen head on. They appear as small

rings—several together give a bunch-of-grapes appearance.

• Tramline shadows: affected bronchi are seen side on. They appear as

short parallel lines.

Pneumonectomy

This is rare. The side from which the lung was removed will appear densely

white (a whiteout) ( Fig. 19.45 ). As such, it should be carefully differenti-

ated from a large pleural effusion or dense consolidation. There may also

be the following:

• Mediastinal shift toward the affected side (An effusion would push the

mediastinum the other way.)

• Total absence of lung markings on the affected side

Fig. 19.44 Radiograph showing an abscess in the left lung—note the distinct air-

ﬂ uid level within the rounded lesion (insert).

CHAPTER 19 Data interpretation634

• d Density of the remaining lung as it expands to ﬁ ll the space available

• Signs of previous surgery (e.g., rib resections, sutures)

Pleural lesions

Lesions in the pleura may be seen to overlie the lung ﬁ eld, or may be seen

laterally at the lung edge. Pleural plaques caused by asbestos exposure are

often seen as a heterogeneous lesion with irregular and spiculated edges

(holly-leaf appearance) (

Fig. 19.46 ).

Remember that the pleura also covers the diaphragm—look for the

linear appearance of plaques seen side-on. Be careful not to mistake

pleural lesions for lung lesions.

Pleural effusion

An effusion will appear as a white area at the base of the lung (if the patient

is standing or sitting up). It often has a well-demarcated upper border with

a meniscal edge as the ﬂ uid tracks up lateral to the lung ( Fig. 19.47 ). As the

overlying lung is unable to inﬂ ate fully, there may be the appearance of

increased lung density with a blurred upper border of the effusion. Look for

mediastinal shift (it will move away from the effusion, if large) ( Fig. 19.48 ).

0 Small effusions may only be seen as a blunting of the costophrenic angle

on the affected side. Remember that 7500 mL of ﬂ

uid can hide behind the

hemidiaphragm before it becomes visible on a PA chest ﬁ lm.

Fig. 19.45 Radiograph showing a previous left pneumonectomy. The mediastinum

has shifted so far to the left that it is almost impossible to distinguish amid the

density of the left side of the chest.

CHEST X-RAYS: INTRODUCTION

635

Fig. 19.46 Radiograph showing extensive pleural plaque disease. Close-up shows

one of the lesions—note the characteristic holly-leaf appearance.

Fig. 19.47 Radiograph showing large pleural effusion on the left. Note the

meniscus as the ﬂ uid tracks laterally beside the lung.

CHAPTER 19 Data interpretation636

Air outside the lung will appear as a black area, often as a sliver between

the lung and the thoracic wall. Look for the following:

• A darker area peripherally, often superior in an erect ﬁ lm

• The lung markings do not reach the edge of the lung ﬁ eld—look

carefully, do not mistake a bulla for a pneumothorax. Examine the rest

of the lung for similar areas.

• A visible, albeit thin, demarcation between the lung and the free air

( Fig. 19.49 )

Small pneumothoraces can be hard to spot, try

• Turning the ﬁ

lm on its side (one can often see horizontal lines easier

than vertical ones).

• Asking for an expiratory ﬁ

lm (the lungs will appear more dense and

the pneumothorax will take up relatively more of the lung ﬁ eld).

Tension pneumothorax

0 This is a medical emergency, as i pressure in the chest reduces venous

return to the heart.

• The lung may appear small and shriveled within the lung ﬁ eld.

• The mediastinum is shifted away from the affected side ( Fig. 19.50 ).

• A lowered hemidiaphragm is on the affected side.

COPD

This is difﬁ

cult to spot on a chest X-ray. The lung ﬁ

elds may appear

less dense than normal with reduced lung markings. The chest may be

hyperinﬂ ated, often with an elongated appearance to the mediastinum.

Look for bullae and be careful to differentiate from a pneumothorax.

2 The key sign is ﬂ

attening of the diaphragms (

Fig. 19.51 ).

Fig. 19.48 Radiograph showing a massive pleural effusion causing almost a

complete whiteout of the left lung ﬁ eld. Note how the mediastinum is shifted away

from the affected side.

CHEST X-RAYS: INTRODUCTION

637

Fig. 19.49 Radiograph showing a right-sided pneumothorax. It is difﬁ cult to spot.

Close-up shows the pleural edge as a tiny but distinct demarcation between the

lung tissue and the free air.

Fig. 19.50 Radiograph showing a right-sided tension pneumothorax. There are no

lung markings on the right of the chest. The mediastinum is shifted to the left and

the right hemithorax is overinﬂ ated.

CHAPTER 19 Data interpretation638

Fig. 19.51 Radiograph showing COPD. Note the d density of the lung ﬁ elds.

(a) (b)

Fig. 19.52 Close-ups of radiographs showing (a) aortic valve replacement and (b)

mitral valve replacement.

Iatrogenic features and foreign bodies

Clothes, buttons, zippers, or even a cigarette packet in a shirt pocket can

give misleading and often amusing appearances on the chest ﬁ lm.

CHEST X-RAYS: INTRODUCTION

639

NG tubes

A correctly placed NG tube ( Fig. 19.53 ) will appear as a thin radio-opaque

line descending through the mediastinum, below the diaphragm, and ending

somewhere in the region of the gastric bubble. If the tube does not reach

the stomach but is seen to pass inferior to the carina, it is almost certainly in

the esophagus and will need to be inserted further rather than reinserted.

Tubes seen entering either major bronchus ( Figs. 19.54 and 19.55 ) should

be removed immediately.

Fig. 19.53 Radiograph showing a correctly placed NG tube.

CHAPTER 19 Data interpretation640

Fig. 19.54 Radiograph showing an NG tube in the right bronchus.

Fig. 19.55 Radiograph showing an NG tube in the left bronchus.

ABDOMINAL X-RAYS: INTRODUCTION

641

Abdominal X-rays: introduction

A systematic viewing strategy will aid you in the interpretation of abdom-

inal ﬁ lms. Certain key points to inspect on every abdominal X-ray include

technical quality, gas pattern, calciﬁ cation, bones, and soft tissue.

Technical assessment

Always begin your inspection by checking the following:

• Name of patient

• DOB

• Age of patient

• Sex of patient

• Date when ﬁ

lm was taken

• Left and right markers

• Note the projection of the ﬁ lm.

•

Almost all abdominal X-rays are AP; other views include upright,

supine, or decubitus—these are usually marked on the ﬁ lm.

Views

• Standard abdominal X-ray: also known as an AXR , ‘ﬂ

at plate,’ or KUB

(kidneys, ureters, bladder); it is a supine view (

Fig. 19.56 ).

• Upright ﬁ

lm is useful in identifying the presence of free intraperitoneal

air and intestinal air-ﬂ uid

levels.

• The left/right lateral decubitus* is especially useful in severely ill patients

who are suspected of having free intraperitoneal air and are unable to

stand or sit.

•

Decubitus ﬁ lms can be identiﬁ ed by ﬂ uid levels lying parallel to

the long axis of the body, instead of at right angles to it as on

conventional erect ﬁ lms.

Penetration

• A ﬁ

lm that is too light (underpenetrated) or too dark (overpenetrated)

is of little diagnostic value (see

Box 19.9 ).

• As a general rule, if you can see the bones in the spine, the technical

quality should sufﬁ ce.

• With overexposed or overpenetrated ﬁ

lms, it is recommended that

you inspect these areas with a bright light behind them (present on

most viewing boxes).

Gas pattern

The large bowel lies around the periphery of the abdomen and normally

shows haustral indentations. It should contain feces and gas.

• In the large bowel, loops are considered dilated if diameter is >5 cm.

The small bowel is more central, shows mucosal folds across its width

(valvulae conniventes), and contains ﬂ

uid and gas.

• The diameter of the normal small bowel should not exceed 2.5–3 cm.

2 Become familiar with the normal gas pattern on an abdominal X-ray.

Abnormal positioning of bowel loops may indicate the presence of an

abdominal mass.

* From the Latin decumbere: ‘to lie down’ on the left or right side.

CHAPTER 19 Data interpretation642

Box 19.9 Densities

2 Be aware that there are ﬁ ve basic densities on X-rays:

• Black: gas

• Dark gray: fat

• Light gray: soft tissues and ﬂ uid

• White: bone and calciﬁ cation

• Intense white: metal

Fig. 19.56 A standard abdominal X-ray showing a normal abdomen. Incidentally,

this patient has a T-shaped copper contraceptive device in her uterus, which is

visible on the ﬁ lm.

Fluid levels

Air-ﬂ uid levels are seen as a clear horizontal demarcation between an area

of light gray ﬂ uid and darker gray or black gas. Small ﬂ uid levels in the small

and large bowel are a normal ﬁ nding.

However, distended loops of bowel with air-ﬂ uid levels in a diffuse pat-

tern are highly suggestive of a mechanical obstruction. The bowel loops

frequently have a hairpin (180° turn) appearance.

ABDOMINAL X-RAYS: INTRODUCTION

643

0 To demonstrate ﬂ uid levels, you need an erect or decubitus ﬁ lm.

Extraluminal gas

Carefully inspect for signs of extraluminal gas (outside the bowel lumen).

This may be either free (pneumoperitoneum) or contained within an

abscess cavity, the retroperitoneum, the bowel wall, or the biliary or por-

tal venous systems of the liver.

Free intraperitoneal air suggests a ruptured viscus in the absence of

immediate previous surgery.

A subtle sign to look for free gas is the double wall sign. Here, both sides

of the wall of loops of bowel become visible because of air on the inside

and outside of the bowel.

Pneumoperitoneum

Request an erect chest ﬁ lm in suspected cases of pneumoperitoneum and

look for bilateral dark crescents of free gas under the hemidiaphragms

( Fig. 19.57 ).

Calciﬁ cation

There are several structures that may become calciﬁ ed, particularly with i

age of the patient. These may sometimes cause confusion if mistaken for

intestinal structures:

• Costal cartilages

• Aorta

• Iliac and splenic arteries

Fig. 19.57 An AXR showing a severe pneumoperitoneum. Note how the bowel

wall can be clearly seen; it has air both on the outside and the inside.

CHAPTER 19 Data interpretation644

• Pelvic phleboliths (small round opacities sometimes containing lucent

centers in the pelvic venous plexus)

• Mesenteric lymph nodes

2 Make careful note of abnormal calciﬁ cations

( Fig.

19.58 ), such as biliary

and urinary calculi, calciﬁ ed aneurysms, tumors, pancreatic calciﬁ cation in

chronic pancreatitis, and calciﬁ ed kidneys in nephrocalcinosis.

Bones

Examine the bones, looking for secondary malignant disease (possibly

seen as rounded lucent lesions), degenerative changes, and osteoporosis

( cortical thinning).

Remember to look at all the bones and joints within the ﬁ eld:

• Pelvis

• Vertebrae

• Lowermost ribs

• Sacroiliac joints

• Femoral heads

Soft tissues

Scan the ﬁ lm and identify the following:

• Lower borders of the liver and spleen

• Renal outlines

• Psoas muscles

Masses

Abdominal masses are frequently revealed by displacements or distortions

of normal viscera.

Distended bladder is the most common mass encountered in the pelvis;

alternatively, a mass here may be ovarian or uterine pathology.

Fig. 19.58 An AXR showing calciﬁ cation in the gall bladder.

ABDOMINAL X-RAYS: INTRODUCTION

645

Gross liver enlargement may be indicated by a large mass in the right side

of the abdomen, which may extend to the iliac crest. Look for an absence

of gut shadows and increased density here.

Gross splenic enlargement is seen as a mass extending inferomedially

from the left upper quadrant. There may be elevation of the left hemidi-

aphragm and downward displacement of the left kidney and stomach.

There may also be associated liver and lymph node enlargement.

Normal renal length is 73–3.5 lumbar vertebrae plus their discs. The left

kidney is usually higher and slightly larger than the right one. A discrep-

ancy of more than 1.5 cm between the two sides should be viewed with

suspicion.

2 The loss of the psoas margin or renal outline generally indicates an

inﬂ

ammatory condition in the retroperitoneum.

CHAPTER 19 Data interpretation646

Radiology: pelvis

Normal

The symphysis pubis joint space should be no wider than 5 mm and there

should be alignment of the pubic rami. Look closely at the main pelvic

ring and the two obturator rings to exclude any abnormality in the bony

cortex. Examine the sacroiliac joints to ensure consistent width on either

side. The sacral foramina should appear symmetrical and undisrupted.

Pelvic fractures

Stable

• Avulsion fractures—e.g., ischial tuberosity (hamstring avulsion)

• Iliac wing fracture: Duverney’s

• Sacral fractures: Denis classiﬁ cation

• Ischiopubic rami fractures

• Acetabular fractures

• Coccygeal fractures: X-rays are not indicated here, as they will not

change management.

0 Avulsion fractures are often due to forceful muscle contraction.

Unstable

The pelvic ring is disrupted in two or more places ( Fig. 19.59 ).

Fig. 19.59 Radiograph showing fractured pubic rami on the left. Note that both

the superior and inferior pubic rami are broken—it is not usually possible to break

only one.

RADIOLOGY: PELVIS

647

• Straddle fracture: both obturator rings

• Bucket-handle fracture: sacroiliac and contralateral ischiopubic rami

(not to be confused with the bucket-handle fracture indicative of child

abuse)

• Malgaigne fracture: sacroiliac and ipsilateral ischiopubic rami

• Open-book fracture: both sacroiliacs and both ischiopubic rami

Hints

2 If you detect a fracture of the main pelvic ring, look hard to exclude a

second disruption to the ring—either a fracture or joint widening at the

symphysis pubis/sacroiliacs.

2 Pelvic fractures can result in severe damage to internal organs.

Pediatrics

• Normal development: be careful not to misinterpret the normal

cartilaginous junction (synchondrosis) between pubic and ischial bones

as a fracture.

CHAPTER 19 Data interpretation648

Radiology: hips and femurs

Normal

The joint space between the femoral head and acetabulum should not

appear narrowed at any point. Examine the femoral neck for a normal

trabecular (bony mesh) pattern and absence of sclerotic areas. Look for a

smooth, undamaged cortex as you trace the outline of the proximal femur

and femoral shaft.

Fractures

Fractures of the proximal femur are common in the elderly and carry

signiﬁ cant mortality risk. Avascular necrosis is a potential complication if

the fracture involves the femoral neck and results from disruption of the

blood supply to the femoral head (retinacular vessels).

Fractures about the hip are typically characterized by location as femoral

neck, intertrochanteric (between the greater and lesser trochanters), and

subtrochanteric ( Fig. 19.60 ).

Femoral neck fractures can be further graded on their radiological

appearance using the Garden classiﬁ cation , presented in Box 19.10.

Hints

2 Ask for lateral as well as AP views when requesting hip X-rays.

0 Hip fracture is used loosely, but incorrectly, to describe all proximal

femoral fractures. Strictly speaking it only relates to intracapsular fractures

(those within the joint capsule).

0 Fractures described as subcapital (just below the femoral head) and

transcervical (across the femoral neck) are both intracapsular fractures.

Degenerative changes

Classical X-ray changes in osteoarthritic degenerative disease at the hip

( Fig. 19.61 ), as with other joints, include the following:

(a) (b)

Fig. 19.60 Close-up of radiographs showing (a) an intertrochanteric fracture on

the left and (b) fractured neck of the femur.

RADIOLOGY: HIPS AND FEMURS

649

Box 19.10 Garden classiﬁ cation*

• I—fracture line across the neck stops short of inferior cortex. No

displacement. Trabecular angulation across fracture

• II—fracture extends right across the neck. No displacement. No

trabecular angulation (no deviation of bony mesh lines)

• III—fracture extends right across the neck. Some displacement and/

or rotation of femoral head

• IV—femoral head severely (often completely) displaced

* The value of this classiﬁ cation is disputed.

Fig. 19.61 Radiograph showing severe degenerative changes at both hips.

• d Joint space

• Osteophyte formation (bony spurs)

• Bone cysts

• Subarticular sclerosis

Dislocation of hip joint

Of all such cases, 90% are posterior dislocations, with the femoral head

seen superior and lateral to the acetabulum. Check for sciatic nerve injury

(10%).

0 Posterior dislocation strongly suggests that major force was applied;

consider trauma elsewhere.

Pediatrics

• Slipped femoral epiphysis: Look for misalignment on lateral X-ray of

the shaft and neck of the femur with the epiphysis (teenagers).

• Legg-Calve-Perthes disease (aseptic necrosis of femoral epiphysis):

Look for sclerosis and ﬂ

attening of the epiphysis and cysts in

metaphysic (preteens).

• Developmental dysplasia of the hip (congenital dislocation): The

femoral head fails to lie within the acetabulum. If missed, osteoarthritis

and gait defects ensue. This is diagnosed neonatally with ultrasound.

CHAPTER 19 Data interpretation650

Radiology: knees

Normal

AP and lateral views are provided as standard. The joint space should be

maintained across the joint. On AP ﬁ lm, the lateral tibial condyle margin

should be no more than 5 mm outside the femoral condyle margin. On

lateral ﬁ lm the distance from the tibial tuberosity to the inferior aspect of

the patella should be similar to the length of the patella.

Abnormal

Distal femur fractures

All of the following fractures are readily identiﬁ able on plain X-ray:

• Supracondylar

• Condylar (medial or lateral)

• Intercondylar

Proximal tibial fractures

These are often a result of being hit by car. Lateral (80%) tibial plateau

fractures are more common (think impact site).

On X-rays, look for an impacted sclerotic area and lateral displacement

of tibial condyle, in addition to fracture itself. A lateral view of the knee

can show a fat-ﬂ

uid (marrow-blood) level in the suprapatellar bursa, which

may be the only sign of intra-articular fracture.

• Depressed plateau fracture—lateral or medial

• Split fracture—proximal ﬁ

bula and lateral tibial condyle both affected

• Combined split depressed fracture—combination of depressed plateau

and split fracture

• Medial condyle fracture—less common

• Comminuted fracture of lateral and medial tibial condyles

• Segond fracture—avulsion fracture superolateral aspect proximal tibia.

Associated with ligamentous and meniscal injury

• Intercondylar eminence fracture (tibial spine)—associated with

anterior cruciate ligament injury

Patella

Transverse, vertical, comminuted, or avulsion fractures can occur. Oblique

or skyline views may be required to identify some vertical fractures. Patella

dislocation is usually lateral. Rupture of patellar ligament leads to superior

displacement of the patella.

Neck of ﬁ bula

fractures

Think about accompanying ligamentous (collateral and cruciate) injury.

Proximal third of ﬁ bula fractures

Look for associated ankle fracture.

Degenerative changes

Knee joint changes are similar to those at the hip.

Knee dislocation

In knee dislocation, 75% of cases are posterior. There is potential for

signiﬁ cant injury to the popliteal and peroneal blood vessels.

RADIOLOGY: KNEES

651

Hints

0 Most meniscal or ligamentous injuries have no X-ray changes.

2 Examine the hip when patients complain of a painful knee—it could be

referred pain.

Pediatrics

• Bipartite patella: normal variant. Secondary ossiﬁ cation center, usually

in superiolateral region. May stay unfused throughout adulthood. Do

not confuse this with fracture.

• Osgood–Schlatter disease: recurrent minor trauma leads to swelling

and pain at quadriceps tendon insertion. Avulsion of tibial tubercle may

be seen on X-ray. Boys are affected more than girls.

• Osteochondritis dissecans: chronic trauma causes articular cartilage

and subchondral bone disruption. Most commonly seen at lateral side

of medial femoral epicondyle. Remember the mnemonic LAME: Lateral

Aspect Medial Epicondyle.

CHAPTER 19 Data interpretation652

Radiology: shoulder

AP and either axial (armpit view), lateral scapular (Y view), or apical

oblique views are usually provided.

Abnormal

Glenohumeral dislocation

• Anterior dislocations: (95%) humeral head lies anterior and inferior to

glenoid

• Posterior dislocation: often missed. Look for a rounded symmetrical

humeral head (due to internal rotation).

• Inferior dislocation (luxatio erecta): rare (neurovascular damage more

likely)

Fractures

• Clavicle fracture: readily identiﬁ

ed on AP ﬁ

lm. 80% lateral 1/3

• Fracture-dislocations: humeral greater tuberosity often involved

• Humeral head or neck fracture: oblique or impacted fractures seen on

X-ray ( Fig. 19.62 )

• Humeral shaft fracture: transverse, spiral, or comminuted

• Scapula fracture: uncommon. May require trans-scapular view.

• Supraspinatus rupture: may see bony avulsion on X-ray

Acromioclavicular (AC) injury

On the AP view, the inferior cortex of the clavicle and that of the acromion

process should be aligned. Normal AC distance should be d8 mm. Look

for widening of the AC joint and any associated fractures.

Fig. 19.62 Radiograph showing fractured neck of humerus on the right.

RADIOLOGY: SHOULDER

653

AC injury is graded according to degree of separation:

• Grade I: ligamentous involvement only. Slight separation

• Grade II: subluxation but with some bony overlap

• Grade III: AC joint fully dislocated. Coracoclavicular ligament ruptured

Adhesive capsulitis (frozen shoulder)

On X-ray, joint space narrowing and osteoporotic changes due to disuse

are apparent.

Sternoclavicular dislocation

Anterior dislocations are more common ( Fig. 19.63 ). There is risk of injury

to large vessels and the trachea with posterior dislocation.

Calciﬁ c

tendonitis

This is exquisitely painful; rapid relief is with local steroidal injections. Look

for abnormal calcium in soft tissues around the joint on X-ray.

Hints

2 AP views of posterior dislocation may appear normal. The axillary view

may be helpful.

• Fracture of the glenoid can be a complication of anterior dislocation.

0 Look for any fracture fragments with anterior dislocation.

Stress views (giving the patient weight to hold on the affected side) can

make AC injury more obvious on X-ray.

Fig. 19.63 Radiograph showing anterior dislocation of the humerus on the left.

CHAPTER 19 Data interpretation654

Radiology: cervical spine

Examining C-spine ﬁ lms

Three views are advisable—lateral, AP, and open mouth (the latter to

get a clear view of the odontoid peg). Remember, the peg is the upward

extension of the body of C2—the axis.

Lateral view

• Can you see all seven cervical vertebrae, including the top of T1?

• Trace three superimposed parallel curved lines running down the neck

to look for steps or misalignments (see Fig. 19.64 ).

• Check the gap between the anterior aspect of the peg and anterior

arch of C1—it should be d3 mm in adults, d5 mm in children.

• Look for prevertebral soft-tissue swelling. This may be only sign

of a C-spine fracture (lack of soft tissue swelling does not exclude

fracture).

• Inspect for narrowing of disc spaces.

Fig. 19.64 Radiograph showing a fractured odontoid peg. Note that the ﬁ rst

cervical vertebra is displaced posteriorly. Several additional lines appear on the ﬁ lm,

caused by the head and neck brace that the patient is wearing.

RADIOLOGY: CERVICAL SPINE

655

AP view

• Ensure that the spinous processes are aligned (some may be biﬁ d).

• Measure the gaps between spinous processes. These should be

approximately equal (but are allowed to be up to 50% wider than the

gaps directly above or below).

Open-mouth (odontoid peg) view

• Check that the peg is intact.

• Are the lateral aspects of C1 and C2 aligned?

• Look for equal gaps on both sides of the peg.

C-spine injuries

Stable

• Unilateral facet dislocation: spinous processes misaligned on AP

• Posterior arch of C1 fracture

• Wedge fracture: d height of anterior vertebral body. Delayed instability

is possible.

• Extension teardrop fracture: avulsion fracture, anteroinferior aspect C2

• Burst fracture: compression fracture between C3 and C7

• Anterior subluxation: fanning (widening) seen between adjacent spinous

processes on lateral view. Delayed instability is possible.

• Clay-shoveler’s fracture: oblique avulsion fracture of lower spinous

process

Unstable

• Bilateral facet dislocation

• Odontoid fracture ( Fig. 19.64 )

• Hangman’s fracture: fracture of C2 pedicles

• Jefferson’s fracture: fracture to anterior and posterior arches of C1

• Flexion teardrop fracture: fracture-dislocation of the vertebral body

• Hyperextension fracture-dislocation: anterior displacement of vertebra is

common

• Atlanto-occipital disassociation (remember, atlanto refers to C1)

Pediatrics

• Normal variant: Particularly in children, the base of C2 spinous process

may lie 2 mm posterior to the curved line linking the other bases.

• Pseudosubluxation: Normal ligamentous laxity causes anterior

displacement of C2 or C3.

Hints

0 If you see one fracture, look for another—20% of cases are multiple.

0 Most C-spine fractures occur near the top (C1–C2) and bottom

(C5–C7) of the neck.

CHAPTER 19 Data interpretation656

Radiology: thoracic and lumbar spine

Examining spinal ﬁ lms

Lateral and AP views are provided as standard.

• Examine the height of each vertebra—they should be approximately

equal and the same front and back.

• Look for the normal concave shape of the back of each vertebral body.

The gaps between vertebrae (the disc spaces) should be equal.

• Trace the lines of the anterior and posterior vertebral bodies. Look for

any steps, ridges, or misalignments.

• On the AP view, the lumbar pedicles should become slightly further

apart going down the spine.

Abnormalities

Thoracic (T) and lumbar (L) spine fractures

• Wedge (compression) fracture ( Fig. 19.65 )

•

d Height of vertebral body with wedge shape

•

Loss of concave shape to posterior vertebral body

Fig. 19.65 Radiograph showing a wedge fracture of a thoracic vertebra.

RADIOLOGY: THORACIC AND LUMBAR SPINE

657

• Burst fracture: vertebral body crushed into >2 pieces (comminuted)

• Fracture-dislocations: high suspicion of spinal cord injury

• Chance fracture: horizontal splitting of vertebra

• Transverse process fracture

• Spinous process fracture

Spondylolysis

• Degeneration of intervertebral discs leads to narrowing of disc space

and osteophyte formation.

Spondylolisthesis

• Anterior subluxation of vertebral body (congenital or after injury)

Hint

• 90% fractures are at T11–L4.

CHAPTER 19 Data interpretation658

Lung function tests

Simple lung function tests can help with the diagnosis and monitoring of

common respiratory diseases, such as asthma and chronic obstructive pul-

monary disease (COPD). Recognizing patterns of abnormality of these

tests is an essential skill in data interpretation.

Peak expiratory ﬂ ow rate

Peak expiratory ﬂ ow rate (PEFR) is the maximum ﬂ ow rate recorded

during a forced expiration. Predicted readings vary according to age, sex,

height, and ethnicity (see Fig. 19.66 ).

Interpreting PEFR

PEFR readings less than the patient’s predicted, or usual best reading, dem-

onstrate airﬂ ow obstruction in the large airways.

PEFR readings are useful in determining the severity and thus most

appropriate treatment algorithm for asthma exacerbations:

• PEFR 80–100% best or predicted—mild asthma attack

• PEFR 50–80% best or predicted—moderate asthma attack

• PEFR <50% best or predicted—severe asthma attack

• PEFR <33% best or predicted—life-threatening asthma attack

0 PEFR readings are subject to considerable personal variation.

0 Note the diurnal variations in PEFR with asthma.

2 Don’t confuse PEFR with forced expiratory volume in 1 second (FEV

1

).

700

650

600

550

500

450

400

350

300

11

10

9

8

7

6

5

1.8 m1.7 m1.6 m1.5 m

71"67"63"59"

1.4 m 1.9 m

Age (yrs):20–25

30

40

50

60

20–25

40

60

Height (m) = metres, " = inches

SD 60 L/min

SD 67 L/min

SD 1 L/s

SD 1.1 L/s

Top 5 lines are for men (black)

Bottom 5 lines are for women (blue)

Peak expiratory flow (L/min)

Peak expiratory flow (L/s)

Fig. 19.66 Predicted values of peak expiratory ﬂ ow rate according to age, sex,

and height. Reproduced with permission from Longmore M, et al. (2004). Oxford

Handbook of Clinical Medicine , 6th ed. Oxford: Oxford University Press.

LUNG FUNCTION TESTS

659

Reversibility testing

Improvement in PEFR or FEV

1

“ 15% following bronchodilator therapy

(e.g., salbutamol) shows reversibility of airﬂ ow obstruction and can help

to distinguish asthma from poorly reversible conditions, such as COPD.

Spirometry

Spirometry is the measurement of airﬂ ow and functional lung volumes.

Fig. 19.67 shows the pattern of lung volumes in a healthy individual during

normal breathing, and maximum inspiration and expiration with a single

breath.

Patients are asked to blow, as fast as possible, into a mouthpiece

attached to a spirometer. This records the rate and volume of airﬂ ow.

Unlike measuring PEFR, patients must continue blowing out for as long as

possible. The test is repeated until two similar readings are achieved.

Two key values are

• FEV

1

: forced expiratory volume in the ﬁ rst second.

• FVC: forced vital capacity—the total lung volume from maximum

inspiration to maximum expiration, in forced exhalation.

Modern machines will often calculate the patient’s predicted values for

FEV

1

and FVC, which, like PEFR, are dependent on age, sex, height, and

ethnicity. Usually 70–85% of the FVC is expired in the ﬁ rst second, giving

the volume–time graph shown in Fig. 19.68.

Volume

Time

RV

FRC

TV FVC

TLC

IC = Inspiratory capacity

TLC = Total lung capacity

RV = Residual volume

FRC = Functional residual capacity

TV = Tidal volume

FVC = Forced vital capacity

IC

Fig. 19.67 Normal pattern of lung volumes.

CHAPTER 19 Data interpretation660

Flow volume loops can also be generated from spirometry data and show

the ﬂ ow at different lung volumes. These are useful in distinguishing intra-

and extrathoracic causes of obstruction as well as in assessing for small

airways obstruction.

2 Spirometry is valuable in assessing anesthetic risk prior to elective sur-

gery and vital for the diagnosis of COPD.

0 Don’t confuse PEFR with FEV

1

. While these may correlate well in

asthma, a normal PEFR does not exclude a reduced FEV

1

in COPD.

Gas transfer

Measuring the capacity of a gas to diffuse across the alveolar–capillary

membrane can provide important information. DLCO (carbon monoxide

diffusion capacity) measures the uptake from a single breath of 0.3% CO.

It is reduced in interstitial lung disease and emphysema.

Other tests

Pulmonology practices calculate static lung volumes with a body plethys-

mograph or through helium rebreath and dilutional techniques:

• TLC—total lung capacity

• RV— residual volume

Both of these can help in identifying patterns of lung disease and assessing

patients prior to lung surgery.

Common patterns of abnormality

Abnormal patterns of lung function fall broadly into two types, obstructive

and restrictive (see Table 19.1 ).

7

6

5

4

3

2

1

0

0123456

FVC

FEV

1

Time (seconds)

Volume (litres)

Fig. 19.68 Spirogram showing normal volume–time graph.

LUNG FUNCTION TESTS

661

Table 19.1 Obstructive v. restrictive spirometry results

Pattern FEV 1 FVC FEV

1

/FVC ratio TLC RV

Obstructive d n/d <75% i (or n) i

Restrictive d d >75% d d

See Fig. 19.69 for spirograms showing obstructive and restrictive volume–

time graphs.

Obstructive

When airﬂ ow is obstructed, although FVC may be reduced, FEV

1

is much

more reduced, hence the FEV

1

/FVC ratio falls. It can also take much longer

to fully exhale.

2 FVC can be normal in mild to moderate obstructive conditions.

Conditions causing an obstructive defect include the following:

• COPD

• Asthma

• Bronchiectasis

• Cystic ﬁ brosis

• Foreign bodies, tumors, and stenosis following tracheotomy (all

localized airﬂ ow

obstruction)

Restrictive

The airway patency is not affected in restrictive lung conditions, so the

PEFR can be normal. But the FEV

1

and FVC are reduced because of the

restrictive picture.

Conditions causing a restrictive defect include the following:

• Fibrosing alveolitis of any cause

• Skeletal abnormalities (e.g., kyphoscoliosis)

• Neuromuscular diseases (e.g., motor neuron disease)

• Connective tissue diseases

• Late-stage sarcoidosis

• Pleural effusion

• Pleural thickening

2 Mixed obstructive and restrictive defects can also be found.

CHAPTER 19 Data interpretation662

Normal

V

FEV

1

–

FVC –

FEV

1

/FVC – 70–80%

FEV

1

– dd

FVC – d

FEV

1

/FVC d

T

Obstructive

V

T

V

Restrictive

T

FEV

1

– d

FVC – d

FEV

1

/FVC

N

Fig. 19.69 Spirograms showing obstructive and restrictive volume–time graphs.

ARTERIAL BLOOD GAS ANALYSIS

663

Arterial blood gas analysis

While clinical examination skills will enable you to detect many important

conditions, at times we all need help from the analysis of blood and other

ﬂ uids. Even the most experienced provider can’t determine the PaCO

2

just by the laying on of hands (although they might tell you otherwise).

A systematic approach

The printout from the ABG machine can have a bewildering number of

results. Initially, just focus on the pH, PaCO

2

, and HCO

3

–

, in that order

(see Box 19.11 ).

pH

Is it low (acidosis) or high (alkalosis)?

PaCO

2

Remember, CO

2

is acidic.

• If PaCO

2

is raised and there is acidosis (pH <7.35), you can deduce a

respiratory acidosis.

• If PaCO

2

is low and there is alkalosis (pH >7.45), then the lack of acid

gas has led to a respiratory alkalosis.

• Conversely, if PaCO

2

is low and there is acidosis, the respiratory

system is not to blame and there must instead be a metabolic acidosis.

•

Conﬁ rm this by looking at the HCO

3

–

; it should be low—remember

it is alkaline and acts as a buffer.

• If PaCO

2

is high or normal and there is alkalosis, then again the

respiratory system will not be to blame and there must instead be a

metabolic alkalosis.

•

Conﬁ rm this by looking at the HCO

3

–

; it should be raised.

PaO

2

0 Note what FiO

2

(fraction of inspired oxygen) the patient was breathing

when the sample was taken.

Hypoxia is PaO

2

of <60 mmHg (8.0 kPa) and can result from

ventilation–perfusion (V/Q) mismatch—e.g., pulmonary embolism—or

from alveolar hypoventilation—e.g., COPD, pneumonia.

• Type I respiratory failure: hypoxia and PaCO

2

d45 mmHg

• Type II respiratory failure: hypoxia and PaCO

2

t50 mmHg

2 If the PaO

2

is very low, consider venous blood contamination.

Box 19.11 Reference ranges

• pH : 7.35–7.45

• PaCO

2

: 35–45 mm Hg

• PaO

2

: 80–100 mm Hg

• HCO

3

–

: 21–28 mEq/L

• Base excess: ±2 mEq/L

CHAPTER 19 Data interpretation664

Compensatory mechanisms

Mechanisms controlling pH are activated when acid–base imbalances

threaten. Thus, renal control of H

+

and HCO

3

–

ion excretion can result

in compensatory metabolic changes. Similarly, blowing off or retaining

CO

2

via control of respiratory rate can lead to compensatory respiratory

changes. This can complicate interpretation of ABG results.

2 A normal pH does not exclude acid–base disturbance ( Table 19.2 )—

there may be adequate compensation or a mixed picture.

2 A compensated picture suggests chronic disease.

Base excess and (standard) HCO

3

–

effectively measure the same thing.

Small variations of above-normal values exist between facilities.

Table 19.2 Some acid–base disturbances

Disturbance pH PaCO

2

HCO

3

–

Respiratory

acidosis

d i n

(i if compensated)

Metabolic acidosis d n

(d if compensated)

d

Respiratory

alkalosis

i d n

(d if compensated)

Metabolic alkalosis i n

(i if compensated)

i

Box 19.12 Example of respiratory acidosis (on room air)

pH 7.29, PaCO

2

56, PaO

2

70, HCO

3

−

25

The cause in this case is acute exacerbation of COPD.

Acidosis

A relative excess of cations (e.g., H

+

), unless adequately compensated, will

result in acidosis (more correctly, acidemia).

Respiratory acidosis

In this condition, pH is d, PaCO

2

i is (HCO

3

–

may i be if compensated)

( Box 19.12 ). Conditions that can lead to respiratory acidosis are as

follows:

• COPD, asthma, pneumonia, pneumothorax, pulmonary ﬁ brosis

• Obstructive sleep apnea

• Opiate overdose (causing respiratory depression)

• Neuromuscular disorders (e.g., Guillain–Barré, motor neuron disease)

• Skeletal abnormalities (e.g., kyphoscoliosis)

• Congestive cardiac failure

0 In COPD, ﬁ

nd patient’s normal PaCO

2

—it may be abnormally high.

ARTERIAL BLOOD GAS ANALYSIS

665

Metabolic acidosis

This involves pH, d HCO

3

–

d (PaCO

2

may be d if compensated) (see

Box 19.13 ).

Anion gap (Na

+

+ K

+

) – (HCO

3

–

+ Cl

–

): Normal range is 8–16 mEq/L

(Note: Reference values vary and an alternative formula is available.)

It is useful to calculate the anion gap to help distinguish causes of metabolic

acidosis. An i anion gap points to i production of unmeasurable anions.

Conditions that can lead to metabolic acidosis involve either an increased

or normal anion.

i Anion gap

• Diabetic ketoacidosis

• Renal failure (urate)

• Lactic acidosis (tissue hypoxia or excessive exercise)

• Salicylates, ethylene glycol, biguanides

Normal anion gap

• Chronic diarrhea, ileostomy (loss of HCO

3

–

)

• Addison’s disease

• Pancreatic ﬁ stula

• Renal tubular acidosis

• Acetazolamide treatment (loss of HCO

3

–

)

A

nion

g

ap

(

Na

+

K

+

)

–

(

HCO

3

–

+ Cl

–

)

: Normal ran

g

e is 8–16 mE

q

/L

(

Note: Reference values vary and an alternative formula is available.

)

Box 19.13 Example of metabolic acidosis (on room air)

pH 7.25, PaCO

2

40, PaO

2

96, HCO

3

–

12

The cause in this case is diabetic ketoacidosis

Box 19.14 Example of respiratory alkalosis (on room air)

pH 7.53, PaCO

2

28, PaO

2

85, HCO

3

–

22

The cause in this example is anxiety.

Alkalosis

A relative excess of anions (e.g., HCO

3

–

), unless adequately compensated,

will result in alkalosis (more correctly, alkalemia)

Respiratory alkalosis

This involves i pH, d PaCO

2

(HCO

3

–

may be d if compensated) ( Box 19.14 ).

Conditions that can lead to respiratory alkalosis are as follows:

• Hyperventilation, secondary to

•

Panic attack (anxiety)

•

Pain

• Meningitis

• Stroke, subarachnoid hemorrhage

• High altitude

CHAPTER 19 Data interpretation666

2 Sensory changes (tingling in hands, face, lips) with hyperventilation are

due to d ionized calcium.

Metabolic alkalosis

This involves i pH, i HCO

3

–

(PaCO

2

may be i if compensated) ( Box 19.15 ).

Conditions that can lead to metabolic alkalosis are as follows:

• Diuretic drugs (via loss of K

+

)

• Prolonged vomiting (via acid replacement and release of HCO

3

–

)

• Burns

• Base ingestion

Mixed metabolic and respiratory disturbance

In clinical practice, patients can develop a mixed picture in which

acid–base imbalance is the result of both respiratory and metabolic fac-

tors ( Box 19.16 ). For example, in critically ill patients, hypoventilation

leads to d PaO

2

, and O

2

-depleted cells then produce lactic acid.

Box 19.15 Example of metabolic alkalosis (on room air)

pH 7.50, PaCO

2

36, PaO

2

92, HCO

3

–

27

The cause in this example is vomiting

Box 19.16 Example of mixed respiratory and metabolic

acidosis (on room air)

pH 7.0, PaCO

2

59, PaO

2

86, HCO

3

–

14

The cause in this example is septic shock.

CEREBROSPINAL FLUID (CSF)

667

Cerebrospinal ﬂ uid (CSF)

CSF is produced by the choroid plexus lining the cerebral ventricles and

helps cushion and support the brain. Samples are usually obtained by

means of lumbar puncture.

Normal adult CSF

Normal values will vary by laboratory.

• Opening pressure

50–200 mm H

2

O

• Red cells 0

• WBC

0–5

• Lymphocytes

40–80%

• Neutrophils 0–6%

• Protein 15–45 mg/dL

• Glucose

60–80% of blood glucose)

• IgG

0–4.5 mg/dL

2 CSF glucose is abnormal if it is < 50% of blood glucose level

0 Premature babies, newborns, children, and adolescents have different

normal ranges

Interpreting CSF

Table 19.3 is only a general guide. Be guided by CSF results (see Box 19.17 )

together with the clinical picture.

Table 19.3 Characteristics of CSF according to underlying pathology

Pathology Appearance Protein

Glucose

CSF–blood

ratio)

Cells

Bacterial

meningitis

Turbid i d Neutrophils

Viral meningitis Clear n /i i/n Lymphocytes

Viral

encephalitis

Clear n /i d Lymphocytes

TB meningitis Fibrin webs i d d Lymphocytes

Neutrophils

Fungal

meningitis

Clear/turbid i d Lymphocytes

Subarachnoid

hemorrhage

Xanthochromia n /i i Red cells

Multiple

sclerosis

Clear n /i n /i Lymphocytes

Guillain–Barré

syndrome

Clear i n /i

Cord

compression

Clear i n

Malignancy Clear i d Malignant

CHAPTER 19 Data interpretation668

Box 19.17 Further CSF tests

• Culture

• Gram stain

• Ziehl–Neelsen stain (TB)

• India ink (cryptococcus)

• Electrophoresis (oligoclonal bands in multiple sclerosis)

• Cytology (malignant cells)

• Serological tests (syphilis)

• Viral polymerase chain reaction (PCR)

URINALYSIS

669

Urinalysis

Dipstick urinalysis offers speedy and noninvasive testing that can help with

the diagnosis of common conditions such as urinary tract infections (UTIs)

and diabetes mellitus (DM). Samples can be sent to the laboratory for

further analysis, including microscopic analysis and culture/sensitivity.

Box 19.18 Methods of collecting urine for analysis

• Random sample (contamination likely)

• Mid-stream sample (less contamination)

• First-void urine (for intracellular organisms—e.g., Chlamydia )

• Early-morning sample (to look for acid-alcohol fast bacilli—TB)

• Suprapubic aspiration

• Via catheter bag

• Via urine bag (pediatrics)

• 24-hour collection

Dipstick

Dipstick testing gives semiquantitative analysis of the following:

• Protein (normally negative)

• Glucose (normally negative)

• Ketones (normally negative)

• Nitrites (normally negative)

• Blood (normally negative)

• Leucocytes (normally negative)

• Bilirubin (normally negative)

• pH (normally acidic with range 4.5–8.0)

• Speciﬁ

c gravity (normal range 1.000–1.030)

2 Test the urine within 15 minutes of obtaining the sample.

0 Color vision must be intact to interpret the dipstick chart.

2 Urine pregnancy-testing is equally convenient and is indicated in females

of childbearing age who present with abdominal symptoms.

2 Various foods (e.g., beets, asparagus, blackberries) and drugs

(e.g., rifampicin, tetracyclines, levodopa, phenytoin, chloroquine, vitamins,

iron supplements) can change the color of urine.

Microscopy, culture, and sensitivity (M,C&S)

Microscopy enables identiﬁ cation of bacteria and other microorganisms,

urinary casts (formed in the tubules or collecting ducts from proteins or

cells), crystals, and cells (including renal tubular and transitional epithelial

cells, leukocytes, and red blood cells). Organism growth and antibiotic

sensitivities and can also be determined.

2 Microscopy and culture/sensitivity may not be indicated for patients

with uncomplicated UTI diagnosed on clinical history and dipstick and

started on antibiotics.

2 Asymptomatic bacteriuria is more common in pregnancy (up to 7%) and

can lead to pyelonephritis and potential fetal complications.

CHAPTER 19 Data interpretation670

Characteristic urinalysis ﬁ ndings

• UTIs: nitrites, leukocytes

• Diabetes mellitus: glucose

• Diabetic ketoacidosis: ketones

• Cholestasis (obstructive jaundice): bilirubin

• Prehepatic jaundice: urobilinogen

• Glomerulonephritis: protein, blood

• Renal stones: blood

• Renal carcinoma: blood

• Nephrotic syndrome: protein ++

• Renal TB: leukocytes, no organisms grown (sterile pyuria)

• Sexually transmitted infections (chlamydia, gonorrhea): sterile pyuria

2 Suspected UTIs in children must be investigated with the consideration

that they may be indicators of anatomical abnormalities or possible sexual

abuse.

PLEURAL AND ASCITIC FLUID

671

Pleural and ascitic ﬂ uid

Pleural effusion

Fluid in the pleural space can be classiﬁ ed as exudate (protein content

>30 g/L) or transudate (protein content <30 g/L). At borderline levels,

if the pleural protein is >50% serum protein, then the effusion is an

exudate. Blood, pus, and chyle (lymph with fat) can also form an effusion.

See b p. 561 for pleural tap guidance.

Box 19.19 Tests for pleural ﬂ uids

• Microscopy, culture (conventional ± TB culture), and sensitivity

(Gram stain, Ziehl–Neelsen stain)

• Cytology (malignant cells)

• Biochemistry

•

Protein

•

Glucose (d if rheumatoid or pneumonia related)

•

Amylase (i in pancreatitis)

•

LDH (i in empyema, malignancy, rheumatoid)

2 A large effusion needs a chest drain.

2 If you suspect malignant pleural disease, consider pleural biopsy.

0 Unilateral effusion suggests localized disease (malignancy, pneumonia).

0 Pleural ﬂ

uid may be purulent (e.g., empyema) and therefore difﬁ cult

to aspirate.

Transudate causes

These involve i venous or d oncotic pressure.

• Heart failure

• Hypoproteinemia (liver failure, malabsorption, nephroticsyndrome)

• Hypothyroidism

• Constrictive pericarditis

• Meig’s syndrome (ovarian ﬁ

broma + pleural effusion)

Exudate causes

These involve i capillary permeability.

• Pneumonia

• Empyema

• Malignancy (lung, pleura, lymph)

• Pulmonary infarction

• TB

• Systemic lupus erythematosus (SLE)

• Rheumatoid arthritis

• Dressler’s syndrome (post-MI)

CHAPTER 19 Data interpretation672

Ascites

Fluid in the peritoneal cavity can result in abdominal distension and short-

ness of breath. As with pleural ﬂ uid, analysis of an aspirated sample can aid

diagnosis. See b p. 569 for ascitic tap guidance.

Box 19.20 Tests for ascites

• MCS (bacterial peritonitis, TB)

• Cytology (malignant cells, macrophages in inﬂ ammatory

diseases)

• Biochemistry (amylase, protein)

2 Spontaneous bacterial peritonitis = neutrophils >250/mm

3

2 Further tests you may consider for a patient with ascites include liver

function tests (LFTs), hepatitis serology, antimitochondrial antibodies (pri-

mary biliary cirrhosis), ultrasound of liver or pelvis, and esophagogastrodu-

odenoscopy (EGD) (varices).

0 It is useful to check platelets and clotting proﬁ

le before inserting drain.

0 Chylous ascites can result from obstruction of lymph drainage.

Causes

• Decompensated liver disease

• Infection (bacterial peritonitis, TB)

• Malignancy (liver, ovary)

• Right-sided heart failure

• Pancreatitis

• Portal vein occlusion

• Nephrotic syndrome

Serum/ascites albumin gradient (SAAG)

• Used to classify ascites as exudate or transudate

• SAAG = serum albumin concentration/ascitic ﬂ uid

albumin

concentration

SAAG >1.1 g/dL (transudate)

• Cirrhosis with portal hypertension

• Cardiac failure

• Nephrotic syndrome

SAAG <1.1 g/dL (exudate)

• Malignancy

• Pancreatitis

• TB

673

Index

A

Abdomen, 203

appetite and weight,

220

applied anatomy,

204–5

auscultation, 231

boundaries, 204

bowel habit, 212–14

contents, 204

dietary history, 222

distension, 229

drug history, 221

in elderly patient, 252

esophageal symptoms,

206–7

and face and chest,

226–7

family history, 222

focal swellings, 229

and gastrointestinal

system, 493

and hand and upper

limb, 224–5

hernial oriﬁ ces, 243–5

inspection of, 229–30

jaundice, 216

nausea, vomiting, and

vomitus, 208

obvious pulsations, 230

outline examination,

223

pain, 210–1

palpating the

abdominal organs,

233–8

palpation, 232

past medical history,

221

percussion, 239–40

peristaltic waves, 230

presenting patterns,

246–51

prominent vasculature,

229–30

pruritus, 216

rectal examination,

241–2

recti, divarication

of, 229

regions, 204–5

scars, 229

skin discoloration, 230

smoking, 221

social history, 222

stomas, 230

striae, 230

swelling in, 217

urinary and prostate

symptoms, 218–19

Abdominal examination

framework for, 223

during pregnancy, 442

Abdominal pain, 210–1

aggravating and

relieving factors,

210

character, 210

ﬁ ndings, 211

in pregnancy, 438

radiation, 210

site, 210

Abdominal reﬂ ex, 305

Abdominal wall, anterior

quadrants of, 205

segments of, 205

Abdominal X-rays,

641–5

bones, 644

calciﬁ cation, 643–4

gas pattern, 641–3

soft tissues, 644–5

technical assessment,

641

Abducens, 280

Abductor pollicis brevis,

64–6

Accessory nerve, 291

applied anatomy, 291

examination, 291

ﬁ ndings, 291

Acid–base disturbances,

664

Acidosis, 664–5

Acoustic neuromas,

142–3

Acromegaly, 99 , 116

Addison’s disease, 83 ,

115–16

Aerochamber, 543

Affect, 458–9

Affective disorders,

473–5

bipolar disorder, 473

depression, 475

hypomania, 475

mania, 473–4

mental state

examination in, 474

Agonal rhythm, 610

Air conduction, testing,

288

Airway management,

547–53

Akathisia, 325–6

Albinism, 83

Alcohol, 37

in common drinks, 37

consumption, 37

Health People

2010, 37

Alcohol and respiratory

system, 189

Alcoholic hepatitis, 247

Alcoholic liver disease,

246–7

extrahepatic

manifestations

of, 247

Alkalosis, 665–6

Allan’s test, 66

Allergic rhinitis, 143

Allergies, 36

Alopecia areata, 80

Alopecia totalis, 80

Alopecia universalis, 80

Alzheimer’s disease

(AD), 472

Amenorrhea, 416 , 417

American Sign Language

(ASL), 12

Amniotic ﬂ uid

volume

estimation,

445

Angina, 148

Angina pectoris. See

Angina

674

INDEX

Angry patients, 15

Angular stomatitis, 226

Ankle, 301

Ankle and foot, 363–4

feel, 363

function, 364

inversion and

eversion, 364

look, 363

measure, 364

move, 363

Thompson or

Simmond test, 364

Ankle clonus, 306

Ankle edema, 151

Ankle examination, 304

Ankylosing spondylitis,

368–9

Anosmia, 128

Antepartum hemorrhage

(APH), 438

Anuria, 219

Anxiety disorders, 470–1

generalized anxiety

disorder (GAD),

470

panic disorder, 470

phobic disorders,

470–1

Aorta, 238

coarctation of, 177

Aortic aneurysm,

dissecting, 149

Aortic regurgitation,

159 , 175

eponymous signs

of, 175

Aortic stenosis, 159 ,

175

Apex beat/PMI, 194

APGAR score, 502

Apley grinding test,

360 , 362

Apocrine sweat glands,

76

Appetite and weight, 220

Apraxic, 321–2

Argyll–Robertson pupil,

274

Arterial blood gas

analysis, 663–6

Arterial blood gas

sampling, 535–6

Arterial ulceration, 91

Arteries

applied anatomy and

physiology of,

146–7

Arthralgia in adults,

causes of, 341

Ascites, 672

examining for, 239–40

Ascitic tap, 569

Asystole, 610

Athetosis, 325–6

Atrial ﬁ brillation

(AF),

603–4

Atrial ﬂ utter, 605

Atrial septal defect

(ASD), 176

Atrioventricular (AV)

conduction

abnormalities,

598–600

Atrophic vaginitis, 448

Attitudes, 4

Auditory hallucinations,

462

Auditory meatus,

external, 285

Augmentation, 304

Auscultation, 198–9 , 231 ,

445 , 486 , 491–2

added sounds, 198–9

bowel sounds, 231

bruits, 231

ﬁ ndings, 198

friction rubs, 231

technique, 198

venous hums, 231

vocal resonance, 199

Autohaler, 539

Automated external

deﬁ brillators

(AED),

584 , 585 , 587

Autonomy, 26

Axillae, 225

Axillary lymph node, 61

B

Background diabetic

retinopathy, 110–1

Bad news, breaking,

17–20

Balanitis, 386

Balanoposthitis, 386

Beau’s lines, 81

Bell’s palsy, 286

Bendroﬂ uazide, 116

Beneﬁ cence, 26

Benign positional

vertigo, 142

Benign prostatic

hyperplasai (BPH),

242

Biceps examination, 302

Bile, 208

Bilevel Positive Airways

Pressure (BiPAP),

559 , 560

Binasal hemianopia, 266

Bioethical principles, 26

Biomedical model, 2

Biopsychosocial model,

2–3

Bipartite patella, 651

Bipolar disorder, 473

Bitemporal hemianopia,

266

Bladder, 237 , 240

Bleeding

abnormal, 415

amenorrhea,

416–17

dysmenorrhea, 415

intermenstrual

bleeding (IMB),

416

menorrhagia, 415

postcoital bleeding,

416

postmenopausal

bleeding, 418

after pregnancy, 438

during pregnancy, 437

in second and third

trimesters, 438

Blepharospasm, 325–6

Blood (hematemesis),

208

Blood pressure (BP), 54

measurement, 531–2

Blue lunulae,

224

Body language, 21–2

emphasis, 22

eye level, 22

open body language,

21–2

touching, 21

watching and

learning, 22

Body mass index (BMI),

56

Body weight and height,

56

Bone conduction,

testing, 288

INDEX

675

Bouchard’s nodes, 63

Boutonniere, 63

Bowel habit, 212–14

constipation, 212

diarrhea, 212

ﬂ atus, 214

mucus, 214

rectal bleeding and

melena, 213–14

Bowel sounds, 231

Brachial artery, 157

Bradycardia, 158–9

Brain, main language

areas of, 261

Brain tumors and

cerebrovascular

events, 476

Branchial cyst, 144

Breast (female), 391

abnormal nipple and

areola, 404

abscesses, 404

anatomy, 392 , 393

cancer,

404

examination, 402 , 403

fat necrosis, 404

ﬁ broadenoma, 404

ﬁ brocystic disease, 404

inspection, 397 , 398

lumps, 396

lymphatic drainage, 392

menstrual history, 394

nipple discharge, 395

normal breast changes

in, 392

pain, 394

palpation, 399–400

symptoms, 394–6

Breast (male), 395

Breast cancer

examination, 404

in females, 396

in males, 395

Breath, 226

Breathlessness and

edema, 150–1

ankle edema, 151

cough, 151

dyspnea, 150–1

Bronchi, anatomy of, 182

Bronchioles, anatomy

of, 182

Brudzinski’s sign, 323

Bruising, 225

Bruits, 231

Bulbourethral glands, 377

C

Cacosmia, 128

CAGE questionnaire, 37

Candidiasis, 227

Capillary reﬁ ll, 54

Cardiac myocytes, 592

Cardiovascular

examination,

framework for, 150 ,

155

Cardiovascular system,

145 , 490–2

abdomen, 173

applied anatomy and

physiology, 146–7

breathlessness and

edema, 150–1

cardiac risk factors,

154

chest pain, 148–9

claudication, 153

congenital heart

disease, 176–7

congestive heart

failure (CHF), 177–8

deep vein thrombosis

(DVT), 178

drug history, 154

in elderly patient,

179

alternative diagnoses,

180

examination, 179–80

history, 179

face and neck, 161–4

fatigue, 153

general inspection,

155–6

hands, 156

hypertrophic

cardiomyopathy,

178

lung bases, 173

palpitations, 152

past medical history,

154

pediatric assessment

of, 490–2

examination, 490–2

murmurs, 492

pericardial effusion, 177

pericarditis, 177

peripheral edema, 173

peripheral pulses,

157–60

peripheral vascular

disease, 178

positioning, 155

precordium,

auscultating,

167–72

precordium,

examining, 165–6

rest pain, 153

social history, 154

syncope, 152

valvular disease,

175–6

varicose veins,

173–4

Carotenemia, 83

Carotid artery, 157

Carotid pulse, 161

Carpopedal spasm, 117

Cartilaginous joints, 338

Cataract treatment,

112–13

Catheters, sizing, 523

Cavernous sinus, 280–1

Celiac disease, 249

Central/branch retinal

artery occlusion, 272

Central/branch retinal

vein occlusion, 272

Central cyanosis, 51

Central scotoma, 266

Central venous

catheterization,

527–30

Central venous pressure

(CVP) kit, 527

Central vestibular

lesions, 126

Cerebellar ataxia, 321–2

Cerebellar lesions, 327

Cerebellum, 295

Cerebrospinal ﬂ uid

(CSF), 667

urinalysis, 669–70

Cervical and

supraclavicular lymph

node, 60

Cervical smears, in

pregnancy, 430

Cervical spine, radiology

of, 654–5

Charles Bonnet

syndrome, 463

Chest, 227

expansion, 194 , 195

inspection of, 193

breathing pattern, 193

INDEX

676

Chest (Cont.)

movement, 193

shape, 193

surface markings, 193

Chest pain, 148–9

angina, 148

aortic aneurysm,

dissecting, 149

esophageal spasm, 149

gastroesophageal

reﬂ ux disease,

149

myocardial infarction

(MI), 149

pericarditis, 149

pleuritic (respiratory)

pain, 149

Chest X-rays, 616–39

clinical interpretation,

620–4

densities on, 618

lungs, 626–39

reporting, framework

for, 616

technical

considerations,

616–18

Childhood coughs,

485

Chin lift, 548 , 549

Cholangitis, 249

Cholesteatoma, 141–2

Chondromalacia

patellae, 340

Chorea, 325–6

Chronic cough, 185

Chronic liver disease,

246

Chvostek’s sign, 103 , 117

Circumoral

pigmentation, 226

Cirrhosis, 247

Clarifying questions, 9

Claudication, 153

Clothing, 4

Clubbing, 63 , 224

causes of, 63

Cluster headache, 329

Cognitive function, 262

Collapse, 200

Color

cyanosis, 51

jaundice, 51

pallor (paleness), 51

Colostomy, 230

Common peroneal

nerve, 319

Communication skills, 1

angry patients, 15

bad news, breaking,

17–20

body language, 21–2

communication

models, 2

conﬁ dentiality, 3

cross-cultural

communication, 13

deaf patients,

communicating

with, 12

essential

considerations, 4–5

essential rules, 6

follow-up

communication, 2

general principles, 9

getting started, 7–8

imparting

information, 15

interpreters, 14

law, ethics, and

communication, 15

patient-centered

communication,

2–3

sex, talking about, 16

silence, importance

of, 15

telephone and e-mail

communication, 16

written

communication, 23

Complete heart block,

600

Conductive dysphasia, 261

Conﬁ dentiality, 3 , 26

breaking, 26

Confusion assessment

method (CAM), 469

Congenital heart disease

(CHF), 176–7 , 177–8

aorta, coarctation

of, 177

atrial septal defect

(ASD), 176

Fallot, tetralogy of,

177

left ventricular failure,

178

patent ductus

arteriosus (PDA),

176–7

right ventricular

failure, 178

ventricular septal

defect (VSD), 176

Congenital heart disease,

176–7

Consent and capacity,

26–7

Consolidation, 200

Constipation, 212

causes of, 213

Continuous murmurs,

170

Continuous Positive

Airways Pressure

(CPAP), 559 , 560

Coordination, 315–16

lower limbs, 316

rebound, 316

upper limbs, 315

Copper, 71

Corneal reﬂ ex, 284

Cortex, 294

Costochondritis, 187

Cough, 151

and abnormal sounds,

190

and expectoration,

185–6

hemoptysis, 186

sputum, 185–6

Courvoisier’s law, 234

Cover–uncover test, 277

Cracking and popping

noises, 124–6

Cranial nerve I. See

Olfactory nerve

Cranial nerve II. See

Ophthalmoscopy;

Optic nerve

Cranial nerves III, IV, and

VI, 276–9

palsies of, 280–2

Cranial nerve V. See

Trigeminal nerve

Cranial nerve VII. See

Facial nerve

Cranial nerve VIII. See

Vestibulocochlear

nerve

Cranial nerves IX and X,

289–90

Cranial nerve XI. See

Accessory nerve

Cranial nerve XII. See

Hypoglossal nerve

Cremasteric reﬂ ex, 305

CREST syndrome, 69

INDEX

677

Creutzfeldt–Jakob

disease (CJD), 473

Crohn’s disease, 250–1

Cross-cultural

communication, 13

Croup (laryngotracheo-

bronchitis), 144

Crystal arthropathies,

367

C-spine ﬁ lms, examining,

654–5

C-spine injuries, 655

C-spine movements, 354

Cullen’s sign, 230

Cultural background and

tradition, 13

Cushing’s syndrome, 115

Cyanosis, 51 , 191

D

Dalrymple’s sign, 106

Data interpretation, 591

abdominal X-rays,

641–5

arterial blood gas

analysis, 663–6

cerebrospinal ﬂ uid

(CSF), 667

cervical spine,

radiology of, 654–5

chest X-rays, 616–39

ECG, 592–615

hips and femurs,

radiology of, 648–9

knees, radiology of,

650–1

lung function tests,

658–61

pelvis, radiology of,

646–7

pleural and ascitic

ﬂ uid, 671

shoulder, radiology of,

652–3

thoracic and lumbar

spine, 656–7

urinalysis, 669–70

Deaf patients,

communicating

with, 12

American Sign

Language (ASL),

12

lip-readers, 12

Deep palpation, 232

Deep vein thrombosis

(DVT), 178

Deﬁ brillation, 584–5

Deformity, in

musculoskeletal

systems, 342–3

Delirium, 467 , 468–70

Delusions, 460–1

Demeanor, 9

Dementia, 471–3

Alzheimer’s disease,

472

Creutzfeldt–Jakob

disease (CJD), 473

frontotemporal, 472

Huntington’s disease,

473

Lewy body, 472

Parkinson’s disease,

473

vascular/multi-infarct,

472

Dentition, 226

Depolarization, 592–3

Depression, 474 , 475

Dermatological history,

78–9

allergies, 78

drug history, 78

FH, 79

PMH, 78

presenting illness,

history of, 78

psychosocial impact,

79

SH, 79

Dermatomes, 308 , 310 ,

311

Dermis, 76

Developmental

assessment, 500

Diabetes, 99

avoiding visual loss

in, 112

examining patient

with, 108–9

diabetic foot, 108–9

ocular manifestations

of, 112

cataract, 112–13

cranial nerve palsy, 112

glaucoma, 112–13

hypertensive retin-

opathy, 112–13

optic neuropathy, 112

Diabetic examination,

108

Diabetic foot

examination,

framework for, 109

Diabetic retinopathy,

110–11

background, 110

classiﬁ cation of, 110

maculopathy, 110

mechanisms of

damage, 110

pre-proliferative

retinopathy,

110

proliferative, 110

Diarrhea, 212

causes of, 213

Diastolic murmurs,

169–70

Dipstick testing, 669

Discussion, setting

during, 4–5

Diskhaler, 540

Diskus, 540

Disaster planning, 509

Disseminated breast

cancer, radiograph

of, 625

Disturbance of higher

functions, 327–8

Dix-Hallpike maneuver,

142

Dizziness, 125–6 , 256

nonotological causes

of, 126

otological causes

of, 125

Dominance, 21

Dorsal interossei, 64–6

Dorsalis pedis, 157

Downbeat nystagmus,

278

Down’s syndrome, 68

Drug history, 36 , 45

Dupuytren’s

contracture, 62 , 224

Dysarthria,

260

Dysfunctional uterine

bleeding (DUB),

415

Dyskinesia, 325–6

Dysmenorrhea, 415

Dyspepsia, 207

Dysphagia, 206 , 260–1

causes of, 207

conductive, 261

expressive, 260–1

INDEX

678

Dysphagia (Cont.)

global, 260

nominal, 261

receptive, 261

Dysphonia, 130 , 260

Dyspnea

(breathlessness),

150–1 , 184

associated symptoms,

184

deﬁ ning, 184

exacerbating and

relieving factors,

184

onset and duration,

184

severity, 184

Dystonia, 325–6

Dysuria, 219

E

Ear

applied anatomy and

physiology of, 120

deformity of, 124–5

examining, 132–4

inspection and

palpation, 132

otoscopy, 132

technique, 132–4

injury to, 124

surface anatomy of,

133

Ear, nose, and throat

(ENT), assessment

of, 488–9

Earache (otalgia), 122

Ear disorders, symptoms

of, 122–3

hearing loss, 122–3

otalgia, 122

otorrhea, 122

Eccrine sweat glands, 76

Edema, 54 , 55

Ejection click, 172

Ejection systolic

murmur, 169

Elbow, 298 , 349–50

examining, 66

feel, 349

function, 350

look, 349

measure, 349

move, 349 , 350

Electrocardiogram

(ECG), 592–615

(AV) conduction

abnormalities,

598–600

axis, calculating, 597–8

axis deviation, 598

cardiac axis, 596–7

heart, electrophysiology

of,

592–3

myocardial infarction,

614–15

paced rhythms, 615

P- and T-wave

abnormalities, 611

sinus rhythms, 602–3

ST segment, 613–14

supraventricular

tachycardias, 603–6

tracing, 596

12 -lead ECG, 593–4

ventricular conduction

abnormalities,

600–2

ventricular rhythms,

607–8 , 610

Wolff–Parkinson–

White syndrome,

607

E-mail

communication, 16

Emergency

preparedness, 509

Emphasis, 22

Endocrine disease,

fundus in, 110–2

diabetes mellitus

(DM), 110

ocular manifestations

of diabetes, 112

Endocrine disorders,

476–7

Endocrine system, 95

abdomen, examination

of, 102

applied anatomy and

physiology, 96–7

axillae, examination

of,

102

chest, examination

of, 102

diabetes, examining

patient with, 108–9

drug history, 100

face and mouth,

examination of, 102

family history, 100

fundus in endocrine

disease, 110–2

general examination,

102–3

hands and arms,

examination of,

102

hypothalamopituitary

axis, 96–7

legs, examination

of, 102

neck, examination

of, 102

past medical history,

100

presenting patterns,

114

symptoms in

endocrinology, 98–9

tetany, signs of, 103

thyroid, 97

examining, 104–5

thyroid disease, eye

signs in, 106

Endocrinology,

presenting symptoms

in, 98–9

appetite and weight

changes, 98

bowel habit, 98

ﬂ ushing, 99

growth, alteration

in, 99

hair distribution, 98–9

headache and visual

disturbance, 99

lethargy/fatigue, 98

pigmentation, 98

sexual function,

changes in, 99

skin and soft tissue

changes, 99

sweating, 98

thirst and

polydipsia, 98

urinary frequency and

polyuria,, 98

Endotracheal (ET)

intubation, 557–8

Enlarged blind spot, 266

Enlarged spleen and

enlarged left kidney,

236

Enteropathic arthritis,

370

Epidermis, 76

INDEX

679

Epididymal cysts, 387

Epididymis, 377

Epiglottis, 120–1

Epiglottitis, 144

Epistaxis, 127

causes of, 127

Epitrochlear lymph

node, 60

Erectile dysfunction,

379–80

Esophageal spasm, 149

Esophageal symptoms,

206–7

dyspepsia, 207

dysphagia, 206

heartburn and acid

reﬂ ux, 206–7

odynophagia, 206

Estimated date of

delivery (EDD), 433

Eversion, 363 , 364

Examination, format of,

48–9

examination

framework, 49

right approach, 48

systems examinations,

48–9

Examination, general, 47

color, 51–2

edema, 55

in elderly patient, 72

ﬁ rst

impressions,

50

hands, 62–6

hydration, 54

lymph nodes, 58–9

nutritional status, 56–7

physical examination,

approaching, 48–9

preparing for, 50

recognizable

syndromes, 68–9

temperature, 53

vitamin and trace

element

deﬁ ciencies, 70–1

Examination drawings,

standard, 24–5

Examination under

special

circumstances, 507

disasters, terrorism,

and public health

emergencies, 509

overview, 508

sexual assault, 510

Expressive dysphasia,

260–1

External ear, 120

External genitalia, 238

examination of, 424

External jugular vein

(EJV), 161–2

External jugular vein

catheterization, 526

Extraluminal gas, 643

Extrapyramidal (indirect)

pathways, 295

Exudates, 671

Eye contact, 10

Eye level, 22

Eyes, 226

F

Face

and chest, 226–7

inspecting, 138

and neck, 161–4

Face masks, 549–50

Facial expression,

muscles of, 285

Facial nerve, 285–6

applied anatomy, 285

examination, 285

ﬁ ndings, 286

Facial sinuses, surface

anatomy of, 121

Fallopian tubes, anatomy

of, 409

Fallot, tetralogy of, 177

Falls and loss of

consciousness

(LOC), 257

Family history (FH), 39

Family tree (genogram),

39–40

Fatigue, 153

Fat malabsorption, 214

Fat necrosis, 404

Fat soluble vitamins,

70

vitamin A (retinol), 70

vitamin D

(cholecalciferol),

70

vitamin E

(alpha-tocopherol),

70

vitamin K, 70

Fatty liver, 247

Fear words, 20

Female breast. See

Breast (female)

Female reproductive

system, 407

abdominal

examination, 442

abnormal bleeding, in

gynecology, 415

cervical (pap) smear,

taking, 430

in elderly patient, 447

external genital

organs, 409

gynecological

examination,

outline of, 423

history-taking, in

gynecology, 413

history-taking, in

obstetrics, 433

internal genital organs,

408

menstrual cycle, 411

obstetric examination,

outline of, 441

obstetrics, presenting

symptoms in, 437

pelvic examination,

424

pelvis, anatomy of, 408

perineum, 409

symptoms, in

gynecology, 419

Female urethral

catheterization,

575–6

Femoral artery, 157

Femoral hernia, 244–5

differential diagnosis

of, 245

Femoral nerve, 319

Femoral nerve stretch

test, 354

Femoral vein, 529

Fetal lie, 442 , 444

Fibroadenoma, 404

Fibrocystic disease, 404

Fibrous joints, 338

Finger, stain in, 191

Finger clubbing, 191 , 192

Finger extension, 64–6

Finger ﬂ exion, 64–6

Finger joint

deformities, 63

Finger–nose test, 315

Fingers, 298

Fingers examination, 302

INDEX

680

Finkelstein’s test, 67

First impressions, 50

bedside clues, 50

consciousness level, 50

ﬁ rst sight, diagnosis

at, 50

vital signs, 50

Flatus, 214

Fluid thrill, testing for,

239

Follicle-stimulating

hormone (FSH), 411

Follow-up

communication, 16

Foot and ankle. See

Ankle and foot

Foot drop, 321–2

Foot tapping, 316

Fornix, anatomy of, 408

Foster–Kennedy

syndrome, 272

Friction rubs, 231

Froment’s sign, 67 , 318

Frontotemporal

dementia, 472

Fundoscopy, abnormal

ﬁ ndings

on,

270–2

central/branch retinal

artery occlusion,

272

central/branch retinal

vein occlusion, 272

Foster–Kennedy

syndrome, 272

optic atrophy, 270 ,

271

optic disc cupping,

270–1

optic disc swelling,

270

retinal hemorrhages,

270–2

Fundus, 269

Furunculosis, 141

G

Gait, 321–2

examination, 321

ﬁ ndings, 321–2

Gallbladder, 234

palpation of, 235

Gallbladder signs, 234

GALS screen, 347

modiﬁ ed, 347–8

Gastroesophageal reﬂ ux

disease (GERD), 149 ,

206–7

Gaze-evoked nystagmus,

279

Generalized anxiety

disorder (GAD), 470

Genital prolapse, 421

Geriatric giants, 73

GI bleeding, lower

causes of, 215

GI bleeding, upper

causes of, 209

Glabellar tap, 307

Glands, applied anatomy

and physiology of, 76

Glasgow Coma Scale

(GCS), 332

Glaucoma, 112–13

Global dysphasia, 260

Globus hystericus

(globus pharyngeus),

130

Glomus jugulare tumor,

143

Glucocorticoid excess

(Cushing’s

syndrome), 115

Glue ear, 141

Gluten, 249

Gonadotrophin-releasing

hormone (GnRH),

411

Gout, 367 , 368

Grasp reﬂ ex, 307

Graves disease, eye signs

of, 107

Gravidity, 434

Greeting, 7 , 21

Grey-Turner’s sign, 230

Growth hormone excess

(acromegaly), 116

Gums, 226

inspecting, 138

Gustatory hallucinations,

462

Gynecological vs.

gastrointestinal pain,

419

Gynecomastia, 227 , 395

H

Haggling and the art of

quantiﬁ cation, 38

Hair

applied anatomy and

physiology of, 77

in elderly patient, 92

Hair disorders and

signs, 80

Hair growth, abnormal,

80

Hair loss, 80

Hair style, 4

Halitosis, 131

Hallpike’s maneuver, 288

Hallucinations, 462

Hand and upper limb,

224–5

axillae, 225

hepatic ﬂ ap (asterixis),

224

nails, 224

palms, 224

upper limb, 225

Handihaler, 541–2

Hands, 62–6

Allan’s test, 66

bedside clues, 62

Dupuytren’s

contracture, 62

elbows, 66

function, 66

inspection, 62

movement, 64–6

palpation, 63–4

preparation, 62

pulses, 66

sensation, 66

shaking, 7

Hand-washing

procedures, 514 , 515

Headaches, 256 , 329–30

cluster headache, 329

meningitis, 329

migraine, 330

raised intracranial

pressure, 329–30

sinusitis, 329

subarachnoid

hemorrhage, 329

temporal (giant cell)

arteritis, 329

tension headache, 329

Head tilt, 548

Health Insurance

Portability and

Accountability Act

(HIPAA), 27

Hearing, simple test

of, 287

Hearing loss, 122–3

INDEX

681

causes of, 123

nonorganic, 123

Heart

applied anatomy and

physiology, 146

electrophysiology of,

592–3

Heart block

ﬁ rst-degree heart

block, 599

second-degree heart

block, 599–600

third-degree heart

block, 600

Heartburn and acid

reﬂ ux, 206–7

Heart sounds, 168

applied anatomy and

physiology, 146

Heberden’s nodes, 63

Heel–shin test, 316

Hematemesis, nature

of, 209

Hematuria, 219

Hemiballismus, 325–6

Hemiplegia, 321–2

Hemochromatosis, 83

Hemoptysis, 186

Hepatic encephalopathy,

248

Hepatic ﬂ ap

(asterixis),

224

testing for, 225

Hepatojugular reﬂ ux,

163

Hepatomegaly,

assessment of,

495–6

Hernial oriﬁ ces, 243–5

femoral hernias, 244–5

hernias, 243

inguinal hernias, 243–4

strangulation, 243

Hernias, 243

Hertel’s

exophthalmometer,

106

High temperature, 53

Hila, radiograph of,

622–4

Hip, 356–7 , 301

examination, 505

feel,

356

function, 357

look, 356

measure, 357

move, 356

Thomas test, 357

Trendelenberg test,

357

Hips and femurs,

radiology of, 648–9

Hirsutism, 98–9

History, 29

alcohol, 37

allergies, 36

chief complaint (CC),

32

drug history, 36

elderly patient, 43–4

family history (FH), 39

history of present

illness (HPI), 33–4

history-taking, 30

past medical history

(PMH), 35

patient proﬁ le

(PP),

31

pediatric patient, 45

review of systems

(ROS), 42

smoking, 38

social history (SH), 41

History-taking, 30 , 480–1

standard history

framework, 30

Hitchhiker’s Thumb, 63

Holmes–Adie pupil, 274

Homonymous

hemianopia, 266

Homonymous

quadrantanopia, 266

Horner’s syndrome, 274

Human chorionic

gonadotrophin

(hCG) hormone, 411

Human papillomavirus

(HPV), 430

Huntington’s disease,

473

Hydration, 54

Hydrocele, 386

Hypercalcemia, 116–17

Hypertension, in

pregnancy,

440

Hypertensive

retinopathy, 112–3

Hyperthyroidism,

114–15 , 99

Hypertrophic

cardiomyopathy,

159 , 178

Hyperuricemia, causes

of, 368

Hypoadrenalism

(Addison’s disease),

115–16

Hypocalcemia, 117

Hypodermis, 76

Hypoglossal nerve, 293

Hypogonadism, 98–9

Hypomania, 475

Hypoparathyroidism, 99

Hypopharynx, 120–1

Hypospadias, 381 , 386

Hypothalamopituitary

axis, of endocrine

system, 96–7

anterior pituitary

hormones, 96

posterior pituitary

gland, 97

Hypothermia,

53

Hypothyroidism, 99 , 114

I

Ileostomy, 230

Illusions, 462

Imparting

information, 15

Infectious diseases, 476

Infertility, 380

Inﬂ ammatory bowel

disease, 250–1

extraintestinal features

of, 251

Information,

imparting, 15

Inguinal hernias, 243–4

differentiation of, 245

Inguinal lymph nodes, 61 ,

238 , 385

Inguinal rings, 244

Inhaler technique,

538–43

autohaler, 539

Diskus, 540

Handihaler, 541–2

metered-dose inhaler

(MDI), 538–9

spacer devices, 542–3

turbohaler, 540–1

Injection techniques,

516–17

Inner ear, 120

Intermenstrual bleeding

(IMB), 416

Intermittent pyrexia, 53

INDEX

682

Internal jugular vein

(IJV), 161–2 , 527–8

Internuclear

ophthalmoplegia, 281

Interpreters, 14

ofﬁ cial interpreter,

using, 14

Interruptions, 11

Interstitial ﬁ brosis, 200

Interview, in psychiatric

assessment, 450

Intradermal (ID)

injections,

procedures for, 517

Intramuscular (IM)

injections,

procedures for,

516–17

Introduction, 7–8

of doctor, 7–8

of patient, 7

Inversion, 363 , 364

Iodine, 71

Irritable bowel

syndrome (IBS), 251

J

Jaundice, 51 , 83 , 216

causes of, 216

Jaw jerk, 284

Jaw thrust, 548 , 549

Joint, 338

Joint deformity, 343

Joint swelling, 342

Jugular venous pressure

(JVP), 54 , 161–4

applied anatomy and

physiology, 146

character of jugular

venous pulsation, 163

differentiating jugular

and carotid

pulsations, 163

examination, 161–2

ﬁ ndings, 164

hepatojugular reﬂ ux, 163

Kussmaul’s sign, 164

theory, 161

Justice, 26

JVP, 191

K

Kernig’s sign, 323

testing for, 324

Kidneys, 236 , 240

Knee, 301 , 358–60

anterior and posterior

drawer tests, 360 ,

361

Apley grinding test,

360 , 362

feel, 358

look, 358

McMurray test, 360 ,

362

measure, 359

medial and lateral

collateral ligament

instability, testing

for, 360 , 361

move, 359

Knee arthralgia, causes

of, 340

Knee clonus, 302

Knee examination, 302

Knees, radiology of,

650–1

abnormal, 650

normal, 650

pediatrics, 651

Koebner’s

phenomenon, 83

Koilonychia, 81 , 224

Kussmaul’s sign, 164

L

Labor pain, 438

Labyrinthitis, 142

Laryngeal mask airway

(LMA), 553

Laryngitis, 144

Late systolic murmur, 169

Law, ethics, and

communication, 26

Learning, 5

Left bundle branch block

(LBBB), 601–2

Left kidney, palpation

of, 237

Legg-Calve-Perthes

disease, 649

Leg swelling, causes

of, 55

Leg ulcers, 91

Lesion, 84–7

conﬂ uence of grouped

lesions, 85

malignant melanoma,

87

primary lesions, 85

secondary lesions, 85

shapes and patterns of

grouped lesions, 86

vascular lesions, 85

Leukonychia, 81 , 224

Lewy body dementia,

472

Lhermitte’s

phenomenon, 323

Libido, 380

Lid lag (von Graefe’s

sign), 106

Light palpation, 232

Limited English

Proﬁ ciency

(LEP)

regulations,

14

Lip-readers, communi-

cating with, 12

Lips, inspecting, 138

Liver, 233–4 , 240

palpation of, 233

Locomotor

musculoskeletal

symptoms, 340–3

deformity, 342–3

extra-articular

features, 343

locking, 342

loss of function, 343

pain,

340

sensory disturbance,

343

stiffness, 342

swelling, 342

weakness, 343

Long-standing problems,

34

Loss of consciousness

(LOC), 257

Loss of function, 343

Lower limb, 319

common peroneal

nerve, 319

femoral nerve, 319

lateral cutaneous

nerve of thigh, 319

sciatic nerve, 319

testing power in, 300

Lower motor neuron

(LMN) lesions, 286 ,

294–5 , 325

Low temperature, 53

Lumbar puncture (LP),

581–2

Lump

INDEX

683

examining, 88–9

auscultation, 88

compressibility, 88

consistency, 88

ﬂ uctuation, 88

ﬂ uid thrill, 88

pulsatility, 88

reducibility, 88

resonance, 88

translucency, 88

in mouth, 129–30

in neck, 130

Lung function tests,

658–61

Lungs

anatomy of, 182

physiology, 182

radiographic examina-

tion of, 626–39

cavitating lesions, 633

coin lesions, 633

collapse, 626–7

consolidation, 629–30

COPD, 636 , 638

ﬁ brosis, 629–30

iatrogenic features

and foreign

bodies, 638

NG tubes, 639–40

normal, 626

pleural effusion,

634–6

pleural lesions, 634

pneumonectomy,

633–4

pulmonary edema,

630–1

tension

pneumothorax,

636–7

ﬁ lm,

examining,

626

surface anatomy of,

183

Luteinizing hormone

(LH), 411–12

Lymphadenopathy,

causes of, 59

Lymph nodes, 58–9

axillary, 61

cervical and

supraclavicular, 60

epitrochlear, 60

ﬁ ndings, 59

inguinal, 61

inspection, 58

palpation, 58–9

M

Macular region, 269

Maculopathy diabetic

retinopathy,

110–11

Magnesium, 71

Malabsorption, 248

Male breast, 395

Male genitalia, pediatric

assessment of, 496

Male-pattern baldness,

80

Male reproductive

system, 375

applied anatomy and

physiology, 376–7

balanitis and

balanoposthitis,

386

in elderly patient, 388

epididymal cysts, 387

examination, 381–4

hydrocele, 386

hypospadias, 386

orchitis, 387

paraphimosis, 386

penile ulcers, 386

phimosis,

386

priapism, 386

sexual history, 378

symptoms, 379–80

testicular carcinoma,

387

testicular torsion, 387

varicocele, 387

Male urethral

catheterization, 573–4

Malignant melanoma, 87

Malignant otitis externa,

141

Malnutrition, conditions

associated with, 57

Mania, 473–4

Manner, adjusting, 10–1

Manual deﬁ brillation,

procedure for, 584

Marche àetits pas, 321–2

Marcus–Gunn swinging

light test, 273

Marfan’s syndrome, 68

Mastalgia, 394

McMurray test, for

meniscal tears

detection, 360 , 362

Median nerve, 317

Mediastinal position, 194

Medical jargon,

avoiding, 6

Medical notes, 23

Melanocytes, 76

Melena, 214

Meni

’s disease,

142

Meningitis, 329

Meniscal tears, testing

for,, 362

Menopause, 392

Menorrhagia, 415

Menstrual cycle, 411–12

luteal/secretory phase,

411–12

menstrual phase, 412

proliferative/follicular

phase, 411

Mental status examina-

tion, 458–65 , 474

appearance and

behavior, 458

cognitive function,

463–5

insight, 465

mood and affect,

458–9

perception, 461–2

speech, 458

thought content,

459–61

Metabolic acidosis, 665

Metabolic alkalosis,

666

Metallic valves, 172

Metered-dose inhaler

(MDI), 538–9

Microscopy, culture, and

sensitivity (M,C&S),

669

Mid-arm circumference,

56–7

Middle ear, 120

Mid-systolic click, 172

Migraine, 330

Mini-Mental State

Examination (MMSE),

463 , 464

Mitral regurgitation,

175

Mitral stenosis, 175

Mixed metabolic and

respiratory

disturbance,

666

Mood, 458–9

Motor neuron disease

(MND), 325

INDEX

684

Motor system, 294–5

cerebellum, 295

cortex, 294

extrapyramidal

(indirect)

pathways, 295

inspection, 296

lower limb power,

300–1

pyramidal (direct)

pathways, 294–5

tone, 296 , 297

upper limb power, 298

Mouth, 226–7

ﬂ oor of

inspecting, 138

lumps in, 129–30

Mouth and throat

applied anatomy and

physiology of,

120–1

examining, 138–40

ﬁ ndings, 139–40

inspection, 138–9

palpation, 139

Movements, abnormal,

325–6

Mucous membranes, 54

Mucus, 214

Muehrcke’s lines, 224

Multiple-choice

questions, 9

Multiple endocrine

neoplasias (MEN)

syndrome, 101

Multiple sclerosis (MS),

476

Murmurs, 492

Murphy’s sign, 234

Muscle wasting, 225

Musculoskeletal system,

337

ankle and foot, 363–4

applied anatomy and

physiology, 338–9

crystal arthropathies,

367

elbow, 349–50

in elderly patient, 334

examination

framework, 346

GALS screen, 347

hip, 356–7

knee, 358–60

locomotor

musculoskeletal

symptoms, 340–3

osteoarthritis, 367

osteoporosis, 370 , 371

Paget’s disease, 370–1

rest of the history,

344–5

rheumatoid arthritis

(RA), 365–6

shoulder, 351–2

spine, 354–5

spondyloarthropathies,

368–70

swollen knee, causes

of, 372

Myaesthenia gravis,

328–9

headaches, 329–30

Myocardial infarction

(MI), 149

Myoclonus, 325–6

Myokymia, 325–6

Myopathies, 328

Myotonias, 328

Myotonic dystrophy,

69 , 328

N

Nail disorders and

signs, 81

Nail/ﬁ nger-tip signs, 63

Nails, 224

applied anatomy and

physiology of, 77

in elderly patient, 92

Nail symptoms, 81

Name badge, 4

Names, remembering, 6

Nasal discharge, 127

causes of, 127

symptoms of, 127–8

epistaxis, 127

nasal and facial pain,

128

nasal deformity, 128

nasal discharge, 127

nasal obstruction, 127

smell, disorders of,

128

sneezing, 128

Nasal polyps, 143–4

Nasal sinuses, examining,

137

Nasopharyngeal airway,

552

Nasopharynx, 120–1

Nausea and vomiting,

208

Neck, 227

lumps in, 130

Neck masses, causes

of, 140

Neck stiffness, 323

Nephrostomy, 230

Nerve palsies, combined,

280–1

Nervous system, 497–9

abdominal reﬂ ex, 305

abnormal movements,

325–6

accessory nerve, 291

ankle clonus, 306

cerebellar lesions, 327

cognitive function, 262

coordination, 315–16

cranial nerves III, IV,

and VI, 276–9

palsies of, 280–2

cranial nerves IX and

X, 289–90

cremasteric reﬂ ex,

305

direct questioning, 258

disturbance of higher

functions, 327–8

drug history, 258

in elderly patient, 334

facial nerve, 285–6

family history, 258

gait, 321–2

general inspection and

mental state, 259

headaches, 329–30

hypoglossal nerve, 293

motor

applied anatomy,

294–5

inspection and tone,

296–7

lower limb power,

300–1

upper limb power,

298

myaesthenia gravis,

328–9

myopathies, 328

neck stiffness, 323

olfactory nerve, 263

ophthalmoscopy,

268–72

optic nerve, 264–6

outline examination, 259

INDEX

685

parkinsonism, 325

past medical history,

258

peripheral nerves,

317–19

plantar response,

305 , 306

primitive reﬂ exes, 307

pupils, 273–4

sensory: applied

anatomy, 308

sensory examination,

312–14

social history, 258

speech and language,

260–1

spinal cord lesions,

326–7

symptoms in

neurology, 256–7

tendon reﬂ exes,

302–4

tobacco and alcohol,

258

trigeminal nerve,

283–4

unconscious patient,

331–3

upper motor and

lower motor nerve

lesions,

323–5

vestibulocochlear

nerve, 287–8

Nervous system,

pediatric assessment

of, 497–9

Neuroﬁ bromatosis, 69

Neurological disorders,

476

brain tumors and

cerebrovascular

events, 476

multiple sclerosis

(MS), 476

Parkinson’s disease,

476

seizure disorder, 476

Newborn, 502

examination of, 502

Nocturia, 218

Nominal dysphasia, 261

Nonallergic (vasomotor)

rhinitis, 143

Noninvasive ventilation

(NIV), 559 , 560

Nonmaliﬁ cence, 26

Nose, examining, 135–6

external inspection,

135

internal examination,

135

olfaction, testing, 135

palpation, 135

Nose and paranasal

sinuses, applied

anatomy and

physiology of, 120

Nostril patency, 135

Numbness and

weakness, 256

Nutritional status, 56–7

body weight and

height, 56

general physical

appearance, 56

mid-arm circumference,

56–7

skin-fold thickness, 56

Nystagmus, 278–9

downbeat, 278

gaze-evoked, 279

optokinetic, 278

pendular, 278

upbeat, 278

vestibular, 278

O

O3PQRST, 33–4

Obesity, conditions

associated with, 57

Obsessive-compulsive

disorder (OCD), 471

Occupational Safety and

Health Administration

(OSHA), 122–3

Oculocutaneous

albinism, 69

Oculomotor nerve, 280

Odynophagia, 206

Ofﬁ cial interpreter,

using, 14

Olfactory hallucinations,

462

Olfactory nerve, 263

applied anatomy, 263

examination, 263

ﬁ ndings, 263

Oliguria and anuria,

219

Onycholysis, 81

Onychomycosis, 81

Open body language,

21–2

Opening snap, 172

Open questions vs.

closed questions, 9

Ophthalmoscopy,

268–72

examination, 268

fundoscopy, abnormal

ﬁ ndings

on,

270–2

normal fundus, 269

Opponens pollicis,

64–6

Optic atrophy, 270 ,

271

Optic disc, 269

Optic disc cupping,

270–1

Optic disc swelling, 270

Optic nerve, 264–6

applied anatomy, 264

color vision, 264

visual acuity, 264

visual ﬁ eld defects,

266 , 267

visual ﬁ elds, 264–5

Optic neuropathy, 112

Optokinetic nystagmus,

278

Oral cavity, 120–1

normal appearance

of, 138

Oral pain, 129

Orbit, 281

Orbital ﬁ ssure,

superior,

281

Orchitis, 387

Oropharyngeal airway,

550–2

Oropharynx, 120–1

inspecting, 138–9

Osgood–Schlatter

disease, 340 , 651

Osler–Weber–Rendu

syndrome, 69

Osteoarthritis, 367

Osteochondritis

dissecans, 340 , 651

Osteoporosis, 370 , 371

Otalgia, 122

causes of, 122

Otitis externa,

141

Otitis media and glue

ear, 141

Otorrhea, 122

Otosclerosis, 142

INDEX

686

Otoscope, 132–3

normal eardrum on,

133

Otoscopy, 132

Ovaries, anatomy of, 409

Ovaries and fallopian

tubes, bimanual

examination of, 428

Oxygen administration,

544–5

P

PaCO2, analysis of, 663

Paget’s disease, 370–1

Painful gait, 321–2

Pallor (paleness), 51

Palmar erythema, 224

Palmar interossei, 64–6

Palmomental reﬂ ex, 307

Palms, 224

Palpating abdominal

organs, 233–8

aorta, 238

bladder, 237

deep palpation, 232

external genitalia, 238

gallbladder, 234

general approach, 232

inguinal lymph nodes,

238

kidneys,, 236

light palpation, 232

liver, 233–4

spleen, 234–5

Palpation of breast,

399–400

Palpation of lymph

nodes, 58–9

axillae, 58

epitrochlear nodes,

59

head and neck, 58

inguinal, 58

popliteal, 59

Palpation of pediatric

assessment, 194 ,

495–6

auscultation, 496

female genitalia, 496

male genitalia, 496

percussion, 496

rectal examination,

496

Palpation of respiratory

system, 194

chest expansion, 194 ,

195

mediastinal position,

194

tactile vocal fremitus,

194

Palpitations, 152

Pancreatitis, acute, 248

Pancreatitis, chronic, 248

Panic disorder, 470

Pansystolic murmur, 169

PaO2, analysis of, 663

Papilledema, 270 , 271

Paraphimosis, 386

Parapontine reticular

formation (PPRF),

lesions of, 281–2

Parinaud’s syndrome,

282

Parity, 434

Parkinsonism, 325

Parkinson’s disease, 69 ,

473 , 476

Paronychia, 81

Past medical history

(PMH), 35

Patent ductus arteriosus

(PDA), 176–7

Patient-centered

communication, 2–3

Patient-centered model,

2–3

key points in, 3

Peak expiratory ﬂ ow

rate (PEFR), 537 ,

658–9

Peak ﬂ ow

measurement,

537

Pediatric assessment,

479

Pediatric history, 481

Pediatric patient, 45

drug history, 45

learning to listen, 45

social history, 45

Pelvis

anatomy, 408

dyspareunia, 419–20

examination, 424–9

pain, 419–20

radiology of, 646–7

Pemberton’s sign, 105

Pendular nystagmus, 278

Penis

anatomy and

physiology,

376

examination, 381–2

ulcers, 386

Percussion, in abdominal

examination, 239–40

ascites, examining for,

239–40

bladder, 240

kidneys, 240

liver, 240

spleen, 240

Percussion, in respiratory

system, 196

ﬁ ndings, 196

technique, 196 , 197

Percussion myotonia,

328

Pericardial effusion, 177

Pericardial rub, 172

Pericarditis, 177 , 149

Perineum, 409

Peripheral cyanosis, 51

Peripheral IV

catheterization,

522–3

Peripheral nerves,

317–19

lower limb, 319

upper limb, 317

Peripheral pulses,

157–60

character/waveform

and volume, 159

irregularly irregular,

159

palpation of, 158

pulse rate, 158–9

radiofemoral delay,

160

radioradial delay, 160

regular, 159

regularly irregular, 159

regular with ectopics,

159

rhythm, 159

technique, 157

Peripheral vascular

disease, 178

Peripheral vestibular

lesions, 125

Peritonitis, signs of, 232

Persistent pyrexia, 53

Personal appearance, 4

Petechiae, 225

Peutz–Jegher’s

syndrome, 69

Pharyngitis, chronic, 129

INDEX

687

Phimosis, 386

Phobic disorders, 470–1

Physical appearance,

general, 56

Physical examination,

approaching

format of examination,

48–9

general conduct, 48

Pinard’s fetal

stethoscope, 445–6

Pitting, 81

Pituitary gland,

posterior, 97

Pituitary hormones,

anterior, 96

Plantar response, 305 ,

306

Pleural effusion, 200 , 671

Pleural ﬂ uids, tests

for, 671

Pleural ﬂ uid sampling,

561–2

Pleuritic (respiratory)

pain, 149

Pleuritic chest pain, 184

Pneumoperitoneum, 643

AXR of,

643

Pneumothorax, 200

Polycystic ovarian

syndrome (PCOS),

115

Polyuria, 219

Popliteal artery, 157

Portal hypertension, 246

Postcoital bleeding, 416

Posterior tibial artery,

157

Postmenopausal

bleeding, 418

Postpartum hemorrhage,

439 , 440

Practical procedures,

511

abdominal

paracentesis, 571–2

anesthetic agents,

inﬁ ltration

of,

512

arterial blood gas

sampling, 535–6

ascitic tap, 569

basic airway

management,

547–53

basic suturing, 579–80

blood pressure

measurement,

531–2

central venous

catheterization,

527–30

chest tube insertion,

563–4

deﬁ brillation, 584–5

endotracheal (ET)

intubation, 557–8

external jugular vein

catheterization,

526

female urethral

catheterization,

575–6

hand-washing, 514

infusion, setting up,

524

inhaler technique,

538–43

injections, 516–17

knee joint aspiration,

588

lumbar puncture (LP),

581–2

male urethral

catheterization,

573–4

nasogastric (NG) tube

insertion, 567–8

noninvasive ventilation

(NIV), 559

oxygen administration,

544–5

peak ﬂ ow

measurement, 537

pericardial aspiration,

583

peripheral IV

catheterization,

522–3

pleural ﬂ uid

sampling,

561–2

rules, 512

sterility and

preparation, 513

suprapubic

catheterization,

577–8

tracheostomy

management,

555–6

12 -lead ECG,

recording, 533–4

venipuncture, 518–20

Prayer position, 65

Precordium, auscultating,

167–72

continuous murmurs,

170

diastolic murmurs,

169–70

dynamic maneuvers,

170

ﬁ ndings extra sounds,

170–2

heart sounds, 168

murmurs, 169

position, 170

radiation, 170

systolic murmurs, 169

technique, 167–8

Precordium, examining,

165–6

inspection, 165–6

percussion, 166

Pregnancy, minor

symptoms of, 440

Pre-proliferative

retinopathy, 110

Presbycusis (senile

deafness), 143

Priapism, 386

Primitive reﬂ exes, 307 ,

499 , 506

Prolactinoma, 116

Proliferative diabetic

retinopathy, 110–11

Pronator drift, 298

Prostate cancer, 242

Prostate gland, 377

Prostatitis, 242

Pruritus, 216

Pseudoathetosis, 325–6

Pseudogout, 367

Pseudohallucinations,

462

Psoriatic arthritis, 369

Psychiatric assessment,

449

affective disorders,

473–5

anxiety disorders,

470–1

confusion assessment

method (CAM),

469

delirium, 468–70

dementia, 471–3

examination, 451

framework for, 451

INDEX

688

Psychiatric assessment

(Cont.)

history, 452–7

medical conditions

with psychiatric

symptoms and

signs, 476

mental status

examination,

458–65

obsessive-compulsive

disorder (OCD),

471

physical examination,

466

preparation and

preliminary

considerations, 450

schizophrenia, 467–8

Ptosis, 277

Public health

emergencies, 509

Pulmonary hypertension,

radiograph of, 623

Pulmonary

regurgitation, 176

Pulmonary stenosis, 176

Pulsatile tinnitus,

124–6

Pulse rate, 54 , 158–9

Pulsus alternans, 159

Pulsus bisferiens, 159

Pulsus paradoxus,

159 ,

191

Pupillary light response,

273

Pupils, 273–4

applied anatomy, 273

Argyll–Robertson

pupil, 274

examination, 273

Holmes–Adie pupil, 274

Horner’s syndrome,

274

Pyramidal (direct)

pathways, 294–5

Q

Questioning, style of, 9

clarifying questions, 9

multiple-choice

questions, 9

open questions vs.

closed questions, 9

Questions, difﬁ cult, 10

R

Radial artery, 157

Radial nerve, 317

Radiofemoral delay, 160

Radioradial delay, 160

Raised intracranial

pressure, 329–30

Ramsay–Hunt syndrome,

286

Rapid alternating

movements, 315 , 316

Reactive arthritis,

369–70

Receptive dysphasia, 261

Recognizable syndromes,

68–9

Down’s syndrome, 68

Marfan’s syndrome, 68

myotonic dystrophy,

69

neuroﬁ bromatosis, 69

oculocutaneous

albinism, 69

Osler–Weber–Rendu

syndrome, 69

Parkinson’s disease, 69

Peutz–Jegher’s

syndrome, 69

systemic sclerosis/

CREST syndrome,

69

tuberous sclerosis,

68–9

Turner’s syndrome, 68

Rectal bleeding and

melena, 213–14

Rectal examination,

241–2

Re-entry tachycardia,

606

Reﬂ ective

comments,

10

Reﬂ exes, 499

Reiter’s syndrome, 370

Relative afferent pupil

defect (RAPD), 273 ,

275

Reproductive system.

See Female

reproductive system;

Male reproductive

system

Respiratory acidosis, 664

Respiratory

alkalosis, 665–6 ,

665 ,Respiratory

system, 181 , 484–6

and alcohol, 189

anatomy, 182

auscultation, 198–9

bedside clues, 190

chest, inspection

of, 193

collapse, 200

common

respiratory condi-

tions and signs, 487

consolidation, 200

cough and abnormal

sounds, 190

cough and

expectoration,

185–6

drug history, 188

dyspnea, 184

ear, nose, and throat

(ENT), 488–9

in elderly patient, 201

family history, 188

hands, face, and neck,

191–2

interstitial ﬁ brosis, 200

pain, 187

palpation, 194

past medical history,

188

pediatric assessment

of,

484–6

percussion, 196

physiology, 182–3

pleural effusion, 200

pneumothorax, 200

respiration, 190

and smoking, 189

social history, 189

speech, 190

stridor, 187

symptoms, 188

wheeze, 187

Rest pain, 153

Retinal hemorrhages,

270–2

Retinal vessels, 269

Reverse prayer

position, 65

Review of systems

(ROS), 42

Rheumatoid arthritis

(RA), 365–6

Right bundle branch

block (RBBB), 600–1

Rinne’s test,

287

Role, deﬁ ning, 9

INDEX

689

Romberg’s sign, 313

Rome III diagnostic

criteria, 251

S

Salivary glands, applied

anatomy and

physiology of, 121

Scarring alopecia, 80

Scenic/panoramic

hallucinations, 462

Schizophrenia, 467–8

Schober’s test, 354–5

Sciatic nerve, 319

Sciatic nerve stretch

test, 354–5

Scissoring, 321–2

Scratch marks, 225

Scrotum

anatomy and

physiology of, 376

examination, 382–3

Seizure disorder, 476

Seizures, 257

Seldinger technique, 563

Self-awareness,

disorders of, 461

Sensory ataxia, 321–2

Sensory examination,

312–14

light touch, 312

pin-prick,

314

proprioception, 313

sensory inattention,

312–13

temperature, 314

vibration sense, 313

Sensory system, 308

sensory cortex, 308 ,

309

somatic sensory

pathways, 308

spinal roots and

dermatomes, 308

Septal perforation, 144

Serum/ascites albumin

gradient (SAAG), 672

Sex hormones, 377

Sexual assault, 510

Sexual assault nurse

examiners (SANE),

510

Sexually transmitted

infection (STI), 378

Sexual questions,

asking, 16

Shaking hands, 21 , 7

Shortness of breath

(SOB). See Dyspnea

Shoulder, 298 , 351–2

feel, 351

function, 352

look, 351

move, 351–2

radiology of, 652–3

special tests, 352

winging of scapula, 353

Silence, importance

of, 15

Sinuses, examining, 137

Sinusitis, 329

Sinus rhythms, 602–3

Skin, applied anatomy

and physiology of, 76

color, 82

dermis, 76

in elderly patient, 92

epidermis, 76

hypodermis, 76

Skin, examining, 82–3

beyond the lesion,

83

general inspection, 82

inspecting a lesion,

82–3

palpation, 83

Skin color

abnormalities, 83

Skin-fold thickness, 56

Skin malignancies, in

elderly patient, 93

Skin turgor, 54

Slipped femoral

epiphysis, 649

Smell, disorders of, 128

Smoking, 38

Smoking and respiratory

system, 189

Sneezing, 128

Snout (or pout) reﬂ ex,

307

Social history (SH), 41

Soft palate, 139

Somatic hallucination,

462

Somatic sensory

pathways, 308

Sore throat, 129

Spacer devices, 542–3

Speech and language,

260–1

dysarthria, 260

dysphasia, 260–1

dysphonia, 260

examination, 260

Speech/thought form,

abnormal, 459

Spermatic cord, 376–7

Spider nevi, 227

Spinal cord lesions,

326–7

Spinal roots and

dermatomes, 308

Spine, 354–5

C-spine movement,

354

feel, 354

femoral nerve stretch

test, 355

look, 354

neurological

examination, 355

Schober’s test, 354–5

sciatic nerve stretch

test, 354–5

T- and L-spine

movement, 354

Spirometry, 659–60

Spleen, 234–5 , 240

palpation of, 235

Splinter hemorrhages, 81

Spondyloarthropathies,

368–70

Spontaneity vs. learned

behaviors, 5

Sputum, 185–6

characteristics of, 186

Squint, 277–8

Standing, 8

Staying on topic, 10

Sterility and preparation

procedures, 513

Stethoscopes, 4

Stiffness, 342

Strabismus, assessment

of, 498

Strabismus/squint, 277–8

Strangulation, 243

Stretch marks, 230

Stridor, 131 , 187

Subarachnoid

hemorrhage, 329

Subclavian vein, 529–30

Subcutaneous (SC)

injections,

procedures for, 516

Subcutaneous layer, 76

Suckling reﬂ ex, 307

INDEX

690

Suicide risk

assessment, 453–5

protective factors

for, 455

risk factors for, 454

Superﬁ cial fascia, 76

Supinator examination,

302

Supraventricular

tachycardias, 603–6

Swan neck, 63

Sweat glands, 76

Swelling, 342

Swollen knee, causes

of, 372

Sympathy, displaying, 21

Symphysial–fundal

height, 422–3

Syncope, 152

Synovial joints, 338–9

Systemic lupus

erythematosus (SLE),

477

Systemic sclerosis, 69

Systolic murmurs, 169

T

Tachycardia, 158–9

Tactile hallucinations,

462

Tactile vocal fremitus,

194

T- and L-spine

movements, 354

Tardive dyskinesia,

325–6

Taste sensation, 285

Technical words,

avoiding, 6

Teeth, inspecting, 138

Telangiectasia, 226

Telephone

communication, 16

Telogen efﬂ uvium, 80

Temperature, 53

Temporal (giant cell)

arteritis, 329

Tendon reﬂ exes, 302–4 ,

499

augmentation, 304

examination, 302–4

technique, 302

theory, 302

Tension headache, 329

Terminal dribbling, 218

Terrorism, 509

Testes

anatomy and

physiology of, 376

carcinoma, 387

testicular pain, 379

Testicular torsion, 387

Tetany, signs of, 103

Thigh, lateral cutaneous

nerve of, 319

Thompson or Simmond

test, 364

Thoracentesis, 561–2

Thoracic and lumbar

spine, radiology of,

656–7

Throat

applied anatomy and

physiology of,

120–1

examining, 138–40

ﬁ ndings, 139–40

inspection, 138–9

palpation, 139

Throat disorders,

symptoms of, 129–31

dysphonia, 130

halitosis, 131

mouth, lumps in,

129–30

neck, lumps in, 130

oral pain, 129

stridor, 131

throat pain, 129

Throat pain, 129

Thudicum speculum, 136

Thyroid, examining, 97 ,

104–5

auscultation, 105

inspection

rest of the neck, 104

thyroid gland, 104

palpation, 104–5

rest of the neck, 105

thyroid gland, 104

Pemberton’s sign, 105

percussion, 105

thyroid status,

assessing, 105

Thyroid disease, eye

signs in, 106

exophthalmos, 106

eye movements, 106

inspection, 106

lid lag, 106

lid retraction, 106

proptosis, 106

thyrotoxicosis and

graves disease, eye

signs of, 107

visual ﬁ elds, 106

Thyroid status, assessing,

105

Thyrotoxicosis, eye signs

of, 107

Thyrotoxicosis and

graves disease, eye

signs of, 107

Tic, 325–6

Tietze’s syndrome,

149 , 187

“Tightness,” 184

Timing, 4

Tinel’s sign, 67 , 318

Tinnitus, 124–6

causes of, 124

deformity of the ear,

124–5

dizziness, 125–6

injury to the ear, 124

Titubation, 325–6

Tongue, 227

Tongue, inspecting, 138

Tonsillitis, 144

Tonsils, 139

Torsades de pointes, 610

Touching, 21

Trace elements, 71

copper, 71

iodine, 71

magnesium, 71

zinc, 71

Trachea, 194

anatomy of, 182

Tracheitis, pain of, 187

Tracheostomy manage-

ment, 555–6

Transudate, 671

Tremor, 191 , 192 , 256–7 ,

325–6

Triceps examination, 302

Tricuspid regurgitation,

176

Tricuspid stenosis, 175

Trigeminal nerve, 283–4

applied anatomy, 283

examination, 283–4

ﬁ ndings, 284

reﬂ exes, 284

Trochlear nerve, 280

Trousseau’s sign, 103 ,

117

INDEX

691

Tuberous sclerosis, 68–9

Tumor plop, 172

Tunnel vision, 266

Turbinates, 120

Turbohaler, 540–1

Turner’s syndrome, 68

12-lead ECG, 593–4

leads, 593–4

orientation, 594

Tympanic cavity, 120

Tympanic membrane,

120

U

Ulcer, examining, 90

base, 90

depth, 90

discharge, 90

edge, 90

leg ulcers, 91

representation of

some ulcer edges,

91

Ulcerative colitis (UC),

250

Ulnar deviation, 63

Ulnar nerve, 317

Ulsatile mass, Palpating,

238

Unconscious patient,

331–3

Unilateral ﬁ eld loss, 266

Upbeat nystagmus, 278

Upper limb, 225 , 317

median nerve, 317

radial nerve, 317

testing power in, 299

ulnar nerve,

317

Upper motor and lower

motor nerve lesions,

323–5

Upper motor nerve

lesion, 286

Upper motor neuron

(UMN), 294–5 , 323

Urinary and prostate

symptoms, 218–19

dysuria, 219

hematuria, 219

hesitancy, 218

incomplete emptying,

219

intermittency, 219

nocturia, 218

oliguria and anuria, 219

polyuria, 219

terminal dribbling, 218

urgency, 218

urinary frequency, 218

urinary incontinence,

218

Urinary bladder, 237

Urinary incontinence,

421

Urinary tract infections

(UTIs), 388

Urostomy, 230

Uterus

anatomy of, 408–9

bimanual examination

of, 427–8

U.S. Centers for Disease

Control and

Prevention (CDC),

509

Uvula, 139

V

Vacutainer®, 518–20

Vagina, anatomy of, 408

Vaginal bleeding, in early

pregnancy, 437

Vaginal discharge, 420

Vaginal examination, 445

Valgus deformity, 343

Valvular disease, 175–6

aortic regurgitation,

175

aortic stenosis, 175

mitral regurgitation, 175

mitral stenosis, 175

pulmonary

regurgitation, 176

pulmonary stenosis,

176

tricuspid

regurgitation, 176

tricuspid stenosis, 175

Variant CJD (vCJD), 473

Varicocele, 387

Varus deformity, 343

Vascular dementia/

multi-infarct

dementia, 472

Vascular

endothelial-derived

growth factor

(VEGF), 110

Veins, applied anatomy

and physiology, 147

Venipuncture, 518–20

Venous hums, 231

Venous hypertension, 91

Ventricular conduction

abnormalities, 600–2

Ventricular escape

rhythm, 610

Ventricular

extrasystoles, 610

Ventricular ﬁ brillation

(VF), 608

Ventricular rhythms,

607–8 , 610

Ventricular septal defect

(VSD), 176

Ventricular tachycardia

(VT), 607

Vestibular neuronitis, 142

Vestibular nystagmus,

278

Vestibulocochlear nerve,

287–8

applied anatomy, 287

examination, 287

hearing, 287

vestibular function,

288

Vestibulocochlear organ,

120

Visual hallucinations, 462

Visual loss avoidance in

diabetes, 112

Visual symptoms, 257

Vitamin A (retinol), 70

Vitamin and trace

element deﬁ ciencies,

70–1

fat soluble vitamins, 70

trace elements, 71

water soluble vitamins,

70–1

Vitamin B1 (thiamine),

70

Vitamin B2

(riboﬂ avin), 70

Vitamin B3 (niacin), 70

Vitamin B6 (pyridoxine),

70–1

Vitamin B9 (folic acid), 71

Vitamin B12

(cyanocobalamin), 71

Vitamin C (ascorbic

acid),

71

Vitamin D

(cholecalciferol), 70

Vitamin deﬁ ciencies, 447

INDEX

692

Vitamin E (alpha-

tocopherol), 70

Vitamin K, 70

Vitilgo, 83

Vomiting, causes of, 209

Vomitus, nature of,

208

bile, 208

blood (hematemesis),

208

Vulva, 409–10

Vulval symptoms, 420

W

Waddling, 321–2

Watching and

learning, 22

Water soluble vitamins,

70–1

vitamin B1 (thiamine),

70

vitamin B2 (riboﬂ avin),

70

vitamin B3 (niacin), 70

vitamin B6

(pyridoxine), 70–1

vitamin B9 (folic

acid), 71

vitamin B12

(cyanocobalamin),

71

vitamin C (ascorbic

acid), 71

Weber’s test, 287

position of tuning fork

for, 288

Wheeze, 187

Whistle-smile sign,

285

White coat, 4

Wolff–Parkinson–White

(WPW) syndrome,

605–6 , 607

Wrist, 298

Wrist extension,

64–6

Wrist ﬂ exion, 64–6

Wrist subluxation,

63

Written

communication, 23

Z

Zinc, 71

Z-shaped thumb

(Hitchhiker’s

Thumb), 63