Assessment, differential diagnosis, and initial clinical evaluation of the pediatric patient with obesity: An Obesity Medical Association (OMA) Clinical Practice Statement 2022

Assessment, differential diagnosis, and initial clinical evaluation of the

pediatric patient with obesity: An Obesity Medical Association (OMA)

Clinical Practice Statement 2022

Suzanne E. Cuda

, Marisa Censani

Alamo City Healthy Kids and Families, 1919 Oakwell Farms Parkway, Ste 145, San Antonio, TX, 78218, USA

New York Presbyterian Hospital, Weill Cornell Medicine, Department of Pediatrics, Division of Pediatric Endocrinology; New York, NY, USA

ARTICLE INFO

Keywords:

Assessment

Clinical evaluation

Differential diagnosis

Obesity

Pediatric patients

ABSTRACT

Background: The Obesity Medical Association (OMA) Clinical Practice Statement (CPS) on the assessment, dif-

ferential diagnosis, and initial clinical evaluation of pediatric patients with obesity is intended to provide clini-

cians with an overview of clinical practices applicable to children and adolescents with body mass indexes greater

than or equal to the 95th percentile for their ages, particularly those with adverse consequences resulting from

increased body mass. The information in this CPS is based on scientiﬁc evidence, supported by the medical

literature, and derived from the clinical experiences of members of the OMA.

Methods: The scientiﬁc information and clinical guidance in this CPS is based upon referenced evidence and

derived from the clinical perspectives of the authors.

Results: This OMA Clinical Practice Statement on assessment, differential diagnosis, and initial clinical evaluation

of pediatric patients with obesity provides clinical information regarding classiﬁcation of children and adolescents

with overweight or obesity, differential diagnoses to consider, and a roadmap for the initial clinical evaluation.

Conclusions: This OMA Clinical Practice Statement on assessment, differential diagnosis, and initial clinical

evaluation of pediatric patients with obesity is an overview of current recommendations. Assessment of pediatric

patients with obesity is the ﬁrst step in determining treatments leading to the improvement of the health of

children and adolescents with obesity, especially those with metabolic, physiological, and psychological

complications.

1. Introduction

The purpose of the CPS on assessment, differential diagnosis, and

initial clinical evaluation of pediatric patients with obesity is to provide

clinicians with a tool to assess children with obesity. The OMA is an

organization of providers in the ﬁeld of obesity medicine dedicated to the

comprehensive care of patients with obesity. OMA members are physi-

cians, nurse practitioners, physician assistants, and other healthcare

providers who take a comprehensive, evidence-based approach to

treating obesity. This approach is comprised of the four pillars of nutri-

tion, physical activity, behavior, and medication. While it is hoped many

clinicians may ﬁnd the recommendations in this CPS helpful, the ﬁnal

decision regarding the optimal care of the patient with overweight or

obesity is dependent upon the individual clinical presentation and the

judgment of the clinician who is tasked with directing a treatment plan

that is in the best interest of the patient.

2. Assessment of pediatric patients

Weight assessment of children is age dependent. For children less

than two years of age, weight percentiles and weight for length charts are

used. Clinicians can choose between growth charts provided by the

Centers for Disease Control and Prevention (CDC) or the World Health

Organization (WHO). The CDC charts are based on a cohort of mainly

white American children who were mostly non-breastfed. The WHO

charts are based on children from diverse racial and ethnic backgrounds,

mostly breastfed [1–3].

For children and adolescents ages 2–20, body mass index (BMI)

percentile is used. For children and adolescents ages 2–20 with BMIs

greater than the 95th percentile, use percent of the 95th percentile [4].

* Corresponding author. 1919 Oakwell Farms Parkway, Ste 145, San Antonio, TX, 78218, USA.

E-mail addresses: [email protected] (S.E. Cuda), [email protected] (M. Censani).

Contents lists available at ScienceDirect

Obesity Pillars

journal homepage: www.journals.elsevier.com/obesity-pillars

https://doi.org/10.1016/j.obpill.2022.100010

Received 23 December 2021; Received in revised form 26 December 2021; Accepted 2 January 2022

(http://creativecommons.org/licenses/by-nc-nd/4.0/).

Obesity Pillars 1 (2022) 100010

Categories of weight status are as follows: less than 5th percentile is

underweight, 5–84th percentile is healthy weight, 85–94th percentile is

overweight, 95th percentile to 119% of the 95th percentile is Class 1

obesity, 120–139% of the 95th percentile or a BMI greater than 35 kg/m

and less than 39 kg/m

is Class 2 obesity, and greater than 140% of the

95th percentile or BMI greater than 40 is Class 3 obesity [5,6]. Any BMI

greater than or equal to 120% of the 95th percentile is severe obesity.

Different charts are used to track BMI for up to the 95th percentile and

above the 95th percentile [4,6–8]. Body mass index categories and per-

centiles are shown in Fig. 1.

BMI z-scores, or BMI standard deviation scores, can be used to adjust

for child age and sex [9] but should not be used to assess BMI changes

among children and adolescents with BMIs greater than or equal to 120%

of the 95th percentile. High BMI z-scores are compressed into a narrow

range, which can result in a clinically signiﬁcant reduction in BMI being

represented by a small reduction in BMI z-score. Change in the percent of

the 95th percentile is the preferred metric to use in the management of

children and adolescents with severe obesity [7,8]. BMI charts for chil-

dren and adolescents with severe obesity are shown in Fig. 2.

A BMI of 35 kg/m

is a higher threshold than a BMI greater than or

equal to 120% of the 95th percentile among most children, but it is a

somewhat lower threshold (and therefore expands the population that is

categorized as severely obese) among boys approximately 18 years of age

and older and girls approximately 16 years of age and older [7,10].

Overall, assessments should consider age as well as BMI status. The top

10 takeaway messages for assessing children and adolescents with

obesity are shown in Table 1.

3. Obesity as a disease

Obesity has been recognized as a disease by the American Medical

Association since 2013 [11]. Response to the disease of obesity manifests

differently in children and adolescents than in adults. A breakdown of

responses into categories of endocrine or immune response, physical

response, and psychological response is a useful way to work through the

clinical presentation [12].

Endocrine and immune responses are due to adiposopathy or “sick

fat.” Common phenomena include impaired fasting glucose, metabolic

syndrome, hypertension, menstrual dysfunction, early onset or a delay in

onset of puberty, nonalcoholic fatty liver disease, dyslipidemia, insulin

resistance, type 2 diabetes, increased uric acid, microalbuminuria, gy-

necomastia, cholecystitis, and accelerated growth [13,14].

Physical response is attributed to fat mass disease. Asthma, immo-

bility, lipomastia, tissue compression (obstructive sleep apnea, gastro-

esophageal reﬂux, hypertension), tissue friction (intertrigo), stress on

weight bearing joints, slipped capital femoral epiphysis, Blount's disease,

scoliosis, and orthopedic disorders are all possible ﬁndings [15].

Psychological responses can impact quality of life and include isola-

tion from peers, decreased ability to participate in normal childhood

activities, victimization (bullying, emotional/physical abuse, or neglect),

lack of social age-appropriate relationships, anxiety, depression, binge

eating disorder, night eating disorder, and bulimia [15,16].

4. Differential diagnosis of children and adolescents with obesity

The diagnosis of exogenous obesity in children and adolescents due to

nutritional origin is a diagnosis of exclusion. Clinicians must consider

endocrinopathies and syndromal obesity as well as both monogenic and

polygenic etiologies.

For approaching the differential diagnosis of childhood obesity, it is

important to assess linear growth. Prepubertal and pubertal children with

exogenous obesity (i.e., related to unhealthful nutrition and physical

inactivity) usually have accelerated or consistent linear growth, in

contrast to those with an endocrinopathy, who frequently present with a

decrease in linear growth [17]. Precocious puberty can occur in both

those with exogenous obesity and those with an endocrinopathy. The

diagnosis of precocious puberty is made in females younger than 8 years

of age with Tanner II breast development and in boys younger than 9

years of age with testicular enlargement greater than 4 cc [18]. In these

children, a bone age assessment may show an advancement of bone age

as compared to chronological age of 1–2 years or more. If a child with

obesity presents with a decrease in linear growth, the clinician should

consider possible hypothalamic/pituitary dysfunction (with growth

hormone deﬁciency), hypercortisolism (consider a dexamethasone sup-

pression test or 24-h urinary free cortisol), hypothyroidism [check thy-

roid-stimulating hormone (TSH), conduct a free thyroxine (T4) test], or

genetic syndromes [19,20].

Syndromal obesity is obesity accompanied by other behavior, func-

tional, or anatomic abnormalities, such as hyperphagia, cognitive delay,

dysmorphic features, and organ-speciﬁc disorders. The clinician should

consider syndromal obesity in children with obesity who present with a

developmental delay. Developmental delay can be associated with

decreased linear growth, and the evaluation of these children is depen-

dent on presentation and family history. A child presenting with severe

obesity (>120% of the 95th percentile) before 5 years of age may indi-

cate a genetic etiology. If hyperphagia and/or a family history of extreme

obesity is present, genetic testing is recommended [21]. The clinical

history may include food-seeking behavior such as searching for or

stealing food, waking at night to eat, and eating food left behind by

others. Neurological causes should be excluded. These dysfunctional

behaviors result from disruption of the hypothalamic pathways involved

in the regulation of energy balance. Genetic testing for multi-gene panels

and referral to a geneticist should be considered [19,22–24]. A summary

of differential diagnoses regarding childhood obesity is shown in Fig. 3.

5. Focused Review of Systems

Children with obesity are commonly seen in primary care for a

problem other than obesity. Therefore, speciﬁc symptoms secondary to

obesity must be carefully assessed. Children may or may not complain of

symptoms, as many have been living with symptoms for years and are not

aware of what life is like without symptoms. Fig. 4 identiﬁes symptoms

with accompanying related co-morbidities.

6. Diagnostic workup

The diagnostic workup is determined by the age at presentation of the

Fig. 1. Body Mass Index Categories in Children

and Adolescents Ages 2–20. BMI categories are

shown for children ages 2–20 who are underweight, at

a healthy weight, overweight, obese, and severely

obese [6]. Note that not all patients with BMI in the

85th percentile or above have excess adiposity, and

many children and adolescents with BMIs below the

5th percentile are healthy and do not need treatment.

The CDC recommends using the WHO growth charts

to monitor growth for infants and children ages 0–2

years of age in the U.S. and using the CDC growth

charts for children ages 2 years and older [2].

S.E. Cuda, M. Censani Obesity Pillars 1 (2022) 100010

child with obesity and the classiﬁcation of obesity presented by the child.

Children with obesity are at risk for glycemic dysregulation [25]. A

fasting blood glucose or a hemoglobin A1c (HbA1c) test will determine

whether glycemic dysregulation is present. Dyslipidemia is the most

common laboratory abnormality found in children with obesity [26].

Either a fasting lipid proﬁle or a non-fasting lipid proﬁle, if fasting is not

feasible, can assess dyslipidemia. Liver function tests, speciﬁcally alanine

aminotransferase (ALT) and aspartate aminotransferase (AST), can

screen for non-alcoholic fatty liver disease. Many children are at risk for

vitamin D deﬁciency, which is detected with a 25-hydroxy (25 OH)

vitamin D test [27]. Blood pressure is checked if the child is older than

three years of age. Other studies are indicated based on history: a sleep

study for any history of snoring, daytime sleepiness, disrupted sleep cycle

or even hyperactivity may be indicated. Liver imaging can be done if the

liver function tests (ALT and AST) are high. Uric acid can be obtained in

those children with diabetes or prediabetes. Uric acid can be elevated

with high intake of high fructose corn syrup and even table sugar. Fig. 5

shows recommended diagnostics based on age ranges, BMIs, and risk

factors [ 19,22–24].

7. Special populations

Turner syndrome (i.e., absence or dysfunction of an X chromosome),

achondroplasia (i.e., mutation of ﬁbroblast growth factor receptor 3

Fig. 2. Body Mass Index Charts for Children and Adolescents Ages 2–20 Years with Severe Obesity. BMI vs. age is shown for children ages 2–20 years.

Table 1

Top 10 Takeaway Messages: Assessment of the Child with Obesity. Shown

are the top 10 messages from the OMA regarding weight assessment of children

[1–8].

1. For children less than two years of age, weight for length percentile is used to

assess weight status.

2. For children 2–20 years of age, BMI is used to assess weight status.

3. Overweight is de ﬁned as a BMI percentile between the 85th percentile and the

94th percentile.

4. Obese is deﬁned as a BMI percentile between the 95th percentile and 119% of

the 95th percentile.

5. Severely obese de ﬁned as is a BMI percentile greater than or equal to 120% of

the 95th percentile.

6. Class 1 obesity is deﬁned as a BMI percentile between the 95th percentile and

119% of the 95th percentile.

7. Class 2 obesity is deﬁned as a BMI percentile that is 120–139% of the 95th

percentile.

8. Class 3 obesity is deﬁned as a BMI percentile greater than or equal to 140% of

the 95th percentile.

9. BMI z-scores should not be used to assess BMI change among children and

adolescents with BMI greater than 120% of the 95th percentile.

10. A BMI of 35 kg/m

is used for adolescent boys at approximately 18 years of age

and adolescent girls at approximately 16 years of age as the threshold for

severely obese and is somewhat lower than 120% of the 95th percentile.

Fig. 3. Childhood Obesity: Differential Diagnosis. Considerations and associations are shown regarding linear growth, developmental delays, and early onset

obesity in children. Abbreviations: TSH: thyroid-stimulating hormone; T4: thyroxine.

S.E. Cuda, M. Censani Obesity Pillars 1 (2022) 100010

gene), and Down syndrome (i.e., trisomy 21 or three copies of chromo-

some 21) are commonly seen populations of children at risk for obesity.

These populations require additional considerations regarding health

impacts and screening tools for obesity.

Children with Turner syndrome have restricted height growth (i.e.,

short stature) and increased adiposity, with an increase in total and

visceral fat mass and a decrease in lean body mass. In addition, 70% of

girls with Turner syndrome have abnormal glucose metabolism leading

to an increased prevalence of both Type 1 and Type 2 diabetes [30,31].

Children with Down syndrome typically have short stature and have

shorter limbs and poor coordination, leading to less activity and a pro-

pensity to gain weight. Growth charts for height and weight are used to

follow children with Down Syndrome, but the American Academy of

Pediatrics (AAP) recommends that clinicians use BMI guidelines from the

CDC for normally developing children to classify BMI status [32–34].

Children with achondroplasia, the most common form of inherited

disproportionate short stature, have no pubertal growth spurt and a

relatively ﬂat growth curve for height from infancy on. They do not have

adiposity rebound and are at high risk for early cardiovascular disease,

obstructive sleep apnea, and difﬁculty with mobility [35,36]. Fig. 6

shows a summary of considerations for children with Turner syndrome,

Down syndrome, and achondroplasia. Table 2 shows the top eight

takeaway messages from the OMA regarding differential diagnoses and

diagnostic workups for special populations.

8. Conclusions

This Clinical Practice Statement on the assessment, differential

diagnosis, and initial clinical evaluation of pediatric patients with obesity

provides clinicians with assessment tools and recommendations

regarding their pediatric patients. Assessment of pediatric patients with

obesity is the ﬁrst step in determining treatments that may lead to im-

provements in the health and wellbeing of children and adolescents with

obesity, especially those with metabolic, physiological, and psychologi-

cal complications.

8.1. Writing Process and ethics statement [38]

8.1.1. Transparency

This manuscript was largely derived and edited from the 2020–2022

Fig. 4. Focused Review of Systems. Symptoms and associated co-morbidities for children with obesity are shown. Children may or may not complain of symptoms,

so a careful assessment of symptoms associated with obesity is necessary.

Fig. 5. Diagnostic Workup: Labs and Studies. Shown are recommended diagnostics based on age ranges, BMIs, and risk factors for pediatric patients [28,29].

Abbreviations: BMI: body mass index; HbA1c: hemoglobin A1c; ALT: alanine aminotransferase; AST: aspartate aminotransferase; GGT: gamma-glutamyl transferase;

25 OH: 25-hydroxy; hs-CRP: high-sensitivity C-reactive protein.

S.E. Cuda, M. Censani Obesity Pillars 1 (2022) 100010

Obesity Medicine Association (OMA) Pediatric Obesity Algorithm.

Beginning in 2016, the OMA created and maintained an online Pediatric

“Obesity Algorithm” (i.e., educational slides and eBook) that underwent

updates approximately every two years by OMA authors and was

reviewed and approved annually by the OMA Board of Trustees. Authors

of prior years’ versions are included in Supplement #1. This manuscript

is the ﬁrst published version of the applicable chapter/s of the

2020–2022 OMA Pediatric Obesity Algorithm.

8.1.2. Group composition

Over the years, the authors of the OMA Pediatric Obesity Algorithm

have represented a diverse range of clinicians, allied health professionals,

clinical researchers, and academicians. (Supplement #1) The authors

reﬂect a multidisciplinary and balanced group of experts in obesity sci-

ence, patient evaluation, and clinical treatment.

8.1.3. Author contributions

SEC transcribed the ﬁrst draft from the 2020–2022 OMA Pediatric

Obesity Algorithm. MC and SEC then reviewed, edited, and approved the

document for pre-peer review submission and post-peer review

publication.

8.1.4. Disclosures (declaration of potential competing interest)

Potential dualities or conﬂicts of interest of the authors are listed in

the Individual Disclosure section. Assistance of a medical writer paid by

the Obesity Medicine Association is noted in the Acknowledgements

section. Neither the prior OMA Pediatric Algorithms nor the publishing

of this Clinical Practice Statement received outside funding. The authors

of prior OMA Pediatric Obesity Algorithms never received payment for

their writing, editing, and publishing work. Authors of this Clinical

Practice Statement likewise received no payment for their writing,

editing, and publishing work. While listed journal Editors received pay-

ment for their roles as Editors, they did not receive payment for their

participation as authors.

8.1.5. Individual Disclosures

SEC declares a relationship with Novo Nordisk as a member of an

Advisory Board and a relationship with Rhythm Pharmaceuticals as a

member of their Gold Panel.

MC reports no disclosures pertaining to this project.

8.1.6. Evidence

The content of the OMA Pediatric Obesity Algorithm and this

manuscript is supported by citations, which are listed in the References

section.

8.1.7. Ethics review

After approval by the authors, a draft manuscript was peer-reviewed

and approved by the OMA Board of Trustees prior to publication. This

submission did not involve human test subjects or volunteers.

8.1.7.1. Conclusions and recommendations. This Clinical Practice State-

ment is intended to be an educational tool that incorporates the current

medical science and the clinical experiences of obesity specialists. The

intent is to better facilitate and improve the clinical care and manage-

ment of patients with pre-obesity and obesity. This Clinical Practice

Statement should not be interpreted as “rules” and/or directives

regarding the medical care of an individual patient. The decision

regarding the optimal care of the patient with overweight and obesity is

best reliant upon a patient-centered approach, managed by the clinician

tasked with directing an individual treatment plan that is in the best

interest of the individual patient.

8.1.7.2. Updating. It is anticipated that sections of this Clinical Practice

Statement may require future updates. The timing of such an update will

depend on decisions made by Obesity Pillars Editorial team, with input

from the OMA members and OMA Board of Trustees.

8.1.7.3. Disclaimer and limitations. Both the OMA Obesity Algorithms

and this Clinical Practice Statement were developed to assist health care

professionals in providing care for patients with pre-obesity and obesity

Fig. 6. Special Populations: Turner Syndrome, Down Syndrome, and Achondroplasia. Children with Turner syndrome, Down syndrome, and achondroplasia

require special considerations regarding health risks and obesity. Takeaways for each condition are shown [30–37].

Table 2

Top Eight Takeaway Messages: Differential Diagnoses and Diagnostic

Workups for Special Populations. The top eight messages from the OMA

regarding differential diagnosis, diagnostic workups, and special populations are

shown [30–37].

1. Although most children with obesity have exogenous obesity of nutritional

origin, endocrinopathies and syndromal obesity must be considered.

2. Not all children with syndromal obesity have developmental delays and/or a

decrease in linear growth, but, if either is present, consider syndromal obesity.

3. Children with severe early-onset obesity and hyperphagia are at increased risk

for genetic etiologies for obesity.

4. The review of systems and initial work up is determined by the age at

presentation and degree of obesity of the child. Glycemic dysregulation,

dyslipidemia, and hepatic function are generally assessed.

5. Other testing is directed by presenting symptoms/physical ﬁndings.

6. Turner syndrome is a special population at high risk for abnormal glucose

metabolism.

7. Children with Down syndrome are at high risk for obesity. BMI is assessed using

the CDC charts for normally developing children; height and weight are followed

using speciﬁc charts for Down syndrome.

8. Achondroplasia is a form of inherited disproportionate short stature in which

there is no pubertal growth spurt, no typical “J” shaped BMI curve, and high rates

of obesity. Speciﬁc height, weight, and BMI curves should be used.

S.E. Cuda, M. Censani Obesity Pillars 1 (2022) 100010

based upon the best available evidence. In areas regarding inconclusive

or insufﬁcient scientiﬁc evidence, the authors used their professional

judgment. This Clinical Practice Statement is intended to represent the

state of obesity medicine at the time of publication. Thus, this Clinical

Practice Statement is not a substitute for maintaining awareness of

emerging new science. Finally, decisions by practitioners to apply the

principles in this Clinical Practice Statement are best made by consid-

ering local resources, individual patient circumstances, patient agree-

ment, and knowledge of federal, state, and local laws and guidance.

Declaration of competing interest

The authors declare the following ﬁnancial interests/personal re-

lationships which may be considered as potential competing interests:

Suzanne Elizabeth Cuda reports ﬁnancial support and travel were pro-

vided by Novo Nordisk Inc. Suzanne Elizabeth Cuda reports a relation-

ship with Novo Nordisk Inc that includes: consulting or advisory and

travel reimbursement.

Acknowledgements

Medical writing support (funded by the Obesity Medicine Associa-

tion) was provided by Savannah Logan, who helped implement author

revisions while adhering to Good Publication Practice (GPP3) guidelines

and International Committee of Medical Journal Editors (ICMJE) rec-

ommendations. Otherwise, this manuscript received no funding.

Appendix A. Supplementary data

Supplementary data to this article can be found online at https

://doi.org/10.1016/j.obpill.2022.100010.

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