Clinical evaluation of the child or adolescent with obesity

INTRODUCTION — 

Obesity is among the most prevalent and consequential public health problems in the United States and many other countries [1]. As the prevalence of obesity increases, so does the prevalence of the associated comorbidities.

The goal of a comprehensive evaluation of the child with overweight or obesity is to identify treatable causes and comorbidities. The evaluation should include a focused history and physical examination, with laboratory and radiologic studies for selected patients.

The clinical evaluation of the child or adolescent with overweight or obesity will be presented here. Other aspects of clinical management of obesity in children are discussed in separate topic reviews:

●(See "Definition, epidemiology, and etiology of obesity in children and adolescents".)

●(See "Overview of the health consequences of obesity in children and adolescents".)

●(See "Prevention and management of childhood obesity in the primary care setting".)

●(See "Surgical management of severe obesity in adolescents".)

BODY MASS INDEX — 

Body mass index (BMI) is equal to the body weight (in kilograms) divided by the height (in meters) squared (table 1). BMI should be calculated at least annually for all children older than two years [2]. The results should be used to determine:

●BMI percentile – The BMI percentile can be determined by plotting points on a BMI growth curve (figure 1A-B). BMI percentiles also can be determined using a calculator for boys (calculator 1) and for girls (calculator 2).

●Weight category – The BMI percentile is used to categorize the weight class (table 2):

•Underweight – BMI <5^th percentile for age and sex.

•Normal weight – BMI between the 5^th and <85^th percentile for age and sex.

•Overweight – BMI ≥85^th to <95^th percentile for age and sex.

•Obesity – Classified by severity, using the following thresholds ( (figure 2A-B) or Centers for Disease Control and Prevention extended BMI growth charts) [1-3]:

-Class I – BMI ≥95^th percentile for age and sex or BMI ≥30 (whichever is lower).

-Class II – BMI ≥120 percent of the 95^th percentile values or a BMI ≥35 kg/m² (whichever is lower). This corresponds to approximately the 98^th percentile.

-Class III obesity – BMI ≥140 percent of the 95^th percentile values or a BMI ≥40 kg/m².

BMI is a clinically practical tool for the assessment of overweight and obesity in children. It correlates with adiposity [2,4-6] and complications of excess childhood weight [7-9]. However, because BMI does not directly measure body fat, it may overestimate adiposity in a child with increased muscle mass (eg, an athlete) and underestimate adiposity in a child with reduced muscle mass (eg, a sedentary child). (See "Measurement of body composition in children", section on 'Estimates of adiposity'.)

HISTORY

Weight history — The child's historical pattern of weight gain should be evaluated based on serial growth measurements (if available) or history.

The rapidity and age of onset is sometimes helpful in determining the cause or contributors to the child's obesity:

●Gradual onset – Gradual onset of obesity is typical for the most common forms of obesity (genetic predisposition combined with excess caloric intake or other environmental contributors).

●Abrupt onset of weight gain – Abrupt onset of obesity with rapid weight gain should prompt investigation of a major psychosocial trigger such as a loss or change in the family or new symptoms of anxiety or depression. (See 'Psychosocial history' below.)

Other possible causes include medication-induced weight gain and neuroendocrine causes of obesity (eg, Cushing disease, hypothalamic tumor, or, rarely, ROHHADNET syndrome [rapid-onset obesity with hypothalamic dysfunction, hypoventilation, autonomic dysregulation, with or without neuroendocrine tumor]) (table 11B) [10]. (See "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Endocrine disorders' and "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Hypothalamic obesity'.)

●Severe early-onset – Severe early-onset obesity is more likely to have a strong genetic component. Some forms of syndromic or monogenic obesity have onset before two years of age, while others (especially Prader-Willi syndrome) tend to have growth failure during infancy followed by rapid weight gain and development of obesity after two years of age (table 3A-B). (See "Prader-Willi syndrome: Clinical features and diagnosis".)

Diet — The dietary history should elicit the following information, as summarized in the table (table 4):

●Caregiver(s) involved in feeding – Including meal planning, shopping, and preparing and being present at meals.

●Eating patterns – Including timing, content, and location of meals and snacks. The possibility of disordered eating is raised by (see "Eating disorders: Overview of epidemiology, clinical features, and diagnosis"):

•Recurrent episodes of consuming large amounts of food with a sense of loss of control (suspect binge eating disorder) [11]

•Inappropriate compensatory behavior to prevent weight gain (self-induced vomiting or other purging, fasting, and/or excessive exercise) associated with binge eating (suspect bulimia nervosa)

Children who eat less frequent meals (eg, those who skip meals) are more likely to have obesity than those who eat more frequently [12], but this association may not be causal and may be due to confounders (eg, increased snacking).

●Food frequency – Preliminary identification of foods high in calories and low in nutritional value that can be reduced, eliminated, or replaced. Common sources of excess calories include:

•Sugar-containing beverages, including soda, juice, sugar-containing "sports" drinks, and flavored milks

•Snack foods (chips, sweets)

•Other eating outside of meals (leftovers, quick-service foods)

●Food preferences and dislikes – While picky eating is not necessarily associated with the development of obesity, several reports indicate higher prevalence of picky eating in children with overweight and obesity [13-15], and addressing picky eating as part of weight management can improve outcomes [13,16]. A picky eating pattern may also be a relevant focus for nutritional and behavioral counseling.

●Restaurants and prepared foods – Fast food service and restaurant meals are often higher in calories and lower in nutritional value compared with foods prepared at home. Identifying the frequency and type of such meals facilitates counseling to reduce frequency and/or optimize food selections. (See "Healthy eating for adolescents", section on 'Fast food'.)

Activity — The activity history should include the following factors, as summarized in the table (table 5) [2,17]:

●Physical activity

•Time spent in play (especially outdoors)

•School recess and physical education (frequency, duration, and intensity)

•Sports participation

•Activity classes, such as dance, yoga, or martial arts

•Afterschool and weekend activities

•Lifestyle activity, such as walking or riding a bike to school; if none, document any barriers to these activities

●Sedentary activity – In most cases, most sedentary behavior involves screen time. Ask the parent or child to estimate total hours of both recreational activities (television, smart phone/device, recreational internet use, and video games) and educational activities (homework, reading, and computer-based learning).

Sleep — The sleep history should include:

●Sleep habits – Assess typical sleep duration, sleep quality, and sleep schedule, and compare with recommended sleep times for children (table 6). Short sleep duration or irregular sleep schedules have been associated with obesity in children and adults; a causal association has been proposed but not established (see "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Sleep'). Strategies for improving sleep are discussed separately. (See "Behavioral sleep problems in children".)

●Symptoms of sleep disorders – Obesity is associated with an increased risk for obstructive sleep apnea. Any child who snores habitually (eg, ≥3 nights per week), has loud snoring, or has pauses in breathing during sleep should be further evaluated. Obstructive sleep apnea also may cause nocturnal enuresis or daytime symptoms including inattention, learning problems, and hyperactivity, with or without sleepiness. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Screening'.)

Medical history — The medical history should include review of all medications, particularly those that are known to be weight-promoting (eg, certain psychoactive drugs such as risperidone, antiseizure medication, and glucocorticoids) (table 7). (See "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Medications'.)

In addition, document any comorbidities of obesity, as outlined in the table (table 8). (See "Overview of the health consequences of obesity in children and adolescents".)

Review of systems — The review of systems should probe for further evidence of comorbidities or underlying causes of obesity (table 9) [2].

Developmental delay or dysmorphic features raise the possibility of a syndromic form of obesity (table 3A). In particular, a history of hypotonia and feeding problems during infancy followed by rapid weight gain during early childhood and developmental delay suggests the possibility of Prader-Willi syndrome. (See "Prader-Willi syndrome: Clinical features and diagnosis".)

Family history — Key elements are:

●Obesity – Inquire about obesity in first-degree relatives (parents and siblings) [2]. Use terms such as "overweight" or "unhealthy weight" because these terms are generally more acceptable to patients than "obesity" (table 10) (see "Prevention and management of childhood obesity in the primary care setting", section on 'Strategies for counseling about weight management'). In particular, obesity in one or both parents is an important predictor for whether a child's obesity will persist into adulthood [18-21]. This association has both genetic and environmental components. (See "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Persistence of obesity'.)

●Comorbidities – Inquire about common comorbidities of obesity in close family members, such as cardiovascular disease, hypertension, diabetes, liver or gallbladder disease, and respiratory problems (severe asthma or sleep apnea) in first- and second-degree relatives (grandparents, uncles, aunts, half-siblings, nephews, and nieces). The presence of such comorbidities predicts the child's future risk, regardless of whether the affected family member has obesity. Maternal gestational diabetes is associated with adverse cardiometabolic outcomes in the offspring [22].

Family dynamics — Information about the family's social context and behavioral habits is valuable background for planning interventions. This includes economic or cultural factors that may affect a family's ability or readiness to make changes in diet or physical activity, parenting style (authoritarian, collaborative, or permissive), and attitudes toward their child's weight problem. These issues are discussed separately. (See "Prevention and management of childhood obesity in the primary care setting", section on 'Understanding the family context'.)

Psychosocial history — Key elements are:

●Anxiety and depression – Anxiety and depression can disrupt eating patterns, promote obesity, and interfere with weight management interventions. (See "Anxiety disorders in children and adolescents: Assessment and diagnosis" and "Pediatric unipolar depression: Epidemiology, clinical features, assessment, and diagnosis".)

●Eating disorders – Suggested by a history of inability to control consumption of large amounts of food, self-induced vomiting or laxative use to avoid weight gain, or dorsal finger lesions. These patients should be evaluated by a therapist with experience in eating disorders and should not participate in weight management programs without the concurrence of a therapist [11,23]. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis".)

●Events – Possible triggering events such as a loss of a loved one (death or relocation), divorce, or changes in primary caregiver(s).

●School function and social issues – Academic performance and trends; social function (eg, does the child have friends, and are they a target for teasing?).

●Smoking or vaping – Cigarette smoking increases long-term cardiovascular risk [24,25]. The risks of vaping nicotine (via e-cigarettes or other electronic devices) have not been established but include nicotine dependence, which may, in turn, promote combustible tobacco use. (See "Overview of the health consequences of obesity in children and adolescents" and "Prevention of smoking and vaping initiation in children and adolescents", section on 'Vaping nicotine'.)

In addition, fear of weight gain may be a barrier to smoking cessation in adolescents and this concern should be addressed specifically in counseling. (See "Management of smoking and vaping cessation in adolescents", section on 'Address barriers to quitting'.)

●Social drivers of health – Key factors include poverty, food insecurity, access to sources of healthy food and recreation, and transportation [26-28]. Exposure to racism is also associated with effects on mental and physical health, including risk of obesity, independent of socioeconomic status [29,30].

PHYSICAL EXAMINATION — 

The physical examination should evaluate for comorbidities and possible causes of the obesity [2]. Key findings to note are shown in the table (table 11A). Details about rare syndromic or endocrine forms of obesity are summarized in these tables (table 3A and table 11B) and described separately. (See "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Etiology'.)

●General examination – Assess the general appearance/mood; look for dysmorphic features, which may suggest a genetic syndrome (table 3A-B) [2]. In addition, assess the fat distribution:

•A markedly Cushingoid fat distribution (concentrated in the interscapular area, face, neck, and trunk) suggests the possibility of Cushing syndrome, although this distribution of fat may also be seen in exogenous obesity (caused by a combination of genetic predisposition and excessive caloric intake). (See "Definition, epidemiology, and etiology of obesity in children and adolescents", section on 'Endocrine disorders' and "Epidemiology and clinical manifestations of Cushing syndrome".)

•Abdominal obesity (also called central, visceral, android, or male-type obesity) is associated with certain comorbidities, including metabolic syndrome, polycystic ovary syndrome, and insulin resistance. Waist circumference or other indices of abdominal obesity are associated with these comorbidities on a population level. However, these measures are weak predictors of cardiovascular risk, so they have limited utility for clinical care of individual patients. Abdominal obesity and measurement of the waist circumference are discussed separately. (See "Measurement of body composition in children", section on 'Fat distribution' and "Overview of the health consequences of obesity in children and adolescents", section on 'Metabolic syndrome' and "Definition, clinical features, and differential diagnosis of polycystic ovary syndrome (PCOS) in adolescents".)

●Blood pressure – Blood pressure should be carefully measured starting at age three years using a properly sized cuff. The bladder of the cuff should cover at least 80 percent of the arm circumference (the width of the bladder will be approximately 40 percent of the arm circumference) (figure 3) [31]. In many children and adolescents with obesity, this will require use of adult-sized or large adult-sized cuffs.

Hypertension is defined as systolic or diastolic blood pressure ≥95^th percentile for children 1 to 13 years and ≥130/80 for adolescents 13 years and older on at least three occasions (table 12) [31]. Blood pressure percentiles can be derived from a calculator (calculator 3) or normative tables. (See "Hypertension in children and adolescents: Definition and diagnosis".)

Hypertension increases the long-term cardiovascular risk in children with excess body weight [2]. Occasionally, hypertension is a sign of Cushing syndrome. (See "Hypertension in children and adolescents: Nonemergency treatment".)

●Stature – Assessment of stature and height velocity provides some clues to help distinguish common exogenous obesity (caused by a combination of genetic predisposition and excessive caloric intake) from obesity that is secondary to genetic or endocrine abnormalities [32,33].

•Children with exogenous obesity are often tall for their age; the mechanism may involve trophic factors such as hyperinsulinemia, which accelerates skeletal maturation. However, they may also have earlier epiphyseal fusion, so the effects on adult height are variable.

•By contrast, children with endocrine and genetic causes of obesity often have short stature. As an example, decreased height velocity is an early sign in Cushing disease (figure 4). Children with Prader-Willi syndrome are often short for their genetic potential and/or fail to have a pubertal growth spurt. A useful (but imprecise and unvalidated) screen for a possible endocrine cause of obesity is the combination of a weight above the 95^th percentile for age and sex but a height below the 50^th percentile, taking into account parental height. (See "Prader-Willi syndrome: Clinical features and diagnosis".)

●Examination of the head, eyes, ears, nose, and throat (HEENT)

•Enlarged tonsils suggest increased risk for obstructive sleep apnea. (See "Evaluation of suspected obstructive sleep apnea in children".)

•Erosion of the tooth enamel may indicate self-induced vomiting in patients with an eating disorder. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis".)

•Blurred optic disc margins (picture 1) may indicate pseudotumor cerebri, an unexplained but not uncommon association with obesity [34]. (See "Idiopathic intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis".)

•Nystagmus or visual complaints raise the possibility of a hypothalamic-pituitary lesion [32]. Other findings that support this possibility are rapid onset of obesity or hyperphagia, decrease in height velocity, precocious puberty, and neurologic symptoms [32]. (See "Clinical manifestations and diagnosis of central nervous system tumors in children".)

•Microcephaly is a feature of Cohen syndrome (in addition to other dysmorphic features).

•Clumps of pigment in the peripheral retina may indicate retinitis pigmentosa, which occurs in Bardet-Biedl syndrome.

●Skin and hair

•Acanthosis nigricans (picture 2A-D) may signify insulin resistance with or without type 2 diabetes [35].

•Hirsutism and acne are common features of polycystic ovary syndrome and Cushing syndrome.

•Striae distensae (stretch marks) are linear atrophic plaques in susceptible sites (eg, abdomen, breasts, thighs). They are initially pink or purple, then evolve to hypopigmented scar-like depressions with fine wrinkling. They are usually the result of rapid weight gain but also may be manifestations of Cushing syndrome. (See "Striae distensae (stretch marks)".)

•Dry, coarse, or brittle hair may be present in hypothyroidism. (See "Clinical manifestations of hypothyroidism".)

•Red hair (in individuals with light skin pigmentation), hyperphagia, and early onset of obesity are features of proopiomelanocortin deficiency. In addition, people with this condition have low levels of adrenocorticotropic hormone with associated adrenal insufficiency. (See "Obesity: Genetic contribution and pathophysiology", section on 'Proopiomelanocortin'.)

●Abdomen

•Abdominal tenderness, particularly in the right upper quadrant, may be a sign of gallbladder disease. Occasionally, tenderness is related to metabolic dysfunction-associated steatotic liver disease (MASLD; formerly known as nonalcoholic fatty liver disease), although this condition is often asymptomatic [2].

•Hepatomegaly may be a clue to MASLD [2]. (See "Metabolic dysfunction-associated steatotic liver disease in children and adolescents".)

●Musculoskeletal

•Limited range of motion at the hip or a gait abnormality may be caused by slipped capital femoral epiphysis. Children with acute symptoms of slipped capital femoral epiphysis should immediately stop all weightbearing activity (including walking) to prevent further displacement pending a full evaluation [2]. (See "Evaluation and management of slipped capital femoral epiphysis (SCFE)".)

•Genu varum (bow legs) or valgus (knock-knees). (See "Overview of the health consequences of obesity in children and adolescents", section on 'Genu varus or valgus'.)

•Nonpitting edema may indicate hypothyroidism. (See "Clinical manifestations of hypothyroidism".)

•Dorsal finger callousness may be a clue to self-induced vomiting in patients with an eating disorder. (See "Eating disorders: Overview of epidemiology, clinical features, and diagnosis".)

•Postaxial polydactyly (an extra digit next to the fifth digit) may be present in Bardet-Biedl syndrome [36], and small hands and feet may be present in Prader-Willi syndrome (table 3A-B) [2]. (See "Prader-Willi syndrome: Clinical features and diagnosis".)

•Pes planus (flat feet) and pronation of the feet are common in children with obesity and frequently give rise to pain during exercise [37-39].

●Genitourinary – Endocrine or genetic causes of obesity are often associated with hypogonadism [2]. Evaluation of pubertal stage is discussed separately. (See "Normal puberty", section on 'Secondary sex characteristics (Tanner stages)'.)

•Undescended testicles, small penis, and scrotal hypoplasia may indicate Prader-Willi syndrome.

•Small testes may suggest Prader-Willi or Bardet-Biedl syndrome [36].

•Delayed or absent puberty may occur in the presence of hypothalamic-pituitary tumors, Prader-Willi syndrome, Bardet-Biedl syndrome, leptin deficiency, or leptin receptor deficiency (table 3A-B).

•Precocious puberty occasionally is a presenting symptom of a hypothalamic-pituitary lesion or dysfunction, including in ROHHAD(NET) syndrome [32]. Children with Prader-Willi syndrome often have premature adrenarche.

(See "Clinical manifestations and diagnosis of central nervous system tumors in children" and "Definition, etiology, and evaluation of precocious puberty" and "Prader-Willi syndrome: Clinical features and diagnosis", section on 'Clinical manifestations'.)

●Development – Most of the syndromic causes of overweight in children are associated with cognitive or developmental delay (table 3A-B). Prader-Willi syndrome is also associated with marked hypotonia during infancy and delayed development of gross motor skills. (See "Prader-Willi syndrome: Clinical features and diagnosis", section on 'Clinical manifestations'.)

FURTHER EVALUATION

Routine blood tests — We suggest routine screening for the following comorbidities (table 13A) [2,33]. Details on evaluation and management are provided through the links below:

●Dyslipidemia – Screening consists of a fasting lipid profile (total cholesterol, triglycerides, and high- and low-density lipoprotein cholesterols). The approach to lipid screening and follow-up is summarized in the algorithms (algorithm 1A-B) and detailed in a separate topic. (See "Dyslipidemia in children and adolescents: Definition, screening, and diagnosis", section on 'Approach to screening'.)

●Type 2 diabetes mellitus – Laboratory testing for diabetes is suggested for children with overweight or obesity and additional risk factors (table 13B). Screening consists of either fasting plasma glucose or hemoglobin A1c. Measurement of a fasting insulin level is not recommended for screening or clinical decision-making [40]. (See "Epidemiology, presentation, and diagnosis of type 2 diabetes mellitus in children and adolescents", section on 'Screening'.)

●Metabolic dysfunction-associated steatotic liver disease (MASLD) – MASLD was previously known as nonalcoholic fatty liver disease. Screening is performed with a serum alanine aminotransferase (ALT) level. Measure starting between 9 and 11 years of age. If normal, repeat at least every two to three years [41]. Sustained elevations of ALT (eg, >2 times the upper limit of normal [ULN] for six months) warrant further evaluation.

For ALT interpretation, use the ULN of 22 units/L for girls and 26 units/L for boys [42]. Note that these values are substantially lower than the ULNs reported in most pediatric hospital laboratories. However, it is important to note that liver transaminases have only moderate sensitivity and specificity for detecting clinically significant MASLD. (See "Overview of the health consequences of obesity in children and adolescents", section on 'Metabolic dysfunction-associated steatotic liver disease (nonalcoholic fatty liver disease)' and "Metabolic dysfunction-associated steatotic liver disease in children and adolescents".)

Tests for selected patients — Additional testing may be warranted for selected patients, as outlined in the table (table 13A) [43-45].

●Tests for causes of obesity

•Hypothyroidism or Cushing syndrome – Routine laboratory screening for hypothyroidism or Cushing syndrome is not recommended [33,46]. However, testing is appropriate if there are suggestive signs or symptoms, particularly evidence of growth attenuation (decreased height velocity). Mildly elevated levels of thyroid-stimulating hormone are more often found in children with obesity compared with normal-weight peers, but this is a consequence rather than a cause of the obesity [47]. (See "Establishing the diagnosis of Cushing syndrome" and "Acquired hypothyroidism in childhood and adolescence".)

•Syndromic obesity – Children with developmental delay or dysmorphic features should be evaluated for syndromic obesity (table 3A), including specific testing for Prader-Willi syndrome for those with suggestive features. (See "Prader-Willi syndrome: Clinical features and diagnosis".)

•Severe early-onset obesity – Screening for genetic obesity syndromes may also be appropriate for children with severe early-onset obesity (younger than five years of age) and especially those with marked hyperphagia, developmental delay, or other syndromic features (table 3A-B); some of these disorders have specific treatments. This approach was suggested in an Endocrine Society guideline, but such testing may be costly and the overall yield is low [33]. This screening can be efficiently performed using a genetic testing panel (ie, a panel for early-onset or monogenic obesity) [48,49]. Interpretation of panel results can be challenging. Variants of uncertain significance are common and generally do not require further evaluation or change in management. Variants identified as "pathogenic" or "likely pathogenic" are probably clinically significant and warrant referral for expert interpretation and management. A list of laboratories that perform such tests is available at the Genetic Testing Registry website. Details about monogenic causes of obesity are discussed separately. (See "Obesity: Genetic contribution and pathophysiology", section on 'Monogenic forms of obesity'.)

●Evaluation for comorbidities

•Vitamin D deficiency – Children with obesity have an increased risk for low vitamin D levels compared with children with healthy weight [50-53]. However, variable assays and cutoffs make classification uncertain, and serum levels may not reflect bioavailability. Therefore, decisions about vitamin D supplementation should be guided by assessment of dietary intake of vitamin D (eg, low milk intake) rather than routine screening of serum vitamin D levels [40,54]. (See "Vitamin D insufficiency and deficiency in children and adolescents", section on 'Obesity'.)

•Hypertension – For children with hypertension, additional laboratory testing may be warranted (eg, serum electrolytes, blood urea nitrogen, creatinine, and urinalysis). (See "Hypertension in children and adolescents: Evaluation".)

•Polycystic ovary syndrome – Laboratory testing is warranted in females with symptoms suggesting polycystic ovary syndrome, ie, an irregular menstrual pattern, hirsutism or treatment-resistant acne, or acanthosis nigricans with central obesity. (See "Diagnostic evaluation of polycystic ovary syndrome (PCOS) in adolescents".)

Imaging — The radiographic evaluation of children with obesity is directed by findings on the history and physical examination.

●Plain radiographs of the lower extremities should be obtained if there are clinical findings consistent with slipped capital femoral epiphysis (hip or knee pain, limited range of motion, abnormal gait) or Blount disease (bowed tibia). (See "Evaluation and management of slipped capital femoral epiphysis (SCFE)", section on 'Radiologic evaluation'.)

●Abdominal ultrasonography may be indicated in children with findings consistent with gallstones (eg, abdominal pain, abnormal transaminases).

●Abdominal ultrasonography is not recommended as a routine screening test for MASLD in children with obesity, because it is not a useful predictor of clinically significant disease. However, for children with persistently elevated serum aminotransferases, ultrasound or other radiographic evaluation may be indicated as part of a full evaluation for suspected MASLD. (See "Overview of the health consequences of obesity in children and adolescents", section on 'Metabolic dysfunction-associated steatotic liver disease (nonalcoholic fatty liver disease)' and "Metabolic dysfunction-associated steatotic liver disease in children and adolescents", section on 'Screening'.)

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Obesity in children".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Weight and health in children (The Basics)")

SUMMARY AND RECOMMENDATIONS

●Body mass index (BMI) – BMI percentile is the accepted standard measure of obesity and overweight in children. "Obesity" is defined by a BMI ≥95^th percentile for age and sex, and "overweight" is defined by a BMI ≥85^th and <95^th percentile for age and sex (table 2). (See 'Body mass index' above.)

Height and weight should be measured and BMI calculated at least yearly in children older than two years. The results should be used to determine the child's weight category (table 2) and plotted on an appropriate growth curve to determine the BMI percentile and trend (figure 1A-B). For children with severe obesity, use of an extended growth chart facilitates tracking (Centers for Disease Control and Prevention extended BMI growth charts or (figure 2A-B)). (See 'Body mass index' above.)

●History – The history should include information about (see 'History' above):

•Onset of obesity and historical patterns of weight gain

•Child's diet and food preferences (table 4)

•Physical activity patterns and sedentary activities (screen time) (table 5)

•Sleep duration compared with recommended sleep time (table 6) and sleep-related symptoms such as snoring

•Review of systems for signs of comorbidities or syndromic obesity (table 9)

•Family history of obesity and comorbidities

•Psychosocial history including possible triggering events, school/social functioning, and social determinants of health (food insecurity and other challenges)

●Physical examination – The physical examination should evaluate for signs and symptoms of comorbidities and genetic and endocrinologic causes of overweight (table 11A-B). (See 'Physical examination' above.)

●Further evaluation – The laboratory evaluation for children with obesity is not standardized. Most experts suggest routine screening for dyslipidemia, hypertension, and metabolic dysfunction-associated steatotic liver disease (MASLD), as well as selective screening for type 2 diabetes in adolescents with risk factors (table 13A-B). Additional testing may be warranted for patients with signs or symptoms suggesting polycystic ovary syndrome, obstructive sleep apnea, hypothyroidism, Cushing syndrome, or orthopedic problems. (See 'Further evaluation' above.)

Screening for genetic obesity syndromes may be appropriate for children with severe early-onset obesity and especially those with marked hyperphagia, developmental delay, or other syndromic features (table 3A-B); some of these disorders have specific treatments. (See 'Tests for selected patients' above.)

●Initial management – Management strategies vary according to the child's age, weight status and trend, comorbidities, and history of interventions. A clinical approach to management in the primary care setting is summarized in the algorithm (algorithm 2) and detailed in a separate topic review. (See "Prevention and management of childhood obesity in the primary care setting".)