Average blood pressures have risen along with BMI in the last 3 decades. The prevalence of hypertension in obese patients is difficult to assess in the current literature as most studies are cross sectional and do not follow recommendations for diagnosing hypertension. Recent studies that follow more rigorous diagnosis protocols suggest that only 0.3–3.4 % are hypertensive [9, 10]. Risk factors for developing hypertension includes African-American or Mexican-American background, male gender, overweight or obese BMI, and family history of hypertension.

Blood pressure measurements should be a routine part of medical visits. Correct measurement requires that the patient be seated for 5 min, the cuff is the correct size, and the patient’s right arm is supported at heart level when the measurement is taken. A small cuff will falsely elevate the reading as will a pressure taken with the patient talking or without adequate rest [11]. A proper cuff size is one in which the bladder width covers 40 % of the arm circumference and the length covers 80–100 % of the arm circumference [12].

Classification of BP is determined by using the American Heart Association (AHA) charts for pediatric blood pressure ranges and is described as normal, pre-hypertensive, Stage 1 and Stage 2 hypertension (see Table 20.1) [13]. Any blood pressures that are >90 percentile should be repeated manually at the end of the visit. A diagnosis of hypertension requires three separate readings done over days or weeks.

Further evaluation differentiates secondary from essential hypertension. Secondary causes are more common in younger children and include renal disease, medication side effects, obstructive sleep apnea, and rarer causes such as pheochromocytoma, Cushing’s syndrome, and congenital adrenal hyperplasia. It is important to evaluate renal function with renal ultrasound with Doppler, renal panel, complete blood count, and urinalysis [13]. Those with Stage 2 hypertension require a more detailed evaluation; in such cases, consider referral to a pediatric hypertension specialist.

Abnormal lipid values in childhood are risk factors for subsequent heart disease [14], and improvements can be achieved through dietary changes [15] as well as with medication [16]. Recent recommendations from NHLBI propose universal screening, regardless of family history, weight, or other risk factors, at two different age periods: 9–11 years and 17–21 years. Screening from age 2 to 8 years should occur when BMI ≥ 95th percentile or in the presence of other risk factors. Screening between ages 17–21 years should be done when BMI ≥ 85th percentile or in the presence of other risk factors. An abnormality in a fasting lipid panel (see Table 20.1 for cut points) should be confirmed with a second panel 2 week–3 months after the first, with results averaged. A non-fasting lipid panel can be performed as a prescreen. If total cholesterol minus HDL is >145 mg/dL, the fasting lipid panel should be evaluated and repeated if any values on that panel are abnormal [17].

Common patterns of dyslipidemia in obesity include combined hyperlipidemia (elevated triglyceride, depressed HDL, and normal or mildly elevated LDL) or elevated LDL alone. Both patterns are associated with initiation and progression of atherosclerotic lesions in children. Both show improvement with diet and activity changes and weight control, which should be the first line of treatment. More aggressive intervention may be needed in severe triglyceride elevation (>500 mg/dL) or severe LDL elevation (>169 mg/dL).

Altered glucose metabolism in the obese patient begins with insulin resistance (IR) and can progress to prediabetes and then diabetes. Current best practices do not recommend routine laboratory screening for IR in obese children. Fasting insulin is not an accurate marker of whole body impairment of glucose metabolism although it may identify compensatory hyperinsulinemia. Physical signs of insulin resistance will be discussed further in the skin subsection. Factors associated with insulin resistance include puberty (a time when insulin sensitivity is lower), Hispanic, and African-American race (blunted compensatory increase in insulin levels), visceral adiposity, polycystic ovary syndrome, and fatty liver disease [18].

The incidence of newly diagnosed Type 2 diabetes mellitus has risen and now accounts for 46 %, 57.8 % of, 69.7 % and 86.2 % of newly diagnosed diabetes cases in Hispanic, African-American, Asian/pacific Islander, and American Indian youth ages 10–19 years, respectively, [10]. Indications for screening include elevated BMI, acanthosis nigricans, and family history of diabetes. Four screening methods are available for screening: random blood glucose, fasting blood glucose, 2-h oral glucose tolerance test, and glycosylated hemoglobin [19]. Per American Diabetes Association guidelines, unless there is “unequivocal hyperglycemia,” one abnormal screening test should be confirmed with repeat testing. Hemoglobin A1C may not be an ideal test in those with anemia or conditions that alter the rate of red blood cell turnover.

Metabolic syndrome (MetS) is a constellation of symptoms that are known to increase the risk of developing cardiovascular disease in adulthood [20]. Other terms for MetS are Syndrome X and cardiometabolic syndrome. Currently recognized components of MetS include elevated blood pressure, impaired glucose metabolism as noted by insulin resistance or glucose intolerance, dyslipidemia noted by low HDL and elevated triglycerides, high waist circumference, and obese BMI. Metabolic syndrome is defined as three abnormal components, but the criteria for abnormal values vary based on patient age and which of the more than eight existing sets of criteria is used [21]. Prevalence of the syndrome ranges from 2 to 39 % depending on the definition used [21–23]. Caution is needed when diagnosing MetS due to instability of the individual components during childhood and adolescence [17, 23]. In addition, cut points considered abnormal in MetS definitions may fall within the normal range on laboratory reports.

Non-alcoholic fatty liver disease (NAFLD) is a silent and serious condition that is challenging to diagnose and treat. NAFLD is the accumulation of triglycerides in liver cells, not related to alcohol or other toxins or metabolic conditions. Simple fat accumulation (steatosis) can progress to inflammation (nonalcoholic steatohepatitis or NASH), which in turn can progress to fibrosis and ultimately cirrhosis. Risk factors are obesity, diabetes or family history of diabetes, and Latino background. Relative to white patients, African-American patients have a low risk despite a high population prevalence of obesity and diabetes. Currently, confirmation and staging of NAFLD require a liver biopsy. An autopsy study found that prevalence among children of all weight categories is low until age 10 years, when it is 11 %, and rises further by mid-teen years. About 25 % of children with NAFLD have NASH, and about 10 % with NAFLD have advanced fibrosis or cirrhosis. Obesity greatly increases the risk [24]. Weight loss can reverse the condition, but effective pharmaceutical treatment has not yet been identified. There is debate about the use of serum alanine aminotransferase (ALT) as a screening tool. Although ALT elevation of 1.5–3 times normal in a high risk patient is suggestive of NAFLD, it is not specific for NAFLD and the degree of elevation does not correlate with stage of NAFLD. Patients with normal ALT can have advanced NAFLD. Those who oppose its use cite its low sensitivity and the lack of treatment options other than weight loss, which generally should be recommended in the presence of obesity. Those who support its use point to NAFLD’s high prevalence and potential severity and to the change in monitoring and management when cirrhosis is identified. Recommendations by an Expert Panel on Child and Adolescent Obesity suggested screening with transaminases every 2 years, starting at approximately 10 years of age, to coincide with recommendations for screening for diabetes [25]. In the absence of underlying evidence, clinicians may use judgment given more recent information about low prevalence among African-American youth. When elevations are in the 1.5–3 times normal range, one approach is to counsel healthy lifestyle and weight control. If elevations persist for 6 months or more, refer to specialist for further management. Specialists will be best positioned to evaluate need for biopsy and also will be aware of emerging studies on medication.

Common skin conditions include acanthosis nigricans, striae distensae, skin infections, and acrochordon (skin tags) [26]. Many skin lesions found in obese patients are in part due to hyperinsulinemia and its effect on IGF-1 receptors in skin. The overgrowth of keratinocytes and fibroblasts results in increased cell growth, which leads to conditions such as acanthosis nigricans, acrochordons, and hidradenitis suppurativa [27]. Often, the lesions are found in intertriginous areas. A close examination of the skin folds of obese patients is important and can be done best when the patient is wearing a gown.

Striae distensae (stretch marks) represent a loss of elasticity in the skin, manifested by linear areas of thinned skin. They are often pink in color and become less pigmented with time. They occur during times of rapid growth, either linear or in girth, and are typically located on upper arms, buttocks, hips, abdomen, and breast. Wide purple striae may be a sign of Cushing’s syndrome.

Acanthosis nigricans is lichenified, velvety, and hyperpigmented lesions of the skin. It is primarily located along the skin folds of the neck, axilla, and groin although it may be present in other areas of the body as well. In the development of acanthosis nigricans, the skin initially looks mildly hyperpigmented (parents may believe their child’s skin is dirty) and then progresses to appear thickened and velvety. As it progresses further, the lesions may involve larger portions of the body. Involvement of the oral mucosa, palms, or soles may be a sign of malignancy or drug-induced acanthosis nigricans. A grading system for acanthosis nigricans located on the neck has been proposed: grade 1 lesions are present only on close observation, grade 2 lesions are at the base of the skull, <3 in. in breadth and do not extend to lateral neck, grade 3 lesions extend to lateral margins of neck but are not visible from front, and grade 4 are visible from the front [28]. Use of a grading system assists with monitoring progression or resolution of lesions.

Acrochordons (skin tags) are commonly seen in obese adults though they may be present in older children and adolescents. They present as soft, flesh-colored, pedunculated growths in intertriginous areas such as the neck, axilla, and groin. If they are present in very young children or in those who are not obesity or insulin resistant, a dermatology referral should be made.

Intertrigo describes superficial skin infections within the skin folds. They appear as painful, moist, macerated areas usually along the abdominal pannus and groin. Common organisms include yeast, bacteria, and dermatophytes. Recurrent deep boils may be a sign of hidradenitis suppurativa.

In obstructive sleep apnea (OSA), the consequences of oxygen desaturation and hypercapnea from the upper airway resistance include systemic hypertension, left ventricular dysfunction, and pulmonary hypertension. In addition, poor sleep compromises neurocognitive function. The incidence of OSA in children is estimated to be 3–4 % in population studies [29, 30]. Among severely obese children, prevalence seems to be much higher [31]. There is not a highly sensitive set of questions that screen for OSA. Most children with OSA snore, but many snorers do not have OSA. Daytime somnolence, assuming child is spending an appropriate amount of time in bed, can be a symptom, and also hyperactivity can reflect disrupted sleep, especially in younger children. A sleep study is a necessary tool to diagnose OSA [32]. Removal of enlarged tonsils and adenoids will improve airway function, but may not resolve the conditions, especially in the severely obese [33].

Obesity impacts the development of secondary sexual characteristics and long-term reproductive health. Obese girls undergo thelarche and menarche earlier than their normal weight peers [34]. Data is conflicting regarding males but also suggests earlier onset of puberty [35]. Males may have exaggerated pubertal gynecomastia or pseudogynecomastia (fatty infiltration of the breast). Obesity is associated with a higher prevalence of true gynecomastia in children and adults, likely because of increased conversion of testosterone to estradiol in adipose tissue [36, 37]. Among males, the increased mons fat pad that surrounds the phallus may result in a buried penis although when extended and measured, the phallus is of normal length. True microphallus and undescended testes may be a sign of Prader–Willi syndrome.

Polycystic ovary syndrome (PCOS) should be given special consideration in adolescent girls with irregular cycles. It is the most common endocrine abnormality in women and a common cause of infertility. Women with PCOS are less successful at losing weight and are at increased risk of developing cardiometabolic comorbidities, regardless of obesity [38]. PCOS is characterized by amenorrhea or oligomenorrhea (fewer than 9 cycles per year in women who have been menstruating for at least 3 years or <6 cycles per year for those menstruating for less than 3 years, physical or biochemical signs of androgen excess and/or polycystic ovaries on ultrasound [39–41]. Physical signs of androgen excess are hirsutism, clitoromegaly, acne, and androgenic alopecia. PCOS is a diagnosis of exclusion; therefore a full evaluation must be done to rule out other causes of androgen excess and oligo-amenorrhea including thyroid dysfunction, hyperprolactinemia, late onset congenital adrenal hyperplasia, premature ovarian failure, androgen-secreting tumor and Cushing’s syndrome. Work-up includes free and total testosterone, sex hormone binding globin, thyroid stimulating hormone, prolactin, dehydroepiandrostenedione sulfate (DHEAS), 17-hydroxyprogesterone, and pelvic ultrasound [42, 43].

Obese pediatric patients not only are prone to several specific musculoskeletal complications but also are at increased risk of fractures and have more complaints of foot and ankle pain then their normal weight peers [44, 45]. Review of systems often notes ankle, knee, hip, groin, and lower back complaints. Physical exam will identify bow-legs, pes planus (flat feet), limb length discrepancies, limited range of motion, and antalgic gait. Special attention should be paid to possible Blount’s disease (tibia vara) and slipped capital femoral epiphysis (SCFE). Blount’s presents with bowing of the legs from tibial torsion in the setting of excessive weight placed on medial tibial growth plate which inhibits growth medially while lateral growth continues unopposed. Blount’s is more common in African-American males [46]. Depending on the severity of obesity, bowing may not be as obvious though patient complains of knee or ankle pain. Diagnosis required X-rays of the lower extremities.

SCFE is the displacement of the femoral head off of the epiphyseal plate. Most cases occur in adolescents and an estimated 60 % of patients have BMI >90 percentile [47]. The incidence of SCFE has increased as BMIs have increased [48]. Chronic, dull hip pain and groin pain may be the presenting complaint. Diagnosis is made based on symptoms and hip radiographs. Anterior-posterior and lateral X-rays of the hips show a classic “ice cream falling off the cone” appearance. Both hips should be imaged because in a significant proportion of cases the condition is bilateral (20–40 %) [47]. Complications of SCFE include a vascular necrosis and loss of the particular cartilage.

Additional complaints include low back pain from an exaggerated lumbar lordosis secondary to weak core muscles and the strain of supporting large abdomens. Adolescent females may complain of shoulder and upper back pain due to heavy, poorly supported breasts. Having the patient walk without shoes will reveal pes planus and other foot deformities resulting from increased weight bearing on developing foot structures [49, 50].

Pseudotumor cerebri is defined as elevated intracranial pressure without an underlying mass, central nervous system infections, or other direct causes of increased pressure. The condition presents with severe headache, often accompanied by nausea, vomiting, and sometimes by neurological symptoms including visual loss from papilledema and diplopia from cranial nerve VI impairment. Visual loss can be permanent. In addition to being associated with medications, including vitamin A, growth hormone, and steroid withdrawal as well as infections, the condition appears to be association with obesity. The evidence for this association is strong in late teens and adults, but the rarity of the condition and the likelihood of an ascertainment bias make incidence and prevalence estimates unreliable. One study estimated an incidence rate of less than 2 per 100,000 for children under age 15, regardless of weight status or gender, but rates increasing to 20 per 100,000 among obese women 15–44 years of age [19]. Not all symptoms may be present [51], but severe headache, visual impairment, abnormal neurological examination, and papilledema should prompt urgent referral to neurology for neuroimaging and lumbar puncture.

Scientific understanding of influences on regulation of appetite, energy expenditure, and body composition is exploding. We now recognize the influences of adipocytes, the hypothalamus, gut and other hormones, and also a number of genes in the development of obesity. Clearly defined genetic syndromes or treatable endocrine disorders are small in number and their prevalence is low, and so the new scientific knowledge of physiologic “causes” for obesity have not yet led to specific treatment strategies. The role of the general clinician is to use the history and physical exam to identify those patients who need further evaluation.

Clinical hypothyroidism has an estimated prevalence of 2 in 1,000 in the US population 12 years and older [52] and is likely somewhat lower in children [53]. In contrast, about 300 of 1,000 children are overweight or obese. Thyroid screening should be limited to children with other symptoms, particularly linear growth cessation or short statue, but also depression, hair thinning, cold intolerance, and other clinical signs and symptoms of low thyroid hormone levels. Primary Cushing’s syndrome is very rare, less than 1 per 100,000 [54]. Screening for Cushing’s syndrome should be limited to children with short stature, hirsutism, striae, and central adiposity with excess weight on back (”buffalo hump”).

The presence of early severe obesity increases the likelihood of a genetic cause of obesity. Some well-recognized syndromes, like Prader–Willi or Bardet–Biedl, are associated with short stature and developmental delay. However, recently identified genetic variations are not uncommon among severely obese children, and they may have normal or accelerated linear growth and normal development. An excellent review article presents an algorithm for investigation of underlying causes of severe early obesity [55]. In contrast to the rarity of metabolic and genetic causes of obesity, medications, especially neuropsychiatric medications, are fairly common contributors to weight gain. If patients and prescribing physicians are aware of this risk and see weight gain, they can sometimes find less obesogenic alternatives. Table 20.2.