Primary care clinicians play an important role in the initial detection, evaluation, and progression of eating disorders. Early detection and management of an eating disorder may prevent or lessen the medical complications and psychological consequences associated with starvation and progression of the illness [57, 58]. Primary and secondary prevention is achieved by screening for eating disorders as part of routine annual health care, providing ongoing monitoring and documentation of weight and height on growth charts, and paying careful attention to the signs and symptoms of an early eating disorder [58]. Screening questions regarding eating patterns and body image that can be used for all adolescents and young adults presenting for routine health care are shown in Table 7.2. In addition, the SCOFF screening questionnaire, although not validated in children and adolescents, can provide a framework for screening (Table 7.3). A recent meta-analysis has shown this to be a very useful screening tool [59].

Concern with weight and body shape is extremely common during adolescence [60, 61]. A significant number of pre-adolescents may also have a desire to be thinner [62, 63]. Canadian, American, and Australian cross-sectional data suggest that more than one in five teenagers are “on a diet” at any given time [60, 62, 64, 65]. Approximately 40–66 % of teenage girls and 20–30 % of teenage boys have attempted dieting in the past [66]. Any evidence elicited on history or physical examination of dieting, excessive concern with weight or shape, weight loss or failure to gain weight as expected for age and developmental stage requires further attention. Careful assessment for the possibility of an eating disorder and close monitoring at intervals as frequent as every 1–2 weeks may be needed until the situation becomes clear [58]. Possible findings on physical examination are detailed in Table 7.4. In addition, when an adolescent is referred to their clinician because of concerns raised by parents, friends, or school that he or she is displaying evidence of an eating disorder, it is most likely that the adolescent does have an eating disorder [58]. These concerns should be taken very seriously even if the adolescent denies all symptoms.

Initial laboratory investigations in an eating disorder evaluation should include a complete blood count and differential, platelet count, electrolytes (including calcium, phosphate and magnesium), glucose, liver function tests, thyroid-stimulating hormone, erythrocyte sedimentation rate, and urinalysis. Markers of nutritional status (albumin, vitamin D, folate, vitamin B12, iron, and other minerals) may also be considered. Additional tests (urine pregnancy, luteinizing and follicle-stimulating hormone, prolactin, and estradiol) should be considered in patients who are amenorrheic or have delayed puberty. An electrocardiogram should be performed on all patients. Bone densitometry should be considered in those females who are amenorrheic for more than 6 months [67]. Other tests such as echocardiogram, upper gastrointestinal tract series, or brain imaging should be considered in select circumstances as guided by the history and physical examination. For example, magnetic resonance imaging and neuropsychological assessment may be needed for patients with atypical features, such as hallucinations, delusions, delirium, and persistent cognitive impairment, despite weight restoration [68]. Normal laboratory investigations in patients with eating disorders do not exclude serious illness or medical instability. A broad differential diagnosis for the adolescent with symptoms of an eating disorder should always be considered (Table 7.5).

Eating disorders in adolescents and young adults can cause serious medical complications in every organ system (Table 7.6) [42, 58, 69]. The medical complications occurring in individuals with an eating disorder are largely related to the effects of starvation, malnutrition, and weight-control behaviors such as vomiting and laxative abuse. The consequences of nutritional deprivation and metabolic impairment on the growing and developing adolescent body also depend on the length, severity, and number of episodes of restriction and, the timing of those episodes in relationship to normal periods of growth and physical development [70, 71].

Although many of the medical complications improve with nutritional rehabilitation and recovery from the eating disorder, some are potentially irreversible [42]. If the eating disorder occurs before the closure of the epiphyses, growth retardation may become potentially irreversible [72–76], resulting in failure to achieve expected adult height. Other potentially irreversible medical complications in adolescents include loss of dental enamel with chronic vomiting [77]; structural brain changes [39, 78]; pubertal delay or arrest [79]; and impaired acquisition of peak bone mass with an increased fracture risk secondary to low bone mineral density [80–83].

Eating disorders are life-threatening illnesses. At least one-third of all deaths in adults with anorexia nervosa are due to cardiac complications [84–86]. Cardiac abnormalities are often present in the early stages of the eating disorder and may be reversible with prompt identification and treatment [87–89]. Common cardiovascular complications include electrocardiographic abnormalities such as sinus bradycardia, decreased voltage and prolonged QTc, orthostatic hypotension, increased vagal tone, poor myocardial contractility, mitral valve prolapse, reduction in left ventricular wall thickness and mass, and silent pericardial effusion [42, 69, 87–92]. Sinus bradycardia is present in 35–95 % of adolescents with anorexia nervosa, and is believed to be due to the reported increased vagal tone and decreased metabolic rate [42, 69, 91, 92]. Electrocardiographic abnormalities may also be due to other secondary causes such as metabolic and electrolyte disturbances, illicit drugs, medications, or complementary and alternative therapies [42].

Cardiovascular complications occur not only in the initial stages of the disorder but also during refeeding. Refeeding syndrome is a term that refers to various metabolic abnormalities that occur in severely malnourished patients following carbohydrate administration [93, 94]. Clinically, refeeding syndrome consists of a constellation of cardiac, hematological, and neurological symptoms. It has been reported in 6 % of hospitalized patients and can include congestive heart failure and pedal edema, a prolonged QT interval with arrhythmia, tachycardia, and sudden cardiac death [68, 89]. Although multiple organ systems may be involved, cardiac and neurologic dysfunction has been noted in those most severely affected [94]. Hypophosphatemia, a potentially life-threatening complication, is recognized as the biochemical hallmark for refeeding syndrome [95]. Refeeding hypophosphatemia has been associated with the degree of malnutrition [96]. Other electrolyte derangements (i.e., hypokalemia, hypomagnesaemia, hypocalcemia) may also occur and generally result from transcellular shifts of fluid and electrolytes as well as total body depletion [95]. Electrolyte disturbances require immediate attention.

The major endocrine abnormalities associated with eating disorders include hypogonadotropic hypogonadism, hypercortisolemia, hypoglycemia, growth hormone resistance, impaired linear growth, and sick euthyroid syndrome [97, 98]. The clinical manifestation of dysfunctional hypothalamic–pituitary–ovarian axis is amenorrhea and pubertal delay [69]. Development of a low bone density is a serious complication in adolescents with eating disorders, as adolescence is a critical period for the attainment of peak skeletal mass [42]. The pathogenesis of bone loss is associated with impaired bone formation and increased bone resorption, hypoestrogenemia, decreased levels of IGF-1, low dehydroepiandrosterone (DHEA) concentrations, increased cortisol levels, physical activity, poor nutrition, reduced leptin levels, low calcium and vitamin D intake, and low body mass [42, 99]. Weight restoration and the resumption of menses is the safest and most effective way to increase bone mineralization in adolescents with anorexia nervosa [80, 100]. Oral estrogen–progesterone combination pills have not been proven to be effective in increasing bone mineral density. Recent data suggests that physiologic estrogen in the form of the transdermal patch in older girls (bone age >15 years) increases spine and hip bone mineral density. However, complete catch-up in bone mineralization did not occur [101]. In addition, a prospective, randomized controlled study using oral micronized DHEA and estrogen–progesterone combination pills prevented bone loss in young women with anorexia nervosa compared to the decrease in areal BMD in women receiving a placebo [102]. Although most of the endocrine changes that occur in anorexia nervosa represent physiologic adaptation to starvation, some may persist after recovery [97, 98].

Alteration in renal function manifesting as abnormal blood urea nitrogen, decreased glomerular filtration rate, hematuria, and proteinuria have been described in patients with eating disorders [69]. Urea and creatinine are generally low and normal concentrations may mask dehydration or renal dysfunction [103]. Further, 17 % of adolescents with anorexia nervosa have been shown to have nocturnal enuresis, which is thought to be related to decreased functional bladder capacity and detrusor instability [104].

Serum pH and electrolyte abnormalities are common and result from starvation, laxative abuse, diuretic use, dehydration, or the practice of water loading to artificially increase weight [69]. Metabolic alkalosis occurs in patients who vomit or abuse diuretics and acidosis in those misusing laxatives [103]. Hypokalemia frequently results from purging by vomiting or laxative abuse. Hyponatremia is often due to excessive water intake, but may also occur in chronic energy deprivation or diuretic misuse [103]. Symptoms of electrolyte abnormalities are rarely present or are denied by patients [69].

Hematologic abnormalities may include anemia, leukopenia, and thrombocytopenia [105, 106]. These changes are generally attributed to starvation-mediated gelatinous bone marrow transformation, which resolves with proper nutritional rehabilitation [105, 106]. Gastrointestinal abnormalities include slowed gastric emptying, constipation, abdominal bloating and pain, and elevated aminotransferases. Abnormalities of liver enzymes may occur before or during refeeding [103]. Hypercholesterolemia is another common finding but its significance for cardiovascular risk is uncertain [103]. Other abnormalities include micronutrient deficiencies, hyperamylasemia, hypercarotenemia, elevated creatine kinase, xerosis, lanugo-like body hair, acrocyanosis, slower wound healing, and reduced fever response [103, 107–109].

Eating disorders are associated with extremely complex medical and psychosocial issues that are best addressed by an interdisciplinary team of medical, nutritional, mental health, and nursing professionals who are skilled and knowledgeable in working with adolescents with eating disorders and their families [57, 110]. Initial evaluation of the adolescent with a suspected eating disorder includes establishment of the diagnosis; determination of severity, including evaluation of medical and nutritional status; and performance of an initial psychosocial evaluation. Depending on the patient and family circumstances, various levels of treatment options are available for adolescents with eating disorders (inpatient, outpatient, day hospital, or residential treatment). The time to full recovery from an eating disorder may take several years [111].

Indications for hospitalization are listed in Table 7.7 [57, 58, 110]. The main goals of inpatient treatment are medical stabilization and weight restoration through nutritional rehabilitation (about 2–3 lbs per week). Recent studies have shown that safe weight gain can occur starting with approximately 1,400—2,000 kcal/day with regular nutritional advancements [96, 112–114]. Close monitoring of weight, vital signs, fluid shifts, and serum electrolytes during the first week of hospitalization is recommended [96, 112–114]. Attempts should be made to achieve weight gain through the oral route; however, short-term nasogastric feeding may be necessary in some patients. Supplementation with calcium (1,300 mg/day), in accordance with the Institute of Medicine recommendations for adolescents [115] and vitamin D (600–1,000 IU) is often necessary. The recommended length of hospitalization has not been established, although risk of relapse is lower in patients who are discharged closer to ideal body weight compared to patients discharged at very low body weight [116].

All adolescents with eating disorders should undergo a mental health evaluation, and be evaluated for potential treatment, which may include the use of anxiolytic or antidepressant medications. Although there remains relatively little research on interventions that address the complex mental and physical needs of adolescents with eating disorders, evidence-based research supports that family-based treatment, also known as the Maudsley approach, is an effective first-line outpatient treatment for adolescents with eating disorders and protective against relapse, particularly in anorexia nervosa [117–120]. Family-based treatment is an intensive outpatient treatment that utilizes parents/caregivers as a primary resource to renourish their affected child or adolescent [121]. Typically, one therapist is involved, along with a physician to provide medical care [122]. Although family-based treatment is effective for adolescents with bulimia nervosa, cognitive-behavioral therapy that focuses on changing the specific eating attitudes and behaviors that maintain the eating disorder may be more effective in older adolescents and young adults [123]. The evidence for binge-eating disorders in adolescents is insufficient to draw any conclusions; however, cognitive-behavioral therapy, interpersonal therapy, and dialectical behavior therapy may be helpful [123]. It is important to note that correction of malnutrition is required for the mental health aspects of care to be effective.

The literature regarding treatment efficacy and outcomes for eating disorders in adults is of highly variable quality [120, 124]. Current evidence does not suggest any one particular psychotherapeutic modality for adults with anorexia nervosa [125]. In bulimia nervosa, cognitive-behavioral therapy is frequently used and may reduce the risk of relapse after weight restoration [110, 124, 126, 127]. Psychological interventions that have shown effective in the treatment of bulimia nervosa also show promise in binge-eating disorder, particularly modified cognitive-behavioral therapy, interpersonal therapy, and dialectical behavior therapy (dialectical behavior therapy, also known as DBT, combines cognitive-behavioral approaches for emotion regulation and reality-testing) [128, 129].

The literature on pharmacologic treatment in either in the acute or maintenance phases of anorexia nervosa remains sparse and inconclusive [38, 130]. There is currently no strong evidence of beneficial effects using antidepressants and antipsychotics in adolescents and adults with anorexia nervosa [130, 131]. Medications, specifically selective serotonin reuptake inhibitors (such as fluoxetine, sertraline, paroxetine, fluvoxamine, and citalopram) may be used to treat comorbid psychiatric disorders such as anxiety, depression, and obsessive compulsive disorder or behavior [132]. There is conflicting evidence as to whether antidepressants reduce the risk of relapse in older adolescents with anorexia nervosa who have attained 85 % of expected body weight [133]. The use of atypical antipsychotics in adolescents with anorexia nervosa is encouraging; however, it is limited to case series and case reports [134–136]. These medications have been shown to be effective in reducing anxiety and obsessional thinking in adolescents with anorexia nervosa.