Chapter 291: Eating Disorders

Eating disorders, such as anorexia nervosa, bulimia nervosa, and binge-eating disorder, are psychological pathologies characterized by disordered relationships with food. Eating disorders are challenging to diagnose in the ED because physical manifestations may be subtle and historical features may not be elicited unless the disorder is suspected from medical complications or comorbidities. It is important for the emergency physician to recognize these conditions, however, because they are among the most deadly of psychiatric illnesses.¹ The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders refines the diagnostic criteria of eating disorders from the previous edition (Table 291-1).²

There are two subtypes of anorexia, restrictive and binge/purge, with crossover between the two subtypes.³ Patients with a predominantly restrictive pattern simply minimize their food intake. Patients with a predominantly binging/purging subtype make up for unaccepTable food intake with diuretics, laxatives, enemas, or vomiting. There are also two subtypes of bulimia: purging and nonpurging. Those who purge do so by the above methods; those classified as nonpurging may use compensatory methods such as fasting or excessive exercise. There is a moderate amount of crossover between anorexia and bulimia, with up to 50% of anorexia patients eventually developing bulimia.⁴ Binge eating disorder is characterized by habitual, recurrent binge consumptions that cause significant distress and is distinct from simple episodic overeating.

Anorexia nervosa has an overall incidence rate of 8 per 100,000 person-years,⁵ with an estimated lifetime prevalence of 0.9% in women and 0.3% in men.⁶ There is no significant difference in prevalence of anorexia between different races or ethnicities.⁷ Bulimia nervosa has an overall incidence rate of 12 per 100,000 person-years,⁵ with an estimated lifetime prevalence of 1.5% in women and 0.5% in men.⁶ Bulimia is more common in Latinos (lifetime prevalence of 2.03%) and African Americans (1.31%) than in whites (0.51%).⁷ Binge eating disorder is relatively more common in older individuals and males than both anorexia and bulimia.⁵ It is also more prevalent in minority groups than in non-Latino whites.⁷ In the United States, the incidence rate for those ≥14 years old is 1010 per 100,000 person-years in females and 660 per 100,000 person-years in males,⁸ with a lifetime prevalence of 3.5% in women and 2.0% among men.⁶ Although it is often associated with obesity, binge eating disorder is a distinct disorder.⁹

There are several biologic and psychosocial factors that predispose toward disordered eating. There is evidence that eating disorders run in families,¹⁰ possibly related to both genetic influences and similar underlying temperaments and behaviors.¹¹ Development of eating disorders has historically been associated with dysfunctional reward processing in relation to food,¹² but the pathogenesis of this abnormal response is not well understood.¹³ MRI studies detect altered subcortical and cortical brain behavior as well as structural brain differences in patients with eating disorders compared to normal controls. Some of these studies implicate differences in brain regions involved in reward processing, but results are inconsistent.^14,15,16 Patients with eating disorders also demonstrate differences in certain peripheral and central chemical modulators involved in eating behavior and energy homeostasis compared to controls, but it is not known if such changes are causal or correlative.¹⁷

HISTORY

Patients with eating disorders often present to the ED with vague signs and symptoms, such as weakness, fatigue, pallor, dizziness, syncope, confusion, bloating, edema, or persistent nausea.¹⁸ Alternatively complaints may be due to medical complications, such as chest pain and hematemesis caused by a Mallory-Weiss tear from purging; palpitations from electrolyte-induced dysrhythmias; dysmenorrhea from disruption of the hypothalamic-pituitary axis; or fractures from osteoporosis or extreme exercise. Depression, anxiety, substance abuse, self-injurious behavior, or suicidality may coexist.^19,20 A meta-analysis of 36 studies reviewing mortality rates for patients with eating disorders reported that one in five individuals with anorexia who died had committed suicide.²¹ Data on patients with bulimia or binge eating disorder are confounded by crossover diagnoses. Therefore, if an eating disorder is suspected, consider screening for depression and suicidality.

If clinical suspicion is raised for an eating disorder based on complaint cluster, physical examination, or family report, explore a more focused history. Important data points to elicit include eating and dieting behavior; desire for weight loss; typical daily dietary intake; presence or absence of calorie counting; compensatory exercise behavior; guilt patterns following eating; menstruation pattern; and use of over-the-counter dietary supplements or laxative agents. Certain sensitive history points may be difficult to elicit in the ED, such as early childhood GI issues or picky eating or obesity, self-esteem issues, societal thinness pressures, teasing, propensity toward perfectionism, or sexual abuse. Certain physical activities raise risk for eating disorders, such as gymnastics, ballet and other dance, wrestling, swimming, and cross-country running.^22,23,24 Because eating disorders are characterized by denial of symptoms and behaviors, when eliciting history, take a nonjudgmental approach to encourage trust and truthful disclosure.¹⁹

PHYSICAL EXAMINATION

Patients with anorexia are typically easily identifiable based on a very thin body habitus. Other possible signs include hypotension (resting or orthostatic); bradycardia or tachydysrhythmia; or hypothermia. Patients may also exhibit signs of vitamin deficiencies such as brittle, flaking, or ridged nails (nonspecific malnutrition); stomatitis or cheilitis (B vitamin deficiency); or perifollicular petechiae (scurvy). They may also develop fine, long hair on the arms and face, acral cyanosis (impaired thermoregulation), and/or pretibial edema secondary to malnutrition.¹⁹

Patients with bulimia or binge eating disorder can be difficult to detect in the ED because they tend to be normal weight or even slightly overweight. Consider eating disorder diagnoses in the presence of other physical indicators, even in normal weight or overweight patients. Self-induced vomiting can cause painless hypertrophy of the parotid glands, dental erosion, and trauma or callous formation to the dorsal hands (Russell's sign),²⁵ as well as pharyngeal erythema or abrasions, gingivitis, facial petechiae or subconjunctival hemorrhage, and halitosis. Laxative abuse may cause peripheral edema, anal fissures, hemorrhoids, perianal dermatitis, and rectal bleeding. Binge eating disorder may have no abnormalities apparent on physical examination.

The SCOFF questionnaire (Table 291-2) is useful for screening for anorexia and bulimia in a brief ED encounter and can be remembered by its acronym: Sick, Control, One stone, Fat, Food.²⁶ Other screening tools are more extensive and are more useful in a primary care setting. For reference, the Eating Disorder Diagnostic Scale is a 22-point questionnaire that is self-administered and can identify risk for all three major eating disorders.²⁷ The Eating Attitudes Test is nonspecific and can identify need for referral to a mental health professional for further evaluation.²⁸ The Questionnaire on Eating and Weight Patterns-Revised is specific for binge eating disorder and displays a reasonable level of concordance between its scores and diagnostic interviews.²⁹

DIFFERENTIAL DIAGNOSIS

Consider organic pathology in the assessment of a patient with a potential eating disorder (Table 291-3).

LABORATORY TESTING

Initial testing should include a full chemistry panel including magnesium, calcium, and phosphorus, CBC, blood glucose, urinalysis, pregnancy test, hepatic function panel, serum albumin, lipase and amylase, and thyroid-stimulating hormone. Electrolyte derangements and other lab abnormalities are more common in purging-type eating disorders. Patients with restrictive-type anorexia may not demonstrate any laboratory abnormalities. Purging results in a metabolic alkalosis and may cause hypokalemia and hypochloremia. Purging and binge eating both may cause elevation of liver and pancreatic enzymes. Habitual vomiting can result in hyperamylasemia. Hyponatremia and hypochloremia are often seen in patients who vomit. Laxative and diuretic abuse and vomiting can lead to potassium depletion. Hyponatremia may develop in patients who abuse diuretics. Laxative abuse may cause a positive fecal occult blood test. Dehydration can lead to hemoconcentration. Malnutrition can cause low albumin. Starvation ketosis may cause spilling of ketones in the urine, and dehydration may cause increased urine specific gravity and urea concentration. In patients with very severe anorexia, anemia, leukopenia, hypoglycemia, and hypophosphatemia can develop.^19,30,31

IMAGING

Obtain imaging to rule out an underlying organic cause of presenting symptoms or to exclude medical complications; for example, obtain chest films to exclude Boerhaave's syndrome or abdominal radiographs to diagnose paralytic ileus or acute gastric dilatation. Radiographic findings in anorexia include decreased muscle mass, paucity of subcutaneous fat, mild small bowel dilatation,³² and osteoporosis.³³ These findings are reversed upon refeeding and appropriate weight gain. There are no specific radiographic findings diagnostic of binge eating disorder or bulimia, but a swallowed toothbrush or similar item suggests purging by induced vomiting.³⁴

Medical complications of eating disorders are many and varied. Medical complications of anorexia are typically more severe than bulimia or binge eating and are directly related to the starvation state. Bulimia medical complications are usually related to purging behaviors and are often the result of chemical derangements or structural damage to the GI tract.³⁵ The most common medical complication of binge eating is obesity, but acute structural complications such as gastric dilatation may also be seen.

CARDIOPULMONARY COMPLICATIONS

Among the most deadly of the eating disorder complications are changes to the cardiovascular system. Malnutrition in eating disorders leads to decreased muscle mass, including cardiac muscle mass, specifically in the interventricular septum and the left ventricle, as well as increased vagal tone. These effects lead to decreased contractility and cardiac output, and therefore result in hypotension, bradycardia, and orthostasis. Relative decreases in cardiac muscle mass compared to valve cross-sectional area can lead to the development of mitral valve prolapse.³⁶ Rarely, patients with anorexia nervosa can develop pericardial effusion, which in a few cases has led to cardiac tamponade requiring urgent pericardiocentesis.³⁷ Purging behavior leading to electrolyte abnormalities can cause cardiac arrhythmias. Syrup of ipecac, used as an emetogenic, is directly cardiotoxic and can cause an irreversible cardiomyopathy.³⁸ Prolongation of the QT interval on ECG has been described in patients with all types of eating disorders relative to controls. QT prolongation is a marker for risk of ventricular tachyarrhythmia, specifically torsades de pointes, and risk of sudden death. QT prolongation as a result of eating disorders is reversed by adequate refeeding and is associated with normalization of heart rate, heart rate variability, and exercise tolerance.³⁹ Therefore, QT normalization has been used as a marker to guide refeeding and rehabilitation.⁴⁰ Most cardiac sequelae are reversible with appropriate weight gain, but there is increased risk of cardiac complications during the first week of refeeding after severe nutrient depletion.^39,41 There are also case reports of pneumothorax and pneumomediastinum as complications of severe anorexia.⁴²

NUTRITIONAL COMPLICATIONS

The proportion of eating disorder patients with vitamin deficiencies is difficult to determine, because many patients take supplementary vitamins. Decreased bone mineral density was reported in 18% of patients age 15 to 54 years old admitted to a specialized eating disorders unit but was not associated with decreased vitamin D levels.⁴³ Deficiencies of other vitamins are rare, and typically merit case reports. Iron and vitamin B₁₂ deficiency can lead to anemia in severely food-restrictive patients. Skin erythema and pruritus with sun exposure, glossitis, epidermal desquamation, and diarrhea should raise suspicion of pellagra.⁴⁴ Confusion, confabulation, ataxia, ophthalmoplegia, and/or nystagmus suggest Wernicke-Korsakoff encephalopathy. Other vitamin deficiencies reported in association with eating disorders include wet beriberi and scurvy, although these are extremely rare.^45,46

Refeeding following prolonged nutrient depletion can cause electrolyte abnormalities, most commonly hypokalemia, hypophosphatemia, and hypomagnesemia, due to redistribution of electrolytes from the extracellular to the intracellular space triggered by insulin release and from depletion of phosphorus during protein synthesis. This can lead to arrhythmias, congestive heart failure, pericardial effusions, and cardiac arrest.⁴¹

GI COMPLICATIONS

Patients with anorexia are at increased risk of constipation, gastroparesis, gastric dilatation, and gastroesophageal reflux.^19,47 Gastroesophageal reflux and laryngopharyngeal reflux commonly occur in patients with bulimia and may result in hoarseness or dysphagia.^19,48 Chronic stimulant laxative abuse can lead to development of rectal prolapse, melanosis coli, or the cathartic colon syndrome.^49,50,51 Other very rare GI complications include superior mesenteric artery syndrome; gastric dilatation, necrosis, and rupture; necrotizing colitis; and gastric bezoar.^{42,52,53,54,55}

ENDOCRINE COMPLICATIONS

Profound food restriction affects the hypothalamic-pituitary axis. Low levels of gonadotropins, loss of the normal pulsatile waves of luteinizing hormone, and estrogen deficiency lead to hypothalamic amenorrhea.⁵⁶ Anorexia is also associated with the "euthyroid sick syndrome" in which thyroid-stimulating hormone is normal or slightly low, T₃ is low, and sometimes T₄ levels are also decreased. Thyroid deficiencies likely contribute to the bradycardia, orthostasis, and hypothermia in anorexia. High cortisol levels and low levels of insulin-like growth factor 1 (somatomedin C), T₃, estradiol, and testosterone contribute to loss of bone mass.⁵⁷ Refeeding and recovery from illness do not fully return bone mass to normal levels, and patients with anorexia remain at an increased risk of fracture for as many as 40 years following initial diagnosis.⁵⁸ The endocrine effects of bulimia and binge eating disorder are less well studied, more variable, and less predictable. Endocrine abnormalities in these disorders may be more related to comorbid obesity than to the eating disorder itself.

The ED treatment of eating disorders is limited to stabilization of urgent medical complications, followed by hospital admission or outpatient referral to a mental health specialist. Tables 291-4 and 291-5 list guidelines for hospital admission.^59,60 Treatment requires a multidisciplinary approach, including medical management with pharmacotherapy, dietary interventions, and psychotherapy.⁵⁹ If pharmacotherapy is indicated, it should be initiated by a psychiatrist or primary care provider. Selective serotonin reuptake inhibitors may alleviate comorbid psychiatric symptoms including depression and anxiety, but are not associated with improved weight gain or longer times to relapse in patients with anorexia.⁶¹ Fluoxetine is approved by the U.S. Food and Drug Administration for use in bulimia, and other antidepressants show some benefit in bulimia.⁶² Avoid bupropion in all patients with eating disorders because it can potentiate weight loss and reduce seizure threshold in patients with electrolyte abnormalities.

PREGNANT WOMEN

Pregnancy can be a particularly stressful time for a woman with an eating disorder, particularly with respect to maintaining adequate and appropriate weight gain for the pregnancy. There are conflicting data on whether the presence of eating disorders increases the risk of complications of pregnancy; certain studies have documented increased risk of miscarriage, lower birth weights, and lower Apgar scores, whereas others have reported no increase in medical complications and normal birth weights. However, the broadest study of its kind to date revealed that the majority of patients with anorexia and bulimia have normal pregnancies and healthy babies. There is, however, an increased risk of birth by cesarean section and an increased risk of postpartum depression following delivery, and these differences remained between groups who had active symptoms of their disease and those with a history of an eating disorder who were asymptomatic during pregnancy.⁶³

MEN

Do not neglect the possibility of eating disorders in males. Men may account for between 10% and 25% of cases of anorexia and bulimia,⁶⁴ but the exact proportion of men with eating disorders is unknown, because men are less likely to be diagnosed and appropriately treated than women. Of the eating disorders, binge eating disorder is more common in men than is anorexia or bulimia. Excessive exercise is a common compensation in men for overeating. Eating disorders in males are typically characterized by the drive to add muscle bulk and increase lean mass. Eating disorders in men are often associated with antecedent obesity, athletic performance concerns, bullying, and occasionally, but not always, sexual abuse. Men with eating disorders are also more likely to abuse steroids and growth hormones, particularly when muscle dysmorphia is present.⁶⁵