Approach to Eating Disorders

Elizabeth A. Lawson

Nancy A. Rigotti

Anorexia nervosa, bulimia nervosa (the binge-purge syndrome), and eating disorder not otherwise specified (i.e., eating disorder that does not meet criteria for anorexia nervosa or bulimia nervosa) are the three DSM-IV eating disorder diagnoses of adolescents and adults. Of the eating disorders not otherwise specified, binge eating disorder has received the most research attention. The lifetime prevalence estimates of anorexia nervosa, bulimia nervosa, and binge eating disorder in the United States are approximately 0.9%, 1.5%, and 3.5%, respectively, among women, and 0.3%, 0.5%, and 2.0%, respectively, among men.

These illnesses are psychiatric disorders that can have serious medical consequences and are associated with a high rate of comorbid anxiety, mood, and substance abuse disorders. They extend beyond racial and socioeconomic boundaries. Because patients with these conditions often hide the problem, a high index of suspicion is required for diagnosis. Primary care physicians need to be able to recognize these disorders, evaluate and treat their medical complications, arrange and coordinate a comprehensive multidisciplinary treatment program, assist in ambulatory monitoring, and determine when a patient requires hospitalization.

PATHOPHYSIOLOGY, CLINICAL PRESENTATION, AND COURSE (1, 2, 3, 4, 5, 6, 7, 8, 9 and 10)

Anorexia Nervosa

Anorexia nervosa is a syndrome characterized by severe weight loss resulting from inadequate food intake by persons with no medical reason to lose weight. A distorted body image and an intense fear of weight gain lead to the relentless pursuit of an unreasonable and unhealthy thinness. Weight is lost in two ways. Patients with restrictive anorexia nervosa starve themselves. In contrast, other patients have symptoms of bulimia nervosa and lose weight by purging after eating, usually by vomiting or taking laxatives. Those with bulimic symptoms may have a graver prognosis and more medical problems as complications of low weight are compounded by purging. Originally more prevalent among persons of high socioeconomic status, anorexia nervosa is now becoming more evenly distributed among socioeconomic groups.

Pathogenesis

The pathogenesis of anorexia nervosa is unknown but appears to be multifactorial. There is a genetic vulnerability to development of anorexia nervosa, though the specific genes involved have not been clearly identified. Neurochemical, psychological, and sociocultural factors have all been suggested as contributing factors. Neuroendocrine abnormalities are well documented (see later discussion). Although many of these hormonal alterations are a consequence of chronic starvation, there is increasing evidence to suggest that some may contribute to symptoms of anorexia nervosa.

Onset frequently coincides with a patient’s time of separation from home or the loss of a loved one. Others attribute anorexia nervosa to problems in emotional development and disturbed family interactions, although these may also be sequelae rather than causes of the eating disorder. Psychological studies find these patients to be bright, compulsive perfectionists who perform well at school and work. The prevalences of comorbid psychiatric disorders, including anxiety, depression, and obsessive-compulsive disorder, are increased among patients with anorexia nervosa. Sociocultural pressure to be thin also contributes to the problem.

Pathophysiology

Restrictive anorexia nervosa is similar to starvation and can be fatal. Diets are deficient in carbohydrates and total calories, but protein and vitamin intake is relatively preserved. Consequently, vitamin deficiencies are unusual. However, inadequate nutrient intake results in a profound loss of weight, fat, and muscle mass, followed by cardiac, metabolic and endocrine, hematologic, and gastrointestinal disturbances.

Cardiovascular Consequences.

Cardiac muscle atrophy is associated with a reduction in left ventricular wall thickness and cardiac output, but, typically, congestive failure does not occur. Sinus bradycardia and hypotension are common. Electrocardiographic changes, primarily low-voltage ST-segment depression, T-wave flattening, and prolonged QT intervals, have been reported. Sudden death, which occurs in anorexia nervosa, is presumably due to ventricular arrhythmias. QT-interval prolongation, which is reversible with refeeding, may herald increased risk of this outcome. Autopsies of some patients performed after sudden death have shown a degeneration of myocardial cells, which may predispose to arrhythmias.

Endocrine and Metabolic Consequences.

Extreme weight loss produces a number of adverse endocrine and metabolic changes. Thyroid hormone metabolism is altered (“sick euthyroid” syndrome), with thyroxine preferentially converted to the inactive reverse 3,5,3′-triiodothyronine (T3) instead of active T3. A compensatory rise in thyrotropin (thyroid-stimulating hormone) does not occur, suggesting dysfunction of the hypothalamic-pituitary axis. Treatment with thyroid hormone replacement is not indicated, and these thyroid function abnormalities normalize with weight recovery. Starvation also produces reversible hypothalamic-pituitary dysfunction that can lead to hypothalamic amenorrhea, infertility, estrogen deficiency, low levels of testosterone, and osteopenia (see Chapter 112).

Besides weight loss, other factors, such as hypercortisolemia and hypoleptinemia, may contribute to suppression of the hypothalamic-pituitary-reproductive axis as menstruation ceases in up to 25% of female patients with anorexia nervosa before weight loss becomes significant, and amenorrhea may persist after weight is regained. Many patients with anorexia nervosa demonstrate excessive secretion of cortisol. Although these patients do not appear cushingoid, with weight gain, they tend to accumulate fat in a central distribution. In addition, hypercortisolemia may contribute to clinical sequelae, such as bone loss and depressive symptoms. Finally, resistance to pituitary growth hormone leads to low levels of insulin-like growth factor (IGF)-1 and contributes to the profound bone loss associated with this disorder.

Posterior pituitary function is also disrupted. Excessive or reduced vasopressin secretion can lead to either hyponatremia (syndrome of inappropriate antidiuretic hormone) or central diabetes insipidus, respectively. Abnormal secretion of oxytocin has also been reported, though the clinical significance of this is unclear. In addition to pituitary consequences, hypothalamic dysfunction in anorexia nervosa can lead to failure to defend core body temperature and resultant hypothermia.

Recent evidence suggests that secretion of hormones implicated in regulation of appetite are abnormal in anorexia nervosa, even after weight recovery. Levels of hormones involved in food
motivation pathways, such as cortisol, oxytocin, and peptide YY, have been found to correlate with severity of disordered eating psychopathology in women. This raises the question of whether endocrine dysfunction may underlie disordered eating behaviors in some patients with anorexia nervosa.

Acquired defects in lipoprotein metabolism may alter serum cholesterol (predominantly increased High density lipoprotein [HDL] and total cholesterol) and raise carotene levels. Blood levels of glucose, protein, amino acids, and insulin are normal or mildly reduced. Severe hypoglycemia and coma have been reported when starvation is very advanced. Electrolyte abnormalities, including hypokalemia, hypophosphatemia, hypomagnesemia, and hyper- or hyponatremia, can occur, particularly in the purging subtype of anorexia nervosa.

Skeletal Consequences.

Osteopenia and osteoporosis occur and predispose to fractures, even vertebral compression fractures in severe cases. Anorexia nervosa-induced bone loss is multifactorial, likely due to estrogen deficiency, cortisol excess, growth hormone resistance, and nutritional deficiencies. Reversal of bone loss is most strongly associated with the restoration of body weight and resumption of menstrual cycles, which have independent effects. Oral estrogen/progestin therapy alone is not an effective treatment for bone loss (see below).

Gastrointestinal Consequences.

Patients may experience delayed gastric emptying, bloating, abdominal pain, constipation, and mild liver function test abnormalities. Those with bulimic subtype are at risk for complications of purging (see below). Refeeding may be followed by gastric dilation, ileus, and transient elevations of serum liver enzymes caused by fatty liver.

Volume Changes.

Dehydration may ensue as a consequence of starvation. Some patients develop hyponatremia from excessive water intake. Refeeding frequently leads to fluid retention, especially in bulimic subtype patients, who may be volume-depleted from purging behaviors. Fluid retention complicates volume status; congestive heart failure may develop as the increase in intravascular volume exceeds the capacity of the weakened heart. Electrolyte abnormalities, such as hypophosphatemia, can also occur from refeeding.

Hematologic Consequences.

Reversible bone marrow depression is noted. Patients may be anemic, leukopenic, and/or thrombocytopenic. Although mild anemia is common, it is rarely a consequence of iron, folate, or B₁₂ deficiency. The anemia may be masked in the setting of concurrent volume depletion and may not appear until rehydration is implemented.

Clinical Presentation

Characteristically, the patient with anorexia nervosa denies she is ill, but her emaciation attracts attention. The patient typically claims to feel well and appears unconcerned about her emaciation. Hunger is not a complaint, but patients may report difficulty sleeping, abdominal discomfort and bloating after eating, constipation, cold intolerance, and polyuria. Amenorrhea is present in female patients. Unlike other persons who are starving, those with anorexia nervosa are often not fatigued until malnutrition becomes very severe. Most are restless and physically active, and some exercise to excess. Listlessness is an ominous sign. The patient may present bundled in clothing because of cold intolerance.

On examination, the patient typically appears extremely thin, if not emaciated. Vital signs may reveal bradycardia, hypotension, and hypothermia. The skin may appear dry, pale, or yellow tinged (a consequence of carotenemia) and covered by fine, downy hair (lanugo) over the face and arms. In women, the female pattern of fat distribution disappears, but axillary and pubic hair is preserved. Acrocyanosis may be present. Bulimic subtype patients may display signs of purging behaviors (see below).

Clinical Course

The disease may occur as a single episode, as repeated episodes separated by remissions, or as a chronic condition. More than half of patients relapse after an initial hospital stay for weight gain. Approximately 50% of patients have a complete recovery (i.e., regain weight and menses), 30% have partial recovery, and 10% to 20% develop a chronic illness. Bulimic symptoms, lower weight, and older age at presentation are associated with poor outcome. Even after weight is restored, the patient with anorexia nervosa may have persistent weight preoccupation, disordered eating patterns, and psychosocial problems. Up to 50% of patients with anorexia nervosa develop bulimia nervosa. The mortality rate is 12 times that of age-matched unaffected persons. Most deaths are sudden, apparently caused by cardiac arrhythmias. Fatal hypoglycemic coma has also been reported. The risk for death appears to be higher in patients whose weight loss exceeds 40% of premorbid weight (or 30% if it has occurred within 3 months). Binge-purge subtype patients with metabolic abnormalities are probably at higher risk. Anorexia nervosa is associated with the highest suicide rate of any psychiatric disorder.

Bulimia Nervosa

This eating disorder is driven by excessive concern about body weight or shape and is characterized by repeated episodes of binge eating (at least once per week for 3 months), during which large amounts of high-calorie foods are consumed, usually in secrecy. The binge is followed by self-deprecating thoughts and purging, excessive exercise, or fasting (at least two times per week for 3 months) to prevent weight gain. Most bulimic patients purge by inducing vomiting or using laxatives, but some use diuretics or exercise excessively. They fear losing control of their eating behavior and are ashamed when it happens. Binges may be repeated several times daily. At other times, people with bulimia nervosa may diet rigorously or take diet pills. Some patients may have no regular eating pattern, fasting, or restricting eating severely outside of bingeing episodes. The result of this behavior is frequent weight fluctuations but not severe weight loss.

In contrast to persons with anorexia nervosa, those with bulimia nervosa are aware that their behavior is abnormal but often conceal the illness because of embarrassment. The bulimic patient’s typically normal weight permits the illness to be hidden. Detection of surreptitious vomiting or laxative abuse can be a challenge (see later discussion).

Pathogenesis

The high prevalence of alcohol and drug abuse among patients with bulimia nervosa has led some to postulate that bulimia nervosa is part of an impulse control disorder. Depression has also been proposed as a precipitant. Changes in neurotransmitter metabolism and a response to antidepressant medication suggest a biochemical component to the condition. Cultural pressure to be thin probably contributes. Patients commonly report that a diet preceded their disease. The bingeing sometimes observed when experimentally starved normal persons resume eating has led to speculation that strict dieting contributes to the onset of bulimia nervosa. Bulimia nervosa is more prevalent in individuals with type 1 diabetes, who can purge by withholding insulin after overeating. Diabetic patients with bulimia nervosa generally have worse glucose control, have poorer quality of life, and may be at greater risk of diabetic complications.

Pathophysiology

The medical consequences of bulimia nervosa usually depend on the specific behaviors present, but menstrual irregularities are common regardless of the purging method.

Bingeing.

Bingeing has few complications, although abdominal pain from distention is common. Acute gastric dilation is rare but has been reported.

Chronic Induced Emesis.

Repeated regurgitation of stomach contents produces volume depletion and a hypochloremic metabolic alkalosis. Dizziness, syncope, thirst, orthostatic changes in vital signs, and an elevated blood urea nitrogen occur in the volumedepleted patient. Renal compensation for the alkalosis and volume depletion causes potassium depletion and hypokalemia, which may predispose to cardiac arrhythmias, muscle cramps and weakness, paresthesias, polyuria, and constipation. T-wave flattening and U waves are seen on the electrocardiogram. Serum and urine chloride levels are low.

Reversible, painless parotid swelling can develop with chronic vomiting and is often accompanied by hyperamylasemia. Irreversible dental problems also occur. Repeated exposure of the teeth to stomach acid causes enamel decalcification and erosion. Teeth diminish in size and become discolored and sensitive to temperature changes. Many vomiters have symptoms of reflux esophagitis, but hematemesis due to a Mallory-Weiss tear is unusual, and esophageal rupture is rare. Some patients use emetine (ipecac) to induce vomiting. Prolonged use may cause a reversible proximal myopathy and a potentially fatal cardiomyopathy.

Laxative Abuse.

Laxative abuse is a common and potentially dangerous form of purging. It may begin as a response to constipation and continue because of the temporary weight loss induced through volume depletion. Stimulant laxatives are used most often. The resultant increase in colonic motility produces abdominal cramps, and electrolytes are lost in a watery diarrhea. Volume depletion, hyponatremia, hypokalemia, and either metabolic acidosis or metabolic alkalosis may result. Calcium and magnesium depletion has also been reported. The irritation of intestinal mucosa or development of hemorrhoids as a result of rapid fecal transit may cause rectal bleeding, and rectal prolapse can occur. When laxative abuse stops, transient fluid retention, edema, and constipation are common.

Diuretic Abuse.

Patients use diuretics more often to prevent fluid retention than to induce weight loss. Use contributes to a hypochloremic metabolic alkalosis, hypokalemia, and volume depletion. Dilutional hyponatremia may also occur. In contrast to vomiters and laxative abusers, patients who use diuretics do not have low urinary levels of sodium and chloride. Fluid retention transiently develops when diuretics are stopped.

Clinical Presentation and Course

Bingeing and purging may be concealed, and no physical signs are characteristic. The clinical presentation is often dominated by one of its medical complications, such as abdominal pain, diarrhea, heartburn, hypokalemia, volume depletion, hyponatremia, or parotid swelling. Findings related to vomiting may also include abrasions and calluses on the back of the hand, cheilosis at the angles of the mouth, and discoloration of teeth.

Patients with concomitant depression, substance use disorders, impulsivity, and personality disorders may have worse prognoses for recovery. Mortality is lower than in anorexia nervosa but higher than in an age-matched control population.

Binge Eating Disorder

This condition, now formally recognized in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) is characterized by recurrent binge eating (at least once weekly for 3 months) accompanied by marked distress and lack of control over eating and associated with eating alone, too rapidly, when not hungry, or until uncomfortably full. The patient has feelings of guilt or disgust after a binge but does not purge, exercise excessively, or fast. Of the several eating disorders, this is the most common among male patients and is more prevalent among the obese.

Night-Eating Syndrome

See Appendix 234-1-234-234.

DIFFERENTIAL DIAGNOSIS (12)

The differential diagnosis spans the array of conditions that may cause unexplained weight loss (see Chapter 9), secondary amenorrhea (see Chapter 112), electrolyte disturbances with volume depletion (see Chapters 59 and 64), and osteoporosis (see Chapter 164). Among them are malignancy, chronic infection, intestinal disorders (malabsorption, inflammatory bowel disease, or hepatitis), and endocrinopathies (e.g., hyperthyroidism, panhypopituitarism, adrenal insufficiency, diabetes mellitus). Tumors of the central nervous system mimic anorexia nervosa in rare cases. Psychiatric illnesses that can be confused with anorexia nervosa include depression, schizophrenia, and obsessive-compulsive neurosis (see Chapters 226, 227, and 230). Binge eating may be a manifestation of depression and, rarely, of an organic brain syndrome.

Only gold members can continue reading. Log In or Register to continue