Chapter 6: Eating Disorders

Adolescents as well as younger children engage in disordered eating behavior at an alarming rate, and many develop partial or full-blown eating disorders (EDs). The spectrum of EDs includes anorexia nervosa (AN), bulimia nervosa (BN), binge-eating disorder (BED), atypical anorexia nervosa, and avoidant/restrictive food intake disorder (ARFID). These disorders are best defined in a biopsychosocial context.

There is strong evidence for a genetic basis for EDs. The incidence of AN is 7% in first-degree relatives of anorexic patients compared with 1%–2% in the general population. The concordance rate in monozygotic twins is 55% compared with 7% in dizygotic twins. Twin studies estimate the heritability of AN as 33%–84% and BN as 28%–83%. Most studies also find a higher incidence of EDs among first-degree relatives of bulimic patients.

There is evidence of altered serotonergic and dopaminergic function and alterations in neuropeptides and gut peptides in AN and BN. It remains unclear whether abnormalities of neurotransmitters contribute to the development of EDs or are a consequence of the physiologic changes associated with the disorders. Patients with BN or BED appear to have a blunted serotonin response to eating and satiety. With a decreased satiety response, patients continue to eat, leading to a binge. Treatment with selective serotonin reuptake inhibitors (SSRIs) tends to equilibrate satiety regulation. An alteration in dopamine has also been recognized, although its significance is not clear. Adiponectin is elevated in AN, although it is unclear whether this is merely secondary to the malnourished state. Cholecystokinin is decreased in BN, perhaps contributing to the lack of postingestion satiety that perpetuates a binge. Ghrelin, a gut peptide, is elevated in patients with AN, and it does not decrease normally after a meal in these patients. Obestatin, a gut peptide that inhibits appetite, is elevated in AN as well.

Leptin physiology is deranged in patients with AN. Abnormalities of leptin may mediate energy changes that affect the hypothalamic-pituitary axis and play a role in perpetuating AN. Leptin levels increase excessively as individuals with AN regain weight. The abnormally high levels of leptin may contribute to the difficulty AN patients have when trying to regain weight, as higher leptin levels signal the body to decrease energy intake. Leptin also plays a significant role in some of the sequelae of AN, with low levels signaling the hypothalamus to inhibit reproductive hormone production.

Some experts have hypothesized that the intrauterine hormonal milieu may explain the differences in prevalence of ED between females and males. Procopio and Marriott have studied the risk of developing AN in the same sex and opposite-sex twin pairs when one twin has AN. There was approximately an eightfold risk of developing AN in males with a female twin with AN compared to the risk of developing AN in males who had a male twin with AN. Though the study could not separate environmental influences, evidence from animal models suggests that increased exposure to estrogen and/or decreased exposure to androgens influence brain development and may play a role in determining which individuals are at risk for AN.

Traditional psychological theory has suggested many environmental factors that might promote the development of EDs. Enmeshment of mother with daughter to the point that the teenager cannot develop her own identity (a key developmental marker of adolescence) may be a predisposing factor. The teenager may cope by asserting control over food, as she senses her lack of control in the developmental realm. A second theory involves father-daughter distancing. As puberty progresses and a girl’s sexuality blossoms, a father may experience difficulty in dealing with his daughter as a sexual being and may respond by withdrawing emotionally and physically. The teenage girl may intuitively recognize this and subconsciously decrease her food intake in order to become prepubertal again. A third theory is related to puberty itself.

Some teenagers may fear or dislike their changing bodies. By restricting food intake they lose weight, stop menstruating, and effectively reverse pubertal development.

Society has promoted the message that being thin or muscular is necessary for attractiveness and success. The ease of access to diet products—foods and diet pills—as well as Internet instructions (proanorexia sites) makes it simple for adolescents to embark on a quest for thinness or muscularity.

Genetic predisposition, environmental factors, and psychological factors likely combine to create a milieu that promotes development of EDs.

Anorexia nervosa is the third most common chronic illness of adolescent girls in the United States. The incidence has been increasing steadily in the United States since the 1930s. Although ascertaining exact incidence is difficult, most studies show that 1%–2% of teenagers develop AN and 2%–4% develop BN. Adolescents outnumber adults 5 to 1, although the number of adults with EDs is rising. Incidence is also increasing among younger children. Prepubertal patients often have associated psychiatric diagnoses. Males comprise about 10% of patients with EDs, though this prevalence appears to be increasing as well, associated with the increased media emphasis on muscular, chiseled appearance as the male ideal.

Preadolescents with EDs, in comparison to teenagers with EDs, are more likely to be male and present with rapid weight loss and lower percentile body weight and less likely to engage in bulimic behaviors.

Teenagers’ self-reported prevalence of ED behavior is much higher than the official incidence of AN or BN. According to the Youth Risk Behavior Survey of US teenagers (2013), 63% of females and 33% of males had attempted to lose weight during the preceding 30 days. Thirteen percent had fasted for more than 24 hours to lose weight, and 5% had used medications to lose weight (6.6% of girls and 3.4% of boys). Self-induced vomiting or laxative use was reported by 6.6% of females and 2.2% of males. Forty-six percent of females and 30% of males reported at least one binge episode during their lifetime. Although the number of youth with full-spectrum EDs is low, it is alarming that so many youth experiment with unhealthy weight control habits. These behaviors may be precursors to the development of EDs, and clinicians should explore these practices with all adolescent patients.

Children involved in gymnastics, figure skating, and ballet—activities that emphasize thin bodies—are at higher risk for AN than are children in sports that do not emphasize body image. Adolescents who believe that being thin represents the ideal frame for a female, those who are dissatisfied with their bodies, and those with a history of dieting are at increased risk for EDs. Sudden changes in dietary habits, such as becoming vegetarian, may be a first sign of anorexia, especially if the change is abrupt and without good reason.

The typical bulimic patient tends to be impulsive and engages in risk-taking behavior such as alcohol use, drug use, and sexual experimentation. Bulimic patients are often an appropriate weight for height or slightly overweight. They have average academic performance. Youth with diabetes have an increased risk of BN. In males, wrestling predisposes to BN, and homosexual orientation is associated with binge eating.

According to the National Eating Disorders Association, the diagnostic criteria for AN, adapted from the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), are described as follows.

There are two major types of AN. In the restricting type, patients do not regularly engage in binge eating or purging. In the binge-purge type, AN is combined with binge eating or purging behavior, or both. Distinguishing between the two is important as they carry different implications for prognosis and treatment. Although patients may not demonstrate all features of AN, they may still exhibit the deleterious symptoms associated with AN. A third form—atypical AN—exists as well, accounting for 18% of all ED diagnoses in one study. These individuals demonstrate typical AN behavior but are within or above normal weight.

Clinical Findings

A. Symptoms and Signs

Clinicians should recognize the early symptoms and signs of AN because early intervention may prevent the full-blown syndrome from developing. Patients may show some typical AN behaviors, such as reduction in dietary fat and intense concern with body image, even before weight loss or amenorrhea occurs.

Making the diagnosis of AN can be challenging because adolescents may try to conceal their illness. Assessing the patient’s body image is essential to determining the diagnosis. Table 6–1 lists screening questions that help tease out a teenager’s perceptions of body image. Other diagnostic screening tools (eg, EDs Inventory) assess a range of eating and dieting behaviors. Parental observations are critical in determining whether a patient has expressed dissatisfaction over body habitus and which weight loss techniques the child has used. If the teenager is unwilling to share his or her concerns about body image, the clinician may find clues to the diagnosis by carefully considering other presenting symptoms or signs. Weight loss from a baseline of normal body weight is an obvious red flag for the presence of an ED. Additionally, AN should be considered in any girl with secondary amenorrhea who has lost weight.

Physical symptoms and signs are usually secondary to weight loss and proportional to the degree of malnutrition. The body effectively goes into hibernation, becoming functionally hypothyroid (euthyroid sick) to save energy. Body temperature decreases, and patients report being cold. Bradycardia develops, especially in the supine position. Dizziness, light-headedness, and syncope may occur as a result of orthostasis and hypotension secondary to impaired cardiac function. Left ventricular mass is decreased, stroke volume is compromised, and peripheral resistance is increased, contributing to left ventricular systolic dysfunction. Patients can develop prolonged QTc syndrome and increased QT dispersion (irregular QT intervals), putting them at risk for cardiac arrhythmias. Peripheral circulation is reduced. Hands and feet may be blue and cool. Hair thins, nails become brittle, and skin becomes dry. Lanugo develops as a primitive response to starvation. The gastrointestinal (GI) tract may be affected; inability to take in normal quantities of food, early satiety, and gastroesophageal reflux can develop as the body adapts to reduced intake. The normal gastrocolic reflex may be lost due to lack of stimulation by food, causing bloating and constipation. Delayed gastric emptying may develop. Nutritional rehabilitation improves gastric emptying and dyspeptic symptoms in AN restricting type, but not in those who vomit. Neurologically, patients may experience decreased cognition, inability to concentrate, increased irritability, and depression, which may be related to structural brain changes and decreased cerebral blood flow.

Determining BMI is critical for assessing degree of malnutrition. A gown-only weight after urination is the most accurate way to assess weight. Patients tend to wear bulky clothes and may hide weights in their pockets or drink excessive fluid (water-loading) to trick the practitioner. BMI below the 25th percentile indicates risk for malnutrition and below 5th percentile indicates significant malnutrition. Median body weight (MBW) should be calculated as it serves both as the denominator to determine what percent weight an individual is and to provide a general goal weight during recovery. MBW for height is calculated by using the 50th percentile of BMI for age.

A combination of malnutrition and stress causes hypothalamic hypogonadism. The hypothalamic-pituitary-gonadal axis shuts down as the body struggles to survive, directing finite energy resources to vital functions. This may be mediated by the effect of low serum leptin levels on the hypothalamic-pituitary axis. Pubertal development and skeletal growth may be interrupted, and adolescents may experience decreased libido.

Amenorrhea will continue to be an important clinical sign that the body is malnourished. Amenorrhea occurs for two reasons. The hypothalamic-pituitary-ovarian axis shuts down under stress, causing hypothalamic amenorrhea. In addition, adipose tissue is needed to convert estrogen to its activated form. When weight loss is significant, there is not enough substrate to activate estrogen. Resumption of menses occurs only when both body weight and body fat increase.

Approximately, 73% of postmenarchal girls resume menstruating if they reach 90% of MBW. An adolescent female needs about 17% body fat to restart menses and 22% body fat to initiate menses if she has primary amenorrhea. Some evidence suggests that target weight gain for return of menses is approximately 1 kg higher than the weight at which menses ceased.

B. Laboratory Findings

All organ systems may suffer some degree of damage in the anorexic patient, related to both severity and duration of illness (Table 6–2). Initial screening should include complete blood count with differential; serum levels of electrolytes, blood urea nitrogen, creatinine, phosphorus, calcium, magnesium, and thyroid-stimulating hormone; liver function tests; and urinalysis. Increase in lipids, likely due to abnormal liver function, is seen in 18% of those with AN, with subsequent return to normal once weight is restored. An electrocardiogram (ECG) should be performed, because significant ECG abnormalities may be present, most importantly prolonged QTc syndrome. Bone densitometry should be done if illness persists for 6 months, as patients begin to accumulate risk for osteoporosis.

Differential Diagnosis

If the diagnosis is unclear (ie, the patient has lost a significant amount of weight but does not have typical body image distortion or fat phobia), the clinician must consider the differential diagnosis for weight loss in adolescents. This includes inflammatory bowel disease, diabetes, hyperthyroidism, malignancy, depression, and chronic infectious disease such as human immunodeficiency virus (HIV). Less common diagnoses include adrenal insufficiency and malabsorption syndromes such as celiac disease. The history and physical examination should direct specific laboratory and radiologic evaluation.

Complications

(Table 6–3)

A. Short-Term Complications

1. Early satiety

Patients may have difficulty tolerating even modest quantities of food when intake increases; this usually resolves after the patients adjust to larger meals. Gastric emptying is poor. Pancreatic and biliary secretion is diminished.

2. Superior mesenteric artery syndrome

As patients become malnourished, the fat pad between the superior mesenteric artery and the duodenum shrinks and compression of the transverse duodenum may cause obstruction and vomiting, especially with solid foods. The upper GI series shows to-and-fro movement of barium in the descending and transverse duodenum proximal to the obstruction. Treatment involves a liquid diet or nasoduodenal feedings until restoration of the fat pad has occurred, coincident with weight gain.

3. Constipation

Patients may be very constipated. Two mechanisms contribute—loss of the gastrocolic reflex and loss of colonic muscle tone. Typically stool softeners are not effective because the colon has decreased peristaltic amplitude. Agents that induce peristalsis, such as bisacodyl, as well as osmotic agents, such as polyethylene glycol-electrolyte solution (MiraLax), are helpful. Constipation can persist for up to 6–8 weeks after refeeding. Occasionally enemas are required.

4. Refeeding syndrome

This syndrome is described in the Treatment section.

5. Pericardial effusion

The degree of malnutrition correlates with increasing prevalence of pericardial effusion. One study demonstrated that 22% of those with AN had silent pericardial effusions, with 88% of effusions resolving after weight restoration.

B. Long-Term Complications

1. Osteoporosis

Approximately 50% of females with AN have reduced bone mass at one or more sites. The lumbar spine has the most rapid turnover and is the area likely to be affected first. Teenagers are particularly at risk as they accrue 40% of their bone mineral during adolescence. Low body weight is most predictive of bone loss. The causes of osteopenia and osteoporosis are multiple. Estrogen and testosterone are essential to potentiate bone development. Bone minerals begin to resorb without estrogen. Elevated cortisol levels and decreased insulin-like growth factor-1 also contribute to bone resorption. Amenorrhea is highly correlated with osteoporosis. Studies show that as few as 6 months of amenorrhea is associated with osteopenia or osteoporosis. Males have similar bone loss related to their degree of malnutrition, likely due to decreased testosterone and elevated cortisol.

The most effective treatment for bone loss in girls with AN has been regaining sufficient weight and body fat to restart the menstrual cycle. Studies do not support the use of hormone replacement therapy delivered orally to improve bone recovery; however, one randomized controlled trial demonstrated that physiologic doses of estrogen, delivered transdermally, over 18 months did improve bone density. Clinicians may consider transdermal estrogen treatment if patients are recalcitrant to intervention and do not restore weight in a timely manner. Bisphosphonates show moderate positive effectiveness for adults with AN, but not for adolescents. Use of dehydroepiandrosterone in combination with oral contraceptive pills is shown to maintain bone mineral density in adolescents with AN compared to controls, though this treatment approach has not been adopted as standard of care.

2. Brain changes

As malnutrition becomes pronounced, brain tissue—both white and gray matter—is lost, with a compensatory increase in cerebrospinal fluid in the sulci and ventricles. Follow-up studies of weight-recovered anorexic patients show a persistent loss of gray matter, although white matter returns to normal. Functionally, there does not seem to be a direct relationship between cognition and brain tissue loss, although studies have shown a decrease in cognitive ability and decreased cerebral blood flow in very malnourished patients. Making patients and family aware that brain tissue can be lost may improve their perception of the seriousness of this disorder.

3. Effects on future children

This area has just recently been studied. Findings suggest that there may be feeding issues for infants who are born to mothers who have a history of either AN or BN. Infants born to mothers with a history of AN have more feeding difficulties at 0 and 6 months and tend to be lower weight (30th percentile on average). Infants born to mothers with current or past BN are more likely to be overweight and have faster growth rates than controls. Pediatricians should ascertain an ED history from mothers of patients who are having feeding issues.

C. Mortality

Patients with EDs are at a higher risk of death than the general population and those with AN have the highest risk of dying among those with EDs. Meta-analysis estimates the standardized mortality ratio associated with AN to be 5.9. Death in anorexic patients is due to suicide, abnormal electrolytes, and cardiac arrhythmias.

Treatment

A. General Approach

Factors that determine treatment interventions are severity of illness, duration of illness, specific manifestations of disease, previous treatment approaches and outcomes, program availability, financial resources, and insurance coverage. Treatment options include outpatient management, day treatment hospitalization, inpatient medical or psychiatric hospitalization, and residential treatment. The key to determining level of intervention is the degree of malnutrition, the rapidity of weight loss, the degree of medical compromise, and the presence of life-threatening electrolyte abnormalities. No absolute criteria determine level of intervention. The practitioner must examine the degree of medical compromise and consider immediate risks and the potential for an individual to reverse the situation on his or her own. Treatment is costly. Many patients do not have insurance benefits that adequately cover the cost of treatment, leaving parents and practitioners with profound dilemmas as to how to best provide treatment in the face of financial constraints. Legally, however, EDs are now recognized as a parity mental health diagnosis similar to the other biologically based mental health illnesses in many states, which has increased the ease of obtaining insurance coverage.

A multidisciplinary approach is most effective and should include medical monitoring, nutrition therapy, and individual and family psychotherapy by experienced practitioners. Family therapy is an important means of helping families understand the development of the disease and addressing issues that may be barriers to recovery. Both types of psychotherapy are encouraged in most treatment programs, and recovery without psychotherapy is unusual. The average length of psychotherapy is roughly 6–9 months, although some individuals continue therapy for extended periods. Adjunctive modalities include art and horticulture therapy, therapeutic recreation, and massage therapy.

Manualized family therapy, developed in Britain by Maudsley and adapted by Lock and LeGrange, has shifted the therapeutic approach to adolescents with AN. Traditional therapy allowed the adolescent to control his or her eating and the parents to remain uninvolved with the food portion of recovery. The manualized approach gives power and control back to parents.

Treatment is prescribed for 20 weekly sessions. The first 10 weeks are devoted to empowering parents, putting them in control of their child’s nutrition and exercise. Parents are educated about the dangers of malnutrition and are instructed to supervise each meal. The next phase, sessions 11–16, returns control over eating to the adolescent once he or she accepts the demands of the parents. The last phase of treatment, sessions 17–20, occurs when the patient is maintaining a healthy weight and shifts the focus away from the ED, examining instead the impact that the ED has had on establishing a healthy adolescent identity. This approach is reported to result in good or intermediate outcomes in 90% of treated adolescents.

Careful instruction in nutrition helps the teenager and family dispel misconceptions about nutrition, identify realistic nutritional goals, and normalize eating. Initially, nutrition education may be the most important intervention as the teenager slowly works through his or her fears of fat-containing foods and weight gain. The teenager begins to trust the nutrition therapist and restore body weight, eventually eating in a well-balanced, healthy manner.

B. Inpatient Treatment

Table 6–4 lists the criteria for hospital admission generally used in the medical community. It is usually quite difficult for a patient who is losing weight rapidly (> 2 lb/wk) to reverse the weight loss because the body is in a catabolic state.

Goals of hospitalization include arresting weight loss and stabilizing hemodynamics. Nutrition is the most vital inpatient medicine. Clinicians can safely begin with a meal plan containing approximately 250 kcal more than the patient has been routinely eating, which can usually be accomplished orally. Studies suggest that meal plans can begin with as high as 1750 kcal regardless of baseline intake. Meal plans should be well balanced with appropriate proportions of carbohydrate, protein, and fat. Oral meals are usually tolerated, although it is important to be supervised by medical staff. If the patient resists, nasogastric or intravenous alimentation can be used. Aside from caloric needs, the clinician needs to consider the patient’s hydration and include the appropriate amount of fluid with the meal plan. Dehydration should be corrected slowly. The oral route is usually adequate. Aggressive intravenous fluid administration should be avoided because left ventricular mass is compromised and a rapid increase in volume may not be tolerated. Regulating fluid intake is important, because water intoxication can contribute to abnormal electrolytes and falsified weights.

During the initial introduction of food, the clinician should monitor the patient for refeeding syndrome, a phenomenon that occurs if caloric intake is increased too rapidly. Signs of refeeding syndrome are decreased serum phosphorus (as the body resumes synthesis of adenosine triphosphate), decreased serum potassium (as increased insulin causes K⁺ to shift from extracellular fluid into K⁺-depleted cells), and, rarely, edema related to fluid shifts or congestive heart failure.

Although specific guidelines do not exist, many practitioners begin phosphorus supplementation if patients are severely malnourished (< 70% MBW) or their intake has been consistently less than 500 kcal/day.

Caloric intake can be increased 250 kcal/day as long as refeeding syndrome does not occur. Weight goals vary depending on programmatic approach. Typically, intake is adjusted to reach a goal of 0.1–0.25 kg/day weight gain.

Overnight monitoring for bradycardia is helpful in assessing degree of metabolic compromise. Usually the more rapid and severe the weight loss, the worse the bradycardia. Improving bradycardia correlates with weight recovery. Orthostatic hypotension is most severe around hospital day 4, improving steadily and correcting by the third week of nutritional rehabilitation. An ECG should be obtained because the patient is at risk for prolonged QTc syndrome and junctional arrhythmias related to the severity of bradycardia.

It usually takes 2–3 weeks to reach the initial goals of hospitalization—steady weight gain, toleration of oral diet without signs of refeeding syndrome, corrected bradycardia (heart rate > 45 beats/min for three consecutive nights), and correction of orthostasis. Specific weight criteria are used by many programs when considering discharge. This depends partly on admission weight. Ideally a patient gains at least 5% of his or her MBW. Some programs set discharge at 80%, 85%, or 90% MBW. Patient outcomes are improved with discharge at a higher body weight. Some evidence exists that patients do better if discharged at 95% MBW. In many practitioners’ experience, relapse rates are high if patients are discharged at less than 75% MBW.

C. Pharmacotherapy

Practitioners frequently use psychotropic medications for treatment of AN, despite the lack of evidence supporting efficacy. Several open-label trials suggest that atypical antipsychotics (risperidone, olanzapine, quetiapine) may be helpful. One review found that olanzapine (2.5–15 mg/day) was associated with improved body weight, decreased delusional thinking, improvement in body image, and decreased agitation and premeal anxiety. However, a randomized controlled trial did not show any difference in outcomes between risperidone and placebo.

SSRIs repeatedly have been shown to not be helpful in the initial therapy of AN. A recent study showed that use of SSRIs may decrease bone mineral density when used in malnourished patients. However, once the patient has achieved approximately 85% MBW, SSRIs (fluoxetine, citalopram, or sertraline) may help prevent relapse.

Zinc deficiency is common in AN, and several studies support its use as a supplement during the initial phases of treatment. Because zinc deficiency adversely affects neurotransmitters, administering zinc helps restore neurotransmitter action to baseline. Additionally, zinc may restore appetite and improve depressive mood. Zinc should be administered for approximately 2 months from the beginning of therapy, with at least 14 mg of elemental zinc daily.

Because of global nutritional deficits, a multivitamin with iron is also recommended daily. Symptomatic treatment for constipation and reflux should be used appropriately until symptoms resolve.

D. Outpatient Treatment

Not all patients with AN require inpatient treatment, especially if parents and clinicians recognize the warning signs early. These patients can receive treatment as outpatients, employing the same multidisciplinary team approach. Manualized family-based treatment is ideal for the outpatient setting if a trained therapist is available. Appropriate nutrition counseling is vital in guiding a patient and family through the initial stages of recovery. As the nutrition therapist is working at increasing the patient’s caloric intake, a practitioner needs to monitor the patient’s weight and vital signs. Often, activity level needs to be decreased to help reverse the catabolic state. A reasonable weight gain goal may be 0.2–0.5 kg/wk. If weight loss persists, careful monitoring of vital signs, including supine heart rate, is important in determining whether an increased level of care is needed. Concomitantly, the patient should be referred to a psychotherapist and, if indicated, assessed by a psychiatrist.

E. Treatment Goals and Outcomes

Goals of treatment include reaching a healthy body weight, elimination of medical sequelae, and resumption of menses. Symptoms can wax and wane over an extended period for several years. Approximately 50% of adolescents recover in a relatively short period of time. Thirty percent may take several years to get back to a state of health, although symptoms may reappear on occasion. About 20% of adolescents can go on to develop chronic, unremitting AN.

The diagnostic criteria for BN are discussed in section Essentials of Diagnosis & Typical Features. Binge eating is either eating excessive amounts of food during a normal mealtime or having a meal that lasts longer than usual. Bulimic individuals feel out of control while eating, unable or unwilling to recognize satiety signals. Any type of food may be eaten in a binge, although typically it includes carbohydrates or junk food. Extreme guilt is often associated with the episode. At some point, either prior to or during a binge, bulimic individuals often decide to purge as a means of preventing weight gain. The most common ways to purge are self-induced vomiting, exercise, and laxative use. Some individuals will vomit multiple times during a purge episode, after using large amounts of water to cleanse their system. This can induce significant electrolyte abnormalities such as hyponatremia and hypokalemia, which may put the patient at acute risk for arrhythmia or seizure. Other methods of purging include diuretics, diet pills, cathartics, and nutritional supplements that promote weight loss, such as Metabolife or Sensa.

Diagnosing BN can be difficult unless the teenager is forthcoming or parents or caregivers can supply direct observations. Bulimic patients are usually average or slightly above average in body weight and have no physical abnormalities. Screening all teenagers for body image concerns is crucial. If the teenager expresses concern about being overweight, the clinician needs to screen the patient about dieting methods. Asking whether patients have binged, feel out of control while eating, or whether they cannot stop eating can clarify the diagnosis. Parents may report that significant amounts of food are missing or disappearing more quickly than normal. If the physician is suspicious, direct questioning about all the ways to purge should follow. Indicating first that the behavior is not unusual can make questioning less threatening and more likely to elicit a truthful response. For example, the clinician might say, “Some teenagers who try to lose weight make themselves vomit after eating. Have you ever considered or done that yourself?” (See Table 6–1 for additional screening questions.)

Clinical Findings

A. Symptoms and Signs

Symptoms are related to the mechanism of purging. GI problems are most prominent. Abdominal pain is common. Gastroesophageal reflux occurs as the lower esophageal sphincter becomes compromised due to repetitive vomiting. Frequent vomiting may also cause esophagitis or gastritis, as the mucosa is irritated by acid exposure. Early satiety, involuntary vomiting, and complaints that food is “coming up” on its own are frequent. Hematemesis and esophageal rupture have been reported. Patients may report diarrhea or constipation, especially if laxatives have been used. Sialadenitis (parotid pain and enlargement) may be caused by frequent vomiting. Erosion of dental enamel results from increased oral acid exposure during vomiting. Because comorbid depression is common in BN, patients may report difficulty sleeping, decreased energy, decreased motivation, and headaches. Light-headedness or syncope may develop secondary to dehydration.

It is important to note that most purging methods are ineffective. When patients binge, they may consume thousands of calories. Digestion begins rapidly. Although the patient may be able to vomit some of the food, much is actually digested and absorbed. Laxatives work in the large intestine, leading to fluid and electrolyte loss, but consumed calories are still absorbed from the small intestine. Use of diuretics may result in decreased fluid weight and electrolyte imbalance.

On physical examination, bulimic patients may be dehydrated and have orthostatic hypotension. Sialadenitis, tooth enamel loss, dental caries, and abdominal tenderness are the most common findings. Abrasion of the proximal interphalangeal joints may occur secondary to scraping the fingers against teeth while inducing vomiting. Rarely, a heart murmur is heard which may be due to mitral valve prolapse. Irreversible cardiomyopathy can develop secondary to ipecac use.

B. Laboratory Findings

Electrolyte disturbances are common. The method of purging results in specific abnormalities. Vomiting causes metabolic alkalosis, hypokalemia, and hypochloremia. Laxatives cause metabolic acidosis, hypokalemia, and hypochloremia. Diuretic use may lead to hypokalemia, hyponatremia, hypocalcemia, and metabolic alkalosis. Amylase may be increased secondary to chronic parotid stimulation.

Complications

A. Short-Term Complications

Complications in normal-weight bulimic patients are related to the mechanisms of purging, and many of these complications are listed under Symptoms and Signs. If the bulimic patient is significantly malnourished, complications may be the same as those encountered in the anorexic patient. Other complications of bulimia include esophageal rupture, acute or chronic esophagitis, and, rarely, Barrett esophagitis. Chronic vomiting can lead to metabolic alkalosis, and laxative abuse may cause metabolic acidosis. Diet pill use can cause insomnia, hypertension, tachycardia, palpitations, seizures, and sudden death.

Patients who stop taking laxatives can have severe constipation. Treating constipation can be difficult psychologically, because the practitioner may need to prescribe agents similar to the drugs of abuse used during the ED.

B. Mortality

The mortality rate in bulimic patients is similar to that in anorexic patients. Death usually results from suicide or electrolyte derangements.

Treatment

Treatment of BN depends on the frequency of bingeing and purging and the severity of biochemical and psychiatric derangement. If K⁺ is less than 3.0 mEq/L, inpatient medical admission is warranted. Typically, extracellular K⁺ is spared at the expense of intracellular K⁺, so a patient may become hypokalemic several days after the serum K⁺ concentration appears to be corrected. Usually cessation of purging is sufficient to correct K⁺ concentration and is the recommended intervention for K⁺ above 3.0 mEq/L. If K⁺ is 2.5–2.9 mEq/L, oral supplementation is suggested. If K⁺ is less than 2.5 mEq/L, intravenous therapy is recommended. Supplements can be stopped once K⁺ levels are more than 3.5 mEq/L. Total body K⁺ can be assumed to be normal when serum K⁺ corrects and remains normal 2 days after supplements are stopped. Continued hospitalization depends on the patient’s psychological status.

Some bulimic patients who abuse laxatives may become chronically dehydrated. The renin-angiotensin-aldosterone axis is activated, and the antidiuretic hormone level may be elevated to compensate. These hormones do not normalize immediately when laxatives are stopped, and fluid retention of up to 10 kg/wk may result. This puts patients at risk for congestive heart failure and can scare them as their weight increases dramatically. Diuresis often occurs after 7–10 days.

Hospitalization of bulimic patients is also recommended if there has been failure of outpatient management. The binge-purge cycle is addictive and can be difficult for patients to interrupt on their own. Hospitalization can offer a forced break from the cycle, allowing patients to normalize their eating, interrupt the addictive behavior, and regain the ability to recognize satiety signals.

Outpatient management can be pursued if patients are medically stable. Cognitive-behavioral therapy is crucial to help bulimic patients understand their disease. Nutrition therapy offers patients ways to regulate eating patterns so that they can avoid the need to binge. Medical monitoring should be done to check electrolytes periodically, depending on the purging method used.

SSRIs are generally helpful in treating the binge-purge cycle. Fluoxetine has been studied most extensively; a dose of 60 mg/day is most efficacious in teenagers. Other SSRIs appear to be effective as well and may be used in patients experiencing side effects of fluoxetine. Treatment for gastroesophageal reflux and gastritis should be used when appropriate. The pain and swelling of enlarged parotid glands can be helped by sucking on tart candy and by the application of heat.

Goals of treatment are to interrupt the binge/purge cycle, with the goal of reaching remission as a targeted outcome.

Binge-eating disorder (BED) is now described in the DSM-5. Studies show that most adults who have BED (a prevalence of 2%–4%) develop symptoms during adolescence. Following are the diagnostic criteria for BED.

Clinical Findings

A. Symptoms and Signs

BED most often is found in overweight or obese individuals. Eighteen percent of such patients report binging at least once in the past year. Patients with BED have an increased incidence of depression and substance abuse. The possibility of BED should be raised for any significantly overweight patient. Specific questionnaires are available for evaluating patients suspected of BED.

B. Laboratory Findings

The clinician should assess causes and complications of obesity, and laboratory evaluation should include thyroid function tests and measurement of cholesterol and triglyceride levels.

Treatment

A combination of cognitive-behavioral therapy and antidepressant medication has been helpful in treating BED in adults. Use of SSRIs for BED in adolescents has not been studied, but in adults fluoxetine and citalopram help decrease binge episodes, improve depressive symptoms, and possibly decrease appetite. This evidence suggests that SSRIs in adolescents with BED may be helpful as well. BED has been recognized only recently, and outcomes have not been studied. Little is known regarding long-term prognosis.

ARFID was added to the DSM-5 that extends the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV) diagnosis of feeding disorder of infancy or early childhood. The hallmark feature is avoidance or restriction of oral food intake, in the absence of criteria for AN (body image disturbance, fear of weight gain/body fat). For teenagers, food avoidance may be associated with more generalized emotional difficulties that do not meet diagnostic criteria for anxiety or depression. Diagnostic criteria for ARFID are discussed in the following section Essentials of Diagnosis & Typical Features. Similar health effects to AN may be found in youth with ARFID, depending on the degree of malnutrition and how an individual became malnourished.

Outcome in EDs, especially AN, has been studied extensively. Prior metrics generally defined remission or recovery as being at a healthy body weight and a return of menses. As diagnostic criteria for AN changed, a national collaborative effort that included 14 ED programs defined AN recovery based on reaching at least 90% median BMI, without consideration of return of menses. Most studies have focused on specific inpatient treatment programs, and few have evaluated less ill patients who do not need hospitalization. About 40%–50% of patients receiving treatment recover, 20%–30% have intermittent relapses, and 20% have chronic, unremitting illness. As time from initial onset lengthens, the recovery rate decreases and mortality associated with AN and BN increases. A study from the Swedish registry of EDs revealed that 55% of the participants were in remission and approximately 85% were within a healthy weight range at the end of treatment (15 months on average). The national collaborative showed that 65% of patients demonstrated recovery at 1 year, with higher BMI at baseline the most significant predictor of recovery.

The course of AN often includes significant weight fluctuations over time, and it may be a matter of years until recovery is certain. The course of BN often includes relapses of bingeing and purging, although bulimic patients initially recover faster than do anorexic patients. Up to 50% of anorexic patients may develop bulimia, as well as major psychological complications, including depression, anxiety, and substance abuse disorders. Bulimic patients also develop similar psychological illness but rarely develop anorexia. Long-term medical sequelae, aside from low body weight and amenorrhea, have not been systematically studied, although AN is known to have multiple medical consequences, including osteoporosis and structural brain changes.

It is unclear whether age at onset affects outcome, but shorter length of time between symptom onset and therapy tends to improve outcome. Various treatment modalities can prove effective. Favorable outcomes have been found with brief medical hospitalization and long psychiatric or residential hospitalization. Higher discharge weight, as well as more rapid weight gain during inpatient treatment (> 0.8 kg/wk), seems to improve the initial outcome. It is difficult to compare treatment regimens, because numbers are small and the type of patient and illness varies among studies. No existing studies compare outpatient to inpatient treatment or the effects of day treatment on recovery.

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