Eating Disorders in Adolescents and Older Children
1999; American Academy of Pediatrics; Volume: 20; Issue: 12 Linguagem: Inglês
10.1542/pir.20-12-410
ISSN1529-7233
AutoresRichard E. Kreipe, Carolyn Piver Dukarm,
Tópico(s)Impact of Technology on Adolescents
ResumoAfter completing this article, readers should be able to:Eating disorders are potentially life-threatening conditions experienced with increasing frequency by older children and adolescents, especially females. These conditions share several features, including dysfunctional eating habits (frequently related to underlying psychosocial issues such as depression, low self-esteem,family dynamics, or environmental problems), disturbance in body image, and change in weight(ranging from extreme loss of weight in anorexia nervosa to fluctuation around a normal to moderately high weight in bulimia nervosa). The feeding patterns may extend from voluntary restriction of food intake to episodic binge eating (often with a compulsive quality) that may be associated with compensatory behaviors ranging from ritualistic exercise to self-induced vomiting. Excessive concerns about negative body image drive many of the daily behaviors exhibited by young people who have eating disorders, who also have few alternative coping mechanisms for various developmental concerns. Once these dysfunctional patterns are established, they can be very difficult to alter because they serve as coping mechanisms and have their own addictive qualities. The pediatric practitioner has a primary role in the early identification and treatment of mild eating disorders and a collaborative role with appropriate colleagues in adolescent medicine, developmental-behavioral pediatrics, psychology, psychiatry,nutrition, and physical therapy to help patients who have established or severe eating disorders.The often extreme weight loss seen in anorexia nervosa (AN) in combination with the associated medical complications facilitates recognition and the early initiation of treatment. Bulimia nervosa (BM)and binge eating disorder (BED) are more likely to go unnoticed because they lack the extreme physiologic manifestations of starvation and typically are associated with normal or high weight. The purpose of this article is to review and clarify the classification, diagnosis,epidemiology, pathogenesis, clinical aspects,and management of eating disorders(with an emphasis on BN and BED)to facilitate successful care and to update an earlier article on the topic(Kreipe RE. Pediatr Rev. 1995;16:370–379). A thorough understanding of these conditions by the pediatric clinician is needed for trust and family involvement. Although the psychiatric aspects of these conditions are prominent, they will not be discussed in detail here.A new classification scheme related to behavioral and mental health concerns for children and adolescents,the Diagnostic and Statistical Manual for Primary Care (DSM-PC),was published in 1996 by the American Academy of Pediatrics to fill a gap in the American Psychiatric Association’s classification of mental illnesses, the DSM-IV. Older children and younger adolescents may exhibit behaviors that do not meet full DSM-IV criteria, yet still deserve attention. The two specific complexes in the DSM-PC related to eating disorders are: 1) dieting/body image behaviors and 2) purging/binge-eating behaviors.There are two levels of pathology for both of these behavior patterns that are not healthy, but do not fulfill DSM-IV criteria for an eating disorder. In DSM-PC, variationsconstitute minor deviations from normal that still might be of concern for a parent or clinician; problemsconstitute more serious manifestations representing the earliest evidence of eating disorders. For clarity, the DSM-PC hierarchical schema has been combined with the DSM-IV diagnostic criteria related to eating disorders in Tables 1, 2, and 3. An adolescent who exhibits dieting and voluntary food limitation in an obsessive pursuit of thinness and a systematic fear of gaining weight that extends beyond a simple dieting/body image variation(V65.49), but that is not yet sufficiently intense to meet criteria for AN (307.10) would be classified as having a dieting/body image problem (V69.1).There is a great deal of overlap between an eating problem in DSM-PC and an eating disorder not otherwise specified (ED-NOS)(Table 3), making the distinction between these two conditions difficult. Complicating the classification of eating disorders further is the frequent use of the term “disordered eating” to include a range of subthreshold deviations from “normal,”which are defined arbitrarily by the individual applying the label, as well as the lack of agreement about what constitutes normal eating habits. Fortunately, it rarely is necessary to make narrow classification distinctions in clinical practice because the majority of attention needs to focus on the presenting attitudes,behaviors, signs, and symptoms, and not on labeling. Throughout this article“eating disorder” or “disordered eating” will be used as generic terms for dysfunctional habits and attitudes related to eating and weight control.The outstanding feature of AN is persistent and severe restriction of energy intake (especially fat),generally in combination with compulsive exercise in an inexorable pursuit of thinness. Patients tend to monitor their intake obsessively, often attempting to limit their overall daily intake to fewer than 1,000 kcal and fewer than 10 g fat. Dieting and exercise frequently begin with reasonable habits and goals, but they quickly escalate and become uncontrollable, even though patients may protest to the contrary. As habits become progressively more unhealthy, parents may attempt to control eating or force weight gain. This adds to the individual’s internal conflict related to the need to lose weight.An outstanding feature of AN is not merely a desire to be thin, but a relentless drive to be thinner; as each goal weight is reached, it is replaced by a lower target, leading to progressive weight loss. These behaviors serve to improve the patient’s sense of self-efficacy, but they also may be associated with depression. Thus, there often is a tendency for patients to defend their habits or to deny that any problem exists—other than the need to lose more weight.Younger patients who have AN may not fit this profile; they are more likely to fail to gain weight as expected than to lose large amounts of weight. In addition, due to cognitive limitations, younger patients may be unable to describe their inner turmoil and merely exercise compulsively or refuse to eat certain categories of food because engaging in these habits lowers their stress levels.Clinically, patients who have AN may be dichotomized into a restrictive type, as just described, or a binge-eating/purging type if they intermittently engage in “bulimic”behaviors. Almost 50% of patients who have AN go through a phase during their illness when they binge eat. However, most do not actually eat large amounts of food. Rather,they feel guilty when they eat“forbidden” foods of high caloric or fat content or when they eat more than they had planned, and they experience these episodes as binges. They interpret such behavior as being “out of control” relative to when they successfully limit their intake to a few hundred calories at a meal. When a patient who has AN reports binge eating, it is important to detail the volume and content of what is eaten at these times. Otherwise, if she or he maintains a low weight(an unexpected occurrence with true binge eating), the clinician may assume erroneously that the patient is purging to prevent weight gain.When true binge eating (eating a large amount of food in a short time period, uncontrollably) dominates the clinical picture, two other diagnoses should be considered: BN and BED. BED is easily distinguished from AN by weight gain, often of significant amounts, and a much weaker drive for thinness. The body image among patients who have BED also may be “distorted,” often in the direction of not seeing themselves as heavy as they really are. In contrast, individuals who have AN perceive themselves as “fat” or“big,” even when extremely emaciated. Depending on the balance between the amount of dieting, the caloric content of binges, and the timing and frequency of vomiting or laxative use, patients who have BN can range from being significantly underweight to being moderately overweight, with a less severely distorted body image than generally is seen in AN.The hallmark of BN is binge eating followed immediately by some compensatory behavior to rid the body of ingested calories. Patients whose BN is full-blown have engaged in these dysfunctional habits at least twice a week for 3 months. Those who have a purging/binge eating problem also engage in these behaviors and have a negative self-evaluation influenced by weight and body shape, but episodes are farther apart temporally,and the behaviors are not as intense as seen in BN (Table 2). Purging is a compensatory mechanism used by more than 90% of patients who have BN to avoid weight gain following binge eating episodes. Types of purging include self-induced vomiting (>85% of adolescents who have BN) using pharyngeal stimulation,pressure on the abdomen, or ipecac and the use of laxatives (<15%) or diuretics (very rare). Patients also may use exercise (about 60%) or fasting (about 30%) as compensatory mechanisms to avoid gaining weight following an episode of binge eating. Although self-induced vomiting is a frequent characteristic,it is binge eating–not vomiting–that is the defining characteristic of BN. Moreover, up to 20% of patients who have AN may vomit intermittently to control weight after eating more than was plannedAn awareness that the eating pattern of BN is abnormal leads to (or may follow) depressed moods and self-deprecating thoughts. Temporary relief of this distress is sought through methods that are intended to rid the body of the effects of calories. However, dieting, exercise, or a combination of both may be the primary methods used to avoid weight gain, often unsuccessfully. Patients who have BN are more likely than those who have AN to be impulsive,not only in eating behavior, but in their use of drugs and alcohol,self-mutilation or self-harm, sexual promiscuity, lying, stealing, and other manifestations of personality disturbance. Patients who have BED also recognize their eating patterns as being abnormal, but demonstrate less of an outward response. However, their internal response of distress may be just as severe; thus,patients who have either BN or BED are at risk of being depressed,often severely.Compensatory mechanisms to avoid weight gain (self-induced vomiting,laxatives, exercise, fasting)distinguish BN from BED. BED involves recurrent binge eating episodes without compensatory mechanisms to avoid weight gain, but with frequent failed attempts at dieting. Therefore,most people who have BED are overweight. Binge eating is associated with eating alone due to a sense of embarrassment and with feelings of disgust or guilt during and after a binge. Thus,intermittently eating large amounts of food in a brief period at social gatherings(such as a party) or to “bulk up at a training table” for sports (such as football) does not necessarily represent pathologic binge eating. However, engaging repeatedly in overeating and in compensatory weight control habits (such as dieting) may predispose vulnerable individuals to develop an eating disorder.An example of this process is represented by a 16-year-old boy who played high school football as a middle linebacker at a weight of 96.76 kg (215 lb), which he attained by intentionally overeating, with reinforcement by his coaches. When he later tried out for the wrestling team, he was informed that the only slot remaining was at 65.25 kg (145 lb). To “make weight,” he developed the habit of fasting,exercising in a plastic suit to stimulate sweating, and vomiting after eating. Of course, he was unhealthy and unable to compete when he finally reached the 65.25 kg (145 lb) level (similar weight control methods recently resulted in the deaths of three collegiate wrestlers in the United States). Moreover, he found it difficult to reverse his established habits and was admitted to the hospital weighing 51.75 kg(115 lb), unable to eat without feeling guilty and vomiting.BED was known formerly as compulsive overeating, but presently it is included as an example of an “Eating Disorder Not Otherwise Specified” (ED-NOS 307.50) in DSM-IV. Proposed criteria for BED include a frequency of binge eating of at least twice a week for 6 months (Table 3). Because it has been identified only recently as a distinct eating disorder, little is known about the prevalence, course,or treatment of BED, especially among children and adolescents. However, it is clear from national surveys that obesity is an emerging problem among patients in the second decade of life, and clinicians should be especially concerned about BED among those patients who gain weight quickly.Eating disorders are not distributed uniformly in the population. More than 90% of patients are female, more than 95% are caucasian,and more than 75% are adolescents when they first develop their eating disorder. Most patients are from middle to upper socioeconomic status families, but patients can be of any gender, race, age, or social stratum. Recent studies suggest that the prevalence of eating disorders among minority females and adolescents of color is much higher than previously suspected. Age- and gender-specific estimates suggest that approximately 0.5% to 1% of teenage females develop AN; up to 5% of older adolescent and young adult females develop BN. BN is more common among high school and college students than among middle or junior high groups, with a peak incidence occurring around 18 years of age. However, a recent population-based study by the Commonwealth Fund estimates that 25% of adolescents regularly engage in self-induced purging as a means of controlling their weight. Although there are no reliable population estimates for BED among children and adolescents,clinical experience with obesity in adults suggests that it is at least as common as the other conditions combined.Mild variants of eating disorders that do not meet full diagnostic criteria but still present a threat to the growth and development of adolescents (variations or problems in the DSM-PC schema) occur in an additional 5% to 10% of postpubertal females. Surveys suggest that many females in late childhood and adolescence feel a need to diet or lose weight and, therefore, are at risk of adopting potentially harmful weight-loss habits. The increase in prevalence rates over time for eating disorders is accounted for primarily by increases in the incidence of BN; increased media attention, improved detection, and less stringent diagnostic criteria also probably contribute to the apparent “epidemic” of eating disorders. Although males constitute a small proportion of adolescents who have eating disorders, most of those who have eating disorders have either BN or BED. Moreover, they are more likely to engage in binge eating and vomiting in association with athletics, as demonstrated by the patient mentioned previously.The etiologies of AN, BN, and BED are not well understood, but a combination of biologic, psychological, and societal factors most likely contribute to the predisposition, precipitation, and perpetuation of these disorders. Emerging data suggest a substantial biologic predisposition to both AN and BN. Strober found the risk of eating disorders (especially subthreshold eating disorders as described in the DSM-PC) in mothers and sisters of probands who had AN to be roughly eight times the lifetime expectancy in the general female population (see Suggested Reading). The Virginia Twin Registry also found a strong association between AN and BN in families. Studies of twins have found heritability estimates in the range of 50% to 90%for AN and 35% to 50% for BN. Genetic studies appear to be converging on the conclusion that there is an underlying biologic diathesis to eating disorders. Cultural, social, and environmental factors undoubtedly play a role, but the majority of individuals exposed to these factors do not develop an eating disorder.Another potential factor predisposing individuals to the development of an eating disorder is imbalance of neurotransmitters, among which serotonin (5-HT) is the most extensively studied. At the medial hypothalamus, higher levels of 5-HT tend to decrease appetite and food intake, and lower levels are associated with decreased satiety. The central nervous system serotonin precursor, 5-hydroxyindolacetic acid(5-HIAA), tends to be reduced significantly in patients who have AN when they are ill, but elevates significantly after recovery. Recovery from BN also is associated with elevated levels of 5-HIAA. Kaye and colleagues interpret these findings as evidence that a disturbance of serotonin activity may create a vulnerability for the expression of a cluster of symptoms that are common to both AN and BN and that nutritional factors (such as dieting or binge eating) may affect symptoms characterized by disturbances in serotonergic pathways (see Suggested Reading). Multiple other neuroendocrine and neurotransmitter abnormalities are recognized in both AN and BN, but these tend to be state-dependent and normalize after nutritional rehabilitation, symptom remission, and weight restoration. Less is known about the role of neurotransmitters in BED. Other factors that predispose to BN and BED include problems with self-esteem and conflictual family dynamics.Psychosocial factors that may precipitate an eating disorder in a predisposed individual include difficulty with the developmental tasks of transition to adulthood, such as acceptance of the physical changes of puberty, peer group involvement, and issues related to the acquisition of a stable identity and adult autonomy. Stressful times of transition (eg, entering high school or college), family conflicts, or ineffective attempts to cope with stress also may precipitate an eating disorder. Patients who have eating disorders report feeling “in control” when engaged in weight control behaviors, especially when those behaviors evoke secondary gains, such as hearing from friends about how much thinner they look or realizing that parents cannot make them eat against their will. Thus, the development of an eating disorder can be precipitated by interpersonal difficulties with friends or parents, but the disorder also can provide a powerful mechanism for coping with these problems.Depression and sexual trauma are two important psychological factors that have been discussed extensively in the pathogenesis of both BN and BED. Patients who have either BN or BED are predisposed to have both a family and a personal history of depression. It often is difficult to determine clinically whether patients are depressed because they have the eating disorder or whether the eating disorder is a clinical manifestation of an affective disorder. Although there appears to be a higher incidence of sexual trauma (eg, incest, rape) among adolescents who have BN than the population at large or than those who have AN,most patients who have BN have no such history. Nonetheless, the presence of either depression or a history of sexual trauma should be sought during patient evaluation because effective treatment generally needs to address these issues as well as the specific concerns raised by the disordered eating.People who go on restrictive diets are at risk for the development of both excessive dieting and binge eating because starvation can trigger obsessive focus on food and feelings of loss of control, with an unintentional and undesired gain in weight and so-called “yo-yo dieting.” A common aphorism in this regard is the warning:“The best way to gain weight is to diet.” Specific groups at risk for the development of eating disorders include athletes (specifically gymnasts and runners) and adolescents who have low self-esteem. Many adolescent girls experience a decrease in self-esteem during the transition from adolescence to adulthood. Although poorly understood,this may represent a societal phenomenon that involves messages related to acceptable body images and conflicting messages about women’s role in society.The symptoms and signs experienced by patients who have eating disorders are related to the various habits used to control weight(Tables 4, 5, 6). Some clinicians question whether patients are honest in answering questions about symptoms, but experience using comprehensive checklists, such as the Guidelines for Adolescent Preventive Services or the Bright Futures, suggests that adolescents generally are honest in completing such surveys or in responding to direct questions. Straightforward questions include:“How do you feel about your weight?” “Are you satisfied with your eating patterns?” “Do you ever eat in secret or eat large amounts of food in a short time?” “Have you tried to lose weight or control your weight by vomiting, taking diet pills or laxatives, or starving yourself?” “Do you exercise?” “Tell me more about your exercise, what do you do, for how long, and how often?” Privacy and confidentiality should be respected, as with any clinical interaction with an adolescent patient. Similarly, the history should be taken with the goal of developing a plan of action to help the patient feel better and not merely to rule out an eating disorder.BN or BED is diagnosed primarily on the basis of the history. Because starvation and malnutrition result in greater physiologic disruption than binge eating, there tend to be fewer physical findings in these two conditions than in AN, and laboratory data contribute more to the determination of physiologic stability than to the diagnosis of an eating disorder. Symptoms are related to recurrent binge eating,purging, chaotic eating patterns, and prolonged starvation. It is important to determine any history of weight loss or of weight cycling. Methods of weight loss can include food restriction (often significantly fewer than 1,000 kcal/d), excessive exercise, and purging (vomiting, ipecac, laxatives, or diuretics). Symptoms of malnutrition and eating disorder behaviors include cold intolerance,fatigue, constipation, sleep, and mood disturbances; binge eating is associated with weight gain and feelings of discomfort after ingesting large amounts of food. Binge eating and vomiting may result in tender,enlarged salivary glands. Amenorrhea is universal among postmenarchal females who have AN, but it occurs in only about 30% of those who have BN and is unusual in BED. Although rare, chest, abdominal, or back pain or hematemesis can signify an esophageal tear due to trauma from vomiting. Determining the presence of a distorted body image is an important part of the history for any patient who is suspected of having an eating disorder because it will suggest the severity of the drive for thinness and for binge eating in addition to the dissatisfaction with physical appearance. Likewise, obtaining a history of eating patterns, using a daily food journal, will provide data for meal planning.The initial physical assessment involves weight and height determinations and vital signs (temperature, blood pressure, and orthostatic pulse measurements). The percent of average weight for height can be calculated by using standard growth charts for patients younger than 10 years of age or the body mass index [BMI =(weight in kg) ÷ (height in m2)] can be used for patients 10 years and older to determine if they are within the normal range of weight for height(FigureF1). A body weight 90% to 110% of average correlates with a BMI of 18.5 to 23 for adults; the BMI for children, however, is different for boys and girls and increases with age up to about age 20. Population weight for height curves are widely available for growing children and are more reliable than BMI at younger ages. Average body weight can be determined for females who have completed their growth by using the formula 45 kg (100 lb) for 152.4 cm (5 ft) and 2.25 kg (5 lb) for each additional 25.4 cm (1 in) of height (eg, 254 cm =45 + 9 kg [64 in = 100 + 20 lb]). Unstable vital signs indicating hypometabolism include an orthostatic pulse differential between supine and standing of more than 30 beats/min, hypothermia (temperature, <35.2°C[96°F]), or hypotension (systolic blood pressure <90 mm Hg). Patients who have hypovolemia from vomiting or using laxatives also have orthostatic pulse changes, but usually do not have hypothermia or hypotension. With excessive weight gain, the blood pressure can become elevated.Several characteristics of BN appear on physical examination. Salivary gland enlargement (parotid, submandibular) can result from stimulation due to recurrent binge eating and vomiting; it usually is not seen with binge eating or vomiting in isolation. Erosion of dental enamel due to exposure to gastric acid can be associated with recurrent vomiting, but it has been related more closely to viscous saliva than to the frequency or duration of vomiting. Russell sign is an abrasion or callus, generally occurring on the skin over the metacarpophalangeal joint of the index or middle finger of the dominant hand, caused by trauma from inducing vomiting by pharyngeal stimulation. Absence of these findings does not preclude the diagnosis of BN, but their presence is strongly suggestive of it. Other signs of BN occur from malnutrition: dry skin, alopecia, acrocyanosis, and decreased capillary refill. When peripheral edema occurs, it is more likely due to rebound fluid retention (due to high levels of vasopressin and aldosterone after repetitive purging) or to poor capillary integrity (due to malnutrition) than to low blood protein and albumin content.There are no specific physical characteristics of BED other than weight gain and its complications (eg, insulin resistance, sleep apnea,daytime somnolence, and pseudotumor cerebri).Because the diagnosis of an eating disorder is a clinical one,there is no confirmatory laboratory test. Laboratory abnormalities in affected patients are due to malnutrition, the weight control habits used by the patient, or the complications thereof. The indicated studies are dictated by the history of weight control methods used and findings on physical examination, but a routine screening battery could include a complete blood count (with differential), erythrocyte sedimentation rate (ESR), and biochemical profile. Patients who are vomiting should have their electrolyte levels monitored, with particular attention to both potassium and carbon dioxide concentrations. Unless the patient has a symptom complex that is consistent with a thyroid disorder, thyroid testing rarely is helpful. For example, low temperature and bradycardia should be associated with weight gain and fatigue in the presence of hypothyroidism. On the other hand, large amounts of magnesium can be lost in diarrheal stools, and hypomagnesemia may be an asymptomatic cause of persistent hypocalcemia as well as a risk factor for cardiac tachyarrhythmias.The results of many blood tests depend on the patient’s state of hydration. Persistently abnormal values should be followed closely and may indicate the presence of an underlying organic illness. Because results of laboratory studies are normal for many patients, it is important to emphasize that studies are obtained as a baseline, not to establish the diagnosis. Management may not be affected by the results,but obtaining a few baseline tests is justifiable. Imaging studies have no place in the routine evaluation of eating disorders, but they may be indicated in individual cases. Electrocardiography (ECG) may be useful to determine the nature of profound bradycardia that generally is associated with weight loss.A low white blood cell count is characteristic of starvation and is seen more commonly in AN than in BN or BED. Because the primary cause of this phenomenon appears to be increased margination of the leukocytes, most patients do not have an increased risk of infection. The ESR, on the other hand, is uniformly normal in all eating disorders; an elevated value should trigger a search for an occult organic illness, such as inflammatory bowel disease. The hemoglobin also is typically normal, although it may be elevated in dehydration or reduced when iron intake is reduced drastically, as in a vegetarian diet. If caloric intake is chronically low, the blood glucose may be low or low-normal due to the lack of glucose precursors in the diet or glycogen stores; hypoglycemia is more common in AN than in either BN or BED. Renal function usually is normal, but the blood urea nitrogen can vary between high (dehydration) and low (low protein intake). With the significant malnutrition typically seen in AN, liver function tests may reveal mildly elevated (1½ to 2 times normal) enzyme levels, but they are not in the hepatitic range. Bilirubin metabolism is normal, so both total and conjugated levels of bilirubin are normal in all forms of eating disorders. Cholesterol levels often are elevated, sometimes dramatically, in starvation states. There appear to be at least three reasons for this: 1) cholesterol breakdown is related to T3 levels, which may be depressed;2) cholesterol binding globulin often is low; and 3) with fatty infiltration (without hepatomegaly), there may be a “leakage”of intrahepatic cholesterol.Laboratory findings in BN may include hypokalemic, hypochloremic metabolic alkalosis due to recurrent vomiting; blood studies also may reflect hemoconcentration. Metabolic alkalosis usually is not seen unless the patient is vomiting at least three times a day, and it corrects quickly with cessation of vomiting. Serum potassium concentrations tend to normalize when blood pH is corrected, as intracellular potassium shifts from the intracellular to the intravascular compartment; persistent hypokalemia in the presence
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