Feeding and Eating Disorders


10


FEEDING AND EATING DISORDERS


DSM-5 (American Psychiatric Association 2013) placed all of the eating and feeding disorders in a single section, whether the typical onset is in early childhood (pica, rumination disorder), at any time in the lifespan (avoidant/restrictive food intake), or in adolescence and young adulthood (anorexia nervosa [AN], bulimia nervosa [BN]). None of these diagnoses has onset restricted to a single developmental period.


PICA


Clinical Description


Pica is the persistent consumption of nonnutritive, nonfood materials that is not developmentally appropriate and not culturally sanctioned or socially normative. Pica in children most often comes to clinical attention in association with other behavior and medical problems.


Epidemiology


Pica can occur at any age, most commonly with childhood onset. A minimum age of 2 years for the diagnosis distinguishes pica from developmentally normative mouthing and ingestion of objects in infants and toddlers. Pica may manifest in pregnancy with cravings for nonfood items such as chalk or clay, but the diagnosis is considered only if the ingestion poses medical risk. Pica may be more prevalent in individuals with intellectual disability, but overall prevalence is unknown.



Etiology


Possible causes include nutritional deficiencies, insufficient stimulation, parent–child relationship difficulties, or cultural tradition, although there is no definitive support for any of these.


Course and Prognosis


Pica usually starts in young children and resolves by school age except in persons with intellectual disability, who may have pica into adulthood. Common nonfood items ingested include ice, chalk, paper, clay, and soil. Delayed motor and mental development, neurological deficits, and behavioral abnormalities may predate (and perhaps contribute to) or result from pica. Pica has numerous potentially severe medical complications, including heavy metal poisoning, parasitic infections, or intestinal obstruction. Lead toxicity (from ingestion of peeling paint, dust from home renovation, plaster, or soil) can lead to learning disorders, hyperactivity, fatigue, weight loss, and constipation, and even to toxic encephalopathy.


Evaluation


Pica should be considered in all cases of developmental delays, learning difficulties, intellectual disability, unusual behavioral symptoms, and chronic constipation. In order to diagnose pica, the clinician must complete a full psychiatric evaluation (see Chapter 2, “Evaluation and Treatment Planning”) as well as determine the child’s nutritional status and feeding history. Inadequate supervision of children or parental neglect should be considered. Questions should be asked about peeling paint or renovation in the home that might increase lead exposure. Periodic blood tests for lead in children with pica are recommended. Consultation with pediatric colleagues is indicated if blood lead levels are greater than 4 micrograms per deciliter.


Treatment


Behavior therapy has been successful in the treatment of pica in individuals with intellectual disability and may be applicable to other children. Components include education of caregivers, rewards for appropriate eating, and teaching how to differentiate edible foods. Appropriate responses to instances of pica include overcorrection (enforced immediate oral hygiene) and negative reinforcement (time-outs, restriction of privileges), combined with a positive reinforcement contingency behavior plan (reward system). Additional interventions include increased supervision, promotion of appropriate stimulation, improvement of play opportunities, or placement in day care. Concomitant treatment of medical complications may be required.


RUMINATION DISORDER


Clinical Description


Rumination is the regurgitation and rechewing or spitting out of recently ingested food, which, when it recurs repeatedly, is called rumination disorder. Once thought to occur only in infants or in individuals with intellectual disability, rumination disorder is now recognized to occur in developmentally typical children and adults. In older children and adults, rumination begins with a rise in intragastric pressure produced by voluntary, but not always intentional, contracture of the abdominal muscles.


Etiology


The etiology is unknown. Rumination is highly associated with gastroesophageal reflux. Clinicians generally presume that the infant, lacking external sources of gratification, uses rumination for self-stimulation or social reinforcement. However, although an understimulating or overstimulating environment can contribute to the appearance of rumination disorder, some infants with the disorder appear happy, are developing normally otherwise, and have emotionally supportive and interactive parents.



Course and Prognosis


Rumination typically occurs during the first year of life, resolving by the second year, or in adolescence, often accompanied by anxiety, depression or other eating disorders. Tooth decay, failure to thrive, dehydration, electrolyte imbalance, and malnutrition can be complications.


Evaluation and Differential Diagnosis


Behavioral and psychiatric evaluation of the child and parents emphasizes developmental history and psychosocial assessment, feeding and eating history, nutritional status, attachment, and observation of parent–child interactions during feeding. Medical conditions, including gastroesophageal reflux and cyclic vomiting, must be considered.


Treatment


Behavioral consultation is highly recommended in treating rumination disorder. In infants, parent training focusing on behavioral techniques, including positive attention and interaction (cuddling and playing with the child before, during, and after mealtimes), will reduce social deprivation and behavioral withdrawal. Negative reinforcement (ignoring) combined with a reward for time not ruminating (parental attention and social interaction, such as playing) can be used in outpatient treatment. In adolescents, behavioral interventions include habit reversal training (HRT), diaphragmatic breathing, and biofeedback (Mousa et al. 2014).


Pediatric hospitalization may be necessary if rumination results in significant malnutrition. Hospitalization can be beneficial by providing a partial separation of the child from the primary caregiver, an alternative feeding environment for the child (to “decondition” the symptoms), and a period of respite for the parent. Continuing treatment facilitates attachment between child and parent, monitors the psychosocial environment at home, and provides support in the event of emerging developmental problems.



AVOIDANT/RESTRICTIVE FOOD INTAKE DISORDER


Clinical Description


DSM-5 (American Psychiatric Association 2013) renamed this disorder and expanded the criteria. Avoidant/restrictive food intake disorder (ARFID) is characterized by restrictive or food avoidant behaviors that result in failure to meet energy or nutritional requirements. These behaviors may result from lack of interest in eating, sensory sensitivities, fear of choking, or history of traumatic experiences such as forceful feeding. They do not, by definition, have fear of gaining weight as a motivation. Limited information is available on this heterogeneous disorder.


Epidemiology


Prevalence data are currently limited to clinical samples. In an eating disorders clinic (patients age 8–18 years), 14% of patients presented with a diagnosis of ARFID (Fisher et al. 2014). Compared with youth with diagnoses of anorexia nervosa or bulimia nervosa, patients with ARFID were younger, more likely to be male, and more likely to have comorbid medical or anxiety disorders, and had a median body weight percentile between that of patients with AN and BN. Eddy et al. (2015) identified 1.5% of patients presenting to a gastroenterology clinic network as having symptoms that met full criteria for ARFID, also with more males than females.


Etiology


Many children who develop ARFID have a history of picky eating from early childhood. The most common underlying pattern in the Eddy et al. (2015) series was lack of interest in food, followed by limited diet due to sensory issues. The aversive/traumatic experience type is least common.



Course and Prognosis


Because the diagnosis of ARFID is relatively new, little is known about the long-term course and prognosis. In a study of children hospitalized with ARFID, a year after admission about half the patients met criteria for readmission and 20% were readmitted. These were similar numbers to patients with AN (Strandjord et al. 2015).


Evaluation and Differential Diagnosis


ARFID must be distinguished from failure to take in adequate nutrients due to medical conditions, including malabsorption, neoplasm, gastroesophageal reflux, or other gastrointestinal disorders. It differs from anorexia nervosa because patients with ARFID are not motivated to lose weight and are not dissatisfied with their weight or body image. ARFID is distinct from normative picky eating in that the child fails to meet nutritional requirements, has substantial weight loss (or, in children, absence of expected weight gain), becomes dependent on enteral feeding or dietary supplements, and/or has significant psychosocial interference.


Evaluation includes medical, dietary, and psychosocial histories and an examination to measure height and weight (and calculate body mass index). Review of a longitudinal growth record is useful. Laboratory evaluation should be done to assess for nutritional deficiencies (e.g., electrolyte abnormalities, anemia).


Treatment


Pediatric hospitalization may be required for individuals with severe nutritional deficiencies. There are very limited data on treatment, but for those individuals who can be managed as outpatients, a multidisciplinary, family-based approach that addresses the restrictive or food-averse behaviors is indicated. Behavioral or cognitive-behavioral treatments should be tailored to the underlying reasons for the disordered eating (Norris et al. 2016).



ANOREXIA NERVOSA AND BULIMIA NERVOSA


Anorexia Nervosa


Clinical Description


Anorexia nervosa is characterized by a refusal to maintain normal weight or a failure to reach expected weight gain as a result of intentional diet restriction or other extreme measures. Patients have either a distorted perception of their body shape and size or a denial of the seriousness of the weight loss. The preoccupation with food and body shape is obsessive. In severe cases, these patients may appear delusional. The appetite is not lost; rather there is an intense fear of gaining weight. DSM-5 (American Psychiatric Association 2013) removed the prior diagnostic requirement for amenorrhea. The restricting type of AN is characterized by strict dieting, fasting, or excessive exercise. In the binge-eating/purging type, huge quantities of food are eaten and then purged.


The physiological process of starvation leads to the development of additional psychological symptoms. Patients may become socially withdrawn, irritable, and anhedonic, with decreased interest in sex, low self-esteem, and recurrent feelings of helplessness and inadequacy. This picture may be consistent with major depression. Depression impairs the individual’s ability to function in the classroom, in social situations, and within the family. Patients tend to be controlling, not only of their own habits but also of those around them. Patients are often preoccupied with personal academic achievement and exercise. An accompanying diagnosis of obsessive-compulsive disorder (OCD) should be made if criteria are met.


Epidemiology


The majority of patients with AN are female, with an estimated prevalence of 0.3%–0.7% of adolescent girls in the United States. Onset of AN prior to puberty is rare. The incidence peaks in the 14- to 24-year age group. Milder forms of eating disorders are even more common. AN is found predominantly in Western industrialized nations, and the prevalence is probably significantly affected by social and societal factors. The prevalence in boys, minority populations, and non-Western countries is lower but increasing.


Etiology


Various biological, psychological, and environmental factors have been associated with AN, although whether these are correlative or etiological is not clear (Le Grange 2016). Genetic and neurophysiological mechanisms contribute to the development of both AN and BN. First-degree relatives of anorexic and bulimic patients are 6–10 times more likely to have an eating disorder than are control populations. However, it remains difficult to separate environmental from heritable causative factors. Patients experience a variety of psychological, physical, academic, and social problems, although distinguishing cause and effect is often difficult. These patients tend to be dissatisfied with their bodies at puberty. Dieting is chosen as a socially acceptable method to improve the patient’s sense of well-being and control. Patients with AN tend to be perfectionistic, cognitively rigid, and detail-oriented, with an obsessive and conflict-avoidant personality style. Some studies have found that societal ideals of beauty (particularly in Western cultures), peer group influences, and engagement in certain activities (e.g., gymnastics, wrestling, dance, modeling) increase the risk of AN.


Family dynamics, including parental over-involvement, lack of appropriate boundaries within the family, and insufficient autonomy, have received much attention in the literature for the past four decades (Minuchin et al. 1978). However, few studies have tested these theories, and these characteristics are also present in families in which eating disorders do not develop. Thus, the etiological role, if any, of family dynamics remains unclear.


Course and Prognosis


AN usually manifests during adolescence, between ages 14 and 18 years, a time of rapid growth with accompanying weight gain and changes in body shape. Although onset before puberty is less common, prepubertal children may develop AN or problem eating behaviors, including food avoidance, body image disturbance, inappropriate dieting, overeating, ritualistic behavior during meals, and selective eating. The first evidence of dissatisfaction with body shape may be found in a preoccupation with dieting. In one community survey, more than half of the girls considered themselves to be overweight, although only 15% were actually overweight (Mellin et al. 1992).


Physiological sequelae are common. Serious medical complications may require hospitalization (Palla and Litt 1988; Table 10–1). The course of AN is typically prolonged, and the disorder does not remit without treatment. Continuing symptoms include low weight for height and age, peak bone mass reduction, excessive concern with weight or appearance, pubertal delay or interruption, amenorrhea, morbidity and mortality associated with serious medical complications, and troubled social and sexual relationships. Poor outcome is associated with longer duration of illness, extreme weight loss, and poor interpersonal relationships. Adolescent patients have a better prognosis, lower mortality, and better response to treatment than do adults.
































































































TABLE 10–1. Physical signs and symptoms and complications associated with anorexia nervosa and bulimia nervosa


Cardiovascular


Hypotension (especially postural)



Bradycardia (rates between 40 and 50 beats per minute)



Arrhythmias (prolonged QT interval may be a marker for risk of sudden death)



Mitral valve prolapse



Cardiac arrest



Edema and congestive heart failure during refeeding



Cardiac failure secondary to cardiomyopathy from ipecac (emetine) poisoning


Neuroendocrine


Amenorrhea or irregular menses (low levels of FSH and LH despite low estrogen levels)



Low basal metabolism rate



Abnormal glucose tolerance test with insulin resistance



Hypothermia



Elevated levels of growth hormone and cortisol



Sleep disturbances


Bone


Osteopenia


Fluid disturbance


Dehydration



Electrolyte imbalance



Abnormal urinalysis


Gastrointestinal


Constipation



Diarrhea


Hematological


Leukopenia



Anemia



Thrombocytopenia



Low sedimentation rate


Dermatological


Dry skin



Lanugo (baby-fine body hair)


Oral, esophageal, and gastric damage from vomiting and/or binge eating


Loss of dental enamel


Gastritis


Enlarged salivary glands


Esophagitis



Esophageal tear



Pancreatitis


Note. FSH = follicle-stimulating hormone; LH = luteinizing hormone.


Source. Adapted from Palla and Litt 1988.


Mortality in part depends on chronicity. Risk of death from medical complications of AN is estimated at between 5% and 7%, with as many as 50% of these deaths due to suicide (Arcelus et al. 2011). Comorbid psychiatric diagnoses contribute to a poor prognosis, and partial remission is common, especially in patients with psychiatric comorbidity.


Evaluation and Differential Diagnosis


A complete history, physical examination, and routine laboratory studies are necessary to rule out other psychiatric or medical causes for loss of weight or appetite. In addition, starvation can produce physiological disturbances that should be identified through laboratory studies (see Table 10–1). An electrocardiogram and DEXA scan (to evaluate for osteoporosis) should be ordered in addition to blood tests. Hypoglycemia is a particularly poor prognostic sign. Dehydration can lead to elevations in blood urea nitrogen, liver function test values, and serum cholesterol levels. Signs of infection may be masked by leukopenia and hypothermia. Abnormal thyroid function studies are classified as “sick-euthyroid syndrome,” with normal to low levels of thyroxine (T4) and free T4 and variable levels of thyroid-stimulating hormone.


The psychiatric interview of a patient with suspected AN includes details about the onset and course of the eating disorder, the highest and lowest weight, and the weight identified by the patient as most comfortable. The clinician should also explore daily eating patterns, including not only amounts of food but also times for meals. Questions about the use of laxatives, emetics, or diuretics and exercise can be incorporated into this eating history. Although anorexic patients learn to disguise their continuing wish to lose weight, hide excessive exercise and purging, and claim to eat more than they do, they may inadvertently reveal important diagnostic information during an eating history. Family members may provide supplementary information, although patients with AN often hide their symptoms.


In addition to individual assessments, a family evaluation is essential in treating young patients. The therapist may ask family members about their impressions of the illness and its origins. A review of at-home treatment attempts uncovers family dynamics and individual perceptions about the problem’s origins and possible solutions. A family eating or weight history may show patterns of behavior imitated by the child or adolescent. Family history of psychiatric illness may suggest similar diagnoses in the patient.


The differential diagnosis of AN is shown in Table 10–2.
















































TABLE 10–2. Differential diagnosis of anorexia nervosa


Normal thinness



Physical disorders causing weight loss


Hyperthyroidism



Cystic fibrosis



Other endocrine disorders, such as Addison’s disease and diabetes mellitus



Gastrointestinal disorders resulting in vomiting, loss of appetite, and/or malabsorption



Malignancy



Chronic infection


Psychiatric disorders causing loss of appetite and weight loss


Depression


Avoidant/restrictive food intake disorder



Rumination disorder



Peculiar eating behavior secondary to obsessive-compulsive disorder or to delusions in schizophrenia or psychotic depression



Avoidance of eating caused by phobia of choking, with or without psychosis



Vomiting secondary to conversion disorder


Hypothyroidism producing hypothermia and amenorrhea



Treatment


The treatment of AN should be comprehensive and emphasize a return to normal eating patterns. In most cases, the initial focus of treatment is on acceptance of the disorder and weight gain. In severe cases, this initial phase may take place on an inpatient unit. Typical indications for inpatient hospitalization include weight more than 25% below ideal body weight, rapid and severe weight loss refractory to outpatient treatment, hypothermia, symptomatic hypotension or syncope, heart rate below 50 beats per minute, severe electrolyte abnormalities, severe dehydration or evidence of arrhythmia, or a prolonged QTc interval. The denial of illness and fears of loss of control and of becoming fat generate severe resistance to treatment, even when the patient and family acknowledge the diagnosis. A firm focus on a target weight within 90% of the ideal body weight is helpful. The patient should reach this goal through gradual weight gain of 1 pound per week as an outpatient or 2–3 pounds per week while hospitalized (Mehler 2001). Too-rapid increase in food intake can lead to medically dangerous “refeeding syndrome.” Appetite stimulants are not recommended and may be contraindicated. Involvement of a primary care physician and a pediatric dietitian with experience in eating disorders is essential, whether treatment is inpatient or outpatient. Psychotherapeutic approaches can act as an adjunct to the refeeding regimen. Forced weight gain alone is futile, and too-rapid weight gain exacerbates fears of loss of control and may be medically hazardous. Tube or intravenous feeding is reserved for medical emergencies, because these methods are viewed by patients as punitive. The patient’s sabotage of these methods can be dangerous (e.g., bleeding from the site of a pulled intravenous line, aspiration of tube feedings). Regardless of the success of refeeding, a comprehensive treatment plan that includes an exploration of underlying psychological factors is essential.


Family therapy is particularly effective in adolescents with AN. The Maudsley model of family-based treatment (FBT) has the strongest empirical support (Lock et al. 2005). Families are affected secondarily by the presence of the eating disorder, and the clinician should not assume that every family has premorbid problems. Psychoeducational programs for family members greatly facilitate treatment and may be done in an individual or group setting (see Appendix, “Resources for Parents”). Family involvement in treatment, whatever the primary modality, clearly benefits young patients. Current FBT emphasizes parents as part of the solution, not the cause of the problem. Parent-focused treatment (PFT) is a modification of FBT in which the therapist meets with the parents only, while a nurse monitors the patient. In a randomized controlled trial, PFT was more efficient at weight restoration in adolescent patients with AN (Le Grange et al. 2016).


Individual psychotherapy is generally a second choice for adolescent patients but may be indicated for patients whose families are unwilling or unable to participate. Adolescent focused therapy (AFT) and cognitive-behavioral therapy (CBT) have demonstrated efficacy in treatment of AN (Lock et al. 2015). CBT initially emphasizes changing incorrect beliefs and dysfunctional cognitions about food and eating. The focus of treatment eventually extends to include issues of body weight, appearance, peer relationships, and individual control. Cognitive-behavioral interventions (e.g., the use of food diaries) have been effective, particularly in preventing relapse in patients once weight has returned to normal.


Once the patient’s eating patterns have normalized, interpersonal psychotherapies may provide insight for the patient that will facilitate long-term recovery. Older patients tend to do well with individual therapies, while younger patients respond best to family interventions.


There is little evidence supporting the use of medication in the treatment of AN. Adjunctive atypical antipsychotic medication prescribed to increase appetite and reduce rumination has not demonstrated significant efficacy in studies. Although use of selective serotonin reuptake inhibitors (SSRIs) has not been systematically studied in adolescents with AN, studies of SSRIs in adults with AN have not been encouraging. However, SSRIs may assist with comorbid anxiety and depression, once weight has stabilized. Current treatment guidelines recommend reserving medications for comorbid conditions and refractory cases (Lock et al. 2015).


Bulimia Nervosa


Clinical Description


Bulimia nervosa is characterized by repeated episodes of uncontrollable binge eating of huge amounts of food in a short time (2-hour period) accompanied by excessive attempts to compensate for this caloric intake. Bingeing and compensatory behaviors occur (on average) at least once a week for at least 3 months. Binge eating is typically done secretly and may initially be pleasurable. The patient may engage in the behavior during a dysphoric episode or in response to a recent stressor. The binge usually brings the patient relief, but self-deprecatory thoughts return. Patients feel that their eating is out of control.


Exercise and strict fasting are the most common compensatory behaviors, followed by induced vomiting. The use of laxatives, enemas, diuretics, or thyroid medication is less common, particularly in the pediatric population.


The frequency of binges increases as the disorder develops. Patients with BN are generally of normal weight but may be slightly over or under their ideal weight, and may have been overweight before the onset of the disorder. The patient’s self-image is unduly influenced by body shape and weight.


Epidemiology


Studies of the prevalence of BN are affected by changing diagnostic criteria, the relative recent definition of the diagnosis, and the secrecy of the behavior. BN is more common than AN. In almost 50% of cases, onset occurs before age 18 years. Binge eating is common among adolescents, but relatively few have signs and symptoms that meet diagnostic criteria for BN. Approximately 1%–2% of adolescent females and 0.5% of adolescent males in the United States had signs and symptoms that met DSM-IV criteria for BN. Males account for 10%–15% of all clinically referred patients with BN. Patients generally become ill in the latter half of adolescence. Risk is increased in ballet dancers and elite athletes whose sport emphasizes thinness. Bulimic patients have increased rates of drug and alcohol use, anxiety, depression, and PTSD. They tend to be of higher socioeconomic status and are typically white or Hispanic. Recent studies have noted increasing rates of BN and purging with laxatives in the African American population, although the prevalence is still lower than in whites or Latinas. Dysfunctional behaviors related to eating and weight are relatively common among adolescent and young adult females. Patients who binge but lack the compensatory behaviors (e.g., purging, excessive exercise) may meet criteria for binge-eating disorder. Studies of adolescent females note that between 40% and 60% are “dieting” to lose weight. This is particularly true among white adolescent girls from high-income families. In more than 10% of these, dieting may include induced vomiting or the use of diet pills and diuretics. Dieting behavior clearly increases the risk for eating disorders.


Etiology


AN and BN frequently present on a continuum, and many patients demonstrate symptoms of each. Approximately 50% of patients with AN will develop bulimic symptoms, and up to a quarter of patients with BN become anorectic. Identical twins of patients with BN have higher rates of the disorder. Monozygotic twins have higher concordance rates than do dizygotic twins. A family history of obesity, depression, or alcoholism is common. Sexual and physical abuse predispose children to various psychiatric disorders but not preferentially to the development of eating disorders.


Course and Prognosis


Dieting usually precedes the development of BN. The patient first begins to binge-eat as a direct result of food restriction; the behavior then becomes a compulsion or an addiction. The patient regards bingeing as abhorrent behavior, which contributes to feelings of depression and self-criticism. The patient once again begins dieting, often augmented with vigorous exercise or purging, in an attempt to undo the damage of the binge. Although these behaviors give the patient temporary relief from the emotional pain, they become part of a vicious cycle that maintains symptoms of BN and depression. A constant state of semi-starvation results, which places the patient at additional risk for mood disorders. The rates of suicidal ideation (53%) and suicide attempts (35%) are elevated in adolescents with BN (Lock et al. 2015).



Few studies have examined either the short- or the long-term prognosis for treated bulimic patients. Relapse rates are 30%–50% when patients are followed for 6 months to 6 years. Some speculate that improvement continues for 10–15 years. Risk factors for relapse include induced vomiting and the use of alcohol or drugs. Patients with milder symptoms at the onset of treatment appear to have a better prognosis. Among bulimic adolescents, comorbid anxiety or mood disorders predict continued eating-disordered behaviors. No factors have been identified as predictive of treatment success. Studies note a BN mortality rate of approximately 5%.


Social complications can be severe, with time and finances depleted by obtaining food, binge eating, and purging. School functioning and peer relationships typically deteriorate. Associated disorders include anxiety, depression, PTSD, substance abuse, and (in adults) borderline personality disorder. The presence of a comorbid medical diagnosis (i.e., diabetes, cystic fibrosis) may cause otherwise benign levels of symptoms to become dangerous. The risk of suicide or death from medical complications is significant. Risk factors for death from bulimia include a greater than 2-year duration; daily vomiting or bingeing; and use of laxatives, diuretics, ipecac, and stimulants (diet pills).


Evaluation and Differential Diagnosis


The clinician should evaluate the patient by 1) obtaining a detailed lifetime history of weight changes, noting periods of greatest fluctuation; 2) inquiring about current eating patterns in a typical day, including the number of calories consumed and any use of diet pills; 3) determining the onset and current status of bingeing and purging behaviors; and 4) asking about possible use of thyroid hormone, excessive exercise, laxatives, and diuretics. The medical history may suggest a neurological, endocrinological, or genetic (e.g., Prader-Willi syndrome) etiology of binge eating. Patients may have medical complications (see Table 10–1). The abuse of laxatives can lead to abdominal cramping, diarrhea, or rectal bleeding. Vomiting or abuse of diuretics or laxatives can produce metabolic alkalosis, elevations in serum amylase, hypomagnesemia and hypophosphatemia, and hypokalemia. A review of psychiatric history focuses on comorbidity and on previous treatment attempts. The individual’s social and personal history may reveal contributing factors. Family assessment considers dynamics; previous attempts to help the patient; eating habits; and a review of significant social, medical, and psychiatric family history.


Treatment


Goals of treatment include eliminating the binge–purge cycle, establishing healthy eating habits, and promoting new strategies and skills to deal with emotions and problematic situations. The treatment plan progresses in a stepwise fashion, beginning with nutritional rehabilitation. Nutritional consultation can facilitate eating of regular, well-balanced meals to avoid the hunger that triggers the urge to binge. Patients with BN who maintain a normal weight generally do not require hospitalization. Hospitalization is indicated when the patient is suicidal, has out-of-control eating and vomiting, is metabolically unstable, or does not respond to outpatient treatment. In the hospital, a behavior contract can be implemented, with activities and privileges contingent on eating regular meals and not vomiting. Patients must be watched closely for hiding or stealing food and for secretive vomiting.


A manualized family-based treatment for BN in adolescents has empirical support (Le Grange et al. 2015). CBT is the most effective treatment for BN in adults and may be preferable to family-based treatment for adolescents from high-conflict families. Case series and one controlled trial support the use of CBT in adolescents (Schmidt et al. 2007). It can help patients overcome feelings of helplessness and the habit of using food to deal with their uncomfortable feelings. The patient learns skills and strategies for problem solving, coping with stress, identifying feelings, and avoiding relapse. Patients are more successful when they have lower weights and do not abuse laxatives or diuretics.


Pharmacological treatment of BN in adolescents does not have research support, although in an open-label medication trial of adolescents with BN, fluoxetine at treatment dosages of 60 mg/day was well tolerated and associated with improvement (Kotler et al. 2003). SSRIs may be useful for comorbid psychiatric disorders. Bupropion increases the risk of seizures and should not be used in these patients.


REFERENCES


American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Arlington, VA, American Psychiatric Association, 2013


Arcelus J, Mitchell AJ, Wales J, Nielsen S: Mortality rates in patients with anorexia nervosa and other eating disorders: a meta-analysis of 36 studies. Arch Gen Psychiatry 68(7):724–731, 2011 21727255


Eddy KT, Thomas JJ, Hastings E, et al: Prevalence of DSM-5 avoidant/restrictive food intake disorder in a pediatric gastroenterology healthcare network. Int J Eat Disord 48(5):464–470, 2015 25142784


Fisher MM, Rosen DS, Ornstein RM, et al: Characteristics of avoidant/restrictive food intake disorder in children and adolescents: a “new disorder” in DSM-5. J Adolesc Health 55(1):49–52, 2014 24506978


Kotler LA, Devlin MJ, Davies M, Walsh BT: An open trial of fluoxetine for adolescents with bulimia nervosa. J Child Adolesc Psychopharmacol 13(3):329–335, 2003 14642021


Le Grange D: Elusive etiology of anorexia nervosa: finding answers in an integrative biopsychosocial approach. J Am Acad Child Adolesc Psychiatry 55(1):12–13, 2016 26703904


Le Grange D, Lock J, Agras WS, et al: Randomized clinical trial of family-based treatment and cognitive-behavioral therapy for adolescent bulimia nervosa. J Am Acad Child Adolesc Psychiatry 54(11):886–94.e2, 2015 26506579


Le Grange D, Hughes EK, Court A, et al: Randomized clinical trial of parent-focused treatment and family-based treatment for adolescent anorexia nervosa. J Am Acad Child Adolesc Psychiatry 55(8):683–692, 2016 27453082


Lock J, Agras WS, Bryson S, Kraemer HC: A comparison of short- and long-term family therapy for adolescent anorexia nervosa. J Am Acad Child Adolesc Psychiatry 44(7):632–639, 2005 15968231


Lock J, La Via MC; American Academy of Child and Adolescent Psychiatry (AACAP) Committee on Quality Issues (CQI): Practice parameter for the assessment and treatment of children and adolescents with eating disorders. J Am Acad Child Adolesc Psychiatry 54(5):412–425, 2015 25901778



Mehler PS: Diagnosis and care of patients with anorexia nervosa in primary care settings. Ann Intern Med 134(11):1048–1059, 2001 11388818


Mellin LM, Irwin CE Jr, Scully S: Prevalence of disordered eating in girls: a survey of middle-class children. J Am Diet Assoc 92(7):851–853, 1992 1624655


Minuchin S, Rosman BL, Baker L: Psychosomatic Families: Anorexia Nervosa in Context. Cambridge, MA, Harvard University Press, 1978


Mousa HM, Montgomery M, Alioto A: Adolescent rumination syndrome. Curr Gastroenterol Rep 16(8):398, 2014 25064317


Norris ML, Spettigue WJ, Katzman DK: Update on eating disorders: current perspectives on avoidant/restrictive food intake disorder in children and youth. Neuropsychiatr Dis Treat 12:213–218, 2016 26855577


Palla B, Litt IF: Medical complications of eating disorders in adolescents. Pediatrics 81(5):613–623, 1988 3162764


Schmidt U, Lee S, Beecham J, et al: A randomized controlled trial of family therapy and cognitive behavior therapy guided self-care for adolescents with bulimia nervosa and related conditions. Am J Psychiatry 164:591–598, 2007 17403972


Strandjord SE, Sieke EH, Richmond M, Rome ES: Avoidant/restrictive food intake disorder: illness and hospital course in patients hospitalized for nutritional insufficiency. J Adolesc Health 57(6):673–678, 2015 26422290


ADDITIONAL READING


Eddy KT, Murray HB, Le Grange D: Eating and feeding disorders, in Dulcan’s Textbook of Child and Adolescent Psychiatry, 2nd Edition. Edited by Dulcan MK. Arlington, VA, American Psychiatric Association Publishing, 2016, pp 435-460


Le Grange D, Lock J: Treating Bulimia in Adolescents: A Family Based Approach. New York, Guilford, 2007


Lock J, La Via MC; American Academy of Child and Adolescent Psychiatry (AACAP) Committee on Quality Issues (CQI): Practice parameter for the assessment and treatment of children and adolescents with eating disorders. J Am Acad Child Adolesc Psychiatry 54(5):412–425, 2015


Lock J, Le Grange D, Agras WS, et al: Treatment Manual for Anorexia Nervosa: A Family Based Approach, 2nd Edition. New York, Guilford, 2013



Rasquin A, Di Lorenzo C, Forbes D, et al: Childhood functional gastrointestinal disorders: child/adolescent. Gastroenterology 130(5):1527–1537, 2006


Rosen DS; American Academy of Pediatrics Committee on Adolescence: Identification and management of eating disorders in children and adolescents. Pediatrics 126(6):1240–1253, 2010

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