Chapter 39 Nutritional Support of Pe Disorders tric Patients With Eating Introduction Eating disorders are psychiatric illnesses defined by behavioral, cognitive, emotional, and physical criteria. The hallmarks of an eating disorder are severe disturbances in eating behavior and in the experience of the body that are associated with psycho- logical distress, Functional impairment, and often physical complications. ‘The current Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition Text Revision (DSM-IV-TR)' recognizes 3 eating disorders: anorexia nervosa (AN), bulimia nervosa (BN), and eating disorder not otherwise specified (EDNOS). The DSM-IV-R provides specific diagnostic criteria for AN and BN; EDNOS is defined by clinically significant eating disorder symptoms that do not meet criteria for either AN or BN and may include subthreshold presentations that resemble AN or BN but fall short by one or more criteria as well as binge eating disorder. Although eating disorders most often occur in females, approximately 10% of patientswith AN or BN are male, and the prevalence of eating disorders may be increasing in male, minority, and younger populations. Often, eating disorder symptoms first appear in childhood or early adolescence, and frank disorders typically have onset in middle or late adolescence or early adulthood. Lifetime prevalence estimates of eating disorders in individuals of all ages range from approximately 19% for AN to 1% to 4% for BN! one recent epidemiologic study of adolescents reported lifetime prevalence rates of 0.3% for AN, 0.9% for BN, and 1.6% For one type of EDNOS (binge eating disorder), and rates of the full range of EDNOS are likely even higher.? Further, all prevalence ratesreported may be underestimates, because eating disorders often go unrecognized, and individuals may be reluctant to acknowledge symptoms or seek treatment because of shame and fear of stigmatization. Early detection and intervention are critical and can lead to improved outcomes.’ Clinical research has focused on AN and BN, although EDNOS is the most common diagnosis in outpatient clinical settings. Children and adolescents, in particular, often do not meet full criteriafor AN or BN, because they may present with failure to gain weight adequately rather than marked weight loss, or they may minimize or deny body image dissatisfaction or overvaluation of weight/shape, for ‘example. ‘Therefore, current DSM-IV-TR descriptions may not fully capture eating disorders in younger populations and often result in the diagnosis of EDNOS, Section VE Nutrition in Acute and Chronic lines 917918 Chapter 39 which is clinically significant but heterogeneous and, therefore, conveys limited specific information. Because of the potential long-term effects of eating disorders ‘on physical and emotional growth, clinicians should lower the threshold for intervention in children and adolescents. Indeed, itis crucial that pediatricians recognize that the medical and psychological complications of EDNOS can parallel those of AN or BN. Given the predominance of empirical information available on AN and BN, this chapter Focuses on nutritional considerations for patients with these primary eating disorders but also provides commentary on how and when modifications may be appropriate or individuals with EDNOS. The goals of this chapter are to provide lnicians working with children and adolescents with practical information regarding the assessment and treatment of eating disorders and, in particular, the assessment and treatment of the common problems that occur related to nutrition and health in these complex disorders. Clinical Features ‘Anorexia Nervosa Diagnostic Criteria AN is characterized in the DSM-IV-T Rby persistent low body weight, marked fear ‘of weight gain, disturbance in the way that body image is experienced (eg, believing ‘one is fat even though underweight), and amenorthea in Females (see Table 39.1). “The Forthcoming Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM.-5), includes a slightly broadened definition of AN, and these proposed revisions are also presented in Table 39.1. Although current criteria provide a guideline for defining low body weight as less than 85% of that expected For age and gender, this threshold is often applied literally. DSM-5 is expected to remove this guideline and instead suggest a more loosely defined weight criterion of less than the minimum expectation for age and gender. When working with children and adolescents, clinicians should review growth charts to ascertain historic growth trajectory to determine whether weight and height have “fallen off” the expected ccurve for the individual patient. Further, the amenorthea eriterion is likely to be climinated in the DSM-5. Pediatric Nutrition, 7th EditionNutritional Support of Pediatric Patients with Eating Disorders 919 Table 39.1. Diagnostic Criteria for Anorexia Nervosa Cente) feet) Body weight | Refusal to maintain a body weight more _ | Restriction ofeneray intake than 85% of expected for height and age; _| relative to requirements leading failure to gain weight during a period of |_| toamarkedly ow body weight arowth with body weightless than 85% | (less than that minimally expected for height and age. expected for age and height) ‘Menstruation | In postmenarchal females, the absence This criterion is ikely to be of three consecutive menstrual cycles deleted. (hormonally induced menstruation is excluded). Fear of ven though underweight, an intense fear _| Intense fear of gaining weight weight gain | of gaining weight or becoming fat. cor becoming fat or persistent behavior that interferes with weight gain, even though at a significantly low weight. Body image | Disturbance in the way one's body weight _ | No change from DSW+WV-TR or shape is experienced; denial ofthe (slight wording change: seriousness of low body weight; an undue | persistent lack of recognition of influence of body weight or shape on self-_| the seriousness of current low evaluation, body weight’). Individuals with AN achieve low weight through dietary restriction and often ‘engage in excessive physical activity and manifest strict food rules. Although all individuals with AN are restricting intake to below nutritional needs, a subset periodically engage in binge cating and/or purging. DSM-IV-TR specifies 2 subtypes of AN: restricting type and binge/purge type. Whereas individuals with the restricting type may appear constricted in affect and personality, those with the binge-cating/purging type may be more likely to have comorbid impulsivity, including substance use disorders, cluster B personality disorders, mood lability, and suicidality. Additionally, those with binge/ purge type AN may develop more severe medical complications, because binge/purge behaviors compound their low weight. Associated Signs and Medical Complications Psychologically, individuals with AN often present with severe body image distor- tion; preoccupation with weight, shape, and eating: restricted or negativeaffect; and limited insight into illness. They may be perfectionistc, obsessive, interpersonally insecure, and unsure of their own identity. Further, they often experience intraper- sonal conflict around maturation, sexual development, separation, and individua- tion, Notably, AN has the highest mortality rate For any mental disorder; suicide and cardiac complications are the leading causes of death, Section VE Nutrition in Acute and Chronic lines920 Chapter 39 In individuals with AN, most systems are affected as weight loss becomes pronounced (see Table 39.2). Physical signs include bradycardia, hypotension, lanugo, alopecia, and edema. ‘Those who self-induce vomiting may exhibie dental crosion and dorsal surface hand lesions. Laboratory findings could include electro- lyte abnormalities, in particular hypokalemia. Gastrointestinal complications, such as constipation, delayed gastric motility, and delayed gastric emptying, are common. High concentrations of blood urea nitrogen may reflect renal abnormalities resulting from dehydration, Polyutia related to an abnormality in vasopressin secretion may also develop. Approximately 20% of patients experience peripheral ‘edema, usually during refeeding. Mild anemia, leukopenia, and thrombocytopenia are often observed but typically reverse with refeeding. Neurologic abnormalities may include reduced gray matter volumes and increased suleal cerebrospinal fluid volumes that persist after recovery. Table 39.2. Associated Signs and Medical Compli Cardiac Bradycardia, orthostatic hypotension, arrhythmia, mitral valve prolapse/ murmur, decreased leftventricular forces, prolonged QT interval corrected for heart rate, increased vagal tone, pericardial effusion, congestive heart failure Endocrine and | Amenorthea, hypothyroidism, delayed puberty, arrested growth, metabolic | hypothermia, osteopenia or osteoporosis, euthyroid sick syndrome, electrolyte disturbances, decreased serum testosterone or estraiol, hypercholesterolemia, hypercortisolsm Skeletal Fractures due to bone mineralization loss, low bone mineral density Breasts Breastatrophy Dermatologic _| Cheiisis, acrocyanosis, hypercarotenemia, alopecia, xerosis, acne, lanugo, pallor Orai/dental | Enamel erosion and gum recession; swelling ofthe parotid gland; salivary gland hypertrophy; elevated serum amylase levels; halitsis Gastrointestinal | Palpable stool secondaryto constipation rectal prolapse, scaphoid abdomen; esophaaitis; chest pain, dyspepsia, gastroesophageal reflux clsease; esophageal rupture; hiatal hernias; irritable bowel syndrome; tmelanosis col; atonic or cathartic colon Pulmonary | Pneumothorax or aspiration secondary to voriting, pulmonary edema during refeeding Neurologic and | Neurocognitive deficit, diminished muscle strength, peripheral neuropathy, mental status _| movernent disorder Hematologic | Anemia, leukopenia, thrombocytopenia Renal increased blood urea nitrogen, calcul Pediatric Nutrition, 7th EditionNutritional Support of Pediatric Patients with Eating Disorders. 921 Electrocardiographic abnormalities (eg, low voltage, bradycardia, T-wave inversions, ST segment depression, and arrhythmias) are common and often normalize with refeeding. Some cardiac problems, including prolonged corrected QT intervals, myocardial damage, and arrhythmias secondary to electrolyte imbalances, may be fatal. Amenorrhea secondary to starvation-induced hypogonad- ism, hypothyroidism, reduction of growth hormones (insulin-like growth factor), and decreased serum leptin concentration are all among the endocrine sequelae.* “The likelihood of these complications increases in adolescents who reach a lower percent of ideal body weight. Although many medical complications resolve when the adolescent achieves weight restoration, bone mineral density (BMD) loss resulting from hypothalamic amenorrhea in female patients or low testosterone in male patients does not necessarily resolve with weight gain. Reductions in BMD tend to occur at multiple skeletal sites in most women with anorexia nervosa, leading to osteopenia and osteoporosis? Although estrogen deficiency is an important cause of low BMD, administration of estrogen as an oral estrogen-pro- gesterone combination pill is not effective in increasing BMD in women or girls with AN. In contrast, physiologic estrogen administration as replacement doses with transdermal estrogen of as small incremental doses of oral estrogen to mimic the early pubertal rise in estrogen does increase BMD in adolescent girls with AN when compared with placebo. However, bone accrual rates remain lower than in normal-weight controls, likely because other hormonal deficits are not addressed by estrogen replacement alone in the absence of weight restorations In low-weight Female athletes, the constellation of low energy availability, with ‘or without an eating disorder, hypothalamic amenorrhea, and osteoporosis, has been termed the “Female athlete triad.”” Energy availability refers to dietary energy intake minus exercise energy expenditure. Energy availability is the amount of dietary energy remaining for other bodily functions. Some athletes resort to abnormal eating patterns, including restriction, fasting, binge eating, and purging, cor may use dict pills, laxatives, diuretics, or enemas and, thus, have low energy availability. Most of these affected athletes manifest with low body fat composition, which contributes to a hypoestrogenic state, causing amenorthea. Adolescent athletes who participate in sports in which leanness is emphasized are at higher risk of decreased bone mineralization. Bulimia Nervosa Diagnostic Criteria In the DSM-IV-TR, BN is characterized by a regular pattern of binge eating and compensatory behaviors and an overvaluation of weight and shape (see Table 39.3). Binge eating and compensatory behaviors occur ata threshold Frequency of twice Section Vi; Nutrition in Acute and Chronic Iliness922 Chapter 39 weekly for at least 3 months. A binge episode is defined as the consumption of an objectively large amount of Food accompanied by a subjective feeling of being out ‘of control during the eating episode, Often, individuals with BN alternate between binge eating and strict dieting. Binge eating typically occurs alone, involves consumption of calorie-dense foods, and is associated with abdominal discomfort and feelings of guilt, disgust, and depression. Individuals with BN engage in compensatory behaviors, including purging (self-induced vomiting, laxative, diuretic, or enema abuse) and nonpurging behaviors (excessive exercise or fasting) in efforts to counteract the effects of the binge and prevent weight gain. In the DSM-IVER, individuals are clasified as purging or nonpurging type on the basis ‘of compensatory behaviors endorsed. Proposed revisions for DSM-5 include lowering the frequency criterion of binge/purge behavior from twice weekly to once weekly and eliminating the nonpurging subtype. Clinical Features of BN are listed in Table 39.4. Table 39.3. Diagnostic Criteria for B eo aro Goce) Binge eating | Recurrent episodes of binge eating, eating ina | No change from discrete petiod of time (eg, within any 2-hour | DSM-N-TR period), an amount of food that is definitely larger than most people would eat during a similar period of time and under similar circumstances. Compensatory | Recurrent inappropriate behaviors in order No change from behaviors | to preventweight gain, such as self-induced DSMAVTR vomiting; misuse of laxatives, diuretics, enemas, or othermedications; fasting; or excessiveexercise. Regularity | Binge eating and compensatory behaviors both | Binge eating and ‘occur on average at least 2times a weekfor3 | compensatory months behaviors both occur Con average atleast once aweek for3 months Body image _| Self-evaluation is unduly influenced by body No change from shape and weight. OSMAV-IR No anorexia | Does not occur exchsively during episodes of | No change from nervosa anorexia nervosa DSM.IV-1R ‘subtype Purging type (has regularly engaged in self-induced | Deletion of subtype. vomiting or the misuse oflaxatives, diuretics,or |Research has shown enemas) or non-purging type (has used other | that individuals with Inappropriatecompensatory behaviors, such as | nonpurging subtype fasting or excessiveexercise, but has not requialy _ | closely resemble ‘engaged in self-induced voriting orthe misuse of | individuals with binge- laxatives, diuretics, or enemas) eating disorder Pediatric Nutrition, 7th EditionNutritional Support of Pediatric Patients with Eating Disorders 923 Table 39.4. Associated Signs and Medical Compl Nervosa Catdiovascuiar | Arrhythmia; mitral vave prolapse; murmur; cardiomyopathy Musculoskeletal | Tetany; skeletal muscle myopathy ions of B Gastrointestinal | Gastric dilation; abdominal fullness; esophagitis; gastroesophageal reflux disease or rupture; hiatal hernias; Barrett esophagus; irritable bowel syndrome; melanosis col; atonic or cathartic colon. Ora/dental | Mouth sores; palatal scratches; dental cares; enamel erosion and gum recession; swelling ofthe parotid gland; submandibular adenopathy; evated serum amylase levels Skin Periorbital petechize, Russell sign (calluses overthe knuckles due to induction ofemesis, swelling ofhands and feet,dryness, lack of hair sheen Metabolic Pitting edema, poor skin turgor,Chvostek signs, Trousseau sign, hypokalemia, metabolic acidosis or alkalosis secondary to purging by vvoriting and/or use of diuretics and laxatives Neurologic _[ Cognitive impairment; iritabiity Associated Signs and Medical Complications Patients with BN may present complaining of bloating, weakness, fatigue, dyspep- sia, chest pain, and dry mouth. Physical signs may include the highly specific findings of facial swelling, sialadenosis (parotid gland hypertrophy, bilateral and nontender) or Russell sign (excoriations on dorsal aspect of hand and fingers). Oral findings may include tooth decay or discoloration, lesions, or bleeding gums. Additional signs include peripheral edema, petechiae in the skin surrounding the eyes, subconjunctival hemorthage (resulting from increased pressure from vomit- ing), or angular cheilitis Angular cheilitis may be secondary to vomiting or vitamin (often B complex) deficiencies. Laboratory findings are not diagnostic but can be helpful in assessing medical complications. Depending on the method of purging, there can be changes in serum electrolyte concentrations. Hypokalemia, hypochloremia, and hyponatremia (associated with excess water ingestion) can be commonly seen. ‘The serum pH can be increased or decreased from purging. There can be an elevated serum amylase, Because of electrolyte disturbances, purging may lead to weakness, tetany, and archythmias, diuretic overuse may cause Pseudo-Barter syndrome (hypokalemia secondary to diuretic or laxative misuse). Further complications include renal failure and electrolyte imbalances, leading to seizures. Albumin concentrations are typically normal in patients with eating disorders; if they are low, clinicians should investi gate a comorbid or alternative diagnosis, such as inflammatory bowel disease. Section VI: Nutrition in Acute and Chronic Iliness924 Chapter 39 Medical complications of BN are varied, often are occult, and carry significant risk of morbidity and mortality. Gastrointestinal tract complications are often secondary to self-induced vomiting and include esophagitis, dyspepsia, gastroesoph- ageal reflux disease, hiatal hernias, and gastric dilatation. In severe cases, self- induced vomiting may lead to Mallory-Weiss tears, aspiration pneumonia, esophageal or gastric rupture, or a pneumothorax. More commonly, delayed gastric emptying and elevated intestinal transit time lead to presenting complaints of bloating, postprandial fullness, and constipation. Ieis very important to inquire about laxative abuse, as this leads to depletion of potassium bicarbonate and a resultant metabolic acidosis, Laxative and diuretic abuse or chronic dehydration may lead to renal stones. Laboratory abnormalities seen with laxative abuse include metabolic acidosis, hyperuricemia, elevated blood urea nitrogen concentration, hypocalcemia, and hypomagnesemia, Laxative abuse may lead to irritable bowel syndrome, melanosis coli, an atonic or cathartic colon, ‘or rectal prolapse. Cessation of chronic laxative abuse may cause rapid increase in ‘weight because of fluid retention and edema. Other times, cessation of laxative abuse leads to constipation and may be managed with increased fluid and fiber intake. All patients with BN, especially purging subtype, should undergo electrocardiog- raphy (ECG), and abnormal results should prompt consideration of hospitalization. Self-induced vomiting and laxative and diuretic abuse may lead to electrolyte and acid base disturbances, and resultant cardiac complications may ensue. Cardiac archythmias and prolonged QT intervals can lead to sudden death in purging patients. T-wave changes may also be noted on ECG, Another cardiac complication noted with increased frequency in patients with BN is mitral valve prolapse. Although no longer commercially available, ipecac abuse is associated with distinct, potentially life-threatening cardiac complications; thus, all patients must be asked about any ipecac abuse. Ipecac containsemetine, which can cause a skeletal muscle myopathy, diffuse myositis, and cardiomyopathy (which could lead to irreversible myocardial damage and cardiac failure). The development of pericardial pain, dyspnea, weakness, hypotension, or tachycardia or abnormalities detected on ECG may suggest ipecac ingestion and requires urgent medical attention. Many endocrine abnormalities are associated with BN. Thyroid function tests may show euthyroid sick syndrome marked by low tri-iodothyronine (T3), elevated reverse Ts, and low to normal thyroxine (T) and thyroid-stimulating hormone (TSH), Cortisol and growth hormone may be increased, Vasopressin depression ‘often leads to polyuria. Patients may have irregular or absent menstruation; this may be seen in normal-weight or even overweight adolescents with BN. Pediatric Nutrition, 7th EditionNutritional Support of Pediatric Patients with Eating Disorders 925 Certain complaints suggest acute complications of BN. Volume depletion may lead to hypotension, dizziness, and syncope. In the case of severe abdominal pain, it is necessary to rule out gastric dilatation (perhaps requiring urgent medical inter- vention). Because ipecac use is associated with cardiomyopathy, any complaints of chest pain, dyspnea, hypotension, or tachycardia or abnormalities detected on ECG require urgent medical attention, In addition, hematemesis or rectal bleeding may require emergent care. Other clinical signs that suggest hospitalization may be necessary include serum potassium concentration less than 3.2 mmol/L, serum chloride concentration less than 88 mmol/L, hematemesis, cardiac arrhythmias (ie, prolonged QT), or hypothermia. Hypokalemia must be carefully corrected in a hospital setting with careful observation for cardiac instability Etiology of AN and BN ‘The etiology of eating disorders is multifactorial, dependent on sociocultural, psychological, biological, and familial factors. Both AN and BN typically have onset during adolescence, although patients Frequently havea history of body image concerns and disordered eating that precede the onset of the illness. Sociocultural factors that may increase risk of eating disorders include the ‘Western emphasis on a thin ideal For women and a muscular ideal for men. Dieting is a behavior that increases risk For eating disorders. Further, certain populations may be at heightened risk of eating disorders, For example, sports such as ballet, gymnastics, long-distance running, ice skating, and wrestling or activities such as ‘modeling or acting all value a slender body shape and may promote thinness and weight loss, In addition, patients with diabetes mellitus represent an at-risk group: patients with type 1 (or insulin-dependent) diabetes mellitus must adhere to strict, diet plans and may underdose insulin to cause intentional weight loss. Diabetic patients with eating disorders more Frequently present with ketoacidosis and vascular complications associated with poor glycemic control. Gay males may also be at increased risk. Environmental factors, including transitions from middle school to high school, the experience of a loss, and physical or sexual abuse, may also precipitate maladaptive coping responses, including eating disorders. Psychological characteristics, such as personality or temperament, as well as comorbid psychopathology may also play a role in the development of eating disorders. Perfectionism, low self-esteem, and difficulty in regulating affect or ‘managing emotions are personality characteristics that may be present in individuals with eating disorders. Further, a subset of patients with eating disorders, particularly those with a bulimic constellation of symptoms, may also demonstrate other impulsive behaviors, such as substance abuse, promiscuity, and self-destructivel injurious behaviors that require their own medical intervention and monitoring. Anxiety and mood disorders also often co-occur with eating disorders, although Section Vi; Nutrition in Acute and Chronic Iliness926 Chapter 39 anxiety disorders most often have onset before eating disorders, mood disorders may be more likely to develop at the same time as or Following the eating disorder onset. Research in the past decade has begun to explore the genetics and heritability of eating disorders. Family and twin studies demonstrate that the risk of AN and/or BN is significantly increased in first-degree relatives of those with eating disorders, with one study indicating the relative risk of eating disorder in female relatives to be 11.3.* Further, there is growing evidence that specific symptoms, such as binge cating and self-induced vomiting, may also be heritable. Biological Factors, such as obesity, may increase vulnerability to eating disorders. Neurobiological research has also demonstrated alterations in hormonal and neurohormonal systems among, individuals with eating disorders. Impaired serotonergic regulation has been implicated in obesity and overeating; studies have shown patients with BN to have dysregulated serotonin Function as wel as lower cerebrospinal 5-HTIA levels. Ghrelin, a hormone that acts on the hypothalamus to stimulate appetite, has been shown to have an abnormal response to normal sized meals in BN patients! Because patients with BN often have an abnormal satiety following normal-sized meals," ghrelin may play a role in the pathogenesis in the lack of satiety that characterizes a binge episode” Yer, the degree to which these neurochemical and hormonal alterations are premorbid risks rather than secondary effects of eating disorders is unclear. Within a biopsychosocial model, the Family environment may also reinforce socioculturally based thin ideal expectations. This influence may occur through modeling of healthful or unhealthful attitudes or behaviors or through direct encouragement of children or adolescents to adopt disordered eating patterns. Further, there is some evidence that a family environment characterized by enmesh- ment or high conflict may also increase vulnerability to eating disorders, although interpretation of this research is challenged by the fact that Family dynamics may change resultant From the eating disorder. Assessment Given thateating disorders often involve private behaviors or secret thoughts that may not be apparent from the outside, careful assessment is critical? Such an assessment involves a medical, nutritional, and psychological evaluation, and itis ‘often pediatricians who are on the front line of screening for eating disorders in children and adolescents. Although eating disorder symptoms may be distressing to patients and often leave them feeling ashamed, lonely, or remorseful, many are ambivalent about seeking treatment and may not readily disclose their symptoms. Further, children and adolescents with eating disorders deny or minimize Pediatric Nutrition, 7th EditionNutvitional Support of Pediatric Patients with Eating Disorders 927 symptoms, either unconsciously because of a distorted perception of their behavior! attitudes or consciously to keep clinicians from recognizing the extent of their symptoms. A strong alliance with a trusted health care professional is crucial in the ‘success of treating the ambivalent patient. Inquiring in a direct yet caring and nonshaming manner can help many patients who are unsure how to disclose their symptoms. Data have shown that patients are more likely disclose their symptoms to aprofessional when directly asked! With young patients, itis often important for the clinician to meet with the adolescent as well as with his or her parents to obtain a more complete perspective on the referral; the Family may cite concerns about the child's diet changes, eating alone, skipping meals, and mood changes. Obtaining a weight history (highest, lowest, current, and desired weight) can shed light on body image concerns and weight uctuations. Evaluation will include inquiry about the amount of time spent thinking about food, calories, and weight, as patients will often report that these topics consume their thoughts and may also interfere with their ability to attend to or enjoy other activities. Detailed assessment of a 24-hour nutritional intake that will alow providers to estimate energy, macronutrient, and micronutrient intake is important to obtain. Are patients restricting or avoiding certain Foods or food groups (eg, fats)? Direct assessment of pattern of eating and frequency of meals consumed provides information about whether some meals/snacks are more challenging than others and whether there may be large gaps between eating episodes. It is important to ascertain whether there are periods of time when the patient eats an unusually large amount of food in an uncontrolled way. If present, gather more details about the episodes (the length of time, feeling during episode, kinds of food eaten). Assessment should include inquiry about all compensatory behaviors, because each is associated with specific medical complications (ie, ipecac abuse and cardiomyopathy), and many patients engage in more than one compensatory behavior. Ask about vomiting, emetic drugs, laxatives, enemas, “recreational” drugs, insulin underdosing, exercise, and skipping meals. Inquiring about all compensatory measures (regardless of whether patient endorses this behavior) provides an opportunity or psychoeduca- tion about the risks associated with each behavior (ie after asking about ipecac use, cexplain risk of cardiac death). Further, it can be important to ask about unusual behaviors, such as hoarding Food, chewing food and spitting it out, eating in secret, and limiting Buid consumption. ‘The initial laboratory evaluation should include a urinalysis; complete blood cell count with sedimentation rate; general chemistries; amylase, lipase, magnesium, phosphorous, calcium, thyroid-stimulating hormone, and serum human chorionic gonadotropin concentration For females. If there are concerns about celiac disease, then an immunoglobulin (Ig) A and serum anti-tissue transglutaminase Section VE Nutition in Acute and Chronic Iliness928 Chapter 39 determination are helpful. A baseline ECG is recommended, Amenorrhea can be further evaluated with determinations of follicle-stimulating hormone, luteinizing hormone, prolactin, and estradiol." Differential Diagnosis Assessment of eating disorders should include carefully ruling out underlying ‘medical causes of changes in weight or eating behavior. Although medical disorders may co-occur with eating disorders ifthe eating disorder symptoms are better accounted for by the medical condition, an eating disorder diagnosis may not be appropriate. One should consider gastrointestinal disorders (such as celiac disease, inflammatory bowel disease, achalasia, or ulcers) and endocrine disorders (such as diabetes mellitus, Addison disease, or pituitary or thyroid dysfunction) as well as pregnancy. ‘The clinician should consider malignancies (eg, lymphoma, central nervous system tumor) or neurologic disorders (eg, Kluver-Bucy syndrome) that may impair appetite regulation. The differential diagnosis should also include depression, substance abuse, and the illicit use of diet pills. Further, conversion disorders, schizophrenia, and mood disorders are among the psychiatric disorders that may manifest weight loss and binge/purge behavior. PsychiatricComorbidity Screening for co-occurring psychiatric disorders is important. Among individuals with eating disorders lifetime prevalence estimates of affective disorders range From 50% to 80%, and those of anxiety disorders, including obsessive compulsive disorder, generalized anxiety disorder, and social phobia, are also high, ranging from 30% to 65%." Substance use disorders co-occur, particularly among individuals with bulimic symptoms, and alcohol use disorder is the strongest predictor of premature death in individuals with AIN.'6 Further, screening for amphetamine misuse and other use of over-the-counter and prescribed drugs used for weight loss is indicated. Although the most commonly recognized abused substance in patients with BN is alcohol, many patients with eating disorders also use caffeine and tobacco to control appetite:”* A toxicology screening is useful in assessment and ‘ongoing monitoring for substance abuse. Personality disorders also Frequently co-occur with eating disorders; avoidant or obsessive compulsive personality disorder may occur among those with AN, and borderline personality disorder has been associated with BN. Personality styles, irrespective of eating disorder diagnosis, including perfectionism, interpersonal avoidance/constriction/restraint, and affectivelbchavioral dysregulation, may also be important to assess, because they can be useful in informing treatment approach. For all patients with eating disorders, assessment of suicidal ideation, intent, and behavior is imperative, Pediatric Nutrition, 7th EditionNutritional Support of Pediatric Patients with Eating Disorders 929 Treatment Eating disorders are complex psychiatric illnesses that require multimodal treat- ments. In addition to medical management, a comprehensive team comprises psychiatric/psychological care and nutrition management.!? Depending on the severity of illness, care may be delivered with variable intensity, ranging from ‘outpatient management to higher levels of care, including intensive outpatient (evening treatment programs), partial hospitalization, residential care, and inpatient treatment. The American Psychiatric Association provides guidelines regarding levels of care2 Psychiatric Treatment Paychotherapy Psychotherapy is an integral component of care for the child or adolescent with an eating disorder. Individual and/or family therapy or parent training can be used to support the medical and nutritional recommendations of the team, which can be challenging for the patient or Family to enact. Therapy also helps the child or adolescent identify and address underlying or associated issues which may include separation-individuation, identity development, comorbidities (such as anxiety or depression), and perfectionism, for example. Although psychotherapy is a mainstay of treatment for eating disorders, few randomized-controlled treatment studies for eating disorders in youth exist. A notable exception to this lack of research is the body of studies supporting the use of family-based treatment for adolescent eating disorders™ Family-based treatment, also known as the Maudsley method because of its initial development at the Maudsley Hospital in London, is an outpatient treatment in which parents are recognized as key resources who are integral participants in the recovery process. “The treatment takes an agnostic approach to the etiology of eating disorders and empowers parents to initially take more control over the child's eating to restore health; as eating disorder symptoms come under better control, the parents step back. ‘Thus, treatment proceeds through 3 phases determined by the patient's progress, beginning wich weight restoration/nutritional rehabilitation, which is managed by the parents, moving to careful return of Food/eating control to the adolescent, and ending with Focus on issues associated with healthy adolescent development. A number of studies have demonstrated the benefits of using, family-based treatment for adolescents with AN”? and more recently for adolescents, with BN®; preliminary work also suggests family-based treatment may be useful in treating children, adolescents, and young adults with a wider range of eating disorders" Section Vi; Nutrition in Acute and Chronic Iliness930 Chapter 39 Individual psychotherapy is helpful for teenagers with eating disorders. A therapist often provides understanding, coaching, praise, and support to generate positive behavioral outcome. When individual psychotherapy is recommended for the adolescent, meetings with the patient's Family must be part of the treatment as well. The goals of individual therapy will include improving nutritional health, modifying unhealthy eating attitudes and behaviors, improving self-esteem and quality of life, and treating co-existing conditions, such as depression and anxiety disorders. Psycho pharmacology Limited data are available on the efficacy of psychiatric medications in adolescents with eating disorders. To date, there has been only one randomized-controlled clinical trial For adolescents with AN, and there have been no such studies for adolescents with BN. In a small study of adolescents with AN, Biederman and colleagues Found that the tricyclic antidepressant amitriptyline was not effective in reducing symptoms of AN of low mood when compared with placebo or psycho- therapy treatment as usual. Instead, among low-weight patients, the mainstay of treatment is weight restoration; psychiatric medications have generally not been shown to improve eating disorder outcomes, and the efficacy of these medications is likely diminished as a result of malnutrition. Hence, nutritional interventions are primary. However, psychiatric medications are often used to treat comorbid conditions, such as depression and anxiety, and are Frequently prescribed, even for underweight patients. More recently, there is some evidence that atypical neurolep- tics, such as olanzapine, may improve distorted body image and may assist with weight gain, although clinicians should be aware that many patients with AN will be resistant to taking a medication associated with weight gain” in addition, atypical neuroleptics have been associated with long-term complications, including, diabetes mellitus and dyslipidemia Better evidence exists For the use of psychopharmacologic interventions in adult BN. Serotonergic medications, such as selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs), and tricyclic antidepressants have been shown to decrease binge/purge behaviors Fluoxetine is the best-studied SSRI and the only medication approved by the Food and Drug Administration for the treatment of BN in adults. Topiramate and other antiepilep- tic medications have also been shown to decrease binge behaviors in those who do not tolerate serotonergic medications; however, topiramate is associated with weight loss and cognitive slowing and should be used cautiously. Pediatric Nutrition, 7th EditionNutritional Support of Pediatric Patients with Eating Disorders. 931 Nutrition Management The nutritional management for AN beginswith the focus on weight restoration; in BN, although weight restoration may be important as well, the treatment Focus is ‘on interrupting and arresting the binge/purge cycle by establishing a regular pattern of eating. Determining Ideal Body Weight Nutritional management of an eating disorder begins with establishment of an initial goal weight. ‘Ihe goal weight is commonly the ideal weight, which is caleu- lated using the following formula: Height (m*) x the 50" percentile body-mass index (BMI) for age and gender BMI information is available on the Centers For Disease Control and Prevention Web site For girls (hetp://www.edegov/growthcharts/data/setl clinical/¢j411024.pdF) and for boys (http:// www.cdegov/growthcharts/data/setlclinical/¢j411023.pdf). Utilizing the 50" percentile BMI for age and gender as the ideal or expected BMI has the advantage of being age specific and accounts For changes in body ‘composition that occur during puberty and adolescence.” However, careful consideration of the individual patient’s BMI chart (and both height and weight charts) prior to the onset of the eating disorder may be informative in guiding determination of initial goal weight. For example, for the adolescent who had always tracked at the 25" percentile BMI curve, it is possible that returning to the 25% percentile would be an appropriate and justifiable goal Calculating Nutrition Requirements Estimating calorie needs for eating disorders varies on the basis of physical state (eg, percent of ideal body weight), patient’s recent energy intake, and risk of refeeding syndrome. Nutrition requirements will change throughout treatment and must be reevaluated frequently on the basis of rate of weight gain, laboratory levels, goal weight, and stage of treatment (inpatient versus outpatient). Overall, many factors such as age, weight, activity level, and overall state of illness can affect calorie needs for weight gain. Indirect calorimetry is the most accurate method to determine energy needs; however, cost and availability make its use difficult. The constant change of metabolic rate during weight restoration in underweight patients would result in requiring indirect calorimetry more frequently than is Feasible to maintain accuracy. “The patient should be Followed carefully by a team for continued monitoring and reevaluation during both inpatient and outpatient treatment. Ifthe patient has severe laboratory abnormalities or is very low weight, an inpatient setting for refeeding is the safest option. Initial calorie prescription for AN can be determined Section VE Nutrition in Acute and Chronic Iliness932 Chapter 39 using a dietary recall andcan begin at estimated intake or 250 keal above estimated intake. It should be noted that patients with AN frequently overestimate intake in a dietary recall If unable to determine actual energy intake, beginning at 1000 to 1250 keal prior to starting the plan is generally safe. For inpatients with AN, it is recommended that 250 kcal be added to the intake prescription every 24 hours because of changes in metabolic rate and postprandial ‘energy expenditure. Resting energy expenditure continues to increase in patients with AN throughout the weight restoration process. An increased thermic effect of food and difficulty with absorption may contribute to greater energy needs. A weight gain of 0.5 Ib daily or 2 to 3 Ib per week is appropriate.” ‘The patient's rate of weight gain should be followed, and energy intake should be adjusted accord- ingly. In an inpatient setting, Femalesoften peak around 3000 to 3500 kcal/day, and males often peak around 4000 keal/day. However, some programs recommend increasing up to 5000 kcal/day, because weight gain may not correlate with the total excess of calories consumed above basal needs. For patients with AN being treated on an outpatient basis, energy intake is advanced at a slower pace. An increase of 500 kcal weekly is usually the maximum, ‘of what can be tolerated for energy intake advancement." A gain of 1 to 2 Ib weekly is appropriate. Once children and adolescents achieve a healthy weight, an increased energy prescription is needed to support future growth and development” Ie may be difficult to determine energy intake in patients with BN, given variability with binge/purge behaviors. Generally, 50% ofkcal consumed in a binge/purge cycle should be added to total calorie count.2”To determine energy intake For normal or overweight patients with BN, the resting energy expenditure equation (REE) covers basal needs and assumes sedentary activity levels and should prevent excessive weight gain in children. REE: Males 3-10 years of age: (22.7 X wt (kg)) + 495 Females 3-10 years of age: (22.5 X wt (kg)) + 499 Males 10-18 years of age: (17.5 X wt (kg)) + 651 Females 10-18 years of age (12.2 X we (kg)) + 746 Weight loss calorie goals should be avoided regardless of overweight/obesity until an eating pattern is stabilized, because caloric restriction may trigger bingeing.® Patients with BN or those with a history of BN may be hypometabolic, requiring less energy intake than typically estimated for a patient of similar weight and height. Notably, patients with BN are most often treated on an outpatient basis; higher level of care may be recommended at times For interrupting the binge/purge cycle ‘or managing medical complications of BN. Pediatric Nutrition, 7th EditionNutvitional Support of Pediatric Patients with Eating Disorders 933 Meal Planning Snacks and/or supplements are helpful to increase energy and protein intake while keeping meals manageable in size. Increasing calorie-dense foods as well as provid- ing luids with calories may be helpful to avoid excessive Fullness after eating. In addition, low-lactose Foods or providing lactase supplements may decrease abdomi- nal discomfort from nutritionally mediated lactase deficiency. Frequently, behav- ioral interventions are necessary to facilitate patients meeting energy intake and ‘weight goals. An eating protocol that provides clear criteria for expected energy intake, weight gain, activity, and behavior and that outlines expectations For the patients, family members, and treatment providers isa valuable tool to help patients to meet goals. The exchange list created by the American Diabetes Association in collaboration with the Academy of Nutrition and Dietetics is a helpful tool to plan meals. The exchange system groups Foods into starch, protein, Fruit, vegetable, milk, and Fat categories and within each category indicates specific portion sizes, which provide similar nutrition content (eg, 1 serving of starch can be Fulfilled by 1 slice ‘of bread or 1/3 cup of pasta). Meals are planned by prescribing a number of ‘exchanges from each Food group. This decreases Focus on calories and fat and increases emphasis on the inclusion of a variety of Foods and food groups In some cases, allowing patients to make Food choices can be empowering and help them to feel in control; yet for other patients, this level of control may Feel overwhelming. Patients with AN may find Food choices difficult despite the method of meal planning or the protocols, and there are no longitudinal outcome data to support ‘one method of meal planning over another.** For normal-weight patients with BN, ‘encouraging 3 meals and snacks daily promotes normal eating and helps the patient break the cycle of restriction and binge/purge behaviors. Nutrition Support Oral feedings are the preferred method of restoring nutrition. The decision to start nutrition support should consider both the patient's immediate physical health and psychological health, ‘The indications For tube feedings include refusing any oral intake, rapid weight loss despite improved oral intake or hypermetabolism, and inability to meet nutritional needs orally?? If enteral nutrition via tube feedings is necessary, starting at 25% of the estimated goal and increasing to initial goal over 3 to 5 days is recommended.® Some patients may need to have both tube Feedings as well as oral nutrition to achieve nutrition and weight gain goals. Bolus feedings or nocturnal feedings are useful to provide uneaten calories or supplement intake. However, continuous feedings are less likely to result in dumping syndrome or purging. If tube feedings are initiated, typically an isotonic, fiber-containing, enteral feeding will be sufficient. Formulas containing high glucose should be avoided. If Section VE. Nutrition in Acute and Chronic Iliness934 Chapter 39 absorption or digestion is impaired, an elemental or peptide-based formula may be indicated. Parenteral nutrition should be used rarely and with caution, because it leads to the continued loss of hunger cues and increases risk of refeeding syndrome. Refeeding Syndrome ‘When starved or severely malnourished patients begin nutrition repletion, they are at risk of refeeding syndrome. As the metabolism shifts, it may result in uid and electrolyte disorders that could cause neurologic, pulmonary, cardiac, neuromuscu- lar, and hematologic complications.» Medical stabilization and safety are the initial concerns, and this stabilization period can last up to 3 weeks. Therefore, substantial ‘weight gain cannot always be expected in this time, especially if medical complica- tions from refeeding arise, To prevent refeeding syndrome, advancement of energy by 250 keal/day in addition to supplementing vitamins and minerals is essential to safely bring the patient from a catabolic to an anabolic state.” Frequent physical examinations as well as determinations of serum phosphorous, magnesium, and electrolyte concen- trations are needed. In addition, there should be careful monitoring of the patient's vital signs, daily weights, fluid intake, and output. During the increase of energy intake, metabolic disturbances may occur, including hypophosphatemia, hypokalemia, and hypomagnesemia. Hypophosphatemia may result from the intracellular shift of serum phosphorus needed for the generation of adenosine triphosphate (ATP) in the cellular anabolic processes, Low serum concentrations of phosphorus are associated with cardiac and neuromuscular dysfunction as well as blood cell dysfunction. Hypokalemia and hypomagnesemia may increase risk of cardiac archythmias and gastrointestinal and neuromuscular complications. During refeeding, extracellular expansion is ‘common, causing peripheral edema; in extreme cases, congestive heart failure may ‘occur.% In the inpatient setting and occasionally in the outpatient setting, supple- mentary phosphorous may be given to prevent the refeeding syndrome. Macronutrients, Fiber, and Fluids No optimal macronutrient intake regimen has been Found to be more beneficial for patients with eating disorders; however, a standard recommendation of 25% to 30% fat, 15% to 20% protein, and 50% to 55% carbohydrate may be helpful to provide a balance of macronutrients In patients at risk of developing refeeding. syndrome, a slightly higher intake of fat and protein calories may be somewhat protective, as carbohydrate metabolism drives refeeding syndrome. Initially, when prescribing a meal plan or tube feedings, 150 to 200 g/day of carbohydrate should not be exceeded and the protein goal should be approximately 1.2 to 1.5 g/kg of Pediatric Nutrition, 7th EditionNutritional Support of Pediatric Patients with Eating Disorders 935 ideal body weight to preserve lean body mass while Feeding hypocalorically. Patient access to simple sugars and sodium should be limited to avoid the risk of refeeding syndrome. The patient's previous intake of fiber should guide how much fiber is prescribed. Excessive fiber may result in discomfort or gastrointestinal distress, and not enough fiber may contribute to constipation. Fluids should start at approxi- mately 20 mL/kg or 1 mL/kcal and be adjusted as needed to prevent dehydration or fluid retention.>” In both AN and BN, the initial diet should be low in sal, lactose, and fat to minimize malabsorption and edema Micronutrients Vitamin deficiencies are not frequently seen in patients with AN and BN. However, it is common practice to supplement the patient with a multivitamin and minerals during treatment.” Because AN often begins during adolescence, the critical period for bone mineral accretion, supplementation with calcium and vitamin D are recommended. The current recommendation for adolescent Females is 1300 mg/ day of calcium and 600 IU/day of vitamin D.* Longitudinal Outcome “The course and outcome of eating disorders is variable; adolescents with a shorter duration of illness have a more favorable outcome compared with adults or those with a longer duration of illness, underscoring the importance of early detection and intervention. A recent meta-analysis of 36 quantitative studies of individuals with eating disorders Found significantly elevated mortality rates,» and AN is associated with the highest risk of mortality among all psychiatric disorders.” Among adults with AN, longitudinal studies suggest the rate of mortality is 0.56% per year, which is more than 12 times higher than that For young women in the general popula- tion.! Further, the rate suicide is also elevated, with one study demonstrating a 57-fold increase in death by suicide among adult women with AN. Yet, the longitudinal course and prognosis is better For adolescents. One recent analysis of multiple outcome studies For adolescents and adults with AN Found that 57% recovered, 26% more had improved substantially, 179% went on to have chronic course of AN, and 2% had died.*t Patients with BN generally havea more favorable course. Longitudinal research suggests that approximately 50% of adult women with BN achieve Full recovery from their eating disorder at 5 to 12 years of follow-up, although approximately one third of these will go on to relapse: In contrast to the high mortality rates in patients with AN, mortality does not appear to be significantly increased in those with BN." One review of 88 studies demonstrated a crude mortality rate of 0.3% during longitudinal follow-up, although the authors cautioned that this may have Section Vi; Nutrition in Acute and Chronic Iliness936 Chapter 39 been an underestimate because of variable lengths of follow-up (6 months to 10 years) and low ascertainment across Follow-up. Conclusions Eating disorders are prevalent problems among adolescents, and to a lesser extent, among chil dren, These illnesses carry the risk of severe medical and psychosocial consequences and poor long-term outcome. As such, early detection and interven- tion involving a multidisciplinary team is required. References 1 10. u" R ‘American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision. Washington, DC: American Psychiatric Publishing; 2000 .. Swanson SA, Crow SJ, Le Grange D, Swendsen J, Merikangas KR. Prevalence and correlates of eating disorders in adolescents. Arch Gen Psychiatry. 2011,68(7):714-723 Rome ES, Ammerman S, Rosen DS, etal. Children and adolescents with eating disorders: the state ofthe art. Pediatrics. 2003;111(1):e98-e107 Misra M, Aggarwal A, Miller KK, etal. Effects of anorexia nervosa on clinical, hematologic, biochemical, and bone density parameters in community-dwelling adolescents girls. Pediatrics. 2004;114(6):1574-1583 Grinspoon 5, Thomas E, Pits S,et a. Prevalence and predictive factors for regional ‘osteopenia in women with anorexianervosa. Ann Intern Med. 2000;133(10)790-794 ‘Misra M, Katzman DK, Miller KK, et al. Physiologic estrogen replacement increases bone density in adolescent girs with anorexia nervosa. J Bone Miner Res. In press NNattiv A, Loucks AB, Manore MM, Sanborn CF, Sundgot-Borgen J, Warren MP. American College of Sports Medicine position stand, The female athlete triad. Med Sci ports Exerc.2007;39(10):1867-1882 ‘Strober M, Freeman R, Lampert C, Diamond J, KayeW. Controlled family study of anorexia nervosa and bulimia nervosa: evidence of shared lability and transmission of partial syndromes. Am J Psychiatry. 2000;157(3}393-401 ‘Strober M, Bulik C. Genetic epidemiology of eating disorders. In: Fairburn C, Brownell K, eds. Eating Disorders and Obesity: A Comprehensive Handbook. 2nd ed, New York, NY: Guilford Press; 2002:238-242 ‘Monteleone P, MartiadisV, Rigamonti AE, etal. Investigation of peptide YY and ghrelin responses toa test meal in bulimia nervosa. Biol Psychiatry. 2005;57(8)926-931 Walsh BT, Kissileff HR, Cassidy SM, Dantzic S. Eating behavior of women with bulimia. ArchGen Psychiatry. 1989;46(1):54-58 Herzog D8, Eddy KT, Beresin EV. Anorexia nervosa and bulimia nervosa. In: Dulcan MK, Wiener JM, eds. Essentials of Child and Adolescent Psychiatry. Washington, DC: ‘American Psychiatric Publishing; 2006:527-560 Pediatric Nutrition, 7th Edition