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Eating disorders (EDs) are characterized by body dissatisfaction related to overvaluation of a thin body ideal, associated with dysfunctional patterns of cognition and weight control behaviors that result in significant biologic, psychological, and social complications. Although usually affecting white, adolescent females, EDs also affect males and cross all racial, ethnic, and cultural boundaries. Early intervention in EDs improves outcome.
Anorexia nervosa (AN) involves significant overestimation of body size and shape, with a relentless pursuit of thinness that, in the restrictive subtype, typically combines excessive dieting and compulsive exercising. In the binge-purge subtype, patients might intermittently overeat and then attempt to rid themselves of calories by vomiting or taking laxatives, still with a strong drive for thinness ( Table 41.1 ).
Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health. Significantly low weight is defined as a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected.
Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight.
Disturbance in the way in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight.
Specify whether:
Restricting type (ICD-10-CM code F50.01): During the last 3 mo, the individual has not engaged in recurrent episodes of binge eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas). This subtype describes presentations in which weight loss is accomplished primarily through dieting, fasting, and/or excessive exercise.
Binge-eating/purging type (ICD-10-CM code F50.02): During the last 3 mo, the individual has engaged in recurrent episodes of binge eating or purging behavior (i.e., self-induced vomiting or the misuse of laxatives, diuretics, or enemas).
Specify if:
In partial remission : After full criteria for anorexia nervosa were previously met, Criterion A (low body weight) has not been met for a sustained period, but either Criterion B (intense fear of gaining weight or becoming fat or behavior that interferes with weight gain) or Criterion C (disturbances in self-perception of weight and shape) is still met.
In full remission : After full criteria for anorexia nervosa were previously met, none of the criteria has been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based, for adults, on current body mass index (BMI) (see below) or, for children and adolescents, on BMI percentile. The ranges below are derived from World Health Organization categories for thinness in adults; for children and adolescents, corresponding BMI percentiles should be used. The level of severity may be increased to reflect clinical symptoms, the degree of functional disability, and the need for supervision.
Mild : BMI ≥ 17 kg/m 2
Moderate : BMI 16-16.99 kg/m 2
Severe : BMI 15-15.99 kg/m 2
Extreme : BMI < 15 kg/m 2
Bulimia nervosa (BN) is characterized by episodes of eating large amounts of food in a brief period, followed by compensatory vomiting, laxative use, exercise, or fasting to rid the body of the effects of overeating in an effort to avoid obesity ( Table 41.2 ).
Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:
Eating, in a discrete period of time (e.g., within any 2 hr period), an amount of food that is definitely larger than what most individuals would eat in a similar period of time under similar circumstances.
A sense of lack of control over eating during the episode (e.g., a feeling that one cannot stop eating or control what or how much one is eating).
Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise.
The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 mo.
Self-evaluation is unduly influenced by body shape and weight.
The disturbance does not occur exclusively during episodes of anorexia nervosa.
Specify if:
In partial remission : After full criteria for bulimia nervosa were previously met, some, but not all, of the criteria have been met for a sustained period of time.
In full remission : After full criteria for bulimia nervosa were previously met, none of the criteria has been met for a sustained period of time.
Specify current severity:
The minimum level of severity is based on the frequency of inappropriate compensatory behaviors (see below). The level of severity may be increased to reflect other symptoms and the degree of functional disability.
Mild : An average of 1-3 episodes of inappropriate compensatory behaviors per week.
Moderate : An average of 4-7 episodes of inappropriate compensatory behaviors per week.
Severe : An average of 8-13 episodes of inappropriate compensatory behaviors per week.
Extreme : An average of 14 or more episodes of inappropriate compensatory behaviors per week.
Children and adolescents with EDs may not fulfill criteria for AN or BN in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and may fall into a subcategory of atypical anorexia nervosa, or a more appropriately defined category of avoidant/restrictive food intake disorder (ARFID). In these conditions, food intake is restricted or avoided because of adverse feeding or eating experiences or the sensory qualities of food, resulting in significant unintended weight loss or nutritional deficiencies and problems with social interactions ( Table 41.3 ).
An eating or feeding disturbance (e.g., apparent lack of interest in eating or food; avoidance based on the sensory characteristics of food; concern about aversive consequences of eating) as manifested by persistent failure to meet appropriate nutritional and/or energy needs associated with one (or more) of the following:
Significant weight loss (or failure to achieve expected weight gain or faltering growth in children).
Significant nutritional deficiency.
Dependence on enteral feeding or oral nutritional supplements.
Marked interference with psychosocial functioning.
The disturbance is not better explained by lack of available food or by an associated culturally sanctioned practice.
The eating disturbance does not occur exclusively during the course of anorexia nervosa or bulimia nervosa, and there is no evidence of a disturbance in the way in which one's body weight or shape is experienced.
The eating disturbance is not attributable to a concurrent medical condition or not better explained by another mental disorder. When the eating disturbance occurs in the context of another condition or disorder, the severity of the eating disturbance exceeds that routinely associated with the condition or disorder and warrants additional clinical attention.
Specify if:
In remission : After full criteria for avoidant/restrictive food intake disorder were previously met, the criteria have not been met for a sustained period of time.
Binge eating disorder (BED) , in which binge eating is not followed regularly by any compensatory behaviors (vomiting, laxatives), is a stand-alone category in DSM-5 but shares many features with obesity (see Chapter 60 ). Eating disorder–not otherwise specified (ED-NOS) , often called “disordered eating,” can worsen into full syndrome EDs.
The classic presentation of AN is an early to middle adolescent female of above-average intelligence and socioeconomic status who is a conflict-avoidant, risk-aversive perfectionist and is struggling with disturbances of anxiety and/or mood. BN tends to emerge in later adolescence, sometimes evolving from AN, and is typified by impulsivity and features of borderline personality disorder associated with depression and mood swings. The 0.5–1% and 3–5% incidence rates among younger and older adolescent females for AN and BN, respectively, probably reflect ascertainment bias in sampling and underdiagnosis in cases not fitting the common profile. The same may be true of the significant gender disparity, in which female patients account for approximately 85% of patients with diagnosed EDs. In some adolescent female populations, ≥10% have ED-NOS.
No single factor causes the development of an ED; sociocultural studies indicate a complex interplay of culture, ethnicity, gender, peers, and family. The gender dimorphism is presumably related to females having a stronger relationship between body image and self-evaluation, as well as the influence of the Western culture's thin body ideal. Race and ethnicity appear to moderate the association between risk factors and disordered eating, with African American and Caribbean females reporting lower body dissatisfaction and less dieting than Hispanic and non-Hispanic white females. Because peer acceptance is central to healthy adolescent growth and development, especially in early adolescence, when AN tends to have its initial prevalence peak, the potential influence of peers on EDs is significant, as are the relationships among peers, body image, and eating. Teasing by peers or by family members (especially males) may be a contributing factor for overweight females.
Family influence in the development of EDs is even more complex because of the interplay of environmental and genetic factors; shared elements of the family environment and immutable genetic factors account for approximately equal amounts of the variance in disordered eating. There are associations between parents' and children's eating behaviors; dieting and physical activity levels suggest parental reinforcement of body-related societal messages. The influence of inherited genetic factors on the emergence of EDs during adolescence is also significant, but not directly. Rather, the risk for developing an ED appears to be mediated through a genetic predisposition to anxiety (see Chapter 38 ), depression (see Chapter 39 ), or obsessive-compulsive traits that may be modulated through the internal milieu of puberty. There is no evidence to support the outdated notion that parents or family dynamics cause an ED. Rather, the family dynamics may represent responses to having a family member with a potentially life-threatening condition. The supportive influence on recovery of parents as nurturing caregivers cannot be overestimated.
The emergence of EDs coinciding with the processes of adolescence (e.g., puberty, identity, autonomy, cognition) indicates the central role of development. A history of sexual trauma is not significantly more common in EDs than in the population at large, but when present makes recovery more difficult and is more common in BN. EDs may be viewed as a final common pathway, with a number of predisposing factors that increase the risk of developing an ED, precipitating factors often related to developmental processes of adolescence triggering the emergence of the ED, and perpetuating factors that cause an ED to persist. EDs often begin with dieting but gradually progress to unhealthy habits that lessen the negative impact of associated psychosocial problems to which the affected person is vulnerable because of premorbid biologic and psychological characteristics, family interactions, and social climate. When persistent, the biologic effects of starvation and malnutrition (e.g., true loss of appetite, hypothermia, gastric atony, amenorrhea, sleep disturbance, fatigue, weakness, depression), combined with the psychological rewards of increased sense of mastery and reduced emotional reactivity, actually maintain and reward pathologic ED behaviors.
This positive reinforcement of behaviors and consequences, generally viewed by parents and others as negative, helps to explain why persons with an ED characteristically deny that a problem exists and resist treatment. Although noxious, purging can be reinforcing because of a reduction in anxiety triggered by overeating; purging also can result in short-term, but reinforcing, improvement in mood related to changes in neurotransmitters. In addition to an imbalance in neurotransmitters, most notably serotonin and dopamine, alterations in functional anatomy also support the concept of EDs as brain disorders. The cause-and-effect relationship in central nervous system (CNS) alterations in EDs is not clear, nor is their reversibility.
Except for ARFID, in which weight loss is unintentional, a central feature of EDs is the overestimation of body size, shape, or parts (e.g., abdomen, thighs) leading to intentional weight control practices to reduce weight (AN) or prevent weight gain (BN). Associated practices include severe restriction of caloric intake and behaviors intended to reduce the effect of calories ingested, such as compulsive exercising or purging by inducing vomiting or taking laxatives. Eating and weight loss habits commonly found in EDs can result in a wide range of energy intake and output, the balance of which leads to a wide range in weight, from extreme loss of weight in AN to fluctuation around a normal to moderately high weight in BN. Reported eating and weight control habits thus inform the initial primary care approach ( Table 41.4 ).
HABIT | PROMINENT FEATURE | CLINICAL COMMENTS REGARDING ED HABITS | ||
---|---|---|---|---|
Anorexia Nervosa | Bulimia Nervosa | Anorexia Nervosa | Bulimia Nervosa | |
Overall intake | Inadequate energy (calories), although volume of food and beverages may be high because of very low caloric density of intake as a result of “diet” and nonfat choices | Variable, but calories normal to high; intake in binges is often “forbidden” food or drink that differs from intake at meals | Consistent inadequate caloric intake leading to wasting of the body is an essential feature of diagnosis | Inconsistent balance of intake, exercise and vomiting, but severe caloric restriction is short-lived |
Food | Counts and limits calories, especially from fat; emphasis on “healthy food choices” with reduced caloric density Monotonous, limited “good” food choices, often leading to vegetarian or vegan diet Strong feelings of guilt after eating more than planned leads to exercise and renewed dieting |
Aware of calories and fat, but less regimented in avoidance than AN Frequent dieting interspersed with overeating, often triggered by depression, isolation, or anger |
Obsessive-compulsive attention to nutritional data on food labels and may have “logical” reasons for food choices in highly regimented pattern, such as sports participation or family history of lipid disorder | Choices less structured, with more frequent diets |
Beverages | Water or other low- or no-calorie drinks; nonfat milk | Variable, diet soda common; may drink alcohol to excess | Fluids often restricted to avoid weight gain | Fluids ingested to aid vomiting or replace losses |
Meals | Consistent schedule and structure to meal plan Reduced or eliminated caloric content, often starting with breakfast, then lunch, then dinner Volume can increase with fresh fruits, vegetables, and salads as primary food sources |
Meals less regimented and planned than in AN; more likely impulsive and unregulated, often eliminated following a binge-purge episode | Rigid adherence to “rules” governing eating leads to sense of control, confidence, and mastery | Elimination of a meal following a binge-purge only reinforces the drive for binge later in the day |
Snacks | Reduced or eliminated from meal plan | Often avoided in meal plans, but then impulsively eaten | Snack foods removed early because “unhealthy” | Snack “comfort foods” can trigger a binge |
Dieting | Initial habit that becomes progressively restrictive, although often appearing superficially “healthy” Beliefs and “rules” about the patient's idiosyncratic nutritional requirements and response to foods are strongly held |
Initial dieting gives way to chaotic eating, often interpreted by the patient as evidence of being “weak” or “lazy” | Distinguishing between healthy meal planning with reduced calories and dieting in ED may be difficult | Dieting tends to be impulsive and short-lived, with “diets” often resulting in unintended weight gain |
Binge eating | None in restrictive subtype, but an essential feature in binge-purge subtype | Essential feature, often secretive Shame and guilt prominent afterward |
Often “subjective” (more than planned but not large) | Relieves emotional distress, may be planned |
Exercise | Characteristically obsessive-compulsive, ritualistic, and progressive May excel in dance, long-distance running |
Less predictable May be athletic, or may avoid exercise entirely |
May be difficult to distinguish active thin vs ED | Males often use exercise as means of “purging” |
Vomiting | Characteristic of binge-purge subtype May chew, then spit out, rather than swallow, food as a variant |
Most common habit intended to reduce effects of overeating Can occur after meal as well as a binge |
Physiologic and emotional instability prominent | Strongly “addictive” and self-punishing, but does not eliminate calories ingested—many still absorbed |
Laxatives | If used, generally to relieve constipation in restrictive subtype, but as a cathartic in binge-purge subtype | Second most common habit used to reduce or avoid weight gain, often used in increasing doses for cathartic effect | Physiologic and emotional instability prominent | Strongly “addictive,” self-punishing, but ineffective means to reduce weight (calories are absorbed in small intestine, but laxatives work in colon) |
Diet pills | Very rare, if used; more common in binge-purge subtype | Used to either reduce appetite or increase metabolism | Use of diet pills implies inability to control eating | Control over eating may be sought by any means |
Although weight control patterns guide the initial pediatric approach, an assessment of common symptoms and findings on physical examination is essential to identify targets for intervention. When reported symptoms of excessive weight loss (feeling tired and cold; lacking energy; orthostasis; difficulty concentrating) are explicitly linked by the clinician to their associated physical signs (hypothermia with acrocyanosis and slow capillary refill; loss of muscle mass; bradycardia with orthostasis), it becomes more difficult for the patient to deny that a problem exists. Furthermore, awareness that bothersome symptoms can be eliminated by healthier eating and activity patterns can increase a patient's motivation to engage in treatment. Tables 41.5 and 41.6 detail common symptoms and signs that should be addressed in a pediatric assessment of a suspected ED.
SYMPTOMS | DIAGNOSIS | CLINICAL COMMENTS REGARDING ED SYMPTOMS | |
---|---|---|---|
Anorexia Nervosa | Bulimia Nervosa | ||
Body image | Feels fat, even with extreme emaciation, often with specific body distortions (e.g., stomach, thighs); strong drive for thinness, with self-efficacy closely tied to appraisal of body shape, size, and/or weight | Variable body image distortion and dissatisfaction, but drive for thinness is less than desire to avoid gaining weight | Challenging patient's body image is both ineffective and countertherapeutic clinically Accepting patient's expressed body image but noting its discrepancy with symptoms and signs reinforces concept that patient can “feel” fat but also “be” too thin and unhealthy |
Metabolism | Hypometabolic symptoms include feeling cold, tired, and weak and lacking energy May be both bothersome and reinforcing |
Variable, depending on balance of intake and output and hydration | Symptoms are evidence of body's “shutting down” in an attempt to conserve calories with an inadequate diet Emphasizing reversibility of symptoms with healthy eating and weight gain can motivate patients to cooperate with treatment |
Skin | Dry skin, delayed healing, easy bruising, gooseflesh Orange-yellow skin on hands |
No characteristic symptom; self-injurious behavior may be seen | Skin lacks good blood flow and ability to heal in low weight Carotenemia with large intake of β-carotene foods; reversible |
Hair | Lanugo-type hair growth on face and upper body Slow growth and increased loss of scalp hair |
No characteristic symptom | Body hair growth conserves energy Scalp hair loss can worsen during refeeding “telogen effluvium” (resting hair is replaced by growing hair) Reversible with continued healthy eating |
Eyes | No characteristic symptom | Subconjunctival hemorrhage | Caused by increased intrathoracic pressure during vomiting |
Teeth | No characteristic symptom | Erosion of dental enamel erosion Decay, fracture, and loss of teeth |
Intraoral stomach acid resulting from vomiting etches dental enamel, exposing softer dental elements |
Salivary glands | No characteristic symptom | Enlargement (no to mild tenderness) | Caused by chronic binge eating and induced vomiting, with parotid enlargement more prominent than submandibular; reversible |
Heart | Dizziness, fainting in restrictive subtype Palpitations more common in binge-purge subtype |
Dizziness, fainting, palpitations | Dizziness and fainting due to postural orthostatic tachycardia and dysregulation at hypothalamic and cardiac level with weight loss, as a result of hypovolemia with binge-purge Palpitations and arrhythmias often caused by electrolyte disturbance Symptoms reverse with weight gain and/or cessation of binge-purge |
Abdomen | Early fullness and discomfort with eating Constipation Perceives contour as “fat,” often preferring well-defined abdominal musculature |
Discomfort after a binge Cramps and diarrhea with laxative abuse |
Weight loss is associated with reduced volume and tone of GI tract musculature, especially the stomach Laxatives may be used to relieve constipation or as a cathartic Symptom reduction with healthy eating can take weeks to occur |
Extremities and musculoskeletal | Cold, blue hands and feet | No characteristic symptoms Self-cutting or burning on wrists or arms |
Energy-conserving low body temperature with slow blood flow most notable peripherally Quickly reversed with healthy eating |
Nervous system | No characteristic symptom | No characteristic symptom | Neurologic symptoms suggest diagnosis other than ED |
Mental status | Depression, anxiety, obsessive-compulsive symptoms, alone or in combination | Depression; PTSD; borderline personality disorder traits | Underlying mood disturbances can worsen with dysfunctional weight control practices and can improve with healthy eating AN patients might report emotional “numbness” with starvation preferable to emotionality associated with healthy eating |
PHYSICAL SIGN | PROMINENT FEATURE | CLINICAL COMMENTS RELATED TO ED SIGNS | |
---|---|---|---|
Restrictive Intake | Binge Eating/Purging | ||
General appearance | Thin to cachectic, depending on balance of intake and output Might wear bulky clothing to hide thinness and might resist being examined |
Thin to overweight, depending on the balance of intake and output through various means | Examine in hospital gown Weight loss more rapid with reduced intake and excessive exercise Binge eating can result in large weight gain, regardless of purging behavior Appearance depends on balance of intake and output and overall weight control habits |
Weight | Low and falling (if previously overweight, may be normal or high); may be falsely elevated if patient drinks fluids or adds weights to body before being weighed | Highly variable, depending on balance of intake and output and state of hydration Falsification of weight is unusual |
Weigh in hospital gown with no underwear, after voiding (measure urine SG) Remain in gown until physical exam completed to identify possible fluid loading (low urine SG, palpable bladder) or adding weights to body |
Metabolism | Hypothermia: temp <35.5°C (95.9°F), pulse <60 beats/min Slowed psychomotor response with very low core temperature |
Variable, but hypometabolic state is less common than in AN | Hypometabolism related to disruption of hypothalamic control mechanisms as a result of weight loss Signs of hypometabolism (cold skin, slow capillary refill, acrocyanosis) most evident in hands and feet, where energy conservation is most active |
Skin | Dry Increased prominence of hair follicles Orange or yellow hands |
Calluses over proximal knuckle joints of hand (Russell's sign) | Carotenemia with large intake of β-carotene foods Russell's sign: maxillary incisors abrasion develops into callus with chronic digital pharyngeal stimulation, usually on dominant hand |
Hair | Lanugo-type hair growth on face and upper body Scalp hair loss, especially prominent in parietal region |
No characteristic sign | Body hair growth conserves energy Scalp hair loss “telogen effluvium” can worsen weeks after refeeding begins, as hair in resting phase is replaced by growing hair |
Eyes | No characteristic sign | Subconjunctival hemorrhage | Increased intrathoracic pressure during vomiting |
Teeth | No characteristic sign | Eroded dental enamel and decayed, fractured, missing teeth | Perimolysis, worse on lingual surfaces of maxillary teeth, is intensified by brushing teeth without preceding water rinse |
Salivary glands | No characteristic sign | Enlargement, relatively nontender | Parotid > submandibular involvement with frequent and chronic binge eating and induced vomiting |
Throat | No characteristic sign | Absent gag reflex | Extinction of gag response with repeated pharyngeal stimulation |
Heart | Bradycardia, hypotension, and orthostatic pulse differential >25 beats/min | Hypovolemia if dehydrated | Changes in AN resulting from central hypothalamic and intrinsic cardiac function Orthostatic changes less prominent if athletic, more prominent if associated with purging |
Abdomen | Scaphoid, organs may be palpable but not enlarged, stool-filled left lower quadrant | Increased bowel sounds if recent laxative use | Presence of organomegaly requires investigation to determine cause Constipation prominent with weight loss |
Extremities and musculoskeletal system | Cold, acrocyanosis, slow capillary refill Edema of feet Loss of muscle, subcutaneous, and fat tissue |
No characteristic sign, but may have rebound edema after stopping chronic laxative use | Signs of hypometabolism (cold) and cardiovascular dysfunction (slow capillary refill and acrocyanosis) in hands and feet Edema, caused by capillary fragility more than hypoproteinemia in AN, can worsen in early phase of refeeding |
Nervous system | No characteristic sign | No characteristic sign | Water loading before weigh-ins can cause acute hyponatremia |
Mental status | Anxiety about body image, irritability, depressed mood, oppositional to change | Depression, evidence of PTSD, more likely suicidal than AN | Mental status often improves with healthier eating and weight; SSRIs only shown to be effective for BN |
In addition to identifying symptoms and signs that deserve targeted intervention for patients who have an ED, a comprehensive history and physical examination are required to rule out other conditions in the differential diagnosis. Weight loss can occur in any condition with increased catabolism (e.g., hyperthyroidism, malignancy, occult chronic infection) or malabsorption (e.g., inflammatory bowel disease, celiac disease) or in other disorders (Addison disease, type 1 diabetes mellitus, stimulant abuse), but these illnesses are generally associated with other findings and are not usually associated with decreased caloric intake. Patients with inflammatory bowel disease can reduce intake to minimize abdominal cramping; eating can cause abdominal discomfort and early satiety in AN because of gastric atony associated with significant weight loss, not malabsorption. Likewise, signs of weight loss in AN might include hypothermia, acrocyanosis with slow capillary refill, and neutropenia similar to some features of sepsis, but the overall picture in EDs is one of relative cardiovascular stability compared with sepsis. Endocrinopathies are also in the differential of EDs. With BN, voracious appetite in the face of weight loss might suggest diabetes mellitus, but blood glucose levels are normal or low in EDs. Adrenal insufficiency mimics many physical symptoms and signs found in restrictive AN but is associated with elevated potassium levels and hyperpigmentation. Thyroid disorders may be considered, because of changes in weight, but the overall presentation of AN includes symptoms of both underactive and overactive thyroid, such as hypothermia, bradycardia, and constipation, as well as weight loss and excessive physical activity, respectively.
In the CNS, craniopharyngiomas and Rathke pouch tumors can mimic some of the findings of AN, such as weight loss and growth failure, and even some body image disturbances, but the latter are less fixed than in typical EDs and are associated with other findings, including evidence of increased intracranial pressure. Mitochondrial neurogastrointestinal encephalomyopathy , caused by a mutation in the TYMP gene, presents with gastrointestinal dysmotility, cachexia, ptosis, peripheral neuropathy, ophthalmoplegia, and leukoencephalopathy. Symptoms begin during the 2nd decade of life and are often initially diagnosed as AN. Early satiety, vomiting, cramps, constipation, and pseudoobstruction result in weight loss often before the neurologic features are noticed (see Chapter 616.2 ). Acute or chronic oromotor dysfunction and obsessive-compulsive disorder may mimic an eating disorder. Fear of choking may lead to avoidance-restrictive food intake disorder .
Any patient with an atypical presentation of an ED, based on age, sex, or other factors not typical for AN or BN, deserves a scrupulous search for an alternative explanation. In ARFID, disturbance in the neurosensory processes associated with eating, not weight loss, is the central concern and must be recognized for appropriate treatment. Patients can have both an underlying illness and an ED. The core features of dysfunctional eating habits—body image disturbance and change in weight—can coexist with conditions such as diabetes mellitus, where patients might manipulate their insulin dosing to lose weight.
Because the diagnosis of an ED is made clinically, there is no confirmatory laboratory test. Laboratory abnormalities, when found, are the result of malnutrition, weight control habits, or medical complications; studies should be chosen based on history and physical examination. A routine screening battery typically includes complete blood count, erythrocyte sedimentation rate (should be normal), and biochemical profile. Common abnormalities in ED include low white blood cell count with normal hemoglobin and differential; hypokalemic, hypochloremic metabolic alkalosis from severe vomiting; mildly elevated liver enzymes, cholesterol, and cortisol levels; low gonadotropins and blood glucose with marked weight loss; and generally normal total protein, albumin, and renal function. An electrocardiogram may be useful when profound bradycardia or arrhythmia is detected; the ECG usually has low voltage, with nonspecific ST or T-wave changes. Although prolonged QTc has been reported, prospective studies have not found an increased risk for this. Nonetheless, when a prolonged QTc is present in a patient with ED, it may increase the risk for ventricular dysrhythmias.
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