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Eating Disorders: Evaluation and Management: Key Points

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37 Eating Disorders: Evaluation and Management

Jennifer J. Thomas, PhD, Diane W. Mickley, MD, FACP, FAED, Jennifer L. Derenne, MD, FACP, FAED,
Anne Klibanski, MD, Helen B. Murray, BA, and Kamryn T. Eddy, PhD

KEY POINTS frequency of binge eating and purging for BN, and frequency
of binge-eating for BED. OSFED (previously termed “eating
Incidence disorder, not otherwise specified” in DSM-IV2) allows for spec-
ification of sub threshold or atypical symptom presentations.
• Eating disorders are prevalent among young women, A change from prior versions of DSM, DSM-5 combines both
but they can occur across diverse ages and feeding and eating disorders into a single section. Feeding
populations. disorders in DSM-5 include pica (persistent ingestion of non-
Epidemiology nutritive, non-food substances), rumination disorder (regular
• Eating disorders are associated with serious medical regurgitation of previously ingested food), and avoidant/
co-morbidity related to nutritional compromise, to restrictive food intake disorder (limited food intake leading to
low weight, and to chronic bingeing and purging nutritional deficiency, in the absence of shape and weight
behaviors. concerns). Because research on the etiology, clinical features,
and treatment of feeding disorders is ongoing, this chapter
Treatment Options will focus specifically on eating disorders (i.e., AN, BN, BED,
• The majority of individuals with an eating disorder and OSFED), which are better understood.
do not access treatment for this illness.
• Leading evidence-based treatments include cognitive- EPIDEMIOLOGY
behavioral therapy for bulimia nervosa and binge-
eating disorder; and family-based treatment for The incidence of eating disorders ascertained by case registries
adolescent anorexia nervosa. probably underestimates the true incidence for several reasons.
Data from the National Comorbidity Survey Replication
• Interdisciplinary team management (including
(NCS-R) indicated that fewer than half of individuals with an
primary/specialty medical care, psychotherapy,
eating disorder access any kind of health care service for their
psychopharmacology, and nutritional counseling) is
illness.3 Many of those affected are known to avoid or to post-
often necessary for optimal treatment.
pone clinical care for the condition. In addition, both BN and
Complications BED may manifest without clinical signs, making them diffi-
• Although many medical complications of anorexia cult, if not impossible, to recognize in a clinical setting without
nervosa resolve with recovery, bone loss may persist patient disclosure of symptoms, which may not be forthcom-
and increase the fracture risk life-long. ing.4 Furthermore, whereas AN may manifest with a variety of
Prognosis clinical signs, including emaciation, many patients effectively
conceal their symptoms; up to 50% of cases of eating disorders
• Anorexia nervosa has among the highest mortality may be missed in clinical settings.5 The lifetime prevalence of
rates of all mental illnesses (comparable to substance AN has been estimated at 0.9% for adult females, 0.3% for
abuse). adult males,3 and 0.3% among adolescent males and females.6
BN is more common than is AN, with a reported lifetime
prevalence in adult women of 1.5% and adult men of 0.5%,3
and 0.9% in adolescent males and females.6 BED appears to
OVERVIEW be the most common eating disorder, with a lifetime preva-
Eating disorders comprise several phenomenologically-related lence ranging from 2.0% for adult males to 3.5% for adult
conditions that are characterized by a disturbance in patterns females3 and 1.6% in adolescents.6 In addition, sub threshold
of eating, often in concert with body image disturbance. Each presentations (captured by OSFED) are at least twice as
of the eating disorder diagnoses is associated with substantial common as AN, BN, and BED combined.7 The prevalence of
distress and psychosocial impairment. Moreover, because the eating disorders appears to vary by gender, ethnicity, and the
behaviors can result in serious medical complications, these type of population studied. Although eating disorders histori-
illnesses can have a catastrophic impact on physiological cally have been reported as more common in females than
health, as well as on psychological function. males,2 males may be under-identified. Eating disorders also
occur in culturally, ethnically, and socioeconomically diverse
populations. It is thus important for clinicians to remain vigi-
CLASSIFICATION lant for possible eating disorder symptoms regardless of
Current Diagnostic and Statistical Manual of Mental Disorders, patient demographics.
Fifth Edition (DSM-5) diagnostic categories for eating disor-
ders include anorexia nervosa (AN), bulimia nervosa (BN), COURSE, CO-MORBIDITY, AND
binge-eating disorder (BED), and other specified feeding or
eating disorder (OSFED).1 AN is further divided into two sub-
MORTALITY RATE
types (restricting and binge-eating/purging). DSM-5 specifiers AN can onset from childhood to adulthood, but it most
for AN, BN, and BED allow for descriptive indicators of rela- commonly begins in post-pubertal adolescence. Likewise,
tive severity (mild, moderate, severe, or extreme) and sympto- the most common time of onset for BN is in post-pubertal
matic improvement (partial vs. full remission). Severity (usually late) adolescence. Both BN and BED can onset in later
is dictated primarily by body mass index (BMI) for AN, decades.3

412

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Eating Disorders: Evaluation and Management 413

Greater than half of those with AN and BN will achieve remains limited. Evolving studies in the area are focusing
recovery over long-term follow-up, and more will have symp- on the genetic underpinnings of symptoms associated 37
tomatic improvement short of full recovery; approximately with the eating disorders (rather than diagnoses), as well as
20-33% will have a chronic course.8,9 Notwithstanding the gene–environment interactions.23,24 Emerging evidence from
data and conventional wisdom that AN, in particular, often neuroimaging research suggests that, compared to healthy
follows a chronic course, the NCS-R study reported that AN controls, individuals with AN experience an over-activation of
had a significantly shorter course than either BN or BED.3 neural circuitry in the fear network when presented with food
These data suggest that there may be more variation in the stimuli.25 In contrast, individuals with BN may binge eat, in
course of AN than previously thought, possibly due to the fact part, due to hypoactivation of reward circuitry and impair-
that some individuals experience remission before seeking ments in neural networks that contribute to impulse control.25
care. Outcomes for BED are somewhat more favorable with
the majority achieving symptom remission over time but still
up to one third remaining more chronically ill.10 Moreover,
DIAGNOSTIC FEATURES
there is also considerable diagnostic migration across eating Considerable phenomenological overlap and diagnostic
disorder categories, typically reflecting crossover from a prima- migration across AN, BN, BED, and OSFED has contributed
rily restrictive to a bingeing and/or purging presentation over to a “transdiagnostic” view of eating disorders that highlights
time.11–13 Eating disorders are associated with high medical similarities in both symptoms and maintaining mechanisms.26
co-morbidity (as nutritional derangement and purging However, by definition, a diagnosis of one eating disorder is
behaviors frequently lead to serious medical complications); mutually exclusive with another at any particular point in time.
they are also associated with a high degree of psychiatric
co-morbidity. The NCS-R study found that a majority of
respondents with each of the full threshold eating disorders
Anorexia Nervosa
(AN, BN, and BED) had a lifetime history of another psychi- AN is characterized and distinguished by a significantly low
atric disorder. Of these, 94.5% of respondents with BN had a body weight. A significantly low body weight is assessed in
lifetime history of a co-morbid mental illness.3 The mortality relation to sex, age, and height. Although the clinical context
risk associated with eating disorders is also elevated.14,15 The guides whether a particular weight is consistent with AN, a
risk of mortality may be increased by co-morbid factors, such commonly recognized guideline for adults is a BMI less than
as substance abuse, and by a longer duration of illness.16 The 18.5 kg/m2 (i.e., the lower limit of the normal range). For
high mortality rate is accounted for by both serious medical children and adolescents, the American Academy of Pediatrics
complications of the behaviors, and by a suicide rate that is and the American Psychiatric Association have set forth prac-
18 times that expected in AN, in particular.17 tice guidelines that encourage providers to determine an indi-
vidual adolescent’s goal weight range using past growth charts,
menstrual history, mid-parental height, and even bone age as
ETIOLOGICAL FACTORS guides. The Centers for Disease Control and Prevention (CDC)
Although the etiology of eating disorders is likely multi- recommends use of normative growth charts, which plot BMI
factorial, causal factors are uncertain.18 Possible sociocultural, percentiles for age (2 to 20 years) and sex. Although children
biological, and psychological risk factors all have been identi- who fall below the fifth percentile in BMI for age are generally
fied, despite methodological limitations that characterize considered underweight,1 children who are above the fifth
many studies. In addition to female gender and ethnicity, percentile may also be considered underweight particularly in
weight concerns and negative self-evaluation have the strong- the instance of deviation from growth trajectory. Of note,
est empirical support as risk factors for eating disorders.18 In many physicians note that children and adolescents can be
particular, risk factors for obesity appear to be associated with sensitive to the medical consequences of eating disorders even
BED,19 and risk factors for dieting appear to be associated with when weight does not appear to be dangerously low.
BN.20 Risk for an eating disorder may also be elevated by In addition to a low body weight, AN is often characterized
generic risk factors for mental illness.18–20 in Western populations by a fear of becoming fat or gaining
Sociocultural factors are strongly suggested by population weight. This may also be manifested in behavior that interferes
studies that have demonstrated that transnational migration, with gaining weight (e.g., restrictive eating, purging, or com-
modernization, and Westernization are associated with an pulsive exercising), particularly for those individuals who do
elevated risk for disordered eating among vulnerable sub- not explicitly endorse a fear of fatness.27 Individuals with AN
populations. Other social environmental factors (such as peer also often exhibit a disturbance in body experience that can
influence, teasing, bullying, and mass media exposure) have range from a lack of insight or recognition of serious medical
been linked with an elevated risk of body image disturbance consequences to a distorted perception of one’s weight and
or disordered eating.21 shape and their importance.
Numerous psychological factors have been identified as Cognitive symptoms can often be assessed by asking about
either risk factors or retrospective correlates of eating disorders. dietary routines, food restrictions, and the patient’s desired
Among these is exposure to health problems (including diges- body weight. Of note, children and adolescents do not always
tive problems) in early childhood, exposure to sexual abuse report cognitive symptoms, possibly due to developmental
and adverse life events, higher levels of neuroticism, low self- factors.28 Binge-eating and purging symptoms are common yet
esteem, and anxiety disorders.18 Furthermore, a cognitive style often overlooked in AN. The binge-eating/purging subtype of
characterized by weak set-shifting (i.e., difficulty switching AN is diagnosed in the setting of recurrent binge-eating and
between tasks) and poor central coherence (i.e., hyper-focus on purging; otherwise the diagnosis of restricting-type AN is
minor details to the detriment of grasping the bigger picture) made. Box 37-1 summarizes diagnostic criteria for AN.
is common in AN and may increase risk for the disorder.22
Genetic influences on eating disorders have also been
studied. Although family and twin studies support a substan-
Bulimia Nervosa
tial genetic contribution to the risk for eating disorders BN is characterized by recurrent episodes of binge-eating
and molecular genetic studies hold promise, our understand- and by behaviors aimed at the prevention of weight gain
ing of the genetic transmission of risk for eating disorders or purging calories. These behaviors, termed “inappropriate

BOX 37-1 DSM-5 Diagnostic Criteria: Anorexia Nervosa BOX 37-2 DSM-5 Diagnostic Criteria: Bulimia Nervosa
(307.1 (F50.01 restricting type, F50.02 (307.51 (F50.2))
binge-eating/purging type))
A. Recurrent episodes of binge eating. An episode of binge
A. Restriction of energy intake relative to requirements, leading eating is characterized by both of the following:
to a significantly low body weight in the context of age, sex, 1. Eating, in a discrete period of time (e.g., within any 2-hour
developmental trajectory, and physical health. Significantly period), an amount of food that is definitely larger than
low weight is defined as weight that is less than minimally what most individuals would eat in a similar period of time
normal or, for children and adolescents, less than that under similar circumstances.
minimally expected. 2. A sense of lack of control over eating during the episode
B. Intense fear of gaining weight or of becoming fat, or (e.g., a feeling that one cannot stop eating or control
persistent behavior that interferes with weight gain, even what or how much one is eating).
though at a significantly low weight. B. Recurrent inappropriate compensatory behaviors in order to
C. Disturbance in the way in which one’s body weight or shape prevent weight gain, such as self-induced vomiting; misuse
is experienced, undue influence of body weight or shape on of laxatives, diuretics, or other medications; fasting; or
self-evaluation, or persistent lack of recognition of the excessive exercise.
seriousness of the current low body weight. C. The binge eating and inappropriate compensatory behaviors
both occur, on average, at least once a week for 3 months.
Specify whether:
D. Self-evaluation is unduly influenced by body shape and
Restricting type: During the last 3 months, the individual has weight.
not engaged in recurrent episodes of binge eating or purging E. The disturbance does not occur exclusively during episodes
behavior (i.e., self-induced vomiting or the misuse of laxatives, of anorexia nervosa.
diuretics, or enemas). This subtype describes presentations in
Specify if:
which weight loss is accomplished primarily through dieting,
fasting, and/or excessive exercise. In partial remission: After full criteria for bulimia nervosa were
Binge-eating/purging type: During the last 3 months, the previously met, some, but not all, of the criteria have been
individual has engaged in recurrent episodes of binge eating met for a sustained period of time.
or purging behavior (i.e., self-induced vomiting or the misuse In full remission: After full criteria for bulimia nervosa were
of laxatives, diuretics, or enemas). previously met, none of the criteria have been met for a
sustained period of time.
Specify if:
Specify current severity:
In partial remission: After full criteria for anorexia nervosa were
The minimum level of severity is based on the frequency of
previously met, Criterion A (low body weight) has not been
inappropriate compensatory behaviors (see below). The level of
met for a sustained period, but either Criterion B (intense fear
severity may be increased to reflect other symptoms and the
of gaining weight or becoming fat or behavior that interferes
degree of functional disability.
with weight gain) or Criterion C (disturbances in self-
perception of weight and shape) is still met. Mild: An average of 1–3 episodes of inappropriate
In full remission: After full criteria for anorexia nervosa were compensatory behaviors per week.
previously met, none of the criteria have been met for a Moderate: An average of 4–7 episodes of inappropriate
sustained period of time. compensatory behaviors per week.
Severe: An average of 8–13 episodes of inappropriate
Specify current severity:
compensatory behaviors per week.
The minimum level of severity is based, for adults, on current
Extreme: An average of 14 or more episodes of inappropriate
body mass index (BMI) (see below) or, for children and
compensatory behaviors per week.
adolescents, on BMI percentile. The ranges below are derived
from World Health Organization categories for thinness in adults; Reprinted with permission from the Diagnostic and statistical manual of
for children and adolescents, corresponding BMI percentiles mental disorders, ed 5, (Copyright 2013). American Psychiatric
should be used. The level of severity may be increased to reflect Association.
clinical symptoms, the degree of functional disability, and the
need for supervision.
Mild: BMI ≥ 17 kg/m2
binge-eating/purging type, although low weight is one helpful
Moderate: BMI 16–16.99 kg/m2
feature to draw a distinction between the two. A binge eating
Severe: BMI 15–15.99 kg/m2
episode is considered to take place in a discrete time period,
Extreme: BMI < 15 kg/m2
consists of the intake of an unusually large amount of food
Reprinted with permission from the Diagnostic and statistical manual of given the social context, and is subjectively experienced as
mental disorders, ed 5, (Copyright 2013). American Psychiatric being out of control. Box 37-2 summarizes the diagnostic
Association. criteria for BN.

compensatory behaviors” in the DSM-5,1 induced self-induced

Binge-eating Disorder
vomiting; laxative, enema, and diuretic misuse; stimulant BED is characterized by recurrent episodes of binge-eating.
abuse; diabetic underdosing of insulin; fasting; and excessive Unlike in individuals with BN, there are no recurrent compen-
exercise. To meet criteria for the syndrome, patients need to satory behaviors. Binge-eating episodes are accompanied by at
engage in both bingeing and inappropriate compensatory least three of five correlates (these include eating rapidly,
behaviors at least once weekly for at least 3 months. In addi- eating until uncomfortably full, eating when not hungry, or
tion, individuals with BN are excessively concerned with body eating alone to avoid embarrassment; and feeling guilty post-
shape and weight. There can be considerable phenomenologi- binge) and are associated with marked distress. In parallel
cal overlap between individuals with BN and AN, with the frequency and duration criteria for BN, individuals

BOX 37-3 DSM-5 Diagnostic Criteria: Binge-Eating Disorder (307.51 (F50.8)) 37

A. Recurrent episodes of binge eating. An episode of binge eating E. The binge eating is not associated with the recurrent use of
is characterized by both of the following: inappropriate compensatory behavior as in bulimia nervosa and
1. Eating, in a discrete period of time (e.g., within any 2-hour does not occur exclusively during the course of bulimia
period), an amount of food that is definitely larger than what nervosa or anorexia nervosa.
most people would eat in a similar period of time under Specify if:
similar circumstances.
In partial remission: After full criteria for binge-eating disorder
2. A sense of lack of control over eating during the episode
were previously met, binge eating occurs at an average
(e.g., a feeling that one cannot stop eating or control what
frequency or less than one episode per week for a sustained
or how much one is eating).
period of time.
B. The binge-eating episodes are associated with three (or more)
In full remission: After full criteria for binge-eating disorder were
of the following:
previously met, none of the criteria have been met for a
1. Eating much more rapidly than normal.
sustained period of time.
2. Eating until feeling uncomfortably full.
3. Eating large amounts of food when not feeling physically Specify current severity:
hungry. The minimum level of severity is based on the frequency of
4. Eating alone because of feeling embarrassed by how much episodes of binge eating (see below). The level of severity may be
one is eating. increased to reflect other symptoms and the degree of functional
5. Feeling disgusted with oneself, depressed, or very guilty disability.
afterward. Mild: 1–3 binge-eating episodes per week.
C. Marked distress regarding binge eating is present. Moderate: 4–7 binge-eating episodes per week.
D. The binge eating occurs, on average, at least once a week for Severe: 8–13 binge-eating episodes per week.
3 months. Extreme: 14 or more binge-eating episodes per week.

TABLE 37-1 Differential Diagnosis of Eating Disorders and Their Subtypes by Signs and Symptoms
Purging or Behaviors to
Body Weight or Typical Dietary Neutralize Perceived or Real
Weight Criterion Shape Concerns Pattern Binge-Eating Excessive Caloric Intake
Anorexia nervosa < Low weight (less Yes Restrictive; Frequently present; Frequently present; binge-
than normal or recurrent binge-eating/ eating/purging subtype
minimally expected) binge-eating purging subtype
Bulimia nervosa No Yes Recurrent Yes Yes
binge-eating
Binge-eating No, but frequently No, but frequently Recurrent Yes No
disorder overweight present binge-eating
OSFED No Frequently present, Varied Frequently present, Frequently present, but not
but not required but not required required for diagnosis
for diagnosis for diagnosis
OSFED: Other specified feeding or eating disorder.

must experience these episodes (on average) once a week for in conjunction with night-time awakenings and is associated
at least 3 months to meet DSM criteria for BED. Although the with distress or functional impairment. Formerly termed
diagnostic criteria for BED do not specifically mention the eating disorders not otherwise specified (EDNOS), individuals
overvaluation of shape and weight that is characteristic of AN with OSFED often have psychiatric symptoms and physical
and BN, individuals with BED who exhibit this feature have complications that are just as severe as those associated with
poorer treatment outcomes.29 Box 37-3 summarizes the diag- full-syndrome disorders.30 Table 37-1 summarizes distinguish-
nostic criteria for BED. ing diagnostic criteria of the eating disorders. Lastly, the diag-
nosis of unspecified feeding or eating disorder subtypes, for
which insufficient information is available to confirm a specific
Other Specified Feeding or Eating Disorder diagnosis (e.g., in an emergency room setting).
This residual category comprises individuals who experience
clinically significant symptoms that do not meet full criteria for
AN, BN, or BED. These include sub threshold categories, such
EVALUATION AND DIFFERENTIAL DIAGNOSIS
as atypical AN (i.e., AN features without low body weight); BN Evaluation of an eating disorder is optimally accomplished
of low frequency and/or limited duration; BED of low fre- with input from mental health, primary care, and dietetic
quency and/or limited duration; purging disorder; and night- clinicians. Team management is advisable and often essential
eating syndrome (NES). Purging disorder resembles BN in to clarify diagnosis, to identify psychiatric and medical
terms of purging, but lacks binge-eating episodes. NES involves co-morbidities, and to establish the modalities and level of
excessive evening eating that occurs after the evening meal or care best suited safe and effective management. Evaluation is

Figure 37-1. Dental erosion resulting from chronic vomiting. (Adapted

and printed with permission from the MGH Department of
Psychiatry.)

often complicated by a patient’s ambivalence about accepting

assistance or engaging in treatment. In other situations, it is
more appropriate to discuss screening for an eating disorder
as a patient may not realize that his or her behaviors are prob-
lematic, or may not have decided whether or how to disclose
his or her symptoms. Figure 37-2. Parotid hypertrophy resulting from chronic vomiting.
Because BN, BED, and OSFED can present with a normal (Adapted and printed with permission from the MGH Department of
weight and physical examination, the diagnosis can be missed Psychiatry.)
if a patient is not forthcoming or queried about symptoms.
Among individuals who acknowledge eating and weight con-
cerns, only a relatively small percentage report being asked by
a doctor about symptoms of an eating disorder.4 Identification especially helpful in deciding whether a patient is well enough
of an occult eating disorder in a primary care or mental health to begin treatment as an outpatient or if he or she would
setting can be challenging if a patient is unreceptive to diag- benefit from a more intensive level of care.
nosis or to treatment. Although screening assessments for The history should elicit the onset of body image and
eating disorders are more frequently used in research than in eating disorder disturbances, specific precipitants, if any, and
clinical settings, offering this screening in a primary care remissions or exacerbations of symptoms. The patient’s history
setting may provide a practical opportunity for a patient to of weight fluctuations, as well as minimum and maximum
discuss eating concerns. However, the validity of these assess- weights and their approximate durations, is useful in gauging
ments rests on a patient’s accurate and truthful responses. how symptomatic the patient has become and where he or
Certain clinical signs (e.g., a history of extreme weight changes, she is in relation to his or her illness history. For assessment
dental enamel erosion (see Figure 37-1), parotid hypertrophy of body image disturbance, it is useful to probe what the
(see Figure 37-2), or elevated serum amylase) may flag the patient’s desired weight is in relation to his or her current
possibility of an eating disorder, although the disorder can weight, as well as any behavioral manifestations of shape and
occur in their absence. Occasionally, certain probes in the weight concerns such as body checking (e.g., seeing if thighs
clinical interview may suggest an eating disorder (Table 37-2). touch, frequent weighing) and experiential avoidance (e.g.,
For example, inquiring about maximum, minimum, and hiding one’s shape with baggy clothes, avoiding being seen in
desired weights often elicits information about body image public). Moreover, probing how preoccupied the patient is
concern, weight loss attempts, and overeating. Next, weighing with calories or his or her weight can include a straightforward
a patient is essential for establishing the weight criterion for question about it (as well as an inquiry about whether the
AN. The appropriateness of weight for height can be surpris- patient keeps a running tally of calories) or questions about
ingly difficult to estimate without this objective data. Although how frequently he or she weighs himself or herself or what
clinicians are sometimes reluctant to inquire about purging effect a weight change has on his or her mood or self-
behaviors, a direct (empathically stated) question has been evaluation. Alternatively, how a patient registers and responds
shown to be useful to elicit a candid response. Data suggest to information about medical complications can also signal
that even patients who have not voluntarily disclosed informa- body image disturbance. Clinicians should ask about current
tion to their doctor about an eating disorder are likely to dietary patterns, including a restrictive pattern of eating (e.g.,
disclose it in response to a direct query.4 fasting, meal-skipping, calorie restriction, or evidence of
Evaluation of a patient with a known eating disorder can restricting intake of specific foods) and overeating (e.g., binge-
also be complicated by incomplete disclosure or misrepresen- eating, grazing, or night-eating). Excess water-drinking to
tation of the frequency or severity of symptoms. For this produce “fullness” should be asked about and can lead to
reason, it is advisable to obtain additional objective data (such hyponatremia. Conversely, dehydration from complete avoid-
as weight and serum electrolytes). Both the type of symptoms ance of fluids (due to fear of weight gain) is also commonly
and their severity or frequency will allow classification into observed.31 In addition to dietary patterns, clinicians should
one of the eating disorder diagnoses. The latter will be inquire about and inventory attempts to compensate for

TABLE 37-2 Useful Probes for Attitudes and Behaviors Associated with the Eating Disorders
37
Topic Suggested Probe Questions
Weight history • Can you give me a sense of your current height and weight?
• Have there been any recent changes in your weight?
• What is the least you have weighed at this height?
• What is the most you have weighed?
Perception of current • Do you see yourself as your friends and family do?
shape and size
Preoccupations • How much time do you spend thinking about food/calories/weight/body shape?
• Has thinking about these things made it difficult to concentrate on other things?
Dietary patterns • Do you count calories (in a given day)?
• What might you eat for meals (and snacks) on a typical day?
• Are there any rules you follow about how much you can eat in a given day?
• Are there certain foods that you feel you should not eat or are fearful of?
• Are there any rules you follow about how much you can eat during the day?
• Are there any rules you follow about certain ways you have to eat?
Binge-pattern eating • Do you have episodes in which you feel you eat an unusual amount of food and it feels like you cannot control it?
• What (amount and kind of food) do you eat during such an episode?
• How long does the episode take?
• How many times might this happen during 1 day (or over a week)?
• How do you feel about it afterward?
• Does anything happen before that might be related? What time of day does it normally happen?
Inappropriate • Have you ever made yourself vomit?
compensatory behaviors • Have you ever used laxatives (especially stimulant type), suppositories, enemas, or diuretics to try to control your
(ask frequency for each) weight or compensate for calories you have taken in? (To be followed with psychoeducational information; i.e., Do
you know that laxatives and diuretics don’t remove any calories from your body and may lead to re-weight gain
from water retention when you try to stop?)
• Have you ever used drugs (prescription or illegal) or caffeine to try to control your appetite or compensate for
calories you have taken in?
• (Assess adequacy of insulin dosing if diabetic; the nature of the probe used here will depend on the clinical
context.)
• How often do you exercise? How much exercise do you get on a typical day or in a typical week?
• How do you feel if you are unable to exercise on a particular day?
• Do you ever skip meals?
• Do you ever go a day or more without eating? Without drinking?

binge-eating or to prevent weight gain (see Table 37-2). Some Other considerations in the evaluation of an eating disor-
clinicians are reluctant to ask about certain symptoms, out of der include the assessment of the supportive or adverse role
concern that they may introduce a weight loss strategy that a of family, peers, team members, and other elements of the
patient may be tempted to try. Unfortunately, patients have psychosocial environment. If the patient is participating in an
access to information through social media platforms (e.g., athletic activity (e.g., skating, gymnastics, track, or wrestling)
Twitter, Tumblr) or “pro-ana” (pro-anorexia) websites about or within an occupation (e.g., dance or modeling) in which
dieting, restrictive pattern eating, purging, and evasion of low weight is considered highly desirable, it is critical to
detection. Patients do not always appreciate how dangerous understand whether there is support for his or her treatment
some behaviors are; therefore, the clinical evaluation provides or pressure to remain slim. In addition to the potential ben-
an invaluable opportunity to intervene in some behaviors that efits of family therapy (especially for adolescents with AN), a
patients use or to suggest that they substitute them for others. family evaluation can play a critical role in psychoeducation
Because untreated or poorly treated diabetes can result in for the family. This is particularly useful for patients who live
weight loss, and because adherence to strict diets and food with, or who continue to be dependent on, their family.
regimens is part of diabetes management, insulin-dependent Parents frequently find themselves in a dilemma, faced with
diabetic patients present a special challenge in an evaluation. expressing concern about their child’s eating (even an adult
Often patients have been specifically referred for evaluation child) and allowing their child autonomy, and often avoiding
and management because their blood sugars are poorly con- a struggle that makes them feel powerless. Some parents
trolled and their inappropriate underdosing or withholding benefit from guidance on what constitutes helpful (and
of insulin has already come to light. For patients in whom unhelpful) input from them, as well as what the signs, symp-
these behaviors have not yet been identified, the most appro- toms, and health risks of an eating disorder are.
priate line of questioning may be more open-ended to deter- Assessment of motivation for change is often critical for
mine how they manage their insulin dosing relative to food individuals with an eating disorder because it can be predic-
intake without necessarily suggesting that intentional hyper tive of treatment outcome.32 Although individuals with BN
glycemia would cause weight loss. Excessive exercise is some- and BED are often distressed by their symptoms, they often
what difficult to assess, as guidelines about the frequency and are fearful or reluctant about relinquishing them. Individuals
duration of exercise for health benefits have shifted upward. with AN are commonly unreceptive to treatment. Cognitive
In this case, it is helpful to determine whether the exercise has distortions that are typical of the illness make it difficult to
a compulsive quality (e.g., does he or she exercise regardless motivate a patient to accept treatment that will restore weight.
of schedule, weather, injury, or illness) or is greatly in excess The prescription for recovery—which starts with weight
of medical or team recommendations. restoration—is exactly what they fear. Moreover, denial of

seriousness of medical complications of their low weight is in anorexia (even in prior athletes), bradycardia reflects cardiac
inherent to the illness; therefore, information that might moti- impairment associated with reduced stroke volume.
vate change under other illness scenarios is not always effective Further changes are seen in cardiac anatomy and conduc-
for AN. In short, patients with AN are frequently highly tion. Compression of the annulus from reduced cardiac mass
invested in their symptoms and unwilling to occupy the con- may result in mitral valve prolapse, and silent pericardial
ventional sick role, in which patients typically agree to treat- effusions are common, but generally not of functional signifi-
ment. In addition to sustaining a particular weight that they cance.35 Electrophysiologically, the QTc interval and QT dis-
find acceptable, individuals with an eating disorder often find persion may be increased,36 and may predispose to ventricular
that their behavioral symptoms (restrictive eating that leads to arrhythmias and be harbingers of sudden death.37 While virtu-
hunger, binge-eating, or purging) contribute to self-soothing ally all aspects of cardiac function normalize with full recov-
and to self-efficacy, and they are reluctant to relinquish these ery, some aspects of cardiac function may actually deteriorate
perceived benefits. during initial treatment.38
Finally, mental health evaluation must take into account Although cardiac complications may be the most danger-
accompanying mood, thought, substance use, personality, and ous for AN patients, low bone mass is among the most per-
other disorders that are frequently co-morbid with eating dis- manent. Loss of bone mass can be rapid and remain low
orders. Excessive use of alcohol and cigarettes should be deter- despite disease recovery; it represents a life-long risk of
mined as well. Behaviors associated with eating disorders are increased fractures. The association of low bone mineral
frequently exacerbated by depression and by anxiety disorders. density (BMD) is established in adolescent girls as well as
Conversely, an increase in the frequency or severity of eating boys.39,40 Of importance, effects on bone mass can be seen
disorder symptoms can exacerbate mood symptoms. More with brief disease duration, with very significant reductions in
over, low weight undermines the efficacy of antidepressants. bone mass being reported in girls who have been ill for less
This may be due to nutritional or other unknown factors. than a year. Skeletal impact can be severe.41 An electron micro-
Substance abuse sometimes waxes and wanes in relation to graph of an osteoporotic female with multiple vertebral com-
disordered eating. A clinician who evaluates a patient with pression fractures is shown in Figure 37-3.
active substance abuse or in early recovery is advised to use Factors that contribute to low BMD in AN include hormo-
particular caution in considering the impact of controlling nal and nutritional abnormalities, as well as risks associated
restrictive eating, bingeing, or purging symptoms if these pat- with excess exercise, smoking, and alcohol use. Endocrine
terns provide an essential coping mechanism for a patient at factors include hypogonadism, low levels of insulin-like
risk of relapse for substance abuse or other self-injurious growth factor-1 (IGF-1), and hypercortisolemia. In AN, normal
behavior. If the symptoms co-exist, generally the more life- puberty is disrupted with prolonged estrogen deficiency, as
threatening of them will require initial treatment. For BN and well as lack of growth hormone (GH) effects mediated by
BED, the substance abuse disorder generally takes precedence, IGF-1. Maximal bone mass is achieved during adolescence and
but the medical and nutritional impact of the eating symp- early adult life. Therefore, suppression of bone formation by
toms requires ongoing surveillance. For severe AN in the under-nutrition during adolescence leaves affected girls par-
setting of substance abuse, it is highly likely that inpatient care ticularly vulnerable to inadequate peak bone mass formation.
is the safest and most effective treatment setting. Finally, Although bone-density measurements in children must be
assessment of suicidal ideation and behavior is critical in the done at a center with access to a normative database, in adults
evaluation of an eating disorder. As noted previously, suicide with AN, a screening bone density dual-energy x-ray absorpti-
rates are elevated in eating disorders and the risk and preven- ometry (DEXA) scan is an important part of the medical evalu-
tion of suicide should always be considered. ation. The results of such a scan in a young woman with AN
showing osteoporosis of the spine are shown in Figure 37-4.
Using high-resolution CT scans, an important new finding is
MEDICAL COMPLICATIONS that bone micro-architecture is also impaired in both girls and
Medical consequences of eating disorders are often occult, yet boys with AN.42 Of note, micro-architectural changes may
dangerous. Even subtle laboratory abnormalities, while not precede a demonstrable change in bone density by traditional
intrinsically harmful or worrisome in other settings, may DEXA readings. Bone strength, as assessed by finite element
reflect physiological tolls indicative of significant illness. analysis techniques, is also decreased compared to healthy-
The devastating physical sequelae of the malnutrition of weight girls.43 A number of neuroendocrine factors, either gut
AN have been well described in the medical literature; chil- derived, such as ghrelin, PYY, and leptin, may also play a role
dren and adolescents are recognized as especially vulnerable. in low bone mass. Oxytocin, a brain-derived peptide stored in
The degree of danger generally parallels the magnitude and the posterior pituitary, has been shown to be associated with
speed of the weight loss. Purging augments the risk in all age the severity of disordered-eating psychopathology and been
groups. Major and potentially irreversible effects exist on shown to relate to low bone mass in AN.44,45
bones and heart, but no organ system is spared. The physical The effects of AN on the brain are still being explored but
damage of BN reflects the modalities of purging employed, include cortical atrophy with enlarged sulci on computed tom-
but frequently affects the gastrointestinal tract, teeth, and ography (CT) scan. Gastrointestinal abnormalities are common
electrolytes. and often symptomatic. Gastroparesis is associated with early
Cardiac consequences of anorexia may be asymptomatic but satiety in AN and can cause significant discomfort during
can turn lethal. Adolescents appear to be particularly at risk.33 re-feeding. About 50% of patients who vomit regularly have
Myocardial hypotrophy occurs, often early, with reduced left mucosal abnormalities on endoscopy,46 and many have symp-
ventricular mass and output.34 The heart of the patient with tomatic esophagitis. Hematemesis may result from Mallory-
anorexia has an impaired ability to respond to the increased Weiss tears, and esophageal or gastric rupture is a rare but fatal
demands of exercise. Hypotension occurs early and orthostasis complication. Hematological abnormalities reflect bone
follows, possibly enhanced by volume depletion. Bradycardia marrow suppression. They parallel severity of weight loss and
is common, probably due to increased vagal tone. This should may cause anemia, neutropenia, or thrombocytopenia, alone
neither be dismissed as innocent, nor be viewed as comparable or in combination.47 In addition, low-weight patients may be
to that in conditioned athletes. Whereas athletes with bradycar- unable to mount a febrile response to infection, causing
dia have increased ventricular mass and myocardial efficiency, delayed recognition and increased severity.48 AN is a risk factor

for acute renal injury and nephrolithiasis, and, if chronic, for

renal failure.49 Patients with co-morbid medical illness present 37
an additional challenge. Individuals with type I diabetes have
a higher risk of eating disorders and may “purge” by omitting
their insulin, resulting in poor glycemic control, rapid develop-
ment of vascular complications, and episodes of ketoacidosis.
The onset of puberty may be delayed in pre-menarchal girls
P with AN. Over one-third of pre-pubertal and peri-pubertal
girls exhibit delayed menarche. Although the effect of AN on
B
final growth is uncertain, abnormalities in the maximum pre-
dicted growth have been reported. Other hormonal abnor-
malities identified in adults and adolescents with AN include
hypercortisolemia, which may have deleterious effects, includ-
ing suppressed bone formation.
Hypothalamic amenorrhea is a hallmark of AN and pre-
cedes the onset of weight loss in a subset of patients. While
some individuals have a reliable menstrual weight threshold,
A others experience a significant delay between weight restora-
tion and the resumption of menses. Normal-weight women
with BN may also have irregular, infrequent, or absent men-
struation. Of note, some women meeting all the psychiatric
criteria of AN may continue to menstruate at very low body
weights; low bone mass may still be seen in such women. With
full resolution of an eating disorder, frequency of pregnancy
has been reported to be comparable to that of the general
population. However, a significant number of anovulatory
women who seek infertility treatment have sub-syndromal, if
not active, eating disorders.
A recent study from Scandinavia documented that more
than 10% of women currently bearing children have a past or
present eating disorder. This high incidence has stimulated
concern about the impact on pregnancy. Although data are
limited and at times conflicting, it would appear that women
with eating disorders have a significantly increased risk of mis-
carriage, obstetrical complications, and Cesarean section.50 Off-
B spring are more likely to show intrauterine growth retardation,
low birth weight, and low Apgar scores at delivery.51 Of addi-
Figure 37-3. (A) Low-power scanning electron micrograph of an
tional concern is the high incidence of post-partum depression
autopsy sample of a normal 44-year-old man. (B) Low-power scanning
among women with current or prior eating disorders, raising
electron micrograph of a 47-year-old osteoporotic woman with multi-
important questions about pharmacologic management.
ple vertebral compression fractures. P, Trabecular plate; B, trabecular
The hypothalamic–pituitary–thyroid axis also shows an
bar; Field width, 2.6 mm in each. (From Dempster DW, Shane E,
adaptation to weight loss. Although thyroid-stimulating hor
Horbert W, Lindsay R. A simple method of correlative light and scan-
mone (TSH) concentrations are typically normal in patients
ning electron microscopy of human iliac crest bone biopsies: qualita-
with AN, total T3 is low (as is leptin), a finding consistent with
tive observations in normal and osteoporotic subjects, J Bone Miner
malnutrition and thought to be part of a complex mechanism
Res 1:15–21, 1986, with permission from the American Society for
to decrease resting energy expenditure.52 T3 concentrations
Bone and Mineral Research.)
increase with weight gain and recovery. It is important not to
erroneously diagnose hypothyroidism in the setting of low T3
levels alone, as administration of thyroid hormone has delete-
rious metabolic and cardiac effects in a euthyroid patient with
AN. Elevations in serum TSH indicate an independent primary
DXA RESULTS SUMMARY cause of hypothyroidism.
The refeeding syndrome is an iatrogenic complication of
Region Area BMC BMD T- Z- vigorous initial refeeding of severely emaciated patients,
(cm2) (g) (g/cm2) score score almost always in-hospital. Rapid introduction of calories, par-
L1 10.41 6.35 0.610 –2.9 –2.7 ticularly carbohydrates, stimulates release of insulin, driving
L2 11.23 8.07 0.718 –2.8 –2.7 glucose, phosphorus, potassium, and magnesium into the
L3 13.34 9.72 0.729 –3.2 –3.1 cells. Precipitous drops in phosphorus, in particular, are
L4 16.32 12.31 0.754 –3.3 –3.1 thought to be responsible for the hemolytic anemia, cardiac
arrhythmias, and death that may occur, typically in the first
Total 51.31 36.45 0.710 –3.1 –2.9
week of re-feeding. Thiamine deficiency can result from the
Total BMD CV 1.0%, ACF = 1.008, BCF = 0.990, rapid increase in utilization with re-feeding and delirium may
TH = 5.555 WHO classification: osteoporosis occur, especially in the second week.
Fracture risk: high
Figure 37-4. Results of lumbar spine scan of a 22-year-old woman
with anorexia nervosa showing marked reduction in bone mass and a
MEDICAL ASSESSMENT
Z-score of -2.9 associated with high fracture risk. BMC, bone mineral Taking a medical history provides a crucial opportunity not
content; BMD, bone mineral density. only to assess but also to educate and engage the patient.

Patients with AN are typically convinced of their well-being heart size. Parotid enlargement (bilateral and non-tender)
despite ominous levels of starvation, and the physician should occurs in some patients with BN (see Figure 37-2). Sub-
use every opportunity to affirm the severity of physical com- mandibular glands may be enlarged as well. Russell’s sign—
promise, even if it is occult and asymptomatic. BN can gener- excoriation on the dorsum of a hand—is considered
ate great shame, and the interviewer can convey acceptance pathognomonic for bulimia. Key potential findings on physi-
with a sensitive, but open, inquiry that includes the relevant cal examination are summarized in Table 37-4.
specifics of purging behaviors. In addition to the patient’s
description of the history of his or her illness (including past
and present treatment), it is useful to pose questions that
LABORATORY FINDINGS
probe for attitudes and behaviors associated with eating dis- Laboratory findings are often not useful in establishing the
orders (see Table 37-2). diagnosis or the severity of an eating disorder. The diagnosis
Patients may deny symptoms, but many describe a plaguing may be self-evident with a classic constellation of symptoms,
preoccupation with food and weight, fatigue or weakness, early though patients may not always be forthcoming. The clinical
satiety, and bloating. Patients with AN may also complain of history and a directed interview are more useful in establishing
cold intolerance, impaired concentration, constipation, and the presence of symptoms of an eating disorder; extensive or
hair loss, while patients with BN may note dental problems invasive testing is generally unnecessary and often counterpro-
and the “puffy cheeks” of parotid enlargement. Symptoms of ductive. Laboratory assessment, though sometimes insensitive,
particular medical significance include dizziness, palpitations, is nonetheless essential to exclude other causes of weight loss,
orthostasis, or syncope that may herald cardiovascular danger. or to identify complications of the eating disorder.
Gastrointestinal symptoms can be moderated. Hematemesis Normal laboratory findings do not exclude a serious eating
or rectal bleeding requires emergency intervention. A gyneco- disorder; however, even subtle laboratory abnormalities may
logical history (including age of menarche, duration of amen- signal a major physical toll from the illness. Hypokalemia is
orrhea, if present, reliable use of contraception, and past or diagnostic for purging behavior but is often absent despite
intended pregnancy) is also important. significant vomiting, or use of laxatives and/or diuretics.
Physical findings may be minimal despite severe medical Hyponatremia is sometimes seen with compulsive water-
compromise. Generally the most crucial medical information drinking. The tests that may be useful are listed in Table 37-5,
comes from the patient’s vital signs. Height and weight, and abnormalities associated with eating disorders are shown
percent loss of total body weight, and the current percent of in Table 37-6.
expected body weight are key barometers of health in AN (Box
37-4 and Table 37-3). Patients who have lost a significant
percent of total body weight, or are far below expected body
TREATMENT
weight (EBW), or whose weight loss is rapid, can be in grave Optimal treatment for an eating disorder includes coordinated
medical danger, despite a normal physical examination, labo- management of psychological, medical, and nutritional issues.
ratory testing, and electrocardiographic findings. Even if the initial evaluation indicates (and the clinical team
Bradycardia and hypotension are significant indicators of believes) that a patient can be safely and effectively managed
cardiovascular compromise, as are orthostatic changes. Hypo- as an outpatient, early treatment frequently focuses on stabi-
thermia is usual with low weight, as is loss of muscle mass lization of psychological and medical symptoms. It is also
and subcutaneous fat. Acrocyanosis is a visible indicator to beneficial to address contingency plans for intensifying the
patients that their smaller, weaker heart is unable to maintain level of care in the initial phase of treatment. At that time, the
circulation to the periphery. Mitral valve prolapse may occur clinical team members can establish their respective roles in
secondary to constriction of the annulus from reduction in care (e.g., who will be weighing the patient), their preferred
mode of communicating, and parameters for hospitalization.
Because it is common for patients to be ambivalent about
certain necessary elements of their treatment (such as medical
BOX 37-4 Calculation of Body Mass Index (BMI) and surveillance or hospital admission), these understandings and
Percent Expected Weight in Adults plans are best arranged before a crisis evolves. A concrete treat-
ment understanding is sometimes very useful, although setting
BMI = Weight (kg) /(Height [m])2 actual parameters can be challenging. Sometimes patients
Expected body weight for adult wome n = misunderstand these as permission to continue symptomatic
(100 lb + 5 lb/inch above 5 ft) ± 10% behaviors without consequences, until they reach the thresh-
old that has been set. Identifying supportive family members

TABLE 37-4 Possible Findings Associated with Eating Disorders on

TABLE 37-3 Relevance of Body Mass Index (BMI) to Health Physical Examination

BMI Weight Category* In Low-Weight Patients In Patients with Induced Vomiting

< 14 At risk for re-feeding syndrome Bradycardia Erosion of dental enamel

< 18.5 Underweight Hypotension Russell’s sign
18.5–24.9 “Normal weight” Orthostasis Parotid or salivary gland (or both)
³ 22 Risk of diabetes, HTN, CHD increases Hypothermia enlargement
25–29.9 Overweight Emaciation
> 30 Obese Flat affect
> 40 Morbidly obese Acrocyanosis
Lanugo
*Reflects weight categories for adults. Click/murmur of mitral
CHD, Coronary heart disease; HTN, hypertension. Valve prolapse

TABLE 37-5 Useful Laboratory Studies for Evaluating Anorexia and securing permission to speak with them (to enlist their
Nervosa and Bulimia Nervosa support) can be useful if the patient is likely to resist a treat- 37
ment plan.
Patient Population Suggested Studies
When treating children and adolescents, clinicians must
All patients Electrocardiogram consider developmental factors. In contrast to adults, children
Complete blood count and teenagers with eating disorders rarely seek treatment on
Glucose their own; worried parents, pediatricians, or teachers most
Blood urea nitrogen, creatinine
often express concerns. Children and adolescents will often
Electrolytes
Calcium, magnesium, phosphorus
deny there is a problem,53 and parents may be reluctant to
Liver function pathologize behavior. Clinicians who treat children and ado-
lescents must be able to coordinate treatment with other
Low-weight patients Erythrocyte sedimentation rate health care providers, while also navigating family and school
Serum albumin
Thyroid-stimulating hormone
systems. Although it is never appropriate or helpful to blame
Testosterone (for men) families for a child’s eating problems, it can be helpful to
identify stressful situations within a family system that may
Patients with Prolactin make recovery difficult. Because parents are the gatekeepers
amenorrhea Estradiol
for treatment, it is important that the clinician help them feel
Luteinizing hormone, follicle-stimulating
hormone
comfortable and understood, while also respecting the child’s
Testosterone privacy. As such, it can be difficult to engage a child or ado-
Dual-energy x-ray absorptiometry (DEXA) lescent in a therapeutic treatment relationship. It is develop-
mentally appropriate for teenagers to rebel against authority
Patients with additional Urinalysis
and to value the opinions of their peers over those of authority
clinical indications Amylase
Brain magnetic resonance imaging (MRI) figures. Often, it is helpful to allow for some flexibility in the
treatment to strengthen the therapeutic alliance, while also
enforcing important limits (such as need for weigh-ins, labo-
ratory studies, and hospitalization if indicated) designed to
ensure patient safety.54

TABLE 37-6 Possible Laboratory Abnormalities in Patients with Anorexia Nervosa or Bulimia Nervosa
Test If Abnormal Details
BLOOD COUNTS
Hct/Hgb Low Normochromic, normocytic
WBC Low Reversed neutrophil : lymphocyte ratio
Platelets Low Often with anemia and/or leukopenia
ESR Very low Helpful in differential
ELECTROLYTES
Glucose Low Especially fasting
Very high Type 1 diabetics omitting insulin to purge
BUN High Pre-renal
Sodium High Dehydration
Low Water-loading
Potassium Low Only seen with purging
Bicarbonate High With vomiting to purge
Low With laxatives to purge
CHEMISTRIES
Magnesium Low Perpetuates hypokalemia
Phosphate Low May fall rapidly in early re-feeding
High In setting of laxative abuse
Transaminases High Starvation; early re-feeding
Amylase Slightly high Especially salivary if purging
Albumin Slightly high Unlike other forms of starvation
Cholesterol ? May rise or fall
ENDOCRINE
Total T3 in the setting of normal TSH Low Compensatory and not to be treated
Estradiol (women) Low Promotes osteopenia/osteoporosis
Testosterone (men) Low Promotes osteopenia/osteoporosis
LH/FSH Low Hypothalamic etiology of amenorrhea
Cortisol High
ELECTROCARDIOGRAM
Findings Low/decreased Voltage
Decreased amplitude P wave
Increased QTc interval (may portend sudden death)
Increased QTc dispersion
Low Heart rate
BUN: Blood urea nitrogen; ESR: erythrocyte sedimentation rate; FSH: follicle-stimulating hormone; Hct: hematocrit; Hgb: hemoglobin; LH: luteinizing
hormone; TSH: thyroid-stimulating hormone; WBC: white blood cell.

Families, however, are often aware of, and gratified by, the
Medical Management returning signs of the patient’s health and pre-morbid persona.
Effective and safe treatment for an eating disorder requires Dietitians experienced with eating-disordered patients can be
immediate attention to medical stability. Medical manage- a valuable asset in the re-feeding process, providing psycho
ment begins with an assessment of the severity of physical educational and cognitive-behavioral treatment, as well as
compromise to determine an appropriate level of care. Though concrete suggestions for incremental increases in the amounts,
there is some variation in the recommendations for hospitali- caloric density, and diversity of intake. Some patients do better
zation, suggested parameters are listed in Table 37-7. Patients with routine foods and others with calorie supplements; many
who require inpatient care should be triaged to an experienced find that they tolerate liquids better than solids. Excess satiety
eating disorders treatment program. may be lessened by frequent small feedings and by elimina-
Nutritional restoration is the immediate focus in low- tion of calorie-free liquids, though some discomfort is gener-
weight patients. Meaningful psychological treatment is not ally unavoidable. Prokinetic agents may be used before meals
possible in an emaciated patient and may engender dangerous for patients with significant distress.
delays. Most patients, even those who require hospitalization, Exercise should be prohibited at less than 90% of EBW for
can be re-fed orally at experienced programs. Nasogastric tube cardiac safety. This is warranted by extensive data on the
feeding and total parenteral nutrition (TPN) are very rarely inability of the anorexic heart to compensate for exercise. It is
required. Calories should be increased incrementally, but not advisable for patients to depart for camp, college, or
rapidly, to achieve desired weight gains of 1 to 2 pounds weekly extended travel below a critical weight, when consistent and
in outpatients and 2 to 3 pounds weekly in hospital settings. intensive monitoring and treatment are still needed. This may
Patients vary widely in their caloric requirements for weight engender intense resistance from patients or families, but it
restoration, but it is not unusual to require up to 4,000 calories should be regarded as a routine and necessary medical recom-
a day as re-feeding progresses. Emaciated patients require mendation, as would be the case after surgery, a significant
phosphorus monitoring the first week and often supplementa- orthopedic injury, or a major infectious illness, such as hepa-
tion of phosphorus and magnesium for several weeks, along titis. The goal is for the patient to restore physical safety so he
with cautious caloric increase to avoid a re-feeding syndrome. or she can return to usual pursuits without danger or damage
Orthostasis has been observed to remit after several weeks, at to health.
about 80% of expected body weight in adolescents. However, Despite the severity of bone loss in those with AN, there is
a return to full health requires restoration of normal weight. no approved effective therapy for prevention or treatment of
Relapse rises steeply as the percent of EBW at discharge falls, low BMD in this population. The single most important factor
with 100% minimizing immediate relapse and re-admission in improving bone density is weight gain and disease recovery.
rising rapidly as discharge weight falls to 95%, 90%, and 85% An improvement in adolescents in bone density is seen after
of EBW. stable weight recovery, but it often remains low despite
Restoration of weight is difficult and uncomfortable for some gains.
patients. Patients may experience improved energy and affect A number of measures can be taken by clinicians to avoid
within several weeks of re-feeding, but generally continue to worsening poor bone health. Calcium and vitamin D intake
fear fatness and maintain a tenacious longing for thinness. should be normal and supplements given as needed. Some

TABLE 37-7 Criteria for Hospitalization

Domain General Symptom* Example†
Weight Substantially low weight for height and age <75%–85% expected body weight
Rapidly falling weight
Behavioral Acute food/water refusal E.g., bingeing and/or vomiting 10–20 times in a day
Episodes of bingeing and purging of very
high or escalating frequency
Other medical compromise Abnormal or unstable vital signs Bradycardia (e.g., < 40 beats per minute)
Orthostatic hypotension (e.g., systolic drop of 30 points, pulse
increase of 20 beats per minute)
Severe medical complications Severe hematemesis
Severe neutropenia or thrombocytopenia
Severe hypokalemia
Uncontrolled type 1 diabetes
Syncope
Psychiatric Substantial risk of self-harm or suicide
Co-morbid substance abuse
Inability to adhere to treatment plan that
will sustain minimal level of safety
Treatment-related Lack of substantial progress E.g., in the setting of chronically low weight and associated
medical complications
Necessity of close supervision to maintain E.g., sustained or persistent inability to eat without supervision
symptom control or to abstain from intractable purging after food intake
Previously agreed-on criterion for E.g., reaching a threshold weight at which the patient
hospitalization based on patient history repeatedly has rapidly deteriorated
*These criteria may be sufficient but not necessary to indicate inpatient care.
†Weight, vital sign, metabolic, and other parameters for hospitalization are best interpreted within the context of the patient’s overall health, medical
and psychiatric history, support systems, and engagement in treatment.

exercise in moderation may be clinically indicated as recovery Fertility may be restored before the first returning men-
progresses, but excess exercise should be avoided, as should strual period, and patients should be advised to attend to 37
forms of exercise that may predispose to fractures in those contraception even while amenorrheic. Patients attempting to
with low bone density. Exogenous oral estrogen has not been conceive, but who experience infertility, should have even sub-
shown to be effective for prevention or management of osteo syndromal eating disorders treated before use of reproductive
porosis in adults and adolescents with AN, despite its well- technology. Pregnancy is a special challenge, with greatest
established role in post-menopausal women.55,56 However, in safety for mother and fetus following complete eating disorder
a randomized placebo-controlled trial, physiologic estrogen recovery. BMI should be no lower than 19 at conception.
administration, primarily given as a transdermal patch, was Women with residual difficulties should be monitored as a
shown to improve bone mass accrual in adolescent girls with high-risk pregnancy, and even women recovered from an
AN.57 This is the first intervention shown to increase bone eating disorder have a high rate of post-partum depression.
density in this population. Bisphosphonates have been used Fortunately, most of the physical tolls of AN and BN, save
in many conditions leading to osteoporosis and have been for bone loss and dental destruction, remit with restoration of
considered for the bone loss of AN. One randomized placebo- normal nutrition and weight and elimination of purging
controlled trial in adults showed improvement in bone mass behaviors. After years of illness, physical deficits, as well as the
using risedronate.58 However, data in adolescents have not eating disorder itself, become more entrenched with progres-
been positive. Because data thus far are few and long-term use sive structural damage to various organ systems.
of bisphosphonates has been associated with complications
(including, very rarely, osteonecrosis of the jaw), and uncer-
tain effects on future pregnancies, their use in treating patients Psychotherapeutic Treatment
with AN is currently not routinely recommended outside of
In addition to medical monitoring and nutritional support,
clinical trials. Several experimental therapies are under
psychotherapy is a critical component of treatment. Although
investigation.
some patients will also benefit from psychopharmacological
Patients who induce vomiting may experience symptomatic
management, psychotherapy is the best-supported treatment
esophagitis and may benefit from proton pump inhibitors.
to address the primary symptoms of an eating disorder. The
Although there is no clinical trial data for validation, various
treatment of choice for adolescent AN is a specialized family-
recommendations have been made to protect the teeth from
based treatment that empowers the parents to take charge of
erosion in patients who vomit. Most involve neutralizing
re-feeding. Interventions for adult AN are less empirically
stomach acid in the mouth after vomiting, using bicarbonate
based. In contrast, the gold standard treatment for BN and
of soda or an alkaline mouthwash. Parotid enlargement,
BED is a specific form of cognitive-behavioral therapy (CBT).
though not painful, can be distressingly obvious. It often
In clinical practice, patients with OSFED are typically treated
remits when vomiting stops, and may be treated with siala-
with the modality corresponding to the most similar full syn-
gogues, if extreme.
drome presentation (e.g., CBT for sub threshold BN; family-
Hypokalemia, from vomiting, laxatives, or diuretics,
based treatment for atypical AN).
requires vigorous correction and careful monitoring, in addi-
tion to testing for concomitant hypomagnesemia. Patients
who are prone to hypokalemia may have their serum potas-
Anorexia Nervosa
sium levels drop precipitously, in part a reflection of total For the treatment of adolescent AN, family-based treatment
body potassium deficits and intracellular shifts. Potassium (FBT) has the strongest evidence base. FBT (sometimes called
chloride should be used under close medical supervision for the “Maudsley method” due to its historical roots at the
replacement, and doses in patients who continue to purge London-based hospital of the same name) consists of 20
may be quite high. Patients with variable purging may need manualized sessions over 12 months.59 In the first phase, the
to titrate doses depending on the frequency of symptoms, therapist provides psychoeducation about the medical and
taking a baseline amount plus an additional dose the morning psychological consequences of malnutrition. Parents take
after a day with extra purging. Patients generally know when control of eating and food-related decisions, limit exercise,
they can hold down potassium or other medication: for resist engaging their child in food-related struggles, and work
example, just before going to sleep at night or just before together to persuade their child to eat. During the second
leaving for work in the morning. Volume depletion will cause phase, as the child engages in treatment and continues to gain
continued renal potassium wasting to spare sodium and pre- weight, the therapist encourages the parents to help their child
serve volume (i.e., secondary hyperaldosteronism), so patients gradually resume independent eating and developmentally
with hypokalemia should be encouraged to have adequate appropriate social activities. When the child is finally able to
dietary salt. Careful attention to maintenance of normal maintain a stable, healthy weight, the therapist shifts the focus
potassium levels is important to avoid both acute cardiac and of treatment away from eating and begins to focus on the
respiratory catastrophe and chronically to avoid hypokalemic impact of AN on the child’s development, particularly around
nephropathy and attendant renal failure. Hyponatremia may identity and autonomy.59 In a large randomized controlled
be seen with compulsive water-drinking or diuretic abuse and trial (RCT) comparing FBT to individual therapy for adoles-
should be carefully monitored because rapidly occurring or cent AN, half of those who took part in FBT were remitted at
very low values can lead to seizures. 12-month follow-up, compared to just one-quarter of those
Laxatives do not appreciably remove ingested calories. who received individual therapy.60 In a smaller uncontrolled
Their futility as a weight loss vehicle notwithstanding, they study, 89% of adolescents treated with FBT were weight-
are the most commonly abused agents used by eating- restored four years after completing treatment.61
disordered patients, second only to vomiting as a form of In contrast, there is much less empirical support for a par-
purging. Patients who try to stop their abuse of laxatives may ticular therapeutic approach in the treatment of adult AN.
experience both rebound edema and refractory constipation. RCTs attempting to identify a treatment of choice have found
Protocols are available for abrupt cessation of laxatives and low overall recovery rates across diverse modalities including
temporary measures to restore normal bowel function. Others CBT, interpersonal therapy (IPT), and specialist supportive
find that gradual tapering of laxatives is better tolerated, espe- clinical management.62,63 Given the norm for adolescent onset,
cially in outpatients. adults are more likely to be those whose illness has followed

a chronic course. Psychotherapy is, therefore, undermined by Binge-Eating Disorder

the long-term effects of starvation and low body weight on
cognition. Low-weight patients often remain perseverative in The psychotherapeutic treatment of BED is very similar to that
their preoccupations with food and weight and relatively rigid of BN, and CBT is also the best-established treatment. In a
in their dietary behaviors. Moreover, persuading patients to study comparing CBT (with either fluoxetine or placebo) to
accept treatment can be challenging due to the ego-syntonic fluoxetine alone, remission rates (defined as abstinence from
nature of the illness; in a randomized therapy study, 46% of binge eating for ≥ 1 month) were 61% for CBT plus placebo,
adults with AN dropped out before treatment completion.64 50% for CBT plus fluoxetine, and 22% for fluoxetine only.71
In practice with adult AN, clinicians usually select a thera- Results were maintained at 12-month follow-up for the major-
peutic modality based on the history, chronicity, co-morbidity, ity of patients who received CBT, but not those who received
and underlying factors that brought the patient into treatment. fluoxetine alone.72
Nonetheless, new interventions are currently being evaluated. Importantly, most individuals with BED are overweight or
A couples-based approach, which enlists a committed partner obese, and come to treatment hoping to reduce weight in
to gently support the patient in his or her re-feeding efforts addition to binge-eating. In one study, two-thirds of obese
has shown preliminary promise.65 Similarly, an enhanced patients seeking treatment for BED had gained a clinically
form of CBT led to weight gain and decreased eating pathology significant amount of weight (i.e., > 5% initial body weight)
in an uncontrolled trial, though only among the two-thirds of in the past year.73 Paradoxically, CBT rarely leads to substantial
patients who completed treatment.66 For patients with more weight loss, even among obese patients who are able to
than 7 years of illness, a therapeutic approach prioritizing become abstinent from binge eating.74 In the study described
improvements in quality of life (rather than weight gain) may above, patients in the CBT plus placebo condition lost an
enhance treatment acceptance.67 average of 5 lb at post-treatment and 10 lb at 12-month
follow-up. It is important for clinicians to be empathically
aware that these modest losses will feel disheartening to
Bulimia Nervosa patients, who may be dazzled by the dramatic but unsubstan-
Because their symptoms cause significant distress, patients tiated claims of commercially available diet plans. However,
with BN are typically more open to psychosocial interventions, in the largest RCT to date comparing behavioral weight loss
and CBT has greater empirical support than any other thera- (BWL) to CBT-guided self-help, CBT was significantly more
peutic approach. Originally developed 20 years ago, the most effective than BWL at eliminating binge-eating, and weight
recent or “enhanced” version (CBT-E) comprises four stages.26 loss was minimal and did not differ significantly between
In the first stage, the therapist co-creates a personalized for- conditions at 2-year follow-up.74
mulation of BN symptoms, highlighting how dieting and nega-
tive affect serve to maintain binge/purge behaviors. During this PHARMACOLOGICAL TREATMENT
stage, the patient begins self-monitoring daily food intake in
order to identify triggers for binge-eating such as under-eating Clinical trials establishing efficacy for pharmacological man-
earlier in the day and/or low mood. In the second stage, the agement of eating disorders include numerous studies on
therapist and patient collaboratively identify barriers to change, adults with AN, BN, and BED. Notwithstanding these studies,
such as perceived benefits of the eating disorder or non- the only agent with Food and Drug Administration (FDA)
adherence with treatment. In the third stage, maintaining approval for the treatment of any of the eating disorders is
mechanisms—such as basing one’s self-worth predominantly fluoxetine for the treatment of BN. There are few clinical trial
on shape and weight—are addressed through behavioral inter- data on adolescents with eating disorders and no clinical trials
ventions, such as reducing body-checking and avoidance. The on OSFED. Despite considerable overlap in symptomatology,
fourth stage focuses on relapse prevention. In a recent waitlist- the respective eating disorders appear to respond differently
controlled trial, half of BN patients achieved remission to medication. Whereas medication has an important adjunc-
(defined as abstinence from bingeing and purging and eating tive role in the treatment of BN and in BED, it has a very
disorder attitudes within one standard deviation of commu- limited role in the treatment of AN.
nity norms) by the end of the 20-session treatment.68 Improve-
ments were well maintained over the 1-year follow-up.68 Pharmacological Management of
To enhance the scalability of this specialized and time-
intensive intervention, self-help versions of CBT (typically
Anorexia Nervosa
using Fairburn’s book Overcoming Binge Eating) have also dem- RCTs of pharmacological agents that address core symptoms of
onstrated some efficacy in reducing binge/purge frequency in AN suggest few benefits to managing the core features of this
BN.69 Furthermore, smartphone “apps” make specific compo- illness with psychotropics. Despite the data available, recent
nents of CBT (e.g., self-monitoring exercises) accessible to a estimates suggest that upwards of 50% of patients undergoing
wider cross-section of individuals who may benefit. Guided treatment for disordered eating are also taking psychotropic
self-help (i.e., featuring a handful of brief meetings with a medications.75 Many of them are working with prescribing
therapist to trouble-shoot roadblocks) appears to be more clinicians to target co-morbid mood and anxiety symptoms,
effective than pure self-help, and self-help is contraindicated which are likely exacerbated by inadequate nutrition. There is
for AN.69 also some speculation that poor nutritional status may impede
Of course, approximately half of patients do not respond response to medications.76 It is noteworthy that a number of
to CBT. Other therapeutic interventions, such as interpersonal RCTs of agents—including chlorpromazine, pimozide, sulpir-
psychotherapy, have also been studied, but treatment response ide, clomipramine, clonidine, and tetrahydrocannabinol77—
is not as rapid as observed in CBT. A new treatment called have not demonstrated efficacy in either promoting weight
integrative cognitive-affective therapy (ICAT), which teaches gain or reducing the cognitive symptoms associated with AN.
emotional coping skills and aims to reduce the discrepancy This is unfortunate, but important to emphasize, since patients
between the patient’s perceived versus ideal self, may be with AN frequently tolerate medication side effects poorly.
worthy of further research. In one study, BN patients treated Researchers and clinicians have been quite interested in
with ICAT had similar abstinence rates after 21 sessions using the atypical antipsychotics to treat AN, owing to the side
(37.5%) compared to those treated with CBT-E (22.5%).70 effect of significant weight gain in psychiatric patients using

these medications for non-eating disorder-related diagnoses.78 The role of selective serotonin reuptake inhibitors (SSRIs)
In addition, the core features of AN (including body image in the treatment of AN is also quite limited and adjunctive to 37
distortion and unreasonable fear of weight gain) are frequently other treatment. Sertraline83 and citalopram84 may improve
compared to psychotic symptoms. Despite this, recruitment symptoms of mood and/or anxiety, but do not promote
for RCTs has been slow, and the data collected so far has been weight restoration. Furthermore, use of citalopram should be
mixed. It is important to note that concerns about weight gain, closely monitored given risk for prolonged QTc in doses >
tardive dyskinesia, and metabolic side effects79 may prevent 40 mg/day. Fluoxetine has not been shown to be beneficial to
patients and families from agreeing to participate in clinical adult or adolescent low-weight inpatients in treating AN.
trials. Others are very motivated to try any adjunctive therapies Fluoxetine has also been studied for stabilization in weight-
that may improve their course of illness. Initial case reports recovered patients with AN in two RCTs. One of these dem-
and trials of olanzapine80 looked promising, but further inves- onstrated some efficacy (when adjunctive to elective
tigation and additional studies looking at risperidone, quetiap- psychotherapy) at a dosage of 20 to 60 mg/day,76 whereas the
ine, and aripiprazole81 have not shown any convincing other failed to show efficacy compared with placebo when
evidence for routine use. Given case reports and anecdotal added to CBT (at a target dosage of 60 mg/day).85
experience, there may be a role for a trial of olanzapine or,
possibly, other atypical or conventional antipsychotics in
some patients with AN. However, these agents should be used
Pharmacological Management of Bulimia Nervosa
with caution (start low and titrate slowly) because of potential Numerous medications have demonstrated efficacy in treating
adverse side-effect profiles (including sedation, prolongation primary symptoms of BN in at least one RCT (Table 37-8).
of the QT interval on the electrocardiogram, hyperprolactine- These include several classes of pharmacological agents,
mia, and reduction in bone mineral density).82 including antidepressants. As a class, antidepressants reduce

TABLE 37-8 Summary of Pharmacological Agents That May Be Useful in Treating Bulimia Nervosa or Binge-eating Disorder Based on Published
RCT Data
Dosage Comments and Caveats
Bulimia Nervosa
Fluoxetine 60 mg/day Best studied; well tolerated; only agent with FDA approval for this indication
Sertraline 100 mg/day
Fluvoxamine* Up to 300 mg/day in divided Utility studied for relapse prevention after inpatient care; a second RCT in
doses combination with stepped-care psychotherapy did not show efficacy in
remission
Imipramine Up to 300 mg/day Potentially undesirable side-effect profile: effects on pulse, blood pressure,
and QT interval that potentiate medical complications seen in BN (e.g.,
QT interval lengthening associated with hypokalemia)
High lethality in overdose
Desipramine Up to 300 mg/day Potentially undesirable side-effect profile: effects on pulse, blood pressure,
and QT interval that potentiate medical complications seen in BN (e.g.,
QT interval lengthening associated with hypokalemia)
High lethality in overdose
Trazodone Up to 400 mg/day Potentially undesirable side-effect profile: sedation
Topiramate Up to 250 mg/day Potentially undesirable side-effect profile:
Up to 400 mg/day Sedation and cognitive changes
Weight loss
Renal calculi
Both studies started at 25 mg/day and titrated upward as tolerated
Naltrexone* 200–300 mg/day Potentially undesirable side-effect profile: hepatotoxicity
Ondansetron 24 mg/day in 6 divided doses High cost
Binge-Eating Disorder
Sertraline 50–200 mg/day
Citalopram 20–60 mg/day
Fluoxetine* 20–80 mg/day
Fluvoxamine* 50–300 mg/day
Topiramate 50–400 mg/day Potentially undesirable side-effect profile: sedation and cognitive changes
Orlistat (in combination with CBT) 120 mg TID
Imipramine (in combination with diet 25 mg TID Studied in patients meeting criteria similar to BED
counseling/psychological support)
*Negative study RCT data also published on this agent for this indication.
BED, Binge-eating disorder; BN, bulimia nervosa; CBT, cognitive-behavioral therapy; FDA, Food and Drug Administration; RCT, randomized clinical
trial; TID, three times daily.
From McElroy SL, Hudson JI, Capece KB, et al; for the Topiramate Binge Eating Disorder Research Group: Topiramate for the treatment of binge
eating disorder associated with obesity: a placebo-controlled study, Biol Psychiatry 61:1039–1048, 2007.

binge and purge frequency by just over half as compared in RCTs, either as a single or as an adjunctive treatment (see
with an approximately 11% reduction with placebo alone.86 Table 37-8). However, none of these medications has FDA
Despite this, medication is generally not as effective as is approval for this indication, and the majority of the studies
psychotherapeutic management of BN, although it has an have investigated only relatively short-term use of the medica-
adjunctive role. For example, augmentation with antidepres- tion (3 months or less) and little is known about maintenance
sants with proven efficacy in BN may further reduce symp- of symptom reduction after the drug is discontinued. Notably,
toms, and fluoxetine (60 mg/day) appears to be beneficial in the majority of these trials also reported a statistically signifi-
reducing symptoms for patients with BN who have not cantly greater weight loss or decrease in BMI in the active drug
responded well to CBT or IPT.87 Finally, fluoxetine has some group compared with placebo, although the weight loss
efficacy for treatment of BN in primary care settings, and thus overall was only modest. Only some of these medications
may have a role in management if psychotherapeutic care is have been assessed in BED without co-morbid overweight or
unavailable.88 obesity.
Fluoxetine (60 mg/day) is the first-line pharmacological
agent in the treatment of BN. It has shown efficacy in the Pharmacological Considerations in Treating
reduction of symptoms of BN compared with placebo in two
large RCTs, is generally well tolerated among individuals with Children and Adolescents
BN, shows efficacy in maintenance therapy over the course of In contrast to the evidence supporting pharmacological man-
a year, and is the only agent with FDA approval for the treat- agement of eating disorders in adults, there are no published
ment of BN.77 Sertraline has also been found to be effective in RCTs in children and adolescents that support psychotropic
reducing the number of binge-eating and purging episodes medication treatment of eating disorders in this age group.
among patients with BN in a small RCT.89 Finally, fluvoxamine Similar to adult populations, many children and adolescents
was superior to placebo in a relapse prevention trial for indi- take psychotropic agents targeting co-morbid conditions. It is
viduals with BN after discharge from inpatient treatment in important to note that interventions have limited effectiveness
one controlled trial.90 The other SSRIs have not been studied when weight is low (re-nourishment is the first priority), and
in RCTs for this indication. child and adolescent patients may be significantly more sus-
Although imipramine, desipramine, and trazodone have ceptible to side effects than are adults. In particular, they may
been found to be effective in reducing symptoms in patients be very sensitive to extrapyramidal symptoms when using
with BN as well, their side-effect profiles limit their utility in antipsychotics (both typical and atypical) aimed at decreasing
this clinical population. Whereas bupropion,91 phenelzine, cognitive distortions. As with adults, there are no studies to
and isocarboxazid have each been found to be effective in the support the routine use of antipsychotic medications in chil-
reduction of bulimic symptoms, the risk of serious adverse dren and adolescents with disordered eating.93 Furthermore,
events (i.e., seizures with bupropion and spontaneous hyper- recent data suggest that children and adolescents may be more
tensive crises with monoamine oxidase inhibitors [MAOIs]) susceptible to activation and to development of suicidal think-
may be elevated in patients with BN, and these agents are not ing when taking antidepressants, which has led the FDA to
appropriate for the management of BN.77 The use of these institute a “black box warning” for all individuals, particularly
medications to manage co-morbid depression in the setting those under the age of 24.94 While not proven effective in the
of BN is relatively contraindicated as well and warrants careful treatment of AN, antidepressants are often used to treat
consideration of risk/benefit ratios in the context of each co-morbid anxiety, depression, obsessive-compulsive disorder
patient’s individualized needs. Other classes of agents also (OCD), and BN. In an open trial, fluoxetine 60 mg was associ-
show promise for the reduction of symptoms of BN; these ated with significant decreases in bingeing and purging, as
include topiramate—shown to significantly reduce symptoms well as improvement on the Clinical Global Impression-
when compared with placebo in two 10-week RCTs92; Improvement scale (CGI-I) in adolescents with BN.83,95
naltrexone (200 to 300 mg/day)—effective in individuals However, when comparing adolescents who have AN (treated
who did not respond to antidepressant therapy; and ondanset- with SSRIs relative to those who had not received antidepres-
ron in patients with severe bulimic symptoms. All are poten- sants), SSRIs did not appear to have significant effects on BMI,
tially limited by side-effect profile and cost. Topiramate, in eating disorder core symptom pathology, depression, or OCD
particular, is associated with significant cognitive slowing and symptoms. Because evidence for these medications is limited,
sedation.92 clinicians should exercise caution when prescribing antide-
Pharmacological management of BN is a reasonable strat- pressants in this population.
egy if psychotherapeutic approaches are ineffective or unavail-
able. Based on tolerability, efficacy in several large studies, and
FDA approval, fluoxetine 60 mg/day is the most appropriate
CONCLUSIONS
first-line choice for a medication management of BN. If fluox- Eating disorders present challenges to effective management
etine is ineffective, is contraindicated, or cannot be tolerated, for several key reasons. First, the diagnosis can be difficult to
consecutive trials of other agents with demonstrated efficacy recognize in the clinical setting. The majority of individuals
can be considered. A patient’s history of response to a particu- with an eating disorder never access care for this problem. This
lar agent, co-morbid psychiatric illness, and cost are other is both because both BN and BED can occur in the absence of
important considerations. A dosing schedule that optimizes clinical signs and because patients are often reluctant to
absorption given a patient’s purging habits should be selected address symptoms and consequently avoid care. Second, they
for maximum efficacy. are associated with serious medical and nutritional complica-
tions that must be addressed concomitantly with the psycho-
logical aspects of the disorders. Optimal patient care thus
Pharmacological Management of almost always requires multi-disciplinary team management.
Third, despite some well-supported treatments for the eating
Binge-eating Disorder disorders, approximately half of patients continue to be symp-
Although psychotherapeutic management is considered the tomatic despite treatment.8,9 There are some data to suggest
first-line treatment of choice for BED, several medications that early intervention is beneficial, and when an eating dis-
have demonstrated efficacy in reducing symptoms of BED order is effectively treated early on, there is a good chance of

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MULTIPLE CHOICE QUESTIONS 2.9%. An estimate of the life-time prevalence of BN-like syn-
dromes is considerably higher (8%).
Select the appropriate answer. The prevalence of eating disorders appears to vary by gender,
Q1 Which of the following disorders is MOST common in ethnicity, and the type of population studied. Eating disorders
the United States? are substantially more common among females than males.
Binge-eating is relatively more common among males (about
○ Anorexia nervosa (AN) 40% of cases), but still is more common in females. Eating
○ Binge-eating disorder (BED) disorders occur in culturally, ethnically, and socioeconomi-
cally diverse populations.
○ Bulimia nervosa (BN)
The incidence of eating disorders ascertained by case registries
○ Schizophrenia probably underestimates the true incidence for several reasons.
○ Somatization disorder Data from the National Co-morbidity Survey Replication
(NCS-R) indicated that fewer than half of individuals with an
Q2 Which of the following conditions is BEST characterized eating disorder access any kind of health care service for their
by a refusal to maintain, or attain, a minimally- illness. Many of those affected are known to avoid or to post-
healthful body weight? pone clinical care for the condition. In addition, both BN and
BED may occur without clinical signs, making them difficult,
○ Anorexia nervosa (AN) if not impossible, to recognize in a clinical setting without
○ Binge-eating disorder (BED) patient disclosure of symptoms, which may not be forthcom-
ing. Furthermore, whereas AN may manifest with a variety of
○ Bulimia nervosa (BN) clinical signs, including emaciation, many patients effectively
○ Schizophrenia conceal their symptoms; up to 50% of cases of eating disorders
may be missed in clinical settings.
○ Somatization disorder
Schizophrenia has a prevalence of 0.2% to 2.0%, and soma-
Q3 Which of the following conditions is MOST closely tization has a prevalence of 0.2% to 2.0% among women and
associated with the development of low bone mineral 0.2% in men.
density (BMD)?
○ Anorexia nervosa (AN) Q2 The answer is: Anorexia nervosa (AN).
○ Binge-eating disorder (BED) Anorexia nervosa (AN) is characterized and distinguished by
a refusal to maintain, or attain, a minimally-healthful body
○ Bulimia nervosa (BN) weight. In addition to a low body weight, AN is characterized
○ Schizophrenia in Western populations by a fear of becoming fat, and by a
disturbance in body experience that can range from a denial
○ Somatization disorder of serious medical consequences to a distorted perception of
one’s size and its importance. For postmenarchal females,
Q4 True or False. Laxatives do not remove ingested calories. amenorrhea of at least 3 months’ duration is a diagnostic
○ True criterion.
○ False Bulimia nervosa (BN) is characterized by recurrent episodes of
binge-eating and behaviors aimed at the prevention of weight
Q5 Which of the following is the MOST accurate equation gain or purging calories. These behaviors, termed “inappropri-
for the calculation of body mass index (BMI)? ate compensatory behaviors, include induced vomiting; laxa-
tive, enema, and diuretic misuse; stimulant abuse; diabetic
○ Weight (in kg)/Height (in meters)2 under-dosing of insulin; fasting; and excessive exercise. To
○ Weight (in kg)/Height (in meters) meet criteria for the syndrome, patients need to engage in both
bingeing and inappropriate compensatory behaviors at least
○ Weight (in lb)/Height (in feet)2 twice weekly for at least 3 months. Two subtypes, “purging
○ Weight (in lb)/Height (in inches) type” and “non-purging type,” are distinguished. Individuals
who prevent weight gain (by exercise or by fasting) fall into
○ Weight (in lb)/Height (in inches)2 the latter subtype. In addition, individuals with BN are exces-
sively concerned with body shape and weight.
Binge-eating disorder (BED) is characterized by recurrent epi-
MULTIPLE CHOICE ANSWERS sodes of binge-eating. Unlike in individuals with BN, there are
no recurrent behaviors to purge calories, or to prevent weight
Q1 The answer is: Binge-eating disorder (BED) gain, from the binge episodes. Binge episodes are accompa-
Binge-eating disorder (BED) appears to be the most common nied by at least three of five correlates (these include eating
eating disorder, with a life-time prevalence ranging between rapidly, until uncomfortably full, when not hungry, alone to
2.9% and 3.5% in females. avoid embarrassment) and are associated with distress. Indi-
viduals must experience these episodes (on average) for once
The life-time prevalence of anorexia nervosa has been esti- each week for at least 3 months to meet provisional DSM
mated from several large international twin cohorts (ranging criteria for BED.
from 0.5% to 2.2% for females). An estimate of the life-time
prevalence of AN combined with Eating Disorder Not Other-
Q3 The answer is: Anorexia nervosa (AN).
wise Specified (ED NOS) resembling AN is over 3%. Bulimia
nervosa (BN) is more common than is AN with a reported Although cardiac complications may be the most dangerous
life-time prevalence in adult women ranging from 1.1% to for patients with anorexia nervosa (AN), osteoporosis is

among the most permanent. Loss of bone mass can be rapid normal bowel function. Others find gradual tapering of laxa-
and remain low despite disease recovery; it represents a life- tives better tolerated, especially in outpatients. 37
long risk of increased fractures. The association of low bone
mineral density (BMD) is established in adolescent girls, as Q5 The answer is: Weight (in kg)/Height (in meters)2.
well as boys. Of importance, effects on bone mass can be seen
with brief disease duration, with significant reductions in A healthful body weight is assessed in relation to age, height,
bone mass being reported in girls who have been ill for less and sometimes gender and frame. Although the clinical
than 1 year. Skeletal impact can be severe. context guides whether a particular weight is consistent with
anorexia nervosa (AN), a commonly recognized guideline is
Factors that contribute to low BMD in AN include hormonal a weight that falls below 85% of that expected for height or a
and nutritional abnormalities, as well as risks associated with body mass index (BMI) less than 17.5 kg/m2 in adults.
excess exercise, smoking, and alcohol use. Endocrine factors Whereas commenting on “ideal weight” in adults is relatively
include hypogonadism, low levels of insulin-like growth fac- straightforward, there are no standardized tables or formulas
tor-I (IGF-1), and hypercortisolemia. In AN, normal puberty available for children and adolescents. This is largely related
is disrupted with prolonged estrogen deficiency, as well as lack to the fact that growth patterns are highly variable and can
of growth hormone (GH) effects. Maximal bone mass is change on a monthly basis. Both the American Academy of
achieved during adolescence and early adult life. Therefore, Pediatrics and the American Psychiatric Association have set
suppression of bone formation by under-nutrition during forth practice guidelines that encourage providers to deter-
adolescence leaves affected girls particularly vulnerable to mine an individual adolescent’s goal weight range using past
inadequate peak bone mass formation. growth charts, menstrual history, mid-parental height, and
Bulimia nervosa (BN), binge-eating disorder (BED), schizo- even bone age as guides. The Centers for Disease Control and
phrenia, and somatization disorder are not closely linked with Prevention (CDC) recommends use of growth charts, which
profound weight loss and osteoporosis. plot BMI for age (2 to 20 years) and gender. Children who fall
below the fifth percentile in BMI for age are considered under-
Q4 The answer is: True. weight, and those who fall between 5% and 85% are deemed
“average weight.” Clearly, there is considerable variation in the
Laxatives do not remove ingested calories. Their futility as a “normal” range. Therefore, following the expected trajectory
weight loss vehicle notwithstanding, they are they most com- for a child based on the pediatrician’s past records is often
monly abused agents by eating-disordered patients, second most helpful.
only to vomiting as a form of purging. Patients who try to stop
their abuse of laxatives may experience both rebound edema The expected body weight for adult women is calculated by
and refractory constipation. Protocols are available for abrupt the following equation: (100 lb + 5 lb/inch above 5 feet)
cessation of laxatives and temporary measures to restore ± 10%.

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Eating Disorders: Evaluation and Management: Key Points

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Eating Disorders: Evaluation and Management: Key Points

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37 Eating Disorders: Evaluation and Management

compensatory behaviors” in the DSM-5,1 induced self-induced

BOX 37-3 DSM-5 Diagnostic Criteria: Binge-Eating Disorder (307.51 (F50.8)) 37

Figure 37-1. Dental erosion resulting from chronic vomiting. (Adapted

often complicated by a patient’s ambivalence about accepting

for acute renal injury and nephrolithiasis, and, if chronic, for

TABLE 37-4 Possible Findings Associated with Eating Disorders on

BMI Weight Category* In Low-Weight Patients In Patients with Induced Vomiting

< 14 At risk for re-feeding syndrome Bradycardia Erosion of dental enamel

TABLE 37-7 Criteria for Hospitalization

a chronic course. Psychotherapy is, therefore, undermined by Binge-Eating Disorder

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