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Anorexia Nervosa

  • Author: Bettina E Bernstein, DO; Chief Editor: Caroly Pataki, MD  more...
 
Updated: May 23, 2016
 

Practice Essentials

Anorexia nervosa (AN) is a potentially life-threatening eating disorder characterized by the inability to maintain a minimally normal weight, a devastating fear of weight gain, relentless dietary habits that prevent weight gain, and a disturbance in the way in which body weight and shape are perceived.

Signs and symptoms

Vital sign changes found in patients with anorexia nervosa include hypotension, bradycardia, and hypothermia. Other changes include the following:[1]

  • Dry skin
  • Hypercarotenemia
  • Lanugo body hair
  • Acrocyanosis
  • Atrophy of the breasts
  • Swelling of the parotid and submandibular glands
  • Peripheral edema
  • Thinning hair

Patients with purging behavior may have callouses to the dorsum of their dominant hand and dental enamel erosion.

Characteristic signs of inadequate energy (caloric) intake observed in patients with anorexia nervosa that are due to starvation-induced changes include the following:

  • Hypothermia
  • Acrocyanosis
  • Resting bradycardia (resting heart rate often 40-49 beats per minute)
  • Hypotension
  • Orthostatic lowered blood pressure or pulse
  • Loss of muscle mass
  • Low blood glucose (impaired insulin clearance)
  • Low parathyroid hormone levels
  • Elevated liver function
  • Low white blood cell (WBC) count

Behaviorally, a patient may demonstrate a flat affect and display psychomotor retardation, especially in the later stages of the disease.

See Clinical Presentation for more detail.

Diagnosis

Because an eating disorder is a clinical diagnosis, no definitive diagnostic tests are available for anorexia nervosa. However, given the multi-organ system effects of starvation, a thorough medical evaluation is warranted. Basic tests include the following:

  • Physical and mental status evaluation
  • Complete blood count (CBC)
  • Metabolic panel
  • Urinalysis
  • Pregnancy test (in females of childbearing age)

Rapid Diagnosis

Rapid diagnosis of anorexia nervosa is crucial to recovery and in some cases can prevent mortality as delay of treatment with persistent starvation from abnormal eating behavior results in treatment resistance due to the neuroadaptive changes, especially increases in angiopoetin-like protein 6 (ANGPTL6), that occur that increase the likelihood that AN will become chronic and persistent.[2]

Electrocardiogram (ECG)

Gastrointestinal signs of anorexia nervosa include intestinal dilation from constipation and diminished intestinal motility.

Fecal occult blood may be indicative of esophagitis, gastritis, or repetitive colonic trauma from laxative abuse. Thyroid function tests, prolactin, and serum follicle-stimulating hormone (FSH) levels can differentiate anorexia nervosa from alternative causes of primary amenorrhea.

See Workup for more detail.

Management

Refeeding

The process of refeeding must be undertaken slowly, with modest increases in metabolic demands, in order to avoid refeeding syndrome (which includes cardiovascular collapse, starvation-induced hypophosphatemia, and dangerous fluctuations in potassium, sodium, and magnesium levels). A nutritionist or dietitian should be an integral part of the refeeding plan.

Electrolyte repletion is necessary in patients with profound malnutrition, dehydration, and purging behaviors. Repletion may be done orally or parenterally, depending on the patient’s clinical state.

Psychological therapy

Various psychological therapies have proven helpful in treating patients with anorexia nervosa, including the following:[3, 4, 5]

  • Individual therapy (insight-oriented)
  • Cognitive analytic therapy
  • Cognitive-behavioral therapy (CBT)
  • Enhanced cognitive-behavioral therapy (CBT-E)
  • Interpersonal therapy (IPT)
  • Motivational enhancement therapy
  • Dynamically informed therapies
  • Group therapy
  • Family-based therapy (FBT)
  • Specialist supportive clinical management (SSCM)
  • Conjoint family therapy
  • Separated family therapy
  • Multifamily groups
  • Relatives and caregiver support groups

Psychopharmacologic therapy

Evidence regarding the efficacy of medication treatment for eating disorders has tended to be weak or moderate. However, fluoxetine, due to effects on serotonin levels, has been found to be generally helpful in patients with anorexia nervosa who have been stabilized with weight restoration. Psychotherapy with adjunctive low-dose olanzapine may be useful for anorexia nervosa during inpatient treatment, especially in the context of anxiety, obsessive eating-related ruminations, and treatment resistance due to failure to engage.[6, 7, 131]

See Treatment and Medication for more detail.

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Background

Anorexia nervosa is an eating disorder characterized by the inability to maintain a minimally normal weight, a devastating fear of weight gain, relentless dietary habits that prevent weight gain, and a disturbance in the way in which body weight and shape are perceived. This condition has potentially life-threatening physiologic effects and causes enduring psychological disturbance. (See Prognosis and Clinical Presentation.)[8, 9]

With the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), changes have occurred in the definition of anorexia nervosa, namely in Criterion A there is a focus on behaviors including restricting calorie intake, and the word “refusal” is no longer included related to weight maintenance because of the incorrect and possibly stigmatizing implication of intention on the part of the patient and because this aspect may be not something that can accurately be assessed.[10]

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) Criterion D requiring amenorrhea, or the absence of at least three menstrual cycles, has been deleted as that criterion cannot be applied to males or premenarchal females, females taking oral contraceptives, and postmenopausal females. In some cases, individuals exhibit all other symptoms and signs of anorexia nervosa but still report some menstrual activity.[10]

Anorexia nervosa may be divided into 2 subtypes:

  • Restricting, in which severe limitation of food intake is the primary means to weight loss
  • Binge-eating/purging type, in which there are periods of food intake that are compensated by self-induced vomiting, laxative or diuretic abuse, and/or excessive exercise

Although the DSM-5 separates anorexia nervosa and bulimia nervosa as two separate disorders, there continues to be consideration that these two disorders may be part of a unified eating disorder. Recent research at the University of Chicago with children and adolescents who met criteria for DSM-5 restrictive type (AN) or binge eating/purging type AN (AN-BE/P) differed in their eating patterns as youths with AN-R consumed meals and snacks more regularly relative to youths with AN-BE/P; youths with AN-BE/P who skipped dinner were associated with a greater number of binge eating episodes, and skipping breakfast was associated with a greater number of purging episodes. Thus, it appeared that youths with AN-R followed a more regular pattern but consumed insufficient amounts of food during meals and youth with AN-BE/P tended to have more irregular eating patterns.[11]

Patients with anorexia nervosa often display such traits as a desire for perfection and academic success, a lack of age-appropriate sexual activity, and a denial of hunger in the face of starvation. Psychiatric characteristics include excessive dependency, developmental immaturity, social isolation, obsessive-compulsive behavior, and constriction of affect. Many patients also have comorbid mood disorders, with depression and dysthymic disorder being most prevalent.(See Clinical Presentation, Workup, Treatment, and Medication.)[12, 13, 14]

Diagnostic criteria (DSM-5)

Diagnostic criteria for anorexia nervosa in the DSM-5 include the following[10] :

  • Restriction of energy intake relative to requirements, leading to a significantly low body weight in the context of age, sex, developmental trajectory, and physical health; significantly low weight is defined as a weight that is less than minimally normal or, for children and adolescents, less than that minimally expected
  • Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though the patient’s weight is already significantly low
  • Disturbance in the way in which one’s body weight or shape is experienced, undue influence of body weight or shape on self-evaluation, or persistent lack of recognition of the seriousness of the current low body weight

The DSM-5, which was published in May 2013, revised the definition of anorexia from the DSM-IV[15] to focus more on behaviors, such as calorie restricting, and removed the qualification of low weight being less than 85% ideal body weight. Additionally, the criterion of amenorrhea in postmenarchal females was completely removed from the definition. (See Clinical Presentation.)

The prevalence of subthreshold eating conditions supports the notion that eating disorders tend to exist along a spectrum and that, if defined by a broader range of symptoms, might be better recognized by doctors. (See Workup, Treatment, and Medication.)[16]

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Pathophysiology

A typical case of anorexia nervosa involves a young person (teenager or young adult) who is mildly overweight or of normal weight and who begins a diet and exercise plan to lose weight. As he or she loses weight and receives initial positive reinforcement for this behavior (eg, compliments by peers on his or her appearance), the reward is high and causes an inability to stop this behavior once an ideal weight is achieved.

Anorexia nervosa may be difficult to resolve due to persistent starvation from abnormal eating behavior resulting in treatment resistance due to the neuroadaptive changes causing increases in angiopoetin-like protein 6 (ANGPTL6) that cause anorexia nervosa to more likely become chronic and persistent.[17, 2]

Malnutrition subsequent to self-starvation leads to protein deficiency and disruption of multiple organ systems, including the cardiovascular, renal, gastrointestinal, neurologic, endocrine, integumentary, hematologic, and reproductive systems.

Cardiovascular complications

Cardiac complications are the most common cause of death; the mortality rate is about 10%. Cardiac effects from anorexia nervosa include profound bradycardia, hypotension, decreased size of the cardiac silhouette, and decreased left ventricular mass associated with abnormal systolic function. Patients with anorexia report fatigue and have an attenuated blood pressure response to exercise and reduction in maximal work capacity. An increased incidence of mitral valve prolapse without significant mitral regurgitation is also observed. Low potassium-dependent QT prolongation increases the risk of ventricular arrhythmia.[18]

The patient's vital signs reflect hypotension with systolic pressures as low as 70 mm Hg and sinus bradycardia with heart rates as low as 30-40 beats per minute. These changes are a response to a decrease in the basal metabolic rate. The mechanism may be due to an autonomic imbalance in heart rate regulation, with increases in vagal activity and a reduction in sympathetic activity. These changes are physiologic cardiovascular responses, and treatment is unnecessary, unless negative clinical sequelae are present.

If electrocardiography (ECG) is performed, evidence of sinus bradycardia, ST-segment elevation, T-wave flattening, low voltage, and rightward QRS axis is apparent. All the aforementioned changes are clinically insignificant; however, the frequency of rhythm disturbances is most concerning, especially QT-interval prolongation that may be an indication for those at risk of cardiac arrhythmias and sudden death.

Cardiac decompensation is greatest during the initial 2 weeks of refeeding, when the myocardium cannot withstand the stress of an increased metabolic demand. However, if the daily weight gain is 0.2-0.4 kg, then complications are limited.

Endocrinologic and metabolic complications

Foremost in the gamut of endocrinologic complications is amenorrhea, although, as previously mentioned, the DSM-5 no longer includes this condition as part of the diagnostic criteria of anorexia nervosa.[19] Amenorrhea results from disorders in the hypothalamic-pituitary-ovarian axis in which levels of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) are low despite low levels of estrogen. Reversion to the prepubertal state occurs; the LH response to gonadotropin-releasing hormone (GnRH) is blunted. This blunted response is insufficient to maintain menstrual integrity, and amenorrhea results.

Weight loss and emotional instability play a role in amenorrhea, although amenorrhea persists in 5-44% of patients in whom weight gain has been documented. The explanation for this wide range has not been elucidated.

Other changes related to endocrine function include a reduction in fertility, multiple small follicles in the ovaries, and decreased uterine volume and atrophy.

Thyroid function is also affected in patients with anorexia nervosa, with laboratory data revealing a decrease in triiodothyronine (T3) and thyroxine (T4) and an increase in reverse T3. These changes are characteristic of the euthyroid sick syndrome and, similar to the cardiac changes, represent an adaptive mechanism; hormonal replacement is not necessary.

An associated impaired release of vasopressin consistent with diabetes insipidus is present. This defect is of the neurogenic type; concentration of urine is observed after administering vasopressin. This condition affects 40% of persons with anorexia nervosa and is reversible with weight gain.

Osteopenia is a serious complication. Cortical and trabecular bone are affected, and osteopenia persists despite estrogen therapy. Low levels of progesterone (accelerates remodeling) formation and decreased insulinlike growth factor-1 (IGF-1) levels, which stimulate type 1 collagen biosynthesis, contribute to bone loss.

Treatment of osteopenia with bisphosphonates is not routinely indicated in adolescents, because of concerns about osteonecrosis of the jaw; however, if this therapy is used, close monitoring is critical.[19, 20] Supplementation with 1000-1500 mg/d of dietary calcium and 400 IU of vitamin D is recommended to prevent further bone loss and to maximize peak bone mass. Although exercise and hormonal replacement therapy have some benefit in perimenopausal women, exercise may be deleterious in patients with anorexia nervosa who have amenorrhea, and hormonal replacement may induce premature closure of bone epiphysis.[19]

Gastrointestinal complications

Patients with anorexia nervosa have fewer gastrointestinal complications than those with bulimia nervosa. Constipation is common. In addition, these patients still have prolonged gastrointestinal transit, alterations in antral motility, and gastric atrophy. Prokinetic agents may accelerate gastric emptying, and the relief from gastric bloating can accelerate resumption of normal eating habits.

Neurologic, integumentary, and renal complications

Cerebral atrophy and loss of brain volume may be observed in patients with anorexia nervosa. Generalized muscle weakness is the most common neurologic symptom.

Patients with anorexia nervosa typically have dry, scaly skin; brittle hair and nails; and increased lanugo-type body hair.

An increase in blood urea nitrogen (BUN) levels, which reflects a level of dehydration and a decreased glomerular filtration rate (GFR), is present. Electrolyte imbalances are secondary to vomiting, and potassium is most often affected. Other abnormalities include disturbances of calcium, magnesium, and phosphorus.

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Etiology

Anorexia nervosa results from a complex interplay between biologic, psychological, and social factors; it tends to affect women more than men, and adolescents more than older women.

Prepubescent patients who subsequently develop anorexia nervosa have a high incidence of premorbid anxiety disorders. The onset of anorexia nervosa during puberty has led to the theory that, by exerting control over food intake and body weight, adolescents are attempting to compensate for a lack of autonomy and selfhood.

Modern preoccupation with slenderness and beauty in the Western world may contribute to the mindset of thinness as a valued quality in adolescents; however, this link has not been proven. A subset of adolescents who are temperamentally incapable of dealing with age-appropriate challenges without extreme reward-seeking behavior (thinness) may be susceptible to anorexia nervosa.[21]

Recognizing the predisposing, precipitating, and perpetuating factors in the disease is important to better facilitate early intervention, especially since nutritional rehabilitation performed simultaneously with family-based treatment (FBT) and the Maudsley method is crucial to recovery.[8, 22, 5]

Predisposing factors

Predisposing factors in eating disorders include the following:

  • Female sex
  • Family history of eating disorders [23]
  • Perfectionistic personality
  • Difficulty communicating negative emotions
  • Difficulty resolving conflict
  • Low self-esteem

Maternal psychopathology (negative expressed emotion, maternal encouragement of weight loss) can also be a risk factor for anorexia nervosa, especially for childhood-onset of this disorder.[24]

Genetic factors

Reported cases of anorexia nervosa in twins and triplets suggest the possibility of an increased genetic predisposition.[25, 26] Indeed, there is evidence from twin studies to suggest that the genetic contribution to the disease is as high as 50-80%, a heritability estimate similar to that for bipolar disorder and schizophrenia.[27, 28]

There may be variations of the 5HTT (serotonin transporter gene) genome (eg, biallelic, triallelic) that are associated with subtypes of eating disorders and that interact with life-history factors.[29, 30, 31]

There is also evidence that an area on band 1p at the DF1153721 locus may be related to a 7% increased incidence of anorexia nervosa in first-degree relatives.[32] Genetic risk factors may also be predictive of specific complications in anorexia nervosa, such as bone loss.[33]

Biochemical factors

Individuals with anorexia nervosa maintain a lifelong increased incidence of anxiety, depressive disorders, and obsessive-compulsive disorder. Neurobiologists hypothesize that disruption of both serotonergic and dopaminergic pathways in the brain mediate the development of anorexia nervosa and may account for the frequent coexistence of other psychological disturbances.[34, 35]

Anorexia nervosa is often heralded by a patient’s desire to lose an insignificant amount of weight through dieting. Once the weight loss is in progress, immunologic and hormonal factors, including leptins (involved with signaling satiety) and alpha-melanocyte–stimulating hormone, may play a role in the downward spiraling and maintenance of anorexia nervosa.[36, 9]

During prolonged food restriction in genetically vulnerable individuals, the ensuing malnutrition perpetuated by the biochemical changes induced by weight loss (ie, ketosis) further magnifies the impact of the malnutrition on the brain, owing to it being in a starvation-illness mode. Thus, it is helpful to conceptualize anorexia nervosa as a developmental condition rather than as a purely mental one. Persistent states of starvation may result in biochemically based treatment resistance due to neuroadaptive changes including increases in angiopoetin-like protein 6 (ANGPTL6) that occur that increase the likelihood that anorexia nervosa will become chronic and persistent.[2]

Age-related factors

Precipitating factors relate most often to developmental tasks that cause intense intrapsychic conflict and unconscious feelings of anxiety, which in turn interact with physiologic and biologic ones.

In individuals aged 10-14 years, such precipitating factors are related to sexual development and menarche, which are associated with a spurt in weight gain. Societal influences, such as a peer group that comments in a rejecting fashion, intensify the fear of becoming "fat." Affected individuals often diet and receive peer acceptance for weight loss; this emotional reinforcement, combined with the physiologic response of the body to the sudden loss of weight (when >5 lb), increases the likelihood of continued weight loss.

Sudden weight loss with loss of fat causes a decrease in body temperature, which physiologically causes a subjective feeling of chills; this discomfort is relieved by increased physical activity, which causes further weight loss. The continuous downward spiraling of weight loss then causes secondary amenorrhea and loss of secondary sexual characteristics, further worsening weight loss.

In adolescents aged 15-16 years, precipitating factors stem from struggles with independence and autonomy. Individuals in this age group with anorexia nervosa typically feel ambivalent about growing up and will transition from dependence to interdependence rather than to independence.

In individuals aged 17-18 years, identity conflicts are more common. These patients do not make healthy transitions from leaving home to going to college or getting married.

Associated diseases

Disorders associated with anorexia nervosa include congenital adrenal hyperplasia[37] and systemic lupus erythematosus.[38]

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Epidemiology

Anorexia nervosa is found in all developed countries and in all socioeconomic classes, occurring around the world at similar rates (0.3-1% in women, 0.1-0.3% in men). It is also found in developing countries such as China and Brazil.[14, 39]

According to Mehler et al, certain groups are especially at risk for anorexia nervosa, including dancers, long-distance runners, skaters, models, actors, wrestlers, gymnasts, flight attendants, college sorority members, and others for whom thinness is emphasized and overly rewarded.[40]

In a European study, a 0.48% lifetime incidence of anorexia nervosa was reported among 21,425 respondents.[41]

The lifetime prevalence of anorexia nervosa in the United States is estimated to be 0.3-1%; however, some studies have shown rates as high as 4% among women. The rates among men are estimated at 0.1-0.3%. As many as 5% of young women exhibit symptoms of anorexia but do not meet the full diagnostic criteria, and some studies show disordered eating behavior in 13% of adolescent girls in the United States.[12, 13, 14, 39]

Using nationally representative, face-to-face interview surveys of 10,123 adolescents in the continental United States, Swanson et al found the following 12-month prevalence rates for eating disorders[16] :

  • Anorexia nervosa (0.2%)
  • Bulimia nervosa (0.6%)
  • Binge-eating disorder (1.6%)
  • Subthreshold anorexia nervosa (0.9%)
  • Subthreshold binge-eating disorder (1.1%)

Race-related demographics

Anorexia nervosa is diagnosed more often in the white (>95%) adolescent (>75%) populations[42, 43] of the middle and upper socioeconomic classes, although it can be observed in either sex and in people of any race, age, or social stratum. (Indeed, a link between socioeconomic class and the prevalence of eating disorders has not been demonstrated in the literature.) This disorder is probably underdiagnosed in black individuals and males because of a low index of suspicion.[44, 45, 46]

Sex-related demographics

Anorexia nervosa is more common in women than in men, with a female-to-male ratio of 10-20:1 in developed countries. In some professions, however, the frequency is much higher among men (wrestling, running, modeling) than it is in the general male population. Treatment plans remain the same for both sexes. Gay and bisexual males are more likely to have an eating disorder than heterosexual males, but they are also more likely to have bulimia than anorexia.[47, 48]

Age-related demographics

Anorexia nervosa has been observed in both the very young and very old, but the disorder is primarily a phenomenon of puberty and early adulthood. Eighty-five percent of patients have onset of the disorder between the ages of 13 and 18 years (although a survey of adolescents by Swanson et al found a median age of onset of 12.3 y).[16, 12, 49] Patients who are older at the time of onset of the disorder have a worse prognosis, as do patients with an onset before age 11 years[50] .

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Prognosis

The prognosis of anorexia nervosa is guarded. Morbidity rates range from 10-20%, with only 50% of patients making a complete recovery. Of the remaining 50%, 20% remain emaciated and 25% remain thin.[51, 52]

The remaining 10% become overweight or die of starvation. However, mortality from the complications of starvation is less frequent in patients with anorexia nervosa than is death from suicide.[53, 54, 55, 52, 56] A history of previous suicide attempts, physical pain, drug use, and laxative use may correlate with a higher likelihood of suicide attempts.[53, 54, 57] Metacognition plays a role in predicting adverse outcomes or suicide, as does alexithymia.[58]

Recovery from anorexia nervosa generally is accompanied by resumption in growth, although there may be residual loss of height that is linear in nature.[59]

Prognostic factors

Onset of anorexia nervosa before adulthood predicts a more favorable outcome, although onset at too young an age, before 11 years, is a poor prognostic factor.[50]

The outcome of anorexia nervosa also depends on the patient’s body mass index (BMI) and his or her weight loss at presentation, as well as the duration of symptoms, duration of inpatient care, and state of family relationships.[60] In addition, patients with the restricting subtype of anorexia nervosa tend to be more refractory to treatment and are at high risk of death.[61]

Body weight and symptom duration

Although the degree of weight loss at the clinically noted onset of the involvement of the patient's organic systems is not predictive of outcome, lower weight (less than 75% of mean body weight [MBW]) and longer duration (more than 19 months) of symptoms were predictors of poorer outcomes in a review of 267 adolescents from 11 different eating disorder programs.[62]

A shorter duration of involvement of the patient's organic systems before admission and a short inpatient treatment period have been associated with a favorable outcome in some studies.

Mental health

Using nationally representative, face-to-face interview surveys of 10,123 adolescents in the continental United States, Swanson et al found that the majority of those with an eating disorder met the criteria for at least 1 other lifetime DSM-4 disorder, as follows[16] :

  • Anorexia nervosa (55.2%)
  • Bulimia nervosa (88%)
  • Binge-eating disorder (83.5%)
  • Subthreshold anorexia nervosa (69.8%)
  • Subthreshold binge-eating disorder (70.1 %)

Psychiatric and somatic comorbidities have been found to worsen the outcome of patients with eating disorders. Psychiatric comorbidities are common with anorexia nervosa, with the following lifetime incidences[63] :

  • Depression (15-60%)
  • Anxiety disorders (20-60%)
  • Substance abuse (12-21%)
  • Personality disorders (20-80%)

Obsessionality and impulsivity in individuals with anorexia nervosa correlate with a lower lifetime BMI, reflecting poorer long-term outcomes, and can be measured with the Yale-Brown-Cornell Eating Disorder Scale (YBC-EDS).[64]

Family involvement

A good relationship between the parent and child tends toward a more favorable outcome. There may be a poorer prognosis among patients from single-parent families, from families in which parents have been married before, and from families in which several generations live together, possibly owing to greater expression of negative emotions in the household.[42, 65] Indeed, joint family therapy is not as effective as separated family therapy if there is a high level of negative emotional expressivity (eg, high levels of maternal criticism).[3]

Mortality

Mortality rates were significantly higher in a well-done 25-year longitudinal study with a standarized mortality ratio (SMR) elevated at 34.5 for females and 16.0 for males with comorbid cluster B personality disorder.[66]

A recent study found that mortality was higher if psychiatric comorbifities such as substance abuse were present. This may be due to the co-occuring shame and isolation that substance abuse disorders engender.[67, 68]

A meta-analysis by Arcelus et al found a weighted annual mortality incidence for anorexia nervosa of 5.1 deaths per 1000 person-years; a lower mortality rate—1.74 deaths per 1000 person-years—was noted in individuals with bulimia nervosa.[69] However, it is possible that because this study was a meta-analysis, individuals with crossover between anorexia and bulimia could not be correctly tracked, causing loss of data in this study.[69]

Patients who misused alcohol, had a low BMI at presentation, or were of older age at first presentation were found to have a higher likelihood of poor outcomes, including death. Comorbid disorders, such as affective disorder or suicidal behavior or self-harm, or a history of mental-health hospitalization for these problems, also strongly predicted patient mortality.[69]

A 25-year study of patients diagnosed with co-morbid substance abuse[67] and with cluster B personality disorders[66] appeared to have much higher rates of mortality with a standardized mortality raio of 34.5 for females and 16.0 for males. 

Suicide

The presence of an eating disorder has been associated with increased levels of suicidal thinking. Using nationally representative, face-to-face interview surveys of 10,123 adolescents in the continental United States, Swanson et al found the incidence of suicidal ideation and behavior in anorexia nervosa to be as follows[16] :

  • Suicidal ideation: Anorexia nervosa (31.4%); subacute anorexia nervosa (30%)
  • Suicide planning: Anorexia nervosa (2.3%); subacute anorexia nervosa (14.2%)
  • Suicide attempts: Anorexia nervosa (8.2%); subacute anorexia nervosa (12.4%)

According to the meta-analysis by Arcelus et al, 1 in 5 individuals with anorexia nervosa who died had committed suicide.[69]

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Complications

Most complications of anorexia nervosa are secondary effects from starvation. Malnutrition subsequent to self-starvation leads to protein deficiency and disruption of multiple organ systems, including the cardiovascular, renal, gastrointestinal, neurologic, endocrine, integumentary, hematologic, and reproductive systems. Endocrine and metabolic disturbances, for example, result in the following[70] :

  • Delayed puberty
  • Amenorrhea
  • Anovulation
  • Low estrogen states
  • Increased growth hormone
  • Decreased antidiuretic hormone
  • Hypercarotenemia
  • Hypothermia
  • Hypokalemia
  • Hyponatremia
  • Hypoglycemia
  • Euthyroid sick syndrome
  • Hypercortisolism
  • Arrested growth
  • Osteoporosis

In addition, decreased gonadotropin levels and hypogonadism may occur among males who are affected.

Cardiovascular effects of anorexia nervosa include the following[71, 21, 72] :

  • Cardiomyopathy
  • Mitral valve prolapse
  • Supraventricular and ventricular dysrhythmias
  • Long QT syndrome
  • Bradycardia
  • Orthostatic hypotension
  • Shock due to congestive heart failure

Renal disturbances include the following:

  • Decreased glomerular filtration rate (GFR)
  • Elevated BUN
  • Edema
  • Acidosis with dehydration
  • Hypokalemia
  • Hypochloremic alkalosis with vomiting
  • Hyperaldosteronism
  • Renal calculi

Gastrointestinal findings in anorexia nervosa include the following:

  • Constipation
  • Decreased intestinal mobility
  • Delayed gastric emptying
  • Gastric dilation and rupture: From binge eating and purging; gastric rupture can lead to pneumothorax and pneumoperitoneum [73, 74]

Neurologic disturbances include the following:

  • Peripheral neuropathy
  • Ventricular enlargement

Integumentary findings include the following:

  • Dry skin and hair
  • Hair loss
  • Lanugo body hair

Hematologic findings include the following:

  • Anemia
  • Leukopenia
  • Thrombocytopenia

Reproductive disturbances include the following:

  • Infertility
  • Low ̶ birth-weight infant

Patients who induce vomiting develop dental enamel erosion, palatal trauma, enlarged parotids, esophagitis, Mallory-Weiss lesions, elevated transaminase levels, and, in extreme cases, seizures (due to electrolyte disturbances). Cases of superior mesenteric artery (SMA) syndrome from loss of intraperitoneal fat in anorexia nervosa have been reported.[73, 74]

Impairment

In the Swanson study, 97.1% of adolescents with anorexia nervosa reporting suffering from some form of impairment (most commonly, social impairment) in the previous 12 months, with 24.2% reporting severe impairment; 11.6% reported a complete inability to carry out normal activities for at least 1 day.[16]

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Patient Education

According to Becker et al, for adequate weight gain, the patient or family requires some "education on nutrition, adjustment of caloric and nutritional intake, and limitations on exercise and other modifications of behavior,” with enteral or parenteral nutrition being used only in patients with severe undernutrition who have not responded to these other methods.

In the moderate stage of anorexia nervosa, in addition to the above recommendations, providing structure to daily activities is necessary. This includes eating 3 meals a day. Also, parents should ensure that healthy food is available, but the patient should assume all responsibility for eating.

For patient education information, see the Women's Health Center, as well as Anorexia Nervosa, Bulimia, and Amenorrhea. Other useful sources of patient information include the following:

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Contributor Information and Disclosures
Author

Bettina E Bernstein, DO Distinguished Fellow, American Academy of Child and Adolescent Psychiatry; Distinguished Fellow, American Psychiatric Association; Clinical Assistant Professor of Neurosciences and Psychiatry, Philadelphia College of Osteopathic Medicine; Clinical Affiliate Medical Staff, Department of Child and Adolescent Psychiatry, Children's Hospital of Philadelphia; Consultant to theVillage, Private Practice; Consultant PMHCC/CBH at Family Court, Philadelphia

Bettina E Bernstein, DO is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Psychiatric Association

Disclosure: Nothing to disclose.

Chief Editor

Caroly Pataki, MD Health Sciences Clinical Professor of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, David Geffen School of Medicine

Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Acknowledgements

Edward Bessman, MD, MBA Chairman and Clinical Director, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University School of Medicine

Edward Bessman, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Tracy A Cushing, MD, MPH, FACEP, FAWM Assistant Professor, Department of Emergency Medicine, University of Colorado School of Medicine; Attending Physician, Denver Health Medical Center

Tracy A Cushing, MD, MPH, FACEP, FAWM is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Angelo P Giardino, MD, PhD, MPH Associate Professor, Baylor College of Medicine; Chief Medical Officer, Texas Children's Health Plan; Chief Quality Officer, Medicine, Texas Children's Hospital

Angelo P Giardino, MD, PhD, MPH is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American Professional Society on the Abuse of Children, Harris County Medical Society, Helfer Society, and International Society for the Prevention of Child Abuse and Neglect

Disclosure: Bayer Honoraria Review panel membership; Pfizer Grant/research funds Independent contractor; Strategic Healthcare Alliance Honoraria Board membership; Health Resources and Services Administration (HRSA) Integrated Community Systems for CSHCN Grant Grant/research funds Other; CLS Bering Grant/research funds Other

Robert Harwood, MD, MPH, FACEP, FAAEM Senior Physcian, Department of Emergency Medicine, Advocate Christ Medical Center; Assistant Professor, Department of Emergency Medicine, University of Illinois at Chicago College of Medicine

Robert Harwood, MD, MPH, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Leah E Jacoby, MD Resident Physician, Department of Emergency Medicine, Denver Health Medical Center, University of Colorado School of Medicine

Leah E Jacoby, MD is a member of the following medical societies: American College of Emergency Physicians and Emergency Medicine Residents Association

Disclosure: Nothing to disclose.

Jennifer DA Liburd, MD Consulting Staff, Assistant Professor of Pediatrics, Department of Pediatric Emergency Medicine, Nyack Hospital

Jennifer Da Liburd is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Siobhan E O'Herron, MD Resident Physician, Department of Psychiatry, Harvard Medical School

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Ron D Waldrop, MD, MS, FAAP, FACEP, FACPE Attending Physician, Pediatric Emergency Medicine, Huntsville Women’s and Children’s Hospital; Assistant Clinical Professor, Georgetown University School of Medicine

Ron D Waldrop, MD, MS, FAAP, FACEP, FACPE is a member of the following medical societies: American Academy of Pediatrics, American College of Emergency Physicians, American College of Physician Executives, and National Association for Healthcare Quality

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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