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Bulimia Nervosa

  • Author: Gagandeep Randhawa, MBBS; Chief Editor: David Bienenfeld, MD  more...
 
Updated: Jun 07, 2016
 

Practice Essentials

Bulimia nervosa is an eating disorder with 5 key characteristics as noted by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM5).[1]

  1. Recurrent episodes of binge eating. Eating more than the average person in a 2-hour period, accompanied by a sense of loss of control.
  2. Repetitive inappropriate compensatory behaviors to avoid weight gain such as excessive exercise, fasting, laxative use, and diuretic use.
  3. This eating behavior occurs at least once a week for a period of 3 months.
  4. Body shape and weight influence self-evaluation.
  5. This does not occur specifically with episodes of anorexia nervosa.

Signs and symptoms

Patients with bulimia nervosa may experience the following symptoms:[2, 3, 4]

  • General - Dizziness, lightheadedness, palpitations (due to dehydration, orthostatic hypotension, possibly hypokalemia), dry skin
  • Gastrointestinal symptoms - Pharyngeal irritation, abdominal pain (more common among persons who self-induce vomiting), blood in vomitus (from esophageal irritation; more rarely, from actual tears, which may be fatal), difficulty swallowing, bloating, flatulence, constipation, obstipation, and gastroesophageal reflux disease (GERD) [5]
  • Reproductive symptoms - Amenorrhea occurs in up to 50% of women with bulimia nervosa; significant proportion of remaining patients have irregular periods; many more will have menstrual irregularity and scanty periods
  • Uncommon symptoms, or in most severe cases
    • Water and electrolytes - Dehydration, hypokalemia, hypochloremia, metabolic alkalosis
    • Cardiac - Edema; EKG changes such as QT prolongation, increased PR interval, increased P wave amplitude, widened QRS, depressed ST segment
    • Gastrointestinal - Gastric dilation, Barrett's esophagus[6]
    • Pulmonary symptoms - aspiration pneumonitis (uncommon), pneumomediastinum (rare)

Physical findings may include the following:

  • Bilateral parotid enlargement (see the image below)
    Parotid hypertrophy. Reprinted with permission fro Parotid hypertrophy. Reprinted with permission from Mandel, L and Siamak, A. Diagnosing bulimia nervosa with parotid gland swelling. J Am Dent Assoc 2004, Vol 135, No 5, 613-616.
  • Dental damage (see the image below)
    Dental caries. Reprinted with permission from Wolc Dental caries. Reprinted with permission from Wolcott, RB, Yager, J, Gordon, G. Dental sequelae to the binge-purge syndrome (bulimia): report of cases. JADA. 1984; 109:723-725.
  • Russell sign (see the image below)
    Russell sign. Reprinted with permission from Glori Russell sign. Reprinted with permission from Glorio R, et al. Prevalence of cutaneous manifestations in 200 patients with eating disorders. Int J Derm, 2000, 39(5), 348-353.
  • Cutaneous manifestations, including sudden, diffuse hair loss, acne, dry skin, nail dystrophy, and scarring resulting from cutting, burning, and other self-induced trauma
  • Bradycardia or tachycardia, hypothermia, and hypotension (often associated with dehydration)
  • Edema
  • Clinical obesity; morbid obesity is rare

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

Lab studies that may be used for diagnosis include:

  • Comprehensive blood chemistry panel
  • Complete blood count (CBC)
  • Urinalysis
  • Urine toxicology screen
  • Pregnancy test
  • Amylase level

Electrocardiography

Because of the potential for arrhythmias and cardiomyopathy as possible complications of bulimia nervosa, an electrocardiogram (ECG) should be performed in patients who are very thin, complaining of palpitations, or have other signs or symptoms of cardiovascular concern.[7]

DEXA

Because of the potential for osteoporosis, a dual-energy radiographic absorptiometry (DEXA) scan may be useful, particularly for patients with irregular menses, who have mood disorders, and/or who smoke cigarettes.

See Workup for more detail.

Management

Core nonpharmacologic interventions for bulimia nervosa include the following:

  • Cognitive-behavioral therapy (CBT)
  • Interpersonal psychotherapy (IPT)
  • Nutritional rehabilitation counseling
  • Family therapy

Pharmacologic agents used in the treatment of bulimia nervosa include the following:

  • Fluoxetine (Prozac) - Approved by the FDA for the treatment of bulimia nervosa
  • Other antidepressants - As a group, antidepressants are the mainstay of pharmacotherapy for bulimia nervosa; [8] they may help patients with substantial concurrent symptoms of depression, anxiety, obsessions, or certain impulse disorder symptoms
  • Mood stabilizers - Topiramate, lithium, and valproic acid have been associated with adverse effects that can make these agents difficult to use in patients with bulimia nervosa; lithium has not been demonstrated to be effective for bulimia nervosa per se

See Treatment for more detail.

Next

Background

Bulimia nervosa is an eating disorder delineated in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5).[1] Among the eating disorders, bulimia nervosa and anorexia nervosa are far more common in young females, while binge-eating disorder, the most common eating disorder overall, is more common in adults.

Bulimia nervosa includes regularly occurring compensatory behaviors that are intended to rid the body of the excess calories consumed during eating binges. Bulimia nervosa is distinguished from the recently delineated syndrome of binge-eating disorder, in which no regular or consistent compensatory behavior accompanies the bingeing episodes. Although the DSM-5 describes that compensatory behaviors may include purging and/or nonpurging behaviors (see below), in contrast to earlier DSM editions, DSM-5 no longer maintains specific purging and nonpurging subtypes. The frequent association of cigarette smoking with bulimia nervosa may at times reflect compensatory behavior, in that nicotine use appears to suppress, whereas smoking cessation provokes, weight gain in some individuals.

In up to 60% of cases, patients with bulimia nervosa report prior histories of anorexia nervosa. In contrast to individuals with uncomplicated binge-eating disorder who tend to be obese, people with bulimia nervosa are more typically of normal weight, although some degree of overlap between nonpurging bulimia nervosa and binge-eating disorder is seen. The natural history of eating disorders is such that individuals may pass through several diagnoses over time, with some meeting criteria for anorexia nervosa, bulimia nervosa, and binge-eating disorder at various points. The development of anorexia nervosa in individuals who initially present with bulimia nervosa is possible, although less common.[9]

Binge eating

Bulimia nervosa is characterized by frequent episodes of binge eating associated with emotional distress and a sense of loss of control.

Binge eating: Eating, in a discrete period of time (eg, 2 hours) an amount of food that is significantly larger than is typical for most people during the same defined period. This behavior is associated with a perceived loss of control of eating during this time.

Overeating episode: The consumption of an unusually large amount of food in a defined period, without concomitant perception of loss of control.

Subjective bulimic episode: The consumption of objectively minimal amounts of food in a defined period with a perception of loss of control.

Compensatory behaviors

Compensatory behaviors used by individuals with bulimia nervosa include self-induced vomiting, laxative abuse, excessive exercise generally experienced as being joyless and/or compulsive, episodes of fasting or strict dieting, diuretic abuse, use of appetite suppressants, failure to use insulin in those with type I diabetes, and/or the use of medications intended to speed up metabolism (eg, thyroid hormone). DSM-5 diagnostic criteria require episodes of binge eating that occur at least once weekly for 3 months. Individuals with bulimia nervosa are also dissatisfied with their body shape, weight, or both.

Self-evaluation

Anorexia nervosa and bulimia nervosa are characterized by abnormalities in eating behaviors associated with a fear of weight gain and usually some degree of body image distortion (believing one looks much fatter than is actually the case). These are accompanied by associated abnormalities in mood and in perceptions of hunger and satiety. Disordered eating and weight control efforts can manifest as dietary restriction, binge eating, and/or other compensatory behaviors intended to prevent weight gain, as noted above.

For more information, see Medscape's Eating Disorders Resource Center.

Diagnostic criteria for bulimia nervosa

DMS-5 diagnostic criteria for 307.51 (F50.2) bulimia nervosa are as follows:[1]

  • Recurrent episodes of binge eating: An episode of binge eating is characterized by both (1) eating, in a discrete period of time (eg, within any 2-hour period), an amount of food that is definitely larger than what most individuals would eat in a similar period of time under similar circumstances and (2) a sense of lack of control over eating during the episode (eg, a feeling that one cannot stop eating or control what or how much one is eating)
  • Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise
  • The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 months
  • Self-evaluation is unduly influenced by body shape and weight
  • The disturbance does not occur exclusively during episodes of anorexia nervosa

Specify if either of the following applies:

  • In partial remission: After full criteria for bulimia nervosa were previously met, some, but not all, of the criteria have been met for a sustained period of time
  • In full remission: After full criteria for bulimia nervosa were previously met, none of the criteria has been met for a sustained period of time

Specify current severity. The minimum level of severity is based on the frequency of inappropriate compensatory behaviors. The level of severity may be increased to reflect other symptoms and the degree of functional disability. Specify current severity as follows:

  • Mild: An average of 1-3 episodes of inappropriate compensatory behaviors per week
  • Moderate: An average of 4-7 episodes of inappropriate compensatory behaviors per week
  • Severe: An average of 8–13 episodes of inappropriate compensatory behaviors per week
  • Extreme: An average of 14 or more episodes of inappropriate compensatory behaviors per week

Case study

A 21-year-old woman is brought into an outpatient clinic by her mother, who complains that her daughter has been demonstrating unusual eating patterns since she moved back home 6 months ago. Her mother observes her to eat large amounts of food, such as desserts, when she is alone, often finding food wrappers hidden in her daughter’s room. She is worried that her daughter may be engaging in vomiting after these episodes of heavy eating. She often isolates herself in the bathroom for 10-20 minutes after a large meal. This case will be discussed in the Clinical History section.

Other problems to be considered

Binge-eating disorder (BED)

BED is characterized by frequent and recurrent binge eating episodes without consistent compensatory behaviors. It is the most common eating disorder overall, with a lifetime prevalence of 2.8%. Binge-eating disorder is known to have several comorbidities with other psychiatric disorders, and is strongly associated with severe obesity. The lifetime prevalence for binge-eating disorder in men is 2%, while the male prevalence of bulimia nervosa is 0.5% and anorexia nervosa is 0.3%. This makes binge-eating disorder the most common eating disorder not only in the general population, but in men, as well.[10]

Night eating syndrome (NES)

NES has only recently been defined and recognized. It is characterized by the consumption of large amounts of food (>20% of the total calorie intake) after evening meals. It is typically associated with early morning drowsiness and anorexia. No significant overlap is seen between binge-eating disorder or bulimia nervosa and night eating disorder.

Several eating disorder syndromes have been described in association with disturbances in disturbances in sleep and circadian patterns. These disorders are diagnosed under the DSM-5 “Other Specified Feeding or Eating Disorders” category.[1]

NES is distinct from sleep-related eating disorder (SRED), another syndrome in which eating and sleep disturbances have been linked. NES and SRED are quite different. NES could be considered an abnormality in the circadian rhythm of meal timing with a normal circadian timing of sleep onset, ie, with individuals eating a substantial part of their daily intake in the evening, after usual dinnertime, before they go to sleep. Conversely, the feeding behavior in SRED is characterized by recurrent episodes of eating after an arousal from nighttime sleep with or without amnesia.

In addition to eating other foods, in SRED episodes, patients will sometimes eat foods that are ordinarily unpalatable, eg, raw flour and raw bacon have been described. Both conditions are often relentless and chronic. SRED is frequently associated with other sleep disorders, in particular parasomnias, eg, sleep-walking. Case reports have linked some cases of SRED to the use of certain psychotropic medications, including tricyclic antidepressants, anticholinergics, lithium, triazolam, olanzapine, risperidone, and zolpidem. Early studies have suggested that the anti-seizure medication topiramate may be an effective treatment for SRED.[11]

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Frequency

United States

Bulimia nervosa is thought to be significantly underrecognized. In the United States, the prevalence of bulimia nervosa is 1%.[10] Lifetime prevalence is 0.5% for males and 1.5% for females. Those who are diagnosed with bulimia nervosa spend approximately 8.3 years with an episode. Approximately 65.3% of patients with bulimia have a body mass index (BMI) between 18.5-29.9 and only 3.5% have a BMI less than 18.5.

Bulimia nervosa is more common among those whose occupation or hobbies require gaining and/or losing weight rapidly, such as wrestlers and competitive bodybuilders.[12] Athletes in certain sports (eg, runners and gymnasts, are particularly prone to eating disorders.[13] The female athlete triad of eating disorders, hypothalamic amenorrhea, and osteoporosis is now well recognized and is particularly common in sports where slimness and body shape are of great importance, such as gymnastics, long distance running, diving, and figure skating. Eating disorders are also being recognized as a problem in predominantly male sports such as cycling, weight lifting, and wrestling. Certain vocations such as acting, modeling, and ballet dancing[14] also appear to be associated with higher risk for these disorders.

While overall epidemiological trends are difficult to assess given the changes in diagnostic criteria over time, most studies report a progressive increase in the prevalence of anorexia nervosa and bulimia nervosa in the last several decades of the 20th century, with the possibility that rates have been leveling off. However, along with increases in obesity, rates of binge eating disorder are believed to be on the rise as well.

Rates of bulimic symptoms (as distinct from the diagnosis of bulimia nervosa per se) may vary across geographic regions in the United States. In one small study, women from North Carolina and Virginia (South Atlantic region) reported more bulimic symptoms than women from Louisiana and Tennessee (South Central region) and Ohio and Missouri (Midwest region).[15]

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Mortality/Morbidity

A meta-analysis conducted of 36 studies by Arcelus et al suggests that individuals with eating disorders have significantly elevated mortality rates. Furthermore, the patients with anorexia nervosa had the highest mortality rate.[16]

Race

Bulimia nervosa is a cosmopolitan disorder that has been described in all ethnic, racial, and socioeconomic groups. Literature is mixed regarding ethnic differences in eating disorders. No clear consensus exists about the relative prevalence of eating disorders and associated symptoms across ethnicities. Clinicians should remain alert for possible ethnic diversity in symptom presentation or distress that could obscure the diagnosis or need for intervention.[17, 18]

Sex

As with other eating disorders, bulimia nervosa occurs predominantly in women. Most reports suggest a female-to-male ratio of 10:1, with reported ranges from 20:1 to 7:1. In some populations (eg, active duty military) body dissatisfaction and subclinical eating disorder rates among males have been reported to be in excess of 20%.

Clinicians should remain aware that men also develop bulimia nervosa and other eating disorders. The psychopathology and attitudes of males with eating disorders appear on the whole to be similar to those of females with eating disorders; both are significantly associated with family histories of these disorders. Although few data are available, evidence suggests that men and women also share significant similarities in clinical course, complications, and response to treatment.

Age

The mean age of onset is 19.7, slightly older than the peak age of onset for anorexia nervosa but generally lower than the age of onset for binge-eating disorder. The prevalence of bulimia nervosa in children younger than 14 years appears to be less than 5%. Bulimia nervosa has also been reported in the elderly.[19]

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Contributor Information and Disclosures
Author

Gagandeep Randhawa, MBBS Resident Physician, Department of Psychiatry, Kaweah Delta Medical Center, University of California, Irvine, School of Medicine

Gagandeep Randhawa, MBBS is a member of the following medical societies: American Psychiatric Association, Indian Doctors for Peace and Development

Disclosure: Nothing to disclose.

Coauthor(s)

Donald M Hilty, MD Chair and Program Director, Department of Psychiatry, Keck School of Medicine of the University of Southern California

Donald M Hilty, MD is a member of the following medical societies: American Psychiatric Association, Association for Academic Psychiatry, American Association for Technology in Psychiatry, American Telemedicine Association

Disclosure: Nothing to disclose.

Joel Yager, MD Professor of Psychiatry, University of Colorado Health Sciences Center; Professor of Psychiatry Emeritus, University of California, Los Angeles, David Geffen School of Medicine; Professor of Psychiatry Emeritus, University of New Mexico School of Medicine

Joel Yager, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Medical Association, American Psychiatric Association, Association for Academic Psychiatry

Disclosure: Nothing to disclose.

 

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

David Bienenfeld, MD Professor, Departments of Psychiatry and Geriatric Medicine, Wright State University, Boonshoft School of Medicine

David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, Association for Academic Psychiatry

Disclosure: Nothing to disclose.

Additional Contributors

Christine I Osterhout, MD Resident Physician, Department of Psychiatry and Behavioral Sciences, University of California, Davis Health System

Christine I Osterhout, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Child and Adolescent Psychiatry, American Academy of Psychiatry and the Law, American Medical Association, American Psychiatric Association

Disclosure: Nothing to disclose.

Lorin M Scher, MD Director, Emergency Psychiatric ServicesHealth Sciences Assistant Clinical ProfessorDepartment of Psychiatry and Behavioral SciencesUniversity of California, Davis, School of Medicine

Lorin M Scher, MD is a member of the following medical societies: Academy of Psychosomatic Medicine, Alpha Omega Alpha, American Medical Association, American Psychiatric Association, Association for Academic Psychiatry

Disclosure: Nothing to disclose.

Acknowledgements

Robert C Daly, MB, ChB, MPH Senior Fellow, Department of Behavioral Endocrinology, National Institute of Mental Health, National Institutes of Health

Disclosure: Nothing to disclose.

Raj K Kalapatapu, MD Fellow, Addiction Psychiatry, Columbia University College of Physicians and Surgeons

Raj K Kalapatapu is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Child and Adolescent Psychiatry, American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association.

Disclosure: Nothing to disclose.

Gabriel I Uwaifo, MD Associate Professor, Section of Endocrinology, Diabetes and Metabolism, Louisiana State University School of Medicine in New Orleans; Adjunct Professor, Joint Program on Diabetes, Endocrinology and Metabolism, Pennington Biomedical Research Center in Baton Rouge

Gabriel I Uwaifo, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, American College of Physicians-American Society of Internal Medicine, American Diabetes Association, American Medical Association, American Society of Hypertension, and The Endocrine Society

Disclosure: Nothing to disclose.

Kelda Harris Walsh, MD Assistant Professor of Clinical Psychiatry, Section of Child and Adolescent Psychiatry, Department of Psychiatry, Indiana University School of Medicine; Chief, Obsessive-Compulsive/Tourette/Anxiety Disorders Clinic, Riley Hospital for Children

Disclosure: Nothing to disclose.

Acknowledgments

The authors would also like to acknowledge the contributions of Rebecca Davis, Librarian at the University of California (UC), Davis and Dr. Eric Rickin, Director for the Center for Overcoming Problem Eating (COPE) at the Western Psychiatric Institute and Clinic, University of Pittsburgh Medical Center. Finally, the authors thank the Department of Psychiatry and Behavioral Sciences at UC Davis.

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Parotid hypertrophy. Reprinted with permission from Mandel, L and Siamak, A. Diagnosing bulimia nervosa with parotid gland swelling. J Am Dent Assoc 2004, Vol 135, No 5, 613-616.
Dental caries. Reprinted with permission from Wolcott, RB, Yager, J, Gordon, G. Dental sequelae to the binge-purge syndrome (bulimia): report of cases. JADA. 1984; 109:723-725.
Russell sign. Reprinted with permission from Glorio R, et al. Prevalence of cutaneous manifestations in 200 patients with eating disorders. Int J Derm, 2000, 39(5), 348-353.
This chest radiograph demonstrates pneumomediastinum, which can occur in association with esophageal rupture from forceful vomiting.
Water-soluble contrast esophagram from a patient with esophageal perforation after esophageal dilation shows contrast leak (arrowheads) and normal esophageal lumen (arrows).
Mallory-Weiss tear. Typical longitudinal mucosal tear with overlying fibrinous exudate extending from the distal esophagus to the gastric cardia. Courtesy of C.J. Gostout, MD.
Differential Diagnosis of Bulimia Nervosa [1]
Anorexia Nervosa AN and BN Bulimia Nervosa
Restriction of energy intake relative to requirement, leading to significantly low body weight in the context of age, sex, developmental trajectory, and physical health   Recurrent episodes of binge eating: a) eating in a discrete period of time, within a 2-hour period, an amount that is definitely larger than what most would eat in that time period; b) a sense of lack of control over eating
Intense fear of gaining weight or of becoming fat, or persistent behavior that interferes with weight gain, even though at a significantly low weight   Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise
  Disturbance 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 binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 months
Two types: Restrictive and Purge/Bing-Eating type   The disturbance does not occur exclusively during episodes of AN
Body Dysmorphic Disorder BDD and BN BN
Preoccupation with one or more perceived defects or flaws in physical appearance that are not observable or appear slight to others Disturbance in which one's body weight or shape is experienced, undue influence of body weight or shape on self-evaluation Recurrent episodes of binge eating: a) eating in a discrete period of time, within a 2-hour period, an amount that is definitely larger than what most would eat in that time period; b) a sense of lack of control over eating
At some point during the course of the disorder, the individual has performed repetitive behaviors or mental acts in response to the appearance concerns The preoccupation causes significant distress or impairment in social, occupational, or other important areas of functioning Recurrent inappropriate compensatory behaviors in order to prevent weight gain, such as self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; or excessive exercise
The appearance preoccupation is not better explained by concerns with body fat or weight in an individual whose symptoms meet diagnostic criteria for an eating disorder   The binge eating and inappropriate compensatory behaviors both occur, on average, at least once a week for 3 months
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