Pediatric Bulimia

No Results

No Results


Bulimia nervosa is an eating disorder characterized by binge eating and purging. It usually begins in adolescence or young adulthood, and is far more common in females than in males.

Symptoms of binge eating include the following:

Lack of control over eating

Secrecy surrounding eating

Eating unusually large amounts of food

Irregular eating habits

Symptoms of purging include the following:

Regularly going to the bathroom after meals

Using laxatives or diuretics

Smelling of vomit

Exercising excessively

Some physical signs and symptoms associated with bulimia include the following:

Normal body weight or increased body weight, with frequent fluctuations

Low body temperature


Dental erosion

Callouses or scars on the knuckles or hands

Menstrual irregularity or amenorrhea

See Clinical Presentation for more detail.

Lab studies and physical findings

No specific diagnostic test for bulimia nervosa currently exists. However, several laboratory abnormalities may occur as a consequence of purging, including:




Metabolic alkalosis (due to vomiting)

Metabolic acidosis (due to laxative and diuretic abuse)

Diagnostic criteria (DSM-5)

Bulimia nervosa is characterized by recurrent episodes of binge eating and inappropriate compensatory behaviors to avoid weight gain, such as self-induced vomiting, using laxatives or diuretics, fasting, or exercising excessively. A third essential feature of the disorder is self-evaluation that is unduly influenced by body shape and weight. [1]

To qualify for the diagnosis of bulimia, the binge eating and inappropriate compensatory behaviors must occur, on average, at least once per week for 3 months.

See Workup for more detail.

Cognitive-behavioral therapy (CBT) is the treatment of choice for bulimia nervosa. [2] In CBT, behavioral approaches to avoiding undesirable eating habits are used, including diary keeping; behavioral analyses of the antecedents, behaviors, and consequences (so-called ABCs) associated with binge eating and purging episodes; and exposure to food paired with progressive response prevention regarding binge eating and purging. Distorted or maladaptive thoughts regarding weight and shape are identified, examined, and addressed, and other dysfunctional irrational beliefs are explored and confronted to allow better understanding, enhanced self-control, and improved body image.

Other therapies that may be helpful include the following:

Interpersonal psychotherapy (IPT)

Nutritional rehabilitation counseling

Family therapy

Group therapy

Inpatient care is indicated for patients who are suicidal, have abnormal ECG findings or electrolyte levels, are dehydrated, or who do not respond to outpatient therapy.

See Treatment and Medication for more detail.

Bulimia nervosa is an eating disorder characterized by binge eating and purging. It usually begins in adolescence or young adulthood, and is far more common in females than in males.

Criteria for the diagnosis of bulimia include preoccupation with eating and overeating large amounts of food in short periods, also described as binge eating. This behavior is then followed by inappropriate behavior to avoid weight gain, most notably, self-induced vomiting. Other methods of avoiding weight gain include laxative/diuretic abuse and excessive exercise. Bulimia nervosa is a disease with a highly focused patient population; it is predominantly found in women and is virtually nonexistent in nonindustrialized countries. [1, 3, 4, 5, 6, 7, 8, 9]

Bulimia nervosa is a disease that most likely emerges from a complex integration of many factors. These factors may be psychological, cultural, environmental, and societal. Many proposed associated factors are involved in the development of bulimia. These factors can include chemical imbalances in neurotransmitters, such as serotonin or pancreatic polypeptides (eg, pancreatic peptide YY [PYY]). Psychological and psychiatric problems are also thought to contribute to the development of bulimia. Another contributing factor is family problems. Participation in extracurricular activities that emphasize body shape and image has also been linked to the development of bulimia.

The binge and purge cycle characteristic of bulimia affects multiple organ systems. The GI system can be affected by the overeating associated with binge episodes. This overeating can stretch the stomach or delay gastric emptying. Purging can induce esophagitis or esophageal rupture due to vomiting. Pancreatitis can also occur. Electrolyte abnormalities can include hypokalemia and hypochloremia. Cardiovascular abnormalities can lead to arrhythmias, arrest, cardiac rupture, or pneumomediastinum. The pulmonary system can be damaged by aspiration of gastric contents upon vomiting. Renal function impairment is also possible. [4, 6, 10, 11, 12, 13]

United States

The lifetime prevalence of bulimia nervosa among women is 1%–3%, and a comparable percentage of women have less severe variants of the disorder. Lifetime prevalence among men is 0.1%. [3, 13]

Although no concrete data are available, bulimia is a disease that is highly culturally dependent. It is found solely in societies in which a high cultural value is placed on slimness and is virtually nonexistent in nonindustrialized countries.

Death is a relatively uncommon outcome for bulimia. Approximately 0-3% of women with the disease eventually die from complications of the disease; however, these numbers may be underestimated owing to low ascertainment rates and short follow-up periods.

The leading cause of death among patients with eating disorders is suicide, which is more common in patients with bulimia nervosa than in those with anorexia nervosa (AN). Factors most strongly associated with suicide attempt or suicidal ideation in patients with eating disorders include concurrent drug use, alcohol use, and tobacco use. [14] Suicide risk should be carefully monitored in patients with eating disorders who also have these risk factors.

One third of patients who present for treatment of bulimia nervosa have past histories of anorexia nervosa.

Bulimia has many complications (see Complications). [3, 10, 14]

Bulimia has traditionally been thought of as a disease that predominantly affects whites. The low incidence of eating disorders among nonwhites has been attributed to differences among ethnic groups in ideal body image. Studies have shown that black women are less likely to develop eating disorders and tend to express more satisfaction with their bodies than white women of similar weight; however, other studies suggest that the incidence of bulimia among minority groups is higher than previously thought. Studies suggest that patients from higher socioeconomic groups are more likely to seek treatment, making the incidence within these groups appear to be higher.

Some population studies suggest an equal incidence of bulimia in blacks and whites. Overall, strong circumstantial evidence suggests that cultural factors play large roles in eating disorder development. Most cases of bulimia nervosa originate in industrialized countries. In general, industrialized countries are places where food is plentiful and a preoccupation with thinness in women is present. [5, 11]

Bulimia primarily occurs in young women. Males comprise only 2-8% of all bulimia cases; however, this number is thought to be on the rise. [15]

Bulimia is most common in adolescents and young adults. Median age of onset is 18 years. [4, 9]

Douglas D. Leptin Levels Tied to Binge Eating in Children. Available at Accessed: August 29, 2013.

Valenzuela F, Lock J, Le Grange D, Bohon C. Comorbid depressive symptoms and self-esteem improve after either cognitive-behavioural therapy or family-based treatment for adolescent bulimia nervosa. Eur Eat Disord Rev. 2018 Feb 15. [Medline].

Behrman RE, Kliegman R, Jenson HB. Nelson’s Textbook of Pediatrics. 16th ed. Philadelphia, Pa: WB Saunders and Co; 2000.

Neinstein LS, Gordon CM, Katzman DK, Rosen DS, Woods ER. Adolescent Health Care, A Practical Guide. 5th ed. Philadelphia, PA: Wolters Kuwer and Lippincott Williams & Wilkins; 2008.

Haly PJ, Bacaltchuk J. Bulimia Nervosa. American Family Physician. June 2007. 75:1699-702.

Walsh BT, Devlin MJ. Eating disorders: progress and problems. Science. 1998 May 29. 280(5368):1387-90. [Medline].

Strasburger VC, Brown RT, Braverman PK, Rogers PD, Holland-Hall C, Coupey SM. Adolescent Medicine, A Handbook for Primary Care. Philadelphia, PA: Lippincott Williams & Wilkins; 2006.

Herpertz-Dahlmann B. Adolescent eating disorders: definitions, symptomatology, epidemiology and comorbidity. Child Adolesc Psychiatr Clin N Am. 2009 Jan. 18(1):31-47. [Medline].

Sigel E. Eating disorders. Adolesc Med State Art Rev. 2008 Dec. 19(3):547-72, xi. [Medline].

Carney CP, Andersen AE. Eating disorders. Guide to medical evaluation and complications. Psychiatr Clin North Am. 1996 Dec. 19(4):657-79. [Medline].

Halmi KA. Models to conceptualize risk factors for bulimia nervosa. Arch Gen Psychiatry. 1997 Jun. 54(6):507-8. [Medline].

Cotran RS, Kumar V, Collins T. Robbins Pathologic Basis of Disease. 6th ed. Philadelphia, Pa: WB Saunders and Co; 1999.

Capasso A, Putrella C, Milano W. Recent clinical aspects of eating disorders. Rev Recent Clin Trials. 2009 Jan. 4(1):63-9. [Medline].

Fedorowicz VJ, Falissard B, Foulon C, Dardennes R, Divac SM, Guelfi JD, et al. Factors associated with suicidal behaviors in a large French sample of inpatients with eating disorders. Int J Eat Disord. 2007 Nov. 40(7):589-95. [Medline]. [Full Text].

Muise AM, Stein DG, Arbess G. Eating disorders in adolescent boys: a review of the adolescent and young adult literature. J Adolesc Health. 2003 Dec. 33(6):427-35. [Medline].

Lilly RZ. Bulimia nervosa. BMJ. 2003 Aug 16. 327(7411):380-1. [Medline]. [Full Text].

Heaner MK, Walsh BT. A history of the identification of the characteristic eating disturbances of Bulimia Nervosa, Binge Eating Disorder and Anorexia Nervosa. Appetite. 2013 Jun 7. [Medline].

Nicholls D, Viner R. Eating disorders and weight problems. BMJ. 2005 Apr 23. 330(7497):950-3. [Medline]. [Full Text].

Spindler A, Milos G. Links between eating disorder symptom severity and psychiatric comorbidity. Eat Behav. 2007 Aug. 8(3):364-73. [Medline].

Mitchell JE. The Outpatient Treatment of Eating Disorders: A Guide for Therapists, Dietitians, and Physicians. University of Minnesota Press; 2001. 32.

Le Grange D, Lock J. Treating Bulimia in Adolescents- A Family Based Approach. New York, NY: The Guilford Press; 2007.

Weddle M, Kokotailo P. Adolescent substance abuse. Confidentiality and consent. Pediatr Clin North Am. April 2002. 49:301-15. [Medline].

Berkman ND, Bulik CM, Brownley KA, Lohr KN, Sedway JA, Rooks A, et al. Management of eating disorders. Evid Rep Technol Assess (Full Rep). 2006 Apr. 1-166. [Medline]. [Full Text].

Ornstein RM, Lane-Loney SE, Hollenbeak CS. Clinical outcomes of a novel, family-centered partial hospitalization program for young patients with eating disorders. Eat Weight Disord. 2012 Sep. 17(3):e170-7. [Medline].

Lock J. Treatment of Adolescent Eating Disorders: Progress and Challenges. Minerva Psichiatr. 2010 Sep. 51(3):207-216. [Medline]. [Full Text].

Linardon J, Wade T, de la Piedad Garcia X, Brennan L. Psychotherapy for bulimia nervosa on symptoms of depression: A meta-analysis of randomized controlled trials. Int J Eat Disord. 2017 Oct. 50 (10):1124-1136. [Medline].

Claudino AM, Van den Eynde F, Stahl D, Dew T, Andiappan M, Kalthoff J. Repetitive transcranial magnetic stimulation reduces cortisol concentrations in bulimic disorders. Psychol Med. 2011 Jun. 41(6):1329-36. [Medline].

Van den Eynde F, Claudino AM, Mogg A, Horrell L, Stahl D, Ribeiro W. Repetitive transcranial magnetic stimulation reduces cue-induced food craving in bulimic disorders. Biol Psychiatry. 2010 Apr 15. 67(8):793-5. [Medline].

Bacaltchuk J, Hay P. Antidepressants versus placebo for people with bulimia nervosa. Cochrane Database Syst Rev. 2003. CD003391. [Medline]. [Full Text].

Hay PJ, Bacaltchuk J, Stefano S. Psychotherapy for bulimia nervosa and binging. Cochrane Database Syst Rev. 2004. (3):CD000562. [Medline]. [Full Text].

Milano W, Siano C, Putrella C, Capasso A. Treatment of bulimia nervosa with fluvoxamine: a randomized controlled trial. Adv Ther. 2005 May-Jun. 22(3):278-83. [Medline].

Milano W, Petrella C, Sabatino C, Capasso A. Treatment of bulimia nervosa with sertraline: a randomized controlled trial. Adv Ther. 2004 Jul-Aug. 21(4):232-7. [Medline].

Aigner M, Treasure J, Kaye W, Kasper S,. World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for the pharmacological treatment of eating disorders. World J Biol Psychiatry. 2011 Sep. 12(6):400-43. [Medline].

March J, Silva S, Petrycki S, Curry J, Wells K, Fairbank J. Fluoxetine, cognitive-behavioral therapy, and their combination for adolescents with depression: Treatment for Adolescents With Depression Study (TADS) randomized controlled trial. JAMA. 2004 Aug 18. 292(7):807-20. [Medline].

Hartman BK, Faris PL, Kim SW, Raymond NC, Goodale RL, Meller WH, et al. Treatment of bulimia nervosa with ondansetron. Arch Gen Psychiatry. 1997 Oct. 54(10):969-70. [Medline].

Waller G, Gray E, Hinrichsen H, Mountford V, Lawson R, Patient E. Cognitive-behavioral therapy for bulimia nervosa and atypical bulimic nervosa: effectiveness in clinical settings. Int J Eat Disord. 2014 Jan. 47(1):13-7. [Medline].

Agüera Z, Riesco N, Jiménez-Murcia S, Islam MA, Granero R, Vicente E. Cognitive behaviour therapy response and dropout rate across purging and nonpurging bulimia nervosa and binge eating disorder: DSM-5 implications. BMC Psychiatry. 2013. 13:285. [Medline].

Zeeck A, Weber S, Sandholz A, Wetzler-Burmeister E, Wirsching M, Hartmann A. Inpatient versus day clinic treatment for bulimia nervosa: a randomized trial. Psychother Psychosom. 2009. 78(3):152-60. [Medline].

Fairburn CG, Cooper Z, Doll HA, O’Connor ME, Bohn K, Hawker DM, et al. Transdiagnostic cognitive-behavioral therapy for patients with eating disorders: a two-site trial with 60-week follow-up. Am J Psychiatry. 2009 Mar. 166(3):311-9. [Medline].

Vaz AR, Conceição E, Machado PP. Early response as a predictor of success in guided self-help treatment for bulimic disorders. Eur Eat Disord Rev. 2014 Jan. 22(1):59-65. [Medline].

Linna MS, Raevuori A, Haukka J, Suvisaari JM, Suokas JT, Gissler M. Reproductive health outcomes in eating disorders. Int J Eat Disord. 2013 Dec. 46(8):826-33. [Medline].

Forman SF, Grodin LF, Graham DA, Sylvester CJ, Rosen DS, Kapphahn CJ, et al. An eleven site national quality improvement evaluation of adolescent medicine-based eating disorder programs: predictors of weight outcomes at one year and risk adjustment analyses. J Adolesc Health. 2011 Dec. 49(6):594-600. [Medline].

Hagan KE, Clark KE, Forbush KT. Incremental validity of weight suppression in predicting clinical impairment in bulimic syndromes. Int J Eat Disord. 2017 Jun. 50 (6):672-678. [Medline].

Eddy KT, Dorer DJ, Franko DL, Tahilani K, Thompson-Brenner H, Herzog DB. Should bulimia nervosa be subtyped by history of anorexia nervosa? A longitudinal validation. Int J Eat Disord. 2007 Nov. 40 Suppl:S67-71. [Medline]. [Full Text].

National Eating Disorders Association. National Eating Disorders Association. Available at Accessed: April 2009.

Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: assessment of a new screening tool for eating disorders. BMJ. 1999 Dec 4. 319(7223):1467-8. [Medline]. [Full Text].

Miller R, Tanofsky-Kraff M, Shomaker LB, Field SE, Hannallah L, Reina SA, et al. Serum leptin and loss of control eating in children and adolescents. Int J Obes (Lond). 2013 Jul 9. [Medline].

Maggie A Wilkes, MD Resident Physician, Department of Psychiatry, Medical University of South Carolina College of Medicine

Maggie A Wilkes, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Medical Association, American Psychiatric Association

Disclosure: Nothing to disclose.

Eve G Spratt, MD, MSc Professor of Pediatrics and Psychiatry, Division of Developmental Pediatrics, Medical University of South Carolina; Director, Pediatric Consultation Liaison Psychiatry, Medical University of South Carolina Children’s Hospital at Charleston

Eve G Spratt, MD, MSc is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry

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.

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.

Angelo P Giardino, MD, MPH, PhD Professor and Section Head, Academic General Pediatrics, Baylor College of Medicine; Senior Vice President and Chief Quality Officer, Texas Children’s Hospital

Angelo P Giardino, MD, MPH, PhD 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, International Society for the Prevention of Child Abuse and Neglect, Ray E Helfer Society

Disclosure: Nothing to disclose.

Libby N Brockman Clinical Research Assistant, Center for Clinical and Translational Research, Seattle Children’s Hospital; Research Assistant, Department of Pediatrics, University of Washington, Seattle

Disclosure: Nothing to disclose.

Robert Judd, MD Associate Professor, Department of Pediatrics, Division of Pediatric Gastroenterology, University of Wisconsin at Madison

Robert Judd, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Megan A Moreno, MD, MEd, MPH Assistant Professor, Department of Pediatrics, Section of Adolescent Medicine, University of Wisconsin-Madison School of Medicine and Public Health

Megan A Moreno, MD, MEd, MPH is a member of the following medical societies: Society for Adolescent Medicine

Disclosure: Nothing to disclose.

Patricia Quigley, MD Resident Physician, Department of Pediatrics, University of Wisconsin Hospital and Clinics

Patricia Quigley, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Pediatric Bulimia

Research & References of Pediatric Bulimia|A&C Accounting And Tax Services