Bulimia Nervosa Clinical Presentation

  • Author: Christine I Osterhout, MD; Chief Editor: David Bienenfeld, MD   more...
 
Updated: Nov 15, 2011
 

History

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.

When the patient was asked about her eating habits, she admitted to a “loss of control.” She described feeling deep remorse when she eats more than she would like. Furthermore, she described feeling so laden with guilt about her eating binges that she purposefully induces vomiting at least once every other day. This act gives her tremendous relief. She admits that she is unhappy with her overall appearance, and feels that she is “fat” and “out of shape.” She is preoccupied with her appearance and says that she compares herself to other women “all day long.” She also admits to feeling sad most days. She endorses experiencing occasional missed menstrual periods, low libido, low energy, and intermittent sore throat.

Historically, the patient has memories of a chaotic childhood. She is an only child whose parents fought often and finally divorced when she was 9 years old. The patient remembers the first time she induced vomiting at 10 years old, after she felt “too full after a large meal.” The mother describes her daughter as having few friends and as tending to isolate herself. However, the mother describes her as very bright; in fact, she was valedictorian of her high school.

On physical examination, the patient’s blood pressure is 90/60, heart rate is 100, and BMI is 19. Her oropharynx appears injected without areas of erosion, and multiple dental caries are seen. Bilateral parotid enlargement with minor tenderness is present. The patient is tachycardic and bowel sounds are hyperactive. The abdomen is soft, nontender, and nondistended. Skin turgor is poor.

On mental status examination, the patient presents as a young Caucasian woman with average body habitus and pale skin. She is meticulously dressed and groomed. She answers questions curtly, makes poor eye contact, and demonstrates mild foot tapping throughout the interview. Her mood is anxious and her affect is mood congruent but restricted to negative emotionality. She is highly articulate. Thought process is linear and goal directed. Methodical about her statements, she often takes time to clarify what she “really means.”

Thought content displays themes of shame, guilt, and self-reproach. No active delusions or hallucinations are present. Her cognition is grossly intact. She denies suicidal thoughts, but sometimes wishes she was “invisible.” She has no violent or homicidal thoughts. Insight is limited regarding her ability to acknowledge her psychiatric illness. Her judgment is impaired considering her inability to recognize the potential negative health consequences of her eating behaviors.

Prior to entering your office, laboratory assessment obtained at the suggestion of her primary care doctor reveals a serum potassium level of 3.8 Meq/L and serum amylase level of 140 Units/L.

Take home points

  1. The differential diagnosis of bulimia nervosa includes depression, anxiety and age-appropriate developmental problems (eg, lack of esteem).
  2. A biopsychosocial treatment plan will be necessary to provide her the care she needs.
  3. Collaboration with primary care providers is often necessary for short-term and sometimes long-term.

History

Bulimia nervosa is often not diagnosed for many months or even years after onset because of the patients' secretiveness about their difficulties, usually associated with a great deal of shame. These patients often see physicians for other problems, such as anxiety, depression, infertility, bowel irregularities, fatigue, or palpitations. Similarly, they may see mental health professionals for mood and anxiety problems, personality issues, relationship issues or substance abuse, without revealing the presence of an eating disorder.

One common presenting scenario is that of a patient who is concerned her about weight who seeks help with weight loss. Symptoms may include bloating, constipation, and menstrual irregularities. Far less often, people may present with palpitations resulting from arrhythmias, which are often associated with electrolyte abnormalities and dehydration. Bulimia nervosa is also characterized by an inappropriate premium placed on slender physical appearance, though less prominently than in anorexia nervosa.

A dietary history may reveal attempts to control weight by dieting and abstaining entirely from high-calorie foods at all times except during binge-eating episodes. Often, a morbid preoccupation with food and eating is present, and recurring cycles of extreme dieting and/or fasting may alternate with gorging behavior. Usually, bingeing episodes are well planned. High-calorie foods that are easy to swallow and to vomit are usually chosen. Patients may rapidly ingest up to 10 times (or more) of the recommended daily calorie allowance in a single binge episode. Understandably, patients often try to avoid social situations in which they might too easily lose control over their food intake (eg, parties, eating out).

Patients with bulimia nervosa frequently engage in physical activity cyclically, in a fashion similar to that of the bingeing episodes. Most patients self-induce vomiting by gagging themselves with their fingers or a toothbrush. Some patients are able to regurgitate reflexively, without requiring external stimulation of the pharynx.[13] A minority of patients will chew, then regurgitate, without actually swallowing the food. One particularly dangerous form of vomiting is via induction through the use of emetics (eg, ipecac). Ipecac is a tightly binding and slowly released myotoxin that may lead to fatal cardiomyopathy in habitual users.

  • Patients with bulimia nervosa may experience the following symptoms:
    • General - Dizziness, lightheadedness, palpitations (due to dehydration, orthostatic hypotension, possibly hypokalemia)
    • Gastrointestinal symptoms - Pharyngeal irritation, abdominal pain (more common among persons who self-induce vomiting), blood in vomitus (from esophageal irritation and more rarely actual tears, which may be fatal), difficulty swallowing, bloating, flatulence, constipation, and obstipation
    • Pulmonary symptoms - Uncommonly aspiration pneumonitis or, more rarely, pneumomediastinum
    • Amenorrhea - Occurs in up to 50% of women with bulimia nervosa; significant proportion of remaining patients have irregular periods
  • A high index of suspicion is required in any depressed or anxious weight-conscious young woman.
    • A set of screening questions, such as the SCOFF mnemonic questionnaire[14] , is useful to obtain a quick impression as to the potential need for further in-depth questioning. The SCOFF questionnaire includes the following 5 questions:
      1. Do you make yourself S ick because you feel uncomfortably full?
      2. Do you worry you have lost C ontrol over how much you eat?
      3. Have you recently lost more than O ne stone (about 14 lbs or 6.35 kg) in a 3-month period?
      4. Do you believe yourself to be F at when others say you are too thin?
      5. Would you say that F ood dominates your life?
    • The Eating Disorder Screen for Primary Care (ESP) questionnaire is an alternative screening tool.[15] It contains the following 5 questions:
      1. Are you satisfied with your eating patterns?
      2. Do you ever eat in secret?
      3. Does your weight affect the way you feel about yourself?
      4. Have family members suffered from an eating disorder?
      5. Do you currently suffer with or have you in the past suffered with an eating disorder?
    • The Eating Attitudes Test (EAT) is a self-report population-based screening instrument that patients can complete in the waiting room prior to seeing the health care provider.[16] (See Psych Central for more information.)
  • Family history of eating disorders, anxiety, mood disorders, and alcohol and/or substance abuse/dependence may contribute to the risk of bulimia nervosa and should be investigated.
    • Generally, patients with bulimia nervosa are more likely than controls to view their families as conflicted, badly organized, noncohesive, and lacking in nurturance and caring. These patients have also been shown to more often appear to be angrily submissive to hostile and neglectful parents.
    • Perceptions of appearance-related teasing by family members may be present.[17]
    • For individuals still living with their parents, careful assessment of the family’s dynamics should be undertaken.

Physiological abnormalities

  • Many physiological abnormalities may be seen in association with eating disorders, but virtually all appear to be consequences of the abnormal behaviors, not their causes. In most cases of bulimia nervosa, laboratory abnormalities are relatively minor. In cases of very frequent purging (eg, daily or multiple times per day), abnormalities in electrolyte and serum amylase levels occur, but these and most other laboratory abnormalities are reversible with weight restoration and cessation of compensatory behaviors.
  • Among the identified metabolic consequences sometimes seen in bulimia nervosa are low plasma insulin, C peptide, triiodothyronine, and glucose values, as well as increased beta-hydroxybutyrate and free fatty acid levels. Both fasting and postbinge/postvomiting hypoglycemia are sometimes seen in some patients with bulimia nervosa. Some studies suggest increased secretory diurnal amplitudes in cortisol and adrenocorticotropic hormone (ACTH) in bulimia nervosa as well as blunted responses to corticotrophin-releasing hormone (CRH). However, these findings have been inconsistent among research studies.
  • Reports have also suggested abnormal responses to dexamethasone suppression similar to those seen in anorexia nervosa and major depressive disorder, more common among individuals with significant dietary restriction. Some authors have attributed these abnormalities to impaired dexamethasone absorption, which is demonstrated in some patients with bulimia nervosa. Similar to findings in anorexia nervosa, patients with bulimia nervosa tend to have higher growth hormone levels at night, while nocturnal prolactin levels tend to be less than those seen in controls.
  • Episodes of amenorrhea may occur in as many as 50% of women with bulimia nervosa.[18] About half of women with bulimia nervosa have anovulatory cycles while about 20% have luteal phase defects. Patients with anovulatory cycles generally have impaired luteinizing hormone pulsatile secretion patterns and associated reduced estradiol and progesterone pulse amplitudes.[18, 19]
  • Although the implications of many research findings are still unclear, and none of the following offer clinical tests of any merit, reports suggest involvement of the serotonin transporter[20, 21] , autoantibodies against neuropeptides[22] , various chromosome regions[23] , brain-derived neurotrophic factor[24] , and peptides leptin and ghrelin.[25] In a few instances, cerebral hemispheric lesions may be involved in pathogenesis.[26] Regional cerebral blood flow abnormalities have been noted in adolescents.[27] Endogenous opioids and beta-endorphins have been implicated in the maintenance of binge eating.

Comorbidity

A national comorbidity study examined lifetime comorbidities of other psychiatric diagnoses in conjunction with bulimia nervosa.[4] In general, the lifetime comorbidity of any psychiatric disorder is 94.5%

  • Affective disorders: The common co-occurrence of eating disorders with affective disorders suggests a possible relationship between them.[28] Major depressive disorder (MDD) is particularly common (approximately 50%) in this regard. Whether the association is causative (primary), secondary to the bulimia nervosa itself, or represents a common set of risk factors for bulimia nervosa and MDD is still unclear. Depressive symptoms can occur during pregnancy and postpartum in women with bulimia nervosa.[29] Bipolar II disorder also appears to be more common in patients with bulimia nervosa than in patients without eating disorders. The lifetime comorbidity for bipolar I or II is 17.7%.
  • Anxiety disorders: Obsessive-compulsive disorder (OCD) is more common in persons with bulimia nervosa (17.4% lifetime comorbidity) than in controls. Panic disorder, social phobia, specific phobias, generalized anxiety disorder (GAD), and posttraumatic stress disorder (PTSD) significantly contribute to comorbidity. Lifetime comorbidities have been reported at approximately 17.4% for OCD, 16.2% for panic disorder, 41.3% for social phobia, 50.1% for specific phobias, 11.8% for GAD, and 45.4% for PTSD.
  • One study suggests that baseline clinical predictors such as female gender and family history of eating disorders might be specific to the later development of eating disorders in the context of childhood OCD.[30]
  • Substance use disorders: Some evidence suggests a relationship between disorders of substance abuse and dependence and bulimia nervosa, including alcohol dependence[31] , nicotine dependence[32] , and drug dependence[33] . Studies on caffeine intake are mixed.[34] Alcohol abuse or dependence has a lifetime comorbidity with bulimia nervosa of 33.7%, whereas illicit drug abuse or dependence has a lifetime comorbidity of 26%.
  • Impulse control disorders: In a study of lifetime prevalence of impulse control disorders in patients with bulimia nervosa, compulsive buying and intermittent explosive disorder were the most frequently reported disorders, at 17.6% and 13.2%, respectively. Higher than expected rates of kleptomania, pathological gambling, and trichotillomania have also been reported in patients with bulimia nervosa.[35]
  • Attention deficit hyperactivity disorder (ADHD): ADHD may be associated with bulimia.[36] In one study of more than 2,000 female inpatients treated for bulimia nervosa, 9% were also diagnosed with ADHD. The average rate of ADHD in the general population of young women is approximately 3.4%.[37] Lifetime comorbidity with ADHD and bulimia nervosa has been reported to be as high as 34.9%.
  • Other psychopathology: The role of sexual abuse in the development of eating disorders is controversial.[38] Some reports suggest a strong association, while others detect no increased association. Borderline personality disorder is found frequently.[39] These patients usually have histories of trauma and abuse and may represent a distinct subgroup. Pathologic narcissism[40] and identity impairment[41] may be present. Features of obsessive compulsive personality disorder (OCPD), particularly perfectionism, may be increased among patients with bulimia nervosa.

Suicidal behavior

Bulimia nervosa is associated with increased risk of suicide attempts and suicidal ideations.[42] In one study, all-cause mortality rate for bulimia nervosa was 3.9%, higher than other reported studies in the past.[43] However, the standardized mortality ratio with respect to suicide was 6.51, a much higher than expected rate.

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Physical

Although patients with bulimia nervosa are often unremarkable in general appearance and frequently have no signs of illness on physical examination, several characteristic findings may occur.

  • Physical findings may include the following:
    • Bilateral parotid enlargement, largely consequent to noninflammatory stimulation of the salivary glands, may be seen.[44] See parotid gland swelling in following image. Parotid hypertrophy. Reprinted with permission froParotid 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.
    • In patients with significant self-induced vomiting, erosions of the lingual surface of the teeth, loss of enamel, periodontal disease, and extensive dental caries may be observed, as in the following image.[45] Dental caries. Reprinted with permission from WolcDental 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 (one of the few physical examination findings in psychiatry) manifests as callosities, scarring, and abrasions on the knuckles secondary to repeated self-induced vomiting.[46] Russell sign. Reprinted with permission from GloriRussell 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.
    • Other cutaneous manifestations can include telogen effluvium (sudden, diffuse hair loss), acne, xerosis (dry skin), nail dystrophy (degeneration), and scarring resulting from cutting, burning, and other self-induced trauma.[47]
    • Other nonspecific but suggestive findings that may reflect the severity of the disease include bradycardia or tachycardia, hypothermia, and hypotension (often associated with dehydration). Edema, particularly of the feet (and less commonly the hands), is found more often among patients with a history of diuretic abuse, laxative abuse, or both or in patients with significant protein malnourishment causing hypoalbuminemia.
    • Some patients may be clinically obese, but morbid obesity is rare. Patients with bulimia nervosa who are overweight may have excessive fat folds that favor humidity and maceration with bacterial and fungal overgrowth, striae due to skin overextension, stasis pigmentation related to peripheral vascular disease, and plantar hyperkeratosis due to increased weight.[47]
  • A typical Mental Status Examination for a patient with bulimia nervosa is detailed below. (The formal Folstein Mini-Mental Status Examination [MMSE] is usually unnecessary in the evaluation of patients with bulimia nervosa because symptoms of dementia and delirium are not common in these patients.)
    • Appearance: Patients are typically neat, well dressed, and show attention to detail. Grooming is often meticulous and may further demonstrate a patient's concern about personal appearance.
    • Behavior: Patients usually do not have kinetic abnormalities, but anxious feelings may heighten psychomotor agitation. Movements are spontaneous, and patients generally are cooperative and able to carry out requested tasks.
    • Cooperation: Patients generally avoid eye contact due to shame and embarrassment.
    • Mood and affect: Patients often demonstrate a depressed mood but may also have significant anxiety.
    • Speech: Content and articulation are generally normal.
    • Thought process: Patients likely have a linear thought process that is goal-directed.
    • Thought content: Thoughts tend to revolve around food and concerns regarding body image and weight.
    • Perceptual disturbances: Delusions and hallucinations are typically absent.
    • Suicidal ideation: Suicidal ideation is a significant consideration, especially in patients with depressed moods. Although suicidal ideation is often restricted to thoughts rather than concrete plans, suicidal thinking should be taken very seriously.
    • Homicidal ideations: Homicidal ideation is not typically associated with those diagnosed with bulimia nervosa.
    • Cognition: Patients are generally alert, and oriented to their surroundings. Attention and concentration typically measured by serial sevens and digit span are generally normal. Immediate memory is normal, as is recent and remote memory recall. Intellect is usually judged as normal, and in some cases, intellect ability may surpass average. Capacity to read and write is within normal limits. Visuospatial functions are also intact.
    • Judgment: Patients generally demonstrate poor judgment regarding self care and treatment. Weight-reducing strategies such as induced vomiting, laxative, and diuretic ingestion are often perceived as legitimate and appropriate methods of weight management.
    • Insight: Insight regarding the presence and significance of disturbances is variable. While patients typically admit to episodes of binge eating, they often do not appreciate their inappropriate fixation on eating or their distorted ideas of body image and weight.
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Causes

Some factors identified as playing potentially important roles in etiopathogenesis are as follows:

Biological factors[48, 49, 50]

  • Neurotransmitters
    • Serotonin: Serotonin is possibly closely related to weight regulation and eating behaviors. There have been documented cases of elevated serotonin in the cerebral spinal fluid in patients with anorexia nervosa and bulimia nervosa.
    • Norepinephrine: Lower levels of serum neurotransmitter are typically thought to be associated with anorexia nervosa.
    • Dopamine: Dopamine activity is thought to be associated with distortion of body image, and a 7 repeat allele of the D4 receptor gene is thought to be associated with both bulimia nervosa and binge eating. This 7 repeat allele is thought to possibly be involved with weight gain in patients with bulimia nervosa.
  • Hormonal: Although many reported abnormalities in bulimia nervosa may reflect consequences of binge eating and purging rather than causal factors, complex irregular interactions exists between orexigenic factors such as neuropeptide Y (NP-Y), peptide Y (PYY), and anorectic factors such as cholecystokinin (CCK) and beta-endorphin. Patients with active bulimia nervosa have normal NP-Y and PYY levels, which do increase after successful treatment. Patients with anorexia nervosa, on the other hand have elevated levels of NP-Y and lower levels of PYY (therefore, less orexigenic peptide action). Furthermore, people with bulimia nervosa have reduced beta-endorphin, normal dynorphin, and low CCK levels.
  • Genetics: Although no definitive inheritance patterns have been identified, a familial component appears to be involved in the development of eating disorders. Patterns of transmission involving monozygotic and dizygotic twins suggest genetic contributions in both anorexia nervosa and bulimia nervosa. There have been proposed genetic links at chromosomes 1, 3, and 10p related to bulimia nervosa. Genome-wide association studies are currently ongoing to further explore this association. Unfortunately, studies to date have been small with poor power. Chromosome 10p may also be linked with obesity in addition to bulimia nervosa.

Developmental factors

Developmental factors include childhood anxiety, (eg, difficulties separating from caretakers).[51] History of childhood trauma and neglect, including subtle degrees of psychological abuse, teasing, and other interactions that generate self-doubt may increase vulnerability.

Psychological factors

Among psychological factors suggested are difficulties with self-esteem, affective self-regulation, impulsivity, perfectionism, body image distortion, susceptibility to triggers of a binge-purge cycle (which may occur around dieting and weight loss), and poor coping skills.

Sociocultural factors

Among the potential precipitating events for a binge/purge cycle in those with bulimia nervosa are anxiety states, emotional tension, boredom, environmental cues about food and eating, alcohol use, substance abuse, and exhaustion. For patients who severely restrict their usual food intake, hunger may precipitate an eating binge (in an “all or none” fashion). Excessive concerns about physical appearance, body image and thinness seem central to both anorexia nervosa and bulimia nervosa.

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Contributor Information and Disclosures
Author

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, and American Psychiatric Association

Disclosure: Nothing to disclose.

Coauthor(s)

Lorin M Scher, MD  Health Sciences Assistant Clinical Professor, Department of Psychiatry and Behavioral Sciences, University 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, and Association for Academic Psychiatry

Disclosure: Nothing to disclose.

Donald M Hilty, MD  Professor of Clinical Psychiatry, Vice-Chair of Faculty Development, Department of Psychiatry and Behavioral Sciences, University of California, Davis School of Medicine

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

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

Disclosure: Gurze publishers Salary editing; Massachusetts Medical Society Salary Writing

Specialty Editor Board

Sarah C Aronson, MD  Associate Professor, Departments of Psychiatry and Medicine, Case Western Reserve School of Medicine/University Hospitals of Cleveland

Sarah C Aronson, MD is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, and American Psychiatric Association

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

Harold H Harsch, MD  Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin

Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association

Disclosure: lilly Honoraria Speaking and teaching; Forest Labs None None; Pfizer Grant/research funds Speaking and teaching; Northstar None None; Novartis Grant/research funds research; Pfizer Honoraria Speaking and teaching; Sunovion Speaking and teaching; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research; Merck Honoraria Speaking and teaching

Chief Editor

David Bienenfeld, MD  Professor of Psychiatry, Vice-Chair and Director of Residency Training, Department of Psychiatry, Wright State University, Boonshoft School of Medicine

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

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors Gabriel I Uwaifo, MBBS and Robert C Daly, MB, ChB, MPH to the development and writing of this article.

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.
Table. Self-Help Books and Internet Resources on Eating Disorders
CBT-oriented workbooksAgras WS, Apple RF: Overcoming Eating Disorders: A Cognitive-Behavioral Treatment for Bulimia Nervosa and Binge-Eating Disorder. New York, Oxford University Press, 1997 (client workbook)
Agras WS, Apple RF: Overcoming Eating Disorders: A Cognitive-Behavioral Treatment for Bulimia Nervosa and Binge-Eating Disorder. New York, Oxford University Press, 1997 (therapist workbook)
Cash TF: The Body Image Workbook: An 8-Step Program for Learning to Like Your Looks. Oakland, CA, New Harbinger, 1997
Fairburn C: Overcoming Binge Eating. New York, Guilford, 1995
Goodman LJ, Villapiano M: Eating Disorders:The Journey to Recovery Workbook. New York, Brunner-Routledge, 2001 (client workbook)
Goodman LJ, Villapiano M: Eating Disorders: Time for Change. Plans, Strategies, and Worksheets. New York, Brunner-Routledge, 2001 (therapist workbook)
Schmidt U, Treasure J: Getting Better Bit(e) by Bit(e): A Survival Kit for Sufferers of Bulimia Nervosa and Binge Eating Disorder. East Sussex, UK, Psychology Press, 1993
Other books reported to be helpful by patients/familiesBulik CM, Taylor N: Runaway Eating: The 8-Point Plan to Conquer Adult Food and Weight Obsessions. New York, Rodale Books, 2005
Ellis A, Abrams M, Dengelegi L: The Art and Science of Rational Eating. Fort Lee, NJ, Barricade Books, 1992
Goodman LJ, Villapiano M: Eating Disorders: The Journey to Recovery Workbook. New York, Brunner-Routledge, 2001 (client workbook)
Hall L: Full Lives: Women Who Have Freed Themselves From Food and Weight Obsessions. Carlsbad, CA, Gürze Books, 1993
Lock J, le Grange D: Help Your Teenager Beat an Eating Disorder. New York, Guilford, 2005
Michel DM, Willard SG: When Dieting Becomes Dangerous. New Haven, CT, Yale University Press, 2003
Walsh BT, Cameron VL: If Your Child Has an Eating Disorder: An Essential Resource for Parents. New York, Guilford, 2005
Zerbe K: The Body Betrayed: A Deeper Understanding of Women, Eating Disorders, and Treatment. Carlsbad, CA, Gürze Books, 1995
Books reported to be helpful for male patientsAndersen AE, Cohn L, Holbrook T: Making Weight: Men's Conflicts With Food, Weight, Shape and Appearance. Carlsbad, CA, Gürze Books, 2000
Internet resources for health care professionalsAcademy for Eating Disorders (http://www.aedweb.org)
Internet resources for patients, families, and professionalsNational Eating Disorders Association (http://www.nationaleatingdisorders.org)National Association of Anorexia Nervosa and Associated Disorders (http://www.anad.org/site/anadweb/)
Eating Disorder Referral and Information Center (http://www.edreferral.com)
Something Fishy (http://www.something-fishy.org; a well-monitored advocacy site)
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