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Bulimia nervosa: Easy to hide but essential to recognize

Ashamed of their behavior, patients with this disorder are more likely to present with vague complaints related to their compensatory weight control practices.

Danielle Kruger, BS, RPA-C

Danielle Kruger is academic coordinator and medicine instructor, Saint John’s University Physician Assistant Program, Fresh Meadows, New York. She has indicated no relationships to disclose relating to the content of this article.

Eating disorders are behavioral patterns that develop within a broad spectrum of emotional, biological, and sociocultural characteristics. Bulimia nervosa, one of the most common and highly secretive of these disorders, is characterized by compulsive eating binges followed by compensatory efforts to purge calories and avoid weight gain.1 This unremitting preoccupation with food and weight control overshadows an underlying psychological struggle with self-image, self-esteem, body satisfaction, and an attempt to maintain personal autonomy and self-discipline. Associated physiologic changes make bulimia a potentially life-threatening condition, especially in persons who present covertly or with apparently unrelated problems. The PA must act as a detective with a high index of suspicion in order to recognize the risk factors, identify psychiatric comorbidities, and provide initial management and referral. The patient with bulimia is best managed by a collaborative, interdisciplinary team of medical providers, mental health professionals, and dietitians who have experience treating eating disorders.

EPIDEMIOLOGY AND ETIOLOGY

Bulimia nervosa has a predominantly female gender predilection approximating 90% to 95% in community-based studies.2,3 The prevalence of this disorder is estimated to be 1% for women and 0.1% for men across western Europe and the United States.3,4 Males affected by bulimia commonly participate in sports that have a weight or body fat requirement, such as wrestling, horse racing, and bodybuilding. Onset usually occurs in adolescence and young adulthood and peaks at age 18 years, but symptoms can begin at any age.2 Eating disorders are more common in whites than in other races, and in industrialized countries. Ashamed of their lack of control, which manifests as a disordered, uncontrolled eating pattern, patients are not likely to admit their problem. Thus, common screening and prevalence estimates may be falsely low.

Cognitive, sociocultural, familial, and environmental factors contribute to the etiology and perseverance of bulimic behaviors (see Table 1). Cognitive models suggest that bulimic activity is precipitated by negative thought patterns and cognitive bias surrounding body image, sadness, and interpersonal problems,3 resulting in cyclical swells of stress and anxiety that further reinforce the binge-purge cycle. Altered physiology and genetics may also play a role. Researchers found that patients with bulimia have impaired satiety, a decreased resting metabolic rate, and abnormal neuroendocrine regulation2 (see Table 2). Identifying and shaping the dynamic puzzle of etiologic factors poses challenges for the clinician and justifies the importance of cognitive-behavioral therapy (CBT), pharmacotherapy, and a multidisciplinary team approach to managing patients.

The prevalence of a coexisting psychiatric disorder in patients with bulimia is approximately 75%; and in most cases, the coexisting disorder precedes the eating disorder5 (see Table 3). Identifying these comorbid conditions is of major clinical and therapeutic importance because they are associated with an increased incidence of attempted suicide, theft, drug and alcohol abuse, and sexual promiscuity.2 Early and effective treatment of coexisting psychiatric disorders in patients with bulimia nervosa promotes a sense of assertiveness, ameliorates depression and anxiety to manageable levels, and increases the efficacy of bulimia treatment.

DIAGNOSIS AND SCREENING

The American Psychiatric Association diagnostic criteria for bulimia nervosa include (1) recurrent episodes of binge eating characterized by consuming more food within a certain time period than most people would in a similar situation or a perceived lack of control during an episode of binge eating; (2) recurrent inappropriate compensatory behavior used to prevent weight gain; (3) binge eating and inappropriate compensatory behavior cycles averaging at least two occurrences a week for 3 months; and (4) self-evaluation unduly influenced by body shape and weight.6 In addition, this behavior must not occur exclusively during episodes of anorexia nervosa.6 Bulimic behaviors are classified as the purging type if the person regularly engages in self-induced vomiting or misuse of laxatives, diuretics, or enemas; and as the nonpurging type if restricted diet, vigorous exercise, or other compensatory behaviors are used.2 Patients may alternate between purging and nonpurging behaviors. Fluctuations in weight are common in patients with bulimia. Patients are usually average or slightly below-average weight, but they may be underweight, overweight, or even obese.5

Considerable overlap exists between the characteristics and clinical presentations of the various eating disorders. The differential diagnosis includes anorexia nervosa, binge-eating disorder, and eating disorders not otherwise specified. Binge eating may occur in any of these disorders; however, anorexia is more characterized by the practice of starvation. Other disorders that may mimic bulimia include upper GI disorders, atypical depression, Klein-Levin syndrome, and Kluver-Bucy syndrome.

The Eating Attitudes Test (EAT-26) is one of the most widely used standardized screening tools to measure the symptoms and concerns characteristic of eating disorders (available at http://studenthealth.missouri.edu/EatingAttitudesTest.doc). EAT-26 was used in the 1998 National Eating Disorders Screening Program, which recommended that patients with a score of 20 points or higher be referred for a diagnostic interview. Other screening tools include the Bulimia Test, the SCOFF questionnaire, and the Eating Disorders Inventory-2.

CLINICAL MANIFESTATIONS

The binge-and-purge cycle characteristic of bulimia nervosa is intimately linked to emotional turmoil, as well as to self-image, and is often provoked by feelings of anxiety, guilt, loneliness, stress, depression, and/or anger. These emotions may be relieved with binging; but after purging, they are replaced with self-criticism and culpability over repeatedly falling victim to the cycle. Before purging, patients may report feeling fat or believe that they have consumed too much food at one time. Binges also can be precipitated by dieting. Caloric restriction leads to increased hunger and stimulates a binge-eating episode. Patients may feel out of control during binges, are usually unaware of hunger, and do not stop eating when satiated.1

Binges vary in frequency and duration. The quantity of food consumed differs per episode but is always large. Most episodes occur spontaneously, but some are planned. Patients report eating sweet, high-calorie, and high-fat “junk foods” they ordinarily deny themselves. The patient will avoid eating with others, skip meals, change dietary preferences, and have an excessive desire for privacy after meals.7 Family members may notice episodic disappearances of large amounts of food and find the wrappers or containers in the garbage.

Binge episodes are commonly compensated for with self-induced vomiting. Patients may stimulate their gag reflex or use an emetic such as ipecac; however, many eventually do not need chemical or mechanical stimulants and can simply vomit at will.1 Patients eat soft foods cut into small pieces or drink large amounts of fluid to facilitate vomiting. Another purging method is the overuse of diet pills, laxatives, or thyroid medications that prevent weight gain. Patients also need to be screened for the use of natural medicines or herbal supplements. These products may contain substances that increase BP or promote electrolyte imbalance.2 Nonpurging patients compensate by alternating binges with long periods of fasting and excessive exercise.

Patients with bulimia often present to their clinician with vague complaints related to their compensatory behaviors.2 Frequent regurgitation of acidic gastric contents and vitamin deficiency may cause dental problems that help distinguish the patient with bulimia nervosa to the dental professional. These problems include tooth enamel erosion, painless enlargement of the parotid salivary glands, dry mouth, decalcification, dental sensitivity, increased cavities, sore throat, and periodontal disease.3 Russell’s sign manifests as a callus or abrasion on the dorsum of the index and middle fingers of the patient’s dominant hand. The condition is caused by repetitive contact with the teeth during self-induced vomiting and is seen in 27% of patients with bulimia.2

Bulimia nervosa also presents a challenge for the obstetric-gynecologic clinician. Weight fluctuations, nutritional deficiency, and stress cause menstrual irregularities. As opposed to persons with anorexia, few bulimic patients experience long-term amenorrhea and generally maintain normal sexual activity.3 Symptoms improve during pregnancy, but few patients recover completely. Many patients with bulimia experience pregnancy complications including miscarriage and premature labor. These patients also have problems feeding and meeting the nutritional needs of their infants.3

COMPLICATIONS

Bulimia nervosa can cause potentially life-threatening metabolic derangements and traumatic injury from forceful, repetitive vomiting. Almost half of patients with severe bulimia demonstrate electrolyte abnormalities including dehydration.3 Hypokalemia can be a sign of recent purging.3 It may coexist with hypochloremic metabolic alkalosis in patients who purge through vomiting and diuretics and coexist with a hyperchloremic metabolic acidosis in those who abuse laxatives. Muscle weakness and cramping, syncope, seizures, cardiac dysrhythmias, or cardiac arrest herald severe metabolic disturbances. Life-threatening cardiomyopathy is associated with the abuse of ipecac. Hypertension in patients with bulimia should raise suspicion of stimulant abuse,2 which has been associated with cerebral hemorrhage.

Chronic vomiting and poor nutrition put the patient with bulimia nervosa at risk for several gastroenterologic problems, including reflux esophagitis, delayed gastric emptying, peptic ulcer disease, irregular bowel movements, pancreatitis, gastric perforation, and hematemesis. Forceful esophageal pressure may result in Mallory-Weiss tears or esophageal rupture characteristic of Boerhaave syndrome. Initial assessment of abdominal pain in bulimic patients involves an upright chest radiograph to evaluate for gastric rupture or pneumomediastinum and serum lipase to screen for pancreatitis. Serum amylase levels are not specific for pancreatitis in patients with bulimia; levels are often elevated because of parotid gland overstimulation.2 Abdominal CT, gastric motility tests, and endoscopy also may be required if further workup is needed.

DIAGNOSTIC ASSESSMENT

Electrolyte measurements and ECG evaluation of electrolyte-related conduction changes are crucial when assessing patients suspected of having bulimia nervosa. A hypochloremic metabolic alkalosis with low potassium and magnesium levels—caused by chronic vomiting—supports a diagnosis of bulimia.2 Diuretic abuse causes decreased sodium, potassium, and magnesium levels with elevated uric acid and calcium levels. Drug screening is recommended because of the high incidence of comorbid substance abuse. In severe cases, liver, thyroid, and renal function should be assessed. Hypercholesterolemia is found in approximately 50% of patients with bulimia.3

For the patient with bulimia presenting with secondary amenorrhea, evaluation begins with a urine pregnancy test and luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, prolactin, and total and free testosterone level measurements. A progesterone challenge test that produces withdrawal bleeding 2 to 7 days after treatment indicates sufficient estrogen levels.8

MULTIDISCIPLINARY TREATMENT

A team approach that involves patients in their care is optimal. Patients should be encouraged to participate in establishing target goals and managing their condition. Most patients with bulimia nervosa can be treated as outpatients. Hospital admission to a specialized eating disorders unit is recommended for those with severe complications, marked dehydration, laboratory or ECG evidence of electrolyte imbalance, family crisis, severe depression, psychosis, current substance abuse behavior, or suicidal ideation.3 The inpatient setting also offers meal supervision with controlled access to the bathroom for 2 hours after meals. In addition, electrolytes, weight, physical activity, psychological state, and nutritional status can be closely monitored.

Bulimia treatment usually involves a combination of cognitive-behavioral therapy, pharmacotherapy, nutritional education, stress-reduction techniques, and group and family therapy. Psychiatric consultation is required for all patients suspected of having an eating disorder. Evidence-based reviews demonstrate that individual CBT reduces purging behavior.3 An important aspect of treatment, CBT helps patients restructure cognitive processes by interrupting the cycle precipitated by low self-esteem, body-image concern, perfectionism, mood changes, and interpersonal deficits.3 Patients develop a self-awareness of their interactions with food, learn to identify binging triggers, and find alternatives to purging. Patient education also includes the dangers of bulimic behavior and how to develop healthy coping strategies.

Interpersonal therapy focuses on the management of role disputes and role transitions and resolution of interpersonal deficits. Emotionally based family therapy aids patients in developing autonomy from their families without severing those connections.3 Patients may also benefit from self-help materials or recovery groups, such as Overeaters Anonymous and Eating Disorders Anonymous. A registered dietician should work with the patient to develop a healthy dietary plan that includes vitamin and mineral supplements. Dieticians also can educate patients about food choices and preparation. Each clinician involved in the patient’s treatment should take care to reinforce the concepts of the collective goals of the treatment plan.

Pharmacotherapy targets predominant biochemical abnormalities associated with bulimia nervosa (see Table 4). In 26 randomized controlled trials, pharmacotherapy reduced anxiety, depression, eating-disorder psychopathology, and binge-purge frequency compared to placebo.3 Antidepressants are effective in treating bulimia and preventing relapse; full therapeutic doses should be maintained for at least 1 year. Selective serotonin reuptake inhibitors are preferred because they have a better side-effect profile and are associated specifically with mood regulation and satiety.

In a 12-week trial, both fluoxetine (Prozac, Sarafem) 60 mg/d plus CBT and CBT alone led to fewer binge-purge episodes than did fluoxetine 60 mg/d alone.4 Similar results were demonstrated in trials with CBT plus tricyclic antidepressants and CBT plus multiple medications. In addition, both nutritional and anxiety-stress management counseling significantly reduces bulimic cycles.

PROGNOSIS AND PREVENTION

The prognosis of patients with bulimia nervosa is variable. One retrospective study of eight female US college students postulated that the majority of patients with bulimia migrate toward atypical eating disorders or remission and that relatively few develop anorexia nervosa.3 Studies identify five prognostic factors that have a similar predictive direction.3 Early progress during therapy and self-directedness are factors that predict a positive response to therapy; lower body mass index at outset, history of childhood obesity, and depression are factors that predict a negative response to therapy. A number of large, long-term follow-up studies of treated and untreated patients cite remission rates ranging from 41% to 70%.3

Children and adolescents should routinely be screened for symptoms of eating disorders, weight dissatisfaction, moodiness, and risk-taking behaviors at primary-care appointments.1 Effective prevention strategies involve the patients and their parents and focus on the context of family and society. Nutritional and general wellness education should be extended to both patients and their families to help prevent unhealthy eating patterns and excess weight gain.

If a patient wants to diet, ask about motivation for losing weight and weight and general health goals, and offer education on nutrition and how to lose weight safely. Education about body weight regulation and the effects of starvation, vomiting, and laxative overuse on the body may be helpful. Patients can also be directed to several online sources of information (see Table 5).

CONCLUSION

The PA plays an imperative role in the diagnosis and management of bulimia nervosa, including recognizing the risk factors, identifying psychiatric comorbidities, and providing initial management and referral. The multifactorial nature of this eating disorder—the struggle with self-esteem, body shape, and autonomy—justifies the need for an interdisciplinary team approach involving medical providers, mental health professionals, and dietitians with experience in treating eating disorders.

REFERENCES

 

1.

Mayo Foundation for Medical Education and Research. Bulimia nervosa. http://www.mayoclinic.com/health/bulimia/DS00607. Published March 13, 2006. Accessed December 5, 2007.

 

2.

Foster T, Smith-Coggins, R. Bulimia. emedicine from WebMD Web site. http://www.emedicine.com/emerg/topic810.htm. Updated February 2, 2007. Accessed December 5, 2007.

 

3.

Bulimia nervosa: efficacy of available treatments. Evidence report. ECRI Health Technology Assessment Information Services. http://www.bulimiaguide.org/summary/detail.aspx?v=1&lid=459&doc_id=9443. Published January 2006. Accessed December 5, 2007.

 

4.

Shapiro JR, Berkman ND, Brownley KA, et al. Bulimia nervosa treatment: a systematic review of randomized controlled trials. Int J Eat Disord. 2007;40(4):321-336.

 

5.

Brewerton TD, Lydiard RB, Herzog DB, et al. Comorbidity of axis I psychiatric disorders in bulimia nervosa. J Clin Psychiatry. 1995;56(2):77-80.

 

6.

Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision; DSM-IV-TR. Washington, DC: American Psychiatric Association; 2000.

 

7.

deBenedictis T, Jaffe J, Segal R, Segal J. Bulimia: signs, symptoms, effects, treatment, and support. Helpguide.org Web site. http://www.helpguide.org/mental/bulimia_signs_symptoms_causes_treatment.htm. Updated January 25, 2007. Accessed December 5, 2007.

 

8.

Seidenfeld ME, Rickert VI. Impact of anorexia, bulimia and obesity on the gynecologic health of adolescents. Am Fam Physician. 2001;64(3):445-450. http://www.aafp.org/afp/20010801/445.pdf. Accessed December 5, 2007.







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