Bulimia Nervosa

Etiology

The precise etiology of bulimia nervosa is unclear but is likely multifactorial. The abnormalities in interoceptive function, particularly of the insula, may contribute to the binging behavior associated with this condition. A 2016 study indicated that patients with anorexia and bulimia nervosa have widespread abnormalities with diffuse alterations in white matter structural and useful connectivity, particularly within appetite-regulating and taste-reward pathways. Other studies have indicated a possible altered function of intrinsic functional brain architecture.[4]

Epidemiology

Bulimia nervosa can affect both sexes but disproportionately affects females. The median age of onset is around 12.4 years old. The estimated prevalence of bulimia nervosa in the United States is 0.9% among adolescents, 1.5% among the general population of women, and 0.5% among the general population of men. While the prevalence of bulimia nervosa is unestablished in developing countries, prevalence estimates from North America, Australia, and Europe range from 0.1% - 1.3% among males and 0.5% - 2.0% among females.[5]

History and Physical

A review of systems in patients with bulimia nervosa demonstrates sore throat, irregular menstruation, constipation, headache, fatigue, lethargy, abdominal pain, and bloating.

When conducting a physical exam on a patient with diagnosed or suspected bulimia nervosa, obtain the height, weight, vital signs, and orthostatic blood pressures. It is also necessary to examine a patient’s skin, mouth, and abdomen. A neurological examination is essential to check for primary neurological causes of weight loss or vomiting before diagnosing bulimia nervosa.[6]

Common physical exam signs associated with bulimia nervosa include hypotension, dry skin, parotid gland swelling, dental erosion, and calluses on the dorsal aspect of the hand (known as “Russel’s sign.”) Bulimia nervosa can also be associated with hair loss, edema, and epistaxis.[6]

Evaluation

A thorough evaluation of a patient with bulimia nervosa should include the following:[7]

• A comprehensive metabolic panel, including electrolytes, liver function tests, blood urea nitrogen, serum creatinine, and calcium.
• Complete blood count with differential. Consider obtaining a vitamin B12 level.
• Urinalysis.
• If severe, also obtain serum magnesium and phosphorous as well as the electrocardiogram.
• Female patients should undergo a pregnancy test. Female patients with secondary amenorrhea should have testing for luteinizing hormone, prolactin, beta-HCG, and a follicle-stimulating hormone to assess for other potential contributors to amenorrhea.
• Lab tests are available to test for stool or urine bisacodyl, emodin, aloe-emodin, and rhein. However, a positive test for a stool or urine laxative is not necessary to establish the diagnosis.

Laboratory abnormalities associated with bulimia nervosa include hypokalemia (including hypokalemic hypochloremic metabolic alkalosis), hyponatremia, and transaminitis.

Treatment / Management

The primary objective of treatment is a cessation of the binging and purging behavior.[7](A1)

Selective serotonin reuptake inhibitors such as fluoxetine, citalopram, and sertraline have shown to reduce symptoms of bulimia nervosa. Fluoxetine is the only FDA approved medication for bulimia nervosa. It appears that a higher dose (60 mg) is significantly better than a placebo in decreasing the frequency of binge and vomiting episodes.[8] Evidence for other medication classes to treat this condition is limited.[9] Trazodone has significantly reduced the frequency of binge-eating episodes when compared to placebo.[10] Monoamine oxidase inhibitors and tricyclic antidepressants are reserved for resistant cases due to their lethality and potential side effects. Bupropion should not be used in patients with bulimia nervosa because of the increased risk of epileptic episodes.[11] One of the antiepileptic medications, topiramate, has shown a reduction in binge episodes, but the side effects should be carefully monitored, especially weight loss and cognitive problems.[12] (A1)

Clinical trials of cognitive-behavioral therapy and interpersonal psychotherapy have also demonstrated a benefit for patients with bulimia nervosa.[13] Patients with bulimia nervosa should be screened for suicidality and comorbid psychiatric illness as they are at higher risk of other mental diseases than the general population.

Bulimia nervosa can lead to a variety of general medical complications, including metabolic alkalosis, dehydration, constipation, and cardiac arrhythmias. The most common cause of metabolic alkalosis in patients with bulimia nervosa is fluid volume depletion, for which saline administration is indicated in addition to the cessation of the purging behavior. For inpatients, consider intravascular administration; however, these patients require monitoring for signs of volume overload. The treatment for dehydration associated with bulimia nervosa is similar. In the uncommon cases of average or increased fluid volume with alkalemia in a patient with bulimia nervosa, intravenous saline has no role. Treatment for constipation associated with bulimia nervosa or with discontinuation of laxatives include adequate hydration, exercise, and dietary fiber. If laxatives are still needed, low doses of polyethylene glycol powder or lactulose may be used. For patients who experience severe or symptomatic cardiac complications of bulimia nervosa, which are generally caused by electrolyte derangements, consider obtaining a cardiology consult.

Differential Diagnosis

The clinician should make a diagnosis of bulimia nervosa after excluding all other medical causes of vomiting and excessive bowel activity, particularly if the patient states that binging or purging behavior is involuntary. Generally, these medical conditions are not associated with a pattern of binge eating or an excessive preoccupation with weight or body image. These medical conditions include the following:

• Biliary disease can cause nausea and vomiting, and it will frequently present with abnormal transaminases or bilirubin on a comprehensive metabolic profile.
• Irritable bowel syndrome can increase the frequency of bowel movements but is usually not associated with episodes of binge eating.
• Neurological conditions, a thorough evaluation should include a neurological examination to rule out a neurological origin for vomiting.

General medical conditions involving increased food intake include the following:

• Prader-Willi syndrome- This is a genetic disorder that can present with hyperphagia and obesity. It is usually associated with mental disability and hypogonadism, angry outbursts, and oppositional behavior. Compensatory purging behavior is typically absent.
• Klein-Levin syndrome- This is a disorder that primarily affects adolescent males and also causes increased appetite, hypersomnia, and behavioral disturbances. As with Prader-Willi syndrome, compensatory purging behavior is not present in this condition.
• Diabetes mellitus- This is a well-established cause of polyphagia. A complete medical workup should check blood glucose.
• Anorexia nervosa- It is essential to distinguish bulimia nervosa from anorexia nervosa because the complications, management, and prognosis of each condition are different. The patient has anorexia nervosa and not bulimia nervosa if binging or purging occurs exclusively during episodes of anorexia nervosa, which includes a binge-eating/purging type. An important distinction is that a diagnosis of anorexia nervosa requires low body weight; BMI<18, whereas this is not a diagnostic criterion for bulimia nervosa. Studies have shown minimal benefits of psychotropic medication for the treatment of anorexia nervosa.
• Binge eating disorder- It is also characterized by episodes of binge eating. However, binge eating disorder does not have the purging behavior, as seen in bulimia nervosa. Patients with bulimia nervosa typically restrict their diet between binge eating episodes to influence their body shape. In contrast, those with binge eating disorder do not limit their intake in between events.
• Major depressive disorder and borderline personality disorder- These may also present with episodes of overeating and with suicidal ideations. However, these conditions do not feature the inappropriate compensatory purging behavior of bulimia nervosa, although both of these conditions can be comorbid with bulimia nervosa.

Prognosis

Most patients who have bulimia nervosa will recover from the condition.

The five-year remission rate for bulimia nervosa using DSM-IV criteria has an estimate of 74%, and among those, 47% also had a relapse within those five years. Another study based on DSM-V criteria listed a 55% five-year recovery rate for bulimia nervosa in the community. At ten years, 52% of patients with bulimia nervosa treated with placebo had fully recovered.

Bulimia nervosa is proven to be associated with an increase in all-cause mortality.[14][15]

Complications

Bulimia nervosa is a psychiatric disorder that can lead to potentially critical complications. Unlike in anorexia nervosa, in which complications are due to weight loss and malnutrition, the type and severity of medical complications of bulimia nervosa can be determined based on the frequency and the method the patient uses to purge.[16]

Complications associated with bulimia nervosa include the following:[7][17][18]

• Salivary gland hypertrophy (sialadenosis) and swollen cheeks - typically in the parotid gland but also has been recorded to cause swelling of the submandibular salivary gland.[6][19]
• Mallory-Weiss syndrome (mucosal and submucosal esophageal tears near the gastroesophageal junction) - at times preceded by gastroesophageal intussusception, caused by forceful contraction of the stomach when a patient vomits. Mallory-Weiss tears can develop into Boerhaave’ syndrome (esophageal rupture)
• GERD - gastroesophageal reflux disease, which can increase the risk of Barrett’s esophagus.[20][21]
• Barrett’s esophagus - a condition in which abnormal columnar mucosa replaces normal squamous cell mucosa as a result of irritation of the tissue by gastric acid. It possibly increases the risk of developing esophageal cancer, although there is only limited evidence for a causal link.
• Laryngopharyngeal reflux - the movement of gastric contents back into the laryngopharynx can manifest as coughing, hoarse voice, sore throat, and dysphagia.[6][19]
• Irritable bowel syndrome (IBS) - one study found that among patients with bulimia nervosa, the prevalence of IBS was about 69%[22]
• Achalasia - the inability of lower esophageal muscles to relax
• Esophageal spasm - irregular contractility of esophageal muscles
• Cardiac arrhythmia - can be caused by hypokalemia due to self-induced vomiting. Hypokalemia can contribute to QTc prolongation. Furthermore, abuse of ipecac is associated with other cardiac complications, including congestive heart failure and death.
• Constipation - chronic abuse of stimulant laxatives, which include senna, cascara, phenolphthalein, or bisacodyl, can result in cathartic colon syndrome.[6][17]
• Dental enamel erosion - result from gastric acid washing over teeth. Exposure of enamel to gastric acid increases the risk of tooth erosion, particularly on the occlusal (“biting”) surfaces of the teeth but can also extend to the buccal-facing and palate-facing surfaces of molars. Gingival recession may also occur for the same reason.
• Rectal prolapse - case reports of rectal prolapse in women with bulimia nervosa are available. The hypothesis is that this is due to constipation or elevated intra-abdominal pressure associated with vomiting.
• Recurrent acute pancreatitis has been documented in several cases of bulimia nervosa, although a single direct mechanism has not been established.
• Diabetes - a meta-analysis of ten studies found that bulimia nervosa was associated with a relative risk of type 2 diabetes of 1.7 (95% CI 1.2-2.5).[16]