Bulimia

Background: Bulimia nervosa (BN) is one of the eating disorders identified in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV). The word bulimia is derived from the Greek words bous (ox) and limos (hunger), indicating a state of excessive hunger. BN is characterized by frequent episodes of binge eating associated with emotional distress and accompanied by compensatory behavioral patterns aimed at preventing weight gain. Among the compensatory behaviors noted in this condition are excessive exercise, self-induced vomiting, diuretic abuse, laxative abuse, use of appetite suppressants, and/or medications intended to speed up the metabolism (eg, thyroid hormone). DSM-IV diagnostic criteria require episodes of binge eating that occur at least twice weekly for 3 months.

Binge eating is defined as eating in a discrete period (eg, 1 hour) an amount of food that is significantly larger than is typical for most people during the same defined period. This is associated with a perceived loss of control of eating during that same time. The mere consumption of an unusually large amount of food in a defined period without concomitant perception of loss of control is defined as an overeating episode. Similarly, the consumption of rather minimal amounts of food in a defined period with a perception of loss of control is referred to as a subjective bulimic episode.

Eating disorders (EDs) as a group are characterized by a fear of weight gain and a distorted body image with associated anomalies in mood, perception, response to physical and emotional cues, and eating behaviors. Within the syndromes of EDs, disordered eating and weight control efforts can manifest as dietary restriction, binge eating, and/or compensatory behaviors intended to prevent weight gain, as noted above. Among the eating disorders, BN and anorexia nervosa (AN) are far more common in young females, while binge-eating disorder (BED) is the most common ED overall, and is more common in adults, with a 2:1 ratio of females to males.

Bulimia is considered distinct from the only recently recognized syndrome of BED, in which no regular or consistent compensatory behavior accompanies the bingeing episodes. The DSM-IV recognizes 2 major variants of BN, as follows: purging and nonpurging (ie, bingeing with use of nonpurging compensatory measures such as excessive exercise, stimulant substances, or fasting).

Many reports suggest that subjects with bulimia often have a prior history of AN. Some reports have suggested this association in as many as 60% of cases. While subjects with uncomplicated BED tend to be obese, subjects with bulimia nervosa more typically are of normal weight. Overlap between nonpurging BN and BED is seen. The natural history of EDs is such that individuals may pass through several diagnoses over time, meeting criteria for anorexia nervosa, bulimia nervosa and binge eating disorder at various points.

Pathophysiology: Among the identified metabolic derangements identified in bulimia 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 seen in some patients with bulimia. The findings regarding the hypothalamo-pituitary-adrenal axis are more inconsistent. Some studies suggest an increased amplitude in cortisol and adrenocorticotrophic hormone (ACTH) during a 24-hour period among persons with bulimia compared to persons without bulimia, as well as a blunted response to corticotrophin releasing hormone (CRH). However, other groups reported normal adrenocortical dynamics in these subjects.

Reports also have suggested abnormal dexamethasone suppression tests akin to those seen in subjects with AN, suggesting that bulimia also may be associated with a pseudo-Cushing state. These findings tend to be more apparent among subjects with significant dietary restriction. Some data suggest that the findings on the dexamethasone suppression test may be the result of impaired dexamethasone absorption, which has been demonstrated in some persons with bulimia. Similar to findings in subjects with AN, patients with bulimia tend to have higher growth hormone levels at night, while the nocturnal prolactin levels tend to be less than those in controls.

Episodes of amenorrhea may occur in as many as 50% of persons with bulimia. About half of patients with bulimia have anovulatory cycles, while about 20% have luteal phase defects. The persons with anovulatory bulimia generally have reduced luteinizing hormone pulsatile secretion frequency and associated reduced estradiol and progesterone pulse amplitudes.

Frequency:

  • In the US: The condition is thought to be significantly underrecognized. Prevalence rates are estimated to be 1-3% of high school- and college-aged women in the US. Even more common, although not meeting criteria for bulimia, is the trend of periodic combined binge eating and purging. Approximately 10-15% of those with bulimia are male, and the disorder is more common in men who are homosexual. Bulimia also is more common among those whose occupation or hobbies require gaining and/or losing weight rapidly, such as wrestlers.

    Athletes as a subgroup are particularly prone to eating disorders; AN has received the greatest public attention. The female athlete triad of eating disorders, hypothalamic amenorrhea, and osteoporosis now is well recognized and is particularly common in sports where slimness and body shape are of great importance, such as gymnastics, diving, and figure skating. As the scope of the problem is more widely recognized, and as more high-profile athletes are identified with the problem, it also is being recognized as a problem in sports such as long-distance running, cycling, weight lifting, and wrestling.

    Certain occupations, such as acting, modeling, and ballet dancing, also appear to be associated with a higher than average risk for these disorders. The most comprehensive study to date suggests that among elite female athletes, the prevalence of eating disorders may be close to 4 times greater than in the general population.

    The rates of BN among patients seeking assistance with weight control are significant. The prevalence of BN and BED among clients of commercial weight loss programs is about 30-50%. Among patients presenting for bariatric surgery, the prevalence reaches 25-70% in some cohorts.

  • Internationally: The overall prevalence of bulimia certainly appears to have increased considerably after World War II, and it has been suggested that this is primarily the result of changing sociocultural expectations for young women. However, it does appear that bulimia specifically and eating disorders as a whole predominantly are Western diseases and occur most often in developed countries. Typically, reports of eating disorders outside of this setting are anecdotal.

    The suggestion that environmental factors play a significant role in the prevalence and incidence of eating disorders also is borne out by the fact that immigrants from underdeveloped countries have a much higher risk for developing eating disorders than do their genetically similar relatives still resident in the countries of origin. Most studies tend to identify bulimia and other eating disorders more frequently among the middle and upper socioeconomic strata of society. Although often described as modern diseases, close review of the older medical literature suggests that similar conditions have been described since antiquity.

Mortality/Morbidity: See Prognosis.

Race: Bulimia is a cosmopolitan disorder that has been described in all ethnic, racial, and socioeconomic groups.

Sex: As with other eating disorders, bulimia occurs predominantly in women. Most reports suggest a female-to-male ratio of 10:1. While some reports suggest the prevalence in men may be as low as 5%, others suggest that it may be as high as 15%.

It is critical to be aware that men also may develop BN and other eating disorders and to maintain a high index of suspicion. Although few data are available, little evidence suggests that men have any significant differences in clinical course, complications, or response to management modalities compared to women.

Age: The typical age of onset for bulimia is in the teenage years and early third decade of life. This is slightly older than the peak age of onset for AN but generally lower than the age of onset of BED. The prevalence of BN in children younger than age 14 years appears to be less than 5%.

CLINICAL

History: A common presenting scenario is concern about weight and seeking help with weight loss. Symptoms may include bloating, constipation, and menstrual irregularities. Far less often, subjects also may present with arrhythmias, which often are the result of electrolyte abnormalities. Though less prominent than in AN, bulimia also is characterized by an inappropriate premium placed on being slender and an associated distorted body image that exaggerates physical appearance.

  • A close dietary inventory may reveal that subjects attempt to control their weight by dieting and abstaining from high-calorie foods (until the binge episode).
    • 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. Foods generally are selected as being easy to swallow, vomit, and regurgitate and tend to have a high caloric value. Up to 10 times the recommended daily allowance for calories (or more) may be rapidly ingested in a single binge episode.
  • Situations in which control over food intake may be lost are avoided (eg, parties, eating out).
  • The level of physical activity that bulimics engage in often is cyclical in a fashion similar to that of the bingeing episodes.
  • While most persons with bulimia induce vomiting, a minority choose to chew the food and then regurgitate it without actually swallowing it. Vomiting usually is achieved by activating the gag reflex through digital stimulation or by ingestion of emetics (eg, ipecac).
  • Common gastrointestinal symptoms that occur in bulimics include abdominal pain (more common among persons who self-induce vomiting), bloating, flatulence, constipation, and obstipation.
  • Pulmonary symptoms in those with bulimia may be due to aspiration pneumonitis or, more rarely, pneumomediastinum.
  • Amenorrhea occurs in about 50% of persons with bulimia, while a significant proportion of remaining patients have irregular periods.

Physical: Eating disorders often are concealed and require a high index of suspicion to diagnose. Patients with bulimia often are unremarkable in general appearance and frequently have no signs of illness or anomalies on physical examination.

  • Bilateral parotid enlargement, largely consequent to noninflammatory stimulation of the salivary glands, may be seen.
  • In patients with significant self-induced vomiting, erosions of the lingual surface of the teeth, periodontal disease, and extensive dental caries may be observed.
  • Russel 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.
  • Other nonspecific but suggestive findings that may reflect the severity of the disease include bradycardia, hypothermia, and hypotension. Edema, particularly of the feet (and less commonly the hands), is found more often among patients with a history of diuretic and/or laxative abuse or in patients with significant protein malnourishment causing hypoalbuminemia. Some patients may be clinically obese, but morbid obesity is rare.

    The evaluation of these subjects is not complete without a comprehensive mental status examination. This is of considerable importance as bulimia often coexists with mood disorders, particularly depression. These patients also commonly have associated neuroses (particularly anxiety neuroses), the management of which may be vital to the adequate management of the bulimia.

    • The mental status examination also helps identify potential psychopathology known to accompany bulimia (and possibly predispose to its development) including alcoholism within the family, family history of eating disorders, and personality disorders.
    • Other areas of concern during the course of the mental status examination include disturbed interpersonal relations and dynamics, difficulties with impulse control, and a history of prior or ongoing substance abuse.

Causes: Among the potential precipitating events for a binge/purge cycle in those with bulimia are anxiety states, emotional tension, boredom, environmental cues about food and eating, alcohol use, substance abuse, and exhaustion. Hunger is a rather uncommon precipitant for the bulimic cycles. Although the exact cause for bulimia and other eating disorders is unclear, some factors identified as playing potentially important roles in its etiopathogenesis are as follows:

  • Psychological factors: Among those suggested are difficulties with self-esteem and affective self-regulation. However, it is difficult to determine the premorbid status that predisposes persons to later develop eating disorders such as bulimia.
  • Sociocultural factors: An inappropriate concern about body image and an excessive preoccupation with thinness seem central to both anorexia and bulimia nervosa. Some evidence suggests an association of bulimia (particularly the bingeing episodes) with disinhibition for food intake.
  • Affective disorders: The rather common association of eating disorders with affective disorders suggests a possible relationship between them. Major depressive disorder (MDD) is particularly common in this regard. It still is unclear whether the association is causative (primary), secondary to the bulimia itself, or represents a common set of risk factors for bulimia and MDD. Furthermore, obsessive-compulsive disorder is more common in persons with bulimia than in those without bulimia. Anxiety disorders, other related neuroses, and phobias also have been noted to be more common.
  • Genetics: Although no definitive inheritance patterns have been identified, a familial component appears to be involved in the development of eating disorders in general. The results of twin studies of both monozygotic and dizygotic twins suggest that the genetic component to the etiology of eating disorders is much greater in anorexia nervosa than in bulimia.
  • Psychopathology: The role of sexual abuse in the development of eating disorders is controversial. Some reports suggest a strong association, while others detect no association. Some evidence suggests a relationship between addictions and eating disorders, particularly in binge-eating disorder. Borderline personality disorder is found frequently, and these patients usually have histories of trauma and abuse and may represent a distinct subgroup. Endogenous opioids and beta-endorphins have been implicated in the maintenance of binge eating.
  • CNS and gastrointestinal peptide interactions: It appears that a complex dysfunctional interaction between orexigenic factors such as neuropeptide Y (NP-Y) and anorectic factors such as cholecystokinin (CCK) and beta-endorphin. The exact details of this interaction are under active investigation, but available data show that bulimics have normal NP-Y levels, which do increase after successful treatment. Furthermore, bulimics have reduced beta-endorphin, normal dynorphin, and low CCK levels. It is suggested that reduced activity of the central serotonin system may have a role in the development of bulimia.


Other Problems to be Considered:

Binge eating disorder

This is characterized by bingeing episodes but without the compensatory behaviors attempted on a consistent basis. It is the most common eating disorder (seen in about 2% of the general population and about 10% of obese subjects) and is more common in men than are the other eating disorders (estimates suggest 30-40% of subjects may be male). Recent reports suggest that BED may be particularly common among African Americans and Hispanics. The mean age at diagnosis also is higher (in the late third decade) when compared to both AN and BN.

Night eating disorder

This is an only recently defined and recognized eating disorder. It is characterized by the consumption of large amounts of food (>20% of the total calorie intake) after evening meals. It typically is associated with early morning drowsiness and anorexia. No significant overlap is seen between BED or BN and the night eating disorder.


WORKUP

Lab Studies:

  • Comprehensive blood chemistry panels are important in detecting possible occult metabolic complications of bulimia.
    • With significant vomiting, hypokalemic metabolic alkalosis is possible.
    • Among patients with significant laxative abuse, normokalemic metabolic acidosis may occur.
    • Hyperamylasemia is found in up to 30% of persons with significant vomiting because of hypersecretion from the salivary glands.
    • Hyponatremia, hypocalcemia, hypophosphatemia, hypomagnesemia, hyperuricemia, and hypoalbuminemia are less common but should be ruled out.
    • Those who have significant intravascular depletion may have elevated blood urea nitrogen levels.

Other Tests:

  • Because of the potential for arrhythmias and cardiomyopathy as possible complications, an electrocardiogram should be performed. In addition, because of the potential for osteoporosis in this group of subjects, a dual energy absorptiometry (DEXA) scan also may be indicated.

TREATMENT

Medical Care: Initial care may be on an inpatient or outpatient basis, depending on the clinical presentation. Factors that may indicate a need for inpatient care include significant metabolic abnormalities, medical complications, risk of suicide, failed outpatient treatment, inability to care for self, and diagnostic uncertainty.

Treatment should be comprehensive and multidisciplinary and may include the following components:

  • Cognitive behavioral psychotherapy (CBT): Distorted or maladaptive cognitions regarding weight and shape are identified and addressed. Irrational beliefs are explored and confronted. Behavioral approaches to avoiding undesirable eating habits are employed, including exposure to food. Cognitive distortions are examined to allow better understanding, enhanced self-control, and improved body image.

  • Interpersonal psychotherapy (IPT): Interpersonal psychotherapy works with specific issues in the interpersonal arena that create the context for the patient’s symptoms; these fall within the categories of grief, role transition, role conflict, or interpersonal deficits. Brief focused therapy in these areas can be effective in producing improvements in those with mood disturbance and low self-esteem, which may trigger and maintain the symptoms of bulimia. Its efficacy is similar to CBT in reducing binge eating but may be somewhat less effective in curbing purging.
  • Supportive-expressive psychotherapy (SEP) or group therapy

  • Family therapy: Explores family dynamics and factors that may precipitate or perpetuate abnormal eating and bingeing behaviors. This technique often views eating as a means of communication within a family.
  • Pharmacotherapy: Antidepressants as a group are the mainstay of pharmacotherapy.

    • Selective serotonin reuptake inhibitors (SSRIs) are among the agents best validated for use in managing bulimia. Both fluoxetine (Prozac) and sertraline (Zoloft) are approved by the Food and Drug Administration (FDA) for treatment of bulimia. Pharmacotherapy generally is recommended as an adjunct to psychotherapy. Antidepressant treatment using SSRIs is suggested regardless of whether the patient appears depressed. The exact mechanism underlying the efficacy of antidepressants in bulimia is unclear, but the effects may be mediated through their salutary impact on cerebral serotonin systems.

    • Bupropion (Wellbutrin) is relatively contraindicated in the treatment of BN because of a higher risk of seizures induced by the medication.

    • Other agents that are being explored for potential utility in bulimia management include anticonvulsants, lithium, L-tryptophan, and naltrexone.
  • Support and self-help groups (guided self-help): These are highly variable in constitution and methods used. While some are run by professionals, others are run by laypersons. Although anecdotal reports exist of their utility, no well-designed studies have confirmed these claims.
  • Inpatient care for the patient with bulimia should be considered when any of the following are present alone or in combination:
    • Diagnostic uncertainty

    • Associated secondary infections

    • Medical comorbidities (eg, arrhythmias, significant electrolyte derangements)

    • Suicidal ideation

    • Absence of a support structure at home

    • Severe impairments in the patient's capacity to function in regular daily activities (ie, severe psychosocial impairment)

    • Failed outpatient treatment

    • Significant concerns over follow-up (whether patient- and/or program-related)
  • With CBP and maintenance treatment with follow-up, as many as 50% of bulimic patients are asymptomatic 2-10 years after completing the treatment period. Evidence for similar improvements from other forms of psychotherapy (eg, IP, SEP) currently is not available.

Surgical Care: Major medical treatment requiring surgical intervention is rare, but medical care providers should be familiar with potential serious complications.

  • Patients may develop an acute gastric obstruction and/or gastric dilatation (possibly resulting in gastric perforation leading to acute peritonitis), which presents with severe, continuous projectile vomiting that occurs soon after any oral intake. This should be considered in individuals with known bulimia who present complaining of uncontrollable vomiting. Those who eat nonfood material during binges or soon after should be considered, as well.
  • When the potential for gastric dilatation and/or outlet obstruction is considered, an urgent surgical consultation is indicated for possible surgical management. This is a surgical emergency and, although uncommon, is the major cause of bulimia-related mortality.
  • Emergency surgical review also is required if symptoms suggestive of esophageal tear (Mallory-Weiss syndrome) develop or in case of esophageal rupture (Boerhaave syndrome), which can precipitate acute mediastinitis.

Consultations:

  • Two subspecialty groups should be involved routinely in the treatment and follow-up care of these patients.
    • Psychiatry and/or psychology for review and treatment. Involvement of a psychotherapist with expertise in the management of eating disorders is strongly recommended.
    • Dietary review and counseling by nutritionist
  • Further subspecialty reviews depend on specific presentations and the presence of specific complications.

Diet: As the disorder is treated, patient education regarding balanced diets, exercise, and long-term maintenance of a healthy weight is important and may reduce the risk of relapse or development of chronic symptoms.

MEDICATION

Various medications have been investigated for treatment of bulimia, with antidepressants proving useful in placebo-controlled double-blind trials. Specifically, SSRIs (eg, fluoxetine) and TCAs (eg, imipramine, desipramine, amitriptyline) may have greater efficacy than placebo. Some reports indicate that mianserin, phenelzine, trazodone, and bupropion may useful in some situations, but such drugs usually are not employed. Bupropion carries a relative contraindication because of the association with seizures when used in the context of eating disorders. Other medications investigated for utility in bulimia (without clear demonstrable efficacy) include lithium, venlafaxine, and naltrexone.

Drug Category: Antidepressants -- Because of their demonstrated efficacy and favorable side effect profiles, SSRIs are the most commonly prescribed medications in bulimia. They are particularly useful in patients with other symptoms such as depression, anxiety, obsession, or certain impulse disorders.
Fluoxetine is the prototypical SSRI for bulimia management. Typically, as with fluoxetine all the other SSRIs generally are prescribed at doses higher than those used for typical depression management.
Drug Name
 Fluoxetine (Prozac) -- Selectively inhibits presynaptic serotonin reuptake with minimal effect in the reuptake of norepinephrine or dopamine. The antidepressant, anti–obsessive-compulsive, and antibulimic actions are presumed to be linked to inhibition of CNS neuronal uptake of serotonin. Efficacy was demonstrated in two 8-week and one 16-week multicenter parallel group studies of adult outpatients meeting DSM-III-R criteria for bulimia. Patients in the 8-week studies received either 20 mg/d or 60 mg/d of fluoxetine or placebo in the morning. Patients in the 16-week study received a fixed fluoxetine dose of 60 mg/d qd or placebo. Patients in these 3 studies had moderate-to-severe bulimia with median binge eating and vomiting frequencies ranging from 7-10 episodes/wk and 5-9 episodes/wk, respectively. Fluoxetine 60 mg (but not 20 mg) was superior to placebo in reducing the number of binge-eating and vomiting episodes/wk.
Adult Dose 60 mg/d PO qd
Pediatric Dose Not established
Contraindications Documented hypersensitivity; concurrently taking MAOIs or taken in last 2 wk
Interactions Increases toxicity of diazepam, alprazolam, midazolam, flecainide, vinblastine, TCAs, and trazodone by decreasing clearance; also increases toxicity of MAOIs, haloperidol, clozapine, phenytoin, carbamazepine, and highly protein-bound drugs (eg, warfarin, digoxin); monitor lithium levels (levels reported to increase or decrease with concurrent use)
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Caution in hepatic impairment and history of seizures; MAOIs should be discontinued at least 14 d before initiating fluoxetine therapy; adverse effects include anxiety, nervousness, insomnia, mania/hypomania, and anorexia
Drug Name
 Desipramine (Norpramin) -- Secondary-amine tricyclic that may increase synaptic concentration of norepinephrine in CNS by inhibiting reuptake by presynaptic neuronal membrane. May have effects in the desensitization of adenyl cyclase, down-regulation of beta-adrenergic receptors, and down-regulation of serotonin receptors.
Adult Dose 100-300 mg/d PO qd
Pediatric Dose Not established
Contraindications Documented hypersensitivity; narrow-angle glaucoma, recent postmyocardial infarction; patients currently receiving MAOIs, fluoxetine, or took them in the previous 2 weeks
Interactions Decreases antihypertensive effects of clonidine and guanethidine but increases effects of sympathomimetics, cimetidine, and benzodiazepines; effects of desipramine increase with phenytoin, phenothiazines, carbamazepine, and barbiturates
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in cardiovascular disease, conduction disturbances, seizure disorders, urinary retention, glaucoma, hyperthyroidism, and patients receiving thyroid replacement; may impair mental and/or physical abilities
Drug Name
 Amitriptyline (Elavil) -- Inhibits reuptake of serotonin and/or norepinephrine at presynaptic neuronal membrane, which increases concentration in CNS. May increase or prolong neuronal activity since reuptake of these biogenic amines is important physiologically in terminating transmitting activity.
Adult Dose 25-150 mg/d PO qd
Pediatric Dose Not established
Contraindications Documented hypersensitivity; MAOIs in past 14 d; acute phase after MI; history of seizures, cardiac arrhythmias, glaucoma, or urinary retention
Interactions Phenobarbital may decrease effects; coadministration with CYP2D6 enzyme (debrisoquin hydroxylase) system inhibitors (eg, cimetidine, quinidine) may increase amitriptyline levels; inhibits hypotensive effects of guanethidine; may interact with thyroid medications, SSRIs, alcohol, CNS depressants, barbiturates, and disulfiram; if given with anticholinergic agents or sympathomimetic drugs, including epinephrine combined with local anesthetics, close supervision and careful adjustment of dosages is required; hyperpyrexia reported with concurrent use of anticholinergic agents or with neuroleptic drugs, particularly during hot weather; caution if patients receive large doses of ethchlorvynol concurrently (transient delirium has been reported)
Pregnancy D - Unsafe in pregnancy
Precautions Caution in cardiac conduction disturbances and history of hyperthyroidism, seizures, urinary retention, angle-closure glaucoma or increased intraocular pressure, and hepatic or renal impairment; avoid using in the elderly
Drug Name
 Imipramine (Tofranil) -- Dibenzazepine antidepressant, referred to as a tricyclic because of its chemical structure. Metabolized to desipramine, which is marketed separately.
Inhibits reuptake of norepinephrine or serotonin (5-hydroxytryptamine, 5-HT) at presynaptic neuron.
Use parenteral administration for starting therapy only in patients unable or unwilling to use oral medication.
Has demonstrated clear superiority over placebo in double-blind trials for treating specific symptoms of bulimia nervosa.
Adult Dose 25 mg PO tid initially and increase 25-50 mg at weekly intervals prn to 200 mg/d; not to exceed 300 mg/d
Pediatric Dose <6 years: Not established
6-12 years: 10-30 mg/d PO or 1-5 mg/kg/d PO in divided doses
Contraindications Documented hypersensitivity; narrow-angle glaucoma; in acute recovery phase following myocardial infarction; avoid in patients taking MAOIs or fluoxetine, or took them in the previous 2 wk
Interactions Decreases antihypertensive effects of clonidine and guanethidine but increases effects of sympathomimetics, cimetidine, and benzodiazepines; effects of desipramine increase with phenytoin, phenothiazines, carbamazepine, and barbiturates
Pregnancy D - Unsafe in pregnancy
Precautions May impair mental or physical abilities required for performance of potentially hazardous tasks including handling machinery, driving; caution in cardiovascular disease, conduction disturbances, seizure disorders, asthma, mental illness, Parkinson disease, increased intraocular pressure or angle-closure glaucoma, benign prostatic hypertrophy, GI disease, gastroesophageal reflux disease (GERD), urinary retention, hyperthyroidism, or receiving thyroid replacement; can induce or exacerbate hiatal hernia, and can cause paralytic ileus or constipation; anticholinergic effects may increase lens discomfort (eg, mydriasis, disturbance of accommodation, dry eyes) for contact lenses wearers; avoid abrupt discontinuation (may cause nausea, vomiting, or diarrhea); agranulocytosis, thrombocytopenia, eosinophilia, leukopenia, and purpura reported; photosensitivity may occur with prolonged exposure to sunlight or tanning equipment

Further Outpatient Care:

  • The proper management of bulimia is with a multidisciplinary approach. Among the bare minimum of care providers who should be involved in the care of these patients are the primary care physician, psychiatrist, psychotherapist, and dietitian. Depending on circumstances and complications, those with bulimia also may require the services of an endocrinologist or surgeon.

Deterrence/Prevention:

  • All eating disorders appear to arise within a cultural context that places too high a value on thinness and engenders unreasonable expectations regarding physical appearance. Awareness of the cultural and social forces and education for both children and their parents regarding the attitudes and behaviors that foster eating disorders may reduce the prevalence of these syndromes. Opportunities for this kind of intervention abound in primary care, athletic, and educational settings.

Complications:

  • Compared to AN, the medical complications associated with bulimia generally are benign, and the mortality rate from bulimia actually is low.
  • While the results of formal gastric emptying studies in bulimic patients have yielded variable results (some suggesting delayed emptying time and others suggesting normal emptying time), acute gastric dilatation is a significant risk. This may result in gastric rupture, which appears to be the most common cause of death related to bulimia.
  • Among the rare potential complications that may follow bulimia (especially in variants associated with vomiting) are Mallory-Weiss tears of the esophagus, esophageal rupture, reflux esophagitis, and cardiomyopathies secondary to ipecac use or from chronic hypokalemia.
  • Ipecac toxicity may be associated with skeletal myopathy, while chronic hypokalemia also may cause intestinal ileus with abdominal distension and/or exertional rhabdomyolysis.
  • Hypokalemia-related distal tubulopathy is very rare but has been described in association with bulimia.
  • Xerosis (dry skin) is a common finding in bulimia, which appears to be related to the chronic dehydration to which persons with bulimia often are prone.
  • In the subgroup of individuals who abuse laxatives, chronic constipation, “cathartic colon,” melanosis coli, steatorrhea, and a protein-losing enteropathy may develop.
  • Obese individuals also may present with any of the various obesity-associated comorbidities.

Prognosis:

  • Relatively little is known about the long-term outcome of bulimia. Research to date suggests that the prognosis is varied.
  • The illness may pursue a long-term, fluctuating course over many years or may be more episodic and may be precipitated by life events and crises. In the shorter term, some reports suggest a 50% improvement in binge eating and purging behavior among patients who are able to engage in treatment.
  • Consistent predictors of outcome have not yet been identified. However, the severity of the purging sequelae may be an important indicator of prognosis; electrolyte imbalances, esophagitis, and hyperamylasemia reflect more severe purging and may predict a poorer outcome.

Patient Education:

  • While still the subject of debate, based on the perspective of interviewed bulimic patients, family psychopathology may play a significant role in the development of the condition.
    • Generally, bulimic patients view their families as conflicted, badly organized, noncohesive, and lacking in nurturance and caring. Detailed psychologic evaluation of these patients generally suggests that they are angrily submissive to rather hostile and neglectful parents.
    • For subjects still resident with their parents, a careful professional evaluation of the family dynamics and family psychotherapeutic and counseling sessions aimed at improving dysfunctional relationships may be of benefit to the patient.
    • The utility of family therapy in the management of bulimia is not as well defined as in AN. A few studies suggest that family therapy is an effective modality of management, while others studies suggest the opposite.
  • Among bulimic subjects in married or other cohabiting consensual adult relationships, the research is limited. The available information is rather sketchy, but overall it is suggested that these relationships generally are suboptimal with the appearance of impaired levels of intimacy in such relationships and suboptimal communication skills. Counseling and openness about these problems may assist with the management of the bulimia.
  • While cognitive behavioral therapy remains the therapeutic method of choice for bulimia, various modifications of this technique currently are being rigorously investigated. Most of these modifications are based on the premise that education about bulimia in a nonthreatening environment has a therapeutic effect. These types of therapy usually are conducted in a group setting. However, no scientifically rigorous studies have been performed comparing the psychoeducational programs in individual or group settings to definitively prove the superiority of one over the other. Whether in the individual, group, or other hybrid educational sessions, these programs should include some instruction on the following:
    • The multifactorial etiology of eating disorders with biologic, genetic, psychologic, familial and sociocultural factors

    • Medical complications related to vomiting, laxative, and diuretic abuse

    • The setpoint theory of weight regulation and the potential consequences of weight cycling and cyclic dieting

    • Basic nutritional information

    • Sociocultural and body image issues

    • Cognitive and behavioral strategies

    • Relapse prevention as distinct from episodic bingeing "slips"
  • More than 70% of published management studies of bulimia involve some form of psychoeducational program. The exact efficacy of these is difficult to determine because most management programs for bulimia are multimodality based. Anecdotal reports and personal experience of many practitioners and subjects suggest that for at least some bulimic patients, they have a significant role in management.

Medical/Legal Pitfalls:

  • One must maintain a high index of suspicion for the condition in at-risk patients. Medical complications should be carefully considered, investigated, and managed, as appropriate.
  • Marked vomiting may be associated with metabolic derangements, which, depending on severity, may require inpatient evaluation and management. Acute medical or surgical emergencies may arise from severe vomiting.
  • Some studies suggest that patients with bulimia have increased rates of substance abuse, anxiety disorders, bipolar 1 disorder, dissociative disorders, and sexual abuse; these conditions should be considered and managed as necessary. Mortality and morbidity associated with depression (suicidal thoughts or self-injury) and poor impulse control (eg, substance abuse, sexually transmitted diseases, unintended pregnancy, accidental injuries) always should be anticipated and assessed.

REFERENCES

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