Medical Complications of Bulimia Nervosa and Their Treatments
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AED INVITED LITERATURE REVIEW Medical Complications of Bulimia Nervosa and Their Treatments Philip S. Mehler, MD* ABSTRACT Results: Extensive and detailed review Objective: To present a cogent and of the medical complications of bulimia practical review of the medical complica- nervosa. VC 2010 by Wiley Periodicals, tions and their treatment in patients Inc. with bulimia nervosa. Keywords: bulimia; medical; compli- Method: Thorough review of the medi- cations; esophagitis; pseudo-barters cal literature from 1990 to current in regards to the medical complications of bulimia nervosa and the therapeutic inter- vention that are effective to treat them. (Int J Eat Disord 2011; 44:95–104) Introduction be healthy and can more easily hide their disorder. It is not uncommon for patient with bulimia nerv- Although DSM-V will likely provide some new defi- 1 osa to engage in bulimic purging behaviors for nitions for bulimia nervosa, currently the purging many years before seeking medical attention. subtype is by far the more common diagnostic cat- To maximize the utility of this review, the manu- egory. The types of compensatory purging behav- script is divided into four main sections: the spe- iors, which individuals engage in most frequently, cific medical complications that emerge as a result include self-induced vomiting, or the misuse of lax- of self-induced vomiting, laxative abuse, and diu- atives or diuretics. There are numerous potentially retic abuse, followed by the fourth section devoted serious medical complications that directly ema- to the therapeutic interventions available to effec- nate from the specific mode and frequency of purg- tively treat these complications. ing that is utilized. Indeed, use of health services are markedly higher for patients with bulimia nerv- osa both in the 12 months leading up to, and in the 12 months following the index visit, probably reflecting, in part, the broad range of medical com- Self-Induced Vomiting plications present as a result of the purging behav- iors.2 In this review, the medical complications of There are a number of oral and gastrointestinal bulimia nervosa will be discussed along with their complications that develop as a result of engaging treatments to help clinicians caring for these in self-induced vomiting. Most patients with buli- patients achieve the most optimal overall results. mia nervosa induce vomiting with their finger, but This is especially important because symptoms of some use ipecac. As the illness progresses, many bulimia nervosa are relatively longstanding and the can vomit reflexively without mechanical stimula- 5-year recovery rate is only in the 50% range.3 tion. Oral complications of bulimia are primarily Thus, the medical complications are of relevance related to the chronic regurgitation of acidic gastric for many years during the course of treatment. contents. Cheilosis, a form of stomatitis character- Although the emaciated state of the patient with ized by pallor and maceration of the mucosa at the angels of the mouth, is seen in some patients with anorexia nervosa immediately suggests that diag- 4 nosis, patients with bulimia nervosa may appear to bulimia nervosa. In severe cases, linear fissures can occur, which may form scars on healing. In Accepted 11 February 2010 addition to the pain associated with cheilosis, *Correspondence to: Philip S. Mehler, Denver Health Medical patients may complain of pharyngeal soreness Center, Denver, Colorado. E-mail: [email protected] related to the chronic irritation created in the back Denver Health Medical Center, Denver, Colorado of the throat from acidic stomach contents. Given Published online 7 May 2010 in Wiley Online Library (wileyonlinelibrary.com). DOI: 10.1002/eat.20825 that dentists may be the first medical providers to VC 2010 Wiley Periodicals, Inc. assess the oral effects of bulimia nervosa, they may International Journal of Eating Disorders 44:2 95–104 2011 95 MEHLER be key in the timely diagnosis of bulimia nervosa after a bingeing-purging episode, and thus the con- and its treatment.5 Oral-dental problems associ- nection to bulimia may not be obvious. ated with self-induced vomiting can be manifested Sialographic computed tomographic scanning of as early as 6 months following the initiation of self- the parotids will demonstrate enlarged glands. His- induced vomiting. The most common dental com- tologically, parotid biopsy specimens are normal plications include dental erosions, dental caries, except for acinar size, which is increased because and periodontal disease. The dental erosions of an increased number of secretion granules.15 Pa- involve erosion of the enamel on the lingual surface rotid salivary flow rates are reduced, but there are of maxillary teeth that manifest as a smooth no derangements of salivary electrolyte or immu- unnatural glossy appearance noticeable with illu- noglobulin levels. mination of the teeth during an examination of the The pathogenesis of parotid swelling in bulimia oral cavity.6 This complication is referred to as peri- is unclear.16 Some investigators think that the swel- myolysis. Enamel erosion is a common manifesta- ling is a direct result of binge eating, which often tion of bulimia. The loss of dentin and tooth involves highly caloric foods consumed in very enamel is seen initially only on the lingual surface but can also involve palatal and posterior occlusal large quantities over short periods. Others postu- surfaces of the maxillary teeth.7 Usually, the lower late that chronic regurgitation of acidic gastric con- anterior teeth have not had significant damage, tents is responsible. Still others believe that pancre- likely because of protective tongue movements.8 It atic proteolytic enzymes brought into the mouth is thought that visible enamel destruction occurs during vomiting stimulate lingual taste receptors; after about 2 years of regular episodes of vomiting. increased autonomic stimulation would thus cause 17 The severity and rate of enamel loss may be related the salivary glands to swell. to a multiplicity of factors, such as duration of buli- In association with sialadenosis, serum amylase mia, frequency of purging, types of food consumed, levels are elevated in 10–20% of patients. Fractiona- quality of tooth structure, and oral hygiene.9 tion of the amylase confirms that it is of salivary Patients with severe cases complain of thermal and not pancreatic origin. Elevated levels are com- tooth sensitivity because of the exposed dentin. mon in patients reporting more frequent binge eat- Gum disease (gingivitis) is also a direct result of ing and vomiting. Amylase levels will usually return chronic irritation from the acidic gastric contents to normal a few days to weeks after cessation of and occurs as pain and erythematous gums. These vomiting. patients also appear to have more periodontitis.10 Esophageal complications run the spectrum There is controversy about whether patients with from mild esophagitis to life-threatening esopha- bulimia have a greater incidence of dental caries.11 geal rupture. Esophagitis, esophageal erosions, It is known that patients with bulimia often binge ulcers, and bleeding are thought to be secondary to on high-carbohydrate foods, but they are often fas- the frequent contact of the esophageal mucosa tidious in the care of their teeth. Older studies, with the regurgitated acidic gastric contents. Thus, however, have suggested an increased risk of caries patients with bulimia nervosa often complain of in patient with bulimia.12 However, the caries that heartburn and acid-reflux symptoms.18 However, patients with bulimia seem to develop include a esophageal motility is normal in bulimia nervosa predisposition to cervical caries and leathery and gastric emptying is not delayed as it often is in lesions of dentine leaving extensive areas of enamel anorexia nervosa.19 Frequent complaints of sore undermined.13 throat and hematemesis are noted. The latter is Another oral complication associated with usually the result of Mallory-Weiss tears at the gas- repeated self-induced vomiting is sialadenosis (hy- tro-esophageal junction and usually only cause pertrophy of the salivary glands). The intensity of minor gastrointestinal bleeds that are self-limited. this seems to correlate with the severity of enamel Spontaneous reflux of acidic gastric contents into erosions. Painless unilateral or bilateral swelling of the lower esophagus can also occur due to laxity of the salivary glands has been reported in 10–50% of the lower esophageal sphincter after months of patients, depending on the frequency of vomiting. repeated vomiting. Similarly, among patients with Initially intermittent, the swelling tends to persist long-standing bulimia nervosa, esophageal stric- as the patient becomes chronically bulimic. tures with resultant dysphagia have been reported. Involvement of the parotid glands is most com- Although Barrett’s esophagus, which is the mon, but some patients will demonstrate subman- replacement of normal squamous epithelium with dibular gland involvement as well.14,15 Clinically, columnar epithelium as a result of chronic gastro- the swelling is generally most pronounced 3–6 days esophageal reflux, has been reported in patients 96 International Journal of Eating Disorders 44:2 95–104 2011 MEDICAL COMPLICATIONS OF BULIMIA with bulimia, it is unclear if this condition has an lar toxicity is not clearly defined, but the alkaloid is increased prevalence among bulimic patients. The known to depress glycolysis, inhibit the Krebs