Medical complications of eating disorders are many and varied. Medical complications of anorexia are typically more severe than bulimia or binge eating and are directly related to the starvation state. Bulimia medical complications are usually related to purging behaviors and are often the result of chemical derangements or structural damage to the GI tract.35 The most common medical complication of binge eating is obesity, but acute structural complications such as gastric dilatation may also be seen.
Among the most deadly of the eating disorder complications are changes to the cardiovascular system. Malnutrition in eating disorders leads to decreased muscle mass, including cardiac muscle mass, specifically in the interventricular septum and the left ventricle, as well as increased vagal tone. These effects lead to decreased contractility and cardiac output, and therefore result in hypotension, bradycardia, and orthostasis. Relative decreases in cardiac muscle mass compared to valve cross-sectional area can lead to the development of mitral valve prolapse.36 Rarely, patients with anorexia nervosa can develop pericardial effusion, which in a few cases has led to cardiac tamponade requiring urgent pericardiocentesis.37 Purging behavior leading to electrolyte abnormalities can cause cardiac arrhythmias. Syrup of ipecac, used as an emetogenic, is directly cardiotoxic and can cause an irreversible cardiomyopathy.38 Prolongation of the QT interval on ECG has been described in patients with all types of eating disorders relative to controls. QT prolongation is a marker for risk of ventricular tachyarrhythmia, specifically torsades de pointes, and risk of sudden death. QT prolongation as a result of eating disorders is reversed by adequate refeeding and is associated with normalization of heart rate, heart rate variability, and exercise tolerance.39 Therefore, QT normalization has been used as a marker to guide refeeding and rehabilitation.40 Most cardiac sequelae are reversible with appropriate weight gain, but there is increased risk of cardiac complications during the first week of refeeding after severe nutrient depletion.39,41 There are also case reports of pneumothorax and pneumomediastinum as complications of severe anorexia.42
The proportion of eating disorder patients with vitamin deficiencies is difficult to determine, because many patients take supplementary vitamins. Decreased bone mineral density was reported in 18% of patients age 15 to 54 years old admitted to a specialized eating disorders unit but was not associated with decreased vitamin D levels.43 Deficiencies of other vitamins are rare, and typically merit case reports. Iron and vitamin B12 deficiency can lead to anemia in severely food-restrictive patients. Skin erythema and pruritus with sun exposure, glossitis, epidermal desquamation, and diarrhea should raise suspicion of pellagra.44 Confusion, confabulation, ataxia, ophthalmoplegia, and/or nystagmus suggest Wernicke-Korsakoff encephalopathy. Other vitamin deficiencies reported in association with eating disorders include wet beriberi and scurvy, although these are extremely rare.45,46
Refeeding following prolonged nutrient depletion can cause electrolyte abnormalities, most commonly hypokalemia, hypophosphatemia, and hypomagnesemia, due to redistribution of electrolytes from the extracellular to the intracellular space triggered by insulin release and from depletion of phosphorus during protein synthesis. This can lead to arrhythmias, congestive heart failure, pericardial effusions, and cardiac arrest.41
Patients with anorexia are at increased risk of constipation, gastroparesis, gastric dilatation, and gastroesophageal reflux.19,47 Gastroesophageal reflux and laryngopharyngeal reflux commonly occur in patients with bulimia and may result in hoarseness or dysphagia.19,48 Chronic stimulant laxative abuse can lead to development of rectal prolapse, melanosis coli, or the cathartic colon syndrome.49,50,51 Other very rare GI complications include superior mesenteric artery syndrome; gastric dilatation, necrosis, and rupture; necrotizing colitis; and gastric bezoar.42,52,53,54,55
Profound food restriction affects the hypothalamic-pituitary axis. Low levels of gonadotropins, loss of the normal pulsatile waves of luteinizing hormone, and estrogen deficiency lead to hypothalamic amenorrhea.56 Anorexia is also associated with the "euthyroid sick syndrome" in which thyroid-stimulating hormone is normal or slightly low, T3 is low, and sometimes T4 levels are also decreased. Thyroid deficiencies likely contribute to the bradycardia, orthostasis, and hypothermia in anorexia. High cortisol levels and low levels of insulin-like growth factor 1 (somatomedin C), T3, estradiol, and testosterone contribute to loss of bone mass.57 Refeeding and recovery from illness do not fully return bone mass to normal levels, and patients with anorexia remain at an increased risk of fracture for as many as 40 years following initial diagnosis.58 The endocrine effects of bulimia and binge eating disorder are less well studied, more variable, and less predictable. Endocrine abnormalities in these disorders may be more related to comorbid obesity than to the eating disorder itself.