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Medical Complications of Anorexia Nervosa and Bulimia
Accepted Manuscript Medical Complications of Anorexia Nervosa and Bulimia Patricia Westmoreland, MD, Mori J. Krantz, MD, Philip S. Mehler, MD, FAED, FACP PII:
S0002-9343(15)00582-3
DOI:
10.1016/j.amjmed.2015.06.031
Reference:
AJM 13081
To appear in:
The American Journal of Medicine
Received Date: 22 May 2015 Revised Date:
19 June 2015
Accepted Date: 19 June 2015
Please cite this article as: Westmoreland P, Krantz MJ, Mehler PS, Medical Complications of Anorexia Nervosa and Bulimia, The American Journal of Medicine (2015), doi: 10.1016/j.amjmed.2015.06.031. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Medical Complications of Anorexia Nervosa and Bulimia
Mori J. Krantz, MD2,4
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Patricia Westmoreland, MD1
Philip S. Mehler, MD, FAED, FACP1,3,4
1
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Eating Recovery Center of Denver, 7351 E Lowry Blvd, Suite 200, Denver, CO 80230 – [email protected] 2
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Cardiology Division, Denver Health Medical Center, Denver, CO, 777 Bannock St., MC0960, Denver, CO 80204 – [email protected] 3
ACUTE at Denver Health, Denver Health Medical Center, 777 Bannock Street, MC4000, Denver, CO 80204 – [email protected] 4
Corresponding Author:
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Department of Medicine, University of Colorado Health Sciences Center
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Philip S. Mehler, MD, FAED, FACP 777 Bannock Street, MC 4000
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Denver, CO 80204 303-602-4972
Email: [email protected] Funding Source – None
Conflict of Interest – None Word Count: 3,888
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ABSTRACT Anorexia nervosa and bulimia nervosa are serious psychiatric illnesses related to
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disordered eating and distorted body images. They both have significant medical
complications associated with the weight loss and malnutrition of anorexia nervosa as well as from the purging behaviors which characterize bulimia nervosa. No body
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system is spared from the adverse sequela of these illnesses, especially as anorexia nervosa and bulimia nervosa become more severe and chronic. Here we review the
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medical complications which are associated with anorexia nervosa and bulimia nervosa as well as the treatment for said complications. We also discuss the epidemiology and
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psychiatric comorbidities of these eating disorders.
Keywords: Anorexia Nervosa, Bulimia, Medical Complications, Hypokalemia,
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Osteoporosis
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INTRODUCTION Anorexia nervosa and bulimia nervosa are serious psychiatric illnesses with substantial morbidity and mortality. It is the psychiatric illness with the highest mortality
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rate.1-7 Mortality is also increased in patients with bulimia nervosa.8 In both anorexia nervosa and bulimia nervosa, much of the increased mortality rate is attributable to the medical complications inherent to these two illnesses.
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Although anorexia nervosa and bulimia nervosa are defined as separate
disorders in the psychiatric Diagnostic and Statistical Manual 5th Edition (DSM-5),9 they
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both fall into the category of disordered eating, driven by an irrational fear of normal body weight, a desire for thinness, and leading to body image distortion.10 Cultural ideals of beauty and thinness may incite the development of disordered eating in vulnerable individuals, who have a genetic predisposition towards anxiety and
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perfectionism.11 Both starvation and purging may initially calm these feelings of anxiety and reduce obsessions and compulsions via a serotonergic neuronal pathway.12, 13 During the course of anorexia nervosa and bulimia nervosa, comorbid mental
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disorders also emerge as a result of altered neurotransmitter metabolism and/ or endocrine changes that result from caloric deprivation.14-17 Almost 50% of adolescent
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patients with anorexia nervosa meet criteria for at least one comorbid psychiatric illness.18 Eating disorders are strongly associated with mood and anxiety disorders, and the type and severity of these comorbidities is increased in patients who have the most severe eating disorders.19-23 In addition, patients with bulimia nervosa who have comorbid borderline personality disorder have poorer outcomes than those without borderline personality
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disorder when both groups are treated with psychotherapy and pharmacotherapy.24,25 Psychiatric comorbidity, as well as a history of suicidal or self-harm ideation, and comorbid mental illnesses all confer an increased risk of death in patients with eating
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disorders.25-28 Problems socializing, and difficulties with being assertive, are factors that contribute to maintaining an eating disorder. 29 Temperament traits of harm avoidance,
patients who recover from eating disorders.30
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combined with high reward dependence, are protective factors seen more commonly in
Treatment of anorexia nervosa and bulimia nervosa is multi-dimensional. In
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addition to nutritional rehabilitation, cognitive-behavioral psychotherapy, along with family therapy, have been shown to be effective in treating patients with anorexia nervosa,31 although the benefit of these therapies have been mostly noted in the weight maintenance phase of treatment.32
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There is only minimal to moderate evidence that psychiatric medications are efficacious in treating patients with anorexia nervosa. Despite the prevalence of mood and anxiety symptoms in patients with anorexia nervosa, medications used to treat
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these conditions are not necessarily useful treatment adjuncts for reducing the symptoms of anorexia nervosa. In one study, fluoxetine assisted in preventing relapse
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in weight-restored patients with anorexia nervosa.33 However this finding was not replicated in a subsequent study.34 While there may be evidence for using antidepressants in the weight maintenance phase, antidepressants do not ameliorate eating disorder pathology in patients who are acutely underweight.35 The poor response to antidepressants is believed to result from starvation-induced abnormalities in serotonin receptors.36
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In addition to concerns regarding the efficacy of antidepressants in patients with anorexia nervosa, there is also considerable debate as to the efficacy of antipsychotics in treating their symptoms. Low-dose antipsychotic medications may be useful in
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treating delusional beliefs regarding body image, intense ruminations about food, and the hyper-arousal and as well as anxiety induced by having to face weight
restoration.37,38 Although atypical antipsychotic medications promote weight gain in
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normal weight individuals, they do not have this effect in patients with anorexia
nervosa.35,39 However, patients with eating disorders may not accept reassurance in
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this regard. Despite the paucity of associated weight gain, there remains concern that the risk of using these medications outweighs their potential benefit.40 First generation antipsychotics (typical antipsychotics) lower the seizure threshold. Side effects of second-generation antipsychotics (atypical antipsychotics), such as orthostasis,
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prolonged QTc, and hepatotoxicity are of concern.
Despite continued debate regarding the usefulness of pharmacotherapy in patients with anorexia nervosa, pharmacotherapy for bulimia is well established.
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Fluoxetine (at doses of 60 mg or higher) is FDA-approved for bulimia nervosa, and other selective serotonin reuptake inhibitors (as well as other classes of
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antidepressants) have been found to be useful in treating patients with bulimia nervosa.32,37 The effect of fluoxetine in treating the symptoms of bulimia nervosa appears to be independent of its effects on mood, and is reportedly related to the effects of the medication on satiety, thereby reducing binge eating.41,42 Cognitive behavioral therapy is a well-established psychotherapeutic treatment for bulimia nervosa.32,43
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MEDICAL COMPLICATIONS - ANOREXIA NERVOSA Anorexia nervosa can adversely affect almost every body system. The complications arise as a direct result of weight loss and malnutrition. However, there
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are no studies which define which body mass index (BMI) is associated with a particular medical complication. The eyes may be affected by lagophthalmos, wherein the eyelids do not totally cover the eye during sleep, resulting in irritation to the cornea and mild
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ocular discomfort.44 Treatment involves taping the eyes shut at night after first applying
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a sterile lubricant.
GASTROINTESTINAL
Dysphagia can frustrate the ingestion of oral calories during the early stages of refeeding. It is due to weakened and uncoordinated pharyngeal muscles. As a result,
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patients may complain of coughing with eating or may have a history of aspiration pneumonia. The diagnosis is made by a modified barium swallow test and the treatment depends on weight restoration and input from a speech therapist to define
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proper food consistencies.45 Patients with anorexia nervosa have significantly slowed gastric emptying at their nadir weights which is accompanied by complaints of early
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satiety, nausea and bloating.46 This gastroparesis ultimately resolves with weight gain, but symptoms may respond early on to low dose, short-term usage of metoclopramide before meals. Acute gastric dilatation is a serious condition which can lead to gastric perforation if not recognized early.47 It can occur independently as an isolated finding in the early phases of refeeding or, it can occur as a result of the superior mesenteric artery syndrome.48 Superior mesenteric artery syndrome is defined by the extrinsic
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compression of the third portion of the duodenum by the superior mesenteric artery, due to loss of a fatty tissue pad which normally maintains the angle between the superior mesenteric artery and the aorta. Significant left upper quadrant abdominal pain with
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eating, emesis during the meal and early satiety should prompt an evaluation for gastric dilatation or superior mesenteric artery syndrome, via an abdominal radiograph or CT scan. Treatment of superior mesenteric artery syndrome is aimed at weight restoration
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to reconstitute the fat pad. This can be achieved by a soft or liquid oral diet or by enteral feeds via a nasojejunal tube or a percutaneously placed one.49 Acute gastric dilation is
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first treated by gastric decompression with a nasogastric tube, followed by similar treatments to those used in superior mesenteric artery syndrome. Just as there is slowing of the proximal gastrointestinal tract, there is also slowing of colonic function, resulting in constipation as an accompanying symptom in anorexia nervosa.50 Osmotic
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laxatives are useful along with reassurance that the patient’s prior bowel pattern should return over a few weeks with ongoing progressive nutritional rehabilitation. Elevated liver transaminases occur frequently at patient’s nadir weights.51 This
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generally represents apoptosis, a programmed hepatocyte death as a result of malnutrition. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT)
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are the most frequently affected in a range of 2-4 times elevated, but severe elevations have also been reported to occur.52 ALT is more elevated than AST. The prevalence of liver enzyme abnormalities correlates with lower BMI’s, hypoglycemia and the development of refeeding hypophosphatemia.53 Progressive nutritional support will resolve these elevations over the first few weeks of refeeding. Alkaline phosphatase and bilirubin are not commonly affected. Less frequently, elevations of the AST and
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ALT may be due to steatosis as a result of actual refeeding. A liver ultrasound can help elucidate the cause since in steatosis, a fatty enlarged liver will be noted.54
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CARDIAC
As noted above, anorexia nervosa has the highest mortality of any psychiatric disorder. Sudden cardiac death along with other medical complications and suicide
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account for about 60% of the deaths. The exact cause of sudden death in anorexia nervosa remains unknown. Autopsy studies do not reveal evidence of obstructive
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coronary artery disease.55 It has been postulated that alterations in cardiac conduction and repolarization contribute to heightened mortality though a single unifying mechanism. Bradycardia is commonly noted in patients and reflects heightened vagal tone in the setting of substantial weight loss. This often recovers with restoration of body
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weight. A resting heart rate of less than 60 beats per minute, for example, was seen in 95% of patients in a consecutive series.56 Sinus bradycardia in and of itself does not require specific therapy, but current guidelines recommend hospitalization for a heart
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rate less than 40 beats per minute. High-grade atrioventricular block is exceedingly rare and suggests underlying structural heart disease that may be unrelated to anorexia
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nervosa itself. Temporary pacemakers are rarely required. Persistent junctional rhythm has been described among patients with severe anorexia nervosa, which may be extinguished with exercise.57,58 Patients may present with prolongation of the rate-corrected QT (QTc) interval on
surface electrocardiography and a commonly held belief was that this is the primary cause of sudden cardiac death. However, this relationship is confounded by concurrent
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QTc-prolonging medications and depletion of serum potassium and magnesium levels. In a series of patients with severe anorexia nervosa, marked QTc interval prolongation (>500 ms) was actually uncommon in the absence of contributing factors.59 Similarly,
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Facchini and colleagues observed 29 patients with anorexia and found marked QTcprolongation in only 2 individuals.60 Both had profound hypokalemia, and after
potassium repletion, the QTc interval normalized. Therefore, to date, an independent
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causal pathway between anorexia nervosa, QTc-prolongation, torsade de pointes, and sudden cardiac death have not been demonstrated. Expectant management of delayed
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repolarization is generally adequate and includes electrolyte repletion, discontinuation of QTc-prolonging medications, and serial 12-lead electrocardiography. Severe anorexia nervosa is also known to change cardiac structure. Many patients develop left ventricular atrophy and subsequent annular changes that lead to
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mitral valve prolapse. Patients occasionally develop pericardial effusions, which are generally self-limited and resolve with weight restoration. Among the most prominent cardiovascular structural abnormalities is a substantial reduction in left ventricular
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myocardial mass with preserved left ventricular systolic function. This is generally reversible with refeeding. One study demonstrated myocardial fibrosis/scar manifested
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by late gadolinium enhancement on magnetic resonance imaging (MRI) in nearly a quarter of patients.61 Although echocardiographic atrophy and fibrosis by MRI have been demonstrated, histologic abnormalities in the heart have been poorly characterized until very recently: a published autopsy report showed left ventricular atrophy with endocardial and interstitial fibrosis, focal myxoid material deposition with mast cells, and increased cytoplasmic lipofuscin.62 Although most cardiac structural
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abnormalities are reversible in this condition, the presence of myocardial scar suggests that malignant arrhythmias remain a possible mechanism of increased mortality in this
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disease.
PULMONARY
As opposed to the cardiac system, the lungs are not adversely affected for the
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most part. There appear to be some pulmonary function test abnormalities associated with anorexia nervosa which are similar to those seen with emphysemia.63 It is not clear
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if this impairment recedes with refeeding. Spontaneous pneumothorax has been reported in anorexia nervosa along with prolonged air leaks.64
HEMATOLOGY
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As anorexia nervosa becomes worse, there is trilinear hypoplasia causing anemia, leukopenia and thrombocytopenia. Anemia occurs in 40% of these patients, with leukopenia noted in 30% and thrombocytopenia in about 10%.65 The cytopenia are
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due to gelatinous marrow transformation with atrophy of the normal fat content in the marrow and replacement by a mucopolysacharide.66 Iron deficiency is not typically
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found and red cell indices are normal. Although often neutropenic, surprisingly, these patients do not appear to be more susceptible to infectious complications.67 However, they also do not manifest a typical febrile response to infections and inflammatory markers are suppressed, which can cause a delay in the diagnosis of an infection.68 The cytopenias resolve with weight restoration; growth factors are not indicated in anorexia nervosa.69 Very recently, plasma levels of vitamin B12 and folate have been
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found to be increased. The increase is artificial as it was found to be due to hepatocyte dysfunction with leakage of the vitamins from these cells.70
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MUSCULOSKELETAL
Osteoporosis is common in anorexia nervosa and occurs early in the disease.71 Decreased bone density is evident after just one year of anorexia nervosa,
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notwithstanding the relatively young age of these patients. The risk of subsequent
fragility fractures is markedly elevated, both in adults and adolescents with anorexia
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nervosa.72,73 Fracture incidence increases soon after diagnosis of anorexia nervosa and remains so many years later. This is one of the rare complications of anorexia nervosa which may leave irreversible damage even after recovery. Thus, the need for obtaining bone density testing in all patients with a disease duration of more than one
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year. In contrast to postmenopausal osteoporosis, in anorexia nervosa the loss of bone mineral density is due to both decreased bone formation along with increased bone resorption. Also, trabecular bone is more affected than cortical bone. Yet, the exact
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etiological factors involved in their loss of bone density is not clear. Putative factors include the overlap between the normal accrual of peak bone mass and the age of
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onset of anorexia nervosa, along with the typical hypogonadal state, elevated cortisol levels and growth hormone resistance found in anorexia nervosa as will be described below.
There are currently no treatments specifically approved for the osteoporosis of
anorexia nervosa. Weight gain and resumption of menses are key and are associated with significant increases in spine and hip bone mineral density.74 However estrogen
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therapy does not appear to be of much value in anorexia nervosa. Many randomized controlled trials have found it to be ineffective, a fact which is underappreciated in the medical community.75-77 Also, the withdrawal bleeding associated with their usage can
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mislead patients into believing they are getting better. Transdermal estrogen patches have shown promising results in adolescents.78 Calcium and vitamin D by themselves do not restore bone density.79 Bisphosphonates have been shown to be effective in
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anorexia nervosa with an increase of 3-4% in spine bone mineral density after twelve months of treatment.80 Teriparatide, a recombinant parathyroid hormone, has recently
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demonstrated very favorable effects in this population.81 There are no data as yet with denosumab.82 Testosterone therapy may be effective in male patients with anorexia nervosa who also have low serum testosterone levels. Males with anorexia nervosa
ENDOCRINE
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actually have more severe degrees of osteoporosis then their female counterparts.83
There are multiple endocrine abnormalities associated with anorexia nervosa.
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Most patients, both female and male, are hypogonadal, due to reversion to a prepubertal state wherein pulsatile hypothalamic gonadotropin releasing hormone
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(GNRH) secretion is reduced, causing low levels of follicle stimulating hormone (FSH) and leutinizing hormone (LH).84 Thus, amenorrhea is commonly noted in most, but not all females with anorexia nervosa. Leptin may have a causal role in the amenorrhea.85 Resumption of menses generally occurs at the weight where the periods ceased or at more than 90% of ideal body weight.86 Some patients, however, have prolonged amenorrhea even after weight restoration, and fertility may be permanently adversely
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affected.87 In males with anorexia nervosa, the low testosterone levels affect potency, libido and muscle strength. Cortisol levels have been noted to be elevated due to both increased adrenal
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production and decreased renal clearance.88 Growth hormone levels are also noted to be elevated, but insulin growth factor-1 (IGF-1) levels are low, indicating a state of
growth hormone resistance.89 Most patients have thyroid function abnormalities which
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closely mimic sick euthyroid syndrome. These resolve with weight gain.90
Hypoglycemia occurs as anorexia nervosa becomes more severe, as a result of
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depleted hepatic glycogen stores. It is a poor prognostic sign which requires close monitoring.91 There is also evidence that Type 1 diabetes may be related to the development of anorexia nervosa, although the specifics are inconclusive.92 However, what is very clear is that some of these insulin-dependent diabetic patients realize that
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they can induce weight loss via reducing their use of insulin, thereby causing hyperglycemia and a resultant osmotic diuresis. This accelerates microvascular
NEUROLOGIC
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complications.93
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Brain atrophy changes occur as a result of the malnutrition of anorexia nervosa.
Neurocognitive functioning may be permanently impaired even though brain atrophy improves with weight restoration.94 Both gray and white matter are affected.
DERMATOLOGIC
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There are multiple skin changes that occur in anorexia nervosa. These include xerosis, lanugo hair growth on the spine and sides of the face, thinning of the hair, acrocyanosis and perinosis. Increased acne and carotenoderma have also been
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described.95 None of these are signs of virilization, but rather are either related to
prevent heat loss. They all resolve with weight gain.
MEDICAL COMPLICATIONS OF BULIMIA
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Self-Induced Vomiting
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reduced subcutaneous tissue or to the body’s attempt to maintain core temperature and
While the mortality rate associated with bulimia is much less than in anorexia nervosa, it is also elevated due to the severe electrolyte and acid base alterations which can be associated with purging behaviors. Ninety percent of the purging behaviors
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found in bulimia are either self-induced vomiting or the abuse of stimulant laxatives. With self-induced vomiting, the complications can be divided into the local adverse effects of vomiting and the electrolyte-acid base abnormalities which can ensue as this
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behavior becomes more extreme. Excessive vomiting can lead to persistent gastric acid reflux leading to dysphagia and dyspepsia. Treatment is cessation of this behavior
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and the administration of proton pump inhibitors. Whether patients with bulimia should be screened for Barrett’s esophagus is not clear.96 There have been reports of esophageal malignancy in bulimia.97 But, even screening for Barrett’s esophagus is the general population with reflux has recently been questioned due to lack of proof of efficicacy.98 Hematemesis is usually due to the limited Mallory-Weiss tears. Epistaxis and subconjunctival hemorrhages are self-limited, but recurrent epistaxis in a young
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female should raise the question of covert bulimia. Perimolysis refers to erosion of the dentin and enamel on the lingual service of the teeth due to repeated exposure to stomach acid.99 Similarly, oral mucositis and cheilitis are found in these patients from
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the recurrent vomiting. Recommended therapies include oral hygiene such as gentle brushing and use of a fluoride mouthwash.100 Acid exposure also causes damage to the larynx with inflammatory changes to the vocal cords and a hoarse voice.101
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Parotid gland enlargement, or sialadenosis, is a common feature of self-induced vomiting, although the precise mechanism remains elusive.102 Tissue examination of
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these parotid glands reveals large acini with prominent zymogen granules without other pathology. Of note, sialadenosis develops 3-4 days after the cessation of chronic excessive self-induced vomiting and can be very distressing to a patient with bulimia whose focus on body image is exaggerated. The swelling is bilateral, with minimal
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tenderness. There may be elevation of the salivary isonmylase enzyme serum level.103 Treatment should ideally be preemptive and comprised of use of sialagogues such as tart candies, along with an anti-inflammatory medication and the frequent application of
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hot packs. Usually this will help prevent, or if started late, said treatment usually resolves the issue within 1-2 weeks. Rarely, oral pilocarpine may be judiciously used to
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help resolve the sialadenosis.104
The most dangerous medical complications of self-induced vomiting relate to the
acid-base and electrolyte changes which ensue as a result thereof. These aberrations are the same which occur with abuse of diuretics as the preferred mode of purging, but in general those encountered with self-induced vomiting are more profoundly abnormal. The most common electrolyte abnormalities are a metabolic alkalosis and hypokalemia.
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With vomiting this is due both to loss of acid and potassium in the vomitus, as well as from the volume depleted state causing increased aldosterone secretion to sustain their blood pressure. This course of compensatory events is referred to as pseudo-Bartter’s
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syndrome.105 It predisposes these patients to a distressing propensity towards edema formation with the cessation of purging behaviors as well as if intravenous saline repletion is required and infused too quickly.106 These patients must be treated
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differently than, for example, a patient with acute gastroenteritis in need of intravenous saline, in whom it can be safely infused rather quickly.107 While the protective elevated
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aldosterone levels will self-normalize after a few weeks of no ongoing purging behaviors, it is often purposeful to initiate spironolactone in a starting dose of 25-50 mg daily, to both prevent and treat edema formation. The finding of hypokalemia, in an otherwise healthy young adult, is highly specific for the diagnosis of covert bulimia.108
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The potentially severe degrees of hypokalemia and metabolic-alkalosis and resulting cardiac arrhythmias which can develop in those who excessively purge, is the likely reason for the elevated mortality rate associated with bulimia nervosa.109 Recently,
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hypokalemia was reported to be especially dangerous in females, which is the gender mostly identified to have bulimia.110
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Most patients with bulimia nervosa use their fingers to provoke vomiting.
However, some abuse syrup of ipecac to accomplish this. This is even more dangerous because, emetine, the alkaloid in ipecac which induces vomiting, is a direct cardiac toxin.111 This toxicity is cumulative. Each bottle of ipecac contains 30 mg of ementine and with a dose of just 1,250 mg, there can be the development of an irreversible cardiomyopathy and severe congestive health failure.112
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Laxative Abuse Excessive laxative abuse is the other main mode of purging.113 Hypokalemia is
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again a potential risk of this behavior. However in contrast to diuretics and self-induced vomiting, laxative abuse is initially associated with a hyperchloremic metabolic acidosis which eventually reverts to a state of metabolic alkalosis after a chronic volume
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depleted state evolves. In addition to the electrolyte abnormalities, laxative abuse causes expected local gastrointestinal adverse effects including rectal prolapse,
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diarrhea, hemorrhoids and hematochezia.114,115 There has long been a debate whether stimulant initiative cause colorectal cancer.116
One final and major complication of laxative abuse is the cathartic colon syndrome.117 For many years it has been known that stimulant laxatives, whose
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mechanism of action is based on stimulation of peristalsis via a direct effect on Auerbach’s plexus in the colon, can cause permanent harm to these nerve plexi.118 As a result of chronic usage, the colon is converted into an inert tube incapable of the
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propagation of fecal material and severe constipation ensues,119 which may necessitate a colectomy. The exact amount of time or quantity of abuse needed to cause the
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cathartic colon syndrome is unknown. Therefore it is important to exhort these patient to cease abuse of laxatives which either contain senna, cascara, phenothalcin or bisocodyl. The aforementioned edema formation which can develop can also be treated with spironolactone and patient concerns about resultant constipation can be allayed with substitution of a judicious amount of an osmotic laxative.120,121 Much less commonly patients with bulimia purge via the usage of enema type products.122 The
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main dangers from them are attributable to the electrolyte abnormalities previously mentioned, but also from the potential for fatal hyperphosphatemia from the sodium-
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phosphate active ingredients.123
CONCLUSION
In summary, both anorexia nervosa and bulimia nervosa inherently have a litany
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of medical complications associated with them. While most of them are treatable after effective medical interventions and psychotherapy. To halt the disease process, these
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are a notable few which are associated with permanent harm. Therefore, given the relatively young age of onset of these illnesses, there is an impelling need for informed
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medical treatment to help achieve a successful treatment outcome.
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70. Corbetta F, Tremolizzo L, Conti E, Ferrarese C, Neri F, Bomba M, Nacinovich R. Paradoxical increase of plasma vitamin B12 and folates with disease severity in anorexia nervosa. Int J Eat Disord. 2015;48:317-322.
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78. Misra M, Katzman D, Miller KK, Mendes N, Snelgrove D, et al. Physiologic estrogen replacement increases bone density in adolescent girls with anorexia nervosa. J Bone Miner Res. 2011;26:2430-2438.
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83. Mehler PS, Sabel AL, Watson T, Andersen AE. High risk of osteoporosis in male patients with eating disorders. Int J Eat Disord. 2008;41:666-672. 84. Devlin MJ, Walsh BT, Katz JL, et al. Hypothalamic-pituitary-gonadal function in
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Clinical Significance
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• •
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•
Anorexia nervosa and bulimia have many medical complications associated with them In anorexia nervosa the medical complications are due to weight loss and malnutrition In bulimia the medical complications are due to the mode and frequency of purging Most complications are reversible with early effective treatment
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•
S0002-9343(15)00582-3
DOI:
10.1016/j.amjmed.2015.06.031
Reference:
AJM 13081
To appear in:
The American Journal of Medicine
Received Date: 22 May 2015 Revised Date:
19 June 2015
Accepted Date: 19 June 2015
Please cite this article as: Westmoreland P, Krantz MJ, Mehler PS, Medical Complications of Anorexia Nervosa and Bulimia, The American Journal of Medicine (2015), doi: 10.1016/j.amjmed.2015.06.031. This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.
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Medical Complications of Anorexia Nervosa and Bulimia
Mori J. Krantz, MD2,4
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Patricia Westmoreland, MD1
Philip S. Mehler, MD, FAED, FACP1,3,4
1
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Eating Recovery Center of Denver, 7351 E Lowry Blvd, Suite 200, Denver, CO 80230 – [email protected] 2
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Cardiology Division, Denver Health Medical Center, Denver, CO, 777 Bannock St., MC0960, Denver, CO 80204 – [email protected] 3
ACUTE at Denver Health, Denver Health Medical Center, 777 Bannock Street, MC4000, Denver, CO 80204 – [email protected] 4
Corresponding Author:
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Department of Medicine, University of Colorado Health Sciences Center
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Philip S. Mehler, MD, FAED, FACP 777 Bannock Street, MC 4000
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Denver, CO 80204 303-602-4972
Email: [email protected] Funding Source – None
Conflict of Interest – None Word Count: 3,888
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ABSTRACT Anorexia nervosa and bulimia nervosa are serious psychiatric illnesses related to
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disordered eating and distorted body images. They both have significant medical
complications associated with the weight loss and malnutrition of anorexia nervosa as well as from the purging behaviors which characterize bulimia nervosa. No body
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system is spared from the adverse sequela of these illnesses, especially as anorexia nervosa and bulimia nervosa become more severe and chronic. Here we review the
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medical complications which are associated with anorexia nervosa and bulimia nervosa as well as the treatment for said complications. We also discuss the epidemiology and
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psychiatric comorbidities of these eating disorders.
Keywords: Anorexia Nervosa, Bulimia, Medical Complications, Hypokalemia,
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Osteoporosis
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INTRODUCTION Anorexia nervosa and bulimia nervosa are serious psychiatric illnesses with substantial morbidity and mortality. It is the psychiatric illness with the highest mortality
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rate.1-7 Mortality is also increased in patients with bulimia nervosa.8 In both anorexia nervosa and bulimia nervosa, much of the increased mortality rate is attributable to the medical complications inherent to these two illnesses.
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Although anorexia nervosa and bulimia nervosa are defined as separate
disorders in the psychiatric Diagnostic and Statistical Manual 5th Edition (DSM-5),9 they
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both fall into the category of disordered eating, driven by an irrational fear of normal body weight, a desire for thinness, and leading to body image distortion.10 Cultural ideals of beauty and thinness may incite the development of disordered eating in vulnerable individuals, who have a genetic predisposition towards anxiety and
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perfectionism.11 Both starvation and purging may initially calm these feelings of anxiety and reduce obsessions and compulsions via a serotonergic neuronal pathway.12, 13 During the course of anorexia nervosa and bulimia nervosa, comorbid mental
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disorders also emerge as a result of altered neurotransmitter metabolism and/ or endocrine changes that result from caloric deprivation.14-17 Almost 50% of adolescent
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patients with anorexia nervosa meet criteria for at least one comorbid psychiatric illness.18 Eating disorders are strongly associated with mood and anxiety disorders, and the type and severity of these comorbidities is increased in patients who have the most severe eating disorders.19-23 In addition, patients with bulimia nervosa who have comorbid borderline personality disorder have poorer outcomes than those without borderline personality
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disorder when both groups are treated with psychotherapy and pharmacotherapy.24,25 Psychiatric comorbidity, as well as a history of suicidal or self-harm ideation, and comorbid mental illnesses all confer an increased risk of death in patients with eating
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disorders.25-28 Problems socializing, and difficulties with being assertive, are factors that contribute to maintaining an eating disorder. 29 Temperament traits of harm avoidance,
patients who recover from eating disorders.30
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combined with high reward dependence, are protective factors seen more commonly in
Treatment of anorexia nervosa and bulimia nervosa is multi-dimensional. In
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addition to nutritional rehabilitation, cognitive-behavioral psychotherapy, along with family therapy, have been shown to be effective in treating patients with anorexia nervosa,31 although the benefit of these therapies have been mostly noted in the weight maintenance phase of treatment.32
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There is only minimal to moderate evidence that psychiatric medications are efficacious in treating patients with anorexia nervosa. Despite the prevalence of mood and anxiety symptoms in patients with anorexia nervosa, medications used to treat
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these conditions are not necessarily useful treatment adjuncts for reducing the symptoms of anorexia nervosa. In one study, fluoxetine assisted in preventing relapse
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in weight-restored patients with anorexia nervosa.33 However this finding was not replicated in a subsequent study.34 While there may be evidence for using antidepressants in the weight maintenance phase, antidepressants do not ameliorate eating disorder pathology in patients who are acutely underweight.35 The poor response to antidepressants is believed to result from starvation-induced abnormalities in serotonin receptors.36
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In addition to concerns regarding the efficacy of antidepressants in patients with anorexia nervosa, there is also considerable debate as to the efficacy of antipsychotics in treating their symptoms. Low-dose antipsychotic medications may be useful in
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treating delusional beliefs regarding body image, intense ruminations about food, and the hyper-arousal and as well as anxiety induced by having to face weight
restoration.37,38 Although atypical antipsychotic medications promote weight gain in
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normal weight individuals, they do not have this effect in patients with anorexia
nervosa.35,39 However, patients with eating disorders may not accept reassurance in
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this regard. Despite the paucity of associated weight gain, there remains concern that the risk of using these medications outweighs their potential benefit.40 First generation antipsychotics (typical antipsychotics) lower the seizure threshold. Side effects of second-generation antipsychotics (atypical antipsychotics), such as orthostasis,
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prolonged QTc, and hepatotoxicity are of concern.
Despite continued debate regarding the usefulness of pharmacotherapy in patients with anorexia nervosa, pharmacotherapy for bulimia is well established.
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Fluoxetine (at doses of 60 mg or higher) is FDA-approved for bulimia nervosa, and other selective serotonin reuptake inhibitors (as well as other classes of
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antidepressants) have been found to be useful in treating patients with bulimia nervosa.32,37 The effect of fluoxetine in treating the symptoms of bulimia nervosa appears to be independent of its effects on mood, and is reportedly related to the effects of the medication on satiety, thereby reducing binge eating.41,42 Cognitive behavioral therapy is a well-established psychotherapeutic treatment for bulimia nervosa.32,43
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MEDICAL COMPLICATIONS - ANOREXIA NERVOSA Anorexia nervosa can adversely affect almost every body system. The complications arise as a direct result of weight loss and malnutrition. However, there
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are no studies which define which body mass index (BMI) is associated with a particular medical complication. The eyes may be affected by lagophthalmos, wherein the eyelids do not totally cover the eye during sleep, resulting in irritation to the cornea and mild
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ocular discomfort.44 Treatment involves taping the eyes shut at night after first applying
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a sterile lubricant.
GASTROINTESTINAL
Dysphagia can frustrate the ingestion of oral calories during the early stages of refeeding. It is due to weakened and uncoordinated pharyngeal muscles. As a result,
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patients may complain of coughing with eating or may have a history of aspiration pneumonia. The diagnosis is made by a modified barium swallow test and the treatment depends on weight restoration and input from a speech therapist to define
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proper food consistencies.45 Patients with anorexia nervosa have significantly slowed gastric emptying at their nadir weights which is accompanied by complaints of early
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satiety, nausea and bloating.46 This gastroparesis ultimately resolves with weight gain, but symptoms may respond early on to low dose, short-term usage of metoclopramide before meals. Acute gastric dilatation is a serious condition which can lead to gastric perforation if not recognized early.47 It can occur independently as an isolated finding in the early phases of refeeding or, it can occur as a result of the superior mesenteric artery syndrome.48 Superior mesenteric artery syndrome is defined by the extrinsic
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compression of the third portion of the duodenum by the superior mesenteric artery, due to loss of a fatty tissue pad which normally maintains the angle between the superior mesenteric artery and the aorta. Significant left upper quadrant abdominal pain with
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eating, emesis during the meal and early satiety should prompt an evaluation for gastric dilatation or superior mesenteric artery syndrome, via an abdominal radiograph or CT scan. Treatment of superior mesenteric artery syndrome is aimed at weight restoration
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to reconstitute the fat pad. This can be achieved by a soft or liquid oral diet or by enteral feeds via a nasojejunal tube or a percutaneously placed one.49 Acute gastric dilation is
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first treated by gastric decompression with a nasogastric tube, followed by similar treatments to those used in superior mesenteric artery syndrome. Just as there is slowing of the proximal gastrointestinal tract, there is also slowing of colonic function, resulting in constipation as an accompanying symptom in anorexia nervosa.50 Osmotic
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laxatives are useful along with reassurance that the patient’s prior bowel pattern should return over a few weeks with ongoing progressive nutritional rehabilitation. Elevated liver transaminases occur frequently at patient’s nadir weights.51 This
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generally represents apoptosis, a programmed hepatocyte death as a result of malnutrition. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT)
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are the most frequently affected in a range of 2-4 times elevated, but severe elevations have also been reported to occur.52 ALT is more elevated than AST. The prevalence of liver enzyme abnormalities correlates with lower BMI’s, hypoglycemia and the development of refeeding hypophosphatemia.53 Progressive nutritional support will resolve these elevations over the first few weeks of refeeding. Alkaline phosphatase and bilirubin are not commonly affected. Less frequently, elevations of the AST and
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ALT may be due to steatosis as a result of actual refeeding. A liver ultrasound can help elucidate the cause since in steatosis, a fatty enlarged liver will be noted.54
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CARDIAC
As noted above, anorexia nervosa has the highest mortality of any psychiatric disorder. Sudden cardiac death along with other medical complications and suicide
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account for about 60% of the deaths. The exact cause of sudden death in anorexia nervosa remains unknown. Autopsy studies do not reveal evidence of obstructive
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coronary artery disease.55 It has been postulated that alterations in cardiac conduction and repolarization contribute to heightened mortality though a single unifying mechanism. Bradycardia is commonly noted in patients and reflects heightened vagal tone in the setting of substantial weight loss. This often recovers with restoration of body
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weight. A resting heart rate of less than 60 beats per minute, for example, was seen in 95% of patients in a consecutive series.56 Sinus bradycardia in and of itself does not require specific therapy, but current guidelines recommend hospitalization for a heart
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rate less than 40 beats per minute. High-grade atrioventricular block is exceedingly rare and suggests underlying structural heart disease that may be unrelated to anorexia
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nervosa itself. Temporary pacemakers are rarely required. Persistent junctional rhythm has been described among patients with severe anorexia nervosa, which may be extinguished with exercise.57,58 Patients may present with prolongation of the rate-corrected QT (QTc) interval on
surface electrocardiography and a commonly held belief was that this is the primary cause of sudden cardiac death. However, this relationship is confounded by concurrent
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QTc-prolonging medications and depletion of serum potassium and magnesium levels. In a series of patients with severe anorexia nervosa, marked QTc interval prolongation (>500 ms) was actually uncommon in the absence of contributing factors.59 Similarly,
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Facchini and colleagues observed 29 patients with anorexia and found marked QTcprolongation in only 2 individuals.60 Both had profound hypokalemia, and after
potassium repletion, the QTc interval normalized. Therefore, to date, an independent
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causal pathway between anorexia nervosa, QTc-prolongation, torsade de pointes, and sudden cardiac death have not been demonstrated. Expectant management of delayed
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repolarization is generally adequate and includes electrolyte repletion, discontinuation of QTc-prolonging medications, and serial 12-lead electrocardiography. Severe anorexia nervosa is also known to change cardiac structure. Many patients develop left ventricular atrophy and subsequent annular changes that lead to
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mitral valve prolapse. Patients occasionally develop pericardial effusions, which are generally self-limited and resolve with weight restoration. Among the most prominent cardiovascular structural abnormalities is a substantial reduction in left ventricular
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myocardial mass with preserved left ventricular systolic function. This is generally reversible with refeeding. One study demonstrated myocardial fibrosis/scar manifested
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by late gadolinium enhancement on magnetic resonance imaging (MRI) in nearly a quarter of patients.61 Although echocardiographic atrophy and fibrosis by MRI have been demonstrated, histologic abnormalities in the heart have been poorly characterized until very recently: a published autopsy report showed left ventricular atrophy with endocardial and interstitial fibrosis, focal myxoid material deposition with mast cells, and increased cytoplasmic lipofuscin.62 Although most cardiac structural
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abnormalities are reversible in this condition, the presence of myocardial scar suggests that malignant arrhythmias remain a possible mechanism of increased mortality in this
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disease.
PULMONARY
As opposed to the cardiac system, the lungs are not adversely affected for the
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most part. There appear to be some pulmonary function test abnormalities associated with anorexia nervosa which are similar to those seen with emphysemia.63 It is not clear
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if this impairment recedes with refeeding. Spontaneous pneumothorax has been reported in anorexia nervosa along with prolonged air leaks.64
HEMATOLOGY
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As anorexia nervosa becomes worse, there is trilinear hypoplasia causing anemia, leukopenia and thrombocytopenia. Anemia occurs in 40% of these patients, with leukopenia noted in 30% and thrombocytopenia in about 10%.65 The cytopenia are
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due to gelatinous marrow transformation with atrophy of the normal fat content in the marrow and replacement by a mucopolysacharide.66 Iron deficiency is not typically
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found and red cell indices are normal. Although often neutropenic, surprisingly, these patients do not appear to be more susceptible to infectious complications.67 However, they also do not manifest a typical febrile response to infections and inflammatory markers are suppressed, which can cause a delay in the diagnosis of an infection.68 The cytopenias resolve with weight restoration; growth factors are not indicated in anorexia nervosa.69 Very recently, plasma levels of vitamin B12 and folate have been
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found to be increased. The increase is artificial as it was found to be due to hepatocyte dysfunction with leakage of the vitamins from these cells.70
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MUSCULOSKELETAL
Osteoporosis is common in anorexia nervosa and occurs early in the disease.71 Decreased bone density is evident after just one year of anorexia nervosa,
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notwithstanding the relatively young age of these patients. The risk of subsequent
fragility fractures is markedly elevated, both in adults and adolescents with anorexia
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nervosa.72,73 Fracture incidence increases soon after diagnosis of anorexia nervosa and remains so many years later. This is one of the rare complications of anorexia nervosa which may leave irreversible damage even after recovery. Thus, the need for obtaining bone density testing in all patients with a disease duration of more than one
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year. In contrast to postmenopausal osteoporosis, in anorexia nervosa the loss of bone mineral density is due to both decreased bone formation along with increased bone resorption. Also, trabecular bone is more affected than cortical bone. Yet, the exact
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etiological factors involved in their loss of bone density is not clear. Putative factors include the overlap between the normal accrual of peak bone mass and the age of
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onset of anorexia nervosa, along with the typical hypogonadal state, elevated cortisol levels and growth hormone resistance found in anorexia nervosa as will be described below.
There are currently no treatments specifically approved for the osteoporosis of
anorexia nervosa. Weight gain and resumption of menses are key and are associated with significant increases in spine and hip bone mineral density.74 However estrogen
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therapy does not appear to be of much value in anorexia nervosa. Many randomized controlled trials have found it to be ineffective, a fact which is underappreciated in the medical community.75-77 Also, the withdrawal bleeding associated with their usage can
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mislead patients into believing they are getting better. Transdermal estrogen patches have shown promising results in adolescents.78 Calcium and vitamin D by themselves do not restore bone density.79 Bisphosphonates have been shown to be effective in
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anorexia nervosa with an increase of 3-4% in spine bone mineral density after twelve months of treatment.80 Teriparatide, a recombinant parathyroid hormone, has recently
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demonstrated very favorable effects in this population.81 There are no data as yet with denosumab.82 Testosterone therapy may be effective in male patients with anorexia nervosa who also have low serum testosterone levels. Males with anorexia nervosa
ENDOCRINE
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actually have more severe degrees of osteoporosis then their female counterparts.83
There are multiple endocrine abnormalities associated with anorexia nervosa.
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Most patients, both female and male, are hypogonadal, due to reversion to a prepubertal state wherein pulsatile hypothalamic gonadotropin releasing hormone
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(GNRH) secretion is reduced, causing low levels of follicle stimulating hormone (FSH) and leutinizing hormone (LH).84 Thus, amenorrhea is commonly noted in most, but not all females with anorexia nervosa. Leptin may have a causal role in the amenorrhea.85 Resumption of menses generally occurs at the weight where the periods ceased or at more than 90% of ideal body weight.86 Some patients, however, have prolonged amenorrhea even after weight restoration, and fertility may be permanently adversely
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affected.87 In males with anorexia nervosa, the low testosterone levels affect potency, libido and muscle strength. Cortisol levels have been noted to be elevated due to both increased adrenal
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production and decreased renal clearance.88 Growth hormone levels are also noted to be elevated, but insulin growth factor-1 (IGF-1) levels are low, indicating a state of
growth hormone resistance.89 Most patients have thyroid function abnormalities which
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closely mimic sick euthyroid syndrome. These resolve with weight gain.90
Hypoglycemia occurs as anorexia nervosa becomes more severe, as a result of
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depleted hepatic glycogen stores. It is a poor prognostic sign which requires close monitoring.91 There is also evidence that Type 1 diabetes may be related to the development of anorexia nervosa, although the specifics are inconclusive.92 However, what is very clear is that some of these insulin-dependent diabetic patients realize that
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they can induce weight loss via reducing their use of insulin, thereby causing hyperglycemia and a resultant osmotic diuresis. This accelerates microvascular
NEUROLOGIC
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complications.93
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Brain atrophy changes occur as a result of the malnutrition of anorexia nervosa.
Neurocognitive functioning may be permanently impaired even though brain atrophy improves with weight restoration.94 Both gray and white matter are affected.
DERMATOLOGIC
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There are multiple skin changes that occur in anorexia nervosa. These include xerosis, lanugo hair growth on the spine and sides of the face, thinning of the hair, acrocyanosis and perinosis. Increased acne and carotenoderma have also been
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described.95 None of these are signs of virilization, but rather are either related to
prevent heat loss. They all resolve with weight gain.
MEDICAL COMPLICATIONS OF BULIMIA
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Self-Induced Vomiting
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reduced subcutaneous tissue or to the body’s attempt to maintain core temperature and
While the mortality rate associated with bulimia is much less than in anorexia nervosa, it is also elevated due to the severe electrolyte and acid base alterations which can be associated with purging behaviors. Ninety percent of the purging behaviors
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found in bulimia are either self-induced vomiting or the abuse of stimulant laxatives. With self-induced vomiting, the complications can be divided into the local adverse effects of vomiting and the electrolyte-acid base abnormalities which can ensue as this
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behavior becomes more extreme. Excessive vomiting can lead to persistent gastric acid reflux leading to dysphagia and dyspepsia. Treatment is cessation of this behavior
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and the administration of proton pump inhibitors. Whether patients with bulimia should be screened for Barrett’s esophagus is not clear.96 There have been reports of esophageal malignancy in bulimia.97 But, even screening for Barrett’s esophagus is the general population with reflux has recently been questioned due to lack of proof of efficicacy.98 Hematemesis is usually due to the limited Mallory-Weiss tears. Epistaxis and subconjunctival hemorrhages are self-limited, but recurrent epistaxis in a young
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female should raise the question of covert bulimia. Perimolysis refers to erosion of the dentin and enamel on the lingual service of the teeth due to repeated exposure to stomach acid.99 Similarly, oral mucositis and cheilitis are found in these patients from
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the recurrent vomiting. Recommended therapies include oral hygiene such as gentle brushing and use of a fluoride mouthwash.100 Acid exposure also causes damage to the larynx with inflammatory changes to the vocal cords and a hoarse voice.101
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Parotid gland enlargement, or sialadenosis, is a common feature of self-induced vomiting, although the precise mechanism remains elusive.102 Tissue examination of
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these parotid glands reveals large acini with prominent zymogen granules without other pathology. Of note, sialadenosis develops 3-4 days after the cessation of chronic excessive self-induced vomiting and can be very distressing to a patient with bulimia whose focus on body image is exaggerated. The swelling is bilateral, with minimal
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tenderness. There may be elevation of the salivary isonmylase enzyme serum level.103 Treatment should ideally be preemptive and comprised of use of sialagogues such as tart candies, along with an anti-inflammatory medication and the frequent application of
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hot packs. Usually this will help prevent, or if started late, said treatment usually resolves the issue within 1-2 weeks. Rarely, oral pilocarpine may be judiciously used to
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help resolve the sialadenosis.104
The most dangerous medical complications of self-induced vomiting relate to the
acid-base and electrolyte changes which ensue as a result thereof. These aberrations are the same which occur with abuse of diuretics as the preferred mode of purging, but in general those encountered with self-induced vomiting are more profoundly abnormal. The most common electrolyte abnormalities are a metabolic alkalosis and hypokalemia.
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With vomiting this is due both to loss of acid and potassium in the vomitus, as well as from the volume depleted state causing increased aldosterone secretion to sustain their blood pressure. This course of compensatory events is referred to as pseudo-Bartter’s
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syndrome.105 It predisposes these patients to a distressing propensity towards edema formation with the cessation of purging behaviors as well as if intravenous saline repletion is required and infused too quickly.106 These patients must be treated
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differently than, for example, a patient with acute gastroenteritis in need of intravenous saline, in whom it can be safely infused rather quickly.107 While the protective elevated
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aldosterone levels will self-normalize after a few weeks of no ongoing purging behaviors, it is often purposeful to initiate spironolactone in a starting dose of 25-50 mg daily, to both prevent and treat edema formation. The finding of hypokalemia, in an otherwise healthy young adult, is highly specific for the diagnosis of covert bulimia.108
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The potentially severe degrees of hypokalemia and metabolic-alkalosis and resulting cardiac arrhythmias which can develop in those who excessively purge, is the likely reason for the elevated mortality rate associated with bulimia nervosa.109 Recently,
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hypokalemia was reported to be especially dangerous in females, which is the gender mostly identified to have bulimia.110
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Most patients with bulimia nervosa use their fingers to provoke vomiting.
However, some abuse syrup of ipecac to accomplish this. This is even more dangerous because, emetine, the alkaloid in ipecac which induces vomiting, is a direct cardiac toxin.111 This toxicity is cumulative. Each bottle of ipecac contains 30 mg of ementine and with a dose of just 1,250 mg, there can be the development of an irreversible cardiomyopathy and severe congestive health failure.112
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Laxative Abuse Excessive laxative abuse is the other main mode of purging.113 Hypokalemia is
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again a potential risk of this behavior. However in contrast to diuretics and self-induced vomiting, laxative abuse is initially associated with a hyperchloremic metabolic acidosis which eventually reverts to a state of metabolic alkalosis after a chronic volume
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depleted state evolves. In addition to the electrolyte abnormalities, laxative abuse causes expected local gastrointestinal adverse effects including rectal prolapse,
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diarrhea, hemorrhoids and hematochezia.114,115 There has long been a debate whether stimulant initiative cause colorectal cancer.116
One final and major complication of laxative abuse is the cathartic colon syndrome.117 For many years it has been known that stimulant laxatives, whose
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mechanism of action is based on stimulation of peristalsis via a direct effect on Auerbach’s plexus in the colon, can cause permanent harm to these nerve plexi.118 As a result of chronic usage, the colon is converted into an inert tube incapable of the
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propagation of fecal material and severe constipation ensues,119 which may necessitate a colectomy. The exact amount of time or quantity of abuse needed to cause the
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cathartic colon syndrome is unknown. Therefore it is important to exhort these patient to cease abuse of laxatives which either contain senna, cascara, phenothalcin or bisocodyl. The aforementioned edema formation which can develop can also be treated with spironolactone and patient concerns about resultant constipation can be allayed with substitution of a judicious amount of an osmotic laxative.120,121 Much less commonly patients with bulimia purge via the usage of enema type products.122 The
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main dangers from them are attributable to the electrolyte abnormalities previously mentioned, but also from the potential for fatal hyperphosphatemia from the sodium-
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phosphate active ingredients.123
CONCLUSION
In summary, both anorexia nervosa and bulimia nervosa inherently have a litany
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of medical complications associated with them. While most of them are treatable after effective medical interventions and psychotherapy. To halt the disease process, these
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are a notable few which are associated with permanent harm. Therefore, given the relatively young age of onset of these illnesses, there is an impelling need for informed
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medical treatment to help achieve a successful treatment outcome.
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59. Krantz MJ, Sabel A, Sagar U, Long CS, Barbey JT, White K, Gaudianni J, Mehler PS. Factors Influencing QT prolongation in Hospitalized Patients with Severe Anorexia Nervosa. Gen Hosp Psychiatry. 2011;34:173-177. 60. Facchini M, Sala L, Malfatto G, Bragato R, Redaelli G, Invitti C. Low-K+ dependent QT prolongation and risk for ventricular arrhythmia in anorexia nervosa. International Journal of Cardiology. 2006;106:170-176.
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Clinical Significance
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Anorexia nervosa and bulimia have many medical complications associated with them In anorexia nervosa the medical complications are due to weight loss and malnutrition In bulimia the medical complications are due to the mode and frequency of purging Most complications are reversible with early effective treatment
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•