Bulimia nervosa presenting as acute cardiogenic shock

Elaine M C Chau 周慕慈，Wing-Hing Chow 周榮興

HK Pract 2005;27:475-477

Summary

Many young people, especially females, have distorted image about their body and become obsessed with dieting. As dieting escalates, this may lead to psychological disorders such as bulimic practices and abuse of laxatives, emetics and appetite suppressant drugs. We present a case of bulimia nervosa presenting with cardiogenic shock and discuss the possible contributing causes of the acute heart failure, including electrolyte abnormalities and drug effects.

摘要

許多年輕人，尤其是女性，因對體形有著不正確的認識而強迫性節食。節食行為的不斷加重， 可導致心理障礙的出現，如暴食和濫用瀉藥、催吐劑和抑制食欲的藥物。 本文報告了一例神經性暴食症(bulimia nervosa)伴心源性休克的病例， 並討論了可能導致急性心力衰竭的原因，包括電解質紊亂和藥物作用。

Introduction

Electrolyte abnormalities are common in patients with eating disorders such as anorexia nervosa or bulimia nervosa and can lead to serious complications, such as muscle weakness, arrhythmias, cardiomyopathy, nephropathy, tetany and rhabdomyolysis. The electrolyte abnormalities can further predispose the patients to adverse side-effects of drugs. We have recently encountered a case of bulimia nervosa with an unusual presentation of acute cardiogenic shock.

Case

A previously healthy 24-year-old female patient presented to the Accident and Emergency Department after collapsing at work. She claimed to have general malaise for 3 to 4 days and had taken some over-the-counter medications, including trimethoprim-sulphamethoxazole and antacids. Furthermore, she had been taking an appetite suppressant, sibutramine, for about 1 week prior to admission. She developed sudden onset of flushing and dyspnoea prior to collapsing. On arrival in hospital, she was found to have severe hypotension and acute pulmonary oedema on Chest X-ray. She required resuscitation with mechanical ventilation and intravenous inotropic agents (dobutamine, dopamine and adrenaline). Echocardiogram showed poor contraction of the left ventricle. An intra-aortic balloon pump was inserted prior to transferring to our hospital for further management of suspected fulminant myocarditis.

On arrival at our hospital, the patient was ventilated and had cold peripheries. She was in sinus tachycardia (160/min) and her blood pressure was 70/50 despite three intravenous inotropic agents and the intra-aortic balloon pump. Cardiac monitor showed frequent non-sustained ventricular tachycardia. Echocardiogram showed a non-dilated left ventricle with globally impaired systolic function (ejection fraction 15%) and normal heart valves. Arterial blood gas showed metabolic acidosis. There was elevation of cardiac enzymes with very high levels of creatinine phosphokinase - MB isoenzyme at 62.3ng/ml (normal < 6ng/ml) and of troponin-I at 6.31 (normal < 0.4 ng/ml). Most remarkable was the presence of severe electrolyte disturbance, including hypokalaemia (potassium 2.0mmol/l), hypochloraemia (chloride 100mmol/l), hypocalcaemia (calcium 1.76mmol/l, corrected calcium 2.04mmol/l) and hypomagnesaemia (magnesium 0.55mmol/l). Her serum amylase level was elevated at 297U/L (normal range 38-119U/L). History from the patient's relatives revealed that, over the past year or so, the patient had regular eating binges with consumption of excessively large amounts of food followed by secretive self-inflicted vomiting, suggestive of a diagnosis of bulimia nervosa. Despite having a body mass index of only 17.7 (height 156cm, weight 43kg), she had a misconceived obsession about her body weight and had been taking sibutramine from a friend for about 1 week prior to admission.

After correction of electrolyte imbalance, her haemodynamics and corresponding left ventricular function improved slowly. On the third day of admission, she underwent transvenous endomyocardial biopsy, during which she developed sustained ventricular tachycardia and required defibrillation. Four large pieces of myocardium were obtained from different sites in the right ventricle using 6-French biopsy forceps. Histology of cardiac biopsy showed diffuse interstitial oedema in all four pieces but no inflammatory cells, including polymorphs, lymphocytes or giant cells. Furthermore, the myocytes were not enlarged or necrotic and did not show any evidence of damage. The patient then developed significant pericardial effusion on day 10 of admission, requiring pericardiocentesis. Pericardial fluid was negative for virus isolation. Serum antibody screening for cardiotropic viruses, mycoplasma, chlamydia and human immunodeficiency virus was also negative. She was successfully extubated when her left ventricular function returned to normal (EF 60%). She was taken off the intra-aortic balloon pump and inotropic support and was fit for discharge at three weeks after admission. She was referred for psychiatric consultation upon discharge.

At follow-up, she was well with normal left ventricular function on echocardiogram. Urinary excretion of potassium, which was initially elevated at 134mmol/day (normal range 15-44mmol/day), returned to normal on follow-up. Urinary excretion of sodium, magnesium and calcium were all within the normal range. Ultrasound scan of the kidneys was normal.

Discussion

We believe that this is the first report of severe electrolyte disturbance presenting as cardiogenic shock in a patient with bulimia nervosa. Frequent vomiting over a prolonged period may manifest as a "pseudo-Bartter's syndrome" electrolyte pattern with hypokalaemic alkalosis and hypochloraemia.¹ In our patient, renal tubular disorder is ruled out because of normal urinary electrolyte excretion. Severe hypocalcaemia and hypokalaemia which was refractory to replacement treatment but responsive to magnesium infusion has been described in a case of anorexia nervosa.² Both hypokalaemia and hypomagnesaemia may lead to cardiac arrhythmias, such as ventricular tachycardia or torsade de pointes. Hypomagnesaemia itself may cause hypokalaemia, which may be refractory to potassium supplementation until correction of magnesium deficiency.³ More importantly, magnesium deficiency can lead to refractory circulatory shock.⁴ It is important to recognize that the serum magnesium level represents <1% of total body stores and may not reflect total-body magnesium concentration. Apart from the severe electrolyte disturbance, another laboratory clue that suggests the diagnosis of bulimia nervosa in our patient is the finding of hyperamylasaemia, which is present in many bulimic patients.⁵ It is said that there is a positive correlation between the frequency of vomiting and the extent of elevated serum amylase level. Another contributing factor to the cardiogenic shock in this patient may be drug-related. Sibutramine, a serotonin and norepinephrine transporter blocker, is an appetite suppressant agent. However, adverse cardiac side-effects such as hypertension, arrhythmias, tachycardia and even death from cardiac arrest have been reported.⁶ Indeed the drug is not only contraindicated in patient with cardiovascular diseases but also in those with anorexia and bulimia nervosa. Patients with eating disorders are also known to abuse diuretics, laxatives, enemas or emetics, the use of which was denied by our patient. Misuse of diuretics, laxatives and enemas can place the bulimic at great risk for electrolyte imbalance. It has been reported that chronic ipecac ingestion for emesis can result in cardiomyopathy, which may or may not be reversible.⁷

Although cardiogenic shock due to acute fulminant myocarditis may present in a similar way, the lack of fever and viral illness symptoms, absence of inflammatory cells on endomyocardial biopsy and negative viral screening make the diagnosis of viral myocarditis unlikely but cannot rule it out. Myocarditis per se cannot account for the severe electrolyte imbalance. To postulate concomitant myocarditis and bulimia-induced severe electrolyte imbalance would be against the principle of Ockham's razor.

The diagnosis of bulimia nervosa was suspected in our patient because of the abnormal eating habits as described by her relatives. According to the World Health Organization, the criteria for making the diagnosis of bulimia nervosa include persistent preoccupation with eating, episodes of overeating, actions to counteract the binging (such as induced vomiting, excessive exercise, laxative or diuretic abuse) and fear of obesity, all of which were present in our patient. Bulimia is further subdivided into the purging type and the non-purging type depending on the presence or absence of self-induced vomiting or misuse of laxatives, diuretics or emetics. The major cardiac complication of eating disorders is arrhythmias which may lead to sudden cardiac death. The markers for fatal arrhythmias in these patients are prolongation of QT interval and QT dispersion on electrocardiogram⁸.

Conclusions

In conclusion, acute cardiogenic shock should be added to the list of potential life-threatening complications of eating disorders. Family physicians should have a high index of suspicion for eating disorders in patients with preoccupation with body weight. Detailed enquiry of eating habits, abnormal behaviour such as purging, possible drug abuse, especially emetics, laxatives and appetite suppressants, is indicated. Unfortunately, due to denial of symptoms, the diagnosis is often delayed. In patients diagnosed with or suspected to have eating disorders, monitoring of electrocardiogram for QT abnormalities or arrhythmias, and periodic measurements of electrolyte levels, including potassium, calcium and magnesium, are recommended.

Key messages

1. Bulimia nervosa is a serious and potentially life-threatening illness affecting mainly young women.
2. The binging and purging activity associated with the purging subtype of bulimia nervosa can lead to electrolyte imbalance, cardiac arrhythmias, heart failure and death among many other medical complications.
3. Abuse of appetite suppressants, laxatives, diuretics and emetics is not unusual in bulimics and side-effects of the drugs may further complicate the clinical picture.
4. Use of sibutramine is contraindicated in patients with eating disorders.
5. Apart from the diagnostic criteria, other features in supporting a diagnosis of bulimia include abnormal ECG findings, electrolyte disturbances and raised serum amylase level.