- Case Report
- Open Access
Life threatening hyperkalemia following cocaine ingestion: a case report
© licensee BioMed Central Ltd. 2009
- Received: 19 April 2009
- Accepted: 8 June 2009
- Published: 30 July 2009
We present a case of life-threatening hyperkalemia after recreational cocaine ingestion. Acute cocaine-induced rhabdomyolysis led to hyperkalemia, cardiac arrhythmias and cardiogenic shock resulting in multi-organ failure.
- Cocaine Abuse
- Cocaine Ingestion
- Bilateral Basal Ganglion
- Prone Ventilation
Cocaine is a popular drug of abuse and there is a tremendous surge in its use because of its stimulant and euphoric properties . It has multi-systemic involvement and there are many reports detailing its harmful effects. Cocaine toxicity normally occurs in chronic abusers and is mainly due to excessive central nervous system stimulation and excessive adrenergic vasoconstriction, the latter resulting in severe hypertension and/or organ ischaemia with associated organ injury . Rhabdomyolysis is a recognised complication of cocaine toxicity . It has been postulated that this results from a combination of sympathetic and muscular overactivity leading to vasoconstriction, micro-infarcts and skeletal muscle necrosis and local pressure necrosis whilst the patient is obtunded . Cocaine-induced hyperpyrexia with fluid loss and inadequate replacement may also precipitate acute renal failure. The cardiovascular complications of cocaine abuse are adrenergic mediated and range from cocaine-associated acute coronary syndromes to aortic dissection and sudden cardiac death . Mortality secondary to cocaine abuse is usually not secondary to single drug overdose but most deaths occur after prolonged drug use, which initiates a series of changes at the molecular, cellular, and tissue levels . All of these changes favour sudden death . Additionally, cocaine use has been associated with spontaneous coronary dissection, mesenteric ischemia, stroke, venous thrombosis, and a variety of pulmonary complications .
Wide complex dysrhythmia due to cocaine in the absence of myocardial Infarction, as happened in our case, is rare and optimum management is undefined . It was postulated that this was due to direct myocardial sodium channel antagonism similar to class I antidysrhythmic drugs and is treated by administration of IV Sodium Bicarbonate. Cocaine ingestion can also lead to Brugada electrocardiographic pattern and can be misleading as it is similar to the ST elevation that occurs in cocaine induced myocardial ischaemia .
Cocaine has also been shown to have caused cerebral infarcts when injected intravenously. Although very rare but it is also implicated in case reports to cause bilateral basal ganglia infarcts .
In this case the patient presented with cardiovascular, renal, neurological, and metabolic effects of cocaine overdosage. The etiology of the cardiogenic shock was either myocardial ischaemia or broad complex tachycardia secondary to sodium channel antagonism and/or hyperkalemia.
The decision to undertake coronary angiography was influenced by the recognised complications of cocaine toxicity . After coronary intervention the focus of treatment was hyperkalemia. At this point a trial of IV sodium bicarbonate would have been worthwhile. Once the serum potassium was corrected the rhythm became normal. The important point is that the DC cardioversion did not restore normal sinus rhythm because of the ongoing hyperkalemia. Earlier vigorous treatment of the hyperkalemia might have improved the cardiac output and may have reduced the severity of the multi-organ failure.
We suggest that patients presented to emergency medicine department with cocaine overdosage and electrolyte abnormality should have this corrected as a priority. Untreated hyperkalemia has a high mortality.
Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
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