Medical Complications of Cocaine Abuse

Medical Complications of Cocaine Abuse

Cardiac toxicity is one of the leading causes of morbidity and mortality associated with cocaine use. The risk of myocardial infarct is well established in cocaine use and is not related to dose, route, or frequency of administration. The risk of acute myocardial infarction is increased 24-fold in 1 hour immediately following cocaine use in persons who are otherwise at relatively low risk for such events (Mittleman et al., 1999). Detection of re-cent cocaine use by urine toxicology screen has been observed in 25% of those reporting to urban emergency departments and 7% of those evaluated at suburban hospitals and found to have evi-dence of myocardial infarct (Hollander et al., 1995). About half of the patients with cocaine-related myocardial infarction have no evidence of atherosclerotic coronary artery disease (Hollander et al., 1997a, 1997b). Identifying and diagnosing cocaine-related myocardial infarction can be difficult. The hallmarks of myocar-dial infarct are a constellation of physical symptoms including chest pain, electrocardiogram (ECG) abnormalities and elevated creatine kinase. Cocaine abusers with chest pain may have ECG abnormalities that are not specific for myocardial infarct (We-ber et al., 2000). Cocaine abusers are also often found to have nonspecific elevations in creatine kinase without myocardial in-farction. Therefore, the diagnosis of cocaine-related myocardial infarction is often based on the physician’s clinical judgment. Evaluation of serum troponin I, a cardiac marker that is not af-fected by recent cocaine use, can be helpful in determination of whether a myocardial infarct has occurred.

The pathophysiology of cocaine-related myocardial inf-arction is probably multifactorial. The sympathomimetic effects of cocaine increase myocardial oxygen demand by increasing heart rate, systemic blood pressure and left ventricular contrac-tility while reducing oxygen supply through its coronary artery vasoconstriction effects (Baumann et al., 2000). According to new treatment guidelines for emergency cardiovascular care, ni-troglycerine and benzodiazepines are first line agents and phen-tolamine is a second line agent for patients with cocaine-related myocardial ischemia or infarction. Propranolol is contraindicated as it exacerbates cocaine-induced vasoconstriction of coronary arteries. Thrombolysis is not recommended unless evidence of evolving myocardial infarction persists despite medical ther-apy and an occluded coronary artery is shown to be present on angiography.

Cocaine use is associated with a wide range of cardiac dysrhythmias including sinus tachycardia, sinus bradycardia, su-praventricular and ventricular tachycardia, ventricular premature contractions, ventricular tachycardia and fibrillation, torsades de pointes and asystole. Life-threatening dysrhythmia caused by cocaine in the absence of myocardial ischemia is rare. In many instances, cardiac dysrhythmias have occurred in the context of profound hemodynamic or metabolic disturbances (Wang, 1999). Intranasal abuse of cocaine has been associated with a number of medical complications including chronic sinusitis, septal perfora-tion, subperiosteal abscess, pneumomediastinum, pneumothorax and pulmonary edema (Gendeh et al., 1998). The presence of pulmonary edema in a young, otherwise healthy patient, without predisposing risk factors, should alert the physician to the pos-sibility of cocaine abuse.

Cerebrovascular accidents related to cocaine use have been well documented in the medical literature. Cerebral infarct, subarachnoid hemorrhage, intraparenchymal hemorrhage and intraventricular hemorrhage have been observed as acute com-plications of cocaine use. Seizures were one of the earliest known complications of cocaine abuse. While anticonvulsants have not been helpful in preventing cocaine-related seizures, intravenous diazepam has been effective in acute management.