The most serious complications of cocaine use and overdose involve the effects on the cardiovascular and cerebrovascular systems.
Significant hyperthermia (core temperature > 40°C [104°F]) should be treated by aggressive cooling mechanisms, including ice water immersion, when feasible, or evaporation of water sprayed directly on the patient with cooling fans, as well as liberal use of benzodiazepines to decrease neuromuscular excitation.
Psychiatric emergencies with agitated delirium and psychosis should be treated with benzodiazepines to control and maintain a safe environment for the patient and emergency department (ED) staff.
Acute myocardial infarction and cerebrovascular accident should be treated as per the standard of care, with specifics of management described below.
Patients with cocaine-indued sympathomimetic toxicity, especially those who have experienced hyperthermia and enhanced neuromuscular excitation, should be closely monitored for the development of rhabdomyolysis and renal failure.
Cocaine is a tropane alkaloid derived from the coca plant (Erythroxylum coca), which is found in South America. Ancient inhabitants of Peru were documented to have chewed or sucked on the leaves of this plant for social and religious reasons, a practice that still occurs today. Therapeutically, cocaine was first used for ophthalmologic procedures in 1884, but toxicity was quickly reported. There is still limited use for cocaine in the otolaryngology setting as an anesthetic and vasoconstrictor, but it is more widely used as a drug of abuse. Its pharmacologic properties are due to its inhibition of catecholamine reuptake at the neuromuscular junction, and toxicity is due to excessive sympathetic nervous system stimulation. Recreational use was made illegal in the United States after the passage of the Harrison Narcotics Act of 1914, but it remains a stimulant commonly seen, with 2.2 million people using cocaine regularly and 1.5 million meeting the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria for cocaine use disorder.
Illegal street cocaine is available in different forms:
- Cocaine salt is water soluble and absorbed through all mucous membranes (intranasal, oral, intravaginal, rectal) or injected. Street names include coke, blow, white lady, white dragon, nose candy, happy dust, aspirin, foo-foo dust, lady, Big C, coconut, Florida snow, devil's dandruff, and flake.
- Cocaine freebase has the ability to be smoked because it melts at a lower temperature. A common method of preparation is combining it with a base such as sodium bicarbonate. Street names include crack (named due to the cracking sound made while being smoked), crack cocaine, rock, freebase, twinkie, gravel, electric kool-aid, purple caps, black rock, scramble, window pane, supercoke, and yam.
- In a paste form, it has been called pasta, basuco, and bazooka.
The effects of cocaine use are described as a state of hyperalertness, energy, and euphoria. Cocaine toxicity, or acute intoxication, refers to the unintended effects of cocaine on the human organs. Cocaine intoxication results in substance-related ED visits second only to those of acute alcohol toxicity. Patients may present with behavioral changes (agitation, psychosis, restlessness, anxiety, and heightened emotions), circulatory changes (hypertension, pallor, irregular pulse, arrythmias), respiratory changes, hyperthermia, and central nervous system signs (sweating, nausea, vomiting, tremor, headache, vertigo, and teeth grinding).
Chest pain is the most common cardiopulmonary complaint of cocaine users presenting to the ED. Dyspnea and diaphoresis are also common. Of these patients, the incidence of cocaine-associated myocardial infarction is estimated at 0.7%-6%, and cocaine appears to be an important contributor to myocardial infarction in young patients. Myocardial ischemia caused by cocaine occurs by multiple mechanisms, including increasing myocardial oxygen demand due to induced tachycardia, hypertension, and increased contractility; decreasing oxygen supply via vasoconstriction, the prothrombotic properties of cocaine; and by accelerating atherosclerosis.
Other adverse effects include delusions, paranoia, hallucinations, impaired judgment, aggressive behavior, depressed mood, sleep disturbance, decreased appetite, weight loss, dyskinesia, dilated pupils, tachycardia, and cravings. Chronic use of cocaine can also result in cardiovascular problems including arrhythmias, myocardial infarction, stroke, dilated cardiomyopathy, and cardiac arrest. Cocaine's ability to increase atherosclerosis and its prothrombotic effect makes the cardiovascular system particularly susceptible to end-organ damage after use and overdose, as mentioned above.
Substance use involving the combination of stimulants and opioids is increasing in incidence. The combination of heroin and cocaine has classically been termed a "speedball." This combination is often taken by individuals physically dependent on opioids who are craving an enhanced sense of euphoria by the addition of cocaine. Not only does this combination place the user at risk for the adverse effects of both stimulants and opioids, but if the user is administered naloxone, there is the potential to have cardiac and neurological toxicity from the unopposed cocaine.
The use of cocaine with ethanol is also a common coingestion. This combination metabolizes to cocaethylene. This metabolite has a longer duration of action than cocaine, with similar effects.
Patients with this disorder may have an increased risk of various general medical conditions and mental health disorders. Cocaine use is associated with increased risk of depression as well as co-occurring substance use disorders. The self-medication hypothesis poses that patients attempt to relieve their psychiatric symptoms with the use of stimulants.
Levamisole is a substance used medically as an anthelmintic drug that has been found as a common adulterant in cocaine. Levamisole is believed to potentiate the effects of cocaine due to mood-elevating properties, as seen by some clinicians when used as an anthelmintic. There is also evidence that levamisole selectively inhibits monoamine oxidase type A and decreases norepinephrine reuptake. Symptoms of levamisole toxicity include skin eruptions, agranulocytosis with neutropenia, and a vasculitis affecting the tips of the ears, nose, and, when most severe, other larger parts of the body.
Related topics: cocaine mucosal ulcer, cocaine-related cardiomyopathy, skin popping substance abuse, sympathomimetic toxicity