Cocaine is one of the most popular drugs of abuse. It may be sniffed into the nose (snorted), smoked, or injected IV. Occasionally, it is combined with other drugs (eg, injected with heroin). Cocaine may contain adulterants including lidocaine or benzocaine, or stimulants such as caffeine, methamphetamine, ephedrine, and phencyclidine. Most illicit cocaine in the United States is adulterated with levamisole, an antiparasitic drug that can cause agranulocytosis and leukocytoclastic vasculitis.

The “free base” form of cocaine is preferred for smoking, because it volatilizes at a lower temperature and is not as easily destroyed by heat as the crystalline hydrochloride salt. Free base is made by dissolving cocaine salt in an aqueous alkaline solution and then extracting the free base form with a solvent such as ether. Fires and explosions can result if heat is applied to hasten solvent evaporation. “Crack” is a free base form of cocaine produced by using sodium bicarbonate to create the alkaline aqueous solution, which is then dried.

The primary actions of cocaine are CNS stimulation, inhibition of neuronal uptake of catecholamines, and local anesthetic effects.

1. Central nervous system stimulation and inhibition of catecholamine uptake result in a state of generalized sympathetic stimulation very similar to that of amphetamine intoxication.
2. Cardiovascular effects of high doses of cocaine, presumably related to blockade of cardiac cell sodium channels, include slowed conduction (QRS prolongation) and depressed contractility. Cocaine-induced QT prolongation also has been described.
3. Pharmacokinetics. Cocaine is well absorbed from all routes, and toxicity has been described after mucosal application as a local anesthetic. Smoking and IV injection produce maximal effects within 1-2 minutes, whereas oral or mucosal absorption may take up to 20-30 minutes. Once absorbed, cocaine is eliminated by metabolism and hydrolysis, with a half-life of about 60 minutes. In the presence of ethanol, cocaine is transesterified to cocaethylene, which has similar pharmacologic effects and a longer half-life than cocaine.

The toxic dose is highly variable and depends on individual tolerance, the route of administration, and the presence of other drugs, as well as other factors. Rapid IV injection or smoking may produce transiently high brain and heart levels, resulting in convulsions or cardiac arrhythmias, whereas the same dose swallowed or snorted may produce only euphoria.

1. The usual maximum recommended dose for intranasal local anesthesia is 100-200 mg (1-2 mL of 10% solution).
2. A typical “line” of insufflated cocaine contains 20-30 mg or more. Crack usually is sold in pellets or “rocks” containing 100-150 mg.
3. Ingestion of 1 g or more of cocaine is likely to be fatal.

1. Central nervous system manifestations of toxicity may occur within minutes after smoking or IV injection or may be delayed for 30-60 minutes after snorting, mucosal application, or oral ingestion.
   1. Initial euphoria may be followed by anxiety, agitation, delirium, psychosis, tremulousness, muscle rigidity or hyperactivity, and seizures. High doses may cause respiratory arrest.
   2. Seizures are usually brief and self-limited; status epilepticus should suggest continued drug absorption (as from ruptured cocaine-filled condoms in the GI tract) or hyperthermia.
   3. Coma may be caused by a postictal state, hyperthermia, or intracranial hemorrhage resulting from cocaine-induced hypertension.
   4. Cocaine is the most common cause of drug-induced stroke. Stroke can be hemorrhagic (related to severe hypertension), embolic (resulting from atrial fibrillation or endocarditis), or ischemic (resulting from cerebral artery constriction and thrombosis). Stroke should be suspected if there is altered mental status and/or focal neurologic deficits.
   5. With chronic cocaine use, insomnia, weight loss, and paranoid psychosis may occur. A “washout” syndrome has been observed after a prolonged binge, consisting of profound lethargy and deep sleep that may last for several hours to days, followed by spontaneous recovery.
2. Cardiovascular toxicity may also occur rapidly after smoking or IV injection and is mediated by sympathetic overactivity.
   1. Fatal ventricular tachycardia or fibrillation may occur. QRS-interval prolongation similar to that seen with other sodium channel blockers (eg, tricyclic antidepressants) may occur.
   2. Severe hypertension may cause hemorrhagic stroke or aortic dissection.
   3. Coronary artery spasm and/or thrombosis may result in myocardial infarction, even in patients with no coronary disease. Diffuse myocardial necrosis similar to catecholamine myocarditis and chronic cardiomyopathy have been described.
   4. Shock may be caused by myocardial, intestinal, or brain infarction; hyperthermia; tachyarrhythmias; or hypovolemia produced by extravascular fluid sequestration caused by vasoconstriction. Intestinal infarction may be complicated by severe, diffuse GI hemorrhage and hemoperitoneum.
   5. Renal failure may result from shock, renal arterial spasm and/or infarction, or rhabdomyolysis with myoglobinuria.
3. Death is usually caused by a sudden fatal arrhythmia, status epilepticus, intracranial hemorrhage, or hyperthermia. Hyperthermia is usually caused by seizures or muscular hyperactivity or rigidity and is typically associated with rhabdomyolysis, myoglobinuric renal failure, coagulopathy, and multiple-organ failure. Severe hyperthermia is more common when the environmental temperature is high, particularly when a high ambient temperature is combined with physical hyperactivity.
4. A variety of other effects have occurred after smoking or snorting cocaine.
   1. Chest pain without ECG evidence of myocardial ischemia is common. The presumed basis is musculoskeletal, and it may be associated with ischemic necrosis of chest wall muscle.
   2. Pneumothorax and pneumomediastinum cause pleuritic chest pain, and the latter is often recognized by a “crunching” sound (“Hamman sign”) heard over the anterior chest.
   3. Chronic exposure to cocaine contributes to premature atherosclerosis.
   4. Chronic insufflation may cause nasal septal perforation.
   5. Accidental subcutaneous injection of cocaine may cause localized necrotic ulcers (“coke burns”) and wound botulism.
   6. Cocaine adulterated with benzocaine can cause methemoglobinemia.
5. Body “packers” and “stuffers.” Persons smuggling cocaine may swallow large numbers of tightly packed cocaine-filled condoms (“body packers”). Attempts to hide evidence from law enforcement may involve an individual quickly swallowing cocaine, often without carefully wrapping or closing the packets or vials (“body stuffers”). Swallowed condoms, packets, or vials may break open, releasing massive quantities of cocaine, causing severe intoxication. Intestinal obstruction may also occur. The packages are sometimes, but not always, visible on plain abdominal radiograph. Likewise, CT imaging of body stuffers or packers does not consistently confirm the presence or absence of ingested packets.

Is based on a history of cocaine use or typical features of sympathomimetic intoxication. Skin marks of chronic IV drug abuse, scarring from coke burns, and nasal septal perforation after chronic snorting suggest cocaine use. Chest pain with electrocardiographic evidence of ischemia or infarction in a young, otherwise healthy person also suggests cocaine use. Note: Young adults, particularly young African-American men, have a high prevalence of normal J-point elevation on ECG, which can be mistaken for acute myocardial infarction. Otherwise unexplained seizures, coma, hyperthermia, stroke, or cardiac arrest should raise suspicion of cocaine poisoning.

1. Specific levels. Blood cocaine levels are not routinely available and do not assist in emergency management. Cocaine and its metabolite benzoylecgonine are easily detected in the urine for up to 72 hours after ingestion and provide qualitative confirmation of cocaine use.
2. Other useful laboratory studies include electrolytes, glucose, BUN, creatinine, creatine kinase (CK), urinalysis, urine myoglobin, cardiac troponin, ECG and ECG monitoring, and CT head scan (if hemorrhage is suspected). Abdominal radiography (plain films or CT scanning) is not reliably sensitive enough to confirm or rule out ingested drug-filled packets.

1. Emergency and supportive measures
   1. Maintain an open airway and assist ventilation if necessary.
   2. Treat coma, agitation, seizures, hyperthermia, arrhythmias, and hypotension if they occur. Benzodiazepines are a good choice for initial management of hypertension and tachycardia associated with agitation.
   3. Angina pectoris may be treated with benzodiazepines, aspirin, nitrates, or calcium channel blockers. For acute myocardial infarction, thrombolysis is controversial. Supporting its use is the high prevalence of acute thrombosis, often superimposed on coronary spasm. Against its use is the excellent prognosis for patients with cocaine-induced infarction, even without thrombolysis, and concerns about increased risks for bleeding caused by intracranial hemorrhage or aortic dissection.
   4. Monitor vital signs and ECG for several hours. Patients with suspected coronary artery spasm should be admitted for cardiac monitoring, and because of reports of persistent or recurrent coronary spasm up to several days after initial exposure, consider the use of an oral calcium antagonist and/or cardiac nitrates for 2-4 weeks after discharge.
2. Specific drugs and antidotes. There is no specific antidote.
   1. While controversial, avoid the use of beta blockers in the management of acute cocaine toxicity. Propranolol, a nonselective beta blocker, can exacerbate cocaine-associated coronary artery vasoconstriction and produce paradoxical worsening of hypertension because of blockade of beta₂-mediated vasodilation. If a beta blocker is needed (eg, for tachycardia and hypertension not responsive to benzodiazepines and IV fluids, especially if associated with myocardial ischemia), current evidence is most supportive of the use of labetalol or carvedilol. Beta blockers may also be used in combination with a vasodilator such as phentolamine for management of hypertension.
   2. QRS prolongation caused by sodium channel blockade can be treated with sodium bicarbonate. Wide-complex tachyarrhythmias may also respond to lidocaine.
3. Decontamination. Decontamination is not necessary after smoking, snorting, or IV injection. After ingestion, perform the following steps:
   1. Administer activated charcoal orally if conditions are appropriate (see Table I-37).
   2. Gastric lavage is not necessary after small-to-moderate ingestions if activated charcoal can be given promptly.
   3. For ingestion of cocaine-filled condoms or packets, give repeated doses of activated charcoal and consider whole-bowel irrigation unless there is evidence of bowel obstruction, bowel perforation, or severe GI hemorrhage. If large ingested packets (eg, Ziploc bags) are not removed by these procedures, laparotomy and surgical removal may be necessary. Surgical intervention to remove ingested packets may also be required for patients with persistent severe symptoms of cocaine intoxication or bowel obstruction.
4. Enhanced elimination. Because cocaine is extensively distributed to tissues and rapidly metabolized, dialysis and hemoperfusion procedures are not effective. Acidification of the urine does not significantly enhance cocaine elimination and may aggravate myoglobinuric renal failure.