Cocaine
GENERAL PRINCIPLES
• Cocaine was historically used as a topical vasoconstrictor and local anesthetic.
• Cocaine is used recreationally by a variety of routes—it may be insufflated, smoked, injected, or taken orally.
Pathophysiology
• Cocaine inhibits the reuptake of serotonin, norepinephrine, and dopamine, producing an excitatory or sympathomimetic state.
• Cocaine is also a local anesthetic with sodium channel antagonist properties and may produce cardiac conduction abnormalities.
• Cocaine is vasculotoxic, enhances platelet aggregation, and accelerates the development of atherosclerotic disease. 27
DIAGNOSIS
Clinical Presentation
• Cocaine poisoning presents with a sympathomimetic toxidrome (see above, amphetamines). Cocaine may also cause choreoathetoid movements and psychomotor agitation.
• Patients may present with symptoms related to end-organ damage from the sympathomimetic toxidrome, including seizures, neurologic deficits from stroke or intracranial hemorrhage, or chest pain.
• The onset of action of cocaine by the usual routes of use is very rapid, and the duration of cocaine intoxication is typically short; symptoms due to cocaine intoxication should resolve within about 8 hours after use.
Diagnostic Testing
LABORATORIES
Have a low threshold to obtain a BMP, troponin, and/or creatinine kinase to evaluate for end-organ damage, including renal injury, myocardial ischemia, and rhabdomyolysis.
ELECTROCARDIOGRAPHY
• Electrocardiography may demonstrate sinus tachycardia or ventricular dysrhythmias and may show ischemic changes in the ST segments or T waves.
• Cocaine may prolong the QRS complex or induce or unmask a Brugada-like pattern. 28
TREATMENT
• The mainstay of treatment is benzodiazepines or other directly GABAergic sedatives, titrated to control of agitation and improvement of vital signs.
• Intravenous fluid resuscitation is necessary in cases of rhabdomyolysis.
• Patients with evidence of sodium channel blockade (QRS prolongation on ECG) should be treated with sodium bicarbonate (bolus of 1-2 mEq/kg followed by infusion, with the goal of normalizing the QRS duration).
• Management of chest pain and myocardial infarction may be complex.
î Cocaine intoxication may cause coronary vasospasm leading to chest pain and myocardial
infarction; this should be treated with benzodiazepines. 27
î Patients who use cocaine are also at risk of type I myocardial infarction due to accelerated atherogenesis and platelet adhesion.
If this occurs, usual treatment with antiplatelet agents, anticoagulants, and potentially cardiac catheterization should be pursued.
î Close discussion with a cardiologist is warranted if objective evidence of myocardial ischemia is present.
• Control of blood pressure and heart rate should be achieved by appropriate titration of benzodiazepines or other sedatives. When tight blood pressure control is required (e.g., aortic dissection, intracranial hemorrhage, acute MI), use agents that are rapidly titratable, such as nicardipine, clevidipine, or nitroglycerin. Consider avoiding beta-adrenergic antagonists due to a theoretical concern that “unopposed alpha” stimulation could cause severe peripheral vasospasm.
• Patients with hyperthermia require aggressive external cooling in addition to aggressive sedation. Paralysis with nondepolarizing neuromuscular blockers may be required in severe cases.