Which agent is recommended for acute cocaine toxicity management?

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Multiple Choice

Which agent is recommended for acute cocaine toxicity management?

Explanation:
Acute cocaine toxicity is driven by surge of central and peripheral sympathetic activity from elevated catecholamines. The most effective first step is rapid relief of this hyperarousal and prevention of seizures, agitation, and cardiovascular complications. A benzodiazepine given IV fits that need perfectly: it quickly sedates, reduces anxiety and agitation, and lowers CNS sympathetic outflow, which in turn lowers heart rate and blood pressure and reduces the risk of seizures. IV lorazepam is preferred because of its reliable onset and smooth titration, allowing rapid control of symptoms in the emergency setting. Beta-blockers are not recommended in this context because blocking beta receptors in the setting of cocaine-induced alpha-adrenergic–mediated vasoconstriction can leave the alpha effects unopposed, potentially worsening hypertension, coronary vasospasm, and other cardiac complications. That’s why they’re avoided in acute cocaine toxicity. Naltrexone targets opioid receptors and does not address cocaine's effects, so it isn’t useful here. Diphenhydramine doesn’t treat the underlying sympathomimetic intoxication and isn’t used as a primary therapy for cocaine toxicity.

Acute cocaine toxicity is driven by surge of central and peripheral sympathetic activity from elevated catecholamines. The most effective first step is rapid relief of this hyperarousal and prevention of seizures, agitation, and cardiovascular complications. A benzodiazepine given IV fits that need perfectly: it quickly sedates, reduces anxiety and agitation, and lowers CNS sympathetic outflow, which in turn lowers heart rate and blood pressure and reduces the risk of seizures. IV lorazepam is preferred because of its reliable onset and smooth titration, allowing rapid control of symptoms in the emergency setting.

Beta-blockers are not recommended in this context because blocking beta receptors in the setting of cocaine-induced alpha-adrenergic–mediated vasoconstriction can leave the alpha effects unopposed, potentially worsening hypertension, coronary vasospasm, and other cardiac complications. That’s why they’re avoided in acute cocaine toxicity.

Naltrexone targets opioid receptors and does not address cocaine's effects, so it isn’t useful here. Diphenhydramine doesn’t treat the underlying sympathomimetic intoxication and isn’t used as a primary therapy for cocaine toxicity.

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