
A cocaine-positive patient rolls into the OR and the monitors look fine—until twenty minutes after induction, when the blood pressure plummets. We unpack that swing from sympathetic surge to sudden crash through two real cases: an emergent trauma laparotomy complicated by asystole and a chronic intranasal user with profound hypotension that only responded to direct-acting vasopressors. From there, we connect the dots to the pharmacology that makes these events predictable and, with the right plan, manageable.We talk candidly about what matters before wheels-in: timing of last use, objective signs of toxicity, and targeted testing. You’ll hear why urine screens can stay positive for weeks, why indirect agents like ephedrine can fail, and how phenylephrine or norepinephrine often become first-line choices. For regional anesthesia, we flag contamination risks and local anesthetic systemic toxicity concerns that call for dose adjustment and intralipid readiness. Chronic cocaine use adds another layer, including left ventricular dysfunction, myocardial infarction and fibrosis, and calcium dysregulation.Hospital policy and equity loom large. Automatic cancellations for cocaine positive patients can worsen pain, delay care, and disproportionately impact patients with limited access. We review current evidence suggesting many asymptomatic, cocaine-positive patients tolerate elective noncardiac surgery under general anesthesia with hemodynamics comparable to controls when vigilant management is in place. The takeaway: build flexible, evidence-informed pathways that prioritize patient safety without reflexive delays, and keep a rescue mindset with careful monitoring and direct vasopressors within reach. If this sparked ideas for your practice, subscribe, share with a colleague, and leave a review so more clinicians can find these insights.
For show notes & transcript, visit our episode page at apsf.org: https://www.apsf.org/podcast/291-managing-anesthesia-risks-for-patients-with-acute-and-chronic-cocaine-use/
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