Recommended Citation
Wojcik C, De Ranieri A, Sumar M. Management of recalcitrant hypotension in cocaine positive trauma patient with ICH. Presented at: Midwest Anesthesia Residents Conference (MARC); April 26, 2025; Indianapolis, IN.
Presentation Notes
Presented at: Midwest Anesthesia Residents Conference (MARC); April 26, 2025; Indianapolis, IN.
Abstract
Introduction: Peri-operative substance abuse presents various substance-specific challenges for anesthesia providers. Cocaine is a sympathomimetic alkaloid with two primary mechanisms of action including inhibition of monoamine re-uptake as well as blockade of sodium channels. Acute intoxication may manifest as agitation, hypertension, hyperthermia, tachycardia and tachyarrhythmias, and myocardial ischemia. At higher doses (3 mg/kg), cocaine has also been shown to have cardiovascular depressant effects. Chronic cocaine abuse results in peripheral catecholamine depletion and may manifest as hypotension or rebound hypertension. Case Presentation: A 30-year-old male with unknown past medical history presents after assault with a crowbar. Vitals showed SBP 150, HR 131. Secondary survey showed pupillary asymmetry. CT Head showed left SDH with mild mass effect, 7 mm midline shift, SAH, and early bilateral tonsillar herniation. Urine drug screen was positive for cocaine. He was then taken emergently to the operating room for left craniotomy. General anesthesia was induced using 100 mcg/kg/min of propofol and 0.07 mcg/kg/min of remifentanil, and muscle relaxation was undertaken with 50 mg of rocuronium. At induction, he was also given 30g of Mannitol. Immediately following induction, he developed hypotension with BP of 88/66, MAP 61. Over the course of the first hour of the case, a phenylephrine infusion was started at 20 mcg/min and quickly titrated up to 140 mcg/min and was given 5,000 mcg of phenylephrine pushes with MAPs of 53 to 84, with only transient modest increases in blood pressure. Ultimately, a 1,500 mcg of phenylephrine bolus was given and produced a MAP increase from 60 to 67, however, after 1 minute MAP had decreased back to 53 and ultimately down to 38. A Levophed infusion was then started at 4 mcg/minute, which maintained MAPs between 50-64 which remained insufficient for adequate cerebral perfusion. Finally, vasopressin pushes were initiated in 2 unit aliquots as pushes and was later started on a 0.04 unit/minute infusion, which was successful in maintaining MAPs >70. Over the course of 3 hours and 10 minutes, he received 29,340 mcg of Phenylephrine, 500 mcg of Levophed, and 19.84 units of Vasopressin. He was transferred intubated to ICU, where Levophed and Vasopressin infusions were continued. Conclusion: Classically, patients with acute cocaine intoxication are expected to display hypertension. Paradoxically, our patient experienced severe recalcitrant hypotension. We suspect this to be due primarily to chronic cocaine abuse causing depletion of peripheral catecholamines. Direct-acting adrenergic vasopressors such as phenylephrine, epinephrine, and norepinephrine are first-line for patients with hypotension in states of chronic catecholamine depletion. Vasopressin, a direct non-adrenergic vasopressor which acts on V1 receptors in vascular smooth muscle resulting in increased peripheral vascular resistance and mean arterial pressure, may be utilized in cases of hypotension refractory to direct-acting adrenergic vasopressors, as was done in our case. 1. Bartels K, et al. (2021) Anesth Analg. 132(2):305-307. 2. Christopher M. Bernards, et al. (1996) Anesthesiology 84:218–220 3. Emerick, Trent D. et al. (2023) Anesth Analg 137(3):474-487.
Type
Oral/Podium Presentation
Affiliations
Advocate Illinois Masonic Medical Center