Anesthetic Management of Patients with Cocaine Intoxication

INTRODUCTION

In 2006, 2.4 million Americans aged 12 or older were current cocaine users.¹ In 2009, nearly 500,000 emergency department visits were attributed to cocaine use, many requiring surgical intervention.² Given the increased risks of arrhythmias, myocardial ischemia, cerebral vasoconstriction, and stroke, anesthesia professionals must understand cocaine’s physiological effects. We present two surgical cases involving recent cocaine use and highlight the perioperative cardiovascular instability that can result. Both patients provided consent to publish their respective case report.

CASE 1

A 28-year-old, 75 kg male with a history of cocaine abuse presented to the emergency department with two abdominal stab wounds. On admission, he was hypertensive (181/85 mmHg), tachycardic (140 bpm), and alert (Glasgow Coma Scale 15), with no respiratory or cardiac complaints. Despite fluids, benzodiazepines, and opioids, he remained tachycardic and in pain. Urine drug screen confirmed recent cocaine use, which the patient admitted to using just prior to injury. Although mildly agitated, the patient remained cooperative. He was scheduled for emergent exploratory laparotomy.

On arrival to the operating room, he was alert with a blood pressure of 140/75 and heart rate of 115 bpm. General anesthesia was induced with intravenous midazolam, propofol, succinylcholine, and fentanyl, and maintained with sevoflurane in 60% oxygen. Although initially stable, over the next 20 minutes his heart rate declined to the 40s before progressing to asystole. Advanced cardiac life support was initiated; following one round of chest compressions and a dose of epinephrine (1 mg IV), return of spontaneous circulation was achieved with blood pressure 100/50 and heart rate 95 bpm.

No intra-abdominal or retroperitoneal injuries were noted, and the abdominal cavity was closed without further cardiovascular events. Postoperatively, he was transported to the intensive care unit without vasopressor or inotropic support, successfully extubated, and discharged three days later after an uneventful recovery. No further cardiac evaluation was performed.

CASE 2

A 46-year-old man with a 20-year history of daily intranasal cocaine use presented for biopsy of a rapidly enlarging nasal lesion. Although he denied cocaine use in the prior two weeks, urine toxicology was positive. Preoperative vital signs were within normal limits, and general anesthesia was induced with propofol and fentanyl. Shortly after induction, the patient became profoundly hypotensive despite repeated boluses of phenylephrine and ephedrine and eventually required a phenylephrine infusion. Postoperatively, the patient remained hypotensive and an echocardiogram revealed left ventricular hypokinesis and a reduced ejection fraction of 40–45%.

The patient was diagnosed with cocaine-induced vasculitis and treated with steroids. He was empirically treated with antibiotics to treat a suspected infection. In the next few months, the patient underwent two otorhinolaryngological procedures. During the first he treated with phenylephrine infusion prior to induction and had no hypotensive episodes. During the second procedure he was not treated preoperatively with phenylephrine, but did have several episodes of intraoperative hypotension that resolved after the initiation of a phenylephrine infusion.

DISCUSSION

These two cases highlight the critical role of anesthesia professionals in managing patients with cocaine use and the need for careful monitoring during the perioperative period. Both patients experienced unexpected intraoperative hypotension resistant to vasopressors, likely due to fluctuating cocaine serum levels. While acute intoxication increases sympathetic tone, rapid declines in cocaine and metabolite levels can lead to cardiovascular collapse, which was seen about 20 minutes after induction in both cases. Additionally, cocaine’s effects may both counteract anesthesia-induced vasodilation and reduce central sympathetic outflow, further contributing to the hypotension and bradycardia noted in these patients.³ Direct-acting vasopressors like phenylephrine or norepinephrine are more likely to be effective than indirect agents such as ephedrine.⁴ Anticipating cardiovascular instability from catecholamine excess or depletion is vital for timely intervention and successful resuscitation.⁴

Anesthetic management for patients with a history of cocaine use depends on the timing of use and comorbidities. Perioperative care should include individualized plans to prevent withdrawal,⁵ and while one study found no increased anesthetic risk in cocaine-intoxicated patients compared to matched controls,⁶ it is reasonable to consider checking cardiac markers such as troponin, chest radiography, electrocardiogram, arterial blood gas, neuroimaging, and other studies in high-risk patients.

Knowing when it is safe to proceed with anesthesia when a patient tests positive for cocaine can be a challenging decision with limited guidance. One survey found that only 16% of hospitals have a formalized policy for screening and treating patients positive for cocaine.⁷ The authors of this survey suggested, when appropriate, non-emergent surgeries be delayed for at least 8 hours after cocaine use, and longer if necessary in patients who exhibit hemodynamic instability.⁷ The authors also note that urine testing may be positive for cocaine up to 20 days after use, limiting the utility of routine urine testing for risk stratification.⁷

When considering a regional anesthetic technique, anesthesia professionals should be aware of possible contamination found in street samples of cocaine. One study found that more than half of a cocaine compound sold was contaminated with other local anesthetics.⁸ This increases the potential for anesthetic toxicity, especially with high-dose regional techniques.

Lastly, while acute intoxication poses challenges, chronic cocaine use also affects anesthetic management. Left ventricular dysfunction is common and may result from myocardial infarction, fibrosis, catecholamine excess, and calcium dysregulation.⁹ Animal studies further link prolonged use to myocardial enzyme depletion and impaired cardiac function.⁹

These cases illustrate how both acute and chronic cocaine use can lead to unpredictable, potentially severe effects on multiple organ systems. Comprehensive screening may be appropriate when the results could impact anesthetic management or surgical timing. Standardized protocols should emphasize individualized care, and further research on chronic use is needed.

Dr. Rahul K. Mishra is an Anesthesiology Resident Physician at the Texas Tech University Health Sciences Center School of Medicine, Lubbock, Texas, United States of America.

Dr. Cooper Phillips is the Division Chief, Anesthesiology Division of Critical Care Medicine; Medical Director, Extracorporeal Membrane Oxygenation Program; ECMO Program Co-Director, Neuro Intensive Care Unit; Assistant Professor, Department of Anesthesiology at the Texas Tech University Health Sciences Center School of Medicine, Lubbock, Texas, United States of America.

Dr. Christiane Vogt-Harenkamp is associate professor of Anesthesiology at the Texas Tech University Health Sciences Center School of Medicine, Lubbock, Texas, United States of America.

Dr. James E. Heavner was the professor Emeritus of Anesthesiology, clinical professor and founding director of the Anesthesiology research program at the Texas Tech University Health Sciences Center School of Medicine, Lubbock, Texas, United States of America.

Or Belkin is a 4^th year medical student at the Texas Tech University Health Sciences Center School of Medicine.

Luis Fernandez-Nava is a PGY-1 at HCA Healthcare Southern Hills.

Elliotte Cannon is a 4^th year medical student at the Texas Tech University Health Sciences Center School of Medicine.

The authors have no conflicts of interests.

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