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DP61: ANESTHETIC MANAGEMENT OF CARCINOID SYNDROME
Rayce Silva, MD; Nathalie Abitbol, MD, MBA
Jackson Health System/University of Miami
Introduction: Carcinoid syndrome is a clinical manifestation of serotonin and vasoactive substance secreting neuroendocrine tumors, most commonly arising from the GI tract with frequent hepatic metastases. During a crisis, patients most commonly present with flushing, diarrhea, bronchospasm, and detrimental hemodynamic instability. While in surgery, physical tumor manipulation, stress, and certain anesthetic agents can precipitate a life-threatening carcinoid crisis. Anesthetic management therefore requires meticulous planning, avoidance of triggering medications, and perioperative somatostatin analog therapy to mitigate this catastrophic risk.
Methods: We describe the case of an 82 year-old male with metastatic small bowel neuroendocrine tumor and active carcinoid syndrome, with symptoms of episodic flushing, secretory diarrhea, and intermittent wheezing who presented for an elective cystolitholapaxy due to kidney stones. He was maintained on long-acting octreotide therapy. Preoperative labs revealed mild hypokalemia secondary to chronic diarrhea and he underwent a preoperative echocardiogram to rule out valve abnormalities. A multidisciplinary perioperative octreotide protocol was designed for his perioperative course.
Results: On day of surgery, patient was administered octreotide (500mcg) subcutaneously. A continuous octreotide infusion (50 mcg/hour) was initiated prior to induction. Induction was achieved with propofol, fentanyl and rocuronium with the goal to avoid histamine-releasing agents. Should any hemodynamic change, such as profound hypotension, have occurred with induction, plan was to use boluses of octreotide (50mcg-100mcg) so as to counteract possible serotonin surges. Maintenance of anesthesia was performed with a propofol and remifentanil drips. Throughout the case, no significant hemodynamic changes occurred, nor did any bronchospasm or arrhythmia arise. Patient was extubated in the operating room and monitored postoperatively in the ICU without further episodes of instability. While in the ICU, the octreotide gtt was weaned over several hours, with an overlap of 500mcg of octreotide being administered subcutaneously every 8 hours. This dose was tapered on POD2 to 250mcg subcutaneously every 8 hours, until it was discontinued in the absence of concerning events. The patient was discharged on POD 4.
Discussion: Carcinoid crisis is a well recognized and potentially life threatening perioperative complication characterized by profound hemodynamic instability, bronchospasm, flushing, and arrhythmias. Intraoperative carcinoid crises occur in up to 20–30% of surgeries, even with prophylactic strategies in place. These events result from sudden massive release of serotonin, histamine, and other vasoactive mediators during tumor manipulation, anesthetic induction, or stress responses. In addition to avoiding anesthetics that release histamine (such as morphine, atracurium, succinylcholine) and avoiding sympathomimetic drugs that may trigger further hormone release, it is imperative to maintain deep anesthesia and use octreotide both prophylactically and as a therapeutic agent. Octreotide, a synthetic somatostatin analog that binds to somatostatin receptors on neuroendocrine tumor cells, inhibits the release of vasoactive substances such as serotonin, bradykinin, histamine, and prostaglandins. During a carcinoid crisis, it reduces further mediator release, stabilizes systemic vascular resistance, and helps prevent bronchospasm. Implementing a perioperative octreotide protocol is essential in patients with carcinoid syndrome, and the anesthesiologist must be familiar with the latter as rapid recognition of hemodynamic instability and treatment with octreotide can be lifesaving.