1433 A Case of Cocaine-Induced Pancreatitis

Abstract

INTRODUCTION: Cocaine-induced pancreatitis is a rare and likely under-reported entity. Physicians must maintain a index suspicion when treating patients with cocaine use who present with abdominal pain especially if they are also on other concomitant medications that increase the risk of acute pancreatitis. CASE DESCRIPTION/METHODS: A 61-year-old male with cocaine abuse and heart failure with reduced ejection fraction (HFrEF) presented with 3 days of epigastric abdominal pain, nausea, and vomiting. His last intranasal use of cocaine was a few days prior to onset of symptoms. Lipase was 2300 (U/L) and computed tomography of the abdomen (CT) demonstrated an edematous and homogeneously enhancing pancreas with a small amount of peripancreatic fluid. Abdominal ultrasound was negative for cholelithiasis. Patient had a remote history of alcohol use but denied recent alcohol abuse. Toxicology was positive for cocaine on day of admission. An ethanol level was not obtained. Triglyceride, IgG4, and calcium levels were within normal limits. Notably, the patient was also hospitalized two months prior to present presentation for new onset left cerebellar stroke. Upon further evaluation, the patient was found to have a left ventricular ejection fraction of 30-35%, consistent with new diagnosis of HFrEF. The patient was started on metoprolol prior to discharge. Based on lack of other identifiable causative factors, patient's pancreatitis was attributed to concurrent cocaine and beta-blocker use. DISCUSSION: Pancreatitis is the most common gastrointestinal diagnosis resulting in admission, costing 2.6 billion dollars annually. The most common etiologies are gallstones and alcohol. Few cases of cocaine-induced pancreatitis have been reported in the literature. Cardiovascular and central nervous system (CNS) toxicities of cocaine such as acute coronary syndromes, chest pain, agitation, and strokes are well documented. Acute gastrointestinal complications of cocaine use are less common however usually include ischemic bowel and related perforation. There are only 5 reported cases of cocaine-induced pancreatitis. The mechanism of action of cocaine is inhibition of noradrenaline re-uptake, which produces vasoconstriction and thrombosis of mesenteric vessels. The pathophysiology of cocaine-induced pancreatitis is postulated to be related to vasoconstriction and thrombotic microangiopathy. In this patient, prior heavy alcohol may have led to underlying parenchymal disease and concomitant use of a beta-blocker were likely additive.