Atypical Gastric Ulcer With Impending Perforation due to Cocaine Use.

CASE REPORT

A 39-year-old man with the history of polysubstance abuse (alcohol, cocaine, heroin, and amphetamine) presented with epigastric abdominal pain and coffee ground emesis for 2 days after recent crack cocaine use. The patient denied nonsteroidal anti-inflammatory drug use. Laboratory test results were significant for leukocytosis of 12,700/μL and hemoglobin of 10 mg/dL. Computed tomography scan showed out-pouching along the stomach's lesser curvature with a possible 3-cm ulcer and concern for a concealed perforation (Figure 1).

Figure 1.

Initial computed tomography abdomen with contrast showing large outpouching defect on lesser curvature area (arrow).

The gastroenterology team was consulted for direct endoscopic visualization. Esophagogastroduodenoscopy showed a large food residue and a >3-cm nonbleeding cratered ulcer with rolled edges and pigmented material extending over the incisura (Figure 2). Biopsies from the ulcer site revealed chronic active gastritis with intestinal metaplasia, negative for Helicobacter pylori organisms and malignancy (Figure 3). The patient was discharged on high-dose proton pump inhibitors with a plan to repeat endoscopy for complete visualization. Three months later, the patient returned with abdominal pain and vomiting. He reported noncompliance with therapy and continued daily cocaine use. Repeat computed tomography scan revealed gastric perforation leading to emergent total gastrectomy with Roux-en-Y esophagojejunostomy. Histopathology findings were consistent with gastric ulcer perforation and negative for dysplasia or malignancy. He had an uneventful postoperative course and was discharged after extensive cocaine abstinence counseling.

Figure 2.

Esophagogastroduodenoscopy showing incisural ulcer (arrow) and thickened rolled margin with large ulcer base. Food residue obscuring the gastric fundus.

Figure 3.

Biopsy from the ulcer site with chronic-active gastritis and intestinal metaplasia (inset: necrotic debris at ulcer base), 100×, hematoxylin & eosin stain.

Cocaine is known to cause gastrointestinal complications including bowel ischemia and gangrene. The knowledge on the endoscopic appearance of cocaine-induced gastric ulcers is limited, mainly because of the presentation of patients with frank perforations.[1] Most common locations of these are in the greater curvature, prepyloric/pyloric regions and the first portion of the duodenum.[2] The presentation of our patient with the endoscopic appearance of cocaine-associated ulcer located at the incisura is unusual.[3,4] The large size of ulcer, rolled edges, and thick pigmented base with eschar is typical of cocaine-associated ulcer as described previously.[4] In addition, the risk of cocaine-induced giant ulcer formation and perforation is increased significantly with concomitant methamphetamine use as seen in our patient.[5] The mechanism of ulceration leading to perforation is caused by focal ischemia from intense vasoconstriction due to agonist activity of cocaine alpha-adrenergic receptors in the gastric and mesenteric arteries. Other factors include direct vasculotoxicity, microthrombi, embolism, gastric motility inhibition, and an increase in intragastric pressure from chronic aerophagia.[1] It is important to remain aware of gastrointestinal complications of cocaine and endoscopically recognize the setting of a cocaine-induced giant ulcer as it may warrant an early aggressive approach, like surgery.

DISCLOSURES

Author contributions: A. Aggarwal wrote and edited the manuscript. VRP Rokkam wrote the manuscript. V. Karasek edited and revised the manuscript. A. Aggarwal is the article guarantor.

Financial disclosure: None to report.

Informed consent could not be obtained for this case report. All identifying information has been removed.