Cocaine use is responsible for approximately 143,000 Emergency Department visits annually; 19% of American, between 18 to 25 years old, have used cocaine: more than 1% of the Americans use cocaine at least once a week; and approximately 50% of all drug-related deaths were secondary to Cocaine. The temporal association between smoking cocaine (crack) and GI tract manifestations include ulceration, perforation, visceral infarction, and retroperitoneal fibrosis. Most ulcer perforations are juxtapyloric or duodenal (D1) however jejunal location has been reported. The physiopathologic hypothesis includes the following mechanisms 1) cocaine blocks the re-uptake of norepinephrine leading to intense vasoconstriction (alpha-adrenergic receptors), mesenteric ischemia, focal tissue ischemia, coagulative necrosis and perforation; and 2) cocaine causes thrombus formation and platelet aggregation mediated by endogenous Thromboxane B2. A few retrospective cohort studies suggest that primary patch repair is the recommended therapeutic option for this type of ulcers. However, Shuster et al reported a high recurrence rate (42%) after omental patch repair compared to a definitive anti-ulcer procedure (0%). Little information exists about the association between crack and gastroduodenal ulcer perforations other than the temporal association reported in small retrospective cohort studies. In a communication, Dr Mason recalls two patients with perforated "stomach ulcers" associated with cocaine use.