Perforated Duodenal Ulcer in High Risk Patients

Abstract

Peptic ulcer disease remains one of the most prevalent disease of the gastrointestinal tract with annual incidence ranging from 0.1% to 0.3% in western countries. There are well-known two major precipitating factors: Helicobacter pylori infection and the use of non-steroidal anti-inflammatory drugs (NSAIDs) and the ulcer incidence increases with age for both duodenal and gastric ulcers. Peptic ulcer disease (PUD) is considered as a mucosal functional derangements due to intraluminal aggressive factors and defects in endogenous defense mechanisms affecting the mucosa and extend through the muscularis mucosa. Some of these functional defects may be caused by the presence of H pylori colonization of the antral mucosa and antral mucosal metaplasia of the proximal duodenum. In vivo and in vitro data support this concept, particularly with reference to the mechanisms of Helicobacter pylori-induced aberrations in gastric and duodenal mucosal function. Standard medical therapy for peptic ulcer disease includes antisecretory medications as well as antibiotics designed to eradicate H pylori colonization. Complications of peptic ulcer disease are bleeding, perforation and obstruction. These complications can occur in patients with peptic ulcers of any etiology. Perforation occurs in about 5% to 10% of patients with active ulcer disease. Duodenal, antral and gastric body ulcers account for 60%, 20% and 20% of perforations, respectively, of peptic ulcers. Open and laparoscopic abdominal exploration are always indicated in gastroduodenal perforation. Hemodynamic instability, signs of peritonitis and free extravasation of contrast material on upper gastrointestinal tract contrast studies make the decision for operation more urgent and imperative. But, the advent of proton pump inhibitors and Helicobacter pylori eradication in the management of chronic peptic ulcer disease has reduced the operative treatment of this condition to its complications. Perforated duodenal ulcer remains a major life threatening complication of chronic peptic ulcer disease. The incidence of peptic ulcer disease in normal populations has declined over the past few years following a more streamlined pharmacological intervention. This can be attributed to the efficiency of histamine 2 (H2) blockers and proton pump inhibitors. Additionally, the diagnosis and eradication of Helicobacter pylori infection, now known to be a major factor in the pathogenesis of peptic ulcer disease, has almost eliminated the role of surgery in the