pylori infection and/or age distribution. The frequency of peptic ulcer and its perforation may change depending on the frequency of H. It occurs most often in elderly patients with co-existent medical problems, who are at increased risk of post-operative complications. The lifetime risk of benign gastroduodenal perforation is 10% in untreated PUD and, 30–50% of ulcer perforations are associated with NSAIDS ( 1, 2). Acute ulcers along the anterior part of first part of duodenum usually perforate, whereas those on posterior aspect tend to cause bleeding as they erode into gastroduodenal artery. pylori and late presentation ( 10– 14).ĭuodenal and gastric ulcers remain the two most common perforations of the gastrointestinal tract due to the increased use of NSAIDS. With the younger population in sub-Saharan Africa, the high mortality of PPU (~20%) is mostly due to the high prevalence of the causative H. This is due to the fact that the age mix of the disease has changed with more elderly females on NSAIDs and many with serious concomitant medical illnesses (poor American Society of Anaesthesiologists score-ASA) ( 9). Despite improvements in resuscitation techniques, antibiotic therapy and anesthesia, the mortality associated with perforated peptic ulcers over the last two decades remains about 25%. The surgical treatment with a simple omental patch closure of the perforation has not changed much over a century and PPU still remains a life-threatening condition with a high mortality of up to 40% being reported ( 8). Although <1% of gastric ulcers is pre-malignant, the percentage of cancer in gastric perforation (9%) is fairly significant ( 7). Ulcers on the greater curve, fundus and in the antrum are more commonly malignant ( 5– 8). Benign gastric ulcers occur predominantly in the elderly, on the lesser curve. Below the age of 40 years duodenal ulcers are four times more common than gastric ulcers and are more common in men. The incidence of peptic ulcer disease (PUD) is estimated to be ~ 1.5–3%, the lifetime prevalence of perforation is ~5% and mortality ranges from 1.3 to 25% ( 5). Other factors include smoking, chronic liver disease, chronic renal failure, especially during dialysis and transplantation, and hyperparathyroidism. The two main factors implicated in the etiology are non-steroidal anti-inflammatory drugs (NSAIDS) and Helicobacter pylori ( H. The majority is from spontaneous perforation due to peptic ulcer disease (PUD) although there are more unusual causes ( 1, 2). Gastric perforation may be spontaneous or traumatic. Gastrointestinal perforation, with leakage of alimentary contents into the peritoneal cavity, is a common surgical emergency and may have life-threatening sequelae. Primary closure is achievable in traumatic perforation, but the management follows the Advanced Trauma Life Support (ATLS) principles. However, non-operative management has a significant incidence of intra-abdominal abscesses and sepsis. Perforated peptic ulcer is an indication for operation in nearly all cases except when the patient is asymptomatic or unfit for surgery. The majority of perforated peptic ulcers are caused by Helicobacter pylori, so definitive surgery is not usually required. The management of perforated peptic ulcer disease is still a subject of debate. The classic sub-diaphragmatic air on chest x-ray may be absent and computed tomography scan is a more sensitive investigation in the stable patient. Improved medical management of peptic ulceration has reduced the incidence of perforation, but still remains a common cause of peritonitis. Gastroduodenal perforation may be spontaneous or traumatic and the majority of spontaneous perforation is due to peptic ulcer disease. Department of Surgery, Faculty of Health Sciences, University of Buea, Buea, Cameroon.
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