[Multiple perforation of peptic ulcer following gastric resection].
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Factors affecting survival were retrospectively analyzed in 89 patients (50 men) operated upon for perforated peptic ulcer. Mean age was 52 years. Only 18 per cent had no history of significant medical illness; almost 26 per cent were termed immune suppressed from high-dose steroid therapy or the presence of diffuse, metastatic cancer. The estimated interval between perforation and operation was over 24 hours in one-third. Preoperative serum creatinine, determined in 83 patients, ranged from 0.1 to 6.4 mg/dl (mean, 1.5 mg/dl); no patients were dialysis-dependent. At celiotomy, 75 per cent underwent ulcer plication only; the remainder had a definitive acid reduction procedure. Stepwise logistic regression analysis revealed that a normal preoperative serum creatinine (less than 1.5 mg/dl) was the most powerful predictor of survival (P less than 0.00001), followed by absence of immune suppression, and age under 60 years. The interval between perforation and operation, the site of perforation, and the type of operation did not statistically affect survival.
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A retrospective study was made based on 243 patients with simple closure of a perforated peptic ulcer in order to analyse factors influencing the results. Complications and mortality showed a good correlation with age, time between onset of symptoms and operation and size of the perforation, but no correlation with ulcer localization and history. Between 1 and 15 years after the operation, 39,4% of the patients were asymptomatic, 34,8% under conservative treatment, whilst 25,8% had to be reoperated on in the meantime. There was no correlation between recurrence and the age of the patients, the time between onset of symptoms and operation, the duration of stay in hospital, inability to work, alcohol and nicotine abuse. Ulcer history was the only factor influencing the late result significantly. Only 11% of patients with a short ulcer history (no longer than 6 months) had to be reoperated on whereas in those with a long ulcer history a recurrence rate of 70% can be expected. The importance of ulcer history for the choice of surgical treatment is emphasized.
BACKGROUND: Perforations of the stomach and duodenum are frequent causes of acute generalized peritonitis in our environment. This is a prospective study of 331 cases of gastric and duodenal perforations. STUDY DESIGN: A consecutive series of adult patients admitted and treated for acute generalized peritonitis due to peptic ulcer perforations was studied prospectively from January 1998 to June 2004. A specially designed proforma was used to record patient characteristics, clinical and operative findings and outcome. Additional information on self-medication and other relevant social habits was obtained and recorded. The data was analysed and the ratio of gastric to duodenal perforations as well as factors associated with perforations determined. RESULTS: More males were affected by a ratio of 3.3:1. For all the patients the median age was 55.0 and the mean age was 52.2 +/- 17.5 years. The mean age of the perforated gastric ulcer patients was 47.7 +/- 17.1 years but higher for perforated duodenal ulcer patients at 64.8 +/- 11.4 years. There were 244 gastric and 87 duodenal perforations giving a ratio of 2.8:1. Most of these perforations were associated with the intake of Non Steroidal Anti Inflammatory Drugs (NSAIDS) 158 (47.7%), habitual ingestion of herbal medicines or concoctions 81 (24.5%) and prolonged fasting for religious reasons, 18 (5.4%). Acute renal failure 32 patients (31.1%), continuing or persistent peritonitis 12 patients (11.6%), wound infection 25 patients (24.3%), and chest infection 12 patients (11.6%), were some of the 103 post-operative complications seen. The overall mortality was 73( 22.1%). The death rate from perforated duodenal ulcer was 27 (32.2%) and that from perforated gastric ulcer was 46 (20.1%). CONCLUSION: In our community perforated gastric ulcer is seen more often than perforated duodenal ulcer. These gastric perforations are related to the widespread use of NSAIDS and herbal medicines.
Cocaine is a potent topical vasoconstrictor that causes nasal mucosal and dermal ulceration. Use of the purified cocaine derivative "crack" has reached epidemic proportions in large cities. In 18 months we operated on 24 patients with perforated peptic ulcers. Five of the patients were young (27-38 years) male crack users without prior history of gastric symptoms who presented with a perforated gastric ulcer related to smoking crack. Three had had symptoms for only 1-5 days before admission. All five were afebrile, had a rigid abdomen, normal leukocyte count, and free intraabdominal air upon radiography. Five other age-matched, non-crack-using patients served as case controls. Their duration of symptoms was 1-24 months, they had elevated leukocyte counts on admission, and, in contrast to the crack users, four of these patients had duodenal perforations. The clinical presentation of the crack smokers and the unusual localization of the perforations imply different pathogenetic mechanisms than are commonly seen in perforated ulcer disease. With increasing abuse of crack, greater numbers of patients with this new complication may be expected to present to emergency services in urban areas.
There has been controversy regarding the relationship between Helicobacter pylori and perforated peptic ulcer, which is known to have a high recurrence rate if only simple patch repair is performed. The aim of this study was to evaluate the association between H. pylori infection and intake of non-steroidal anti-inflammatory drugs (NSAIDs) in patients with perforated duodenal ulcers. Of the 73 patients recruited over a 16-month period, 51 (70 per cent) had evidence of H. pylori infection by intraoperative gastroscopy and antral biopsies. The infection rate rose to 80 per cent if NSAID users were excluded. The H. pylori-infected group was significantly younger (mean 47.6 versus 62.5 years), with a male preponderance (49 of 51 versus 14 of 22 patients), and had significantly less NSAID consumption (three of 51 versus ten of 22) and more prolonged dyspepsia (40 of 51 versus ten of 22), compared with H. pylori-negative patients. H. pylori infection probably plays an important role in the causation of non-NSAID-induced duodenal ulcer perforation. Whether eradication of the bacteria can alleviate the strong ulcer diathesis in this subgroup of patients is unknown.
The eradication of Helicobacter pylori in patients with peptic ulcer disease has greatly diminished the need for antiulcer surgery. However, in societies where such drug therapy is considered too expensive and because occasional patients remain refractory to optimal medical therapy, elective surgery for duodenal ulcer disease is still carried out. If the required expertise is available, it can be undertaken laparoscopically. The advent of endoscopic therapies such as heater probe therapy and injection sclerotherapy has also greatly diminished the need for emergency surgery in bleeding peptic ulcer disease. Once again, however, when such therapy fails surgery is still indicated. Even with perforated peptic ulcer disease the role of surgery has receded somewhat, but here not because of changes in drug therapy. Nonoperative management of perforation is indicated in fit patients if the diagnosis is in doubt, in any patient when surgical facilities are unavailable (e.g., remote geographic areas, on board ship), or when a patient is extremely ill either because of co-morbidity or late presentation of the disease. Operation should be considered in all patients when the perforation is established to be unsealed, particularly after
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