Search

Background: Salmonella typhi infection continues to be a significant problem worldwide. Patients suffering from "typhoid" in endemic regions such as West Africa often present late in the course of the disease with symptoms of malnutrition and peritonitis. Clinical peritonitis in these patients is invariably associated with perforation of the terminal ileum and purulent peritonitis. Operative intervention and its success have not been well documented. The purpose of this article is to review the experience of 1 hospital in West Africa and the efficacy of operative management of perforated intestine from typhoid., Methods: A retrospective review of all patients admitted between January and October of 2003 to the Carolyn Kempton Memorial Hospital in Togo, West Africa, with the diagnosis of typhoid. Demographic data including age, sex, number of perforations, and outcome were obtained. All patients were treated with ampicillin, gentamycin, and flagyl or chloramphenicol as the sole antibiotic therapy along with operative management., Results: One hundred ninety-one patients with typhoid were admitted. One hundred twelve patients underwent laparotomy for perforation, 18 of whom died from persistent typhoid septicemia for a mortality rate of 16%. Reoperative management was used in some patients who did not respond immediately., Conclusions: Primary repair of typhoid perforation is a safe and effective treatment. Patients with persistent septicemia after laparotomy most likely have resistant Salmonella typhi infection. Availability of second-line antibiotic therapy in these third world countries would likely improve outcomes. Prospective studies on appropriate antibiotic therapy along with operative management in endemic areas are necessary until resources are available for preventative measures.

Intestinal motility, absorption, and secretion are altered after intestinal obstruction, but at what point the normal bacterial barrier function of the viable gut fails after intestinal obstruction is unclear. Thus, we tested whether after simple intestinal obstruction bacteria would translocate across the viable intestinal wall to cause systemic infection. Within 6 hours of intestinal ligation 1 cm proximal or distal to the ileocecal valve, bacteria had translocated to the mesenteric lymph nodes, and by 24 hours after intestinal obstruction, bacteria had spread to the liver, spleen, and blood stream. Bacterial translocation rarely occurred in the animals undergoing laparotomy and sham intestinal ligation, indicating that bacterial translocation was not due to surgical stress. Based on the results of these studies, bacterial translocation induced by intestinal obstruction appears to be due to disruption of the ecology of the normal gut microflora, leading to intestinal overgrowth with certain enteric bacilli and mucosal damage. Although the exact mechanism(s) by which simple mechanical obstruction injures the intestine is not known, the fact that mucosal injury did not occur in germ-free mice suggests that bacteria may play a role in the pathogenesis of obstruction-induced intestinal injury.

The objective of this experimental study of small bowel obstruction was to investigate luminal bacterial colonization and assess the most likely mediator substances responsible for the pathophysiologic alterations, those being endogenous endotoxin and prostaglandins. Eighteen pigs with small bowel obstruction and 11 sham-operated control animals given constant infusion therapy were investigated over 7 days. Bacteria determinations were performed at operation and at sacrifice. Endotoxin levels were determined three times and prostaglandin levels, twice daily in portal and central venous blood. In the pigs with small bowel obstruction, greatly increased microflora with a predominance of E. coli bacteria was observed in the obstructed bowel. Endotoxin measurements proved general release into the circulation, with potentially toxic levels in the systemic circulation arising relatively late on the fourth postobstruction day. Beginning on the first postobstruction day, stimulation of the prostaglandin system occurred which was initially limited to the gastrointestinal tract but spread systemically when the obstruction persisted for more than 5 days. Vasoactive eicosanoids were predominantly involved. The control animals showed none of the alterations seen in the animals with small bowel obstruction.