ANTIBIOTICS FOR THE ACUTE ABDOMEN

Abstract

Antibiotics are only an adjunct to proper surgical therapy for the treatment of the acute abdomen associated with bacterial secondary peritonitis. Upon presentation, all patients require a preoperative dose of antibiotics for prophylaxis against infection of remaining sterile tissues. Patients found intraoperatively to have an established peritoneal infection benefit from an immediate postoperative course of therapeutic antibiotics. A regimen that adequately covers facultative and aerobic gram-negative bacilli and anaerobic organisms is essential. The duration of therapeutic antibiotics is probably best decided on an individual patient basis. The goal of antibiotics is to reduce the concentration of bacteria invading tissues. The pathogens of bacterial peritonitis are influenced by such factors as the patient's pre-existing chronic diseases, state of acute physiologic debilitation, immunocompetence, recent antibiotic use, recent hospitalization, and neutralization of gastric acidity. Intraoperative peritoneal cultures are most useful in patients suspected of having impaired local host defenses. In these patients, all identified organisms, such as Enterococcus or Candida, may be potential pathogens. The common practice of administering empiric and prolonged courses of broad-spectrum antibiotics in patients who manifest persistent signs of inflammation may be more harmful than beneficial. These patients warrant an exhaustive search for extra-abdominal and intraperitoneal sources of new infection. Otherwise, such use of antibiotics may continue to promote the selection of bacteria that are highly resistant to conventional antibiotics and permit the overgrowth of organisms commonly seen with tertiary peritonitis. The best chance of resolving bacterial peritonitis is through early, aggressive surgical management complemented by short courses of potent antibiotics and appropriate physiologic support. Through these efforts, the clinician tries to help the systemic inflammatory response to benefit the host and not become unregulated, result in MOFS, and produce a high mortality.