Abdominal catastrophe: visceral injury as a cause of peritonitis in patients treated by peritoneal dialysis.

OBJECTIVE: Peritonitis is considered an acceptable and controllable risk in patients undergoing chronic peritoneal dialysis (PD). In contrast, peritonitis due to visceral leakage represents a true "abdominal catastrophe" because of striking morbidity and mortality. To delineate the incidence, causes, and outcomes of catastrophic peritonitis, we compared patients who developed peritonitis due to documented visceral leakage with patients who developed peritonitis due to enteric organisms without evidence of visceral leakage. DESIGN: Retrospective chart review. SETTING: PD Unit located in tertiary care referral center. PATIENTS: 230 patients treated by PD between January 1988 and June 1996. MAIN OUTCOME MEASURES: All episodes of PD-related peritonitis occurring over an 8-year period. Hospital course of all patients with or without renal failure who were treated at University Hospitals of Cleveland for ischemic bowel disease, cholecystitis, viscus perforation, or diverticulitis. RESULTS: Anatomically documented visceral injury caused 32.5% of episodes of enteric bacterial peritonitis in 72 patients between January 1988 and June 1996. The overall incidence of this "abdominal catastrophe" was 11.3%, or 26 of a total of 230 patients treated by PD. Of the 26 patients, 50% died, 30.7% survived but switched permanently to hemodialysis, and only 19.2% remained on, or returned to, PD. Compared to renal failure patients treated by hemodialysis or transplantation and to non-renal failure patients, the incidence of abdominal catastrophe was 20-60 times greater in patients treated by PD. CONCLUSIONS: Evidence for injury of an abdominal organ should be sought in all patients treated by PD who develop peritonitis with enteric organisms. Surgical intervention is definitive for diagnosis, and if performed early may reduce morbidity and mortality.

Fetal catecholamine responses to maternal hypoglycemia.

The present studies were designed to determine the fetal catecholamine and metabolic responses to insulin-induced maternal hypoglycemia. Maternal hypoglycemia was induced by a primed constant infusion of insulin and glucose administered to pregnant ewes to maintain maternal glucose at 20-25 mg/dl. Maternal and fetal samples for measurement of catecholamine, glucose, and free fatty acid levels and arterial blood gas analysis were collected before insulin infusion and at intervals thereafter for 6 h. Maternal and fetal plasma catecholamine levels increased significantly in response to hypoglycemia (analysis of variance, P less than 0.01). Fetal insulin and glucagon levels did not change despite a 50% reduction in fetal whole blood glucose concentration. Fetal free fatty acid levels increased significantly during hypoglycemia (P less than 0.05). There were no significant changes in maternal or fetal heart rate, blood pressure, or arterial blood gases during hypoglycemia. These results suggest that the fetus is capable of responding to hypoglycemia with an increase in catecholamine and free fatty acid levels. These results are consistent with the interpretation that the fetus is able to mobilize alternative energy substrates in response to maternal insulin-induced hypoglycemia.