ABSTRACT
Spontaneous bacterial peritonitis (SBP) is an ascitic fluid infection as a complication of end stage liver disease. The outcome is related to the severity of hepatorenal function, gastrointestinal bleeding, and many others; however it is not well known whether the infection acquisition sites have an effect on the prognosis of SBP. In order to identify the prognostic significance of the acquisition sites, we studied 106 patients who were diagnosed as culture positive SBP between October 1998 and August 2003. Thirty-two episodes were nosocomial and 74 were community acquired. Gramnegative bacilli such as Escherichia coli were dominant in both of the nosocomial and community-acquired SBPs. Despite significantly higher resistance to cefotaxime in nosocomial isolates compared to community-acquired isolates (77.8% vs. 13.6%, p=0.001), no difference was found regarding short or long term prognosis. Infection acquisition sites were not related to short or long term prognosis either. Shock, gastrointestinal bleeding and renal dysfunction were related to short term prognosis. Only Child-Pugh class C was identified as an independent prognostic factor of long-term survival.
Subject(s)
Middle Aged , Male , Humans , Female , Aged , Time Factors , Survival Rate , Shock/etiology , Prognosis , Peritonitis/complications , Multivariate Analysis , Klebsiella pneumoniae/drug effects , Kidney Diseases/etiology , Gastrointestinal Hemorrhage/etiology , Escherichia coli/drug effects , Drug Resistance, Bacterial , Cross Infection/complications , Community-Acquired Infections/complications , Ciprofloxacin/pharmacology , Cefotaxime/pharmacology , Bacterial Infections/complications , Anti-Bacterial Agents/pharmacologyABSTRACT
BACKGROUND: The purpose of this study was to define morphine's effects on resting ventilation and the ventilatory response to hypoxia and hypercarbia. METHODS: Six healthy nonsmoking young adult males were tested for the respiratory effects of intravenous morphine (0.15 mg/kg). Test began with baseline measurement of resting ventilation, isocapnic hypoxic ventilatory response (HVR), and normoxic hypercapnic ventilatory response (HCVR). After baseline measurement, morphine was administered and ventilatory responses were determined 20 and 40 min postinfusion. RESULTS: Morphine significantly decreased resting ventilation, hypoxic ventilatory response, and hypercarbic ventilatory response. Resting hypoventilation manifested as a peak rise in PETCO2 from 38.0+/-1.4 to 42.8+/-1.0 mmHg ( SEM) at 20 min (p<0.05). Hypoxic ventilatory response, measured as the slope of the ventilatory response to hypoxia, decreased from a control of 20.7+/-3.8 to 14.5+/-7.2 at 20 min after morphine (p<0.05). Hypercapnic ventilatory response, measured as the slope of the ventilatory response to hypercarbia, also decreased from 34.9+/-7.5 to 11.1+/-4.9 (p<0.05) 20 min after morphine. CONCLUSION: These decreased responsiveness to the chemical stimuli to breathing may contribute to the ventilatory depression frequently seen after administration of morphine.