Combined spontaneous bacterial empyema and peritonitis in cirrhotic patients with ascites and hepatic hydrothorax

Background and study aims: Spontaneous bacterial empyema [SBEM] is an underestimated condition in patients with ascites and hepatic hydrothorax with a high mortality. This study aimed to find whether spontaneous bacterial peritonitis [SBP] is a prerequisite for SBEM

Patients and methods: 3000 HCV-related cirrhotic patients with ascites and hydrothorax were screened for the presence of SBP [ascitic fluid neutrophils >250/mm[3]] and SBEM [positive pleural fluid culture and neutrophils >250/mm[3] or negative pleural fluid culture and neutrophils >500/mm[3] with no evidence of pneumonia/parapneumonic effusion on chest radiograph or CT]

Results: The prevalence of SBEM in cirrhotic patients was 1.2% [36/3000] unlike SBP [1.6%; 48/3000]. SBEM was detected in 51.4% of the patients with hepatic hydrothorax [36/70]. A total of 70 patients had concomitant ascites and hydrothorax, namely SBP [n = 17], SBEM [n = 5], and dual SBP and SBEM [n = 31], whereas 17 patients had sterile concomitant ascites and hydrothorax. Age, sex, liver function, kidney function tests, complete blood count, INR, MELD, MELD-Na, blood chemistry, and culture/sensitivity for ascitic and pleural fluid were statistically not different [p > 0.05] between SBP and dual SBP and SBEM patients. Escherichia coli and Klebsiella pneumoniae were detected in the culture. From univariate analysis, no predictors of dual SBP and SBEM were detected

Conclusion: SBEM is a part of SBP in cirrhotic patients with ascites and hydrothorax

The impact of paracentesis flow rate in patients with liver cirrhosis on the development of paracentesis induced circulatory dysfunction

BACKGROUND/AIMS: Ascites is a dreadful complication of liver cirrhosis associated with short survival. Large volume paracentesis (LVP) is used to treat tense or refractory ascites. Paracentesis induced circulatory dysfunction (PICD) develops if no plasma expanders are given with ominous complications. To study the effect of ascites flow rate on PICD development. METHODS: Sixty patients with cirrhosis and tense ascites underwent LVP of 8 L were randomized into 3 equal groups of different flow rate extraction; group I (80 mL/minute), group II (180 mL/minute) and group III (270 mL/minute). Plasma renin activity (PRA) was measured baseline and on day six. PICD was defined as increase in PRA >50% of the pretreatment value. RESULTS: In group I through 3; the mean age was (52.5±9.4 vs. 56.4±8.5 vs. 55.8±7.1 years; P>0.05), mean arterial pressure (81.4±5.6 vs. 81.5±7 vs. 79.5±7.2 mmHg; P>0.05), MELD (17.6±4.1 vs. 15.8±4.1 vs. 14.7±4.5). Baseline PRA was comparable (1,366.0±1244.9 vs. 1,151.3±1,444.8 vs. 951.9±1,088 pg/mL; P>0.05). There was no statistically significant (P>0.05) flow mediated changes (Delta) of creatinine (0.23±0.27 vs. 0.38±0.33 vs. 0.26±0.18 mg/dL), MELD (1.25±5.72 vs. 1.70±2.18 vs. 1.45±2.21) or PRA (450.93±614.10 vs. 394.61±954.64 vs. 629.51±1,116.46 pg/mL). PICD was detected in a similar frequency in the three groups (P>0.05). On univariate logistic analysis only female sex was a fairly significant PICD predictor (Wald 3.85, odds ratio 3.14; P=0.05). CONCLUSIONS: The ascites flow rate does not correlate with PICD development.