Pre-surgical risk assessment in patients with cirrhosis.

Over the last decades, significant improvements in the clini- cal management of patients with cirrhosis have increased their life expectancy. Thus, indications for surgical procedures other than liver transplantation are becoming more frequent. However, patients with advanced liver disease are at high risk of perioperative morbidity and mortality. This is the consequence of multiple factors that include the presence of portal hypertension, alterations on hemostasis and coagulation, the immune dysfunction that entails an increased risk of infections, and the impaired synthesis of proteins that impacts on the nutritional status and the wound healing. Surgical outcomes are not only determined by the severity of the liver disease, but also by the type of surgery and the presence of other comorbidities. Different models to predict mortality have been proposed, including the MELD score, the Child-Pugh classification, the hepatic venous pressure gradient, and the Mayo postoperative mortality risk calculator, among others. Multidisciplinary committees including surgeons, anesthesiologists, hepatologists, critical care physicians and other specialties involved in each case, should assess individually the risk-benefit of the surgical procedure, also considering patient`s expectations and will.

Accuracy of portal and forearm blood flow measurements in the assessment of the portal pressure response to propranolol.

BACKGROUND/AIMS: The portal pressure response to propranolol varies significantly in individual patients with cirrhosis. At present, propranolol responders can be identified only by measuring the hepatic venous pressure gradient. The aims of this study were: 1) to investigate whether the noninvasive monitoring of portal blood flow by pulsed Doppler ultrasound and forearm blood flow by strain-gauge plethysmography can predict the hepatic venous pressure gradient response to propranolol in patients with cirrhosis, and 2) to analyze the factors that may influence this response. METHODS: Hemodynamic measurements were undertaken in 80 patients with cirrhosis before and after receiving propranolol (0.15 mg/kg i.v., n = 60) or placebo (n = 20). RESULTS: No changes were observed in the placebo group. Propranolol lowered (p < 0.01) hepatic venous pressure gradient from 17.6 +/- 3.8 to 14.7 +/- 3.8 mmHg, portal blood flow from 1122 +/- 363 to 897 +/- 332 ml/min and forearm blood flow from 7.52 +/- 3.1 to 6.12 +/- 2.3 ml/min%. Changes in hepatic venous pressure gradient were correlated (p < 0.01) with those of portal blood flow (r = 0.82) and forearm blood flow (r = 0.54). The reduction in hepatic venous pressure gradient was > 20% in 23 patients ("responders"). The accuracy of portal Doppler flowmetry in identifying responders was higher than that of forearm plethysmography (88.3 vs. 68.3%, p < 0.05). Multivariate analysis proved that previous variceal bleeding was the only factor independently associated with a lack of response to propranolol (relative risk 3.42, 95% CI 1.5-7.4, p < 0.01). Hepatic venous pressure gradient reduction by propranolol was higher in non-bleeders than in bleeders (-19.9 +/- 9.4 vs. -11.3 +/- 8.6%, p < 0.01). CONCLUSIONS: Portal Doppler ultrasound can be used as a reliable surrogate indicator of the hepatic venous pressure gradient response to acute propranolol administration. In addition, our study indicates that this response is mainly influenced by previous variceal hemorrhage.