Journal of hepatology
-
Cirrhotic patients are prone to develop life-threatening complications that require emergency care and ICU admission. They can present specific decompensations related to cirrhosis such as variceal bleeding and hepatorenal syndrome (HRS) or other critical events also observed in the general population such as severe sepsis or septic shock. Clinical management of all these entities requires a specific approach in cirrhosis. ⋯ Cirrhotic patients are also at a high risk for development of other bleeding complications and are more susceptible to nosocomial infections. This extreme complexity of critically-ill cirrhotic patients requires a specific medical approach that should be known by general intensivists since it has a negative impact on patient prognosis. This review will focus on the diagnostic approach and treatment strategies currently recommended in the critical care management of patients with cirrhosis.
-
Journal of hepatology · Jan 2012
Chronic intermittent hypoxia is a major trigger for non-alcoholic fatty liver disease in morbid obese.
Morbid obesity is frequently associated with low grade systemic inflammation, increased macrophage accumulation in adipose tissue (AT), obstructive sleep apnea (OSA), and nonalcoholic fatty liver disease (NAFLD). It has been suggested that chronic intermittent hypoxia (CIH) resulting from OSA could be an independent factor for early stage of NAFLD in addition to other well-recognized factors (dyslipidemia or insulin resistance). Moreover, macrophage accumulation in AT is associated with local hypoxia in fat tissue. We hypothesized that the association between CIH and morbid obesity could exert additional specific deleterious effects both in the liver and adipose tissues. ⋯ In morbidly obese patients, CIH was strongly associated with more severe liver injuries but did not worsen obesity induced macrophage accumulation in adipose tissue depots.
-
Journal of hepatology · Jan 2012
Prospective evaluation of the prognostic scores for cirrhotic patients admitted to an intensive care unit.
Cirrhotic patients admitted to an Intensive Care Unit (ICU) have a poor prognosis. Identifying patients in whom ICU care will be useful can be challenging. The aim of this study was to assess the predictive value of prognostic scores with respect to mortality and to identify mortality risk factors. ⋯ For cirrhotic patients admitted to the ICU, SAPS II, and SOFA scores predicted ICU mortality better than liver-specific scores. Mechanical ventilation or vasopressor therapy, bilirubin levels at admission and infection in patients with advanced cirrhosis were associated with a poor outcome.
-
Journal of hepatology · Jan 2012
Assessment of portal hypertension by transient elastography in patients with compensated cirrhosis and potentially resectable liver tumors.
Patients with cirrhosis and small hepatocellular carcinoma with normal bilirubin and hepatic venous pressure gradient (HVPG) <10 mm Hg have >70% 5-year survival after hepatic resection. On the contrary, patients with HVPG ≥10 mm Hg (clinically significant portal hypertension, CSPH) frequently develop decompensation following surgery, with around 50% 5-year survival. Liver stiffness (LS) evaluation by transient elastography might non-invasively identify CSPH. We investigated the usefulness of LS predicting CSPH in patients with compensated cirrhosis and potentially resectable liver tumors. ⋯ These data suggest that in real-life scenarios half of patients with potentially resectable liver nodules can be non-invasively classified as having or not CSPH by LS. However, in the remaining half, LS is either not applicable or inaccurate. In this last population HVPG is still a non replaceable method to detect CSPH.
-
Journal of hepatology · Jan 2012
Threshold for toxicity from hyperammonemia in critically ill children.
Hyperammonemia results from reduction of hepatocyte function or enzyme of urea cycle deficiency. Hyperammonemia contributes to cerebral edema that may lead to cerebral herniation. The threshold of toxicity of ammonemia is unknown. ⋯ Our study identifies a threshold of exposure to ammonia (≥200 μmol/L) above which mortality increases significantly, especially in liver failure. Specific treatments of hyperammonemia are rarely used in liver failure when compared with urea cycle defect even though use of ammonia scavengers may help to decrease ammonemia.