Hepatitis E virus infection is a major cause of acute hepatitis, typically self-limiting but occasionally leading to liver failure. Understanding disease progression factors could inform prevention strategies. This study aimed to analyse the characteristics of a large cohort of hospitalised hepatitis E patients in Tianjin, China, and explore factors influencing their progression to liver failure. A total of 1279 hospitalised patients with hepatitis E were included in this cross-sectional study in Tianjin, China. Student's t-test and the Mann–Whitney U-test were used for comparisons. Multiple logistic regression analysis was used to explore the association. Among these 1279 patients, 107 (8.4%) developed liver failure. Patients with diabetes mellitus (DM) (95% confidence interval [CI] 1.150–2.887, p = 0.011), liver cirrhosis (95% [CI] 2.229–7.224, p < 0.001), and hepatitis B (95% [CI] 1.159–4.512, p = 0.017) were more likely to progress to liver failure. Hepatitis E patients with comorbid DM, liver cirrhosis, or hepatitis B virus co-infection have higher risks of developing liver failure. Hepatitis E vaccination may be recommended for these vulnerable patients to curb disease severity.

The amino acid arginine and one of its metabolites NO have gathered broad attention in the last decade. Although arginine is regarded as a conditionally essential amino acid in disease, L-arginine supplementation in severe illness has not found its way into clinical practice. This might be due to the invalid interpretation of results from studies with immune-enhancing diets containing L-arginine amongst other pharmaconutrients. However, not much attention is given to research using L-arginine as a monotherapy and the possibility of the alternative hypothesis: that L-arginine supplementation is beneficial in disease. The present review will discuss data from studies in healthy and diseased animals and patients with monotherapy of L-arginine to come to an objective overview of positive and negative aspects of L-arginine supplementation in disease with special emphasis on sepsis, cancer, liver failure and wound healing.

Improvement in surgical techniques, technology and perioperative assessment has dramatically simplified the anaesthetic care for elective liver resection. Patients with a non-tumorous healthy liver should only need the usual preoperative assessment. Patients with pre-existing parenchymal liver disease should be specifically assessed for gas exchange impairment, alcoholic or nutritional-associated cardiomyopathy, infection, cirrhosis decompensation, acute alcoholic hepatitis, and kidney impairment. The type of anaesthetic management does not influence the intra- and postoperative courses. Intermittent clamping of the portal vascular triad is better tolerated than prolonged continuous periods of ischaemia—especially in patients with abnormal liver parenchyma. Intraoperative antibiotic prophylaxis must be administered to prevent translocation of intestinal enterobacteria to the systemic circulation in patients with both healthy and diseased livers. Blood-salvage techniques have limited indications in liver resection. Systematic invasive haemodynamic monitoring is no longer warranted. An arterial cannula should only be considered in procedures of long duration and in selected situations likely to cause anticipated circulatory impairment: total liver vascular occlusion, repeat surgery, combined organ resection, and surgery conducted on tumours >10 cm in size or in connection with the vena cava. In a recent large series of liver resections, 60% of patients did not need a blood transfusion, only 2% of transfused patients received >10 units of blood and cirrhosis was not predictive of increased intraoperative bleeding. Postoperative ascites, which always develops at the expense of circulating fluid, is a frequent occurrence in patients with healthy or diseased livers. Intra- and postoperative fluid limitation does not prevent postoperative ascites. Volume expansion, diuretics and vasopressor therapy should be initiated early to prevent kidney failure.

Background and objective: The removal of the non-functioning liver in cases of fulminant liver failure has been advocated by some authors as a means of improving haemodynamic instability and acid-base disturbances associated with acute liver failure.

Methods: The aim of the present experimental study was to investigate whether maintaining a non-functioning liver is preferable over removing it in terms of haemodynamic variables, after acute hepatic failure has been surgically induced. Twenty Landrace pigs were used in the study. All of them underwent portocaval anastomosis and ligation of the hepatic artery. After an 18-h period and with biochemical indices of fulminant hepatic failure clearly demonstrated, the animals were randomly assigned to one of two groups: in 10 pigs (Group A) the ischaemic liver was left in situ and no further surgical intervention was undertaken. The other 10 (Group B) underwent total hepatectomy. Haemodynamic monitoring was the same in both groups. No inotropes were administered throughout the whole period of observation.

Results: Haemodynamic deterioration was observed in the hepatectomized pigs (Group B) whereas the group with the ischaemic liver in situ (Group A) remained stable in terms of the haemodynamic variables evaluated until the end of the experiment. (Cardiac index in Group A 7.59 ± 1.25 Lmin−1 m-2 vs. 2.92 ± 0.68 Lmin−1 m−2 in Group B, P < 0.05.)

Conclusions: The concept of salvage hepatectomy in cases of acute liver failure should be redefined since there seems to be some experimental evidence that it may not be as beneficial as originally thought.