Management in Acute Liver Failure

Abstract

Acute liver failure (ALF) is a rare, potentially fatal complication of severe hepatic illness resulting from various causes. In a clinical setting, severe hepatic injury is usually recognised by the appearance of jaundice, encephalopathy and coagulopathy. The central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique and multifactorial. Ammonia plays a central role in the pathogenesis. The role of newer ammonia lowering agents is still evolving. Liver transplant is the only effective therapy that has been identified to be of promise in those with poor prognostic factors, whereas in the others, aggressive intensive medical management has been documented to salvage a substantial proportion of patients. A small fraction of patients undergo liver transplant and the remaining are usually treated with medical therapy. Therefore, identification of the complications and causes of death in such patients, and use of appropriate prognostic models to identify those who need liver transplant and those who can be managed with medical treatment is a vital component of therapeutic strategy. In this review, we discuss the various pathogenetic mechanisms and treatment options available. ( J CLIN EXP HEPATOL 2015;5:S104-S115)A cute liver failure (ALF) can be a fatal complication of acute hepatic injury and occurs unpredictably. It is a rare clinical entity marked by the sudden loss of hepatic function and a severe life-threatening course in a person with no prior history of liver disease. ALF represents a syndrome rather than a specific disease, having multiple causes that vary in course and outcome. ALF is difficult to identify in its early stages, resulting in frequent delays in initiation of treatment. The causes of ALF include viral hepatitis, drug induced and toxin-induced liver damage, metabolic errors, ischemia, and miscellaneous rare causes.ALF is defined by three criteria: (1) rapid development of hepatocellular dysfunction (jaundice, coagulopathy), (2) encephalopathy, and (3) absence of a prior history of liver disease. 1 However, the interval between onset of acute hepatic injury (jaundice) and onset of liver failure (encephalopathy with or without coagulopathy) in such patients (icterus-encephalopathy interval; IEI) has been described to be between 4 weeks (Indian definition) 2-4 to 24 weeks (AASLD-ALF study group). 5 Further, due to the diverse natural course, ALF has been sub-classified as hyperacute (IEI # 7 day), acute (IEI # 4 weeks) and sub-acute ALF (IEI $ 5 week to #12 weeks) by British authors. 6 Despite these differences in definitions, the central and most important clinical event in ALF is occurrence of hepatic encephalopathy (HE) and cerebral edema which is responsible for most of the fatalities in this serious clinical syndrome. The pathogenesis of encephalopathy and cerebral edema in ALF is unique an...

Mesenchymal stem cells prolong survival and prevent lethal complications in a porcine model of fulminant liver failure

“…During liver injury, hemodynamic changes and electrolyte and metabolic imbalance are frequently presented . Electrolytes and blood gas were monitored within 24 hours after surgery.…”

“…During liver injury, hemodynamic changes and electrolyte and metabolic imbalance are frequently presented. 6,[42][43][44][45] Electrolytes and blood gas were monitored within 24 hours after surgery. Before I-R injury, the blood samples of pigs from infra-renal vena cava were collected to provide parameters of average baseline data for each biomarker in Figure 4C).…”

Patient With Nonalcoholic Steatohepatitis Posttransplant Develops Acute Hepatitis B Virus Causing Graft Failure

“…Currently, use of a combination of NAs with HBIG is considered the most effective way to prevent reinfection of HBV after transplant . Shalimar and Acharya note that for the patient with hepatitis B–related ALF, antivirals (i.e., entecavir or tenofovir) are recommended . In the case study mentioned earlier, once active HBV infection was known, she was prescribed renally adjusted tenofovir for HBV treatment and was given HBIG at the time of her second transplant.…”

Hepatobiliary Quiz (Answers)—15 (2015)

“…ICP .40 mmHg for .2 h or CPP \50 mmHg preclude liver transplantation in patients with ALF. 56,57 A jugular bulb catheter may be used to sample the jugular venous blood. Saturation of \55% represents an ischemic brain, and indicate need to improve oxygenation of the patient.…”

“…Its ICP lowering action is optimal in cases of mild to moderate ICH, and is less effective when the ICP is greater than 60 mmHg. 56,59 Moderate hypothermia (32 C-35 C) leads to a reduction in intracranial pressure in patients with ALF. The cerebral metabolism, ammonia uptake by the brain, and glutamine synthesis are also reduced.…”