Liver failure

Author(s):  
George F. Mells ◽  
Graeme J.M. Alexander

Case History—A 53 yr old man, known to have alcoholic liver cirrhosis, now presenting with jaundice, ascites and deteriorating renal function. Case History—A 62 yr old man presenting with confusion and ascites. Liver failure occurs when loss of hepatic parenchymal function exceeds the capacity of hepatocytes to regenerate or repair liver injury. Acute liver failure is characterized by jaundice and prolongation of the prothrombin time in the context of recent acute liver injury. Acute liver failure is the syndrome of hepatic encephalopathy occurring within 8 weeks of the first onset of liver disease. Chronic liver failure is characterized by a chronic liver injury with one or more features of liver failure....

2020 ◽  
pp. 3089-3100
Author(s):  
Jane Macnaughtan ◽  
Rajiv Jalan

Liver failure occurs when loss of hepatic parenchymal function exceeds the capacity of hepatocytes to regenerate or repair liver injury. Acute liver failure is characterized by jaundice and prolongation of the prothrombin time in the context of recent acute liver injury, with hepatic encephalopathy occurring within 8 weeks of the first onset of liver disease. Acute-on-chronic liver failure is characterized by hepatic and/or extrahepatic organ failure in patients with cirrhosis associated with an identified or unidentified precipitating event. The commonest causes of acute liver failure are acute viral hepatitis and drugs. Acute-on-chronic liver failure is most commonly precipitated by infection, alcohol abuse, and superimposed viral infection. The main clinical manifestations are hepatic encephalopathy, coagulopathy, jaundice, renal dysfunction, and haemodynamic instability. Infection and systemic inflammation contribute to pathogenesis and critically contribute to prognosis. Specific therapy for the underlying liver disease is administered when available, but this is not possible for most causes of liver failure. Treatment is predominantly supportive, with particular emphasis on (1) correction or removal of precipitating factors; (2) if encephalopathy is present, using phosphate enemata, nonhydrolysed disaccharide laxatives, and/or rifaximin; (3) early detection and prompt treatment of complications such as hypoglycaemia, hypokalaemia, cerebral oedema, infection, and bleeding. The onset of organ failure should prompt discussion with a liver transplantation centre. The mortality of acute liver failure (without liver transplantation) is about 40%. Patients with acute liver failure who do not develop encephalopathy can be expected to recover completely. Those who recover from an episode of acute-on-chronic liver failure should be considered for liver transplantation because otherwise their subsequent mortality remains high.


Author(s):  
Daniel Marks ◽  
Marcus Harbord

Definitions of acute liver failure Aetiology Presentation Investigation Initial management Subsequent management Markers of disease severity Paracetamol overdose Acute presentations of Wilson’s disease Acute-on-chronic liver failure Hepatic encephalopathy Criteria for emergency liver transplantation Acute liver failure (ALF) is defined as potentially reversible severe liver injury with impaired synthetic function (INR 〉1.5) and hepatic encephalopathy, developing within 28d from the onset of jaundice, in the absence of pre-existing liver disease or with well-compensated chronic liver disease (...


2018 ◽  
Vol 146 (3-4) ◽  
pp. 200-202
Author(s):  
Dragan Delic ◽  
Nikola Mitrovic ◽  
Aleksandar Urosevic ◽  
Jasmina Simonovic ◽  
Ksenija Bojovic

Introduction. Acute liver failure is rare and very complex clinical syndrome, the consequences of the sudden and severe liver dysfunction. There are several causes of this condition (viruses, medications, toxins, metabolic, autoimmune and malignant diseases), but etiological agent often remains undiscovered. Case Outline. A 40-year-old male patient got ill suddenly with signs and symptoms relevant for acute hepatitis, which was confirmed with biochemical analysis. The cause of acute liver failure was not determined. Despite all therapeutic measures, clinical course of the disease was bad: severe icterus, decreased synthetic function of the liver and hepatic encephalopathy developed. In the later, subacute course of the disease, developed ascites, episodes of hepatic encephalopathy and biochemical findings of chronic hepatocellular failure. After three months treatment, in hepatic coma, there was lethal outcome. Histopathological findings confirmed the diagnosis of decompensated liver cirrhosis of unknown origin. Conclusion. The cause of acute liver failure often remains unclear; potential causes should be looked for in infections with unknown viruses or in toxins exposure. The disease is most commonly presented as subacute failure with the development of liver cirrhosis. Survival rate is low.


Author(s):  
Carl Waldmann ◽  
Neil Soni ◽  
Andrew Rhodes

Jaundice 348Acute liver failure 350Hepatic encephalopathy 352Chronic liver failure 354Abnormal liver function tests 356Jaundice (icterus) is the accumulation of bile pigments in serum and tissues including sclerae and skin. Jaundice is usually clinically detectable once serum bilirubin exceeds 50...


2019 ◽  
Vol 18 (3) ◽  
pp. 514-516
Author(s):  
Magdalena Arłukowicz-Grabowska ◽  
Maciej Wójcicki ◽  
Joanna Raszeja-Wyszomirska ◽  
Monika Szydłowska-Jakimiuk ◽  
Bernard Piotuch ◽  
...  

2021 ◽  
Author(s):  
Anıl Delik ◽  
Yakup Ülger

Chronic liver disease and decompensated cirrhosis are the major causes of morbidity and mortality in the world. According to current data, deaths due to liver cirrhosis constitute 2.4% of the total deaths worldwide. Cirrhosis is characterized by hepatocellular damage that leads to fibrosis and regenerative nodules in the liver. The most common causes of cirrhosis include alcohol consumption, hepatitis C, hepatitis B, and non-alcoholic fatty liver disease. Dysbiosis and intestinal bacterial overgrowth play a role in the development of complications of cirrhosis through translocation. In liver cirrhosis, ascites, gastrointestinal variceal bleeding, spontaneous bacterial peritonitis infection, hepatic encephalopathy, hepatorenal syndrome, hepatocelluler carcinoma are the most common complications. In addition, there are refractory ascites, hyponatremia, acute on-chronic liver failure, relative adrenal insufficiency, cirrhotic cardiomyopathy, hepatopulmonary syndrome and portopulmonary hypertension. In the primary prophylaxis of variceal bleeding, non-selective beta blockers or endoscopic variceal ligation are recommended for medium and large variceal veins. In current medical treatment, vasoactive agents, antibiotics, blood transfusion, endoscopic band ligation are the standard approach in the treatment of acute variceal bleeding. Sodium-restricted diet, diuretics and large-volume paracentesis are recommended in the management of ascites. In the treatment of hepatic encephalopathy, lactulose, branched chain amino acids, rifaximin and L-ornithine L-aspartate can be used. New therapeutic approaches such as ornithine phenyl acetate spherical carbon and fecal microbiota transplantation have shown beneficial effects on hepatic encephalopathy symptoms. In addition to their antioxidative, anti-proliferative and anti-inflammatory properties, statins have been shown to reduce the risk of decompensation and death by reducing portal pressure in compensated cirrhosis. In the treatment of liver failure, some artificial liver devices such as molecular adsorbent recirculating system, the single albumin dialysis system, fractionated plasma separation and adsorption are used until transplantation or regeneration. The purpose of this chapter is to review the most up-to-date information on liver cirrhosis and to explain the complications assessment, current management and potential treatment strategies in decompensated cirrhosis.


2016 ◽  
Vol 31 (10) ◽  
pp. 642-653 ◽  
Author(s):  
Carmi S. Punzalan ◽  
Curtis T. Barry

Acute liver failure is life threatening liver injury with coagulopathy and hepatic encephalopathy within 26 weeks and generally, in the absence of preexisting liver disease. Fulminant liver failure occurs when hepatic encephalopathy occurs within 8 weeks of jaundice. The majority of patients with ALF are women with the median age of 38 years. In the United States, drug induced liver injury including acetaminophen causes the majority of ALF cases. The etiology of ALF should be determined, if possible, because many causes have a specific treatment. The mainstay for ALF is supportive care and liver transplantation, if necessary. There are multiple prognostic criteria available. Prognosis can be poor and patients should be referred to a liver transplantation center as soon as possible.


Sign in / Sign up

Export Citation Format

Share Document