Acute-On Chronic Liver Failure: The Relationship with Underlying Liver Disease Severity and Portal Hypertension

2016 ◽  
Vol 64 (2) ◽  
pp. S278
Author(s):  
M.Y. Kim ◽  
Y.L. Lim ◽  
S.K. Baik ◽  
Y.O. Jang
Author(s):  
James Y. Findlay ◽  
Eelco F. M. Wijdicks

Acute liver failure (ALF) is an uncommon condition in which an acute insult results in a rapid deterioration of liver function, encephalopathy, and coagulopathy in the absence of prior underlying liver disease. It is differentiated from rapid deterioration in the setting of underlying liver disease (acute on chronic liver failure) and from the gradual deterioration in liver function that can occur in chronic liver failure.


2020 ◽  
Vol 19 (1) ◽  
pp. 85-95
Author(s):  
Ton Lisman ◽  
Bethlehem Arefaine ◽  
Jelle Adelmeijer ◽  
Ane Zamalloa ◽  
Eleanor Corcoran ◽  
...  

2020 ◽  
Vol 73 ◽  
pp. S496-S497
Author(s):  
Ton Lisman ◽  
Bethlehem Arefaine ◽  
Jelle Adelmeijer ◽  
Ane Zamalloa ◽  
William Bernal ◽  
...  

2021 ◽  
Author(s):  
Nidhi Nautiyal ◽  
Deepanshu Maheshwari ◽  
Dhananjay Kumar ◽  
Rekha Kumari ◽  
Suchi Gupta ◽  
...  

Abstract Background and Aims: Acute-on-chronic liver failure (ACLF) is a distinct clinical entity with high probability of organ failure and mortality. Experimental models of ACLF are needed to understand the pathophysiology and natural course of the disease.Methodology and Results: To mimic the syndrome of ACLF, chronic liver disease was induced by intra-peritoneal administration of carbon tetrachloride (CCl4) for 10 weeks, followed by acute injury with acetaminophen (APAP) and lipopolysaccharide (LPS) administration. Blood, ascitic fluid and organs were collected to study cell death, regeneration and fibrosis. APAP/LPS induced second insult to the CCL4 animals showed progressive and significant increase in bilirubin (p < 0.05), prothrombin time (P < 0.0001) and blood ammonia (p < 0.001) post-acute injury similar to human ACLF. Ascites was noticed by day 11 (median serum-ascites albumin gradient, SAAG ((1.2(1.1–1.3) g/dL) suggestive of portal hypertension. At 24 hours post-APAP/LPS infusion, the liver tissue showed increased hepatocyte ballooning and endothelial cell TUNEL positivity. This was followed by progressive hepatocyte necrosis from perivascular region at day 7 to lobular region by day 11 acute injury. They also showed regression in fibrous septa (p < 0.005) in comparison to cirrhosis. A progressive loss of hepatic regeneration (proliferating cell nuclear antigen; p < 0.005) was also seen following APAP/LPS injury. These animals also showed a significant increase in serum creatinine (p < 0.05) levels and renal tubular injury by day 11 which was not present in cirrhotic animals.Conclusion: The CCL4/APAP/LPS (CALPS) model of ACLF mimics the clinical, biochemical and histological features of ACLF with demonstrable progressive hepatocyte necrosis, liver failure, impaired regeneration, development of portal hypertension and organ dysfunction in an animal with chronic liver disease.


2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Giovanni Marasco ◽  
Sinan Sadalla ◽  
Giulio Vara ◽  
Rita Golfieri ◽  
Davide Festi ◽  
...  

Sarcopenia is gaining attention as a negative prognostic factor in different fields of medicine, including chronic liver failure. However, the assessment of sarcopenia in patients with liver diseases is often neglected due to unawareness of reliable tools and methods and thus is limited to research studies. Cross-sectional imaging is a diffuse diagnostic tool and is commonly performed in patients with chronic liver failure. The last advancements in radiology image analysis using dedicated software allow an easy and standardized method to assess skeletal muscle volume. Several measures can be obtained from cross-sectional imaging analysis to evaluate sarcopenia in patients affected by chronic liver disease. We aimed to review the recent advances in imaging-based sarcopenia assessment, in particular in patients with chronic liver diseases. As a result, we found that the skeletal muscle index (SMI) seems to be a reliable method to assess sarcopenia in cirrhotic patients. Even if further studies are needed to validate proper cut-offs for each clinical endpoint, physicians are invited to consider the assessment of sarcopenia in the work-up of patients with chronic liver disease.


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.


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