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Acute Liver Failure

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  • Acute liver failure

     Acute liver failure (ALF) is a rare syndrome defined by a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease.The interval from the onset of jaundice to the development of encephalopathy occurs within 24 to 26 weeks and may further classify ALF into categories based on hyperacute, acute, or subacute presentations.Although clinical jaundice is considered a defining feature of ALF, it may not always be present, particularly in hyperacute presentations. The term acute liver failure is preferred over fulminant hepatic failure or acute hepatic necrosis, although these terms have been used historically to classify hepatic failure.

    Typical symptoms

    Yellowing of your skin and eyeballs (jaundice), Pain in your upper right abdomen, Abdominal swelling, Nausea, Vomiting, A general sense of feeling unwell (malaise), Disorientation or confusion, Sleepiness.

  • Acute liver failure

     Therapeutic aspects

    Treatments for acute liver failure Acute liver failure treatments may include: Medications to reverse poisoning. Acute liver failure caused by acetaminophen overdose or mushroom poisoning is treated with drugs that can reverse the effects of the toxin and may reduce liver damage. Liver transplant. When acute liver failure can't be reversed, the only treatment may be a liver transplant. During a liver transplant, a surgeon removes your damaged liver and replaces it with a healthy liver from a donor. Treatments for complications Control signs and symptoms you're experiencing and try to prevent complications caused by acute liver failure. This care may include: Relieving pressure caused by excess fluid in the brain. Cerebral edema caused by acute liver failure can increase pressure on your brain. 

  • Acute liver failure

     Statistics

    The median (minimum, maximum) age was 33.5 (17, 47) years with 50% female. The median (minimum, maximum) duration from the onset of fever to development of ALF was 7.5 (5, 13) days and the maximum hepatic encephalopathy (HE) grade were III in five patients and II in three patients. Three patients had systemic inflammatory responses (SIRS) on admission and were in grade III HE. The presence of SIRS on admission was associated with higher grade of HE and its development during the course of hospitalization was associated with worsening HE grade. The hepatitis was characterized by marked elevations in: alanine transaminase [median admission 1140.5 u/L (639, 4161); median peak 2487 u/L (998, 5181)], serum bilirubin [median admission 29 μmol/L (23, 291); median peak 127 μmol/L (72, 592)], and prothrombin time [median admission 16.8 s (15.3, 26.2); median peak 22 s (15.3, 40.7)]. The survival rate with standard medical therapy alone was 100%.

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