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Liver Failure. Mackay Memorial Hospital Department of Internal Medicine Division of Gastroenterology R4 陳泓達. 97/6/22. Liver failure: Clinical syndrome: sudden loss of liver parenchymal and metabolic function Manifest as coagulopathy and encephalopathy. Acute liver failure : - PowerPoint PPT Presentation


  • Liver FailureMackay Memorial Hospital Department of Internal MedicineDivision of GastroenterologyR4 97/6/22

  • Liver failure:Clinical syndrome: sudden loss of liver parenchymal and metabolic functionManifest as coagulopathy and encephalopathy

  • Acute liver failure :Defined as interval between onset of the illness and appearance of encephalopathy < 8 weeks

  • Etiology:Western countries: heterogenous, drugs (acetaminophen, NSAID), virusesDeveloping countries: viruses, regional Difference (endemic area ?)

  • Journal of Gastroenterology and Hepatology(2002)17,S268S273

  • Acetaminophen toxicityIdiosyncratic drug toxicityHepatotropic virusesMiscellaneous causesIndeterminate acute liver failure (viruses can not be demonstrated ? )

  • Uncommon causes:Wilsons disease, other infections (CMV, HSV, EBV), vascular abnormality, toxin, acute fatty liver of pregnancy, antoimmune hepatitis, ischemia, malignant infiltration

  • Symptoms and signs:Jaundice, altered mental status, nausea/ vomiting, anorexia, fatigue, malaise,myalgia/arthralgiaMost of them present hepatoencephalopathy and icteric appearance.

  • Non-specific ManagementHypoglycemiaEncephalopathyInfectionsHemorrhageCoagulopathyHypotension(hypovolemia, vascular resistance )Respiratory failureRenal failurePancreatitis

  • Hypoglycemia: monitoring blood glucose, IV glucose supplement.Infection: aseptic care, high index of suspicion, preemptive antibiotic.Hemorrhage (i.e. GI): NG placement, H2 blocker or PPI.Hypotension: hemodynamic monitoring or central pressures, volume repletion

  • Respiratory failure (ARDS): mechanical ventilation.Renal failure (hypovolemia, hepatorenal syndrome, ATN): hemodynamic monitor, central pressure, volume repletion, avoid nephrotoxic agent

  • Encephalopathymajor complication precise mechanism remains unclearHypothesis: Ammonia productionTreatment toward reducing ammonia productionWatch out airway, prevent aspiration

  • EncephalopathyStage 1: day-night reversal, mild confusion, somnolenceStage 2: confusion, drowsinessStage 3: stuporStage 4: coma

  • EncephalopathyPredisposing factor of hepatic encephalopathy:GI bleeding, increased protein intake, hypokalemic alkalosis, hyponatremia, infection, constipation, hypoxia, infection, sedatives and tranquilizers

  • EncephalopathyTX upon ammonia hypothesisCorrection of hypokalemiaReduction in ammoniagenic substrates:cleansing enemas and dietary protein restriction.Lactulose: improved encephalopathy, but not improved outcome. Dose 2-3 soft stools per day

  • EncephalopathyOral antibiotics: neomycin lack of evidence nephrotoxicity limited use.

  • Cerebral EdemaCerebral edema develops in 75 - 80 % of patients with grade IV encephalopathy. precise mechanism : not completely understoodPossible contributing factor: osmotic derangement in astrocytes changes in cellular metabolism alterations in cerebral blood flow

  • Cerebral EdemaClinical manifestations:intracranial pressure (ICP) and brainstem Herniation the most common causes of death in fulminant hepatic failureischemic and hypoxic injury to the brainhypertension, bradycardia, and irregularrespirations, muscle tone, hyperreflexia

  • Cerebral EdemaMonitoring of ICP:routinely used by more than one-half of liver transplantation programs in the United States Tx: to maintain ICP below 20 mmHg and the CPP above 50 mmHg.

  • Coagulopathydiminished capacity of the failing liver to synthesize coagulation factors.The most common bleeding site: GI tract.Prophylactic administration of FFP: not recommended. performed before transplant or invasive procedure

  • Specific TreatmentACT intoxication: charcol followed by NACDrug induced hepatotoxicity: discontinue drugs supportive treatmentViral hepatitis: HBV: anti-HBV treatment, lamivudine HSV/varicella zoster: acyclovir others: supportive care

  • Wilsons disease: early diagnosis liver transplantautoimmune hepatitis: confirm diagnosis (liver biopsy), corticosteroid liver transplantacute fatty liver of pregnancy or the HELLP syndrome: obstetrical services, and expeditious delivery are recommended

  • Acute ischemic injury (shock liver): cardiovascular support Malignant infiltration: liver biopsy for diagnosis treat underlying disease.Indeterminate etiology: consider biopsy for diagnosis and further guide of treatment

  • Liver transplantLiver transplant: remain backbone of treatment of fulminant hepatic failure reliable criteria to identify these patients who really need transplant. remain unresolved in fulminant hepatic failure.

  • At Kings College hospital in London (not due to ACT)either PT>100 second or the presence of any three of the following variables: 1. age < 10 or > 40 years ;2. an etiology of non-A, non-B hepatitis, halothane, drug induced liver failure; 3. duration of jaundice before onset of encephalopathy > 7 days, prothrombin time >50 s, and serum bilirubin > 300 mmol/L.

  • EncephalopathyCoagulopathy (PT)

  • Liver transplantCriteria: In chronic liver diseasemost commonly used prognostic model MELD score (Model for End-stage LiverDisease )3.8[Ln serum bilirubin (mg/dL)] + 11.2[Ln INR] + 9.6[Ln serum creatinine (mg/dL)] + 6.4 Ln: natural logarithm.

  • Liver transplantCONTRAINDICATIONS: Cardiopulmonary disease can not be corrected, or preclude surgery.Malignancy outside of the liver within 5 years of evaluation, or can not be cured.Active alcohol and drug use

  • Advanced age and HIV disease: relative contra-indication (site-specific management)

  • Liver support systemNon-cell-based: plasmapheresis and charcoal-based hemoabsorption Cell-based systems: known as bioartificial liver support systems

  • Liver support systemNon-cell-based: not improved survival.Available systems: molecular adsorbents recirculation system (MARS)Cell-based systems: undergoing trial.