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DESCRIPTIONLiver 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.
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.