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8/13/2019 970622 Pre-ICU training Liver failure( ) (1)
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Liver Failure
Mackay Memorial HospitalDepartment of Internal Medicine
Division of GastroenterologyR4
97/6/22
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Liver failure:
Clinical syndrome: sudden loss of liver
parenchymal and metabolic function
Manifest as coagulopathy and
encephalopathy
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Acute liver failure :
Defined as interval between onset of the illnessand appearance of encephalopathy < 8 weeks
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Etiology:
Western countries: heterogenous, drugs
(acetaminophen, NSAID), virusesDeveloping countries: viruses, regional
Difference (endemic area ?)
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Journal of Gastroenterology and Hepatology(2002)17,
S268S273
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Acetaminophen toxicity
Idiosyncratic drug toxicity
Hepatotropic virusesMiscellaneous causes
Indeterminate acute liver failure (viruses can not
be demonstrated ? )
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Uncommon causes:
Wilsons disease, other infections (CMV, HSV,
EBV), vascular abnormality, toxin, acute fatty liverof pregnancy, antoimmune hepatitis, ischemia,
malignant infiltration
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Symptoms and signs:
Jaundice, altered mental status, nausea/
vomiting, anorexia, fatigue, malaise,myalgia/arthralgia
Most of them present hepatoencephalopathy
and icteric appearance.
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Non-specific Management
Hypoglycemia
Encephalopathy
Infections
HemorrhageCoagulopathy
Hypotension(hypovolemia, vascular resistance )
Respiratory failureRenal failure
Pancreatitis
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Hypoglycemia: monitoring blood glucose, IVglucose supplement.
Infection: aseptic care, high index of suspicion,preemptive antibiotic.
Hemorrhage (i.e. GI): NG placement, H2blocker or PPI.
Hypotension: hemodynamic monitoring orcentral pressures, volume repletion
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Encephalopathy
major complication
precise mechanism remains unclear
Hypothesis: Ammonia productionTreatment toward reducing ammonia
production
Watch out airway, prevent aspiration
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Encephalopathy
Stage 1: day-night reversal, mild confusion,somnolence
Stage 2: confusion, drowsiness
Stage 3: stupor
Stage 4: coma
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Encephalopathy
Predisposing factor of hepatic encephalopathy:
GI bleeding, increased protein intake, hypokalemic
alkalosis, hyponatremia, infection, constipation,hypoxia, infection, sedatives and tranquilizers
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Encephalopathy
TX upon ammonia hypothesis
Correction of hypokalemia
Reduction in ammoniagenicsubstrates:cleansing enemas and dietary proteinrestriction.
Lactulose: improved encephalopathy, but notimproved outcome.
Dose2-3 soft stools per day
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Encephalopathy
Oral antibiotics: neomycinlack of evidence
nephrotoxicitylimited use.
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Cerebral Edema
Cerebral edema develops in 75 - 80 % ofpatients with grade IV encephalopathy.
precise mechanism : not completely understood
Possible contributing factor:
osmotic derangement in astrocytes
changes in cellular metabolismalterations in cerebral blood flow
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Cerebral Edema
Clinical manifestations:
intracranial pressure (ICP) and brainstem
Herniation
the most common causes of deathin fulminant hepatic failure
ischemic and hypoxic injury to the brain
hypertension, bradycardia, and irregularrespirations, muscle tone, hyperreflexia
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Cerebral Edema
Monitoring of ICP:
routinely used by more than one-half of liver
transplantation programs in the United StatesTx: to maintain ICP below 20 mmHg and the
CPP above 50 mmHg.
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Coagulopathy
diminished capacity of the failing liver tosynthesize coagulation factors.
The most common bleeding site: GI tract.
Prophylactic administration of FFP: notrecommended.
performed before transplant or invasiveprocedure
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Specific Treatment
ACT intoxication: charcol followed by NAC
Drug induced hepatotoxicity: discontinue drugs
supportive treatmentViral hepatitis:
HBV: anti-HBV treatment, lamivudine
HSV/varicella zoster: acyclovirothers: supportive care
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Wilsons disease: early diagnosislivertransplant
autoimmune hepatitis: confirm diagnosis (liver
biopsy), corticosteroidliver transplant
acute fatty liver of pregnancy or the HELLPsyndrome: obstetrical services, and expeditiousdelivery are recommended
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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
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Liver transplant
Liver transplant: remain backbone of treatmentof fulminant hepatic failure
reliable criteria to identify these patients whoreally need transplant.
remain unresolved in fulminant hepaticfailure.
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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, druginduced liver failure;
3. duration of jaundice before onset of encephalopathy >7 days, prothrombin time >50 s, and serum bilirubin >300 mmol/L.
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Encephalopathy
Coagulopathy (PT)
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Liver transplant
Criteria:
In chronic liver disease
most commonly used prognostic model
MELD score (Model for End-stage Liver
Disease)
3.8[Ln serum bilirubin (mg/dL)] + 11.2[Ln INR]
+ 9.6[Ln serum creatinine (mg/dL)] + 6.4
Ln: natural logarithm.
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Liver transplant
CONTRAINDICATIONS:
1. Cardiopulmonary disease can not be corrected,or preclude surgery.
2. Malignancy outside of the liver within 5 yearsof evaluation, or can not be cured.
3. Active alcohol and drug use
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Advanced age and HIV disease: relative contra-indication (site-specific management)
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Liver support system
Non-cell-based: plasmapheresis and charcoal-based hemoabsorption
Cell-based systems: known as bioartificial liversupport systems
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Liver support system
Non-cell-based: not improved survival.
Available systems:
molecular adsorbents recirculation system (MARS) Cell-based systems: undergoing trial.
Recommended