Liver Failure
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Transcript Liver Failure
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 :
Defined as interval between onset of the illness
and appearance of encephalopathy < 8 weeks
Etiology:
Western countries: heterogenous, drugs
(acetaminophen, NSAID), viruses
Developing countries: viruses, regional
Difference (endemic area ?)
Journal of Gastroenterology and Hepatology(2002)17,
S268–S273
Acetaminophen
toxicity
Idiosyncratic drug toxicity
Hepatotropic viruses
Miscellaneous causes
Indeterminate acute liver failure (viruses can not
be demonstrated ? )
Uncommon causes:
Wilson’s 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/arthralgia
Most of them present hepatoencephalopathy
and icteric appearance.
Non-specific Management
Hypoglycemia
Encephalopathy
Infections
Hemorrhage
Coagulopathy
Hypotension(hypovolemia, vascular resistance ↓)
Respiratory failure
Renal failure
Pancreatitis
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
Encephalopathy
major complication
precise mechanism remains unclear
Hypothesis: Ammonia production
Treatment toward reducing ammonia production
Watch out airway, prevent aspiration
Encephalopathy
Stage 1: day-night reversal, mild confusion,
somnolence
Stage 2: confusion, drowsiness
Stage 3: stupor
Stage 4: coma
Encephalopathy
Predisposing factor of hepatic encephalopathy:
GI bleeding, increased protein intake, hypokalemic
alkalosis, hyponatremia, infection, constipation,
hypoxia, infection, sedatives and tranquilizers
Encephalopathy
TX upon ammonia hypothesis
Correction of hypokalemia
Reduction in ammoniagenic
substrates: cleansing enemas and dietary protein
restriction.
Lactulose: improved encephalopathy, but not
improved outcome.
Dose 2-3 soft stools per day
Encephalopathy
Oral antibiotics: neomycin lack of evidence
nephrotoxicity limited use.
Cerebral Edema
Cerebral edema develops in 75 - 80 % of
patients with grade IV encephalopathy.
precise mechanism : not completely understood
Possible contributing factor:
osmotic derangement in astrocytes
changes in cellular metabolism
alterations in cerebral blood flow
Cerebral Edema
Clinical manifestations:
↑intracranial pressure (ICP) and brainstem
Herniation the most common causes of death
in fulminant hepatic failure
ischemic and hypoxic injury to the brain
hypertension, bradycardia, and irregular
respirations, ↑ muscle tone, hyperreflexia
Cerebral Edema
Monitoring 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.
Coagulopathy
diminished 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 Treatment
ACT intoxication: charcol followed by NAC
Drug induced hepatotoxicity: discontinue drugs
supportive treatment
Viral hepatitis:
HBV: anti-HBV treatment, lamivudine
HSV/varicella zoster: acyclovir
others: supportive care
Wilson’s disease: early diagnosis liver
transplant
autoimmune hepatitis: confirm diagnosis (liver
biopsy), corticosteroid liver transplant
acute 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 transplant
Liver 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 King’s 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.
Encephalopathy
Coagulopathy
(PT)
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.
Liver transplant
1.
2.
3.
CONTRAINDICATIONS:
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 contraindication (site-specific management)
Liver support system
Non-cell-based: plasmapheresis and charcoalbased hemoabsorption
Cell-based systems : known as bioartificial liver
support systems
Liver support system
Non-cell-based: not improved survival.
Available systems:
molecular adsorbents recirculation system (MARS)
Cell-based systems: undergoing trial.