970622 pre-icu training liver failure(陳泓達) (1)

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.

970622 pre-icu training liver failure(陳泓達) (1)

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