Download - 20 hepatic enchephalopathy
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HEPATIC ENCEPHALOPATHY
GAO XIANGDepartment of Gastroenterology
The First Affiliated Hospital
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DEFINITION
Hepatic encephalopathy is a reversible neuro-psychiatric state that complicates severe liver disease(HE).
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AETIOLOGY
Encephalopathy associated with Cirrhosis and portal hypertension
Encephalopathy associated with portal-systemic Bypass without hepatocellular disease
Encephalopathy associated with Acute liver failure
Concensus in Hepatic Encephalopathy, WCOG, 2001; in press
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Hepatic encephalopathy-A complication of cirrhosis of the liver
0 20 40 60 80 100 120 140 1600
20
40
60
80
100Pr
obab
ility
of c
ompl
icat
ions
(%)
Gines et al. Hepatology (1987) 7, 1:122-128
Months
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Key questions Mechanism: clearance of toxins central system --- treatment
Clinical manifestation: neuro-psychiatric changes --- diagnosis and clinical grading
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PATHOGENETIC MECHANISM
Ammonia toxicity theory False neurotransmitters theory & amino acid imbalance theory Gama-aminobutyric aicd and endogenou
s benzodiazepines (GABA/BZ ) receptor complex theory
Others
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intestinal Precipitating factors bacteria/protein GI bleeding
infection
liver removed hypokalemia and/or alkalosis
portal-systemic shunt hypovolemia and/or hypoxia
large protein meal
blood-brain barrier constipation drugs(sedatives )
cerebral toxicity hypoglycemia
Ammonia intoxication theoryNH3 NH4
urea&
H+
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Branched-chain amino acid /Aromatic amino acids 3-3.5 :1 (normal)
<1 : 1 (cirrhosis)------ the use of branched-chain amino acid
Amino acid metabolic imbalance
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Tyrosine intestinal bacterial decarboxylase
L-dopa Tyrosine Phenylalanine
Dopamine (Liver)
Noradrenaline Octopamine -phenylethanolamine true false Sympathetic transmitter
Brain function disturbed
False neurotransmitterColon: protein
x(Brain)
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GABA/BZ receptor complex theory
•GABA (from intestine produced by bacteria)
•Endogenous BZ
--- the use of benzodiazepine antagonist
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CLINICAL MANIFESTATION
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DIAGNOSIS AND
DIFFERENTIAL DIAGNOSIS
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• Severe liver disease or portal-systemic shunt
• Neuropsychiatric manifestation• Precipitants that induce HE• Obvious impaired liver function tests, eleva
ted blood ammonia level, flapping tremor and typical EEG change indicate the possible diagnosis
Diagnosis
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Coma induced by other causes
Differential diagnosis
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TREATMENT
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1. Identification & correction of the precipitating cause: Precipitating factors Drugs! Electrolyte imbalance – hypokalemia/metabolic alkalosis (diuretics, vomiting, diarrhea, infusion) GI Bleeding Infection Constipation Large protein meal …….
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2. Intervention to reduce the production & absorption of gut-derived ammonia & other toxins:
1) Diet: reduce and modify dietary protein and maintain Calorie intake
2) Enemas (mild acid) and/or purgation3) Lactulose or lactitol4) Inhibition of gut bacteria: Antibiotics: neomycin(oral), metronidazone?5) Modification of colonic flora: probiotics?
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Modify colonic flora, resulting in displacement of urease-containing bacteria with lactobacillus
Cathartic effect
Lower the colonic pH, resulting in the formation of nonabsorbable NH4 from NH3 in the colon
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3. Stimulation of metabolic ammonia metabolism: 1) Ornithine-aspartate: enhancing the metabolism
of ammonia to glutamine 2) Sodium glutamate or potassium glutamate,
Arginine? 3) Sodium benzoate(oral): acting with glycine in
the colon to form hippurate which can be excreted in the urine
- applied in chronic HE, particularly in those with elevated blood ammonia
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4. Correct amino acid metabolic imbalance: infusion or oral administration of BCAA (branched-chain amino acid)
5. GABA/BZ complex antagonist: flumazenil ( particularly if patient has been given
banzodiazepines )
6. Other drugs
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7. Miscellaneous treatment
Prevention and treatment of cerebral edema
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8. Temporary hepatic support
9. Liver transplantation
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PROGNOSIS
Acute hepatic failure (+++) Cirrhosis - with precipitant (++) Cirrhosis - portal-systemic shunt (+) Cirrhosis - end stage (++++)
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