Hepatic Encephalopathy

Hepatic Encephalopathy
A syndrome characterized by personality changes, intellectual impairment and depressed level of consciousness Present in 50 to 70 percent of patients with cirrhosis Appro ! "0# of patients dying of end$stage liver disease e perience significant encephalopathy, approaching coma

Precipitating Factors
%astrointestinal &leeding &lood loss of '00 ml absorbed as '($)0 g Protein Azotemia *onstipation High protein dietary inta+e Hypo+alemic acidosis *,- depressants .e!g! &enzodiazepines/ Hypo ia Hypercarbia -epsis

Pathophysiology
-evere liver disease resulting in liver failure .Acute fulminant hepatitis/ 0nability to deto ify *,- to ins .false neurotransmitter/ Ammonia 1ercaptans 2atty acids %amma$aminobutyric acid .%A&A/

PATHOGENESIS OF HEPATIC ENCEPHALOPATHY Hypothesis : - Hyperammonemia - False Neurotransmitter - GABA (Gamma Amino Butyric Acid)
'! 2ischer, 3!E, &ernardini P, Amino Acid 0mbalance and Hepatic Encephalopathy 4 Ann!5ev!,utr! '67),)8('6$ (5( )! -teven -chen+er,19,*harles E!&rady,000,19,Pathogenesis of Hepatic Encephalopathy 8 ("$ :'

Symptom and signs

1ild 9isease 9ay$night reversal -omnolence *onfusion Personality change Asteri is .2lapping ;remor/ -evere 9isease -tupor *oma 9ementia E trapyramidal signs 2etor hepaticus .<dor of breath from mercaptans/

Clinical Signs of Hepatic Encephalopathy

Mental status disorders

Clinical Signs of Hepatic Encephalopathy

Flapping tremor= asterixis

Diagnosis
Electroencephalogram (EEG)

Da4idson.s Classification of H7 E7
ST GE !E"T # ST TE F# PP$"G T&E!'& %& $" ( )ES Tendency for slo, ,a4e Slo, ,a4e+ rhythmic high 4oltage 5 ,a4e+ triphasic ,a4e
$ (Prodrome) $$ ($mpending Coma)

E*phoria+ occasional depression+ slo, mentation + arrhythmic sleep E*phoria+ disorientation+ dyscalc*lia+ mental conf*sion+ a-le to follo, physician.s instr*ct/ ions Deliri*m+ excitement + dro,siness (aro*sa-le) + *na-le or ref*ses to follo, physician.s instr*ctions 0nconscio*sness + (1) 2 (/) reaction to noxio*s stim*li

(3) / (1) (11)

$$$ (St*por)

(11)

$) (Semicoma or Coma)

Disappearance of dominant rhythm6 rhythmic high 4oltage 5 ,a4e+ triphasic ,a4e Flattening

(/)

P TH'GE"ES$S
0nsulin sensitivity =atabolisme protein
%C

BCAA

AAA

NH3

NH3

CIRRHOSIS

Harold <!*onn,Hepatic Encephalopathy 4 -yndromes and ;herapies

&*AA
AAA BCAA

2alse adrenergic neurotransmitter

( Tyr + Phe )

#/D'P

Tyr
Tyramine

Phe
Phenylethylamine

Dopamine

"orepinephrine

'ctopamine Phenylethanolamine .2alse ,eurotransmitters/

3!E!2ischer > 5!3!&aldessarini ,?ancet '67'

;E51-

$ &*AA .&ranched$chain Amino Acid/ 4 @aline, ?eucine, 0soleucine $ AAA .Aromatic Amino Acid/ 4 ;yrosine, Phenylalanine $ 2alse ,eurotransmitter 4 <ctopamine, Phenylethanolamine $ ;rue ,eurotransmitter 4 9opamine and ,oradrenaline

F i s c h e r.s & a t i o
BCAA ( Val + Leu + Ile ) mol
<

AAA ( Phe + Tyr ) mol

A P B 0!00'
:

A P B 0!00'

*ontrols . ,o! C 57 /

*irrhosis without encephalopathy .,o! C )0 /

*irrhosis with encephalopathy . ,o! C "0 /

A 4 student t$ test

Sheila Sherlock, 1993

!anagement
$nitial !eas*res Avoid precipitating factors listed above 5educe blood ammonia 9ecrease protein inta+e .limit to )0$"0 gDday/ ?actulose &efractory cases ,eomycin ' g P< bid *onsider unproven or e perimental methods 0@ branched chain amino acids &romocriptine 2lumazenil ?actilol .alternative to ?actulose/

T&E T!E"T 'F HEP T$C E"CEPH #'P TH=

9iagnosis4 ?2;, EE%, ammonia, blood coagulation 1onitor4 @ital signs, &lood gas analysis, @entilation, o yigen saturation

-EPP<5; <5%A, 2E,*;0<,?ung function4 1aintain <) saturation F 60# Protect airways 1aintain Pa*<) F "0 mmHg Ese antacid to raise pH F (,5 1aintain .5anitidine/ -erum ,a F'"0 .careful diuresis/ Prevent aggravation of encephaloptahy

maintain blood glucose .hypertonic glucose )0#/

?actulosa, ,utrition4 *ontrol %0; bleeding ,eomycin &*AA *aurious use of ?avage, 2resh 2rozen AAA *,- depressant Plasma 2at emulsion *arbohydrate Ref: Demling.RH, Wilson RF. Decision making in Surgical Critical care. BC. Decker 1998. pp 9!

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