Kedaruratan

di bidan g
G a s troentero-Hepatol g
oi
dr. Gde Somayana,Sp-PD-KGE H

D ivi GGaassttrrooeenntteerroolog i
Dep. Ilmu Pssieny
i aak o-k-iH Daep
DHe l at
alpa FFtoKK /-/- SJ UP Sanglah
itt aaDrm n pp D
DneenUNU R-:
aassaarr A
 OUTLINE

• Abdominal pain
• GI Bleeding
Upper GI Bleeding
Middle GI Bleeding
Lower GI Bleeding

• Hepatic Encephalopathy
• Acute Liver Failure
• Acute on Chronic Liver Failure
 Acute Abdomen
• Acute abdomen : nye ri p·erruutt yyaannqg ttiibbaa--ttibibaa
• ~ (
Acute abdominal pain : onss( << 2 2 44 jjaa m m ) )

• Perlu diagnosis yg tepat &eem ttma

ddaananrraiiajj aaw yyaa b aik, krn sebagian besar tdk
bbe
e eembmbeeeernranapwpa allhnhnagagrrlib
aa
memerlukan pembed ahann
• Ada 3 pola nyeri abd omieenn:: ssoormnaattoo l referred pain
vviisscceerra ppaarrleiettaat ddaa
• Pada hollow organ loka....1 rreseeppttoorr
a l , n n
mukosa, muskularis mukosa,
l ,
...s_i aaffffeerreenntt
dlm otot polos, serosa dan meesseenntt
n t teee
e rrrrill
iueuemt t a
m a kk dii
• Pada organ solid, affere teerrbba d kkaap oorrg shg nyeri akan muncul bila tjd
n a t t a a ss d i p ss u u l g aa nn
peregangan kapsul or n gatssbb
n i l
t
Nyeri Viscer al
• Nyeri visceral terutama ddiittrraannssmmisisikika myelinated c fibre yg
dirangsang oleh bahan kaklnim n ododlle iiseshthteeuukn kooraalk traksi atau torsi
mesenterium miiaa, nnssi,i, nnttr otot, si
,, kkrraa ssuu ddiilloo si·,
• Nyerinya tumpul, dalam onsetnya gradual dan
bisa disertai dgn m ua eme, m m
es ,
s,i i s l
s l,i,i tt k k a a li li r
da , gelisah
• Lokasi nyeri sesuIai
l,,_dendgdaia iaaapapshshaoaollrreessisi se~- n embriologi, yi:
snonorrgogorrggaann22 ddca _ ra
• Epigastrium: utk ffoorre I i proksimal lig Treitz yi.
duodenum, gast...., a a n ntts s b b
ssiisgsut ubtbi
eg t il/lii i nkreas, lien
...... h e
• Periumbilical: utk oorrggaann
er
, e p p t i i m m ese r
spr,p, t tp..aenum, ileum, kolon kanan
a a r
dan midtransversu mmkidiqguutt r,, j j e e j j a
• Hipogastrium: orrg mgma hhiinnd ssp ccooll transversum distal, c
descenden, sigm a n n d g gu u t t pt t .. a on
ooiid
d
Nyeri somato parietal
• Diperantarai oleh serrabb ssaar A ddee . Sifat nyerinya tajam dan
terlokalisir. uut raaff A ltltaa
• Struktur somatoparietal ddiiiinnee uun.niilla l ddar dermatom T6-L1
• Reseptor peritoneum pI prrar vvriaieasdsdi i adtd teiierrraraannrgi oleh organ di dekatnya
yg inflamasi atau ir itta e
a tkkiimmi sseegcscsaanung,
t a a l l p p t a gl n , shg menimbulkan nyeri
yg tajam, lateralisasiiiss daiaallw w it
ookki alla asanjjnegegllsa Tetapi lokasi nyeri bisa juga
nn yg _-nggaala iinanaflflaaasm
jauh dari organ me s i i n n y ys s. .ssp peerfor duodenum yang
akan dirasakn nyeri- di am ppamairi raamkakaasan si,i,kkrptrnnasi grasi gastric content
• Contoh klasik pa da ·accuc o
u oali l
apc ic
pp n
p a
e a
e n n
n d md imi
ic ciiiada ....walnya berupa nyeri
viscera di paraum bilica tteelI — ttiiskske ,, eym ygm g upp,, ddiirsakan.... nyeri di daerah Mc
l > > u d d i ia a n n
krn inflamasi s ssaam d sseerr d..n mengenai peritoneum r a a ..
Burney ddhh mppaai di oossa d .. a
parietal i i a ..
a
Nyeri Alih / Refer rree ppaai
dd i nn
• Nyeri yang dirasakan j· uuhh llookkaassi i Y y- sakit
• a nddvavairisrisi cocorrogogra
Nyeri alih tjd bila affere rgagnn
yy sakinga I masuk ke spinal cord
di level yang sama dgg nt e er
a r a
af afflfl
e earan n g g
ssoom k —> t · dirasakan di
pa t
dermatom kulit da seggmm ssppiil ym
n n r e e n n tt y asastatiai nyeri
eueknka
• Dirasakan nyeri di permm na nknku
aaul gg mma
u a an n l l i
• Polanya tetap / stereot i p sseehhiin
i p i tt bbeaerrgg untuk diagnostik
ee nggggaa uunnaa u
Diagnosis

• Nyeri abdomen akut harruuss sseeggeerraa pe nyebabnya

• Pengetahuan ttg ana..ododiittededgagaiin
aknkekekrariandnda organ abdomen akan
membantu menegakka .... tn
..mnm ann vvaassi arrti
• _ i i
d
( i
Anamnesis yang telit (dbibiaaaagg no
ffo n & ssaaccr seven) dan pemeriksaan
i o
s o
fisik yang benar akan meemmbub
s isi s
ccis is urrm&
mere
eemdm
d pmpit diagnosis diferensial
aannttuu peerrssee
 Epigastric
Right upper quadrant Left u
pper quadrant
Pulmonary: pneumonia, pleural
Cardiovascular: ischemi
myocardial pericarditis a,
effusion, nary embolism Pulmonary: pneumonia, pleural
pulmo and pulmonary emeffusion
Esophagus: esophagitis,
infarction, yema empyema bolism and infarction,
Boorhaeve
emp
Liver: hepatitis, congestive
Stomach/ dyspepsia,
hepatopathy, Cardiovascular: myocardial
gastritis, gastric outletPUD,
Duodenum:
abscess, benign or malignant ischemia
obstruction
mass Spleen: infarction, abscess,
Pancreas: pancreatitis,
lesion,
Biliary: hematoma
cholecystitis, pseudocyst, rupture,
cholangitis choledocholithiasis, neoplasm splenomegaly
Vascular: aortic aneurysm rupture, Stomach: perforated
Duodenum: p erforated aortic PUO
PUO dissection

Right midabdome Peri Left

n umbilical midabdomen

Small bowel: gastroenteritis,

obstruction, Spleen: infarction, abscess,
mesenteric ischemia, Crohn's rupture,
Urological/ pyelonephritis disease,early
Colon: ileus coliti cec splenomegaly
Renal:
perinephric ,
abscess, appendicitis, s, al Urological/Renal:
infarction volvulus pyelonephritis,
nephrolithiasis Vascular aortic rupture, aorti perinephric abscess,
: aneurysm c infarction, nephrolithiasis
dissecti
on

Right lower quadrant Hypogastriu Left lower quadrant

m
Small bowel: late ileitis, Colon: diverticulitis, mesenteric
mesenteric appendicitis,
emia, mesenteric ischemia, colitis (IBD, infectious),
isch Colon: adenitis sigmoid
right-sid ed diverticulitis, Colon: mesenteric colitis volvulus, IBS
ischemia, mesenteric ischemia,
(IBD, infectious), diverticulitis, GYN: ectopic pregnancy, ruptured
colitis (IBO, infectious), large ovarian
IBS GYN: ectopic pregnancy, bowel obstruction, IBS cyst, torsion, PID, tuboovarian abscess
ruptured ovariannephrolithiasis,
UrologidRenal: cyst, torsion, Urological: cystitis, urinary Urological/Renal: nephrolithiasis,
pyelonephriti
PIO, TOA perinephric retention pyelonephritis, perinephric
s, abscess, GYN: PIO, ectopic pregnancy abscess,
infarction infarction
a, Inguinal: hernia,
Inguinal: lymphadenopathy lymphadenopthy
herni
I
t
Figure 43.5 Differential diagnosis of acute abdominal pain by region of pain presentation. GYN, gynecological; IBD, inflammatory bowel disease; IBS,
irritable bowel syndrome; PID, pelvic inflammatory disease; PUD, peptic ulcer disease; TOA, tuboovarian abscesses.
 Acute abdomin
.
al
pain

Unstable Hemodynamica
vital lly
Sign stable
s
Fluid resuscitation, blood
&
No Evidence of Surgical
urine culture, bedside US overt peritoniti consult
+/- upright XR
peritoniti s ation
Urgent s
surgical
consultation
Assess
pain
location

RUQ/right LUQ/
Epigastric Periumbilical RL Hypogastru m LL
mid left
Q Q
quadrant mid
quadrant
Lipase, Lipase, Lipase, Pregnancy Pregnancy Pregnancy test,
LFTs Lipase, UA, CT
LFTs, LFTs, test, test, UA, CT vs
UA, CXR, XR, US XR,CT UA, CT vs US UA, CT vs US
US, US
Figure 43.6 algorithm for acute abdominal CT, computed tomography; CXR, chest x- LFTs, function tests; LLQ, left
DiagnosticLUQ, left upper
quadrant; pain.
RLQ, right lower RUQ, right ray; UA, urinalysis;liver
quadrant; lower
US, ultrasound; XR, x-
 Perdarahan Saluran Cerna
• Sering dijumpai dgn sppeekkttrruumm erdarahan samar
sampai berat m enga knklnc
liin
canisam ism ddaarri i pp
• nny y aaww aa
Harus dinilai be ratnyaa mbernya
• Hematemesis: muntptah ped erdradadrara ararhahahhaann g atau spt warna
d d a
bubuk kopi ---> sumbeerrnnyy pra
h a
m n
men sueru prarhohokks l gam entum Treitz
• a t
d t
Bila berwarna m era teerraanngigim—
a ed ei i r rans n m>a>al lIii an a ktif , dan bila
h gelapppe aatertra da dauaurraahh —> perdarahan tidak
warnanya merah p hhiittaamm sspptt ~
• aktif
Melena: kotoran atau ffeesseess k ko o p p i i ...eperti ter dan
berbau busuk, dgn suuum bbe mebrbrw eewrraarrnnaase~----- s~an besar dari
~- S
saluran cerna at as p h
pe hi
e it
r rad ad ~
a m
a r ra ah ha an---
n bagi"-
r a.s..a, l dari perdarahan
usus halus atau ·ko. . eebbaaggiiaann .....,,
• Hematochezi a : pe.._ l k ke e c c i i l l b b ii s sa a bbe r ,___
berwarna merah terang
oonn kkaannaann
pprrookkssiimmaal l
• Obscure bleedi nng ((OOGG ppeerrddhan saluran
cerna yang summb g bIeIB erBr )t)t:i:iddaadrdi
raikakhehui walaupun
nn...
sudah dilak uk ynyaatatiinnddaaaakdkdiieatatagagnn endoskopi dan
radiologi _ n kkaann oossti tik
• Occult bleediinn pprreesse i kklliis b erupa anemia
def besi, atrauagdgda :: ehnha nttaasassilsili inni test
• Overt bleediuna nrgrigi f:f:p
eepcecearardlld ssaaraa n cerna yang
a a ra rao
visible (melenn hheemmaatoto h o
h cancc cu
an ult lluur
aa, cchheezizai)a)
,
A. Perdarahan Saluran CCeerrnnaa pper GI Bleeding)
n AAttaass ((UUP.
• Secara garis b esarr 22 vvaerrii d an non-variceal
bleeding ddiibba yyaaiit cceeael
• Etiologi : a g gi i t u u
Table 3.1 Major cause of uppe gastrointestin bleedin
(0/o [4] s r al g
frequency) .

Source of bleeding Frequency{%)

Pepti u 35-62°/o
c leer
Gastroesophage varice 4-31 o/
al
Mallory-Weiss tears 4- o
Gastroduode erosio 13o/o
3-11 °/o
nal
Erosiv esophagins 2-8o/o
e tis
Malignanc 1-4o/o
y sourc 7-
Unidentifie e 25o/o
d
• Anamnesis & Pemeriksaan fisik

Harus digali apakah ada p-eem- - ian NSAID,

antikoagulan, alkohol, rok·ooaak ari riwayat p enyakit hati
dd
ka
Pada pemerik saan fisik dikccaa ntanda2 pe ny hati kronis,
lakukan peme riksaan reccm arrit (Rectal Tou cher)
mencari sumber perda u(m untuk
rraha
Stratifikasi risiko dgn sisti1 sskking dikerj akan untuk
m
a n
menilai risiko rebleeding m or Imortalitas
Evaluasidda 1
ana2 syok sep eer taakikar ia, tekanan darah
•
tand
sistolik <90 mmHg , ekstrrertiemiI ditItaa s da n sinkop. Bila
disertai dengan syok m din gi1asnya
! n di atas 30 %
Lab : darah lengkap , fun ogorgrtahaaliatitd
taan fung si ginjal
ssii tii d
Risk stratification : iiddeennttiififikk sus dengan tingkat
1

morbiditas & maoaor ss i kaka

rti ta l yayaa tinggi / rendah
:

liittaass ngg
Table 3.3 Rocka risk score [6]
ll scheme .
Value Scor
e
0 1 2 3

Age <60 60-79 >80

(years) None BP > Tachycar Hypotensio (systol
Shock (systolic 100, dia n ic
BP > puls
pulse (systoli 100, e BP<
<100) c 100)
Comorbidit No major Cardia failure, Renal live failure
y comorbidity >100) c ischemic failure, r malignanc
,
diseas an
hear e, y disseminat y
comorbidit
y of ed
Diagnosi Mallory- tear Al other diagnose t
Malignanc
s Weiss
no ,
identifi l s y gastrointestin
maj upper tract
lesion
and ed
no SRH al
or
Majo stigmat None or dark spot Bloo in
r of recent
a only d gastrointestin
upper tract,
haemorrhag al
adhere clot visibl
e nt spurting
or , e
vessel
The total is calculated by additio of each Maximu additiv score prior to is 7, additiv
score simple
endoscop is BP n pressur
variable.
SR stigmatm of recente endoscopy maximum e
score y 11. blood e, H a hemorrhage.
following
Rockall score : untuk m en i1 lai1 pprrooggnnoossisis I/
rriissiikkoo mmoorrttaalliittaas.
Skor : - 2 : rendah .
0 -4 : ediate
3 keatas inter alitas
5 : mor tinggi
Clinical Rockall score: j umlI ahh sskkoorr l eennddoopi ,
nilai maksimal 7 ttaannppaa osskko
vvaarriiaabbeel
Blatchford score : untuk memmpprreeddikikssi i leb ih
lanjut sseepppe peeerrrlltutiu
i tntrnryayaananssffuussii,, at a
teerrbed
tpem aapapahim etta
ena
ih nenedrrduvo
unvoesnestn
tkunkusoksopi
kl i I d arau
ber ulangn —>> mmeenncceeggaahh han
pp errd
Table 3.5 Blatchford admission risk markers [8].

Admissionrisk marker Score componentvalue

Blood urea (mmol!L)

6.5-8 2
8.0-10.0 3
10.0-25.0 4
>25 6

Hemoglobin (gldL) for men

12-13 1
10-12 3
<10 6

Hemoglobin (gldL) for women

10-12 1
<10 6

Systolic blood pressure (mmHg)

100-109 1
90-99 2
<90 3

Other markers
Pulse > 100 1
bpm 1
Presentin with melena
g 2
Presentatio with syncop
n e 2
Hepatic
failure 2
Cardia failure
c
(a) (b) (c)

(d) (e) (f)

Figure 44.1 Endoscopic stigmata of recent hemorrhage in ulcers. (a) Arterial spurting; (b) nonbleeding
vessel; (c) adherent clot; (d) oozing
visible ulcer.
without other stigmata; (e) flat pigmented spot; (f) clean-base
Table 2.1 Comparison of the most commonly used scoring system for peptic ulcer
bleeding.

Characteristi Baylo Cedars- Rockal Blatchfor

cs Ris Score
of r Sinai l d
k s Scor Score Score Score
e
Primar outcom variabl Rebleedin Rebleedin Mortalit Cl inica I
y e e g g/ y Interventio
Mortalit n
Patien cohor PU UGI
y UGIB
tEndoscopi
t finding B B
UGIB
cPatient's ages + +
+ + +
Comorbi condition + +
d s
Hemodynam statu + + + +
ic
Tim sinc onses of symptom + +
e e t s
• Manajemen:

Resusitasi : adala h langkah pertama harus dike untuk

menstabilkan hemodinamik . Pemberian rjakan
cairan kristaloid, koloid atau
transfusi darah
Menghentikan sumber perdara h an :
h I

A). Non-variceal bleeding

1. Endoscopic hemostasis dalam 24 jam perta ma
2. Farmakologi: PI
3. Pembedahan ( berdasarkan haasil angiografi)
B). Variceal bleeding:

1. Medical therapy:
Obat vasoactive: men runkan
u tekanan portal dg vasokonstriksi di
sistim splanknik —>n somatostatin, octreotide , vasopressin,
terlipressin
Balloon tampona de : Sengstaken-Blakemore tub e, Minnesota tube
atau Linton-Nachl es tube

2. Endoscopic therapy: skleroterappi endoscopic b ligation (EBL)

,,e and
3. Pembedahan: TIPS (Transjugular Intrahepatic Portosystemic Shunt)
• Fig. 16-10 Small esophageal varices. A, Longitudinal varices in the lower of the esophagus with
third
diameter less than 5 B, Small with red wale sign (arrow).
mm. varix

• Fig. 16-27 Control of gastric variceal bleeding with cyanoacrylate glue injection. A, Actively
bleeding gastric varix
(pentagon arrow) with large amount of blood (arrowhead) pooling in
) (black stomach.
gastri varix C, Gastri varix after obliteratio Earlie appearance of
B,
cyanoacrylat casts of
(arrow) (arrow). c . c n. r
Injection
e bleeding

• Fig. 16-11 Large esophageal varices. view of the lower third of the esophagus Fig. 2. Endoscopic techniques for treating esophageal varices. Endoscopic
Endoscopic
strating varices greater than 5 mm in diameter. A, Large varix (arrow)demon-
with red wale sign. B, sclerotherapy
Red wale (right) and endoscopic band ligation (left). (Courtesy of AGA GastroSlides,with permission.
sign-longitudinal whip mark on varix (arrow). C, Large varix with hematocystic spot (arrow). Copyright © AGA Institute, all rights reserved.)
nton
 \ Length marks

G
a
s
t
r
i
c

b
a
l
l
o
o
n

p
o
r
t Esophagal balloon in11mion --
/ e
Oesophageal
aspiration port

~ strlc b Uoon , 11
~
Gastric aspiration
openings

/ /
Oesophageal
open"ngs

A B

V fl · ~~M

C er

Banded Clot f t r
vances •
"'J • C •
O , _ _.,
B. Middle GI Bleeding

• Sumber perda rahan dari ampula vateri - ileocecal valve

• Perlu dicurigai MGIB bila ditemukan adany anemia pada
occult OGIB at a au overt OGIB dgn hasil oskopi yang
normal / tidak adaend
kelainan

Manajemen:
• Diagnostik:e ndoskopi (up ppe ll wer, enteroscope, capsule),
angiography err,, o
o
• Terapi: endo scopic therapy: APC, clippi ng, surgery
 • Vascular
Etiologi: o Angiodysplasias
• Anticoagulation
• Chronic renal failure
o Arteriovenous malformations
• Prior abdominal radiotherapy
o Dieulafoy's lesions
• Aortic stenosis (Heyde's syndrome)
o Ischemic enteritis • Aortic aneurysm repair
o Varices
• Inflammatory bowel disease
• Inflammatory • Celiac disease
o Anastomotic ulcers
• Acquired immune deficiency syndrome
o Crohn's disease • Hemorrhagic hereditary telangiectasias
o Eosinophilic enteritis • Blue rubber nevus syndrome
o NSAID enteropathy • Plummer-Vinson syndrome
o Radiation enteritis • Tylosis
o Ulcers • Pseudoxanthoma elasticum
• Autoimmune • Ehlers-Danlos syndrome
o Amyloidosis • Schonlein-Henoch syndrome
o Behcet's disease • Neurofibromatosis
• Tumors • Malignant atrophic papulosis
o Adenocarcinoma • Klippel-Trenaunav syndrome
o Gastrointestinal stromal tumor • Behc;et's disease.
 Box 10.5 Aetiology of occult gastrointestinal
Box 44.1 Causes of overt obscure gastrointestinal bleedinq". bleeding

Oesophagus
Upper gastrointestinal tract" • Camero erosions
n
Stomach
Cameron lesions
• Porta hypertensiv gastropathy
Dieulafoy lesion • lDieulafoy's
e disease
Gastric antral vascular ectasia (GAVE, "watermelon stomach") • Gastric antral vascular ectasia (watermelon
stomach)
Small intestine • Arteriovascular malformation
(angiodysplasia
Aortoenteric fistula )
Biliary tree
• Haemobilia (trauma or stone)
Dieulafoy lesion
Pancreas
Meckel • Aneurysm (haemosuccus pancreaticus)
diverticulum Small intestine
Neoplasm • Portal hypertensive intestinal vasculopathy
• Neoplasi (GIST, carcinoma)
Pancreatidbiliary a
• Crohn's disease
disease • Arteriovenous malformation (angiodysplasia)
Ulcer • Aortoenteric fistula
Vascular ectasia • Radiation ileitis
• Meckel's diverticulum
Colon • Polyposis and Peutz-Jeghers syndrome
• Medication-induced mucosa! lesions
Dive rt i cu I os (NSAIDs)
is • Jejuna! diverticula
• Carcinoma
Hemorrhoids • Carcinoid tumour
Rectal varices Colon
Vascular Arteriovascular malformation (angiodysplasia)
C. Perdarahan Saluran Cerna Bawah (Lower GI Bleeding)
Box 10.4 Causes of rectal bleeding

In patients under 40 years old

Very common
• Haemorrhoids
• Anal fissure
• Inflammatory bowel disease
(mainly proctitis)
Less common
• Polyps (hamartomatous or
adenomatous)
• Infective colitis
• Meckel's diverticulum
• lntussusception
Rare
• Colorectal cancer
In patients over 40 years old
• Haemorrhoids
• Anal fissure
• Colorectal cancer
• Colorectal polyps (mostly adenomas)
• Angiodysplasia
• Diverticular disease
• Inflammatory bowel disease
• lschaemic colitis
• Radiation colitis
• Infective colitis
 • Diverticulosis
• Etiologi
• Cancers/Polyps

• Colitis (inflammatory,
ischemic, infectious and
radiation)
D Angiodysplasia

o Miscellaneous

D Anorectal conditions (e.g.

hemorrhoids, fissures and
idiopathic rectal ulcer)
D Unknown

Figure 1. 4 Common causes of lower gastrointestinal bleeding (Modified from Zuckerman

and Prakash (35) with permission from Elsevier.)

• Manajemen:
- Resusitasi
- Mencari sumbe r ppeerrdda : ko
olonoskopi,
angiografi terap iIr ataauu
arraahhaa
nn:
ppeemmbbeedaaha
an
 HEPATIC ENCEPHALOPATHY
• Definisi menurut AASLD (2014): disfungsi otak ok insuffisiensi hati atau
akibat hipertensi porto-sistemik
• Klasifikasi HE:
Table 16.1 Classificati of hepatic
on encephalopathy.
Based on of Base on Based time Based on
Base on etiology severity d scal on precipitatingfactors
d WHC scale ISHE e course
Typ A MHE N
CH Episodi Precipitate
e Grad 1 E c d

Typ B e 2 OH Recurren
e Grad E t Nonprecipitate
e d
Grad 3
Typ C e 4 Persisten
e Grad t
e
WHC Wes Have Criteria ISHE Internation Societ for Hepatic and Nitroge Metabolism MH minim
,hepatict n ; CH N,coveralhepati encephalopath
y Encephalopathy
OH E, hepatic n ; E, al
encephalopathy;
Adapte fro [27] E, t c y; overt encephalopathy.
 Clinically detectable, Figure 16.1 Spectrum of neurocognitive impairment in
spanning from cirrhosis (SONIC) (Adapted from [31] with permissio from

__ _
conf
r
us ion
,..,,.
.._
to
1
John Wiley. & Sons.
)
n

Unimpaired
CHE
com
_ Grad atose

(MH e OH
2,3,
E+ 4 E
L Gra J
de1
Clinically undetectable
OH
E)

Worsening mentation
 3
UJ
Q.) I Q.)
"O 0 "O
~
2 ~
0)
0)

UJ UJ
I I
1
UJ
UJ I
I o
o

Days to months
Days to months
Figure 16.3 Recurrent hepatic encephalopathy showing regular frequency
Figure 16.2 Episodic hepatic encephalopathy, showing complete recovery
of episodes with possible continuing hepatic
in between HE, hepatic encephalopathy; CH, covert hepatic covert/minimal
episodes. encephalopathy between HE, encephalopath CHE
encephalopathy; OH overt hepatic encephalopathy. episodes. hepatic y; encephalopathy.
,
E, covert hepatic encephalopathy OHE, overt hepatic
;

3
Q)
w
I
"'C
~
0 2
0)
w
I 1

iu

Days to months
Figure 16.4 hepatic encephalopath showing a continued
overt hepatic encephalopathyy lasting for weeks
Persistent
of state
to months with
no
return to normalcy. HE, hepatic CH, covert
encephalopathy; OHE, overt hepatic
encephalopath hepatic
y; encephalopathy
Patogenesis

• Ada 2 kondisi yang menyebabkan

terjadinya HE, yi: kegagalan fungsi
hati dan porto-systemic shunt

• Akibatnya tjd gangguan kliren di hati

terhadap neurotoksin dari usus —>
ggn astrocyte di otak
 Healthy Cirrhosis

. .•
..• ••
...
..•
. .•
.••
.•

Ammonia
' .....- A -m-m..-__,on ;
1 I

+- -i~

,/ It.._
• .
.
•• ...
..
------------·
• .
...
•

..
I Glutamine
•• . Urea Glutamine Urea
.•
• .
..........
Ammonia

!l
..........
Glutamine
..........
Urea
Fig. 10.8 A simple schematic of inter-organ trafficking of ammonia both in healthy individuals and in patients with cirrhosis. Ammonia
is
produced in the intestine from dietary protein, deamination of glutamine via glutaminase, and bacterial action in the colon. It is also
produced in the kidney from glutamine via glutaminase. In healthy individuals, the ammonia generated in the gut and kidney is
metabolized in the liver to urea, which is then excreted in the urine. A small proportion of the ammonia produced in the kidney is also
excreted in the urine. Ammonia is also to glutamine in the liver, muscle, and, to a much lesser extent, the brain, via glutamine
detoxified
synthetase. The glutamine is released back into the circulation and undergoes degradation by glutaminase in the gut and
subsequently
kidney to form ammonia. In patients with cirrhosis, ammonia levels are Under these circumstances the synthesis of
circulating via glutamine synthetase becomes the most important,
glutamine increased.
though temporary, pathway for ammonia detoxification. Thus, a
greater proportion of the ammonia generated in the kidney is released into the urine reducing the amount released into the
circulation. Additional ammonia is also systemic
in muscle and, to a much lesser extent, in the brain. Source: Adapted from Wright et
[66]. Reproduced with permissiondetoxified
of John Wiley & al.
Sons.
Fig. 10.12 A possible unifying hypothesis
Precipitating factors
for the pathogenesis of hepatic
encephalopathy. A number of factors,
Ammonia I Hyponatraemia lnflamatory cytokins Benzodiazepines
predominantly ammonia, induce astrocytic
swelling which results in activation of the
N-methyl-o-aspartate (NMDA) receptor and
the generation of reactive oxygen/nitrogen
species ROS/RNS; the Astrocyte
mechanisms
underlying the NMDA receptor activation
are unclear. Astrocyte function is
Swelling
compromised as a result of both the effects
of cell swelling and oxidative/nitrosative
stress and as a result of the direct
neurotoxic effects of ammonia. The
resultant dysfunction causes in
alterations NM DA-receptor
gene transcription, modification of
proteins and RNA, zinc mobilization,
disturbances andin intracellular signa
transduction and l ROS/ANS
neurotransmission.
Astrocytic-neuronal communication and
neuronal function may be compromised,
resulting in disruption of multiple
neurotransmitter systems,
synaptic
plasticity, oscillatory networks, and Gene Protein/mRNA Zinc
functional network connectivity. Source: expression modification mobilization
Adapted from Haussinqer & Sies • Signalling
[87].
Reproduced with permission of
Elsevier.
Astrocytic/neuronal dysfunction

J. ±
i
Synaptic plasticity Disturbed oscillatory networks Functional connectivity
Diagnosis
• Overt HE ditegakkan secara klinis.
• Bila curiga adanya ensefalopati harus dibuat diagnosis bandingnya
• Pemeriksaan laboratorium: pemeriksaan kadar amonia darah tidak
direkomendasikan krn OHE ditegakkan secara klinis. Sedangkan
pada CHE ada korelasi dgn onset dan terapi, tetapi tdk untuk
diagnostik
• Pemeriksaan lab lebih ditujukan untuk mencari faktor pencetus atau
mencari kemungkinan lain penyebab ggn kesadarannya

• Beberapa test yg digunakan untuk diagnosis CHE dan OHE:

Table 16.4 Tests for overt and covert hepatic encephalopathy. Table 16.2 West Haven Criteria
scale.
Special Trained Time
ISHEN classification WHC grade Description Operative definition
equipment personnel Advantages Disadvantages required

Tests for OH E CH Minima Normal mentation clinically Abnormal results of psychometric

E l and/or
neurophysiologic tests
WHC No No Quick bedside test High interobserver variability, <5 min Abnormal psychometric and
especially for early stages al .
neurophysiological tests. No set number
HES No Yes Accurate with low Time consuming for clinical -10-20 min Example:
A of tests PHES >2 SD in 2 or more tests
interobserver variability practice
and requires expertise ICT abnormal-
MO-Log test No No Quick bedside accurate -10 min
test Requires patient cooperation and C FF of 39 Hz or less
CHES No No restricted in unconscious patients Grad 1 Trivial lack of Oriented to time and place
Accurate and detailed with - 20 min
S Can be time consuming for clinical e awareness
good sensitivity However, change in cognition/behavior
FOUR No Yes Short test with excellent practice -10 min Euphoria or anxiety with
score Needs expertise for neurological
Shortened span respect to patient's baseline caregiver
sensitivity attention per s
assessment addition or subtractio
Tests for CHE n
Impairment of
Paper and psychometric tests
pencil OH Grad 2 basic Altered sleep Oriented to place
No Yes Good Predicts Not suitable in the USA due to lack -15-20 min
PHES validity. poor of E e rhythm Lethargyfor or
Disorientatio time Disoriented to time (>3 items), day of the
outcomes normative data n
apathy i.e.,
RB No Yes Applicable in the USA Incorporates domains not affected in -30-35 min Obvious personality change week, day of the month and year
ANS CHE but not fully to
Inappropriate behaviors month, ,
applicable
hepatic encephalopathy Dyspraxia and asterixis
Computerized psychometric tests
Grad 3 Somnolence to semi- Disoriented in place (>2 items) country
ICT Yes No Sensitive and easily Requires highly functional patient -15-20 min
e stuporous i.e., ,
available. and lacks repeatability state/ city or place in addition to
Can predict driving Responsive to stimuli region, above
CDR Yes No
impairment and
Not applicable if hearing -20-25 min Confused symptoms
OHE impaired.
Sensitive and predicts Gross
Not validated in the USA
resolution of cognitive Grad 4 disorientation Unresponsiv to painful
dysfunction post e Bizarre behavior e stimuli
CR Yes No Unavailable in the USA and not -20-25 min
transplant and post TIPS
T
applicable to deaf patients •Lure and targets are captured by ICT of whichComasubjects need avoid respondin to lures and need to respond to targets. A high lure rate
Ease of administration and
s to
of which is indicative of g indicates
sensitivity but not
SCAN test Yes No Unavailable in the USA -20 min failure inhibition, CHE.
validated in the USA West Haven Criteria; ISHEN, International Hepati Encephalopath and Nitrogen Metabolism; covert encephalopath OHE
WHC, Society for
Sensitive in detecting overt hepatic PHE Psychometri Hepati cEncephalopat
y Score IC Inhibitory CHE,
Contro Test; Critical Flicke y;
hepatic ,
neuropsychological encephalopathy; S, c c hy ; T, l CFF, r Frequency.
E ncepha IApp-S No No Cannot be applied in color-blind -5min
troop abnormalities Adapted from [27].
patients
Short and easy to administer.
Neurophysiological tests Can predict OHE
CFF test Yes No Short sensitive bedside test. Equipment, requires binocular -10-15 min
vision
Can predict
OHE and a highly functional patient
EE Yes Yes Can be administered in Long duration
G Needs neurological support and can
advanced hepatic
be confounded easily
encephalopathy. With
MELD, can predict
OHE
Evoked potentials Yes Yes Insufficient evidence, - 30-60 min
Has sensitivity in needs
general. cooperation from patient,
Predicts OHE confounded easily

CHE, covert hepatic encephalopathy; OHE overt hepatic encephalopathy; WHC, West Haven Criteria; HESA, Hepatic Scoring Algorithm;
, Encephalopathy
CHESS, Clinical Hepatic Encephalopathy Staging Scale; MO-Log, Modified-Orientation Log; FOUR, Full Outline of Unresponsiveness Score; PHES,
Psycho-
metric Hepatic Encephalopathy Score; RBANS, Repeatable Battery for the Assessment of Neurophysiological Status; ICT, Inhibitory Control Test;
CDR,
Cognitive Drug Research; CRT, Continuous Reaction Time; CFF, Critical Flicker Frequency; EEG, electroencephalogram; MELD, Model of End-stage
Manajemen
A. Umum
• Nutrisi: kalori 35-45 kkal/bb/hari, protein 1,2-1,5 gr/bb/hari. Protein
nabati lebih disarankan
• Jangan puasa berkepanjangan, cukup 24-36 jam..misalnya bila
mengalami perdarahan saluran cerna
• Jangan terlambat makan > 3-6 jam

• Atasi faktor pencetus

• Bowel cleansing: untuk mengekskresi amonia
• phosphate netral dan laktulosa
Manajemen (2)

B. Khusus
1. Non-absorbable disaccharides
• lgs di metabolisme di kolon menjadi asam lemak+hidrogen
• bermanfaat menurunkan produksi dan absorpsi amonia
• laktulosa: 15-30 ml, 2-4 x/hari —> bab 2x/hari. Bisa juga per-rektal
250 ml/750 cc air.
• laktitol: generasi ke-2 berupa powder dg dosis 10-90 gr/hari
2. Antibiotika: utk eliminasi bakteri penghasil urease (menghasilkan
amonia :
I. Neomycine
II. Rifaximin 1100-1200 mg/hari dosis terbagi
Manajemen (3)
3. BCAA : meningkatkan detoksifikasi amonia & menurunkan influks
asam amino aromatik ke otak
4. Probiotik
5. LOLA : efeknya untuk meningkatkan aktifitas siklus urea di hati
(amonia —> glutamin) dan meningkatkan sintesis glutamin di tempat
lainnya => kadar amonia darah menurun
6. Ammonia scavenging agents
7. Zinc : sbg kofaktor enzim di siklus urea dan enzim glutamine
synthetase di otot
8. Bromocriptine
9. Flumazenil
10.Liver support system
11. hati
Transplantasi
Table 10.6 Management of recurrent or episodic hepatic
encephalopathy
Acute events:
• General supportive measures
• Identify and treat precipitating factors
• Enema ta every 6-12 hours for 48- 72 h
• Maintain adequate protein and energy intakes
• Non-absorbable disaccharides:
- Lactulose 40-120 mL daily or
- Lactitol 20-40 g daily
If response inadequate, add:
• Non-absorbable antibiotic for 5-7 days
- Rifaximin 400 mg tds or
- Neomycin 4-6 g daily
Between episodes (if necessary):
• Avoid precipitating factors
• Maintain adequate protein and energy intakes
• Non-absorbable disaccharides
- Lactulose 20-60 mL daily or
- Lactitol 20-40 g daily and/ or
• Non-absorbable antibiotics
- Rifaximin 400 mg tds
Table 10.7 Management of persistent hepatic encephalopathy
General
• Avoid precipitating factors
• Maintain adequate protein and energy intakes
• Increase protein intake from vegetable sources
• Consider probiotics
• Non-absorbable disaccharides
- Lactulose 40-120 mL daily or
- Lactitol 20-40 g daily
If response incomplete, consider:
- Rifaximin 1.2 g daily
- BCAA supplements
- Bromocriptine 7.5 mg daily (if no fluid retention)
- LOLA 6g tds
- Sodium benzoate 2 g bd (if no fluid retention)
- Daily enemata
Continuing poor response, consider:
- Revision of surgical shunts or TIPS
- Blockage of large spontaneous shunts
If situation unresolved:
- Hepatic transplantation, if there are other indications
BCAA, branched-chain amino acids; LOLA, L-ornithine L-
TIPS, transjugular intrahepatic portal-systemic shunt. aspartate;
 Box 16.4 Pharmacotherapies for acute overt
Table 10.8 Management of minimal hepatic encephalopathy hepatic encephalopathy and for prophylaxis.
First-line therapy
• Avoid constipation Lactulose or lactito/
•• Acute hepatic encephalopathy
Acute hepatic encephalopathy grade 2/3: 30-45 ml orally every
• Avoid other precipitating factors gr
2-3 bowel movements a day till
2-3 hours with goal of minimum
• Maintain adequate protein and energy intakes improves clinically
• Acute hepatic encephalopathy grade 3/4: 300 ml every 2-3 hours
• Acute hepatic encephalopathy gr
• Non-absorbable disaccharides per rectally till clinically
improved orally two or three times
daily
Lactulose 20-40 mL daily or • Prophylaxis/outpatient:
15-45 ml
Lactitol 10-20g daily for 2-3 bowel movements a day

• Recurrent
Second-line hepatic encephalopathy/first line for OHE if
therapy to
intolerant
Rifaximin
lactulose Add on to 400-550 mg two times daily
• :
Recurrent hepatic encephal es daily
lactulose: Add on to 400-550
• Outpatient: 400-550 mg two tim
g orally every 6 hours for up to
Neomycin
• Acute hepatic encephalopathy: 1
6 days
• Outpatient: 1-2 g orally daily
• Outpatient: 250 mg orally two times
Metronidazole daily
• Outpatient: 250 mg orally two

Third-linetherapy
Branched-chainamino acids
• Outpatient: ,..., 12 g orally daily
erapy. Dose
L-OrnithineL-aspartate variable
• Acute hepatic encephalopathy th
 Acute Liver Failure
• Difinisi
Acute liver injury yang ditandai dgn ensefalopati dan koagulopati
(INR >= 1,5), pada pasien tanpa riwayat penyakit hati sebelumnya
dalam waktu < 26 mgg
• Klasifikasi:
 Table 2
Etiology of acute liver failure

Infections Viral hepatitis A, B, C, D, E

Herpes simple x virus, varicel la zoster virus
Epstein-Barr Epstein-Barr virus, cytomegalovirus
Tropical ions (eg, Dengue virus, leptospirosis, scrub typhus, malaria)
Drug and toxins Acetaminophen
infect
Carbon tetrachloride
Drug and toxins Idiosyncratic drug reactions (eg, modern medications, a herbal supplements)
Carbon
Mushroom poisoning (eg, Amanita pha/loides)
Idiosyncratic sting
Mushroom
lschemia lschemic hepatitis, hypoperfusion, cardiogenic shock
Sea anemone
lschemia Cocaine, methamphetamines, ephedrine, ecstasy
lschemic
Vascular
Heat stroke Acute Budd-Chiari syndrome
Cocaine, struction syndrome

Vascular Acute hepatitis

Wi Ison disease
Budd-
Sinusoidal Reye syndrome
Malignant infiltration
ob
Acute fatty liver of pregnancy, eclampsia, HELLP
Miscellaneous Autoimmune nonfunction after syndrome
Indeterminate liver
Wi Ison Reye
transplantation
Malignant
Abbreviation: HELLP, hemolysis,
Acute fatty liver enzymes, low platelets.
a lsoniazid, elevated
rifampicin, pyrazinamide, sulfonamides, trimethoprim-sulfamethoxazole, amoxi-
Primary graft
cillin-clavulanate, dapsone, ketoconazole, ofloxacin, didanosine, efavirenz, allopurinol, diclofe
nac, halothane, isoflurane, phenytoin, valproic acid, nicotinic acid, statins, imipramine, -
propylthiouracil, disulfiram, lisinopril, labetalol, methyldopa, amiodarone, flutamide, metformin,
etoooside. aemtuzumab.
• Patofisiologi:
Acute insult

Apoptosis Necrosis

Complement depletion,
Immune activation
impaired phagocytosis

Proinflammatory cytokines
TNF-a, IL 1 ~'
IL6 Anti-inflammatory cytokines

l
IL4, IL 10, TGF-
~
Microthrombi, tissue
hypoxia SIRS Infections

Artery
Venule Arteriol
e
Capillaries
Vasodilatation/Hyperdynamic Cerebral edema* Renal failure
circulation

Figure 17 .1 mechanisms in acute liver An acut impairment in predisposing to In combination,

Pathophysiologic failure.causes hepatocyte injury and death
insult from a multitude of etiologies e phagocytosis
these pathways can result infections.
in systemic inflammatory response
via syndrome
two main pathways: apoptosis and necrosis, which in turn triggers the (SIRS) leading to formation of microthrombi, tissue hypoxia and
release
can oflead
also bothtopro- and anti-inflammatory
immune activation, cytokines. Hepatocyte
depletion, and eventual multiorgan system failure. * Additional pathophysiologic
 • Diagnosis: mencari etiologi & menilai beratnya penyakit
D1agnost1 tests to etermine t e etio ogy Assessment of severity of liver injury"
c Liver chemistries (tota and
Suspected Serum level urin Serum AST, ALT,
l direct),
overdose acetaminophen
toxicolog scree , e bilirubin alkaline
Liver function INphosphatase
factor V,
Viral y
Anti-HAV n
lgM, anti- HB synthetic injur R, Blood
fibrinogen
Metaboli glucose, serum electrolytes,
hepatitis HBsAg,
DNA anti- HCV-HBc, anti-V lg
c y calcium,
magnesium, phosphate, arterial
Nonhepatotrophi virus ,
HSV HCV,
EBV- RNA,
C MV- HEV M gas, ammoni and
blood
leve
Infectio arterial
Chest a, and urine
X-ray, blood lactate l
c
Wilso disea es DNA, DNA,24-
Ceruloplasmi DNA
urin copper n cultures,
peritonea flui cultur (if
n se n, genetic testing,
hour
and e lamp, Neurologi statu l
Bedside d exam,
neuro e ascites)
Com
c s Glasgow a
ANA, anti-slit Ab, quantitativ
exam Scor CT scan of head (if >HE grade
Autoimmun hepatiti e,
ICP 2), if grade 4
e s Sm e
immunoglobulin live biops monitor HE

Vascular s,
Liver with rDopple
y aobtai every 8- hour earl on and daily
n 12 transaminas
s y ANAthereafter.
disorder ultrasound
20 cardiac with r EK
ALT, alanine antinuclea antibod AST aspartat
transaminas e;BUN bloo ,
urea r y; cytomegaloviru
CMV , e EB
lschemia echo Doppler G, e; , d nitrogen; , s; V,
, Epstein- virus; HAV, A HCV, C virus;
volume Barr hepatitis HSV, virus; hepatitisIN HE, hep
Pregnancy- Pregnancy platele count atic simplex
related status
test, t , encephalopathy;
malized LOH, herpes virus;
dehydrogenas Sm, R,
internationa -
muscle
LDH, test ratio; lactate e; smooth l .
nor
haptoglobin, Coombs
Malignanc History imaging live biops -
y , , r y
Manajemen
A. Umum
• Nutrisi: terjadi hipoglikemia akibat insulin yang meningkat, ggn
glukoneogenesis & hiperkatabolik state. Kalori enteral 20-25 kkal/
bb/hari, protein 1-1,5 gr/bb/hari.
• Atasi ensefalopati & udem cerebri. Ensefalopati hepatik tjd krn udem
cerebri dan peningkatan tekanan intrakranial—> manitol atau saline
hipertonik
• Infeksi insidennya 90 %, atasi dengan antibiotika broad spektrum.
Pertimbangan pemberian antibiotika: leukositosis, demam,
kesadaran makin menurun

B. Khusus
• ECLS
• Transplantas hati
 Acute on Chronic Liver Failure

• Difinisi:
Suatu dekompensasi hati akut pada pasien dengan CLD yang disertai
dengan gagal organ
• Definisi ACLF berbeda di berbagai negara (APASL, AASLD/EASLD,
NACSELD)
Table 2 of the existing ACLF definitions commonly accepted
Comparison
APASL EASL/CLIF NASCELD

Definitio Acute hepatic insult manifesting as jaundice and An acute of pre-existing chronic liver A syndrome characterized
n coagulopathy deterioration
disease usually related to a precipitating event by acute deterioration in a patient of cirrhosis due
Complicated within 4 weeks by ascites and/or and
associated with increased mortality at 3 months due to
encephalopathy in a patient with previously diag- to multisystem organ failure infection presenting with two or more extrahepatic
nosed or undiagnosed chronic liver disease organ failure.
associ-
Study cohort ated with high mortality. Prospectively studied in 1343 Prospectively studied in 507 patients
First consensus was the expert opinion, patients
subsequently
prospectively evaluated in 1402 patient, subse-
Inclusion Compensated Cirrhosis (diagnosed or non-diagnosed) Cirrhosis only Cirrhosis only
CLD but innot
quently 3300 patients.
cirrhosis Compensated or decompensated Compensated or decompensated
Acute insult directed to liver Renal failure is mandatory (not liver failure for defin- Two extrahepatic organ failure
Presentation with liver failure to start with ing ACLF) Presentation not necessarily be liver failure
Index presentation Presentation not necessarily be liver failure Can be repeated episodes of ACLF
Can be repeated episodes ACLF
Diagnosi Early, reversibility is and thus may affect Too late, is unlikely and thus may not Too late, reversibility is and thus may not
s likely reversibility unlikely
outcome affect outcome affect outcome
Exclusion Criteria Patients who had infections but did not require hospital
Prior decompensation HCC admission.
HCC Cirrhosis without infection.
Immune-compromised patients with human immunode-
ficiency virus (HIV) infection, prior organ transplant,
and disseminated malignancies
Homogeneity Yes. Index previously unknown or com- No. Any with prior decompensatio or No. Any presentation, with prior or
presentation,
pensated, hepatic insult leadin to liver failure presentation, ongoing n ac decompensation ac
acute g recent
insult isworsening of decompensation,
not directed to liver, in particular ( 40%ut recent worsening of ongoing ut
as the driver. are e decompensation, e
of unknown acute insult), not liver but extrahepatic insult is not directed to liver in particular
organ failure, i.e., renal failure is must, systemic Any extrahepatic organic failure
inflammation but not the liver as driver.
Time frame 4 weeks Not defined
Acute insult 4-12 weeks (variable)
Hepatic Infection, i.e., systemic
Sepsis Consequence/complication Hepatic or Systemic (extrahepatic) (extrahepatic)
Organ failure Liver is primary to start Cause/precipitant Cause/precipitant organic
with Systemic inflammation leading to kidney failure Systemic inflammation leading to
Others subsequently as extrahepatic
Disease severity score CLIF-C SOFA, Prospective but only expert opinion
AARC Score-prospective as well as validated the primary with or without other organ failure failure
MELD
Golden window Well defined for therapy, i.e., by 7 days SIRS or No such
sepsis CLIF-CSOFA
as well as for decision regarding Liver Transplant No such
Pediatric cohort None None
Yes
Therapy Regenerative and bridging therapy with good result No such No such
Reversibility of ACLF Yes Not described Not described
syndrome
APASL
• Definisi ACLF: acute hepatic insult berupa ikterus (bilirubin >= 5) dan
koagulopati (INR >= 1,5) yang kmd diikuti dgn komplikasi asites dan
atau ensefalopati dlm waktu 4 mgg, pada orng yg diketahui atau tidak
menderita peny hati kronis atau sirosis kompensata

• Insult : bisa alkohol, reaktifasi hep B, infeksi virus hepatotropik, DILI,

autoimun

• Dibedakan dengan acute decompensation, yi: suatu perburukan akut

(asites, HE, ikterus, perdarahan varises, AKI atau sepsis) pada pasien
sirosis dlm waktu 3 bln. Faktor pencetusnya 48 % hepatik dan 46 %
non-hepatik
35 Hepatolog Internationa (2019 13:353-
6 y l ) 390

Fig. 1 Concept of ACLF and

the cohorts included in different I Normal liver
Chronic Liver
Disease
definitions. The figure describes
the response of the liver to an I
acute hepatic injury, depend-
ing on the underlying hepatic
injury, prior decompensation,
time frame from ins ult to pres-
entation with decompensation
and reversibility with mitigation
of the acute insult. The spec-
Acute 'Liver F Failure' First/repeated Further
trum extends from acute liver Liver Acute-on-chronic
Acute liver Decompensation worsening of
failure, acute-on-chronic liver
Failur -on-cfailure as GI decompensate
failure, acute decompensation, e
JAUNDICE~fa ASCITE bleed, HE, ascites, d
end-stage liver disease. ACLF HRS,
S cirrhosis/
is distinct like ALF when the
sepsis or sepsis/bleed/ AKI
APASL definition is considered. combinations
APASL definition is simple and Homogenous •
m any sequence
homogenous and is distinct
Heterogenous CLI
F
Table 3 Differentiating ACLF from acute
decompensation
Parameter( s) Acute-on-chronic liver failure (ACLF) Acute decompensation (AD)

Presentation Hepatic insult Hepatic or non-hepatic

Index Can be index or subsequent
Identifiable precipitant In up-to 95 cases In up to 70% cases
Time from insult to presentation % Up to 12 weeks
Within 4 weeks
Underlying cirrhosis May or may not be present Always present
Prior decompensation No With or without Prior Decompensation
Mortality at 1 and 3 33-51 % 23-29%
Reversal months In half of cases Uncommon
or recovery
Faktor predisposisi ACLF:
• Genetik
• Umur : berisiko pada usia lebih muda —> respon imun lebih kuat
• Gaya hidup : alkohol, obese, pemakaian PPI
• Beratnya portal hipertensi dan asites —> berbanding lurus dgn
permeabilitas usus —> translokasi bakter
i
Faktor pencetus : 20-40 % ACLF tjd tanpa faktor pencetus yg jelas —>
diduga krn perburukan inflamasinya
Table 18.2 Precipitan of acute-on- live failure in patient with from different part of the world
ts chronic r s s .
CANONIC study [9] Shi et al. [19] Shalimar et al. [59]

Patients 303 405 1049

enrolled
Region/ of Eur Chi Indi
country origin ope na a
Precipitant:
Hepatit exacerbation 145 (35.8°/ 224 (21.4°/
is " 98 (32.6°/ 113 o) 174 o)
Bacteri infection
Activ alcoholis ( < mo) 69 o) 25 (27.9°/
(6. °/ 374 (16.6°/
al o)
e m 3
Gastrointestin hemorrha 40 (24. 5 40 1 o)
(9.8°/ 88 o)
°/o)
al ge 2 9 o) 85 (35.7°/
(8. o/
Others 5 (1 3.2 80 (2°/o) 10 1
o) o)
(9.9o/
Unidentifiable
°/o)
More than 1 precipitan 12 (20.4°/o)
36 (8.9°/ 4 o)
(8.4o/o)
6 (8.6°/o)
t o)
39 (43.6°/
a exacerbatio include either B or
o) acut hepatiti E Th categor of "Others include surger
Hepatitis n acut alcoholi
TIPS s hepatitisdrug- flare liver
hepatitis e injury,
s and autoimmun
. e y " exacerbation
hepatitis s y,
(13.5°/
insertion,
TIPS, e intrahepati
c ,portosystemi
induced
shunt o) e .
transjugular c c .
Manajemen

A. Faktor predisposisi
B. Faktor pencetus
C. Faktor inflamasinya
D. Terapi spesifik thd organ failure

————————-