CASE PRESENTATION

Tuesday, February 11th 2014

Mrs. T , 45 Y.O.
MC :

Abdominal enlargement

HI

: She has been suffering from

abdominal
enlargement since 3 months
ago, accompanied by pain of the
abdomen, nausea, and loss of
appetite.Micturation and bowel habit were
normal.

HPI

DM (-), HT (-)

She has been suffering from liver

2
cirrhosis since 1 year ago.

Physical examinations
Weak, BP : 110/70 mmHg,
RR : 20 x/min ,
Head / Neck : A+/J-/C-/D-

HR: 88 x/min ,
t: 36.9C

Chest: Heart: S1S2 single, murmur/gallop(-)

Lung : ves/ves, Rh -/-, Wh -/Abd
: enlarge, ascites +
Liver : not palpable
Spleen: S II
Ext: warm, oedema - + +
3

LABORATORY RESULT

Hematology Results
CBC

2/2/14

5/2/14

7/2/14

WBC (103/L)

2.57

2.11

2.07

% Neu (%)

66.1

61.71

58.2

% Lym (%)

22.2

17.97

22.5

% Mo

(%)

8.6

13.09

9.94

% Eos

(%)

3.1

3.58

4.08

%Baso (%)

0.1

3.63

1.96

RBC (106/L)

2.64

4.26

4.31

6.5

9.24

9.58

18.0

30.47

31.2

MCV (fl)

68.2

71.50

72.3

MCH (pg)

17.0

21.69

22.2

MCHC (g/dL)

25.0

30.33

30.7

RDW (%)

20.4

21.22

20.9

85

54.49

56.9

Hb

(g/dL)

Hct

(%)

Plt

(103/L)

Clinical Chemistry Result

2/2/14

05/2/14

RBG (mg/dL)
AST (IU/L)
ALT (IU/L)
Albumin (g/dL)
Creatinin (mg/dL)
BUN (mg/dL)
Na (mmol/L)
Cl (mmol/L)
Ca (mg/dL)

70
27
39
3.6
0.7
7
143
113

72
27
22
4.1
0.8
10
134
104

K (mmol/L)
T.Prot (g/dL)

4.2

TIBC (g/dL)

372

SI (g/dL)

14

9.2
4.1

5.7

T.Cholesterol (mg/dL)

205

Trigliserid (mg/dL)

116

HDL (mg/dL)

55

LDL (mg/dL)

118

D.Bilirubin (mg/dl)

0.2

T.Bilirubin (mg/dl)

0.7

Imunology Result
2/2/2014
HBsAg stick

negative

Coagulatio
n Study

2/2/2014

PPT

14.0 (control : 12.8)

APTT

26.8 (control 26.5)

Urinalysis
Sedimen :
Color : yellow
Clarity : clear
Glu : neg
Bil : Keton : SG : 1.013
Bld : pH : 7.0
Prot : Uro :Nitrit :Leu: -

Ery : 0-2
Leu : 0 - 2
Epith : few

10

Chest X ray : nad

Endoscopy : Varices esophagus grade II-III

11

BSE :
E : Hypochromic,anisopoikilocytosis
(normocytes,macrocytes,microcytes, ovalocytes,
helmet cell), polychromatophilic cell -, normoblast L : seems to be decrease in number,
dominated by segmented neutrophils,
no immature cells.
T : seems to be decrease in number,
giant platelet (-)
12

DX/: Liver Cirrhosis + Ascites

Treatment :
Diet H1 1900 kcal/day
Furosemid 2x1 amp iv
Cefotaxime inj 3 x 1 g iv
Omeprazole tab 2 x 1
PRC transfusion 2 bag/day,until Hb 10 g/dL
Propanolol 3 x 20 mg

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THANK YOU

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15

Clinical Sign of Cirrhosis

1. Liver failure
2.
edema
icterus
coma
spyder nevi
gynecomasti
ascites
erythema palmaris
atrophy testis
anemia,hematom/
bleeding easily

Hipertensi portal
varices
oesophagus
splenomegali
caput meduse
asites
collateral -vein
anemia, leukopeni
dan
trombocytopenia
17

DIAGNOSA
Pembesaran limpa biasanya bisa dirasakan/diraba melalui
dinding perut.
Cairan di perut bisa diketahui dari adanya pembengkakan
perut dan pemeriksaan perkusi perut memberikan hasil
suara yang tumpul.
USG dilakukan untuk memeriksa aliran darah di dalam
pembuluh darah portal dan bisa menunjukkan adanya
pengumpulan carian di perut.
CT scan juga bisa digunakan untuk memeriksa pelebaran
pembuluh vena.
Tekanan dalam sistem portal bisa diukur secara langsung
dengan memasukkan jarum melalui dinding perut ke
dalam hati atau limpa.
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19

SAAG
Serum ascites albumin gradient
Untuk menentukan cairan transudat atau
eksudat
>1.1 = high gradient

22

Klasifikasi derajat keparahan SH

Klasifikasi
Parameter
(Pugh)

A
1

B
2

C
3

Bilirubin (mg/dL)
Albumin (g/dL)
Ascites (g/dL)
Encefalopati
Nutrisi

< 2.0
>3.5
Baik

2.0 3.0
3.0 3.5
Terkontrol
Stadium I/II
Sedang

> 3.0
< 3.0
Tidak terkontrol
Stadium III/IV
Jelek

Total Skor

5-7

8 - 10

11 - 15

Klasifikasi Child A : Sirosis hati ringan

Klasifikasi Child B : Sirosis hati sedang
Klasifikasi Child C : Sirosis hati berat
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25

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ASCITES
Cirrhosis
Portal
hypertension
Splanchnic
vasodilatation
Splanchnic
pressure

Lymph
formation
Formation of
ascites
Plasma volume
expansion

Arterial
underfilling
Activation of
vasoconstrictors
and antinatriuretic
factors
Sodium
retention
27

Hepatic Encephalopathy

29

30

Complications of
Cirrhosis

Portal Hypertension
Variceal Bleeding
Ascites
Spontaneus Bacterial Peritonitis (SBP)
Hepatorenal Syndrom
Hepatic Encephalophaty

31

Patogenesis sindrom hepatorenal

Sirosis Hati derajat berat

Hipertensi portal

Vasodilatasi arterial splanknik

hipovolemi arteri sentral

Aktivasi simpatis renin/Angiotensin/

Aldosteron hormon anti diuretik

Vasokonstriksi renal

Intra Renal Vasokonstriksi meningkat

Vasodilator menurun

Vasokonstriksi renal lebih meningkat

Sindrom Hepatorenal

32

Hepatitis B akut

Gambar 7. Karakteristik hepatitis B akut dengan kesembuhan

2/16/15

dr.Siswanto D Sp.PK(K)

34

SEROLOGI HBV

Hepatitis kronik
aminotransferase > 6 bulan
Hepatitis C akut 80% menjadi
kronik
( B: 1-2% ) Cirrhosis (C:30%,B:40%,
C&B %>, atau dgn HIV %>)
Px Cirrhosis: 3-5%/ tahun HCC
Tanpa cirrhosis, virus B dgn replikasi
virus aktif HCC
36

LOKASI ENZIM DALAM HEPATOSIT

Hepatocyte with cell organelles
(schematic representation)
and localization of the
diagnostically most important
enzymes etc

AST,ALT,LDH

ALP
GGT

1. Stellate Kupffer cell

2. Space of Disse
3. Granular endopl. retic:ChE
4. Smooth endopl. retic
5. Mitochondrion: GlDH,ASAT
6. Bile canaliculi:ALP,LAP,G-GT
7. Nucleus
8. Lysosomes :hydrolases
9. Cytoplasm:LDH,ALAT,ASAT Iron

AST
ChE

37

37

AST dan ALT

Dalam sitoplasma hepatosit:
- AST 1,5 2 x ALT
Waktu paruh : - AST ~ 18 jam
- ALT ~ 48 jam
awal hepatitis akut AST > ALT
> 48 jam kmd ALT > AST

38

38

Kerusakan sel hati ringan terutama

ALT meningkat.
Kerusakan sel hati berat/nekrosis
terutama AST meningkat.

Aminotransferase :
enzim yang mengkatalisis perpindahan
reversibel satu gugusan amino dari
asam amino ke asam alfa-keto.

39

39

KERUSAKAN SEL HATI

HEPATITIS VIRUS TRANSAMINASE
NEKROSIS OLEH KARENA TOKSIN
TRANSAMINASE
CHOLESTASIS, SIROSIS TRANSAMINASE
YANG BANYAK DIPAKAI :

SGOT ( Serum Glutamic Oxalocetic Transaminase ) =

AST ( Aspartate Transaminase )

JANTUNG, HATI, OTOT-OTOT SKELET,
GINJAL, PANKREAS.
SGPT ( Serum Glutamic Pyruvic Transaminase) =
ALT ( Alanine Transaminase )
HATI, JANTUNG, GINJAL, OTOT SKELET.
22

Tes untuk diagnosis penyakit hati

Gangguan fungsi hati :
Uptake : bilirubin
Konjugasi : bilirubin
Ekskresi : bilirubin
Sintesis : albumin, kolin esterase, faktor pembekuan
Integritas sel : SGOT, SGPT, LDH
Kolestasis : alkali fosfatase, gamma
glutamiltranspeptidase (GGT), 5 Nukleotidase
Etiologi : petanda hepatitis virus, Alfa fetoprotein,
CEA
41

PEMERIKSAAN LABORATORIK
Gambaran lab sirosis hepatis :
AST dan ALT
tak begitu tinggi.
AST lebih daripada ALT, bila transaminase normal
tidak mengenyampingkan adanya sirosis.
GGT pada penyakit hati alkoholik kronik --> alkohol
menginduksi GGT mikrosomal hepatik dan
menyebabkan bocornya GGT dari hepatosit.
Bilirubin bisa normal pada sirosis hati kompensata,
tapi bisa meningkat pada sirosis yang lanjut.
Albumin sesuai dengan perburukan sirosis.
42

PEMERIKSAAN LABORATORIK
Globulin
--> sekunder dari by pass ke liver: antigen
bakteri dari sistem porta ke jaringan limfoid-->
menginduksi produksi imunoglobulin.
Waktu protrombin --> memanjang
Natrium serum
dengan asites--> ketidakmampuan
ekskresi air bebas
Kelainan hematologi: anemia penyebabnya bisa
bermacam-macam, anemia monokrom, normositer,
hipokrom mikrositer atau hipokrom makrositer.
Anemia + trombositopenia, lekopenia, dan netropenia
--> splenomegali kongestif ok hipertensi porta
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METABOLISME BILIRUBIN
Destruksi eritrosit (RES 80-85%,SuTul

15-20%)

Hb

Pool

Fe

oksidase,katalase

Heme

Globin

Protein

myoglobin,sitokrom

Biliverdin
Bilirubin bebas

albumin
(unconjugated bilirubin)
protein y,z
UDP glukuronyltransferase

2-5%

as.glukuronat

s
fece
e
k
80%
conjugated

n)
e
g
o
ilin(
b
o
c
ter
n

bilirubin
20%

Sirkulasi enterohepatik

44

44

urobilin(ogen)

Esophageal Varices
Esophageal varices (or oesophageal varices) are extremely dilated submucosal veins in the lower third [1] of the esophagus. They are most often a
consequence of portal hypertension, commonly due to cirrhosis; patients with
esophageal varices have a strong tendency to develop bleeding

They result from the higher than normal

pressure in the system of veins that arise
from the region of the liver, and which are
known to be affected by liver disease.
They are particularly seen in conditions
that scar the liver, such as cirrhosis.

Gastroscopy image of
esophageal varices
with prominent
cherry-red spots
45

Normal portal pressure is approximately 9 mmHg

compared to an inferior vena cava pressure of 2-6
mmHg. This creates a normal pressure gradient of 3-7
mmHg. If the portal pressure rises above 12 mmHg,
this gradient rises to 7-10 mmHg.[3] A gradient greater
than 5 mmHg is considered portal hypertension. At
gradients greater than 10 mmHg, blood flow though
the hepatic portal system is redirected from the liver
into areas with lower venous pressures. This means
that collateral circulation develops in the lower
esophagus, abdominal wall, stomach, and rectum.
The small blood vessels in these areas become
distended, becoming more thin-walled, and appear as
varicosities.

Varices can also form in other areas of the body,

including the stomach (gastric varices), duodenum (
duodenal varices), and rectum (rectal varices).
46
Treatment of these types of varices may differ.

Esophageal varices
In the cirrhotic liver, the scar tissue
blocks the flow of blood returning to the
heart from the intestines and raises the
pressure in the portal vein (portal
hypertension).
As a result of the increased flow of blood
and the resulting increase in pressure,
the veins in the lower esophagus and
upper stomach expand and then are
referred to as esophageal and gastric
varices.
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Jenis
pemeriksaan

Transudat

Eksudat

Kadar protein
serum

< 0,5 g/dL

> 0,5 g/dL

lekosit

< 1000/mm3

> 1000/mm3

Rivalta

Negatif

Positif

58

 Splenomegaly
The spleen normally acts as a filter to
remove older red blood cells, white blood
cells, and platelets.The blood that drains
from the spleen joins the blood in the
portal vein from the intestines. As the
pressure in the portal vein rises in
cirrhosis, it increasingly blocks the flow of
blood from the spleen. The blood "backsup," accumulating in the spleen, and the
spleen swells in size, a condition referred
to as splenomegaly.
59

 As the spleen enlarges, it filters out

more and more of the blood cells and
platelets until their numbers in the
blood are reduced. Hypersplenism is
the term used to describe this
condition, and it is associated with a
low red blood cell count (anemia),
low white blood cell count
(leucopenia), and/or a low platelet
count (thrombocytopenia).

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