CASE PRESENTATION

Tuesday, February 11th 2014

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Mrs. T , 45 Y.O.

MC : Abdominal enlargement

H I : 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 cirrhosis since 1 year ago.

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Physical examinations

Weak, BP : 110/70 mmHg, HR: 88 x/min , RR : 20 x/min , t: 36.9°C

Head / Neck : A+/J-/C-/D-

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

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Hematology Results

CBC 2/2/14 5/2/14 7/2/14

WBC (103/µL) 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/µL) 2.64 4.26 4.31

Hb (g/dL) 6.5 9.24 9.58

Hct (%) 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

Plt (103/µL) 85 54.49 56.9 5

Clinical Chemistry Result2/2/14 05/2/14

RBG (mg/dL) 70 72

AST (IU/L) 27 27

ALT (IU/L) 39 22

Albumin (g/dL) 3.6 4.1

Creatinin (mg/dL) 0.7 0.8

BUN (mg/dL) 7 10

Na (mmol/L) 143 134

Cl (mmol/L) 113 104

Ca (mg/dL) 9.2

K (mmol/L) 4.2 4.1

T.Prot (g/dL) 5.7

TIBC (µg/dL) 372

SI (µg/dL) 14

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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

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Imunology Result

2/2/2014

HBsAg stick negative

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Coagulation Study

2/2/2014

PPT 14.0 (control : 12.8)

APTT 26.8 (control 26.5)

Urinalysis

Color : yellow Clarity : clearGlu : negBil : -Keton : -SG : 1.013Bld : -pH : 7.0Prot : -Uro :-Nitrit :-Leu: -

Sedimen :

Ery : 0-2

Leu : 0 - 2

Epith : few

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Chest X ray : nad

Endoscopy : Varices esophagus grade II-III

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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 (-)

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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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Clinical Sign of Cirrhosis1. Liver failure

• edema• icterus• coma• spyder nevi• gynecomasti• ascites• erythema palmaris• atrophy testis• anemia,hematom/

bleeding easily

2. Hipertensi portal• varices oesophagus• splenomegali• caput meduse• asites• collateral -vein• anemia, leukopeni dan

trombocytopenia

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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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SAAG Serum ascites albumin gradientUntuk menentukan cairan transudat atau

eksudat>1.1 = high gradient

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Klasifikasi derajat keparahan SHKlasifikasi Parameter

(Pugh)

A1

B2

C3

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

Nutrisi

< 2.0>3.5

--

Baik

2.0 – 3.03.0 – 3.5Terkontrol

Stadium I/IISedang

> 3.0< 3.0

Tidak terkontrolStadium III/IV

Jelek

Total Skor 5 - 7 8 - 10 11 - 15

Klasifikasi Child A : Sirosis hati ringanKlasifikasi Child B : Sirosis hati sedangKlasifikasi Child C : Sirosis hati berat

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ASCITESCirrhosis

Portal hypertension

Splanchnic vasodilatation

Splanchnic pressure Arterial underfilling

Formation of ascitesActivation of

vasoconstrictors and antinatriuretic factors

Plasma volume expansionSodium retention

Lymph formation

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Hepatic Encephalopathy

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Complications of Cirrhosis

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

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

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Patogenesis sindrom hepatorenal

Hepatitis B akut

Gambar 7. Karakteristik hepatitis B akut dengan kesembuhan

April 19, 2023 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

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Hepatocyte with cell organelles(schematic representation)and localization of thediagnostically most importantenzymes etc

1. Stellate Kupffer cell2. Space of Disse3. Granular endopl. retic:ChE4. Smooth endopl. retic5. Mitochondrion: GlDH,ASAT6. Bile canaliculi:ALP,LAP,G-GT7. Nucleus8. Lysosomes :hydrolases9. Cytoplasm:LDH,ALAT,ASAT Iron

LOKASI ENZIM DALAM HEPATOSIT

ChEAST

ALP

GGT

AST,ALT,LDH

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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

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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.

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.

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Tes untuk diagnosis penyakit hati

Gangguan fungsi hati :

Uptake : bilirubin

Konjugasi : bilirubin

Ekskresi : bilirubin

Sintesis : albumin, kolin esterase, faktor pembekuan

Integritas sel : SGOT, SGPT, LDHKolestasis : alkali fosfatase, gamma

glutamiltranspeptidase (GGT), 5 NukleotidaseEtiologi : petanda hepatitis virus, Alfa fetoprotein,

CEA 41

PEMERIKSAAN LABORATORIKGambaran 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.

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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

20%

Sirkulasi enterohepatik urobilin(ogen)

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0% ke feces

Stercobilin(ogen)

urobilinogen

Destruksi eritrosit (RES 80-85%,SuTul 15-20%)

Hb Globin Protein Pool Fe Heme myoglobin,sitokrom oksidase,katalase

Biliverdin

Bilirubin bebas albumin (unconjugated bilirubin)

protein y,z UDP glukuronyltransferase as.glukuronat 2-5% conjugated bilirubin

Esophageal Varices

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Gastroscopy image of esophageal varices with

prominent cherry-red spots

Esophageal varices (or oesophageal varices) are extremely dilated sub-mucosal 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.

• 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). Treatment of these types of varices may differ.

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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

• SplenomegalyThe 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 "backs-up," accumulating in the spleen, and the spleen swells in size, a condition referred to as splenomegaly.

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• 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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