liver cirrhosis - USU OCW [PDF]

Cardiac failure. • Autoimmune chronic active hepatitis. • Drug and toxins. DIAGNOSIS. 1.SPIDER NAEVI. 2.ERITHEMA PAL

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Idea Transcript


LIVER CIRRHOSIS

leonardo dairi Departemen Penyakit Dalam

DEFINITION ANATOMICALLY AS A DIFFUSE PROCESS WITH FIBROSIS AND NODULE FORMATION

CLASSIFICATION: MICRONODULAR CIRRHOSIS MACRONODULAER CIRRHOSIS MIXED

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Causes of Cirrhosis • • •





• •

Viral hepatitis; B, D, and C Alcohol Metabolic Haemochromatosis Wilson’s disease Alpha-1-antitrypsin deficiency Chronic biliary obstruction Extrahepatic biliary obstruction Intrahepatic biliary obstruction Venous outflow obstruction Veno-occlusive disease Budd-Chiari syndrome Cardiac failure Autoimmune chronic active hepatitis Drug and toxins

DIAGNOSIS. 1.SPIDER NAEVI 2.ERITHEMA PALMARIS 3.COLLATERAL VEIN 4.ASITES 5.SPLENOMEGALI 6.INVERTED ALBUMIN GLOBULIN 7.HEMATEMESIS/MELENA

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CLINICAL CIRRHOSIS IN CLINICAL TERM,COMPENSATED AND DECOMPENSATED CLINICAL APPERANCE RESULT,  HEPATOCELLULER FAILURE  PORTAL HYPERTENSION CHRONIC ACTIVE HEPATITIS and EARLY CIRRHOSIS  NON SPECIFIC, DECOMPENSATED CIRRHOSIS

INVESTIGATION: 1. HAEMATOLOGY - HAEMOGLOBIN,LEUCOCYTE, PLATELET COUNT and PROTHROMBIN TIME. 2. BIOCHEMICAL BILLIRUBIN,TRANSAMINASE (ALT/AST),ALKALINI PHOSPATASE,ALBUMIN GLOBULIN,IMMUNOGLOBULINT, GAMMA GT,

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- ASCITES PRESENT, SERUM SODIUM,POTASSIUM, BICARBONATE,CHLORIDE,UREA AND CREATININE LEVEL,WEIHLY DAILY AND 24 HOUR URINE VOLUME

3.USG,HEPATIC CT SCAN 4.LEVER BIOPSY GOLD STANDART 5.ENDOSCOPY 6.EEG IF

EXMINATION: NURITION,FEVER,FETOR HEPATICUS,JAUNDICE,PIGMENTATION,PURPURA, FINGER CLUBBING,WHITE NAILS,SPIDER NAEVI,PALMAR ERYTHEMA,GYNECOMASTIA,TESTICULAR ATROPHY,DISTRIBUTION OF BODY HAIR,PAROTID ENLARGMENT,DUPUYTREN CONTRACTURE,BLOOD PRESSURE ABDOMEN  ASCITES, COLLATERAL VEIN, LIVER, SPLEEN PERIPHERAL OEDEMA NEUROLOGICAL CHANGES  MENTAL FUNCTIONS, STUPOR, TREMOR.

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MODIFIED CHILD-PUGH CLASSIFICATION OF THE SEVERITY LIVER DISEASE CHILD

A

B

C

BILIRUBIN

< 2 gr %

2,0 - 3,0 gr %

> 3,5 gr %.

KADAR ALBUMIN

> 3,5 gr %

2,8 - 3,5 gr %

< 2,8 gr %.

ASCITES

-

SLIGHT

MODERATE

ENSEFALOPATI

-

GRADE 1/2

GRADE 3/4

4-6

>6

PROTHROMBINE

1–3

TOTAL SCORE ,! – 6 (grade A), 7 – 9(grade B), 10 – 15(grade C)

PORTAL HYPERTENSI Continuing Liver damage

Nodular regeneration

Fibrosis Increased sinusoidal pressure Portal Hypertension

Splancnic vasodilatation

Increased gastroesophageal collateral

Decreased effective blood volume

Formation of oesophagogastric varices

Increased sodium retention

Variceal rupture

Ascites

Variceal bleeding

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MANAGEMENT

TERGANTUNG STADIUMNYA.

1. STD. KOMPENSASI - KONTROL TERATUR, ISTIRAHAT CUKUP, DIET TINGGI KALORI / PROTEIN, LEMAK SECUKUPNYA, DIIT HATI III/IV - HINDARI FAKTOR PENYEBAB ( ALKOHOL, OBAT ). - LIVER PROTEKTIF.

2. STAD. DEKOMPENSATA: - ISTIRAHAT TOTAL. - BATASI MASUKKAN CAIRAN < 1000 cc / HARI. - DIURETIK HEMAT KALIUM / SPIRONOLAKTON. BILA GAGAL  + FUROSEMID. - DIET RENDAH GARAM : 0,5 gr / HR. - BILA TERJADI ENSEFALOPATI  PROTEIN . - BERI LIVER PROTEKTIF. - HINDARKAN PENYEBAB PENCETUS ENSEFALOPATI.

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PROGNOSA : PROGNOSA JELEK, 1. ASITES REFRAKTER. 2. BILIRUBIN MENETAP > 1,5 - 2 gr %. 3. KADAR ALBUMIN < 2,5 gr %. 4. HATI MENGECIL. 5. MASA PROTROMBIN RENDAH. 6. KADAR NATRIUM DARAH RENDAH. 7. TERJADI PSCA. 8. GANGGUAN KESADARAN.

MORTALITAS PENDERITA S.H. BERDASARKAN KRITERIA CHILD PADA OPERASI:

A : 10 – 15 %. B : 30 %. C : DIATAS 60 %.

PENYEBAB KEMATIAN : - 43 %  DARI LUAR HATI. - 57 %  DARI HATI.

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Causes of death • • • • • • •

Variceal hemorrhage Spontaneous bacterial peritonitis Sepsis Liver failure Hepatic coma Functional renal failure Hepatocelluler carcinoma

Complications of Cirrhosis • • • • • •

Variceal bleeding Ascites, refractory ascites Hepatorenal syndrome(HRS),HPS Hepatic encephalopathy Spontaneous bacterial peritonitis Hepatocelluler carcinoma

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Variceal Bleeding

A. Bleeding from – varises is reported in about 20 – 60 % of case with cirrhosis. cirrhosis. B. Mortality of the first bleeding episode is around 50 % Prevention measure Prevention measuress rational to avoid development of Varices bleeding (Primary proph prophyla ylax xis). C. Up to 70 % Of Patient who do not receive treatment die within 1 year of the initial bleeding episode

The Efforts in preventing bleeding seems to be crucial (secondary, prophylaxis)

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Consensus in Portal Hypertension Baveno III Monitoring for the Development of Varices in the Portal Hypertensive Patient. 1. All cirrhotic patients should be screened for the presence of varices at the time of the initial diagnosis of cirrhosis. 2. In compensated patients without varices, endoscopy should be repeated at 2-3 year intervals to evaluate the development of varices. 3. In compensated patients with small varices, endoscopy should be repeated at –2 year intervals to evaluate progression of varices. 4. There is no indication for subsequent evaluations once large varices are detected.

Algorithm for cirrhosis Without Bleeding

Algorithm For Cirrhosis Without Bleeding Cirrhosis Established Upper Endoscopy

No varices

Observe

(2 – 3 years Evaluation)

Small or Medium Varices

Observe (1 – 2 years Evaluation)

Large Varices

Primary Bleeding Prophylaxis Reguler Interval Usually one week

Non Selectne Blockers (and /or long actmy Nitrates)  Ligation 

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Algorithm For Bleeding Cirrhotis

Algorithm For Bleeding Cirrhotis  Resuscitae

 Begin Octreotide (or Vasopressin) Early endoscopy Esophagel Non-Portal Gastric Varices Portal Hypertensive Cause Varices Hypertensive Gastropathy

Continue octreotide 5 days

Treat appropriately

Begin beta-blocker when stable

Band ligation or injection Sclerotheraphy Ballon Tamponade Rebleeding

No rebleeding

Continue treatment Shunt (Child A) Preventation of Rebleeding TiPSS. or • Pharmacological Treatment Liver transplantation (Child B or C) • Ligation /Sclerotheraphy Reguler Interval Usually one week Eradication Repeated Endoscopy 3 – 6 month Rebleeding Shunt (Child A) TIPSS or Liver transplantation (Child B or C)

Dosis dan cara pemberian obat-obat vasoaktif pada perdarahan varises Obat

Cara pemberian Dosis

Lama pemberian

Vasopressin (VP) + Nitroglyserin (NG)

VP: i.v infus NG: percutaneus, bolus

VP: 0,4UU/menit

48 jam

Terlipressin

i.v, bolus

Somatostatin

i.v bolus dan infus

2 mg/4 jam 2-5 hari selama 24-48 jam pertama, kemudian 1 mg/ 4 jam 250 ug diikuti 2-5 hari 250-500 ug/jam

Octreotide

i.v, bolus dan infus

50 ug diikuti 50 ug/jam

2-5 hari

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ASCITES

Pathophysiology of Ascites Portal Hypertension

Splanchnic arteriolar vasodilatation "Forward" increase of splancnic capillary pressure and permeability

Arterial vascular underfilling and activation of sodium retaining mechanism

Lymph formation > lymph return

Sodium and water retention

Ascites

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Management of cirrhotic patients with moderate uncomplicated ascites • Start with a low sodium diet (80 mmol /day) and anti aldosteronic drug (100-200 mg/day) ⌫ monitoring body weight • Low doses of furosemide (20-40 mg/day, in case of poor response to the anti aldosteronic drug. • The goal of treatment : weight loss of 500 g /day in patients without peripheral edema, and 1 kg/day in patients with peripheral edema. • Maximum dose of anti aldosteronic drug 400 mg/day, and 160 mg of furosemide. • Sodium restriction.

Management of cirrhotic patients with tense or large uncomplicated ascites • Total paracentesis is the most effective and safest procedures to mobilize large ascites • Blood volume with intravenous albumin (8 g/L of ascite removed) is required if the volume of ascites is more than 5 liter. • Start with a low sodium diet and diuretics soon after paracentesis

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Management of refractory ascites • Paracentesis • Peritovenous shunt • Transjugular intrahepatic porto-systemic stent-shunt (TIPSS) • Liver Transplantation

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Hepatic Encephalophathy

Common Precipitant of Hepatic encephalopathy •



• •

Increased Nitrogen Load Gastrointestinal bleeding Excess dietary protein Azotemia Constipation Electrolyte and Metabolic Imbalance Hypokalemia Alkalosis Hypoxia Hyponatremia Drugs Narcotics, transquilizers, sedatives, Diuretics. Miscellaneous Infection, Surgery, Superimposed liver disease

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Clinical Stages of Hepatic Encephalopathy Stage

Mental status

Asterixis

EEG

I

Euphoria or depression, mild confusion, slured speech, disordered speech Lethargy, moderate confusion

+/-

Normal

+

Abnormal

Marked confusion, + incoherent speech, sleeping but arousable Coma, initially responsive to noxious stimuli, later unresponsive

Abnormal

II III

IV

Abnormal

Approach to the patient with hepatic encephalopahty Initial Evaluation * Exclude other causes of disordered mentation * Identify precipitant and correct * Determinant electrolytes, BUN, creatinine, NH3, Glucose Protein restriction Laxative, e.g., Lactulose 30-120 ml, 1 to 4 times daily until 4 stools/day Inadequate response?

Broad-spectrum antibiotics (e.g., neomycin 500 mg qid, or metronidazole 250 mg tid)

Inadequate response?

Consider liver transplatation

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Spontaneus Bacterialis Peritonitis

Cirrhotic patients at high risk of SBP • Cirrhotic patients with gastrointestinal hemorrhage • Cirrhotic patients with low ascitic fluid total protein (< 1 g/dL) and / or high serum bilirubin (>2.5 mg/dl) • Survivors of an episode of SBP. • Hospitalized cirrhotic patients with ascites and low ascitic fluid total protein (< 1 g/dl)

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Diagnosis Peritonitis Bakterialis Spontan Pasien sirosis hati dengan asites

Pungsi asites

Gejala menyertai: Syok, perdarahan, gangguan kesadaran, gangguan motilitas, hipotensi, dll Asimtomatik.

Nyeri perut panas

Pungsi asites: periksa: PMN Kultur

Sel PMN > 250

Sel PMN < 250 Ulangi pungsi 24 jam

Kultur + Monomikrobial Kultur + Monomikrobial PBS

BMNN (Bakterasites Monomikrobial Non-Neutrosistik)

Penatalaksanaan Peritonitis Bakterialis Spontan PBS simtomatik

Profilaksis PBS

Antibiotik pilihan : Sefotaksim 1-2 gram/hari selama 5-7 hari Amoksisilin+Asam klavulanat selama 5-7 hari

Ofloksasin Siprofloksasin Dosis standar 5-7 hari

Parasentesis ulang setelah 24 jam antibiotik

Sel PMN

Sel PMN

Antibiotik diteruskan

Ganti antibiotik

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HEPATORENAL SYNDROME

Pathogenesis of Hepatorenal Syndrome Cirrhosis Sinusoidal portal hypertension

Splanchnic vasodilatation

Arterial underfilling

Reduced renal vasodilator factors

Baroreceptor-mediated activation of systemic Vasoconstriction factors

Increased intrarenal vasoconstriction factors

Renal vasoconstriction

Hepatorenal syndrome

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HEPATOCELLULAR CARCINOMA

• Treatment of HCC depends on 1. Local resources 2. Stage of the disease 3. Presence of cirrhosis

• Liver Transplantation • Hepatic resection  treatment of choice for the few patients with HCC and normal liver. • Trans Arterial Chemo Embolization • Cytostatica • Interferon

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Five years survival of pts with HCC treated by transplantation in 82 Europeans centers between 1988 and june 1994 •

Indication to transplantation

Patients

% Alive

HCC with Cirrhosis HCC without cirrhosis Cirrhosis with HCC

361 446 176

46 34 54

p = 0.0004 from European Transplantation Register

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