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 •
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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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