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  • *LIVER CIRRHOSISLeonardo dairyDivisi Gastroentero-HepatologiDepartemen Ilmu Penyakit DalamFK-USU/ RSUP H. Adam Malik Medan

  • LIVER CIRRHOSISchronic progressive liver disease leading to necroinflammatory reactionfibrosisloss of the lobular and vascular architecture of liver lobule regenerating nodulesLIVER CIRRHOSIS, is common end results from chronic injury to liver cells with variety causes INTRODUCTION

  • The prevalence of liver cirrhosis is 3.6 per 1000 individuals in North America. Liver Cirrhosis is the 12th leading cause of death in the United States, It accounted for 29,165 deaths in 2007, with a mortality rate of 9.7 per 100,000 persons. Alcohol abuse and viral hepatitis are the most common causes of cirrhosis, although NAFLD is emerging as an increasingly important cause. Portal hypertension develops as a consequence of cirrhosis,is present in 60% at the time of diagnosisMorphology Classification Micronodular cirrhosis, Macronoduler cirrhosis and Mixed cirrhosis

    INTRODUCTION

  • DEFINITION

    Cirrhosis is derived from Greek kirros = orange or tawny and osis=conditioDefinition: a diffuse process characterized by liver necrosis, fibrosis and conversion of normal liver architechture into structurally abnormal nodules

    Healthy LFibrosisCirrhosis

  • CAUSES OF CIRRHOSISViral hepatitis; B, D, and CAlcoholMetabolic Haemochromatosis Wilsons disease Alpha-1-antitrypsin deficiencyChronic biliary obstruction Extrahepatic biliary obstruction Intrahepatic biliary obstructionVenous outflow obstruction Veno-occlusive disease Budd-Chiari syndrome Cardiac failureAutoimmune chronic active hepatitisDrug and toxins

  • NATURAL HISTORY OF CHRONIC LIVER DISEASE

  • CLINICAL FEATURES The clinical features of cirrhosis have been known since ancient timesCompensated CirrhosisDecompensated CirrhosisCirrhotic patient may develop Hepatocellular carcinoma

  • CLINICAL HISTORYFatique and weight lossAnorexia and dyspepsiaAbdominal painJaundiceSwelling of legs or abdomenHaemorrage- nose, gums, skin, alimentary tractLoss of libidoPast health, Jaundice, Hepatitis, Drug ingested, Blood transfusionSocial, Alcohol consumptionHereditary

  • EXAMINATION

    Nutrition, 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, SpleenPeripheral edemaNeurological changes mental functions, stupor, tremor

  • INVESTIGATION

    HAEMATOLOGY Haemoglobin, Leucocyte, Platelet count and Prothrombine time .BIOCHEMICALSerum Billirubin, Transaminase, Alkaline phospatase, Albumin, Globulin, ImmunoglobulinsASCITES Serum sodium, Potassium, Bicarbonate, Chloride, Urea and Creatinine levelsWeight daily24 hours urine volume and sodium secretion

  • INVESTIGATION

    Ultrasonografi, Hepatic CT ScanLiver Biopsy EndoscopyEEG if neuropsychiatric changesSerum immunologocal, smoothmuscle,mitochondrial and nucleus antibodiesHbsAg, Anti HCV and other marker of HepatitisAlpha fetoprotein

  • Clinical apperance result Hepatocelluler failure Portal Hypertension

  • PORTAL HYPERTENSION

  • MODIFIED CHILD - PUGH CLASSIFICATIONOF THE SEVERITY LIVER DISEASE

    CHILD -PUGH 1 2 3---------------------------------------------------------------------------------------BILIRUBIN < 2 gr % 2,0 - 3,0 gr % > 3,0 gr %.ALBUMIN > 3,5 gr % 2,8 - 3,5 gr % < 2,8 gr %.ASCITES NONE SLIGHT MODERATEENSEFALOPATI NONE GRADE 1/2 GRADE 3/4PROTHROMBINE 1 3 4 - 6 >6 TIME ============================================================TOTAL SCORE ( 5 6 grade A ) ( 7 9 grade B ) ( 10 15 grade C) ----------------------------------------------------------------------

    MELD SORE,3.78ln[serum bilirubin (mg/dL)] + 11.2 ln[INR] + 9.57ln[serum creatinine (mg/dL)] + 6.43 aetiology(0: cholestatic or alcoholic, 1- otherwise)

  • COMPLICATION OF CIRRHOSISVariceal bleedingAscites, refractory ascitesHepatorenal syndromeHepatic encephalopathySpontaneous bacterial peritonitisHepatocelluler carcinomaGastropathyOsteopenia, osteoporosis

  • MANAGEMENT

    The new concept in management of patients with cirrhosis should be prevention and early intervention to stabilise disease progression and to avoid or delay clinical decompensation and the need for liver transplantation General ManagementSpecific TreatmentTreatment of complication CirrhosisOrthotopic Liver Transplantation

  • General Management

    Good nutritionAvoid protein excessLow salt dietAlcohol abstinenceAvoid NSAID, Sedative, and OviatCholestyramine for pruritus

  • Specific Treatment

    Interferon and Ribavirin improve liver biochemistry and may retard development of HCC in HCV induced CirrhosisUCLA in PBC with little benefitPenicillamine for Willson diseaseVena section for Haemochromatosis

  • Variceal Bleeding

  • *Methode Non Farmakology

    SB Tube(Sengstaken-Blackmore Tube)Methode Farmacology

    Non selektif Beta blokersEndoscopic Injection Sclerotherapy (EIS)Endoscopic VaricealLigation (EVL)TIPPSSurgical Porto Systemic ShuntOLT Treatment options for Esophageal VaricesNitratVasopressinSomatostatin & Analog(Octreotide)

  • TREATMENT OPTIONS FOR ESOPHAGEAL VARICES PURPOSE OFTHERAPY FIRST-LINE THERAPY SECOND-LINE OR ALTERNATIVE PRIMARY PROPHYLAXIS BETA-BLOCKER ALONE BETA-BLOCKER AND LONG-ACTING NITRATE (ISOSORBIDE MONONITRATE) BAND LIGATION ACUTE VARICEAL BLEED SANDOSTATIN, (OR TERLIPRESSIN OR VASOPRESSIN) AND ENDOSCOPIC THERAPY TIPS* SHUNT SURGERY SECONDARY PROPHYLAXIS BAND LIGATION ALONE BAND LIGATION BETA-BLOCKER ( NITRATES) TIPS* SHUNT SURGERY Treatment options for Esophageal Varices

  • Algorithm for Cirrhosis without bleedingCirrhosis WithoutBleedingCirrhosisEstablishedReguler IntervalUsually one weekUpper EndoscopyNo varicesSmall or MediumVaricesLarge VaricesObserveObserve 1 2 years Evaluation)Primary BleedingProphylaxis Non Selectne Blockers (and /or Nitrates) Ligation

    2 3 years Evaluation

  • Algorithm for Cirrhosis with bleedingAlgorithm ForBleeding Cirrhotis Resuscitae Begin Octreotide or VasopressinEarly endoscopyNon-PortalHypertensive CauseGastric VaricesEsophagelVaricesPortalHypertensiveGastropathyTreat appropriatelyContinue octreotide 5 daysBegin beta-blocker when stableBand ligation or injectionSclerotheraphyBallon TamponadeRebleedingNo rebleedingShunt (Child A)TiPSS. orLiver transplantation (Child B or C)Continue treatmentPreventation of Rebleeding Pharmacological Treatment Ligation /Sclerotheraphy Reguler IntervalUsually one weekRepeated Endoscopy3 6 monthEradicationShunt (Child A)TIPSS Or OLT (Child B or C)Rebleeding

  • Ascites

  • Grading ascites

    grade 1: detectable only by careful physical examination grade 2: easily detected but relatively small amount grade 3: obvious but not tense grade 4: tense

  • Management of cirrhotic patients with moderate uncomplicated ascitesStart with a low sodium diet (80 mmol /day) and anti aldosteronic drug (100-200 mg/day) monitoring body weightLow 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 ascitesBlood 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

  • Management of refractory ascitesParacentesisPeritovenous shuntTransjugular intrahepatic porto-systemic stent-shunt (TIPSS)Liver Transplantation

  • Spontaneus Bacterialis Peritonitis

  • Spontaneus Bacterial PeritonitisSpontaneous bacterial peritonitis is an infection of ascitic fluid without a known source of infection. It occurs in 10% to 30% of patients with cirrhotic ascites and is frequently recurrent (70% recurrence rate in 1 year)Cirrhotic patients at high risk of SBPCirrhotic patients with gastrointestinal hemorrhageCirrhotic 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

  • Liver cirrhosis with ascitesAscites functureabdominal pain

    accompanying symptom, shock, disturbances of consciousness,disturbances of motility,hypotension.etc,asymptomatic Ascites funtionCheck PMN, culturePMN cell > 250PMN cell < 250Culture + MonomikrobialCulture + MonomikrobialSBPBMNNBakterisida Monomikrobial Non Nerro toxicDiagnosis of SBP

  • SBP SYMPTOMATICSBP PROPHYLAXISANTIBIOTIC CHOICECefotaxime 1-2gr/day (5-7)daysAmoxillin+ Clavulanic Acid (5-7)daysREPEAT PARASINTESIS AFTER 24 HOURS ANTIBIOTICSANTIBIOTIC FORWAREDPMN CELL PMN CELL MANAGEMENT OF SBPNorfloxacinCyprofloks