LIVER CIRRHOSIS - USU OpenCourseWare
LIVER CIRRHOSISleonardo dairiDepartemen Penyakit DalamDEFINITION ANATOMICALLY AS A DIFFUSEPROCESS WITH FIBROSIS AND NODULEFORMATIONCLASSIFICATION:MICRONODULAR CIRRHOSISMACRONODULAER CIRRHOSISMIXED1
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Causes of Cirrhosis Viral hepatitis; B, D, and CAlcoholMetabolicHaemochromatosisWilson’s diseaseAlpha-1-antitrypsin deficiencyChronic biliary obstructionExtrahepatic biliary obstructionIntrahepatic biliary obstructionVenous outflow obstructionVeno-occlusive diseaseBudd-Chiari syndromeCardiac failureAutoimmune chronic active hepatitisDrug and toxinsDIAGNOSIS.1.SPIDER NAEVI2.ERITHEMA PALMARIS3.COLLATERAL VEIN4.ASITES5.SPLENOMEGALI6.INVERTED ALBUMIN GLOBULIN7.HEMATEMESIS/MELENA3
CLINICAL CIRRHOSISIN CLINICAL TERM,COMPENSATED ANDDECOMPENSATEDCLINICAL APPERANCE RESULT, HEPATOCELLULER FAILURE PORTAL HYPERTENSIONCHRONIC ACTIVE HEPATITIS andEARLY CIRRHOSIS NON SPECIFIC,DECOMPENSATED CIRRHOSISINVESTIGATION:1. HAEMATOLOGY- HAEMOGLOBIN,LEUCOCYTE,PLATELET COUNT and PROTHROMBINTIME.2. NIPHOSPATASE,ALBUMINGLOBULIN,IMMUNOGLOBULINT,GAMMA GT,4
- ASCITES PRESENT,SERUM SODIUM,POTASSIUM,BICARBONATE,CHLORIDE,UREA ANDCREATININE LEVEL,WEIHLY DAILY AND 24HOUR URINE VOLUME3.USG,HEPATIC CT SCAN4.LEVER BIOPSY GOLD STANDART5.ENDOSCOPY6.EEG E,PIGMENTATION,PURPURA,FINGER CLUBBING,WHITE ICULARATROPHY,DISTRIBUTION OF BODY HAIR,PAROTIDENLARGMENT,DUPUYTRENCONTRACTURE,BLOOD PRESSUREABDOMEN ASCITES, COLLATERAL VEIN, LIVER,SPLEENPERIPHERAL OEDEMANEUROLOGICAL CHANGES MENTAL FUNCTIONS,STUPOR, TREMOR.5
MODIFIED CHILD-PUGH CLASSIFICATIONOF THE SEVERITY LIVER DISEASECHILDABCBILIRUBIN 2 gr %2,0 - 3,0 gr % 3,5 gr %.KADAR ALBUMIN 3,5 gr %2,8 - 3,5 gr % 2,8 gr %.ASCITES-SLIGHTMODERATEENSEFALOPATI-GRADE 1/2GRADE 3/44-6 6PROTHROMBINE1–3TOTAL SCORE ,! – 6 (grade A), 7 – 9(grade B), 10 – 15(grade C)PORTAL HYPERTENSIContinuing Liver damageNodular regenerationFibrosisIncreased sinusoidalpressurePortal HypertensionSplancnic vasodilatationIncreased gastroesophagealcollateralDecreased effective bloodvolumeFormation ofoesophagogastric varicesIncreased sodium retentionVariceal ruptureAscitesVariceal bleeding6
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MANAGEMENTTERGANTUNG STADIUMNYA.1. STD. KOMPENSASI- KONTROL TERATUR, ISTIRAHAT CUKUP,DIET TINGGI KALORI / PROTEIN, LEMAKSECUKUPNYA, 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 PENCETUSENSEFALOPATI.9
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. BERDASARKANKRITERIA CHILD PADA OPERASI:A : 10 – 15 %.B : 30 %.C : DIATAS 60 %.PENYEBAB KEMATIAN :- 43 % DARI LUAR HATI.- 57 % DARI HATI.10
Causes of death Variceal hemorrhageSpontaneous bacterial peritonitisSepsisLiver failureHepatic comaFunctional renal failureHepatocelluler carcinomaComplications of Cirrhosis Variceal bleedingAscites, refractory ascitesHepatorenal syndrome(HRS),HPSHepatic encephalopathySpontaneous bacterial peritonitisHepatocelluler carcinoma11
Variceal BleedingA. 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 measurePreventionmeasuress rational to avoid developmentof Varices bleeding (Primary prophprophylaylaxxis).C. Up to 70 % Of Patient who do not receive treatmentdie within 1 year of the initial bleeding episodeThe Efforts in preventing bleeding seems to becrucial (secondary, prophylaxis)12
Consensus in Portal Hypertension Baveno IIIMonitoring for the Development of Varices in thePortal Hypertensive Patient.1. All cirrhotic patients should be screened for thepresence of varices at the time of the initialdiagnosis of cirrhosis.2. In compensated patients without varices, endoscopyshould be repeated at 2-3 year intervals toevaluate the development of varices.3. In compensated patients with small varices,endoscopy should be repeated at –2 year intervalsto evaluate progression of varices.4. There is no indication for subsequent evaluationsonce large varices are detected.Algorithm for cirrhosis Without BleedingAlgorithm ForCirrhosis WithoutBleedingCirrhosisEstablishedUpper EndoscopyNo varicesObserve(2 – 3 years Evaluation)Small or MediumVaricesObserve(1 – 2 years Evaluation)Large VaricesPrimary BleedingProphylaxisReguler IntervalUsually one weekNon Selectne Blockers(and /or long actmy Nitrates) Ligation 13
Algorithm For Bleeding CirrhotisAlgorithm ForBleeding Cirrhotis Resuscitae Begin Octreotide(or Vasopressin)Early endoscopyEsophagelNon-PortalGastric VaricesPortalHypertensive CauseVaricesHypertensiveGastropathyContinue octreotide 5 daysTreat appropriatelyBegin beta-blocker when stableBand ligation or injectionSclerotheraphyBallon TamponadeRebleedingNo rebleedingContinue treatmentShunt (Child A)Preventation of RebleedingTiPSS. or Pharmacological TreatmentLiver transplantation (Child B or C) Ligation /SclerotheraphyReguler IntervalUsually one weekEradicationRepeated Endoscopy3 – 6 monthRebleedingShunt (Child A)TIPSS or Liver transplantation(Child B or C)Dosis dan cara pemberian obat-obat vasoaktif padaperdarahan varisesObatCara pemberian DosisLamapemberianVasopressin(VP) Nitroglyserin(NG)VP: i.v infusNG:percutaneus,bolusVP:0,4UU/menit48 jamTerlipressini.v, bolusSomatostatini.v bolus daninfus2 mg/4 jam2-5 hariselama 24-48jam pertama,kemudian 1mg/ 4 jam250 ug diikuti 2-5 hari250-500 ug/jamOctreotidei.v, bolus daninfus50 ug diikuti50 ug/jam2-5 hari14
ASCITESPathophysiology of AscitesPortal HypertensionSplanchnic arteriolar vasodilatation"Forward" increase ofsplancnic capillary pressureand permeabilityArterial vascular underfillingand activation of sodiumretaining mechanismLymph formation lymphreturnSodium and water retentionAscites15
Management of cirrhotic patients with moderateuncomplicated ascites Start with a low sodium diet (80 mmol /day) and antialdosteronic drug (100-200 mg/day) monitoring bodyweight Low doses of furosemide (20-40 mg/day, in case of poorresponse to the anti aldosteronic drug. The goal of treatment : weight loss of 500 g /day inpatients without peripheral edema, and 1 kg/day inpatients with peripheral edema. Maximum dose of anti aldosteronic drug 400 mg/day, and160 mg of furosemide. Sodium restriction.Management of cirrhotic patients with tense or largeuncomplicated ascites Total paracentesis is the most effective and safestprocedures to mobilize large ascites Blood volume with intravenous albumin (8 g/L of asciteremoved) is required if the volume of ascites is more than5 liter. Start with a low sodium diet and diuretics soon afterparacentesis16
Management of refractory ascites Paracentesis Peritovenous shunt Transjugular intrahepatic porto-systemicstent-shunt (TIPSS) Liver Transplantation17
Hepatic EncephalophathyCommon Precipitant of Hepatic encephalopathy Increased Nitrogen LoadGastrointestinal bleedingExcess dietary proteinAzotemiaConstipationElectrolyte and Metabolic ugsNarcotics, transquilizers, sedatives, Diuretics.MiscellaneousInfection, Surgery, Superimposed liver disease18
Clinical Stages of Hepatic EncephalopathyStageMental statusAsterixisEEGIEuphoria or depression,mild confusion, sluredspeech, disordered speechLethargy, moderateconfusion /-Normal AbnormalMarked confusion, incoherent speech, sleepingbut arousableComa, initially responsive to noxious stimuli, laterunresponsiveAbnormalIIIIIIVAbnormalApproach to the patient with hepatic encephalopahtyInitial Evaluation* Exclude other causes of disordered mentation* Identify precipitant and correct* Determinant electrolytes, BUN, creatinine, NH3,GlucoseProtein restrictionLaxative, e.g., Lactulose 30-120 ml, 1 to 4 timesdaily until 4 stools/dayInadequate response?Broad-spectrum antibiotics (e.g., neomycin 500mg qid, or metronidazole 250 mg tid)Inadequate response?Consider liver transplatation19
Spontaneus BacterialisPeritonitisCirrhotic patients at high risk of SBP Cirrhotic patients with gastrointestinal hemorrhage Cirrhotic patients with low ascitic fluid total protein ( 1g/dL) and / or high serum bilirubin ( 2.5 mg/dl) Survivors of an episode of SBP. Hospitalized cirrhotic patients with ascites and low asciticfluid total protein ( 1 g/dl)20
Diagnosis Peritonitis Bakterialis SpontanPasien sirosis hati dengan asitesPungsi asitesGejala menyertai:Syok, perdarahan, gangguankesadaran, gangguanmotilitas, hipotensi, dllAsimtomatik.Nyeri perut panasPungsi asites:periksa: PMNKulturSel PMN 250Sel PMN 250Ulangi pungsi24 jamKultur MonomikrobialKultur MonomikrobialPBSBMNN(Bakterasites MonomikrobialNon-Neutrosistik)Penatalaksanaan Peritonitis Bakterialis SpontanPBS simtomatikProfilaksis PBSAntibiotik pilihan :Sefotaksim 1-2 gram/hari selama 5-7 hariAmoksisilin Asam klavulanat selama 5-7 hariOfloksasinSiprofloksasinDosis standar5-7 hariParasentesis ulang setelah 24 jamantibiotikSel PMNSel PMNAntibiotikditeruskanGanti antibiotik21
HEPATORENAL SYNDROMEPathogenesis of Hepatorenal SyndromeCirrhosisSinusoidal portalhypertensionSplanchnic vasodilatationArterial underfillingReduced renalvasodilator factorsBaroreceptor-mediatedactivation of systemicVasoconstriction factorsIncreased intrarenalvasoconstrictionfactorsRenal vasoconstrictionHepatorenal syndrome22
HEPATOCELLULARCARCINOMA Treatment of HCC depends on1. Local resources2. Stage of the disease3. Presence of cirrhosis Liver Transplantation Hepatic resection treatment of choice for thefew patients with HCC and normal liver. Trans Arterial Chemo Embolization Cytostatica Interferon23
Five years survival of pts with HCC treated by transplantationin 82 Europeans centers between 1988 and june 1994 Indication to transplantationPatients% AliveHCC with CirrhosisHCC without cirrhosisCirrhosis with HCC361446176463454p 0.0004from European Transplantation Register24
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
veloped to grade the liver status in cirrhosis. This review will focus on these topics. Keywords Liver cirrhosis.Liver, MR imaging Introduction Hepatic cirrhosis is a chronic inflammatory liver disorder associated with fibrosis. Although fibrosis is considered the hallmark of cirrhosis, regeneration, necrosis and inflamma-
Cirrhosis of the liver Sclerosing cholangitis. Liver transplant candidate Liver transplant . Other liver conditions: Hepatitis C. Primary biliary cirrhosis Other diagnosis #1: NOTE: Determination of these conditions requires documentation by appropriate serologic testing, abnormal liver function tests, and/or abnormal liver biopsy or imaging .
Chronic Hep C can cause liver inflammation and scarring that can lead to moderate liver damage (fibrosis) and severe liver damage (cirrhosis). People with cirrhosis are at high risk for liver failure, liver cancer and even death. Liver damage often happens slowly, over 20 to 30 years. Hep C and Liver Health Tests
CIRRHOSIS What is Cirrhosis: Cirrhosis is the end stages of a liver disease. Over time, from years to decades, fibrosis (or scar tissue) progresses through stages while your liver attempts to repair itself. Eventually, if left untreated, fibrosis replaces normal liver tissue and eventually results in cirrhosis.
lead to liver failure. Viral hepatitis C has emerged as the leading cause of liver cirrhosis surpassing alcoholic liver disease in the last decade. Incidence Liver cirrhosis is an important public health concern in the United States. According to the Centers for Disease Control and Prevention (CDC) chronic liver disease and
care for better symptom control and improved health. 8–10 In liver cirrhosis, management of patients with liver cirrhosis is traditionally taken care of by physicians, while nurse-led clinics are still rare. However, previous studies on liver cirrhosis, nurse-led clinics have suggested that nurse-led clinics will contribute to better patient .
Liver transplantation Anesthesia Liver Cirrhosis End stage liver disease Coagulopathy KEY POINTS Each program appoints a director of liver transplant anesthesia, who must meet the re-quirements of the American Society of Anesthesiologists and the United Network for Or-gan Sharing. Liver cirrhosis may cause major dysfunction in all organ systems.
Central Bank Survey of Foreign Exchange and Derivatives Market Activity—FR 3036. Turnover Survey as of April 2019. This report is authorized by law (12 U.S.C. §§ 225a and 263). Your voluntary cooperation in submitting this report is needed to make the results comprehensive, accurate, and timely. The Federal Reserve may not conduct or sponsor, and an organization . is not required to .
