Download - CIRRHOSIS OF LIVER
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CIRRHOSIS OF CIRRHOSIS OF LIVERLIVER
Dr.Vemuri ChaitanyaDr.Vemuri Chaitanya
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Cirrhosis Cirrhosis Chronic generalized liver diseaseChronic generalized liver disease
A condition that is defined histopathologically and A condition that is defined histopathologically and has a variety of clinical manifestations and has a variety of clinical manifestations and complications, some of which can be life threatening.complications, some of which can be life threatening.
Pathologic features : development of fibrosis to the Pathologic features : development of fibrosis to the point that there is architectural distortion with point that there is architectural distortion with formation of regenerative nodules ( micronodular / formation of regenerative nodules ( micronodular / macronodular )macronodular )
This results in decrease in hepatocellular mass, thus This results in decrease in hepatocellular mass, thus function . function .
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NORMALNORMAL
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Micronodular CirrhosisMicronodular Cirrhosis
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Macronodular CirrhosisMacronodular Cirrhosis
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EpidemiologyEpidemiology
40% cases asymptomatic40% cases asymptomatic
It is the 12It is the 12thth leading cause of death in United leading cause of death in United
States.States.
Approximately 30,000 to 50,000 deaths per Approximately 30,000 to 50,000 deaths per
yearyear
Additional 10,000 deaths due to liver cancer Additional 10,000 deaths due to liver cancer
secondary to cirrhosissecondary to cirrhosis
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This end stage of CLD is This end stage of CLD is characterised by :characterised by :
Bridging Fibrous SeptaBridging Fibrous Septa Parenchymal nodules Parenchymal nodules Disruption of the architecture of the Disruption of the architecture of the
entire liverentire liver
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pathogenesispathogenesis Hepatocellular deathHepatocellular death Regeneration Regeneration Progressive fibrosisProgressive fibrosis
The induction of fibrosis occurs with activation of hepatic The induction of fibrosis occurs with activation of hepatic stellate cells, resulting in formation of increased amounts stellate cells, resulting in formation of increased amounts of collagen & other components of extracellular matrix.of collagen & other components of extracellular matrix.
Stimuli : 1.Chr.inflammation – cytokines like TNF, Stimuli : 1.Chr.inflammation – cytokines like TNF, Lymphotoxin, IL-1 Lymphotoxin, IL-1 2.Cytokine production by injured Kupffer cells, 2.Cytokine production by injured Kupffer cells, endothelial cells, hepatocytes, bile duct endothelial cells, hepatocytes, bile duct
epithelial cellsepithelial cells 3.Disruption of ECM3.Disruption of ECM 4.Direct stimulation of stellate cells by toxins4.Direct stimulation of stellate cells by toxins
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EtiologyEtiology AlcoholismAlcoholism Chronic Viral Hepatitis – Hepatitis BChronic Viral Hepatitis – Hepatitis B Hepatitis CHepatitis C Autoimmune HepatitisAutoimmune Hepatitis Nonalcoholic steatohepatitisNonalcoholic steatohepatitis Biliary Cirrhosis – Primary biliary cirrhosisBiliary Cirrhosis – Primary biliary cirrhosis Primary sclerosing Primary sclerosing
cholangitischolangitis Autoimmune Autoimmune
cholangiopathycholangiopathy
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EtiologyEtiology Cardiac CirrhosisCardiac Cirrhosis Budd Chiari SyndromeBudd Chiari Syndrome Inherited metabolic liver disease :Inherited metabolic liver disease : HemochromatosisHemochromatosis Wilson’s DiseaseWilson’s Disease Alpha 1 Antitrypsin deficiencyAlpha 1 Antitrypsin deficiency Cystic FibrosisCystic Fibrosis Cryptogenic CirrhosisCryptogenic Cirrhosis Others : Galactosemia , Tyrosinemia, Others : Galactosemia , Tyrosinemia, Drug induced : alpha methyldopaDrug induced : alpha methyldopa SyphilisSyphilis
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Clinical FeaturesClinical Features
Asymptomatic for long periods.Asymptomatic for long periods. Onset of symptoms – insidious , less Onset of symptoms – insidious , less
often abrupt.often abrupt. Non specific symptoms – vague right Non specific symptoms – vague right
upper quadrant pain, fever, nausea, upper quadrant pain, fever, nausea, vomiting,diarrhea,anorexia & malaise.vomiting,diarrhea,anorexia & malaise.
Or they may present with more Or they may present with more specific complication of CLD – specific complication of CLD – ascites,upper GI bleed etc…ascites,upper GI bleed etc…
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Signs Signs Loss of hair ( alopecia )Loss of hair ( alopecia ) IcterusIcterus Pallor Pallor KF Ring KF Ring Parotid enlargementParotid enlargement Fetor hepaticusFetor hepaticus Loss of axillary & pubic hairLoss of axillary & pubic hair Spider neviSpider nevi GynecomastiaGynecomastia Atrophy of breasts in femalesAtrophy of breasts in females Wasting of musclesWasting of muscles
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SignsSigns Glossitis, cheilitisGlossitis, cheilitis Palmar erythemaPalmar erythema Clubbing Clubbing LeuconychiaLeuconychia Dupuytren’s contracture Dupuytren’s contracture AscitesAscites In 70 % cases liver is enlarged, firm if not In 70 % cases liver is enlarged, firm if not
hard and nodularhard and nodular SplenomegalySplenomegaly Caput medusaeCaput medusae
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SignsSigns Bleeding tendencies : deficiency of clotting Bleeding tendencies : deficiency of clotting
factors – check PT /INRfactors – check PT /INR FeverFever HyperpigmentationHyperpigmentation Hyperdynamic circulatory stateHyperdynamic circulatory state EdemaEdema HerniaHernia Testicular atrophyTesticular atrophy DeliriumDelirium Constructional apraxiaConstructional apraxia Flapping tremorsFlapping tremors Inversion of sleep rhythmInversion of sleep rhythm
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Palmar erythemaPalmar erythema
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Alcoholic CirrhosisAlcoholic Cirrhosis
Accurate history regarding amount & Accurate history regarding amount & duration of alcohol consumption is required.duration of alcohol consumption is required.
Lab tests : Lab tests : • Completely normal in early compensated Completely normal in early compensated
alcoholic cirrhosisalcoholic cirrhosis• Hb: Anemia + ( chr.GI loss, nutritional def, Hb: Anemia + ( chr.GI loss, nutritional def,
hypersplenism )hypersplenism )• Platelet count : reduced early in disease, Platelet count : reduced early in disease,
portal htn with portal htn with hypersplenismhypersplenism
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Alcoholic CirrhosisAlcoholic Cirrhosis S.Bilirubin – normal / elevated S.Bilirubin – normal / elevated PT – often prolongedPT – often prolonged S. Transaminases – elevatedS. Transaminases – elevated AST / ALT = > 2/1AST / ALT = > 2/1 Liver biopsy Liver biopsy Treatment :Treatment : Abstinence is the cornerstone of therapy.Abstinence is the cornerstone of therapy. Treatment of any complicationsTreatment of any complications Glucocorticoids – if DF > 32 Glucocorticoids – if DF > 32 Oral PentoxiphyllineOral Pentoxiphylline
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Cirrhosis d/t Chr.Hepatitis Cirrhosis d/t Chr.Hepatitis B & CB & C
Of patients exposed to HCV, approximately 80% Of patients exposed to HCV, approximately 80% develop Chronic hepatitis and of those, about 20 –develop Chronic hepatitis and of those, about 20 –30 % will develop cirrhosis over 20-30 yrs.30 % will develop cirrhosis over 20-30 yrs.
Here , liver is small & shrunken with a Here , liver is small & shrunken with a characteristic features of mixed micro and macro characteristic features of mixed micro and macro nodular cirrhosis seen on biopsy.nodular cirrhosis seen on biopsy.
Of patients exposed to HBV, about 5 % develop Of patients exposed to HBV, about 5 % develop chronic hepatitis & about 20% of those patients go chronic hepatitis & about 20% of those patients go on to develop cirrhosis.on to develop cirrhosis.
Liver is small & shrunken and has mixed micro & Liver is small & shrunken and has mixed micro & macronodular cirrhotic pattern.macronodular cirrhotic pattern.
Invg : Routine investigations + HCV RNA, HBsAg, Invg : Routine investigations + HCV RNA, HBsAg, anti – HBs, HBeAg, anti – HBe, HEV DNA.anti – HBs, HBeAg, anti – HBe, HEV DNA.
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Cirrhosis d/t Chr.Hepatitis Cirrhosis d/t Chr.Hepatitis B & CB & C
Specific Treatment :Specific Treatment : HBV : Lamivudine, Adefovir, HBV : Lamivudine, Adefovir,
Entecavir, TenofovirEntecavir, Tenofovir HCV: Pegylated Interferon, Ribavirin HCV: Pegylated Interferon, Ribavirin
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Primary Biliary CirrhosisPrimary Biliary Cirrhosis Female preponderanceFemale preponderance Median age of around 50 yrs Median age of around 50 yrs Etiology : unknownEtiology : unknown Portal inflammation & necrosis of Portal inflammation & necrosis of
cholangiocytes in small and medium cholangiocytes in small and medium sized bile ducts.sized bile ducts.
Antimitochondrial antibodies in 90% of Antimitochondrial antibodies in 90% of ptspts
Pathology : earliest lesion- Chronic Pathology : earliest lesion- Chronic Nonsuppurative Destructive CholangitisNonsuppurative Destructive Cholangitis
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Primary Biliary Cirrhosis Primary Biliary Cirrhosis
FatigueFatigue PruritisPruritis On ex: hepatomegalyOn ex: hepatomegaly splenomegalysplenomegaly ascitesascites edemaedema Unique to PBC : Unique to PBC :
Hyperpigmentation,Xanthelasma,XaHyperpigmentation,Xanthelasma,Xanthomatanthomata
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Primary Biliary CirrhosisPrimary Biliary Cirrhosis
LAB :LAB : Elevated GGT, ALP with mild elevations of Elevated GGT, ALP with mild elevations of
AST & ALTAST & ALT HyperbilirubinemiaHyperbilirubinemia Thrombocytopenia, leukopenia, anemiaThrombocytopenia, leukopenia, anemiaTREATMENT :TREATMENT : UDCA @ 13 – 15 mg/Kg per dayUDCA @ 13 – 15 mg/Kg per day Liver TransplantationLiver Transplantation CholestyramineCholestyramine Bisphosphonates – Bisphosphonates –
osteopenia/osteoporosisosteopenia/osteoporosis
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Primary Sclerosing Primary Sclerosing CholangitisCholangitis
Etiology : unknownEtiology : unknown Diffuse inflammation & fibrosis of entire biliary tree – Diffuse inflammation & fibrosis of entire biliary tree –
chronic cholestasis – obliteration of intra & chronic cholestasis – obliteration of intra & extrahepatic biliary tree – biliary cirrhosis – portal htn extrahepatic biliary tree – biliary cirrhosis – portal htn – liver failure– liver failure
Cli fea : fatigue, pruritis, steatorrhea, fat sol vitamin Cli fea : fatigue, pruritis, steatorrhea, fat sol vitamin deficienciesdeficiencies
Lab: 2 fold rise in ALP, elevated aminotransferases, p-Lab: 2 fold rise in ALP, elevated aminotransferases, p-ANCA ( 65%)ANCA ( 65%)
Diagnosis : MRCP , CholangiogramDiagnosis : MRCP , Cholangiogram Treatment : No proven treatment. Treatment : No proven treatment. High dose 20 mg/kg/day UDCA.High dose 20 mg/kg/day UDCA. Endoscopic dilatation of dominant Endoscopic dilatation of dominant
stricturesstrictures Liver TransplantationLiver Transplantation
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Cardiac CirrhosisCardiac Cirrhosis
Pts with long standing right sided Pts with long standing right sided CHF may develop chronic liver CHF may develop chronic liver disease & cardiac Cirrhosisdisease & cardiac Cirrhosis
Cli fea : symptoms of Rt.Heart.Failure Cli fea : symptoms of Rt.Heart.Failure + Hepatomegaly+ Hepatomegaly
Lab : ALP raised,Lab : ALP raised,
AST > ALT – normal / raised AST > ALT – normal / raised Diagnosis : cardiac case with elevated Diagnosis : cardiac case with elevated
ALP & enlarged liverALP & enlarged liver
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Cirrhosis – other causesCirrhosis – other causes
HemochromatosisHemochromatosis Wilson’s DiseaseWilson’s Disease Alpha1 Antitrypsin DeficiencyAlpha1 Antitrypsin Deficiency Cystic FibrosisCystic Fibrosis
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InvestigationsInvestigations
Complete Hemogram Complete Hemogram
Peripheral SmearPeripheral Smear
Platelet CountPlatelet Count
PT INRPT INR
LFT – S. Bilirubin, S. Albumin, S. Globulin, SGPT, LFT – S. Bilirubin, S. Albumin, S. Globulin, SGPT,
SGOT, ALPSGOT, ALP
Hepatitis ProfileHepatitis Profile
Alpha FetoproteinAlpha Fetoprotein
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InvestigationsInvestigations
Blood sugarBlood sugar
Urea, CreatinineUrea, Creatinine
Sodium, PotassiumSodium, Potassium
Ascitic fluid examinationAscitic fluid examination
X-Ray chestX-Ray chest
USG / CT AbdomenUSG / CT Abdomen
Confirmation by Liver BiopsyConfirmation by Liver Biopsy
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Complications of Complications of CirrhosisCirrhosis
Portal HTN – Gastroesophageal VaricesPortal HTN – Gastroesophageal Varices Portal hypertensive GastropathyPortal hypertensive Gastropathy Splenomegaly, HypersplenismSplenomegaly, Hypersplenism Ascites – SBPAscites – SBP Hepatorenal Syndrome – Type 1 & 2Hepatorenal Syndrome – Type 1 & 2 Hepatic EncephalopathyHepatic Encephalopathy Hepatopulmonary SyndromeHepatopulmonary Syndrome Portopulmonary HypertensionPortopulmonary Hypertension MalnutritionMalnutrition
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Complications of Complications of CirrhosisCirrhosis
Coagulopathy : Factor deficiencyCoagulopathy : Factor deficiency FibrinolysisFibrinolysis ThrombocytopeniaThrombocytopenia Bone Disease : Osteopenia/Osteoporosis/ Bone Disease : Osteopenia/Osteoporosis/
OsteomalaciaOsteomalacia Haematological abn : AnaemiaHaematological abn : Anaemia HemolysisHemolysis ThrombocytopeniaThrombocytopenia NeutropeniaNeutropenia
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Portal HypertensionPortal Hypertension Prehepatic :Portal Vein thrombosisPrehepatic :Portal Vein thrombosis Splenic Veinf ThrombosisSplenic Veinf Thrombosis Massive SplenomegalyMassive Splenomegaly Hepatic : Presinusoidal – SchistosomiasisHepatic : Presinusoidal – Schistosomiasis Cong.hepatic Cong.hepatic
fibrosisfibrosis Sinusoidal – CirrhosisSinusoidal – Cirrhosis Alcoholic hepatitisAlcoholic hepatitis Postsinusoidal – Veno-occlusive Postsinusoidal – Veno-occlusive
DiseaseDisease
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Posthepatic : Budd Chiari syndromePosthepatic : Budd Chiari syndrome
Inferior vena caval websInferior vena caval webs
Cardiac Causes –Cardiac Causes –
Restrictive Restrictive CardiomyopathyCardiomyopathy
Constrictive PericarditisConstrictive Pericarditis
Severe CHFSevere CHF
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Portal Hypertension Portal Hypertension Elevation of hepatic venous pressure gradient to > 5mm Hg.Elevation of hepatic venous pressure gradient to > 5mm Hg. It is caused by combination of 2 simultaneously occuring It is caused by combination of 2 simultaneously occuring
hemodynamic processes :hemodynamic processes :1.1. Increased intrahepatic resistance to passage of blood flow Increased intrahepatic resistance to passage of blood flow
through liver through liver 2.2. Increased splanchnic blood flow secondary to vasodilation. Increased splanchnic blood flow secondary to vasodilation.
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Portal HypertensionPortal Hypertension
Portal HTN directly responsible for 2 Portal HTN directly responsible for 2 complications – variceal complications – variceal haemorrhage and asciteshaemorrhage and ascites
Also hypersplenism, Also hypersplenism, congestive gastropathy, congestive gastropathy, renal failure and renal failure and hepatic encephaopathyhepatic encephaopathy
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CLINICAL FEATURESCLINICAL FEATURES
Splenomegaly – Hypersplenism – Splenomegaly – Hypersplenism – Thrombocytopenia, Neutropenia, Thrombocytopenia, Neutropenia, AnemiaAnemia
Dilated Abdominal Veins, Caput Dilated Abdominal Veins, Caput Medusae, Ascitis.Medusae, Ascitis.
Oesophageal varicesOesophageal varices
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Variceal BleedVariceal Bleed Approx 5 – 15 % of cirrhotics per year develop Approx 5 – 15 % of cirrhotics per year develop
varices and it is estimated that majority of patients varices and it is estimated that majority of patients with cirrhosis will develop varices over their lifetimewith cirrhosis will develop varices over their lifetime
1/31/3rdrd of patients with varices develop bleeding. of patients with varices develop bleeding. Factors predicting variceal bleed :Factors predicting variceal bleed : Severity of cirrhosis ( Child’s Class )Severity of cirrhosis ( Child’s Class ) Ht of wedged hepatic vein pressureHt of wedged hepatic vein pressure Size and location of varixSize and location of varix Endoscopic stigmata : red wale sign, hematocystic Endoscopic stigmata : red wale sign, hematocystic
spots, diffuse erythema, bluish color, cherry red spots, diffuse erythema, bluish color, cherry red spot & white nipple spotspot & white nipple spot
Tense ascitesTense ascites
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Variceal BleedVariceal Bleed
Diagnosis : identified by endoscopyDiagnosis : identified by endoscopy Pt with a gradient of >12 mm Hg – are at a Pt with a gradient of >12 mm Hg – are at a
greater risk for variceal bleed.greater risk for variceal bleed. Precipitating Factors – Precipitating Factors – AAlcohol, lcohol, AAspirin, spirin, AAnalgesics nalgesics
(NSAIDs), (NSAIDs), AAdrenal Corticosteroidsdrenal Corticosteroids Assessment – Drop in systolic BP > 10 mmHg, rise in Assessment – Drop in systolic BP > 10 mmHg, rise in
pulse > 15 beats / minute on sitting up – 10 to 20% pulse > 15 beats / minute on sitting up – 10 to 20% Supine Hypotension - > 20%Supine Hypotension - > 20% Systolic BP < 100 mmHg / Baseline Tachycardia > Systolic BP < 100 mmHg / Baseline Tachycardia >
25%25%
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RESUSCITATION RESUSCITATION Stabilize BP – 2 large bore IV line – Stabilize BP – 2 large bore IV line –
Isotonic saline / Ringer Lactate / fresh blood / Isotonic saline / Ringer Lactate / fresh blood / packed RBC transfusion – Maintain ½ hour packed RBC transfusion – Maintain ½ hour pulse, BP, respiration chart (In emergency pulse, BP, respiration chart (In emergency situation – O-ve blood)situation – O-ve blood)
MEASURE URINE OUTPUTMEASURE URINE OUTPUT Correction of coagulopathy – FFP, Correction of coagulopathy – FFP,
parenteral Vit K 10 mg parenteral Vit K 10 mg Platelet transfusion – if count < 50,000Platelet transfusion – if count < 50,000 Airway protection – endotracheal intubation Airway protection – endotracheal intubation
to prevent aspirationto prevent aspiration
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RESUSCITATIONRESUSCITATION
Nasal Gastric AspirationNasal Gastric Aspiration OCTREOTIDEOCTREOTIDE Infusion 50 to 100 Infusion 50 to 100 µgm µgm
bolusbolus
25 to 50 25 to 50 µgm / hour infusionµgm / hour infusion VASOPRESSINVASOPRESSIN 0.3 unit / minute IV – 0.3 unit / minute IV –
gradually increased to 0.9 units/minute – gradually increased to 0.9 units/minute – Side-effects : Myocardial ischemia, Side-effects : Myocardial ischemia, infarction, arrhythmia, cardiac arrest, infarction, arrhythmia, cardiac arrest, mesenteric ischemia mesenteric ischemia
( now not preferred ) ( now not preferred )
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ResuscitationResuscitation Endoscopic Therapy : Variceal band ligationEndoscopic Therapy : Variceal band ligation Variceal sclerotherapyVariceal sclerotherapy Balloon tamponade ( Sengstaken-Blakemore Balloon tamponade ( Sengstaken-Blakemore
tube or Minnesota tube ) – in pts who cannot tube or Minnesota tube ) – in pts who cannot get endoscopic therapy or those who need get endoscopic therapy or those who need stabilization prior to endoscopic therapystabilization prior to endoscopic therapy
TIPS – When esophageal varices extend into TIPS – When esophageal varices extend into proximal stomach proximal stomach
In Pts eho fail endoscopic / medical In Pts eho fail endoscopic / medical treatmenttreatment
and also poor subjects for surgery.and also poor subjects for surgery.
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prophylaxisprophylaxis
Beta blockers – propranolol – resting Beta blockers – propranolol – resting heart rate to be reduced by 25 %.heart rate to be reduced by 25 %.
Repeated variceal band ligation until Repeated variceal band ligation until varices are obliterated.varices are obliterated.
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Splenomegaly & Splenomegaly & HypersplenismHypersplenism
Congestive splenomegaly is common in pts Congestive splenomegaly is common in pts with portal htn.with portal htn.
Clinical features include enlarged spleen, Clinical features include enlarged spleen, thrombocytopenia, leukopeniathrombocytopenia, leukopenia
Some – significant left sided/ left upper Some – significant left sided/ left upper quadrant abdominal painquadrant abdominal pain
No specific treatmentNo specific treatment Splenectomy Splenectomy Hypersplenism with development of Hypersplenism with development of
thrombocytopenia – first indicator of portal thrombocytopenia – first indicator of portal hypertensionhypertension
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AscitesAscites Accumulation of fluid within the peritoneal cavityAccumulation of fluid within the peritoneal cavity M.C cause : cirrhosis with portal hypertensionM.C cause : cirrhosis with portal hypertension Clinical features : increase in abdominal girthClinical features : increase in abdominal girth peripheral edemaperipheral edema dyspnea – if massivedyspnea – if massive bulging flanksbulging flanks shifting dullness shifting dullness fluid thrillfluid thrill Hepatic hydrothorax – more common on rt.side Hepatic hydrothorax – more common on rt.side implicates rent in diaphragm implicates rent in diaphragm
withwith free flow of ascitic fluid into free flow of ascitic fluid into
thoracic cavity thoracic cavity
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AscitesAscites
Diagnostic paracentesisDiagnostic paracentesis SAAG :SAAG : >1.1g/dL – portal hypertension>1.1g/dL – portal hypertension <1.1g/Dl – neoplasm,Tb, pancreatitis,<1.1g/Dl – neoplasm,Tb, pancreatitis, Ascitic fluid proteins low – high chance of Ascitic fluid proteins low – high chance of
developing SBPdeveloping SBP Ascitic fluid – high RBCs – traumatic tap, Ascitic fluid – high RBCs – traumatic tap,
HCC, ruptured omental varixHCC, ruptured omental varix Ascitic fluid – PMN >250 /cu.mm - SBPAscitic fluid – PMN >250 /cu.mm - SBP
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Ascites - TreatmentAscites - Treatment Small amounts of ascites – dietary sodium Small amounts of ascites – dietary sodium
restriction ( <2g/day )restriction ( <2g/day ) Moderate : diuretic is essentialModerate : diuretic is essential Spiranolactone 100-200 mg/day Spiranolactone 100-200 mg/day
ODOD Furosemide 40-80 mg/day Furosemide 40-80 mg/day - if peripheral edema +- if peripheral edema + Pt is compliant but ascitic fluid + , thenPt is compliant but ascitic fluid + , then Spiranolactone 400 -600 mg/daySpiranolactone 400 -600 mg/day Furosemide 120-160 mg/dayFurosemide 120-160 mg/day If ascites still + , then it is REFRACTORY If ascites still + , then it is REFRACTORY
ASCITESASCITES
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Ascites - treatmentAscites - treatment
Refractory ascites – Large volume Refractory ascites – Large volume paracentesisparacentesis
TIPSTIPS
Liver Liver TransplantationTransplantation
Prognosis – pts of cirrhosis with Prognosis – pts of cirrhosis with ascites- poorascites- poor
<50 % of pts survive 2 yrs after the <50 % of pts survive 2 yrs after the onset of ascites.onset of ascites.
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Spontaneous Bacterial Spontaneous Bacterial PeritonitisPeritonitis
Spontaneous infection of ascitic fluid without Spontaneous infection of ascitic fluid without any intraabdominal source.any intraabdominal source.
Bacterial translocation – gut flora transversing Bacterial translocation – gut flora transversing the intestine into mesenteric lymph nodes, the intestine into mesenteric lymph nodes, leading to bacteremia and seeding of ascitic leading to bacteremia and seeding of ascitic fluidfluid
MC : E.coliMC : E.coli Others : Step.viridans, Staph.aureusOthers : Step.viridans, Staph.aureus If > 2 organisms are identified – secondary If > 2 organisms are identified – secondary
bacterial peritonitis d/t perforated viscus to be bacterial peritonitis d/t perforated viscus to be consideredconsidered
Ascitic fluid PMN > 250/cu.mmAscitic fluid PMN > 250/cu.mm
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SBPSBP
Pt can present with altered Pt can present with altered sensorium, elevated WBC, sensorium, elevated WBC, abdominal pain/discomfortabdominal pain/discomfort
Treatment : cephalosporinsTreatment : cephalosporins In pts with an episode(s) of SBP and In pts with an episode(s) of SBP and
recovered , once –weekly- recovered , once –weekly- administration of antibiotic as administration of antibiotic as prophylactic measureprophylactic measure
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Hepatorenal SyndromeHepatorenal Syndrome Functional renal failure without renal pathology Functional renal failure without renal pathology 10% of pts with cirrhosis / advanced liver failure10% of pts with cirrhosis / advanced liver failure Diagnosis : presence of large amount of ascitesDiagnosis : presence of large amount of ascites progressive rise in creatinineprogressive rise in creatinine urinary sodium <10 mEqurinary sodium <10 mEq Type 1 HRS : progressive impairment of renal Type 1 HRS : progressive impairment of renal
function & significant reduction in creatinine function & significant reduction in creatinine clearance within 1- 2 wks . BAD PROGNOSISclearance within 1- 2 wks . BAD PROGNOSIS
Type 2 HRS : reduction in GFR, with rise in Type 2 HRS : reduction in GFR, with rise in S.CreatS.Creat
BETTER PROGNOSISBETTER PROGNOSIS
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Hepatorenal SyndromeHepatorenal Syndrome
Seen in refractory ascitesSeen in refractory ascites Exclude causes of ARF Exclude causes of ARF Treatment:Treatment: Midodrine, an alpha agonist along Midodrine, an alpha agonist along
with Octerotide and IV Albuminwith Octerotide and IV Albumin Liver transplantationLiver transplantation
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HEPATIC HEPATIC ENCEPHALOPATHYENCEPHALOPATHY
Precipitating factors Precipitating factors
GI BleedingGI Bleeding
Excess protein intakeExcess protein intake
Electrolyte abnormalities, Ascitic AspirationElectrolyte abnormalities, Ascitic Aspiration
UremiaUremia
Dehydration, ConstipationDehydration, Constipation
AlcoholAlcohol
Viral infections, SBPViral infections, SBP
Anaesthetic agents, Surgery, Narcotics, TranquilisersAnaesthetic agents, Surgery, Narcotics, Tranquilisers
Hepatic toxins, Portosystemic shunts - TIPSHepatic toxins, Portosystemic shunts - TIPS
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HEPATIC HEPATIC ENCEPHALOPATHYENCEPHALOPATHY
Treatment–CORRECT/ AVOID Treatment–CORRECT/ AVOID
PRECIPITATING FACTORSPRECIPITATING FACTORS
Dietary protein restriction-30 - 40 gm protein / dayDietary protein restriction-30 - 40 gm protein / day
Non absorbable disaccharide – LACTULOSE – 15 Non absorbable disaccharide – LACTULOSE – 15
to 45 ml BID / QIDto 45 ml BID / QID
Lactulose enema Lactulose enema
Neomycin 1 gm 6Neomycin 1 gm 6thth hrly hrly
Metronidazole 250 mg 8Metronidazole 250 mg 8thth hrly hrly
Bowel wash / LactobacillusBowel wash / Lactobacillus
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GRADING OF HEPATIC GRADING OF HEPATIC ENCEPHALOPATHYENCEPHALOPATHY
0 – Normal0 – Normal 1 – Inverted sleep rhythm, restless1 – Inverted sleep rhythm, restless 2 – Lethargy, slow response2 – Lethargy, slow response 3 – Drowsy, arousable but confused3 – Drowsy, arousable but confused 4 - Coma4 - Coma
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HEPATOPULMONARY HEPATOPULMONARY SYNDROMESYNDROME
Clubbing, cyanosis, spider nevi, orthodeoxiaClubbing, cyanosis, spider nevi, orthodeoxia Hypoxia in standing position-ORTHODEOXIAHypoxia in standing position-ORTHODEOXIA Hypoxia is due to intrapulmonary shunting Hypoxia is due to intrapulmonary shunting
through direct arteriovenous communications through direct arteriovenous communications Intra Pulmonary Vascular dilatation in the Intra Pulmonary Vascular dilatation in the
absence of intrinsic cardio pulmonary diseaseabsence of intrinsic cardio pulmonary disease Resistant hypoxaemia (Resistant hypoxaemia (PaPaO2 < 9.3 kPa or 70 O2 < 9.3 kPa or 70
mmHg), intrapulmonary vascular dilatation and mmHg), intrapulmonary vascular dilatation and chronic liver disease with portal hypertension chronic liver disease with portal hypertension
Treatment : liver transplantationTreatment : liver transplantation
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Portopulmonary Portopulmonary HypertensionHypertension
Similar to 'primary pulmonary Similar to 'primary pulmonary hypertension‘hypertension‘
defined as pulmonary hypertension with defined as pulmonary hypertension with increased pulmonary vascular resistance increased pulmonary vascular resistance and a normal pulmonary artery wedge and a normal pulmonary artery wedge pressure in a patient with portal pressure in a patient with portal hypertension hypertension
caused by vasoconstriction and obliteration caused by vasoconstriction and obliteration of the pulmonary arterial system and leads of the pulmonary arterial system and leads to breathlessness and fatigue. to breathlessness and fatigue.
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MALIGNANT MALIGNANT TRANSFORMATIONTRANSFORMATION
Rapid, unexplained weight lossRapid, unexplained weight loss
Unexplained feverUnexplained fever
Pain in the right HypochondriumPain in the right Hypochondrium
Rapid enlargement of liver / one of the nodulesRapid enlargement of liver / one of the nodules
Hepatic Rub / Hepatic BruitHepatic Rub / Hepatic Bruit
Hemorrhagic ascitic fluidHemorrhagic ascitic fluid
Malignant cells in cytology of Ascitic fluidMalignant cells in cytology of Ascitic fluid
Confirmation by USG / CT / AFP / BiopsyConfirmation by USG / CT / AFP / Biopsy
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HCCHCC
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CHILD – PUGH ScoringCHILD – PUGH Scoring
Clinical and biochemical Clinical and biochemical measurementsmeasurements
Points scored for increasing Points scored for increasing abnormalityabnormality
11 22 33
Albumin (g/dl)Albumin (g/dl) > 3.5> 3.5 2.8 to 3.52.8 to 3.5 < 2.8< 2.8
Bilirubin (mg/dl)Bilirubin (mg/dl) 1 to 21 to 2 2 to 32 to 3 > 3> 3
For cholestatic For cholestatic diseases : bilirubin diseases : bilirubin (mg/dl)(mg/dl)
< 4< 4 4 to 104 to 10 > 10> 10
PT (secs prolonged)*PT (secs prolonged)*
Or Or
INR*INR*
1 to 41 to 4 4 to 64 to 6 > 6> 6
< 1.7< 1.7 1.7 to 2.31.7 to 2.3 > 2.3> 2.3
AscitesAscites AbsentAbsent SlightSlight ModeratModeratee
Encephalopathy (grade)Encephalopathy (grade) NoneNone 1 & 21 & 2 3 & 43 & 4
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CHILD -PUGH SCORING CHILD -PUGH SCORING SYSTEMSYSTEM
Class A – 5 to 6 pointsClass A – 5 to 6 points Class B – 7 to 9 pointsClass B – 7 to 9 points Class C – 10 to 15 pointsClass C – 10 to 15 points B & C – Potential candidates for B & C – Potential candidates for
Hepatic transplantationHepatic transplantation
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THANK YOUTHANK YOU