CIRRHOSIS OF CIRRHOSIS OF LIVERLIVER

Dr.Vemuri ChaitanyaDr.Vemuri Chaitanya

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 .

NORMALNORMAL

Micronodular CirrhosisMicronodular Cirrhosis

Macronodular CirrhosisMacronodular Cirrhosis

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

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

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

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

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

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…

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

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

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

Palmar erythemaPalmar erythema

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

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

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.

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

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

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

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

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

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

Cirrhosis – other causesCirrhosis – other causes

HemochromatosisHemochromatosis Wilson’s DiseaseWilson’s Disease Alpha1 Antitrypsin DeficiencyAlpha1 Antitrypsin Deficiency Cystic FibrosisCystic Fibrosis

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

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

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

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

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

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

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.

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

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

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

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%

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

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 )

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.

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.

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

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

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

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

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.

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

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

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

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

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

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

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

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

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.

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

HCCHCC

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

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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