ANAESTHESIA AND ANAESTHESIA AND LIVER DISEASES LIVER DISEASESBY BYDR.D.KIRUBAKARAN DR.D.KIRUBAKARAN11.08.08 11.08.08Introduction Introduction Largest organ in the body ( 1.2 Largest organ in the body ( 1.2 1.5kg). 1.5kg). Liver has unparlleled regenerative capacity i.e it has Liver has unparlleled regenerative capacity i.e it hasability to regenerate even when 80 oI is resected. ability to regenerate even when 80 oI is resected. Plays a critical role in the mainataince oI haemostasis. Plays a critical role in the mainataince oI haemostasis. Primary regulatory site Ior metabolism. Primary regulatory site Ior metabolism. Vital organ as evidenced Irom the Iact that the human Vital organ as evidenced Irom the Iact that the humanbeing can survive only Ior 24 being can survive only Ior 24 - - 48hours in the 48hours in the anhepatic state despite Iull supportive therapy. anhepatic state despite Iull supportive therapy. Hepatic lobule Hepatic lobule -- Anatomical unit Anatomical unit onsist oI 50,000 onsist oI 50,000 1,00,000 lobules. 1,00,000 lobules. Hepatocytes arranged cylindrically around Hepatocytes arranged cylindrically aroundthe central vein. the central vein. 4 to 5 portal tracts surround each lobule. 4 to 5 portal tracts surround each lobule. !ortal triad !ortal triad hepatic artery, portal vein hepatic artery, portal vein and bile canaliculi. and bile canaliculi. Hepatic acinus Hepatic acinus- - functional unit functional unit ormed by portal tract in the middle and central ormed by portal tract in the middle and central vein at the periphery. vein at the periphery. zones zones one I (Periportal) one I (Periportal) one II(mid zonal) one II(mid zonal) one III(pericentral) one III(pericentral) one 3 one 3 more susceptible Ior hypoxic iniury more susceptible Ior hypoxic iniury..etabolic diversity within zones etabolic diversity within zonesZone 1(periportal) Zone 1(periportal) Zone (pericentral) Zone (pericentral)Rich in oxygen and the Rich in oxygen and thenutrients nutrientsRelatively poor in O2 and Relatively poor in O2 andnutrients nutrientsLess prone to hypoxia and Less prone to hypoxia anddrug toxicity drug toxicityMore prone Ior hypoxic & More prone Ior hypoxic &drug induced damage drug induced damageOxidative/phaseII reaction Oxidative/phaseII reaction Anaerobic/phaseI reaction Anaerobic/phaseI reactionGlycogen snthesis as well Glycogen snthesis as wellas gluconeogenesis as gluconeogenesisGlycolysis GlycolysisBile salt Iormation Bile salt Iormation Lipolysis LipolysisHepatic blood flow Hepatic blood flow Receives 25 oI cardiac output. Receives 25 oI cardiac output. haracteristic dual blood supply through haracteristic dual blood supply through hepatic artery and portal vein. hepatic artery and portal vein. THB THB 25 to 30 by hepatic artery and 25 to 30 by hepatic artery and70 to 75 by portal vein. 70 to 75 by portal vein. Hepatic oxygen consumption Hepatic oxygen consumption - -45 to 50 45 to 50 by hepatic artery and 50 to 55 by the by hepatic artery and 50 to 55 by theportal vein portal vein Hepatic sinusoids Hepatic sinusoids --- --- central vein central vein --- ------ ---sublobular vein sublobular vein--- --- hepatic vein hepatic vein---- ----ivc ivceatures eatures H.A H.A P.V P.VBl supply Bl supply 25 25- -30 30 70 70- -75 7502 supply 02 supply 45 45- -50 50 50 50- -55 55Spo2 Spo2 98 98 60 60- -75 75Mean BP Mean BP 40 40- -70 70 55- -10 10Intrinsic Regulation Intrinsic Regulation FLOW AUTOREGULATION FLOW AUTOREGULATIONExist even when the SB! reaches 80mmhg. Exist even when the SB! reaches 80mmhg.Myogenic reIlex Myogenic reIlexHigh TM pressure High TM pressure decreases Ilow decreases IlowLow TM pressure Low TM pressure - - increases Ilow increases IlowAutoregulation Doesn`t exist in portal circulation. Autoregulation Doesn`t exist in portal circulation. FOOD RELATED FOOD RELATEDPostprandial hyperosmolarity increases both portal & HB. Postprandial hyperosmolarity increases both portal & HB.Hepatic arterial system undergoes Ilow autoregulation best when the liver is Hepatic arterial system undergoes Ilow autoregulation best when the liver is very active metabolically(postprandial) but not during Iasting state . Hence very active metabolically(postprandial) but not during Iasting state . HenceIlow autoregulation is not likely to be an important mechanism during Ilow autoregulation is not likely to be an important mechanism duringmost anaesthetics, given that they are perIormed in Iasted patients. most anaesthetics, given that they are perIormed in Iasted patients. Intrinsic regulation Intrinsic regulation Hepatic arterial buffer response Hepatic arterial buffer responseDecrease in portal biood Ilow and oxygen Decrease in portal biood Ilow and oxygen tension will increase the hepatic arterial blood Ilow tension will increase the hepatic arterial blood Ilow thru increased periarteriolar adenosine whereas thru increased periarteriolar adenosine whereasincrease in portal blood Ilow decrease the HAB thru increase in portal blood Ilow decrease the HAB thrudecrease in periarteriolar adenosine. decrease in periarteriolar adenosine.In portal HT In portal HT Liver depend upon Liver depend upon hepatic arterial blood Ilow as HABR reaches its hepatic arterial blood Ilow as HABR reaches its upper limit.(oxygen supply and demand should upper limit.(oxygen supply and demand should be careIully maintained) be careIully maintained) Extrinsic regulation Extrinsic regulation Circulatory regulation Circulatory regulationBlood Ilow through portal vein is indirectly regulated by vasoconstriction and Blood Ilow through portal vein is indirectly regulated by vasoconstriction and vasodilatation oI splanchnic arterial bed whereas hepatic arterial Ilow is vasodilatation oI splanchnic arterial bed whereas hepatic arterial Ilow isdirectly regulated thro sympathetic system. directly regulated thro sympathetic system.Hepatic artery Hepatic artery both alpha and beta receptors. both alpha and beta receptors.Portal vein Portal vein - - contains only alpha receptors. contains only alpha receptors. Hormonal regulation Hormonal regulationglucagon glucagon - - increases hepatic arterial blood Ilow. increases hepatic arterial blood Ilow.angiotensin angiotensin - - decreases both portal and hepatic blood Ilow. decreases both portal and hepatic blood Ilow.vasopressin vasopressin - - decreases both portal and hepatic blood Ilow. decreases both portal and hepatic blood Ilow.Extrinsic regulation Extrinsic regulationatecholamines atecholaminesPortal vein Portal vein - - vasoconstriction. vasoconstriction.Hepatic artery Hepatic artery - - vasoconstriction in low vasoconstriction in low dose. dose.vasodilatation in high vasodilatation in highdose. dose. Decreased hepatic blood flow Decreased hepatic blood flow Upright posture Upright posture Hypocarbia Hypocarbia Hypoxia Hypoxia IPPV/PEEP IPPV/PEEP Sepsis Sepsis Haemorrhage Haemorrhage Mesentric traction Mesentric traction Increased IA pressure Increased IA pressure Alpha agonist Alpha agonist Beta blockers Beta blockers Vasopressin Vasopressin Octreotide Octreotide Volatile anaesthetics Volatile anaesthetics Intravenous induction Intravenous inductionagents agents Regional anaesthesia Regional anaesthesiaIncreased hepatic blood flow Increased hepatic blood flow Supine posture Supine posture Postprandial state Postprandial state Hypercarbia Hypercarbia Acidosis Acidosis Acute hepatitis Acute hepatitis Beta agonist Beta agonist Phenobarbitone Phenobarbitone Glucagon Glucagon Dopamine Dopamine Dopeximine Dopeximine Functions of liver Functions of liverA. Albumin synthesis A. Albumin synthesisB. Bilirubin secretion B. Bilirubin secretion. oagulation Iactor synthesis . oagulation Iactor synthesis D. Drug metabolism D. Drug metabolismE. Excretion E. Excretion . at metabolism . at metabolismG. Glucose & Glycogen metabolism G. Glucose & Glycogen metabolismH. Hormone metabolism H. Hormone metabolismI . Immunological Iunction I . Immunological Iunction Drug metabolism Drug metabolism !hase I reaction !hase I reactionarried out by cyto P450 enzyme system. arried out by cyto P450 enzyme system.one 3 rich in cytochrome enzyme system. one 3 rich in cytochrome enzyme system.AIIected early by ageing and liver disease. AIIected early by ageing and liver disease.Most drug hepatotoxicity is mediated by the Most drug hepatotoxicity is mediated by thephase I toxic metabolite. phase I toxic metabolite.Drug metabolism Drug metabolism Phase II Phase II reaction reactionconiugation reaction (glucuronic acid &sulIate). coniugation reaction (glucuronic acid &sulIate).one 1 rich in enzymes involved in coniugation. one 1 rich in enzymes involved in coniugation.AIIected least by ageing and liver disease. AIIected least by ageing and liver disease.Products oI phase 2 reaction are usually less Products oI phase 2 reaction are usually lesstoxic when compared to phase I reaction. toxic when compared to phase I reaction. Extraction ratio Extraction ratio Extraction ratio is the proportion oI the drug that is extracted Extraction ratio is the proportion oI the drug that is extracted in single passage through the liver. in single passage through the liver.ER intrinsic clearance/ HB ER intrinsic clearance/ HBHigh extraction ratio High extraction ratio ( 0.7 ) ( 0.7 )It is aIIected by the hepatic blood Ilow but not by Iactors It is aIIected by the hepatic blood Ilow but not by Iactorsthat increase Iree Iraction oI drug. that increase Iree Iraction oI drug. Dose has to be reduced by as much as 50 but not the Dose has to be reduced by as much as 50 but not theIrequency oI dosing. Irequency oI dosing. Extraction ratio Extraction ratio Low extraction ratio Low extraction ratioIt is aIIected by intrinsic metabolic capacity But it is Ilow independent.i.e It is aIIected by intrinsic metabolic capacity But it is Ilow independent.i.eincrease in Ilow doesn`t increase extraction. increase in Ilow doesn`t increase extraction.AIIected by Iactors that increase Iree Iraction oI the drug. AIIected by Iactors that increase Iree Iraction oI the drug.Reduction in protein binding oI highly protein bound drug causes almost Reduction in protein binding oI highly protein bound drug causes almostdoubling oI Iree Iraction but with poorly bound drug it doesn`t have doubling oI Iree Iraction but with poorly bound drug it doesn`t havemuch eIIect. much eIIect.or low extraction drugs ,interval between the doses should be increased but or low extraction drugs ,interval between the doses should be increased but the drug dosage should not be altered. the drug dosage should not be altered. Capacity limited drugs Capacity limited drugs Thiopentone Thiopentone NM agents( most oI NM agents( most oI the agents the agents Benzodiazepine Benzodiazepine AlIentanil/ methadone AlIentanil/ methadone NSAID NSAID Diuretics Diuretics Anticonvulsant( most oI Anticonvulsant( most oI the drug ) the drug ) Amiodarone/ digitoxin Amiodarone/ digitoxin Antithyroid drugs Antithyroid drugs SulIonyl ureas SulIonyl ureas Steroids Steroids Theophylline Theophylline Flow limited drugs Flow limited drugs Bupivacaine Bupivacaine Lidocaine Lidocaine PropoIol PropoIol Ketamine Ketamine alcium channel alcium channel blockers blockers Beta blockers Beta blockers Nitrates Nitrates Statins Statins Opioid( most oI the Opioid( most oI the opioid) opioid) Naloxone Naloxone SSRI SSRI Tricylic A.Depressant Tricylic A.Depressant Antipyschotic AntipyschoticVolatile agent on HBF Volatile agent on HBFV.Agent V.Agent .bolism .bolism HABF HABF HABR HABR O2 deli O2 deliHalothane Halothane 20 20 46 46 - - - - - - - - Lost Lost Decrease DecreaseEnflurane Enflurane 2.5 2.5- - 8.5 8.5 - - - - - - Lost Lost Decrease DecreaseDesflurane Desflurane 0.02 0.02 - - - - Lost Lost Decrease Decreaseisoflurane isoflurane 0.2 0.2 22 prved prved prved prved preserved preservedsevoflurane sevoflurane 2 2 - - 55 prved prved prved prved preserved preservedNitrous oxide on HBF Nitrous oxide on HBF Nitrous oxide containing anaesthetics does not Nitrous oxide containing anaesthetics does notcause liver iniury in the absence oI impaired cause liver iniury in the absence oI impairedhepatic oxygenation. hepatic oxygenation. Nitrous oxide may exacerbate hepatic damage Nitrous oxide may exacerbate hepatic damage in the presence oI impaired hepatic oxygenation in the presence oI impaired hepatic oxygenation through sympathetic stimulant action and through sympathetic stimulant action andmethionine synthase inhibition. methionine synthase inhibition. Effect of induction agents on Effect of induction agents on hepatic blood flow hepatic blood flow Rapid sequence induction more likely to cause hypotension Rapid sequence induction more likely to cause hypotensionthan conventional induction. than conventional induction. Slow titrated dose oI induction agents cause less hypotension Slow titrated dose oI induction agents cause less hypotension All iv induction agents (single dose) can be saIely given in pt All iv induction agents (single dose) can be saIely given in ptwith liver dysIunction. with liver dysIunction. Ketamine cause decrease in HB thru sympathetic stimulation Ketamine cause decrease in HB thru sympathetic stimulationwhereas other thru dose related decrease in .O & B.P. whereas other thru dose related decrease in .O & B.P.Etomidate Etomidate least decrease least decreaseThiopentone sodium Thiopentone sodium moderate decrease moderate decreasePropoIol PropoIol - - maximum decrease ( 17 ) maximum decrease ( 17 )Effect of hepatic dysfunction on the Effect of hepatic dysfunction on thedrug pharmacokinetics drug pharmacokineticsLiver dysfunction Liver dysfunction Effect on the drug Effect on the drugDecreased PB & Iraction Decreased PB & IractionoI shunt increased oI shunt increasedirst pass metabolism Ior the irst pass metabolism Ior the oral drug decreased oral drug decreasedHypoalbuminemia Hypoalbuminemia Increased unbound Iraction Increased unbound IractionAscites Ascites Increased VOD Increased VODEnzyme content Enzyme content Metabolism either can be Metabolism either can beincreased or decreased increased or decreasedObstructive iaundice Obstructive iaundice Decreased biliary excretion Decreased biliary excretionoI drugs oI drugsEffect of hepatic dysfunction on Effect of hepatic dysfunction on drug pharmacodynamics drug pharmacodynamics Increased sensitivity to NS depressants. Increased sensitivity to NS depressants. Decreased sensitivity to vasopressors. Decreased sensitivity to vasopressors. Enhanced eIIect to anticoagulation. Enhanced eIIect to anticoagulation. Enhanced Na retention Enhanced Na retention NSAID/ Steroid. NSAID/ Steroid. Ascites /oedema may be resistant to diuretics. Ascites /oedema may be resistant to diuretics. Duration oI action oI single dose wont be prolonged Duration oI action oI single dose wont be prolonged as the maior determinant oI 1 dose is redistribution. as the maior determinant oI 1 dose is redistribution. Thiopentone Thiopentone capacity limited drug. Dose has to be capacity limited drug. Dose has to bereduced Ior induction because oI decreased protein reduced Ior induction because oI decreased proteinbinding & reduction in enzyme activitity. binding & reduction in enzyme activitity. Thiopentone Thiopentone- - Higher dose is needed in alcoholic with Higher dose is needed in alcoholic withcompensated liver disease because oI cytoch P450 compensated liver disease because oI cytoch P450enzyme induction by alcohol( Reversed in ESLD). enzyme induction by alcohol( Reversed in ESLD).Effect of hepatic dysfunction on Effect of hepatic dysfunction on induction agents induction agents PropoIol & ketamine in contrast to thiopentone is a PropoIol & ketamine in contrast to thiopentone is aIlow limited drug. Ilow limited drug. PropoIol in contrast to other iv induction agents has PropoIol in contrast to other iv induction agents hasextrahepatic metabolism. extrahepatic metabolism. PropoIol cause the maximum decrease in HB among PropoIol cause the maximum decrease in HB amongthe induction agents. the induction agents. Slow titrated dose oI induction agents with smooth Slow titrated dose oI induction agents with smoothintubation will have little impact on the HB. intubation will have little impact on the HB. Effect of hepatic dysfunction on Effect of hepatic dysfunction on induction agents induction agents Suxamethonium Suxamethonium - - DOA rarely gets prolonged despite DOA rarely gets prolonged despitereduced pseudocholinesterase level. reduced pseudocholinesterase level. DOA oI pancuronium and rocuronium gets prolonged DOA oI pancuronium and rocuronium gets prolongedbecause oI increased VOD and impaired hepatic because oI increased VOD and impaired hepaticmetabolism (altered pharmacokinetics). metabolism (altered pharmacokinetics). DOA oI vecuronium 0.15mg/kg unaIIected. DOA oI vecuronium 0.15mg/kg unaIIected. DOA oI mivacurium gets prolonged because oI the DOA oI mivacurium gets prolonged because oI thereduced plasma cholinesterase level. reduced plasma cholinesterase level.Effect of hepatic dysfunction on Effect of hepatic dysfunction onmuscle relaxants muscle relaxants Atracurium and cis Atracurium and cis- -atracurium atracurium DOA oI both the drug are not DOA oI both the drug are notaIIected as both the drug can undergo organ independent aIIected as both the drug can undergo organ independentelimination thru ester hydrolysis and HoIImans degradation. elimination thru ester hydrolysis and HoIImans degradation. DOA oI above drugs are inIact reduced because oI increased DOA oI above drugs are inIact reduced because oI increased VOD & increased binding to globulins. VOD & increased binding to globulins.To prevent residual muscle weakness in the p.o.period To prevent residual muscle weakness in the p.o.periodbecause oI altered pharmacokinetics, careIul monitoring oI the because oI altered pharmacokinetics, careIul monitoring oI theneuromuscular Iunction is needed. neuromuscular Iunction is needed.Effect of hepatic dysfunction on Effect of hepatic dysfunction onmuscle relaxants muscle relaxants entanyl and suIentanil entanyl and suIentanil - - DOA oI single dose DOA oI single dose is not altered in compensated liver disease. is not altered in compensated liver disease. AlIentanil AlIentanil - - DOA is prolonged because oI the DOA is prolonged because oI theincreased Iree Iraction oI the drug. increased Iree Iraction oI the drug. RemiIentanil duration oI action is unaIIected RemiIentanil duration oI action is unaIIected as it is metabolised by nonspeciIic esterace. as it is metabolised by nonspeciIic esterace. Effect of hepatic dysfunction on Effect of hepatic dysfunction onopioids opioids Drugs in Liver failure Drugs in Liver failureDrugs Drugs Safe Safe Caution Caution!remedication !remedication Lorazepam LorazepamOxazepam OxazepamMidazolam MidazolamDiazepam DiazepamInduction agents Induction agents Single dose all Single dose all are saIe are saIeVolatile agents Volatile agents Nitrous oxide Nitrous oxideIso/sevoIlurane Iso/sevoIluraneDesIlurane DesIluraneEnIlurane EnIluraneDrugs in Liver failure Drugs in Liver failureDrugs Drugs Safe Safe Caution Cautionuscle relaxants uscle relaxants Atracurium Atracuriumcisatracurim cisatracurimSuxamethonium SuxamethoniumPancuronium PancuroniumVecuronium VecuroniumOpioids Opioids entanyl entanyl SuIentanil SuIentanil RemiIentanil RemiIentanil Remaining drug Remaining drugAnalgesics Analgesics Paracetamol Paracetamol Other NSAID Other NSAIDLidocaine LidocaineBupivacaine Bupivacaine Liver function tests Liver function tests Quantitative Quantitative - - assess hepatic blood Ilow and assess hepatic blood Ilow andthe metabolic capacity. the metabolic capacity. Qualitative Qualitative - - assess hepatocellular necrosis. assess hepatocellular necrosis.assess cholestasis. assess cholestasis.assess synthetic Iunction. assess synthetic Iunction.assess excretory Iunction. assess excretory Iunction. Quantitative liver test Quantitative liver test Hepatic blood flow or perfusion Hepatic blood flow or perfusion Bromosulphothalein clearance Bromosulphothalein clearance Indocyanine green clearance Indocyanine green clearance Rose bengal clearance test Rose bengal clearance test Hepatic drug metabolising capacity Hepatic drug metabolising capacity Galactose elimination capacity Galactose elimination capacity Aminopyrine breath test Aminopyrine breath test Antipyrine clearance Antipyrine clearance Monoethylglycinexylidide(MEGX) clearance Monoethylglycinexylidide(MEGX) clearance aIIeine clearance aIIeine clearancemore expensive & time consuming more expensive & time consumingAminotransferace(ALT &AST) Aminotransferace(ALT &AST)Alanine transaminase Alanine transaminase Aspartate transaminase Aspartate transaminaseRelatively liver speciIic Relatively liver speciIic Non speciIic Non speciIicytosol ytosol ytosol and mitochondria ytosol and mitochondriaone 1~3 one 1~3 one 3~1 one 3~1N.value O N.value O 45 IU/L 45 IU/L N.Value 0 N.Value 0 35IU/L 35IU/LHalI liIe is 18hrs HalI liIe is 18hrs HalI liIe is 36hrs HalI liIe is 36hrsExamples for raised ALT &AST Examples for raised ALT &AST inor < 100 IU inor < 100 IU hronic hepatitis B/ hronic hepatitis B/ NASH NASHatty liver atty liver oderate 100 oderate 100- -00IU 00IU Alcoholic hepatitis Alcoholic hepatitisAutoimmune hepatitis Autoimmune hepatitisAcute viral hepatitis Acute viral hepatitisExacerbation oI chronic viral hepatitis Exacerbation oI chronic viral hepatitisplus all the above condition plus all the above condition arked > 00 IU arked > 00 IU Drugs and toxins Drugs and toxinsAcute viral hepatitis Acute viral hepatitisIschaemic hepatitis Ischaemic hepatitisAcute exacerbation oI chronic Acute exacerbation oI chronic hepatitis hepatitisExtrahepatic cholestasis with Extrahepatic cholestasis with cholangitis. cholangitis.Eventhough it is a marker oI hepatocellular necrosis, the degree Eventhough it is a marker oI hepatocellular necrosis, the degreeoI elevation does not correlate with the extent oI necrosis.(no oI elevation does not correlate with the extent oI necrosis.(noprognostic value). prognostic value).Examples for raised ALT &AST Examples for raised ALT &AST Aminotransferace(ALT &AST) Aminotransferace(ALT &AST) AST/ALT ratio may be oI value in diIIerential diagnosis. AST/ALT ratio may be oI value in diIIerential diagnosis. ~4 (wilsons hepatitis) ~4 (wilsons hepatitis)22- -4 (alcoholic liver disease) 4 (alcoholic liver disease)1 (NASH) 1 (NASH) Episodic elevation oI aminotransIeraces is characteristics oI Episodic elevation oI aminotransIeraces is characteristics oI chronic hepatitis . chronic hepatitis . Suspicion oI cirrhosis once AST value exceeds ALT in patient Suspicion oI cirrhosis once AST value exceeds ALT in patientwith chronic hepatitis. with chronic hepatitis. all in aminotransIerace level indicates recovery unless it is all in aminotransIerace level indicates recovery unless it isaccompanied by rise in bilirubin & PT. accompanied by rise in bilirubin & PT.Alkaline phosphatase Alkaline phosphatase Normal value Normal value 30 to 100IU/L(liver and bone contributes more 30 to 100IU/L(liver and bone contributes morethan 80 percent oI the total value). than 80 percent oI the total value). Value 3Iold elevation can be seen in almost any type oI liver Value 3Iold elevation can be seen in almost any type oI liverdisease i.e.elevation oI liver derived ALP is not totally disease i.e.elevation oI liver derived ALP is not totallyspeciIic Ior cholestasis. speciIic Ior cholestasis. Degree oI elevation doesn`t diIIerentiate extrahepatic Irom the Degree oI elevation doesn`t diIIerentiate extrahepatic Irom theintrahepatic cholestasis. intrahepatic cholestasis. ALP elevation in cholestasis is usually ~ 3Iold normal value ALP elevation in cholestasis is usually ~ 3Iold normal value but the level remain elevated Ior 7 but the level remain elevated Ior 7- -10days even aIter the 10days even aIter the obstruction resolves as the halI liIe oI ALP is 7days. obstruction resolves as the halI liIe oI ALP is 7days. Alkaline phosphatase Alkaline phosphatase Value 3 Iold elevation Irom normal value can be seen in normal people. Value 3 Iold elevation Irom normal value can be seen in normal people. Age~ 60yrs Age~ 60yrs upto 1.5 times increase upto 1.5 times increasehildren hildren - - upto 2 times increase upto 2 times increasePregnancy Pregnancy - - upto 3 times increase upto 3 times increaseB.G O & B B.G O & B - - upto 3 times increase aIter a Iatty meal upto 3 times increase aIter a Iatty meal Only recomended use oI GGT & 5 Only recomended use oI GGT & 5- -nucleotidase (most speciIic) is to exclude or to nucleotidase (most speciIic) is to exclude or tosubstantiate, liver is the source oI raise ALP iI the electrophoretic Iractionation substantiate, liver is the source oI raise ALP iI the electrophoretic IractionationoI ALP is not available. oI ALP is not available. Elevated ALP along with 5 Elevated ALP along with 5- -nucleotidase is speciIic Ior the hepatobiliary diseases nucleotidase is speciIic Ior the hepatobiliary diseasesand also helps to R/O physiological ALP elevation. and also helps to R/O physiological ALP elevation. Disproportinate elevation oI ALP and bilirubin suggest the presence oI inIiltrative Disproportinate elevation oI ALP and bilirubin suggest the presence oI inIiltrativeliver disease ( tumour, sarcaidosis,tuberculosis etc). liver disease ( tumour, sarcaidosis,tuberculosis etc). LFT Differentiation of Obstructive LFT Differentiation of Obstructive & &Hepatocellular jaundice Hepatocellular jaundice AST/ALT AST/ALT ALP ALP OBS iaundice OBS iaundice H..iaundice H..iaundice~6 ULN ~6 ULN 2.5ULN 2.5ULN 10 10 90 906 ULN 6 ULN ~2.5ULN ~2.5ULN 90 90 10 10!rothrombin time !rothrombin time Normal prothrombin time 11 Normal prothrombin time 11- -14secs. 14secs. PT ~3 PT ~3- -4s over control value is signiIicant. 4s over control value is signiIicant. Increasing PT is a ominuos sign in patient with acute Increasing PT is a ominuos sign in patient with acutehepatocellular disease (impending hepatic Iailure). hepatocellular disease (impending hepatic Iailure). Prothrombin time in contrast to s.albumin is a useIul Prothrombin time in contrast to s.albumin is a useIul prognostic indicator in acute hepatocellular disease. prognostic indicator in acute hepatocellular disease.( as halI liIe oI is short I to albumin) ( as halI liIe oI is short I to albumin) !rothrombin time !rothrombin time Mild Mild moderate hepatic disease may not be detected by PT as moderate hepatic disease may not be detected by PT as only 30 oI is needed Ior maintaining haemostasis. only 30 oI is needed Ior maintaining haemostasis. holestatic iaundice holestatic iaundice - -correction oI PT by atleast 30within 24 correction oI PT by atleast 30within 24hr oI vit k administration suggest hepatic synthetic Iunction hr oI vit k administration suggest hepatic synthetic Iunction is intact ( prolonged PT due to vit k deIiciency alone). is intact ( prolonged PT due to vit k deIiciency alone). Prolonged PT ~5sec above control not corrected by vitamin k Prolonged PT ~5sec above control not corrected by vitamin k administration is a poor prognostic sign ( in both acute and administration is a poor prognostic sign ( in both acute andchronic liver disease). chronic liver disease). INR is a better indicator than PT because it is a standardized INR is a better indicator than PT because it is a standardizedvalue and is not subiected to lab variability as PT. value and is not subiected to lab variability as PT.Albumin Albumin Normal value Normal value 3.5 to 5.5gm/dl. 3.5 to 5.5gm/dl. Blood level depends upon rate oI synthesis(10 Blood level depends upon rate oI synthesis(10- -15gm/day),rate 15gm/day),rate oI degradation and plasma volume. oI degradation and plasma volume. HalI liIe oI serum albumin is about 21 days. HalI liIe oI serum albumin is about 21 days. Not a good indicator oI acute hepatic dysIunction because oI Not a good indicator oI acute hepatic dysIunction because oIslow turnover ( long halI liIe with 4 degredation per day). slow turnover ( long halI liIe with 4 degredation per day). Albumin Albumin In patients with hepatitis, albumin 3gm/dl should In patients with hepatitis, albumin 3gm/dl shouldraise the possibility oI chronic liver disease. raise the possibility oI chronic liver disease. Decreasing albumin level in patient with chronic liver Decreasing albumin level in patient with chronic liver disease indicates worsening oI liver Iunction in the disease indicates worsening oI liver Iunction in theabsence oI other causes oI hypoalbuminemia. absence oI other causes oI hypoalbuminemia. As long as albumin level is more than 2.5gm per dl, As long as albumin level is more than 2.5gm per dl,Iree or unbound Iraction oI the drug wont be Iree or unbound Iraction oI the drug wont bealtered. altered.Bilirubin Bilirubin Normal total bilirubin value is 1mg/dl.Out oI these, upto Normal total bilirubin value is 1mg/dl.Out oI these, upto0.3mg is coniugated bilirubin. 0.3mg is coniugated bilirubin. Unconiucated bilirubin is toxic Ior neuronal cell whereas the Unconiucated bilirubin is toxic Ior neuronal cell whereas theconiucated bilirubin is responsible Ior renal dysIunction in coniucated bilirubin is responsible Ior renal dysIunction in patient with obstructive iaundice. patient with obstructive iaundice. Bilirubin value rarely exceeds 6mg/dl in Haemolytic anaemia. Bilirubin value rarely exceeds 6mg/dl in Haemolytic anaemia. Intrahepatic cholestasis to cause rise in bilirubin, drainage oI Intrahepatic cholestasis to cause rise in bilirubin, drainage oI bile in ~75 parenchyma should be blocked. bile in ~75 parenchyma should be blocked.Bilirubin Bilirubin In choledocholithisis caused by BD stone, the bilirubin value rarely In choledocholithisis caused by BD stone, the bilirubin value rarelyexceeds 10mg/dl.Sepsis or renal Iailure should be excluded iI the bn exceeds 10mg/dl.Sepsis or renal Iailure should be excluded iI the bn exceeds 30mg/dl in patient with BD stone. exceeds 30mg/dl in patient with BD stone. In cholestatic iaundice due to malignancy, the bilirubin value is ~10mg but In cholestatic iaundice due to malignancy, the bilirubin value is ~10mg butbut less than 30mg/dl. but less than 30mg/dl. ommon bile duct obstruction iI persist Ior more than 30 days will result in ommon bile duct obstruction iI persist Ior more than 30 days will result inliver damage and can lead to the development oI cirrhosis. liver damage and can lead to the development oI cirrhosis. Serum bilirubin will take atleast 1 Serum bilirubin will take atleast 1- -2 weeks to return to normal Iollowing 2 weeks to return to normal Iollowingthe relieI oI obstruction ( halI liIe oI delta bn is 2weeks). the relieI oI obstruction ( halI liIe oI delta bn is 2weeks).Antibodies in liver disease Antibodies in liver diseaseAntimitochondrial AB Antimitochondrial AB Primary biliarycirrhosis Primary biliarycirrhosisP P - - ANA ANA Prm sclerosing cholangitis Prm sclerosing cholangitisAntinuclear antibody Antinuclear antibody Type 1 A.I. Hepatitis Type 1 A.I. HepatitisAnti LKM 1 Anti LKM 1 hronic hep & Type 11 hronic hep & Type 11autoimmune hepatitis autoimmune hepatitisAnti LKM2 Anti LKM2 Drug induced chr hepatitis Drug induced chr hepatitisAnti LKM3 Anti LKM3 hronic hepatitis D hronic hepatitis DLiver biopsy Liver biopsyGold standard Ior evaluation oI patient with chronic liver disease . Liver Gold standard Ior evaluation oI patient with chronic liver disease . Liverbiopsy helps in biopsy helps in# Diagnosis oI various chronic liver disease. # Diagnosis oI various chronic liver disease.#Assessing the severity(grade) and stage oI liver #Assessing the severity(grade) and stage oI liverdisease. disease.#Predicting the prognosis and #Predicting the prognosis and# monitoring the response to treatment. # monitoring the response to treatment. Histological activity index Histological activity index(knodell Ishak score) (knodell Ishak score) Periportal necrosis Periportal necrosis( no necrosis to MLN) ( no necrosis to MLN) Intralobular necrosis Intralobular necrosis(no to marked necrosis) (no to marked necrosis) Portal inIlammation Portal inIlammation(none to marked inIm) (none to marked inIm) ibrosis ibrosis(none to cirrhosis) (none to cirrhosis) Score 0 Score 0- -10 10 Score 0 Score 0- -44 Score 0 Score 0- -44 Score 0 Score 0- -4 total22 4 total22Normal LFT Values Normal LFT ValuesTotal bilirubin Total bilirubin 0.3 0.3- -1mg/dl (DB 0.1 1mg/dl (DB 0.1- -0.3) 0.3)Urine urobilinogen Urine urobilinogen 1 1 4 mg/day 4 mg/day Stercobilinogen Stercobilinogen 40 40 280 mg/day 280 mg/dayAminotransIerases AminotransIerases 0 0 35 IU/L 35 IU/LAlkaline phosphatase Alkaline phosphatase 35 35 100 IU/l 100 IU/lLactate dehydrogense Lactate dehydrogense 90 90 300 IU/L (6 300 IU/L (6- -16) 16)5 5 Nucleotidase Nucleotidase 1 1 18 IU/L 18 IU/LGG Transpeptidase GG Transpeptidase 11 11 64 IU/L 64 IU/L Normal LFT values Normal LFT valuesS.Albumin S.Albumin 3.5 3.5 5.5 gm/dl 5.5 gm/dlS.globulin S.globulin 2.0 2.0 3.5 gm/dl 3.5 gm/dl S.ibrinogen S.ibrinogen 175 175 400mg/dl 400mg/dlPlasma Ammonia Plasma Ammonia 10 10 80 micg/dl 80 micg/dlInternational N ratio International N ratio 1 1 - - 1.3 1.3 Partial thromboplastin Time Partial thromboplastin Time 25 25 - - 35 seconds 35 secondsProthrombin time Prothrombin time 11 11 - - 14 seconds 14 secondsClinical presentation Clinical presentation1. 1. Asymptomatic patient with abnormal LT Asymptomatic patient with abnormal LT2. 2. Acute hepatitis/Acute liver Iailure Acute hepatitis/Acute liver Iailure3. 3. hronic hepatitis hronic hepatitis4. 4. irrhosis(compensated & decompensated) irrhosis(compensated & decompensated)5. 5. Obstructive iaundice(Benign & malignant) Obstructive iaundice(Benign & malignant)Asymptmatic patient with abnormal Asymptmatic patient with abnormalLiver function tests Liver function tests Biochemical screening oI healthy asymptomatic Biochemical screening oI healthy asymptomaticpeople has revealed that upto 6 have abnml people has revealed that upto 6 have abnmlliver enzyme level but the prevalance oI liver liver enzyme level but the prevalance oI liverdisease in the Gen population is around 1. disease in the Gen population is around 1. Liver test must always interpretated along with Liver test must always interpretated along withcareIul history and examination as well as to careIul history and examination as well as toconIirm each abnormal test with another test. conIirm each abnormal test with another test.Evaluation of Isolated Evaluation of IsolatedRaised AST/ALT Raised AST/ALTEvaluation of Isolated Evaluation of IsolatedALT Elevation ALT ElevationAsymptomatic patient with Asymptomatic patient withabnormal LFT abnormal LFT AminotransIerace elavation 3times ULN is not a AminotransIerace elavation 3times ULN is not acontraindication Ior elective surgery iI bilirubin is contraindication Ior elective surgery iI bilirubin iswithin normal limits. within normal limits. Liver ALP 3times ULN is not a /I Ior elective Liver ALP 3times ULN is not a /I Ior elective surgery iI bilirubin is within normal limits. surgery iI bilirubin is within normal limits. Delay surgery when a patient without any risk Iactors Delay surgery when a patient without any risk Iactorsor stigmata oI liver disease is having more than one or stigmata oI liver disease is having more than oneabnormal LT. abnormal LT.II.Acute hepatitis & liver failure II.Acute hepatitis & liver failure Drug induced Drug induced - - Acetiminophen ,Halothane etc Acetiminophen ,Halothane etc Viral inIection Viral inIection Toxins Toxins Autoimmune hepatitis Autoimmune hepatitis Alcoholic hepatitis Alcoholic hepatitis Acute Iatty liver oI pregnancy Acute Iatty liver oI pregnancyOut oI these , Drugs is the most common cause oI acute hepatitis/hepatic Iailure. Out oI these , Drugs is the most common cause oI acute hepatitis/hepatic Iailure.Elective surgery postponed until atleast 30days aIter the liver Iunction tests have Elective surgery postponed until atleast 30days aIter the liver Iunction tests havereturned to normal because oI high perioperative mortality. returned to normal because oI high perioperative mortality.anagement of acute liver failure anagement of acute liver failure Airway control should be done with HE 3 or 4. Airway control should be done with HE 3 or 4. Management oI raised IT. Management oI raised IT. Management oI acid base imbalance. Management oI acid base imbalance. Management oI electrolyte imbalance/hypoglycemia. Management oI electrolyte imbalance/hypoglycemia. Management oI coagulopathy by vit k & P. Management oI coagulopathy by vit k & P. ardiac support with vasopressors. ardiac support with vasopressors. Renal support by HaemoIiltration. Renal support by HaemoIiltration. Respiratory support with mechanical ventilation. Respiratory support with mechanical ventilation.Despite best supportive measures in IU attached to the Despite best supportive measures in IU attached to the LT centre, m.rate approaches 50 LT centre, m.rate approaches 50 - - 80. 80.Indication for OLT in acute Indication for OLT in acutehepatic failure hepatic failureKINGS OLLEGE RITERIA KINGS OLLEGE RITERIAA) Non acetominophen patients A) Non acetominophen patientsPT ~6.5 (INR) or PT ~6.5 (INR) orAny 3 oI the Iollowing variables Any 3 oI the Iollowing variablesNon A Non A- -nonB hepatitis/Drug induced nonB hepatitis/Drug induced Age 10 or ~ 40 yrs Age 10 or ~ 40 yrs S.Bilirubin ~17.6mg/dl S.Bilirubin ~17.6mg/dl PT ~ 3.5 (INR) PT ~ 3.5 (INR) Duration oI icterus beIore HE ~ 7days. Duration oI icterus beIore HE ~ 7days. Acute liver failure(cont) Acute liver failure(cont)B) Acetaminophen patients B) Acetaminophen patientsPH 7.3 or PH 7.3 orPT 6.5 (INR) and PT 6.5 (INR) and S.reatinine~3.4mg/dl. S.reatinine~3.4mg/dl. Acute liver failure (cont) Acute liver failure (cont)Paul Brousse hospital criteria Paul Brousse hospital criteriaHepatic encephalopathy and Hepatic encephalopathy and actor V 20 in patients 30yrs. actor V 20 in patients 30yrs.or oractor V30 in patients ~30yrs. actor V30 in patients ~30yrs.Contraindication for OLT in acute Contraindication for OLT in acuteliver failure liver failure Improving hepatic Iunction Improving hepatic Iunction PP 40mmhg Ior ~2hrs PP 40mmhg Ior ~2hrs Sustained elevation oI IT ~50mmhg Sustained elevation oI IT ~50mmhg Irreversible brain damage Irreversible brain damage Active alcohol or drug abuse Active alcohol or drug abuse Seropositivity Ior HIV Seropositivity Ior HIV Advanced cardiopulmonary disease Advanced cardiopulmonary disease Uncontrolled sepsis Uncontrolled sepsis Widespread thrombosis oI portal/mesentric vein Widespread thrombosis oI portal/mesentric vein III. Chronic liver disease III. Chronic liver diseaseMost common causes oI chronic liver disease (in descending Most common causes oI chronic liver disease (in descendingorder) are order) are hronic hepatitis hronic hepatitis Alcoholic liver disease Alcoholic liver diseaseNASH NASH hronic hepatitis B hronic hepatitis BAutoimmune hepatitis Autoimmune hepatitisSclerosing cholangitis Sclerosing cholangitisPrimary Biliary cirrhosis Primary Biliary cirrhosisHaemochromotosis Haemochromotosis Wilsons disease Wilsons diseaseor chronic hepatitis, Hepatitis c is the most common cause (Alcoholism Ior cirrhosis). or chronic hepatitis, Hepatitis c is the most common cause (Alcoholism Ior cirrhosis).Chronic hepatitis old classification Chronic hepatitis old classification Chronic persistent hepatitis. Chronic persistent hepatitis. Chronic lobular hepatitis. Chronic lobular hepatitis. Chronic active hepatitis. Chronic active hepatitis.hronic active hepatitis in contrast to other two subtypes is a hronic active hepatitis in contrast to other two subtypes is aprog disorder in which the symptoms range Irom recurrent prog disorder in which the symptoms range Irom recurrentmild to severe acute exacerbation that eventually progress mild to severe acute exacerbation that eventually progress to cirrhosis. to cirrhosis. Chronic hepatitis Chronic hepatitisategorization based only on histopathological Ieatures has been ategorization based only on histopathological Ieatures has beenreplaced by classiIication that is much more inIormative based replaced by classiIication that is much more inIormative based upon a combination oI upon a combination oIlinical Ieatures linical IeaturesSerological SerologicalBiochemical and Biochemical and Histological activity index. Histological activity index.Chronic hepatitis new classification Chronic hepatitis new classificationGrade stage Grade stage C!H C!H Mild None or mild Mild None or mild CLH CLH Mild or mod Mild Mild or mod Mild CAH CAH Mild to severe Mild to cirrhosis Mild to severe Mild to cirrhosis hronic hepatitis is said to be active iI there is hronic hepatitis is said to be active iI there is HBV DNA ~ 1o5 copies/ml HBV DNA ~ 1o5 copies/mlchronic active hepatitis picture on LB chronic active hepatitis picture on LBAminotransIeraces~ 2 times ULN. AminotransIeraces~ 2 times ULN.Above Ieatures should be present Ior starting medical Above Ieatures should be present Ior starting medical management. management. Chronic hepatitis B Chronic hepatitis BChronic hepatitis C Chronic hepatitis C Indication Ior medical management is like that oI Indication Ior medical management is like that oIchronic hepatitis B inIection but HV RNA will be chronic hepatitis B inIection but HV RNA will betaken into account. taken into account. HV more likely to progress HV more likely to progress genotype 1& 4 genotype 1& 4chronic active hepatitis picture on LB chronic active hepatitis picture on LBLonger duration oI inIection & Longer duration oI inIection &Immunocompromised states. Immunocompromised states. Alcoholic hepatitis Alcoholic hepatitisAlcoholic hepatitis (acute or acute on chronic) is considered severe iI there Alcoholic hepatitis (acute or acute on chronic) is considered severe iI thereis Ascites is Ascites variceal bleeding variceal bleedingRenal Iailure Renal IailureS.Bilirubin~8mg/dl S.Bilirubin~8mg/dlS.Albumin2.5gm/dl S.Albumin2.5gm/dlAnaemia AnaemiaPT ~ 5 sec over control PT ~ 5 sec over controlPMN~ 5,500cells/mm3 PMN~ 5,500cells/mm3Alcohol discriminant Iunction ~32. Alcohol discriminant Iunction ~32.Alcoholic hepatitis occurs in 10 Alcoholic hepatitis occurs in 10- -20 oI patient with chronic alcoholic 20 oI patient with chronic alcoholiceventhough Iatty liver is present in 90 oI alcoholics. eventhough Iatty liver is present in 90 oI alcoholics. Autoimmune hepatitis Autoimmune hepatitisAutoimmune hepatitis (acute or acute on chronic) in symptomatic patient is said Autoimmune hepatitis (acute or acute on chronic) in symptomatic patient is saidto be severe iI there is to be severe iI there isS.bilirubin~3mg/dl S.bilirubin~3mg/dl. . prolonged PT prolonged PTDecreased S.Albumin Decreased S.AlbuminAminotransIerace~10times ULN. AminotransIerace~10times ULN.S.globulin~2 times ULN in association S.globulin~2 times ULN in associationwith aminotransIeraces~5times ULN. with aminotransIeraces~5times ULN.Bridging necrosis or multilobular collapse Bridging necrosis or multilobular collapse or cirrhosis on LB. or cirrhosis on LB.Anaesthetic consideration for Anaesthetic consideration forChronic Hepatitis Chronic Hepatitis Surgical risk correlate with clinical Ieatures,biochemical Surgical risk correlate with clinical Ieatures,biochemicalIeatures and histological severity oI the disease. Ieatures and histological severity oI the disease. Elective surgery has been reported to be saIe in asymptomatic Elective surgery has been reported to be saIe in asymptomaticpatient with mild patient with mild- -moderate chronic hepatitis. moderate chronic hepatitis. Symptomatic and histological severe H have increased Symptomatic and histological severe H have increasedsurgical risk particularly iI hepatic synthetic or excretory surgical risk particularly iI hepatic synthetic or excretoryIunction is impaired,PHT iI present or bridging/MLN Iunction is impaired,PHT iI present or bridging/MLNnecrosis is seen on liver biopsy. necrosis is seen on liver biopsy. Anaesthetic consideration for Anaesthetic consideration forChronic Hepatitis Chronic Hepatitis hronic alcoholic patient should be abstinent Irom alcohol hronic alcoholic patient should be abstinent Irom alcohol Ior atleast 6 mon to undergo elective procedure. Ior atleast 6 mon to undergo elective procedure. NASH not a contraindication Ior elective surgery ( ~30 NASH not a contraindication Ior elective surgery ( ~30 hepatocytes iI contain Iat hepatocytes iI contain Iat increased mortality) increased mortality) Hemochromatosis Hemochromatosis Evaluate Ior complication such as Evaluate Ior complication such asdiabetes,hypothyrodism and cardiomyopathy. diabetes,hypothyrodism and cardiomyopathy. Wilsons disease Wilsons disease Antipsychiatric medication has to be Antipsychiatric medication has to becontinued(surgery can ppt or aggravate neurological continued(surgery can ppt or aggravate neurologicalsymptoms). symptoms).IV.Complication of Decompensated IV.Complication of Decompensated cirrhosis cirrhosis !ortal HT !ortal HT - - GE Varices GE VaricesPH gastropathy PH gastropathyHyperspleenism HyperspleenismAscites including SBP Ascites including SBP Respiratory Respiratory - - HPS HPS PPHT PPHTHepatic hydrothorax Hepatic hydrothorax Haematological Haematological - - Anaemia AnaemiaThrombocytopenia (qualitative deIect Thrombocytopenia (qualitative deIectalso present) also present)oagulopathy oagulopathy Complication of Decompensated Complication of Decompensated cirrhosis(cont) cirrhosis(cont) Kidney Kidney - - Hepatorenal syndrome Hepatorenal syndrome VS VS - - ardiomyopathy ardiomyopathy NS NS - - Hepatic encepalopathy Hepatic encepalopathy MSK MSK - - Osteoporosis OsteoporosisOsteopenia Osteopenia Nutrition Nutrition - - Malnutrition Malnutrition Respiratory system Respiratory system Ventilation Ventilation- -perIusion mismatch caused by perIusion mismatch caused byimpaired HPV,pleural eIIusion,ascites impaired HPV,pleural eIIusion,ascites& diaphragm dysIunction. & diaphragm dysIunction. Decreases in diIIusion capacity due to intersitial Decreases in diIIusion capacity due to intersitialoedema,increased E & pulmonary HT. oedema,increased E & pulmonary HT. Incidence oI coexisting pulmonary abnormalities Incidence oI coexisting pulmonary abnormalitiesHepatic hydrothorax Hepatic hydrothorax 5 to10 5 to10H.P.synrome H.P.synrome - - 40 to 50 40 to 50PP hypertension PP hypertension - - 4 to 6 4 to 6 ABG & PT ABG & PT - - 40 to 50 40 to 50 Anaesthetic consideration(R.S) Anaesthetic consideration(R.S) Ascites Iluid to be drained preoperatively with simultaneous colloid Ascites Iluid to be drained preoperatively with simultaneous colloid replacement to reduce the splinting eIIect. replacement to reduce the splinting eIIect. oexistent OPD should be optimised & hydrothorax should be oexistent OPD should be optimised & hydrothorax should be treated. treated. hest tube drain is /I in hepatic hydrothorax. hest tube drain is /I in hepatic hydrothorax. Increased risk Ior aspiaration(aspiration prophylaxis & rapid Increased risk Ior aspiaration(aspiration prophylaxis & rapid sequence induction). sequence induction). Avoid PEEP as Iar as possible. Avoid PEEP as Iar as possible. Avoid N2O in patient with OPD & PPH. Avoid N2O in patient with OPD & PPH. Avoid hypoxia(High inspired 02) & hypocarbia. Avoid hypoxia(High inspired 02) & hypocarbia. Response oI OLT is poor in PPH when compared to HPS. Response oI OLT is poor in PPH when compared to HPS. Elective postoperative ventilation Ior maior surgery. Elective postoperative ventilation Ior maior surgery. Extubation should be done when the patient is Iully awake. Extubation should be done when the patient is Iully awake. HPS & hepatic hydrothorax iI present is indication Ior OLT. HPS & hepatic hydrothorax iI present is indication Ior OLT.Cardiovascular system Cardiovascular system Decreased peripheral vascular resistance. Decreased peripheral vascular resistance. Increased cardiac output. Increased cardiac output. Increased blood volume but redistributed. Increased blood volume but redistributed. Low Low- - normal blood pressure with mildly elevated normal blood pressure with mildly elevatedheart rate. heart rate. Decreased eIIective circulatorary volume. Decreased eIIective circulatorary volume. Diminished response to catecholamines. Diminished response to catecholamines. Possible cirrhotic & alcoholic cardiomyopathy. Possible cirrhotic & alcoholic cardiomyopathy.Anaesthetic consideration(CVS) Anaesthetic consideration(CVS) Pain and light plane oI anaesthesia cause decreased HB through Pain and light plane oI anaesthesia cause decreased HB throughsympathetic nervous system. sympathetic nervous system. Hypotensive eIIect oI volume depletion is exacerbated because oI Hypotensive eIIect oI volume depletion is exacerbated because oI impaired vasoconstrictor response to catecholamines. impaired vasoconstrictor response to catecholamines. Redistribution oI blood Ilow Irom splanchnic as well as Skeletal Redistribution oI blood Ilow Irom splanchnic as well as Skeletalmuscle to central circulation is also impaired. muscle to central circulation is also impaired. Blunted vascular response to exogenous vasopressors and volume Blunted vascular response to exogenous vasopressors and volumeexpansion. expansion. Volume assessment and Iluid management thro cvp are oIten misleading Volume assessment and Iluid management thro cvp are oIten misleadingas cvp are oIten elevated despite relative hypovolumia Irom increased as cvp are oIten elevated despite relative hypovolumia Irom increased back pressure in the IV Irom hepatic enlargement,scarring and ascites back pressure in the IV Irom hepatic enlargement,scarring and ascitesinduced increased IA pressure. induced increased IA pressure.Anaesthetic consideration(CVS) Anaesthetic consideration(CVS) PWP/VP guided Iluid management. PWP/VP guided Iluid management. Low threshold Ior starting vasopressors as haemorrhage Low threshold Ior starting vasopressors as haemorrhageis poorly tolerated. is poorly tolerated. Low threshold Ior volume overload as well as to v.presor Low threshold Ior volume overload as well as to v.presor induced pulmonary oedema. induced pulmonary oedema. Propranolol iI used Ior prophylaxis Ior GE varices may Propranolol iI used Ior prophylaxis Ior GE varices maymask the signs oI haemorrhage. mask the signs oI haemorrhage. Diuretics should be used with caution in ascites patient Diuretics should be used with caution in ascites patientwithout oedema (protective eIIect Irom intersitial Iluid without oedema (protective eIIect Irom intersitial Iluidwont be there as in patient with oedema). wont be there as in patient with oedema). irrhotic cardiomyopathy iI present is an indication Ior irrhotic cardiomyopathy iI present is an indication Iorliver transplantation. liver transplantation.Renal system Renal system Decreased renal perIusion and GR. Decreased renal perIusion and GR. Reduction in Iree water clearance. Reduction in Iree water clearance. Reduction in sodium excretion. Reduction in sodium excretion. Hepatorenal syndrome occurs in 10 oI patients with decompensated Hepatorenal syndrome occurs in 10 oI patients with decompensated cirrhosis(100 mortality iI OLT not done). cirrhosis(100 mortality iI OLT not done).Anaesthetic consideration( Kidney) Anaesthetic consideration( Kidney) Urea Ialsely low due to decrease hepatic production. Urea Ialsely low due to decrease hepatic production. Bilirubin lowers the measured s.creatinine(underestimation oI renal Bilirubin lowers the measured s.creatinine(underestimation oI renaldysIunction) dysIunction) Renal Iunction assesed by inulin ,125 I iothalamate or 51 cr Renal Iunction assesed by inulin ,125 I iothalamate or 51 cr- - EDTA clearance. EDTA clearance. Avoid aggressive diuretic therapy.(Precipitate HE & HRS) Avoid aggressive diuretic therapy.(Precipitate HE & HRS) Absence oI response to spironolactone400mg/day & Iurosemide160mg/day Absence oI response to spironolactone400mg/day & Iurosemide160mg/day indicates ascites becomes reIractory (consider LVP or TIPS). indicates ascites becomes reIractory (consider LVP or TIPS). catheterise evening beIore surgery and start iv Iluids while Iasting ( 1 catheterise evening beIore surgery and start iv Iluids while Iasting ( 1- - 2ml/kg/h to 2ml/kg/h to maintain u.o.oI atleast 1ml/kg/hr.( to prevent HRS ) maintain u.o.oI atleast 1ml/kg/hr.( to prevent HRS ) Avoid morning dose oI diuretics beIore elective surgery. Avoid morning dose oI diuretics beIore elective surgery.Kidney(cont) Kidney(cont) PWP/VP guided I.O.Iluid management. PWP/VP guided I.O.Iluid management. I.O chart in the P.O.period. I.O chart in the P.O.period. Avoid hypotension in the P.O.period (meanB.P.10 Avoid hypotension in the P.O.period (meanB.P.10- -20 0I preop value). 20 0I preop value). U.O.oI atleast1ml/kg/hr must be achieved in the I.O.period (iI not mannitol U.O.oI atleast1ml/kg/hr must be achieved in the I.O.period (iI not mannitol or Iurosemide inIusion). or Iurosemide inIusion). Avoid NSAID & aminoglycosides in the I.O.period. Avoid NSAID & aminoglycosides in the I.O.period. irrhotics are also at risk Ior ATN in the postoperativeperiod. irrhotics are also at risk Ior ATN in the postoperativeperiod. HRS iI present is an indication Ior OLT. HRS iI present is an indication Ior OLT.Gastrointestinal system Gastrointestinal system Development oI GE varices & spleenomegaly signiIy Development oI GE varices & spleenomegaly signiIythe development oI portal hypertension. the development oI portal hypertension. Development oI ascites indicates the onset oI hepatic Development oI ascites indicates the onset oI hepatic decompensation. decompensation. GE varices more likely to bleed iI the portal vein GE varices more likely to bleed iI the portal vein pressure exceeds 12mmhg. pressure exceeds 12mmhg. Prognosis aIter development oI ascites is poor.( 50 Prognosis aIter development oI ascites is poor.( 50die within 3years Irom the onset oI diagnosis) die within 3years Irom the onset oI diagnosis)Anaesthetic consideration regarding Anaesthetic consideration regardinggatroesophageal varices gatroesophageal varices Blood loss in GE varices is haemodynamically sgnIt Blood loss in GE varices is haemodynamically sgnItand patient should be managed in IU. and patient should be managed in IU. Propranolol used Ior prophylaxis will mask the signs Propranolol used Ior prophylaxis will mask the signsor haemodymamic eIIects oI haemorrhage. or haemodymamic eIIects oI haemorrhage. Airway should be protected to prevent the risk Irom Airway should be protected to prevent the risk Iromaspiration. aspiration. rystalloid and colloid resuscitation along with the rystalloid and colloid resuscitation along with thepharmacological measures such as vasopressin, pharmacological measures such as vasopressin,somatostatin or octreotide. somatostatin or octreotide. Alteast 8 Alteast 8- -12 units oI blood should be crossmatched 12 units oI blood should be crossmatchedduring the resucscitation period. during the resucscitation period. P should be given iI the PT is 1.5 times more than P should be given iI the PT is 1.5 times more thanthe control value. the control value. are should be taken to prevent volume overload as are should be taken to prevent volume overload as the baseline SBP oI most cirrhotics is 85 to 95mmhg the baseline SBP oI most cirrhotics is 85 to 95mmhg(volume overload increases hge). (volume overload increases hge). Endoscopy should be done within 12hrs once the Endoscopy should be done within 12hrs once thepatient is haemodynamically stable. patient is haemodynamically stable. Anaesthetic consideration regarding Anaesthetic consideration regardinggatroesophageal varices gatroesophageal varices Ascites increases the risk oI aspiration by increasing intra Ascites increases the risk oI aspiration by increasing intra- -abdominal pressure ( also decreased GITmotility & GERD abdominal pressure ( also decreased GITmotility & GERDdue to hiatal hernia in the cirrhotics). due to hiatal hernia in the cirrhotics). PID can be prevented by concurrent administration oI salt PID can be prevented by concurrent administration oI saltpoor albumin or other colloid. poor albumin or other colloid. Ascites is said to be reIractory iI there is no response to the Ascites is said to be reIractory iI there is no response to themaximum dose oI Iurosemide and spiranolactone. maximum dose oI Iurosemide and spiranolactone. TIPS should be considered Ior patient with reIractory ascites TIPS should be considered Ior patient with reIractory asciteswho is listed Ior OLT. who is listed Ior OLT. Tense and reIractory ascites should be drained adequately Tense and reIractory ascites should be drained adequately beIore surgery ( signiIicant intra and postop comp.). beIore surgery ( signiIicant intra and postop comp.).Anaesthetic consideration regarding Anaesthetic consideration regardingascites ascitesAscites Anaesthetic consideration Ascites Anaesthetic consideration !reoperative !reoperative Respiratory distress Respiratory distressHypotension iI inadeq replaced Hypotension iI inadeq replacedaIter LVP aIter LVPHepatic hydrothorax Hepatic hydrothoraxRisk Ior SBP (50 mortality) Risk Ior SBP (50 mortality)Intraoperative Intraoperative Risk Ior aspiration Risk Ior aspirationalse high VP alse high VPHaemodynamic instability Haemodynamic instabilitySplinting eIIect to diaphragm Splinting eIIect to diaphragmIncreased volume oI distribution Increased volume oI distributionPostoperative Postoperative - - Wound dehiscence Wound dehiscenceAbdominal wall herniation Abdominal wall herniationAtelectasis Atelectasis1 litre oI ascitic Iluid 50ml oI 25 albumin( i.e 1 litre 1 litre oI ascitic Iluid 50ml oI 25 albumin( i.e 1 litreroughly contains 10gm oI protein). roughly contains 10gm oI protein).Albumin should be idealy used in case oI LVP(~5L/day). Albumin should be idealy used in case oI LVP(~5L/day).HalI oI the albumin during the procedure and the other 6 hrs HalI oI the albumin during the procedure and the other 6 hrs later. later. Ascites Anaesthetic consideration Ascites Anaesthetic consideration Haematological system Haematological system Anaemia is common with chronic liver disease. Anaemia is common with chronic liver disease. Thrombocytopenia(qualitative as well). Thrombocytopenia(qualitative as well). Mild thrombocytopenia is oIten the Iirst maniIestation oI worsening oI Mild thrombocytopenia is oIten the Iirst maniIestation oI worsening oI Iibrosis in patient with chronic hepatitis. Iibrosis in patient with chronic hepatitis. Prothrombin time & partial thromboplastin time is prolonged (mild Prothrombin time & partial thromboplastin time is prolonged (mild- -moderate prolongation). moderate prolongation). ibrinogen level will be normal ( low Iibrinogen level with severe ibrinogen level will be normal ( low Iibrinogen level with severethrombocytopenia R/O DI ). thrombocytopenia R/O DI ). Drugs used to treat chronic hepatitis can cause anaemia. Drugs used to treat chronic hepatitis can cause anaemia.RiIampin RiIampin Hemolytic anaemia Hemolytic anaemiaInterIeron InterIeron- - bone marrow suppression bone marrow suppressionAnaes.consideration(Haematology) Anaes.consideration(Haematology) Liver biopsy can be saIely perIormed iI plateletcount~50,000/mm3 and PT as well Liver biopsy can be saIely perIormed iI plateletcount~50,000/mm3 and PT as wellas APTT do not exceed 1.5 times the control value( BT not a reliable indicator). as APTT do not exceed 1.5 times the control value( BT not a reliable indicator). Avoid drugs that precipitate bleeding such as NSAID/ WarIarin. Avoid drugs that precipitate bleeding such as NSAID/ WarIarin. Avoid IM iniection to prevent haematoma. Avoid IM iniection to prevent haematoma. Haematocrit should be maintained around 30 in the perioperative period. Haematocrit should be maintained around 30 in the perioperative period. Anaemia should corrected preoperatively preIerably with packed cell or Iresh Anaemia should corrected preoperatively preIerably with packed cell or Ireshwhole blood ( Balanced against the risk oI inducing HE Irom haemolysed RB). whole blood ( Balanced against the risk oI inducing HE Irom haemolysed RB). Thrombocytopenia in hyperspleenism as a rule is mild( severe thrombocytopenia Thrombocytopenia in hyperspleenism as a rule is mild( severe thrombocytopenia indicates the development oI DI). indicates the development oI DI). Haematology (Cont) Haematology (Cont) Thrombocytopenia iI present should be preoperatively corrected. Thrombocytopenia iI present should be preoperatively corrected.Exploratory laprotomy~50,000/mm3 Exploratory laprotomy~50,000/mm3losed space surgery~1Lakh/mm3 losed space surgery~1Lakh/mm3 PT and APTT becomes abnormal only with severe deIiciency oI (abnormal PT and APTT becomes abnormal only with severe deIiciency oI (abnormalwith 30 oI normal level). with 30 oI normal level). PT and APTT iI prolonged should be corrected to be within 1.5times the control PT and APTT iI prolonged should be corrected to be within 1.5times the controlvalue.(Risk oI Hge increases iI PT & APTT exceeds 1.5 times the control value). value.(Risk oI Hge increases iI PT & APTT exceeds 1.5 times the control value). ailure oI PT and APTT to respond to vitK/P indicates poor prognosis. ailure oI PT and APTT to respond to vitK/P indicates poor prognosis. P must be transIused iust prior to procedure and repeated every 8 P must be transIused iust prior to procedure and repeated every 8- -12hrs to 12hrs tomaintain acceptable coagulation parameters( chance oI volume overload maintain acceptable coagulation parameters( chance oI volume overload- -Exchange plasma transIusion). Exchange plasma transIusion). Haematology(cont) Haematology(cont) Adequate blood/ blood component should be arranged prior to surgery. Adequate blood/ blood component should be arranged prior to surgery. Invasive arterial BP preIerable than NIBP(repeated NIBP cause bruises). Invasive arterial BP preIerable than NIBP(repeated NIBP cause bruises). Blood loss should be closely monitored &should be corrected immedietly Blood loss should be closely monitored &should be corrected immedietly(Hematocrit maintained around 30). (Hematocrit maintained around 30). P should be given when crystalloid,colloid or packed cells are given to P should be given when crystalloid,colloid or packed cells are given toreplace blood loss.( 1unit P1unit packed cells250ml crystalloid) replace blood loss.( 1unit P1unit packed cells250ml crystalloid) Hypothermia should be avoided (humidiIied gases,warm ivI,warming Hypothermia should be avoided (humidiIied gases,warm ivI,warming blankets,Iorced air warming devices & blood warmer). blankets,Iorced air warming devices & blood warmer).Haematology(cont) Haematology(cont) Blood loss can be minimised by perioperative administration oI tranexemic Blood loss can be minimised by perioperative administration oI tranexemic acid (prostate & ortho surgeries). acid (prostate & ortho surgeries). orrect/prevent I.O. Iactors that increases bleeding(dilution,hpypothermia orrect/prevent I.O. Iactors that increases bleeding(dilution,hpypothermiahypocalcemia & acidosis). hypocalcemia & acidosis). Thromboelastography Ior I.O. assesment oI coagulation parameters. Thromboelastography Ior I.O. assesment oI coagulation parameters. Universal precautions in patients with hepatitis (30 Universal precautions in patients with hepatitis (30 - - HepB & 3 HepB & 3 - -Hep) Hep) Even 0.04ml blood may be enough to inIect an anaesthesiologist. Even 0.04ml blood may be enough to inIect an anaesthesiologist. RA not contraindicated iI coagulation parameters are within normal. RA not contraindicated iI coagulation parameters are within normal.Causes of bleeding in liver Causes of bleeding in liver disease disease Anatomical Iactors Anatomical Iactors gastroesophageal varices gastroesophageal varicespeptic ulcer peptic ulcergastritis gastritishaemoorhoid haemoorhoid Thrombocytopenia Thrombocytopenia Hepatic Iunction abnormalities Hepatic Iunction abnormalitiesDecreased synthesis oI procoagulant protein Decreased synthesis oI procoagulant proteinDecreased synthesis oI coagulation inhibitors Decreased synthesis oI coagulation inhibitors Causes of bleeding in liver Causes of bleeding in liver disease(cont) disease(cont)ailure to clear activated coagulation Iactors ailure to clear activated coagulation IactorsImpaired absorbtion and metabolism oI vit k Impaired absorbtion and metabolism oI vit kSynthesis oI abnormal Iibrinogen Synthesis oI abnormal Iibrinogen Intraoperative Iactors Intraoperative Iactors Hypothermia HypothermiaDilution DilutionHypocalcemia HypocalcemiaAcidosis Acidosis !latelet count. !latelet count.~1lakh/mm ~1lakh/mm saIe saIe70,000 70,000- -1lakh 1lakh - - saIe iI cg scn is wnl saIe iI cg scn is wnl 70,000/mm3 70,000/mm3 - - unsaIe unsaIe !rothrombin time !rothrombin timeINR~1.5 INR~1.5 - - unsaIe unsaIe Activated partial thromboplastin time Activated partial thromboplastin timeAPTT~40sec APTT~40sec - -unsaIe unsaIeCoagulation parameters and Coagulation parameters and neuraxial block neuraxial blockNeuraxial anaesthesia(cont) Neuraxial anaesthesia(cont) Epidural preIerred than spinal anaesthesia. Epidural preIerred than spinal anaesthesia. LA dose should be titrated.(Ilow limited drug) LA dose should be titrated.(Ilow limited drug) Hypotension more likely with high spinal( T4 level Hypotension more likely with high spinal( T4 level 20 decrease in HB) but saIe Ior lower limb 20 decrease in HB) but saIe Ior lower limbprocedures. procedures. Strict aseptic precautions Strict aseptic precautions increased susceptiblity increased susceptiblityIor inIection. Ior inIection. Epidural UseIul Ior postopanalgesia/decreases P.O Epidural UseIul Ior postopanalgesia/decreases P.Opulmonary complication. pulmonary complication.Indication for OLT in chronic Indication for OLT in chronicliver disease liver diseaseA) holestatic condition (speciIic) A) holestatic condition (speciIic)S.bilirubin~10mg S.bilirubin~10mgRecurrent bacterial cholangitis Recurrent bacterial cholangitisprogressive cholestatic bone disease progressive cholestatic bone diseaseIntractable pruritus. Intractable pruritus.B) Parenchymal condition (speciIic) B) Parenchymal condition (speciIic)S.Albumin 3gm/dl S.Albumin 3gm/dlPT ~ 3 sec above control PT ~ 3 sec above control Indication for OLT in chronic Indication for OLT in chronicliver disease liver disease) ommon to both condition ) ommon to both conditionRecurrent or severe HE Recurrent or severe HEReIractory ascites ReIractory ascitesSpontaneous bacterial peritonitis Spontaneous bacterial peritonitisRecurrent PHT bleeding Recurrent PHT bleedingHepatorenal syndrome Hepatorenal syndromeHPS / H. Hydrothorax HPS / H. Hydrothoraxirrhotic cardiomyopathy irrhotic cardiomyopathyDetection oI small H Detection oI small HProgressive malnutrition Progressive malnutritionSevere chronic Iatique & weakness. Severe chronic Iatique & weakness.V.Cholestatic jaundice V.Cholestatic jaundice Diff. Features Diff. Features Intrahepatic Intrahepatic Extrahepatic ExtrahepaticFever Fever Absent Absent Present PresentAbdominal pain Abdominal pain Absent Absent Present Present!rodromal symptom !rodromal symptom Present Present Absent AbsentH/O of surgery H/O of surgery Absent Absent Present PresentCirrhosis stigmata Cirrhosis stigmata Present Present Absent Absent Cholestatic jaundice Cholestatic jaundiceDiff. Features Diff. Features Intrahepatic Intrahepatic Extrahepatic Extrahepatic!alpable gallbladder !alpable gallbladder Absent Absent Present PresentTotal bilirubin Total bilirubin Variable Variable 30mg/dl 30mg/dlB.Dilatation on USG B.Dilatation on USG Absent Absent Present PresentERC! ERC! Not needed Not needed Needed NeededVit K treatment Vit K treatment Variable Variable Responsive ResponsiveBenign vs alignant surgical Benign vs alignant surgical jaundice jaundiceDiff.Features Diff.Features Benign Benign alignant alignant ode of onset ode of onset Acute Acute Insidious InsidiousFever with chills Fever with chills Present Present Absent AbsentAbdominal pain Abdominal pain Present Present Absent Absent!alpable gallbladder !alpable gallbladder Absent Absent Present PresentTotal bilirubin Total bilirubin 10mg/dl 10mg/dl 10 10- -30mg/dl 30mg/dlAnaesthetic consideration in Anaesthetic consideration inobstructive jaundice obstructive jaundiceIt includes It includesoagulopathy oagulopathyEndotoxemia EndotoxemiaHaemodynamic instability Haemodynamic instabilityRenal Iailure Renal IailureAltered drug handling due to cholestasis Altered drug handling due to cholestasisImpaired wound healing. Impaired wound healing. Measures taken to to reduce the renal Iailure is responsive better in benign Measures taken to to reduce the renal Iailure is responsive better in benign rather than malign condition.In malignancy only way to reduce the rather than malign condition.In malignancy only way to reduce theincidence oI renal Iailure is to maintain adequate iv volume and incidence oI renal Iailure is to maintain adequate iv volume andperIusion pressure. perIusion pressure.Effect of obstructive jaundice on the Effect of obstructive jaundice on thecardivascular system cardivascular system Negative inotropic eIIect by bile salt. Negative inotropic eIIect by bile salt. Negative chronotropic eIIect by bile salt. Negative chronotropic eIIect by bile salt. Altered haemodynamic response to haemorrhage. Altered haemodynamic response to haemorrhage. Blunted vascular response to vasopressor and volume Blunted vascular response to vasopressor and volumeexpansion. expansion. Jaundiced induced cardiomyopathy. Jaundiced induced cardiomyopathy. Haemodynamic instability caused by the bile salts & Haemodynamic instability caused by the bile salts &endotoxin on the cardovascular Iunction. endotoxin on the cardovascular Iunction. Diuretic and the natriuretic eIIect oI bile salt. Diuretic and the natriuretic eIIect oI bile salt. Reduced renal perIusion because oI enhanced renal Reduced renal perIusion because oI enhanced renalvascular reactivity to endogenous vasopressors. vascular reactivity to endogenous vasopressors. Direct nephrotoxic eIIect by bile salt and coniugated Direct nephrotoxic eIIect by bile salt and coniugatedbilirubin (controversial) bilirubin (controversial) Renal tubule blockade oI bilirubin cast may Iurther Renal tubule blockade oI bilirubin cast may Iurtherpotentiate the renal iniury. potentiate the renal iniury. Effect of obstructive jaundice on the Effect of obstructive jaundice on theRenal function Renal function easures to prevent perioperative easures to prevent perioperativerenal failure renal failure Maintainence oI adequate iv volume( most important oI all the Maintainence oI adequate iv volume( most important oI all themeasures). measures). Avoid NSAID & AMINOGLOSIDES. Avoid NSAID & AMINOGLOSIDES. Oral lactulose/ ursodeoxycholic acid. Oral lactulose/ ursodeoxycholic acid. Endoscopic internal biliary drainage. Endoscopic internal biliary drainage. Preoperative and postoperative mannitol iI the Bn~8mg per dl Preoperative and postoperative mannitol iI the Bn~8mg per dl (controversial role). (controversial role).Dopamine/ Iurosemide has no role. Dopamine/ Iurosemide has no role.Except Ior maintainence oI adequate iv volume and avoidance oI Except Ior maintainence oI adequate iv volume and avoidance oINSAID, all other measures are controversial in malignant NSAID, all other measures are controversial in malignantiaundice. iaundice.Antiendotoxin measures Antiendotoxin measures Avoid oral antibiotics. Avoid oral antibiotics. Avoid percutaneous external drainage. Avoid percutaneous external drainage. Oral lactulose. Oral lactulose. Oral ursodeoxycholic acid. Oral ursodeoxycholic acid. Endoscopic internal biliary drainage. Endoscopic internal biliary drainage. Experimental drugs Experimental drugs Taurolidine TaurolidineRiIaximin RiIaximinPolymyxin. Polymyxin. !reoperative evaluation !reoperative evaluation omplete history with clinical examination. omplete history with clinical examination. Investigation. Investigation. Risk assesment. Risk assesment. Management oI complication due to liver disease. Management oI complication due to liver disease. Preoperative optimisation oI modiIiable risk Iactors Preoperative optimisation oI modiIiable risk Iactorsin hild B status patient and obstructive iaundice. in hild B status patient and obstructive iaundice. Premedication and instruction beIore surgery(include Premedication and instruction beIore surgery(includethe inIormed high risk consent). the inIormed high risk consent). !reoperative investigation !reoperative investigation Haematological Blood grouping/typing Haematological Blood grouping/typingHaemoglobin/ HT Haemoglobin/ HTWB count WB countPlatelet count Platelet countBleeding Time Bleeding TimePT / INR PT / INRAPTT APTT Liver Iunction tests. Liver Iunction tests. Serology Ior viral hepatitis. Serology Ior viral hepatitis. !reoperative investigation(cont) !reoperative investigation(cont) etabolic / Renal etabolic / RenalBlood glucose Blood glucoseS.Electrolytes / S.alcium S.Electrolytes / S.alciumBlood urea Blood ureaS.reatinine S.reatinineU.Electrolytes U.Electrolytes Cardiorespiratory Cardiorespiratoryhest x hest x- -ray rayEG EGEHO ( iI needed) EHO ( iI needed)PT/ABG ( iI needed) . PT/ABG ( iI needed) . Risk assesment Risk assesment hild hild Pugh score Pugh score MELD score ~ 18 years MELD score ~ 18 years PELD score 18 years PELD score 18 years Garrisons score Garrisons score Dixon Dixon reidman score reidman score Knodell Knodell Ishak score Ior chronic hepatitis Ishak score Ior chronic hepatitis ASA lassiIication ASA lassiIication POSSUM score POSSUM scoreodified Child odified Child- -!ugh Score !ugh Score!arameters !arameters 11 22 Albumin(g/dl) Albumin(g/dl) ~3.5 ~3.5 2.8 2.8 - - 3.5 3.5 2.8 2.8INR INR 1.7 1.7 1.7 1.7 - - 2.3 2.3 ~2.3 ~2.3Bilirubin(mg/dl) Bilirubin(mg/dl) 2 2 2 2 - - 33 ~3 ~3Ascites Ascites Absent Absent Moderate Moderate Tense TenseEncephalopathy Encephalopathy None None Grade I Grade I- -II II Grade III Grade III- -IV IVClass Classortality ortalityA 5 to 6 A 5 to 610 10B 7 to 9 B 7 to 931 3110 to 15 10 to 1576 76CHILD SCORE AND SURGERY CHILD SCORE AND SURGERY hild A hild A - - saIely undergo elective surgery. saIely undergo elective surgery. hild B hild B - - may undergo elective surgery aIter may undergo elective surgery aIteroptimisation with caution. optimisation with caution.accepted criterion Ior listing to OLT. accepted criterion Ior listing to OLT. Child C Child C - - contraindication Ior elective surgery. contraindication Ior elective surgery.ELD SCORE ELD SCORE Obiective score ( no interindividual variation in contrast Obiective score ( no interindividual variation in contrastto child to child pugh score that has 2 subiective component). pugh score that has 2 subiective component). Designed to predict survival aIter TIPS 2 control bleeding Designed to predict survival aIter TIPS 2 control bleedingvarices but now used Ior prioritizing patients Ior OLT. varices but now used Ior prioritizing patients Ior OLT.eld score eld score 3.78 x Log (BN) 11.2 x Log (INR) 3.78 x Log (BN) 11.2 x Log (INR) 9.57x Log(cr) 6.43 (x 0 Ior alcoholic and 9.57x Log(cr) 6.43 (x 0 Ior alcoholic andcholestatic condition , x 1 Ior remainder) cholestatic condition , x 1 Ior remainder) ELD SCORE AND SURGERY ELD SCORE AND SURGERY Meld 10 Meld 10 - - saIely undergo elective surgery. saIely undergo elective surgery. Meld10 Meld10 - -15 15 - - may undergo elective surgery aIter may undergo elective surgery aIteroptimisation with caution. optimisation with caution.accepted criterion Ior listing to OLT. accepted criterion Ior listing to OLT. Meld ~ 15 Meld ~ 15 - - contraindication Ior elective surgery. contraindication Ior elective surgery.Garrison risk factors for Garrison risk factors forcirrhosis cirrhosis GARRISON et al GARRISON et al Iactors associated with increased Iactors associated with increasedpost operative mortality post operative mortalityS.albumin 3gm/dl S.albumin 3gm/dlpresence oI inIection presence oI inIectionWB ~10.000/cu.mm WB ~10.000/cu.mmTreatment with more than two antibiotics Treatment with more than two antibioticsS.bilirubin~3mg/dl S.bilirubin~3mg/dlPT~1.5sec over control PT~1.5sec over control Presence oI ascities Presence oI ascitiesMalnutrition MalnutritionEmergency surgery Emergency surgeryRisk factors in obstructive jaundice Risk factors in obstructive jaundiceDIXON DIXON REIDMAN RISK ATORS REIDMAN RISK ATORS S.Bilirubin ~ 11mg/dl S.Bilirubin ~ 11mg/dl Malignant obstruction Malignant obstruction Haematocrit 30 Haematocrit 30 Renal Iailure Renal Iailure holangitis holangitis Hypoalbuminemia Hypoalbuminemia II at least 3 oI above mortality 60 II at least 3 oI above mortality 60 II none oI above mortality 5 II none oI above mortality 5ASA physical status classification ASA physical status classification ASA I ASA I Normal healthy patient. Normal healthy patient. ASA II ASA II Patient with mild systemic disease. Patient with mild systemic disease. ASA III ASA III Patient with severe systemic disease. Patient with severe systemic disease. but is not incapacitating. but is not incapacitating. ASA IV ASA IV Patient with severe systemic disease Patient with severe systemic diseasethat is a constant threat to liIe. that is a constant threat to liIe. ASA V ASA V Moribund patient who is not expected Moribund patient who is not expectedto survive without the operation. to survive without the operation. ASA VI ASA VI Brain dead patient. Brain dead patient. EXA!LES FOR ASA CLASSES EXA!LES FOR ASA CLASSESASA II ASA II - - igarette smoking without OPD igarette smoking without OPDMore than minimal drinking More than minimal drinkingMild obesity Mild obesityWell controlled HT or DM without systemic Well controlled HT or DM without systemicor end organ involvement or end organ involvementASA III ASA III Morbid obesity Morbid obesityActive hepatitis Active hepatitishronic renal Iailure/ ESRD hronic renal Iailure/ ESRDMild OPD ( well controlled) Mild OPD ( well controlled)Poorly controlled HT or DM with systemic Poorly controlled HT or DM with systemic involvement involvementStable angina, MI, VA, H, coronary Stable angina, MI, VA, H, coronarystent over 6 months ago stent over 6 months agoEiection Iraction 40 Eiection Iraction 40 EXA!LES FOR ASA CLASSES EXA!LES FOR ASA CLASSESASA IV ASA IV Hepatorenal syndrome Hepatorenal syndromeUnstble angina, MI,VA,oronary stent Unstble angina, MI,VA,oronary stentoI 6 months duration oI 6 months durationSymptomatic H Symptomatic H Eiection Iraction 25 Eiection Iraction 25 Moderate to severe OPD Moderate to severe OPDASA V ASA V - - MODS/Sepsis with HD instability MODS/Sepsis with HD instabilityPoorly controlled coagulopathy Poorly controlled coagulopathy EXA!LES FOR ASA CLASSES EXA!LES FOR ASA CLASSESASA I & II ASA I & II - - 0.3 0.3 ASA III ASA III - - 4 to 5 4 to 5ASA IV ASA IV - - 25 to 30 25 to 30ASA V ASA V - - ~ 70 ~ 70 ORTALITY IN ASA SUBCLASS ORTALITY IN ASA SUBCLASSContraindication for elective surgery Contraindication for elective surgery Acute viral hepatitis Acute viral hepatitis Acute alcoholic hepatitis Acute alcoholic hepatitis ulminant hepatic Iailure ulminant hepatic Iailure Severe chronic hepatitis Severe chronic hepatitis hild's class cirrhosis hild's class cirrhosis Severe coagulopathy (pl count 3s despite oI vitamin k administration) Hypoxia(Po260mmhg) Hypoxia(Po260mmhg) ardiomyopathy/ heart Iailure ardiomyopathy/ heart Iailure Hepatorenal syndrome Hepatorenal syndromeHigh risk factors for surgery High risk factors for surgeryA) Type oI surgery A) Type oI surgeryEmergency ~ Elective Emergency ~ ElectiveIntraabdominal ~ Extraabddominal Intraabdominal ~ ExtraabddominalUpperabdomen ~ Intraabdomen Upperabdomen ~ IntraabdomenNonlaproscopic ~ laprascopic Nonlaproscopic ~ laprascopicEmergency T ~ Elective T Emergency T ~ Elective THepatic resection with MELD Hepatic resection with MELD score~8/PS~6 score~8/PS~6Prior abdominal surgery Prior abdominal surgery High risk factors for High risk factors for surgery(cont) surgery(cont)BB) haracteristics oI patient ) haracteristics oI patienthild class ~B~A. hild class ~B~A.Meld score ~ 15. Meld score ~ 15.High ASA status. High ASA status.S.bilirubin ~3mg/dl(~11mg in obstructive LD). S.bilirubin ~3mg/dl(~11mg in obstructive LD).Malignant ~ Benign iaundice. Malignant ~ Benign iaundice.S.Albumin 3gm/dl. S.Albumin 3gm/dl.HT 30. HT 30.Acute ~ chronic encephalopathy. Acute ~ chronic encephalopathy.Grade 3 or 4 encephalopathy. Grade 3 or 4 encephalopathy.Prolonged PT ~3 sec above control(not corrected with vit K) Prolonged PT ~3 sec above control(not corrected with vit K)complication oI cirrhosis(Ascites,GE Varices,HRS,HPS,PPHT complication oI cirrhosis(Ascites,GE Varices,HRS,HPS,PPHTHydrothorax,ardiomyopathy). Hydrothorax,ardiomyopathy).Abnormal quantitative liver Iunction tests. Abnormal quantitative liver Iunction tests.Optimisation before surgery Optimisation before surgery Ascites to be drained beIore surgery iI possible. Ascites to be drained beIore surgery iI possible. Hydrothorax should be treated beIore surgery. Hydrothorax should be treated beIore surgery. Encephalopathy should be corrected beIore surgery. Encephalopathy should be corrected beIore surgery. Anemia should be corrected beIore surgery. Anemia should be corrected beIore surgery. oagulopathy should be corrected beIore surgery. oagulopathy should be corrected beIore surgery. Electrolyte imbalance should be corrected beIore the surgery. Electrolyte imbalance should be corrected beIore the surgery. Nutrional needs should be addressed by either enteral or by Nutrional needs should be addressed by either enteral or byparentral route beIore surgery. parentral route beIore surgery. Alcohol abstinence Ior atleast 6 months is needed Ior elective Alcohol abstinence Ior atleast 6 months is needed Ior elective suregery. suregery. Antiendotoxin measures to reduce the renal dysIunction. Antiendotoxin measures to reduce the renal dysIunction. oexisting illness( OPD, HT & DM) should be optimised. oexisting illness( OPD, HT & DM) should be optimised.Ascites Treatment Ascites Treatment Salt restriction Salt restriction luid restriction luid restriction spiranolactone spiranolactone urosemide urosemide Albumin Albumin Not ~ 2 gm per day Not ~ 2 gm per day 800 800- -1000ml/day iI serum 1000ml/day iI serum sodium 125meq/L sodium 125meq/L Dose 100mg per day Dose 100mg per day (max dose 400mg) (max dose 400mg) Dose 40mg per day Dose 40mg per day(max dose 160mg) (max dose 160mg) 88- -10g/L oI Iluid removed 10g/L oI Iluid removed(iI ~ 5L removed) (iI ~ 5L removed) Coagulopathy Treatment Coagulopathy Treatment Vit K 10 mg sc or slow iv over 20 minutes Ior 3 Vit K 10 mg sc or slow iv over 20 minutes Ior 3days(altered PT due to vit K deI iI there is 30 days(altered PT due to vit K deI iI there is 30improvement in the Iirst 24 hours). improvement in the Iirst 24 hours). P in case oI emergency rapid correction or in P in case oI emergency rapid correction or invit K unresponsive patients. vit K unresponsive patients. Platelet transIusion in case oI thrombocytopenia. Platelet transIusion in case oI thrombocytopenia. ryoprecipitate iI Iibrinogen75mg/dl. ryoprecipitate iI Iibrinogen75mg/dl. DDAVP iI BT ~ 12 minutes. DDAVP iI BT ~ 12 minutes.Hepatic encephalopathy treatment Hepatic encephalopathy treatment are oI airway,haemodynamic,metabolic are oI airway,haemodynamic,metabolicand acid base status. and acid base status. IdentiIy and correct precipitating Iactors. IdentiIy and correct precipitating Iactors. Restriction oI protein Irom the diet. Restriction oI protein Irom the diet. Avoid narcotics and sedatives. Avoid narcotics and sedatives. Reduction oI blood ammonia by lactulose Reduction oI blood ammonia by lactuloseand neomycin. and neomycin. !remedication !remedication Oral premedication preIIered than intramuscular. Oral premedication preIIered than intramuscular.HE absent HE absent lora / oxazepam (small dose) lora / oxazepam (small dose)HE present HE present - - avoid sedative avoid sedative Aspiration prophylaxis. Aspiration prophylaxis. Vit k slow iv continue till morning oI surgery. Vit k slow iv continue till morning oI surgery. P should be given immedietly beIore surgery. P should be given immedietly beIore surgery. Mannitol inIusion iI bilirubin ~ 8mg/dl Mannitol inIusion iI bilirubin ~ 8mg/dl Steroidal supplemenation in autoimmune hepatitis. Steroidal supplemenation in autoimmune hepatitis.!remedication !remedication Antipyschotic medication to be continued in pt with wilsons disease. Antipyschotic medication to be continued in pt with wilsons disease. ontinue other optimisation measures Ior ascites ,HE etc except Ior ontinue other optimisation measures Ior ascites ,HE etc except Iormorning dose oI diuretics. morning dose oI diuretics. Large bore iv cannulae with cvp line aIter excluding coagulopathy. Large bore iv cannulae with cvp line aIter excluding coagulopathy. atheterise evening beIore surgery and start iv Iluids (1 atheterise evening beIore surgery and start iv Iluids (1- -2ml/kg/hr 2ml/kg/hr while Iasting to maintain u.o. oI atleast 1ml/kg/ hr. while Iasting to maintain u.o. oI atleast 1ml/kg/ hr.Induction agents Induction agentsAll the induction agents (single dose) are saIe. All the induction agents (single dose) are saIe.Dose has to be reduced and given slowly except in Dose has to be reduced and given slowly except in alcoholics with compensated liver disease. alcoholics with compensated liver disease. Haemodynamically stable Haemodynamically stable - - thiopentone/propoIol thiopentone/propoIolHaemoynamically unstable Haemo