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  • 1. ANAESTHESIA AND LIVER DISEASES BY DR.D.KIRUBAKARAN 11.08.08
  • 2. Introduction
    • Largest organ in the body ( 1.2 – 1.5kg).
    • Liver has unparlleled regenerative capacity i.e it has
    • ability to regenerate even when 80% of is resected.
    • Plays a critical role in the mainataince of haemostasis.
    • Primary regulatory site for metabolism.
    • Vital organ as evidenced from the fact that the human
    • being can survive only for 24 - 48hours in the
    • anhepatic state despite full supportive therapy.
  • 3. Hepatic lobule – Anatomical unit
    • Consist of 50,000 – 1,00,000 lobules.
    • Hepatocytes arranged cylindrically around
    • the central vein.
    • 4 to 5 portal tracts surround each lobule.
    • Portal triad – hepatic artery, portal vein
    • and bile canaliculi.
  • 4. Hepatic acinus- functional unit
    • Formed by portal tract in the middle and central
    • vein at the periphery.
    • 3 zones
        • Zone I (Periportal)
        • Zone II(mid zonal)
        • Zone III(pericentral)
    • Zone 3 – more susceptible for hypoxic injury .
  • 5. Metabolic diversity within zones Relatively poor in O2 and nutrients Rich in oxygen and the nutrients Lipolysis Bile salt formation Glycolysis Glycogen snthesis as well as gluconeogenesis Anaerobic/phaseI reaction Oxidative/phaseII reaction More prone for hypoxic & drug induced damage Less prone to hypoxia and drug toxicity Zone 3(pericentral) Zone 1(periportal)
  • 6. Hepatic blood flow
    • Receives 25% of cardiac output.
    • Characteristic dual blood supply through
    • hepatic artery and portal vein.
    • THBF – 25 to 30% by hepatic artery and
    • 70 to 75% by portal vein.
    • Hepatic oxygen consumption - 45 to 50%
    • by hepatic artery and 50 to 55% by the
    • portal vein
    • Hepatic sinusoids --- central vein ---
    • ---sublobular vein--- hepatic vein----
    • ivc
    5-10 40-70 Mean BP 60-75% 98% Spo2 50-55% 45-50% 02 supply 70-75% 25-30% Bl supply P.V H.A Features
  • 7. Intrinsic Regulation
    • FLOW AUTOREGULATION
    • Exist even when the SBP reaches 80mmhg.
      • Myogenic reflex
      • High TM pressure – decreases flow
      • Low TM pressure - increases flow
      • Autoregulation Doesn’t exist in portal circulation.
    • FOOD RELATED
    • Postprandial hyperosmolarity increases both portal & HBF.
    • Hepatic arterial system undergoes flow autoregulation best when the liver is
    • very active metabolically(postprandial) but not during fasting state . Hence
    • flow autoregulation is not likely to be an important mechanism during
    • most anaesthetics, given that they are performed in fasted patients.
  • 8. Intrinsic regulation
    • Hepatic arterial buffer response
      • Decrease in portal biood flow and oxygen tension will increase the hepatic arterial blood flow
      • thru increased periarteriolar adenosine whereas
      • increase in portal blood flow decrease the HABF thru
      • decrease in periarteriolar adenosine.
      • In portal HT – Liver depend upon hepatic arterial blood flow as HABR reaches its upper limit.(oxygen supply and demand should be carefully maintained)
  • 9. Extrinsic regulation
    • Circulatory regulation
    • Blood flow through portal vein is indirectly regulated by vasoconstriction and
    • vasodilatation of splanchnic arterial bed whereas hepatic arterial flow is
    • directly regulated thro sympathetic system.
    • Hepatic artery – both alpha and beta receptors.
    • Portal vein - contains only alpha receptors.
    • Hormonal regulation
    • glucagon - increases hepatic arterial blood flow.
    • angiotensin - decreases both portal and hepatic blood flow.
    • vasopressin - decreases both portal and hepatic blood flow.
  • 10. Extrinsic regulation
    • Catecholamines
    • Portal vein - vasoconstriction.
    • Hepatic artery - vasoconstriction in low
    • dose.
    • vasodilatation in high
    • dose.
  • 11. Decreased hepatic blood flow
    • Upright posture
    • Hypocarbia
    • Hypoxia
    • IPPV/PEEP
    • Sepsis
    • Haemorrhage
    • Mesentric traction
    • Increased IA pressure
    • Alpha agonist
    • Beta blockers
    • Vasopressin
    • Octreotide
    • Volatile anaesthetics
    • Intravenous induction
    • agents
    • Regional anaesthesia
  • 12. Increased hepatic blood flow
    • Supine posture
    • Postprandial state
    • Hypercarbia
    • Acidosis
    • Acute hepatitis
    • Beta agonist
    • Phenobarbitone
    • Glucagon
    • Dopamine
    • Dopeximine
  • 13. Functions of liver
    • A. Albumin synthesis
    • B. Bilirubin secretion
    • C. Coagulation factor synthesis
    • D. Drug metabolism
    • E. Excretion
    • F. Fat metabolism
    • G. Glucose & Glycogen metabolism
    • H. Hormone metabolism
    • I . Immunological function
  • 14. Drug metabolism
    • Phase I reaction
    • Carried out by cyto P450 enzyme system.
    • Zone 3 rich in cytochrome enzyme system.
    • Affected early by ageing and liver disease.
    • Most drug hepatotoxicity is mediated by the
    • phase I toxic metabolite.
  • 15. Drug metabolism
    • Phase II reaction
    • conjugation reaction (glucuronic acid &sulfate).
    • Zone 1 rich in enzymes involved in conjugation.
    • Affected least by ageing and liver disease.
    • Products of phase 2 reaction are usually less
    • toxic when compared to phase I reaction.
  • 16. Extraction ratio
    • Extraction ratio is the proportion of the drug that is extracted
    • in single passage through the liver.
    • ER = intrinsic clearance/ HBF
    • High extraction ratio ( 0.7 )
    • It is affected by the hepatic blood flow but not by factors
    • that increase free fraction of drug.
    • Dose has to be reduced by as much as 50% but not the
    • frequency of dosing.
  • 17. Extraction ratio
    • Low extraction ratio
    • It is affected by intrinsic metabolic capacity But it is flow independent.i.e
    • increase in flow doesn’t increase extraction.
    • Affected by factors that increase free fraction of the drug.
    • Reduction in protein binding of highly protein bound drug causes almost
    • doubling of free fraction but with poorly bound drug it doesn’t have
    • much effect.
    • For low extraction drugs ,interval between the doses should be increased but
    • the drug dosage should not be altered.
  • 18. Capacity limited drugs
    • Thiopentone
    • NM agents( most of
    • the agents
    • Benzodiazepine
    • Alfentanil/ methadone
    • NSAID
    • Diuretics
    • Anticonvulsant( most of
    • the drug )
    • Amiodarone/ digitoxin
    • Antithyroid drugs
    • Sulfonyl ureas
    • Steroids
    • Theophylline
  • 19. Flow limited drugs
    • Bupivacaine
    • Lidocaine
    • Propofol
    • Ketamine
    • Calcium channel
    • blockers
    • Beta blockers
    • Nitrates
    • Statins
    • Opioid( most of the
    • opioid)
    • Naloxone
    • SSRI
    • Tricylic A.Depressant
    • Antipyschotic
  • 20. Volatile agent on HBF preserved prved prved 0.2 – 2 isoflurane preserved prved prved 2 - 5 sevoflurane Decrease Lost - - 0.02 Desflurane Decrease Lost - - - 2.5- 8.5 Enflurane Decrease Lost - - - - 20 – 46 Halothane O2 deli HABR HABF M.bolism V.Agent
  • 21. Nitrous oxide on HBF
    • Nitrous oxide containing anaesthetics does not
    • cause liver injury in the absence of impaired
    • hepatic oxygenation.
    • Nitrous oxide may exacerbate hepatic damage
    • in the presence of impaired hepatic oxygenation
    • through sympathetic stimulant action and
    • methionine synthase inhibition.
  • 22. Effect of induction agents on hepatic blood flow
    • Rapid sequence induction more likely to cause hypotension
    • than conventional induction.
    • Slow titrated dose of induction agents cause less hypotension
    • All iv induction agents (single dose) can be safely given in pt
    • with liver dysfunction.
    • Ketamine cause decrease in HBF thru sympathetic stimulation
    • whereas other thru dose related decrease in C.O & B.P.
    • Etomidate – least decrease
    • Thiopentone sodium – moderate decrease
    • Propofol - maximum decrease ( 17 % )
  • 23. Effect of hepatic dysfunction on the drug pharmacokinetics Decreased biliary excretion of drugs Obstructive jaundice Metabolism either can be increased or decreased Enzyme content Increased VOD Ascites Increased unbound fraction Hypoalbuminemia First pass metabolism for the oral drug decreased Decreased PBF & fraction of shunt increased Effect on the drug Liver dysfunction
  • 24. Effect of hepatic dysfunction on drug pharmacodynamics
    • Increased sensitivity to CNS depressants.
    • Decreased sensitivity to vasopressors.
    • Enhanced effect to anticoagulation.
    • Enhanced Na retention – NSAID/ Steroid.
    • Ascites /oedema may be resistant to diuretics.
  • 25.
    • Duration of action of single dose wont be prolonged
    • as the major determinant of 1 dose is redistribution.
    • Thiopentone – capacity limited drug. Dose has to be
    • reduced for induction because of decreased protein
    • binding & reduction in enzyme activitity.
    • Thiopentone- Higher dose is needed in alcoholic with
    • compensated liver disease because of cytoch P450
    • enzyme induction by alcohol( Reversed in ESLD).
    Effect of hepatic dysfunction on induction agents
  • 26.
    • Propofol & ketamine in contrast to thiopentone is a
    • flow limited drug.
    • Propofol in contrast to other iv induction agents has
    • extrahepatic metabolism.
    • Propofol cause the maximum decrease in HBF among
    • the induction agents.
    • Slow titrated dose of induction agents with smooth
    • intubation will have little impact on the HBF.
    Effect of hepatic dysfunction on induction agents
  • 27.
    • Suxamethonium - DOA rarely gets prolonged despite
    • reduced pseudocholinesterase level.
    • DOA of pancuronium and rocuronium gets prolonged
    • because of increased VOD and impaired hepatic
    • metabolism (altered pharmacokinetics).
    • DOA of vecuronium <0.15mg/kg unaffected.
    • DOA of mivacurium gets prolonged because of the
    • reduced plasma cholinesterase level.
    Effect of hepatic dysfunction on muscle relaxants
  • 28.
    • Atracurium and cis-atracurium – DOA of both the drug are not
    • affected as both the drug can undergo organ independent
    • elimination thru ester hydrolysis and Hoffmans degradation.
    • DOA of above drugs are infact reduced because of increased
    • VOD & increased binding to globulins.
    • To prevent residual muscle weakness in the p.o.period
    • because of altered pharmacokinetics, careful monitoring of the
    • neuromuscular function is needed.
    Effect of hepatic dysfunction on muscle relaxants
  • 29.
    • Fentanyl and sufentanil - DOA of single dose
    • is not altered in compensated liver disease.
    • Alfentanil - DOA is prolonged because of the
    • increased free fraction of the drug.
    • Remifentanil duration of action is unaffected
    • as it is metabolised by nonspecific esterace.
    Effect of hepatic dysfunction on opioids
  • 30. Drugs in Liver failure Enflurane Nitrous oxide Iso/sevoflurane Desflurane Volatile agents Single dose all are safe Induction agents Midazolam Diazepam Lorazepam Oxazepam Premedication Caution Safe Drugs
  • 31. Drugs in Liver failure Other NSAID Lidocaine Bupivacaine Paracetamol Analgesics Remaining drug Fentanyl Sufentanil Remifentanil Opioids Suxamethonium Pancuronium Vecuronium Atracurium cisatracurim Muscle relaxants Caution Safe Drugs
  • 32. Liver function tests
    • Quantitative - assess hepatic blood flow and
    • the metabolic capacity.
    • Qualitative - assess hepatocellular necrosis.
    • assess cholestasis.
    • assess synthetic function.
    • assess excretory function.
  • 33. Quantitative liver test
    • Hepatic blood flow or perfusion
        • Bromosulphothalein clearance
        • Indocyanine green clearance
        • Rose bengal clearance test
    • Hepatic drug metabolising capacity
        • Galactose elimination capacity
        • Aminopyrine breath test
        • Antipyrine clearance
        • Monoethylglycinexylidide(MEGX) clearance
        • Caffeine clearance
      • more expensive & time consuming
  • 34. Aminotransferace(ALT &AST) Zone 3>1 Zone 1>3 Half life is 36hrs Half life is 18hrs N.Value 0 – 35IU/L N.value O – 45 IU/L Cytosol and mitochondria Cytosol Non specific Relatively liver specific Aspartate transaminase Alanine transaminase
  • 35. Examples for raised ALT &AST
    • Minor < 100 IU – Chronic hepatitis B/ C
    • NASH
    • Fatty liver
    • Moderate 100-300IU – Alcoholic hepatitis
    • Autoimmune hepatitis
    • Acute viral hepatitis
    • Exacerbation of chronic viral hepatitis
    • plus all the above condition
  • 36.
    • Marked > 300 IU – Drugs and toxins
    • Acute viral hepatitis
    • Ischaemic hepatitis
    • Acute exacerbation of chronic
    • hepatitis
    • Extrahepatic cholestasis with
    • cholangitis.
    • Eventhough it is a marker of hepatocellular necrosis, the degree
    • of elevation does not correlate with the extent of necrosis.(no
    • prognostic value).
    Examples for raised ALT &AST
  • 37. Aminotransferace(ALT &AST)
    • AST/ALT ratio may be of value in differential diagnosis.
    • >4 (wilsons hepatitis)
      • 2-4 (alcoholic liver disease)
      • <1 (NASH)
    • Episodic elevation of aminotransferaces is characteristics of
    • chronic hepatitis C.
    • Suspicion of cirrhosis once AST value exceeds ALT in patient
    • with chronic hepatitis.
    • Fall in aminotransferace level indicates recovery unless it is
    • accompanied by rise in bilirubin & PT.
  • 38. Alkaline phosphatase
    • Normal value – 30 to 100IU/L(liver and bone contributes more
    • than 80 percent of the total value).
    • Value < 3fold elevation can be seen in almost any type of liver
    • disease i.e.elevation of liver derived ALP is not totally
    • specific for cholestasis.
    • Degree of elevation doesn’t differentiate extrahepatic from the
    • intrahepatic cholestasis.
    • ALP elevation in cholestasis is usually > 3fold normal value
    • but the level remain elevated for 7-10days even after the
    • obstruction resolves as the half life of ALP is 7days.
  • 39. Alkaline phosphatase
    • Value < 3 fold elevation from normal value can be seen in normal people.
    • Age> 60yrs – upto 1.5 times increase
    • Children - upto 2 times increase
    • Pregnancy - upto 3 times increase
    • B.G O & B - upto 3 times increase after a fatty meal
    • Only recomended use of GGT & 5-nucleotidase (most specific) is to exclude or to
    • substantiate, liver is the source of raise ALP if the electrophoretic fractionation
    • of ALP is not available.
    • Elevated ALP along with 5-nucleotidase is specific for the hepatobiliary diseases
    • and also helps to R/O physiological ALP elevation.
    • Disproportinate elevation of ALP and bilirubin suggest the presence of infiltrative
    • liver disease ( tumour, sarcaidosis,tuberculosis etc).
  • 40. LFT Differentiation of Obstructive & Hepatocellular jaundice 10% 90% >2.5ULN <6 ULN 90% 10 % <2.5ULN >6 ULN H.C.jaundice OBS jaundice ALP AST/ALT
  • 41. Prothrombin time
    • Normal prothrombin time 11-14secs.
    • PT >3-4s over control value is significant.
    • Increasing PT is a ominuos sign in patient with acute
    • hepatocellular disease (impending hepatic failure).
    • Prothrombin time in contrast to s.albumin is a useful
    • prognostic indicator in acute hepatocellular disease.
    • ( as half life of CF is short IC to albumin)
  • 42. Prothrombin time
    • Mild – moderate hepatic disease may not be detected by PT as
    • only 30% of CF is needed for maintaining haemostasis.
    • Cholestatic jaundice -correction of PT by atleast 30%within 24
    • hr of vit k administration suggest hepatic synthetic function
    • is intact ( prolonged PT due to vit k deficiency alone).
    • Prolonged PT >5sec above control not corrected by vitamin k
    • administration is a poor prognostic sign ( in both acute and
    • chronic liver disease).
    • INR is a better indicator than PT because it is a standardized
    • value and is not subjected to lab variability as PT.
  • 43. Albumin
    • Normal value – 3.5 to 5.5gm/dl.
    • Blood level depends upon rate of synthesis(10-15gm/day),rate
    • of degradation and plasma volume.
    • Half life of serum albumin is about 21 days.
    • Not a good indicator of acute hepatic dysfunction because of
    • slow turnover ( long half life with 4% degredation per day).
  • 44. Albumin
    • In patients with hepatitis, albumin< 3gm/dl should
    • raise the possibility of chronic liver disease.
    • Decreasing albumin level in patient with chronic liver
    • disease indicates worsening of liver function in the
    • absence of other causes of hypoalbuminemia.
    • As long as albumin level is more than 2.5gm per dl,
    • free or unbound fraction of the drug wont be
    • altered.
  • 45. Bilirubin
    • Normal total bilirubin value is < 1mg/dl.Out of these, upto
    • 0.3mg is conjugated bilirubin.
    • Unconjucated bilirubin is toxic for neuronal cell whereas the
    • conjucated bilirubin is responsible for renal dysfunction in
    • patient with obstructive jaundice.
    • Bilirubin value rarely exceeds 6mg/dl in Haemolytic anaemia.
    • Intrahepatic cholestasis to cause rise in bilirubin, drainage of
    • bile in >75% parenchyma should be blocked.
  • 46. Bilirubin
    • In choledocholithisis caused by CBD stone, the bilirubin value rarely
    • exceeds 10mg/dl.Sepsis or renal failure should be excluded if the bn
    • exceeds 30mg/dl in patient with CBD stone.
    • In cholestatic jaundice due to malignancy, the bilirubin value is >10mg but
    • but less than 30mg/dl.
    • Common bile duct obstruction if persist for more than 30 days will result in
    • liver damage and can lead to the development of cirrhosis.
    • Serum bilirubin will take atleast 1-2 weeks to return to normal following
    • the relief of obstruction ( half life of delta bn is 2weeks).
  • 47. Antibodies in liver disease Chronic hep C & Type 11 autoimmune hepatitis Anti LKM 1 Chronic hepatitis D Anti LKM3 Drug induced chr hepatitis Anti LKM2 Type 1 A.I. Hepatitis Antinuclear antibody Prm sclerosing cholangitis P - ANCA Primary biliarycirrhosis Antimitochondrial AB
  • 48. Liver biopsy
    • Gold standard for evaluation of patient with chronic liver disease . Liver
    • biopsy helps in
    • # Diagnosis of various chronic liver disease.
    • #Assessing the severity(grade) and stage of liver
    • disease.
    • #Predicting the prognosis and
    • # monitoring the response to treatment.
  • 49. Histological activity index (knodell Ishak score)
    • Periportal necrosis
    • ( no necrosis to MLN)
    • Intralobular necrosis
    • (no to marked necrosis)
    • Portal inflammation
    • (none to marked infm)
    • Fibrosis
    • (none to cirrhosis)
    • Score 0-10
    • Score 0-4
    • Score 0-4
    • Score 0-4 total=22
  • 50. Normal LFT Values 1 – 4 mg/day Urine urobilinogen 11 – 64 IU/L GG Transpeptidase 1 – 18 IU/L 5 – Nucleotidase 90 – 300 IU/L (6-16%) Lactate dehydrogense 35 – 100 IU/l Alkaline phosphatase 0 – 35 IU/L Aminotransferases 40 – 280 mg/day Stercobilinogen 0.3-1mg/dl (DB 0.1-0.3) Total bilirubin
  • 51. Normal LFT values 25 - 35 seconds Partial thromboplastin Time 11 - 14 seconds Prothrombin time 1 - 1.3 International N ratio 10 – 80 micg/dl Plasma Ammonia 175 – 400mg/dl S.Fibrinogen 2.0 – 3.5 gm/dl S.globulin 3.5 – 5.5 gm/dl S.Albumin
  • 52. Clinical presentation
    • Asymptomatic patient with abnormal LFT
    • Acute hepatitis/Acute liver failure
    • Chronic hepatitis
    • Cirrhosis(compensated & decompensated)
    • Obstructive jaundice(Benign & malignant)
  • 53. Asymptmatic patient with abnormal Liver function tests
    • Biochemical screening of healthy asymptomatic
    • people has revealed that upto 6% have abnml
    • liver enzyme level but the prevalance of liver
    • disease in the Gen population is around 1%.
    • Liver test must always interpretated along with
    • careful history and examination as well as to
    • confirm each abnormal test with another test.
  • 54. Evaluation of Isolated Raised AST/ALT
  • 55.  
  • 56. Evaluation of Isolated ALT Elevation
  • 57. Asymptomatic patient with abnormal LFT
    • Aminotransferace elavation < 3times ULN is not a
    • contraindication for elective surgery if bilirubin is
    • within normal limits.
    • Liver ALP < 3times ULN is not a C/I for elective
    • surgery if bilirubin is within normal limits.
    • Delay surgery when a patient without any risk factors
    • or stigmata of liver disease is having more than one
    • abnormal LFT.
  • 58. II.Acute hepatitis & liver failure
    • Drug induced - Acetiminophen ,Halothane etc
    • Viral infection
    • Toxins
    • Autoimmune hepatitis
    • Alcoholic hepatitis
    • Acute fatty liver of pregnancy
    • Out of these , Drugs is the most common cause of acute hepatitis/hepatic failure.
    • Elective surgery postponed until atleast 30days after the liver function tests have
    • returned to normal because of high perioperative mortality.
  • 59. Management of acute liver failure
    • Airway control should be done with HE 3 or 4.
    • Management of raised ICT.
    • Management of acid base imbalance.
    • Management of electrolyte imbalance/hypoglycemia.
    • Management of coagulopathy by vit k & FFP.
    • Cardiac support with vasopressors.
    • Renal support by Haemofiltration.
    • Respiratory support with mechanical ventilation.
    • Despite best supportive measures in ICU attached to the
    • LT centre, m.rate approaches 50% - 80%.
  • 60. Indication for OLT in acute hepatic failure
    • KINGS COLLEGE CRITERIA
    • A) Non acetominophen patients
    • PT >6.5 (INR) or
    • Any 3 of the following variables
    • Non A-nonB hepatitis/Drug induced
    • Age < 10 or > 40 yrs
    • S.Bilirubin >17.6mg/dl
    • PT > 3.5 (INR)
    • Duration of icterus before HE > 7days.
  • 61. Acute liver failure(cont)
    • B) Acetaminophen patients
    • PH < 7.3 or
    • PT 6.5 (INR) and
    • S.Creatinine>3.4mg/dl.
  • 62. Acute liver failure (cont)
    • Paul Brousse hospital criteria
    • Hepatic encephalopathy and
    • Factor V <20% in patients < 30yrs.
    • or
    • Factor V<30% in patients >30yrs.
  • 63. Contraindication for OLT in acute liver failure
    • Improving hepatic function
    • CPP <40mmhg for >2hrs
    • Sustained elevation of ICT >50mmhg
    • Irreversible brain damage
    • Active alcohol or drug abuse
    • Seropositivity for HIV
    • Advanced cardiopulmonary disease
    • Uncontrolled sepsis
    • Widespread thrombosis of portal/mesentric vein
  • 64. III. Chronic liver disease
    • Most common causes of chronic liver disease (in descending
    • order) are Chronic hepatitis C
    • Alcoholic liver disease
    • NASH
    • Chronic hepatitis B
    • Autoimmune hepatitis
    • Sclerosing cholangitis
    • Primary Biliary cirrhosis
    • Haemochromotosis
    • Wilsons disease
    • For chronic hepatitis, Hepatitis c is the most common cause (Alcoholism for cirrhosis).
  • 65. Chronic hepatitis old classification
    • Chronic persistent hepatitis.
    • Chronic lobular hepatitis.
    • Chronic active hepatitis.
    • Chronic active hepatitis in contrast to other two subtypes is a
    • prog disorder in which the symptoms range from recurrent
    • mild to severe acute exacerbation that eventually progress
    • to cirrhosis.
  • 66. Chronic hepatitis
    • Categorization based only on histopathological features has been
    • replaced by classification that is much more informative based
    • upon a combination of
    • Clinical features
    • Serological
    • Biochemical and
    • Histological activity index.
  • 67. Chronic hepatitis new classification
    • Grade stage
    • CPH Mild None or mild
    • CLH Mild or mod Mild
    • CAH Mild to severe Mild to cirrhosis
  • 68.
    • Chronic hepatitis is said to be active if there is
    • HBV DNA > 1o5 copies/ml
    • chronic active hepatitis picture on LB
    • Aminotransferaces> 2 times ULN.
    • Above features should be present for starting medical
    • management.
    Chronic hepatitis B
  • 69. Chronic hepatitis C
    • Indication for medical management is like that of
    • chronic hepatitis B infection but HCV RNA will be
    • taken into account.
    • HCV more likely to progress
    • genotype 1& 4
    • chronic active hepatitis picture on LB
    • Longer duration of infection &
    • Immunocompromised states.
  • 70. Alcoholic hepatitis
    • Alcoholic hepatitis (acute or acute on chronic) is considered severe if there
    • is Ascites
    • variceal bleeding
    • Renal failure
    • S.Bilirubin>8mg/dl
    • S.Albumin<2.5gm/dl
    • Anaemia
    • PT > 5 sec over control
    • PMN> 5,500cells/mm3
    • Alcohol discriminant function >32.
    • Alcoholic hepatitis occurs in 10-20% of patient with chronic alcoholic
    • eventhough fatty liver is present in 90% of alcoholics.
  • 71. Autoimmune hepatitis
    • Autoimmune hepatitis (acute or acute on chronic) in symptomatic patient is said
    • to be severe if there is
    • S.bilirubin>3mg/dl
    • .
    • prolonged PT
    • Decreased S.Albumin
    • Aminotransferace>10times ULN.
    • S.globulin>2 times ULN in association
    • with aminotransferaces>5times ULN.
    • Bridging necrosis or multilobular collapse
    • or cirrhosis on LB.
  • 72. Anaesthetic consideration for Chronic Hepatitis
    • Surgical risk correlate with clinical features,biochemical
    • features and histological severity of the disease.
    • Elective surgery has been reported to be safe in asymptomatic
    • patient with mild-moderate chronic hepatitis.
    • Symptomatic and histological severe CH have increased
    • surgical risk particularly if hepatic synthetic or excretory
    • function is impaired,PHT if present or bridging/MLN
    • necrosis is seen on liver biopsy.
  • 73. Anaesthetic consideration for Chronic Hepatitis
    • Chronic alcoholic patient should be abstinent from alcohol
    • for atleast 6 mon to undergo elective procedure.
    • NASH not a contraindication for elective surgery ( >30%
    • hepatocytes if contain fat – increased mortality)
    • Hemochromatosis – Evaluate for complication such as
    • diabetes,hypothyrodism and cardiomyopathy.
    • Wilsons disease – Antipsychiatric medication has to be
    • continued(surgery can ppt or aggravate neurological
    • symptoms).
  • 74. IV.Complication of Decompensated cirrhosis
    • Portal HT - GE Varices
    • PH gastropathy
    • Hyperspleenism
    • Ascites including SBP
    • Respiratory - HPS
    • PPHT
    • Hepatic hydrothorax
    • Haematological - Anaemia
    • Thrombocytopenia (qualitative defect
    • also present)
    • Coagulopathy
  • 75. Complication of Decompensated cirrhosis(cont)
    • Kidney - Hepatorenal syndrome
    • CVS - Cardiomyopathy
    • CNS - Hepatic encepalopathy
    • MSK - Osteoporosis
    • Osteopenia
    • Nutrition - Malnutrition
  • 76. Respiratory system
    • Ventilation-perfusion mismatch caused by
    • impaired HPV,pleural effusion,ascites
    • & diaphragm dysfunction.
    • Decreases in diffusion capacity due to intersitial
    • oedema,increased ECF & pulmonary HT.
    • Incidence of coexisting pulmonary abnormalities
    • Hepatic hydrothorax – 5 to10%
    • H.P.synrome - 40 to 50%
    • PP hypertension - 4 to 6%
    • ABG & PFT - 40 to 50%
  • 77. Anaesthetic consideration(R.S)
    • Ascites fluid to be drained preoperatively with simultaneous colloid
    • replacement to reduce the splinting effect.
    • Coexistent COPD should be optimised & hydrothorax should be
    • treated.
    • Chest tube drain is C/I in hepatic hydrothorax.
    • Increased risk for aspiaration(aspiration prophylaxis & rapid
    • sequence induction).
    • Avoid PEEP as far as possible.
    • Avoid N2O in patient with COPD & PPH.
    • Avoid hypoxia(High inspired 02) & hypocarbia.
    • Response of OLT is poor in PPH when compared to HPS.
    • Elective postoperative ventilation for major surgery.
    • Extubation should be done when the patient is fully awake.
    • HPS & hepatic hydrothorax if present is indication for OLT.
  • 78. Cardiovascular system
    • Decreased peripheral vascular resistance.
    • Increased cardiac output.
    • Increased blood volume but redistributed.
    • Low- normal blood pressure with mildly elevated
    • heart rate.
    • Decreased effective circulatorary volume.
    • Diminished response to catecholamines.
    • Possible cirrhotic & alcoholic cardiomyopathy.
  • 79. Anaesthetic consideration(CVS)
    • Pain and light plane of anaesthesia cause decreased HBF through
    • sympathetic nervous system.
    • Hypotensive effect of volume depletion is exacerbated because of
    • impaired vasoconstrictor response to catecholamines.
    • Redistribution of blood flow from splanchnic as well as Skeletal
    • muscle to central circulation is also impaired.
    • Blunted vascular response to exogenous vasopressors and volume
    • expansion.
    • Volume assessment and fluid management thro cvp are often misleading
    • as cvp are often elevated despite relative hypovolumia from increased
    • back pressure in the IVC from hepatic enlargement,scarring and ascites
    • induced increased IA pressure.
  • 80. Anaesthetic consideration(CVS)
    • PCWP/CVP guided fluid management.
    • Low threshold for starting vasopressors as haemorrhage
    • is poorly tolerated.
    • Low threshold for volume overload as well as to v.presor
    • induced pulmonary oedema.
    • Propranolol if used for prophylaxis for GE varices may
    • mask the signs of haemorrhage.
    • Diuretics should be used with caution in ascites patient
    • without oedema (protective effect from intersitial fluid
    • wont be there as in patient with oedema).
    • Cirrhotic cardiomyopathy if present is an indication for
    • liver transplantation.
  • 81. Renal system
    • Decreased renal perfusion and GFR.
    • Reduction in free water clearance.
    • Reduction in sodium excretion.
    • Hepatorenal syndrome occurs in 10% of patients with decompensated
    • cirrhosis(100% mortality if OLT not done).
  • 82. Anaesthetic consideration( Kidney)
    • Urea falsely low due to decrease hepatic production.
    • Bilirubin lowers the measured s.creatinine(underestimation of renal
    • dysfunction)
    • Renal function assesed by inulin ,125 I iothalamate or 51 cr- EDTA clearance.
    • Avoid aggressive diuretic therapy.(Precipitate HE & HRS)
    • Absence of response to spironolactone400mg/day & furosemide160mg/day
    • indicates ascites becomes refractory (consider LVP or TIPS).
    • catheterise evening before surgery and start iv fluids while fasting @ 1- 2ml/kg/h to
    • maintain u.o.of atleast 1ml/kg/hr.( to prevent HRS )
    • Avoid morning dose of diuretics before elective surgery.
  • 83. Kidney(cont)
    • PCWP/CVP guided I.O.fluid management.
    • I.O chart in the P.O.period.
    • Avoid hypotension in the P.O.period (meanB.P.10-20% 0f preop value).
    • U.O.of atleast1ml/kg/hr must be achieved in the I.O.period (if not mannitol
    • or furosemide infusion).
    • Avoid NSAID & aminoglycosides in the I.O.period.
    • Cirrhotics are also at risk for ATN in the postoperativeperiod.
    • HRS if present is an indication for OLT.
  • 84. Gastrointestinal system
    • Development of GE varices & spleenomegaly signify
    • the development of portal hypertension.
    • Development of ascites indicates the onset of hepatic
    • decompensation.
    • GE varices more likely to bleed if the portal vein
    • pressure exceeds 12mmhg.
    • Prognosis after development of ascites is poor.( 50%
    • die within 3years from the onset of diagnosis)
  • 85. Anaesthetic consideration regarding gatroesophageal varices
    • Blood loss in GE varices is haemodynamically sgnft
    • and patient should be managed in ICU.
    • Propranolol used for prophylaxis will mask the signs
    • or haemodymamic effects of haemorrhage.
    • Airway should be protected to prevent the risk from
    • aspiration.
    • Crystalloid and colloid resuscitation along with the
    • pharmacological measures such as vasopressin,
    • somatostatin or octreotide.
  • 86.
    • Alteast 8-12 units of blood should be crossmatched
    • during the resucscitation period.
    • FFP should be given if the PT is 1.5 times more than
    • the control value.
    • Care should be taken to prevent volume overload as
    • the baseline SBP of most cirrhotics is 85 to 95mmhg
    • (volume overload increases hge).
    • Endoscopy should be done within 12hrs once the
    • patient is haemodynamically stable.
    Anaesthetic consideration regarding gatroesophageal varices
  • 87.
    • Ascites increases the risk of aspiration by increasing intra-
    • abdominal pressure ( also decreased GITmotility & GERD
    • due to hiatal hernia in the cirrhotics).
    • PICD can be prevented by concurrent administration of salt
    • poor albumin or other colloid.
    • Ascites is said to be refractory if there is no response to the
    • maximum dose of furosemide and spiranolactone.
    • TIPS should be considered for patient with refractory ascites
    • who is listed for OLT.
    • Tense and refractory ascites should be drained adequately
    • before surgery ( significant intra and postop comp.).
    Anaesthetic consideration regarding ascites
  • 88. Ascites Anaesthetic consideration Risk for aspiration False high CVP Haemodynamic instability Splinting effect to diaphragm Increased volume of distribution Intraoperative Respiratory distress Hypotension if inadeq replaced after LVP Hepatic hydrothorax Risk for SBP (50% mortality) Preoperative
  • 89.
    • Postoperative - Wound dehiscence
    • Abdominal wall herniation
    • Atelectasis
    • 1 litre of ascitic fluid = 50ml of 25% albumin( i.e 1 litre
    • roughly contains 10gm of protein).
    • Albumin should be idealy used in case of LVP(>5L/day).
    • Half of the albumin during the procedure and the other 6 hrs later.
    Ascites Anaesthetic consideration
  • 90. Haematological system
    • Anaemia is common with chronic liver disease.
    • Thrombocytopenia(qualitative as well).
    • Mild thrombocytopenia is often the first manifestation of worsening of
    • fibrosis in patient with chronic hepatitis.
    • Prothrombin time & partial thromboplastin time is prolonged (mild-
    • moderate prolongation).
    • Fibrinogen level will be normal ( low fibrinogen level with severe
    • thrombocytopenia R/O DIC ).
    • Drugs used to treat chronic hepatitis can cause anaemia.
    • Rifampin – Hemolytic anaemia
    • Interferon- bone marrow suppression
  • 91. Anaes.consideration(Haematology)
    • Liver biopsy can be safely performed if plateletcount>50,000/mm3 and PT as well
    • as APTT do not exceed 1.5 times the control value( BT not a reliable indicator).
    • Avoid drugs that precipitate bleeding such as NSAID/ Warfarin.
    • Avoid IM injection to prevent haematoma.
    • Haematocrit should be maintained around 30% in the perioperative period.
    • Anaemia should corrected preoperatively preferably with packed cell or fresh
    • whole blood ( Balanced against the risk of inducing HE from haemolysed RBC).
    • Thrombocytopenia in hyperspleenism as a rule is mild( severe thrombocytopenia
    • indicates the development of DIC).
  • 92. Haematology (Cont)
    • Thrombocytopenia if present should be preoperatively corrected.
    • Exploratory laprotomy>50,000/mm3
    • Closed space surgery>1Lakh/mm3
    • PT and APTT becomes abnormal only with severe deficiency of CF (abnormal
    • with CF < 30% of normal level).
    • PT and APTT if prolonged should be corrected to be within 1.5times the control
    • value.(Risk of Hge increases if PT & APTT exceeds 1.5 times the control value).
    • Failure of PT and APTT to respond to vitK/FFP indicates poor prognosis.
    • FFP must be transfused just prior to procedure and repeated every 8-12hrs to
    • maintain acceptable coagulation parameters( chance of volume overload-
    • Exchange plasma transfusion).
  • 93. Haematology(cont)
    • Adequate blood/ blood component should be arranged prior to surgery.
    • Invasive arterial BP preferable than NIBP(repeated NIBP cause bruises).
    • Blood loss should be closely monitored &should be corrected immedietly
    • (Hematocrit maintained around 30%).
    • FFP should be given when crystalloid,colloid or packed cells are given to
    • replace blood loss.( 1unit FFP=1unit packed cells=250ml crystalloid)
    • Hypothermia should be avoided (humidified gases,warm ivf,warming
    • blankets,forced air warming devices & blood warmer).
  • 94. Haematology(cont)
    • Blood loss can be minimised by perioperative administration of tranexemic
    • acid (prostate & ortho surgeries).
    • Correct/prevent I.O. factors that increases bleeding(dilution,hpypothermia
    • hypocalcemia & acidosis).
    • Thromboelastography for I.O. assesment of coagulation parameters.
    • Universal precautions in patients with hepatitis (30% - HepB & 3% -HepC)
    • Even 0.04ml blood may be enough to infect an anaesthesiologist.
    • RA not contraindicated if coagulation parameters are within normal.
  • 95. Causes of bleeding in liver disease
    • Anatomical factors – gastroesophageal varices
    • peptic ulcer
    • gastritis
    • haemoorhoid
    • Thrombocytopenia
    • Hepatic function abnormalities
    • Decreased synthesis of procoagulant protein
    • Decreased synthesis of coagulation inhibitors
  • 96. Causes of bleeding in liver disease(cont)
    • Failure to clear activated coagulation factors
    • Impaired absorbtion and metabolism of vit k
    • Synthesis of abnormal fibrinogen
    • Intraoperative factors – Hypothermia
    • Dilution
    • Hypocalcemia
    • Acidosis
  • 97.
    • Platelet count.
    • >1lakh/mm – safe
    • 70,000-1lakh - safe if cg scn is wnl
    • <70,000/mm3 - unsafe
    • Prothrombin time
    • INR>1.5 - unsafe
    • Activated partial thromboplastin time
    • APTT>40sec -unsafe
    Coagulation parameters and neuraxial block
  • 98. Neuraxial anaesthesia(cont)
    • Epidural preferred than spinal anaesthesia.
    • LA dose should be titrated.(flow limited drug)
    • Hypotension more likely with high spinal( T4 level –
    • 20% decrease in HBF) but safe for lower limb
    • procedures.
    • Strict aseptic precautions – increased susceptiblity
    • for infection.
    • Epidural Useful for postopanalgesia/decreases P.O
    • pulmonary complication.
  • 99. Indication for OLT in chronic liver disease
    • A) Cholestatic condition (specific)
    • S.bilirubin>10mg
    • Recurrent bacterial cholangitis
    • progressive cholestatic bone disease
    • Intractable pruritus.
    • B) Parenchymal condition (specific)
    • S.Albumin < 3gm/dl
    • PT > 3 sec above control
  • 100. Indication for OLT in chronic liver disease
    • C) Common to both condition
    • Recurrent or severe HE
    • Refractory ascites
    • Spontaneous bacterial peritonitis
    • Recurrent PHT bleeding
    • Hepatorenal syndrome
    • HPS / H. Hydrothorax
    • Cirrhotic cardiomyopathy
    • Detection of small HCC
    • Progressive malnutrition
    • Severe chronic fatique & weakness.
  • 101. V.Cholestatic jaundice Absent Present Cirrhosis stigmata Present Absent H/O of surgery Absent Present Prodromal symptom Present Absent Abdominal pain Present Absent Fever Extrahepatic Intrahepatic Diff. Features
  • 102. Cholestatic jaundice Present Absent Palpable gallbladder Responsive Variable Vit K treatment Needed Not needed ERCP Present Absent B.Dilatation on USG <30mg/dl Variable Total bilirubin Extrahepatic Intrahepatic Diff. Features
  • 103. Benign vs Malignant surgical jaundice 10-30mg/dl <10mg/dl Total bilirubin Present Absent Palpable gallbladder Absent Present Abdominal pain Absent Present Fever with chills Insidious Acute Mode of onset Malignant Benign Diff.Features
  • 104. Anaesthetic consideration in obstructive jaundice
    • It includes
    • Coagulopathy
    • Endotoxemia
    • Haemodynamic instability
    • Renal failure
    • Altered drug handling due to cholestasis
    • Impaired wound healing.
    • Measures taken to to reduce the renal failure is responsive better in benign rather than malign condition.In malignancy only way to reduce the
    • incidence of renal failure is to maintain adequate iv volume and
    • perfusion pressure.
  • 105. Effect of obstructive jaundice on the cardivascular system
    • Negative inotropic effect by bile salt.
    • Negative chronotropic effect by bile salt.
    • Altered haemodynamic response to haemorrhage.
    • Blunted vascular response to vasopressor and volume
    • expansion.
    • Jaundiced induced cardiomyopathy.
  • 106.
    • Haemodynamic instability caused by the bile salts &
    • endotoxin on the cardovascular function.
    • Diuretic and the natriuretic effect of bile salt.
    • Reduced renal perfusion because of enhanced renal
    • vascular reactivity to endogenous vasopressors.
    • Direct nephrotoxic effect by bile salt and conjugated
    • bilirubin (controversial)
    • Renal tubule blockade of bilirubin cast may further
    • potentiate the renal injury.
    Effect of obstructive jaundice on the Renal function
  • 107. Measures to prevent perioperative renal failure
    • Maintainence of adequate iv volume( most important of all the
    • measures).
    • Avoid NSAID & AMINOGLCOSIDES.
    • Oral lactulose/ ursodeoxycholic acid.
    • Endoscopic internal biliary drainage.
    • Preoperative and postoperative mannitol if the Bn>8mg per dl
    • (controversial role).
    • Dopamine/ furosemide has no role.
    • Except for maintainence of adequate iv volume and avoidance of
    • NSAID, all other measures are controversial in malignant
    • jaundice.
  • 108. Antiendotoxin measures
    • Avoid oral antibiotics.
    • Avoid percutaneous external drainage.
    • Oral lactulose.
    • Oral ursodeoxycholic acid.
    • Endoscopic internal biliary drainage.
    • Experimental drugs – Taurolidine
    • Rifaximin
    • Polymyxin.
  • 109. Preoperative evaluation
    • Complete history with clinical examination.
    • Investigation.
    • Risk assesment.
    • Management of complication due to liver disease.
    • Preoperative optimisation of modifiable risk factors
    • in Child B status patient and obstructive jaundice.
    • Premedication and instruction before surgery(include
    • the informed high risk consent).
  • 110. Preoperative investigation
    • Haematological Blood grouping/typing
    • Haemoglobin/ HCT
    • WBC count
    • Platelet count
    • Bleeding Time
    • PT / INR
    • APTT
    • Liver function tests.
    • Serology for viral hepatitis.
  • 111. Preoperative investigation(cont)
    • Metabolic / Renal
    • Blood glucose
    • S.Electrolytes / S.Calcium
    • Blood urea
    • S.Creatinine
    • U.Electrolytes
    • Cardiorespiratory
    • Chest x-ray
    • ECG
    • ECHO ( if needed)
    • PFT/ABG ( if needed) .
  • 112. Risk assesment
    • Child –Pugh score
    • MELD score > 18 years
    • PELD score < 18 years
    • Garrisons score
    • Dixon – Freidman score
    • Knodell – Ishak score for chronic hepatitis
    • ASA Classification
    • POSSUM score
  • 113. Modified Child-Pugh Score C=10 to 15 76% B= 7 to 9 31% A =5 to 6 10% Class Mortality Grade III-IV Grade I-II None Encephalopathy Tense Moderate Absent Ascites >3 2 - 3 <2 Bilirubin(mg/dl) >2.3 1.7 - 2.3 <1.7 INR <2.8 2.8 - 3.5 >3.5 Albumin(g/dl) 3 2 1 Parameters
  • 114. CHILD SCORE AND SURGERY
    • Child A - safely undergo elective surgery.
    • Child B - may undergo elective surgery after
    • optimisation with caution.
    • accepted criterion for listing to OLT.
    • Child C - contraindication for elective surgery.
  • 115. MELD SCORE
    • Objective score ( no interindividual variation in contrast
    • to child –pugh score that has 2 subjective component).
    • Designed to predict survival after TIPS 2 control bleeding
    • varices but now used for prioritizing patients for OLT.
    • Meld score = 3.78 x Log (BN) + 11.2 x Log (INR) +
    • 9.57x Log(cr) +6.43 (x 0 for alcoholic and
    • cholestatic condition , x 1 for remainder)
  • 116. MELD SCORE AND SURGERY
    • Meld < 10 - safely undergo elective surgery.
    • Meld10 -15 - may undergo elective surgery after
    • optimisation with caution.
    • accepted criterion for listing to OLT.
    • Meld > 15 - contraindication for elective surgery.
  • 117. Garrison risk factors for cirrhosis
    • GARRISON et al –factors associated with increased
    • post operative mortality
    • S.albumin <3gm/dl
    • presence of infection
    • WBC >10.000/cu.mm
    • Treatment with more than two antibiotics
    • S.bilirubin>3mg/dl
    • PT>1.5sec over control
    • Presence of ascities
    • Malnutrition
    • Emergency surgery
  • 118. Risk factors in obstructive jaundice
    • DIXON – FREIDMAN RISK FACTORS
    • S.Bilirubin > 11mg/dl
    • Malignant obstruction
    • Haematocrit < 30%
    • Renal failure
    • Cholangitis
    • Hypoalbuminemia
    • 􀂄 If at least 3 of above mortality 60%
    • 􀂄 If none of above mortality 5%
  • 119. ASA physical status classification
    • ASA I – Normal healthy patient.
    • ASA II – Patient with mild systemic disease.
    • ASA III – Patient with severe systemic disease.
    • but is not incapacitating.
    • ASA IV – Patient with severe systemic disease
    • that is a constant threat to life.
    • ASA V – Moribund patient who is not expected
    • to survive without the operation.
    • ASA VI – Brain dead patient.
  • 120. EXAMPLES FOR ASA CLASSES
    • ASA II - Cigarette smoking without COPD
    • More than minimal drinking
    • Mild obesity
    • Well controlled HT or DM without systemic
    • or end organ involvement
  • 121.
    • ASA III – Morbid obesity
    • Active hepatitis
    • Chronic renal failure/ ESRD
    • Mild COPD ( well controlled)
    • Poorly controlled HT or DM with systemic
    • involvement
    • Stable angina, MI, CVA, CHF, coronary
    • stent over 6 months ago
    • Ejection fraction < 40 %
    EXAMPLES FOR ASA CLASSES
  • 122.
    • ASA IV – Hepatorenal syndrome
    • Unstble angina, MI,CVA,Coronary stent
    • of < 6 months duration
    • Symptomatic CHF
    • Ejection fraction < 25 %
    • Moderate to severe COPD
    • ASA V - MODS/Sepsis with HD instability
    • Poorly controlled coagulopathy
    EXAMPLES FOR ASA CLASSES
  • 123.
    • ASA I & II - 0.3 %
    • ASA III - 4 to 5%
    • ASA IV - 25 to 30%
    • ASA V - > 70 %
    MORTALITY IN ASA SUBCLASS
  • 124. Contraindication for elective surgery
    • Acute viral hepatitis
    • Acute alcoholic hepatitis
    • Fulminant hepatic failure
    • Severe chronic hepatitis
    • Child's class C cirrhosis
    • Severe coagulopathy (pl count ≤50.000/mm3 &
    • PT↑≥3s despite of vitamin k administration)
    • Hypoxia(Po2<60mmhg)
    • Cardiomyopathy/ heart failure
    • Hepatorenal syndrome
  • 125. High risk factors for surgery
    • A) Type of surgery
    • Emergency > Elective
    • Intraabdominal > Extraabddominal
    • Upperabdomen > Intraabdomen
    • Nonlaproscopic > laprascopic
    • Emergency CT > Elective CT
    • Hepatic resection with MELD
    • score>8/CPS>6
    • Prior abdominal surgery
  • 126. High risk factors for surgery(cont)
    • B ) Characteristics of patient
    • Child class C>B>A.
    • Meld score > 15.
    • High ASA status.
    • S.bilirubin >3mg/dl(>11mg in obstructive LD).
    • Malignant > Benign jaundice.
    • S.Albumin <3gm/dl.
    • HCT <30%.
    • Acute > chronic encephalopathy.
    • Grade 3 or 4 encephalopathy.
    • Prolonged PT >3 sec above control(not corrected with vit K)
    • complication of cirrhosis(Ascites,GE Varices,HRS,HPS,PPHT
    • Hydrothorax,Cardiomyopathy).
    • Abnormal quantitative liver function tests.
  • 127. Optimisation before surgery
    • Ascites to be drained before surgery if possible.
    • Hydrothorax should be treated before surgery.
    • Encephalopathy should be corrected before surgery.
    • Anemia should be corrected before surgery.
    • Coagulopathy should be corrected before surgery.
    • Electrolyte imbalance should be corrected before the surgery.
    • Nutrional needs should be addressed by either enteral or by
    • parentral route before surgery.
    • Alcohol abstinence for atleast 6 months is needed for elective
    • suregery.
    • Antiendotoxin measures to reduce the renal dysfunction.
    • Coexisting illness( COPD, HT & DM) should be optimised.
  • 128. Ascites Treatment
    • Salt restriction
    • Fluid restriction
    • spiranolactone
    • Furosemide
    • Albumin
    • Not > 2 gm per day
    • 800-1000ml/day if serum
    • sodium < 125meq/L
    • Dose 100mg per day (max dose 400mg)
    • Dose 40mg per day
    • (max dose 160mg)
    • 8-10g/L of fluid removed
    • (if > 5L removed)
  • 129. Coagulopathy Treatment
    • Vit K 10 mg sc or slow iv over 20 minutes for 3
    • days(altered PT due to vit K def if there is 30%
    • improvement in the first 24 hours).
    • FFP in case of emergency rapid correction or in
    • vit K unresponsive patients.
    • Platelet transfusion in case of thrombocytopenia.
    • Cryoprecipitate if fibrinogen<75mg/dl.
    • DDAVP if BT > 12 minutes.
  • 130. Hepatic encephalopathy treatment
    • Care of airway,haemodynamic,metabolic
    • and acid base status.
    • Identify and correct precipitating factors.
    • Restriction of protein from the diet.
    • Avoid narcotics and sedatives.
    • Reduction of blood ammonia by lactulose
    • and neomycin.
  • 131. Premedication
    • Oral premedication preffered than intramuscular.
    • HE absent – lora / oxazepam (small dose)
    • HE present - avoid sedative
    • Aspiration prophylaxis.
    • Vit k slow iv continue till morning of surgery.
    • FFP should be given immedietly before surgery.
    • Mannitol infusion if bilirubin > 8mg/dl
    • Steroidal supplemenation in autoimmune hepatitis.
  • 132. Premedication
    • Antipyschotic medication to be continued in pt with wilsons disease.
    • Continue other optimisation measures for ascites ,HE etc except for
    • morning dose of diuretics.
    • Large bore iv cannulae with cvp line after excluding coagulopathy.
    • Catheterise evening before surgery and start iv fluids @1-2ml/kg/hr
    • while fasting to maintain u.o. of atleast 1ml/kg/ hr.
  • 133. Induction agents
    • All the induction agents (single dose) are safe.
    • Dose has to be reduced and given slowly except in
    • alcoholics with compensated liver disease.
    • Haemodynamically stable - thiopentone/propofol
    • Haemoynamically unstable - ketamine/etomidate
  • 134. Inhalational agents
    • Halothane & Enflurane has to be avoided because of its
    • effect on hepatic blood fow and its metabolism.
    • Maintainence with Isoflurane-O2-N20 / isoflurane – O2
    • and fentanyl or remifentanyl if N20 has to be avoided.
    • PEEP may have to be given to prevent hypoxemia but
    • care should be taken to maintain C.O & B.P.
  • 135. Muscle relaxants
    • Muscle relaxants
    • Suxamethonium single dose doesn’t need dose reduction.
    • Maintaince with Atracurium in titrated doses under neuromuscular
    • monitoring if available.
    • Loading dose larger than normal but the maintainence dose is smaller
    • than normal.
    • Reversal can be given for minor procedures but for major procedures
    • elective postoperative ventilation is often needed.
  • 136. Intraoperative considerations
    • Goal is to maintain the adequate blood flow and oxygen content in the blood so as to maintain the
    • oxygen supply – demand relation in the liver.
    • High inspired O2 to prevent hypoexemia.
    • Maintainence of adequate cardiac output and B.P.(PCWP/CVP guided
    • fluid management)
    • Avoid hepatotoxic drug / NSAID.
    • Avoidance of relative overdose of anaesthetics.
    • Maintainence of normocarbia and normothermia.
    • Maintainence of adequate haematocrit.
    • Adequate blood & volume replacement to prevent hypotension.
    • Monitoring of u.o/coag parameters/glucose/calcium and electrolytes.
  • 137. Intraoperative monitoring and equipment
    • Pulse oximetry
    • NIBP/INVASIVE B.P.
    • Electrocardiography
    • PCWP/ CVP
    • ETCO2
    • Temperature
    • NM monitoring
    • Urine output
    • Blood loss(swab,suction,drape
    • & floor)
    • Input – output
    • Rapid infusion system
    • Forced air warmers
  • 138. Biochemical/Haematological Monitoring
    • Haematocrit
    • Serum electrolytes / ionised calcium
    • Blood glucose
    • Arterial blood gas analysis
    • Coagulation parameters / TEG
  • 139. Postoperative management
    • Patient with child B grade who has undergone a major surgery
    • should be shifted to ICU and may need to be electively
    • ventilated.
    • Fluid , electrolyte, acid base balance, coagulation parameters
    • temperature, u.o and cvs stability should be maintained like
    • that of i.o.period.
    • Sedation and pain medication should be carefully titrated.
    • Chest x-ray should be immedietly taken to see the lung fields
    • and to check central as well as pulmonary catheter.
    • Monitor the patient for features of hepatic decompensation.
  • 140. Summary
  • 141. Thank you