copy of kiruba liver1

1.ANAESTHESIA AND LIVER DISEASES BY DR.D.KIRUBAKARAN 11.08.08

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 onlyfor24 - 48hoursinthe

anhepatic state despite full supportive therapy.

Consistof 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.

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 .

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----

FLOW AUTOREGULATION

Exist evenwhen the SBP reaches80mmhg.

Myogenic reflex

High TM pressure decreases flow

LowTM pressure -increases flow

Autoregulation Doesnt 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 likelyto be animportant mechanismduring

most anaesthetics, given that they are performed in fasted patients.

Hepatic arterial buffer response

Decrease in portal biood flow and oxygen tensionwillincrease the hepatic arterial blood flow

thru increased periarteriolar adenosine whereas

increase in portal blood flow decrease the HABF thru

decrease in periarteriolar adenosine.

Inportal HT Liver depend upon hepatic arterial blood flow as HABRreaches its upper limit.(oxygen supply and demand should be carefully maintained)

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.

Catecholamines

Portal vein- vasoconstriction.

Hepatic artery- vasoconstriction in low

vasodilatation in high

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

Supine posture

Postprandial state

Hypercarbia

Acidosis

Acute hepatitis

Beta agonist

Phenobarbitone

Glucagon

Dopamine

Dopeximine

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

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.

Phase IIreaction

conjugation reaction (glucuronic acid &sulfate).

Zone 1 rich in enzymes involved in conjugation.

Affected least by ageing and liver disease.

Products of phase 2 reactionare usually less

toxic when compared to phase I reaction.

Extraction ratio is the proportion ofthe drug that is extracted

in single passage through the liver.

ER = intrinsic clearance/ HBF

High extraction ratio( 0.7 )

It is affectedby 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.

Low extraction ratio

Itis affected by intrinsic metabolic capacity But it is flow independent.i.e

increase in flow doesnt 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 poorlybound drug it doesnt have

much effect.

For low extraction drugs ,interval between the doses should be increased but

the drug dosage should not be altered.

Thiopentone

NM agents( most of

the agents

Benzodiazepine

Alfentanil/ methadone

Diuretics

Anticonvulsant( most of

the drug )

Amiodarone/ digitoxin

Antithyroid drugs

Sulfonyl ureas

Steroids

Theophylline

Bupivacaine

Lidocaine

Propofol

Ketamine

Calcium channel

blockers

Beta blockers

Nitrates

Statins

Opioid( most of the

opioid)

Naloxone

Tricylic A.Depressant

Antipyschotic

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 sympatheticstimulant action and

methionine synthase inhibition.

Rapid sequence induction more likely to cause hypotension

than conventional induction.

Slow titrated dose of induction agentscause 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 relateddecrease in C.O & B.P.

Etomidate least decrease

Thiopentone sodium moderate decrease

Propofol-maximum decrease ( 17 % )

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.

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 ofcytoch P450

enzyme induction by alcohol( Reversed in ESLD).

Propofol & ketamine in contrast to thiopentoneis a

flow limited drug.

Propofol in contrast to other iv induction agentshas

extrahepatic metabolism.

Propofol cause the maximum decrease in HBF among

the induction agents.

Slow titrated dose of induction agents withsmooth

intubation will have little impact on the HBF.

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 1 Zone 1>3 Half life is 36hrs Half life is 18hrs N.Value0 35IU/L N.valueO 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


Ischaemic hepatitis

Acute exacerbation of chronic

hepatitis

Extrahepatic cholestasis with

cholangitis.

Eventhough it is a marker ofhepatocellular 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)

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 afatty meal

Only recomended use of GGT & 5-nucleotidase(most specific) is to exclude orto

substantiate, liveris the source of raise ALPiftheelectrophoreticfractionation

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 thepresence of infiltrative

liver disease ( tumour, sarcaidosis,tuberculosis etc).

40. LFT Differentiation of Obstructive & Hepatocellular jaundice10% 90% >2.5ULN 3-4s over controlvalueis 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% ofCF is neededfor maintaining haemostasis.

Cholestatic jaundice -correction of PT by atleast 30%within 24

hr of vit k administrationsuggest 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 uponrate 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 worseningof 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

Normaltotal 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% parenchymashould be blocked.

46. Bilirubin

In choledocholithisis caused by CBD stone,the bilirubin valuerarely

exceeds 10mg/dl.Sepsis or renal failureshould be excluded if the bn

exceeds30mg/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 developmentof cirrhosis.

Serum bilirubin will take atleast 1-2 weeks to return to normal following

the reliefof 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 AntimitochondrialAB 48. Liver biopsy

Gold standard for evaluation of patient with chronic liver disease . Liver

biopsyhelpsin

# 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 0-4total=22

50. Normal LFT Values 14mg/dayUrine urobilinogen11 64IU/LGG Transpeptidase 1 18IU/L 5 Nucleotidase90 300 IU/L (6-16%) Lactate dehydrogense 35 100 IU/l Alkaline phosphatase035IU/L Aminotransferases40 280 mg/day Stercobilinogen0.3-1mg/dl (DB 0.1-0.3) Total bilirubin 51. Normal LFT values 25-35 seconds Partial thromboplastin Time 11-14 seconds Prothrombin time 1-1.3International N ratio 1080 micg/dl Plasma Ammonia 175 400mg/dl S.Fibrinogen 2.0 3.5 gm/dlS.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 thatupto 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 < 3timesULN 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


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 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


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 othertwo subtypes is a

prog disorder in which the symptoms range from recurrent

mild to severe acute exacerbationthateventually progress

tocirrhosis.

66. Chronic hepatitis

Categorization based only on histopathological features has been

replaced by classification that is much moreinformative based

upon a combination of

Clinical features

Serological

Biochemical and

Histological activity index.

67. Chronic hepatitis new classification

Gradestage

CPH MildNone or mild

CLH Mild or modMild

CAH Mild to severeMild to cirrhosis

68.

Chronic hepatitis is said to be active if thereis

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

isAscites

variceal bleeding

Renal failure

S.Bilirubin>8mg/dl

S.Albumin 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 ifthere 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

Chronicalcoholic 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 diseaseAntipsychiatric medication hasto 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 asSkeletal

muscle to central circulation is also impaired.

Blunted vascular response toexogenous vasopressors and volume

expansion.

Volume assessment and fluid management thro cvp are oftenmisleading

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 ofportal hypertension.

Development of ascites indicates the onset ofhepatic

decompensation.

GE varices more likely to bleed iftheportal 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 prophylaxiswill mask the signs

or haemodymamic effects of haemorrhage.

Airway should be protected to preventthe 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 increasingintra-

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 considerationRisk 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 ofLVP(>5L/day).

Half ofthe 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 suchas 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 ofPT and APTT to respond to vitK/FFP indicates poorprognosis.

FFP must be transfused just prior to procedure andrepeated every 8-12hrs to

maintain acceptable coagulation parameters( chanceof volume overload-

Exchange plasma transfusion).

93. Haematology(cont)

Adequate blood/ blood component shouldbe arranged prior to surgery.

Invasive arterial BP preferable than NIBP(repeated NIBP causebruises).

Blood loss should be closely monitored &should be corrected immedietly

(Hematocrit maintained around 30%).

FFP should be given when crystalloid,colloid or packed cells aregiven 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/mmsafe

70,000-1lakh-safe if cg scn is wnl

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 jaundiceAbsentPresent Cirrhosis stigmata Present Absent H/O of surgeryAbsent 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 18 years

PELD score < 18 years

Garrisons score

Dixon Freidman score

Knodell Ishak score for chronic hepatitis

ASA Classification

POSSUM score

GARRISON et al factors associatedwith increased

post operative mortality

S.albumin 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

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%

ASA INormal healthy patient.

ASA IIPatient 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 VMoribund patient who is not expected

to survive without the operation.

ASA VI Brain dead patient.

ASA II-Cigarette smoking without COPD

More than minimal drinking

Mild obesity

Well controlled HT or DM without systemic

or end organ involvement

ASA III Morbidobesity

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 over6 months ago

Ejection fraction < 40 %

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

ASA I & II-0.3 %

ASAIII-4to 5%

ASAIV-25 to 30%

ASAV-> 70 %

Acute alcoholic hepatitis

Fulminant hepatic failure

Severe chronic hepatitis

Child's class C cirrhosis

Severe coagulopathy (pl count 50.000/mm3 &

PT3s despite of vitamin k administration)

Hypoxia(Po2 Elective

Intraabdominal> Extraabddominal

Upperabdomen > Intraabdomen

Nonlaproscopic > laprascopic

Emergency CT> Elective CT

Hepatic resection with MELD

score>8/CPS>6

Prior abdominal surgery

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 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.

Ascites to be drained before surgery if possible.

Hydrothoraxshould 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 byeither 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.

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)

Dose40mg per day

(max dose 160mg)

8-10g/L of fluid removed

(if > 5L removed)

Vit K10 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 12 minutes.

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.

Oral premedication preffered than intramuscular.

HEabsent 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.

Antipyschotic medication to be continued inpt with wilsons disease.

Continue other optimisation measures for ascites ,HE etc except for

morning dose ofdiuretics.

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.

All the induction agents (single dose) are safe.

Dose has to be reduced andgivenslowly exceptin

alcoholics with compensated liver disease.

Haemodynamically stable-thiopentone/propofol

Haemoynamically unstable-ketamine/etomidate

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 hypoxemiabut

care should be taken to maintain C.O & B.P.

Muscle relaxants

Suxamethonium single dose doesntneed 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.

Goalis to maintain the adequate blood flow and oxygen content in the blood so as to maintainthe

oxygen supply demand relation in the liver.

High inspired O2 to prevent hypoexemia.

Maintainence of adequate cardiac output and B.P.(PCWP/CVP guided

fluidmanagement)

Avoid hepatotoxic drug / NSAID.

Avoidance of relative overdose of anaesthetics.

Maintainence of normocarbia and normothermia.

Maintainence of adequate haematocrit.

Adequate blood & volume replacementto prevent hypotension.

Monitoring of u.o/coag parameters/glucose/calcium and electrolytes.

Pulse oximetry

NIBP/INVASIVE B.P.

Electrocardiography

PCWP/ CVP

Temperature

NM monitoring

Urine output

Blood loss(swab,suction,drape

& floor)

Input output

Rapid infusion system

Forced air warmers

Haematocrit

Serum electrolytes / ionised calcium

Blood glucose

Arterial blood gas analysis

Coagulation parameters / TEG

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 ofi.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.

copy of kiruba liver1

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