ANAESTHESIA AND

LIVER DISEASES
BY
DR.D.KIRUBAKARAN
11.08.08
 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.
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.
 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 .
 Metabolic diversity within zones
Zone 1(periportal) Zone 3(pericentral)

Rich in oxygen and the Relatively poor in O2 and

nutrients nutrients
Less prone to hypoxia and More prone for hypoxic &
drug toxicity drug induced damage
Oxidative/phaseII reaction Anaerobic/phaseI reaction

Glycogen snthesis as well Glycolysis

as gluconeogenesis
Bile salt formation Lipolysis
 Hepatic blood flow
 Receives 25% of cardiac output.
Features H.A P.V
 Characteristic dual blood supply through
hepatic artery and portal vein. Bl supply 25-30% 70-75%
 THBF – 25 to 30% by hepatic artery and
70 to 75% by portal vein.
02 supply 45-50% 50-55%
 Hepatic oxygen consumption -45 to 50%
by hepatic artery and 50 to 55% by the
portal vein
Spo2 98% 60-75%
 Hepatic sinusoids --- central vein ---
---sublobular vein--- hepatic vein----
ivc Mean BP 40-70 5-10
 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.
 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)
 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.

 Extrinsic regulation
Catecholamines

Portal vein - vasoconstriction.

Hepatic artery - vasoconstriction in low

dose.
vasodilatation in high
dose.
 Decreased hepatic blood flow
 Upright posture  Alpha agonist
 Hypocarbia  Beta blockers
 Hypoxia  Vasopressin
 IPPV/PEEP  Octreotide
 Sepsis  Volatile anaesthetics
 Haemorrhage  Intravenous induction
 Mesentric traction agents
 Increased IA pressure  Regional anaesthesia
 Increased hepatic blood flow
 Supine posture  Beta agonist

 Postprandial state  Phenobarbitone

 Hypercarbia  Glucagon
 Acidosis  Dopamine
 Acute hepatitis
 Dopeximine
 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
 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.
 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.
 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.
 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.

 Capacity limited drugs
 Thiopentone  Anticonvulsant( most of
the drug )
 NM agents( most of
the agents  Amiodarone/ digitoxin

 Benzodiazepine  Antithyroid drugs

 Alfentanil/ methadone  Sulfonyl ureas

 NSAID  Steroids

 Diuretics  Theophylline
 Flow limited drugs
 Bupivacaine  Statins
 Lidocaine  Opioid( most of the
 Propofol opioid)
 Ketamine  Naloxone
 Calcium channel  SSRI
blockers  Tricylic A.Depressant
 Beta blockers  Antipyschotic
 Nitrates
 Volatile agent on HBF
V.Agent M.bolism HABF HABR O2 deli

Halothane 20 – 46 ---- Lost Decrease

Enflurane 2.5- 8.5 --- Lost Decrease

Desflurane 0.02 -- Lost Decrease
isoflurane 0.2 – 2 prved prved preserved

sevoflurane 2-5 prved prved preserved

 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.
 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 % )
 Effect of hepatic dysfunction on the
drug pharmacokinetics
Liver dysfunction Effect on the drug
Decreased PBF & fraction First pass metabolism for the
of shunt increased oral drug decreased
Hypoalbuminemia Increased unbound fraction

Ascites Increased VOD

Enzyme content Metabolism either can be

increased or decreased
Obstructive jaundice Decreased biliary excretion
of drugs
 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.

 Effect of hepatic dysfunction on
induction agents
 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
 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
muscle relaxants
 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
 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
opioids
 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.
 Drugs in Liver failure
Drugs Safe Caution
Premedication Lorazepam Midazolam
Oxazepam Diazepam
Induction agents Single dose all
are safe
Volatile agents Nitrous oxide Enflurane
Iso/sevoflurane
Desflurane
 Drugs in Liver failure
Drugs Safe Caution

Muscle relaxants Atracurium Suxamethonium

cisatracurim Pancuronium
Vecuronium
Opioids Fentanyl Remaining drug
Sufentanil
Remifentanil
Analgesics Paracetamol Other NSAID
Lidocaine
Bupivacaine
 Liver function tests
 Quantitative - assess hepatic blood flow and
the metabolic capacity.

 Qualitative - assess hepatocellular necrosis.

assess cholestasis.
assess synthetic function.
assess excretory function.
 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
Aminotransferace(ALT &AST)
Alanine transaminase Aspartate transaminase

Relatively liver specific Non specific

Cytosol Cytosol and mitochondria

Zone 1>3 Zone 3>1

N.value O – 45 IU/L N.Value 0 – 35IU/L

Half life is 18hrs Half life is 36hrs

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
Examples for raised ALT &AST
 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).
 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.
 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.
 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).
 LFT Differentiation of Obstructive
&
Hepatocellular jaundice
AST/ALT ALP OBS jaundice H.C.jaundice

>6 ULN <2.5ULN 10 % 90%

<6 ULN >2.5ULN 90% 10%

 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)
 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.
 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).
 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.
 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.
 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).
 Antibodies in liver disease
Antimitochondrial AB Primary biliarycirrhosis

P - ANCA Prm sclerosing cholangitis

Antinuclear antibody Type 1 A.I. Hepatitis
Anti LKM 1 Chronic hep C & Type 11
autoimmune hepatitis

Anti LKM2 Drug induced chr hepatitis

Anti LKM3 Chronic hepatitis D

 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.

 Histological activity index
(knodell Ishak score)
 Periportal necrosis  Score 0-10
( no necrosis to MLN)

 Intralobular necrosis  Score 0-4

(no to marked necrosis)

 Portal inflammation
(none to marked infm)
 Score 0-4

 Fibrosis
(none to cirrhosis)  Score 0-4 total=22
 Normal LFT Values
Total bilirubin 0.3-1mg/dl (DB 0.1-0.3)
Urine urobilinogen 1 – 4 mg/day
Stercobilinogen 40 – 280 mg/day

Aminotransferases 0 – 35 IU/L
Alkaline phosphatase 35 – 100 IU/l
Lactate dehydrogense 90 – 300 IU/L (6-16%)
5 – Nucleotidase 1 – 18 IU/L
GG Transpeptidase 11 – 64 IU/L
 Normal LFT values
S.Albumin 3.5 – 5.5 gm/dl
S.globulin 2.0 – 3.5 gm/dl

S.Fibrinogen 175 – 400mg/dl

Plasma Ammonia 10 – 80 micg/dl

International N ratio 1 - 1.3

Partial thromboplastin Time 25 - 35 seconds

Prothrombin time 11 - 14 seconds

 Clinical presentation
1. Asymptomatic patient with abnormal LFT

2. Acute hepatitis/Acute liver failure

3. Chronic hepatitis

4. Cirrhosis(compensated & decompensated)

5. Obstructive jaundice(Benign & malignant)

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.
Evaluation of Isolated
Raised AST/ALT
Evaluation of Isolated
ALT Elevation
 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.
 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.
 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%.
 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.
 Acute liver failure(cont)
B) Acetaminophen patients

PH < 7.3 or

PT 6.5 (INR) and

S.Creatinine>3.4mg/dl.
 Acute liver failure (cont)
Paul Brousse hospital criteria

Hepatic encephalopathy and

Factor V <20% in patients < 30yrs.

or
Factor V<30% in patients >30yrs.
 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
 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).
 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.
 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.
Chronic hepatitis new classification
Grade stage

 CPH Mild None or mild

 CLH Mild or mod Mild

 CAH Mild to severe Mild to cirrhosis

 Chronic hepatitis B
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 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.
 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.
 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.
 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.
 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).
 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
 Complication of Decompensated
cirrhosis(cont)
 Kidney - Hepatorenal syndrome

 CVS - Cardiomyopathy

 CNS - Hepatic encepalopathy

 MSK - Osteoporosis
Osteopenia

 Nutrition - Malnutrition
 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%
 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.
 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.
 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.
 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.
 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).

 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.

 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.

 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)
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.
Anaesthetic consideration regarding
gatroesophageal varices
 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
ascites
 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.).
Ascites Anaesthetic consideration
Preoperative Respiratory distress
Hypotension if inadeq replaced
after LVP
Hepatic hydrothorax
Risk for SBP (50% mortality)
Intraoperative Risk for aspiration
False high CVP
Haemodynamic instability
Splinting effect to diaphragm
Increased volume of distribution
Ascites Anaesthetic consideration
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.
 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

 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).
 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).
 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).
 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.

 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

 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
 Coagulation parameters and
neuraxial block
 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
 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.
 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
 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.
 V.Cholestatic jaundice
Diff. Features Intrahepatic Extrahepatic

Fever Absent Present

Abdominal pain Absent Present

Prodromal symptom Present Absent

H/O of surgery Absent Present

Cirrhosis stigmata Present Absent

 Cholestatic jaundice
Diff. Features Intrahepatic Extrahepatic

Palpable gallbladder Absent Present

Total bilirubin Variable <30mg/dl

B.Dilatation on USG Absent Present

ERCP Not needed Needed

Vit K treatment Variable Responsive

 Benign vs Malignant surgical
jaundice
Diff.Features Benign Malignant
Mode of onset Acute Insidious
Fever with chills Present Absent
Abdominal pain Present Absent
Palpable gallbladder Absent Present
Total bilirubin <10mg/dl 10-30mg/dl
 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.
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.

Effect of obstructive jaundice on the
Renal function
 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.
 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.
 Antiendotoxin measures
 Avoid oral antibiotics.
 Avoid percutaneous external drainage.
 Oral lactulose.
 Oral ursodeoxycholic acid.
 Endoscopic internal biliary drainage.

 Experimental drugs – Taurolidine

Rifaximin
Polymyxin.
 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).
 Preoperative investigation
 Haematological Blood grouping/typing
Haemoglobin/ HCT
WBC count
Platelet count
Bleeding Time
PT / INR
APTT
 Liver function tests.

 Serology for viral hepatitis.

 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) .
 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
 Modified Child-Pugh Score
Parameters 1 2 3

Albumin(g/dl) >3.5 2.8 - 3.5 <2.8

INR <1.7 1.7 - 2.3 >2.3

Bilirubin(mg/dl) <2 2 - 3 >3

Ascites Absent Moderate Tense

Encephalopathy None Grade I-II Grade III-IV

Class A =5 to 6 B= 7 to 9 C=10 to 15
Mortality 10% 31% 76%
 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.

 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)

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.

 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
 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%
 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.
 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
 EXAMPLES FOR ASA CLASSES
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
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
MORTALITY IN ASA SUBCLASS

ASA I & II - 0.3 %

ASA III - 4 to 5%

ASA IV - 25 to 30%

ASA V - > 70 %
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
 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
 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.
 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.
 Ascites Treatment
 Salt restriction  Not > 2 gm per day

 Fluid restriction  800-1000ml/day if serum

sodium < 125meq/L
 spiranolactone  Dose 100mg per day
(max dose 400mg)
 Furosemide  Dose 40mg per day
(max dose 160mg)
 Albumin  8-10g/L of fluid removed
(if > 5L removed)
 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.
 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.
 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.

 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.
 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

 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.
 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.
 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.

 Intraoperative monitoring and
equipment
 Pulse oximetry  NM monitoring

 Urine output
 NIBP/INVASIVE B.P.
 Blood loss(swab,suction,drape
 Electrocardiography & floor)
 Input – output
 PCWP/ CVP
 Rapid infusion system

 ETCO2  Forced air warmers

 Temperature
 Biochemical/Haematological
Monitoring
 Haematocrit

 Serum electrolytes / ionised calcium

 Blood glucose

 Arterial blood gas analysis

 Coagulation parameters / TEG

 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.
Summary
Thank you