Postoperative jaundice - Dr PSN Raju

Approach to Jaundice
Dr.Ashok.K.

Jaundice factfile
 Approximately 1 out of 80 healthy
patients who undergo cardiac surgery
and anaesthesia may have clinically
significant post operative liver
dysfunction that is totally unrelated to
surgery or anaesthesia

Key Learning Objectives
 What is jaundice?
 Bilirubin metabolism
 Implications of hyperbilirubinemia
 D/D of post operative jaundice
 Appropriate workup.
 Management

Definition of Jaundice
 Jaundice from French word “jaune” for yellow.
 Yellow discoloration of skin, M/M and sclera -
secondary to hyperbilirubinemia.
 Bilirubin is yellow tetrapyrrole.
 Clinical Jaundice when total bilirubin is > 2.0-
3.0 mg.

PREHEPATIC
- HAEMOLYTIC
HEPATOCELLULAR POST HEPATIC-
OBSTRUCTIVE

Cardiovascular implications of
hyperbilirubinemia
 Cholemia can impair myocardial
contractility
 Direct depressant effect on the SA node.
 Blunts response to vasopressors
 Hyperdynamic circulation
 More susceptible to hypotension from
blood loss.

HYPERBILIRUBINEMIA
Production Clearance

Increased Bilirubin production
 Hemolysis
 Massive blood transfusion
 Incompatible transfusions
 Ineffective erythropoiesis
 Large hematoma absorption

Hemolytic Jaundice
 Unconjugated hyperbilirubinemia due
- hemolysis,
- resorption of hematoma,
- minor/ major incompatibility
- massive transfusion
 10% of transfused RBCs hemolyse within the
first 24 hours following transfusion.
 Each unit of blood provides a bilirubin load of
250 mgs/100 cc of blood

Hemolytic Jaundice
 Seen in caged ball valves, multiple
prosthetic valves, periprosthetic leaks,
prosthetic valve endocarditis.
 Diagnosis is by elevated LDH, reticulocyte
count, unconjugated bilirubin, and urinary
haptoglobin.
 ECHO- abnormal rocking of prosthesis,
regurgitant jets.

Hemolytic Jaundice
 Medical therapy: Blood transfusion.
Iron and folate
supplements.
Avoid hepatotoxic drugs.
 Surgical therapy: Repair of perivalvular leaks
or valve replacement in patients with severe
hemolysis in patients requiring repeated blood
transfusions or those with CCF.

Decreased clearance of Bilirubin
Decreased uptake by hepatocytes
- Gilberts Syndrome
- Criggler Najjar Type I,II
Impaired excretion of conjugated Bile
from Hepatocytes
- Dubin Johnson Syndrome
- Rotor Syndrome

Acute Liver Diseases
Viral infections
Parasitic infections- Malaria, Leptospirosis
Reye’s Syndrome
Alcoholism

Chronic Liver Diseases
Viral ( Hep B & C )
Alcohol
Vinyl chloride, CCl 4
Metabolic Liver Diseases
- Wilson’s,
- Hemochromatosis,
- Alpha-1antitrypsin deficiency.

Viral hepatitis
 Hepatitis A-E
 They can elude peri op detection during
their incubation periods.
 Diagnosis made by clinical symptoms,
signs, and serology
 Mainstay of therapy is supportive
 Appropriate preventive measures to be
taken to prevent cross infection

Benign postoperative cholestasis
 Mild self - limiting conjugated
hyperbilirubinemia
 Reactive hepatitis - multifactorial origin
- reduced HBF
- hypoxia, hypercarbia
- breakdown of transfused cells
- temporary hepatocellular
dysfunction

Benign postoperative cholestasis
 Warrants assessment of the patient’s
condition and sequential biochemical
profiles.
 Coagulopathy corrected with Vit K.
 Usually subside within 3-4 weeks.
 Failure of Vit K to correct a prolonged
PT typically indicates the presence of
hepatic parenchymal dysfunction

Progressive severe jaundice
 Primary biliary tract problem
 Significant liver disease
 Severe sepsis

Sepsis
 Early - Increased splanchnic blood flow
as a consequence of increased hepatic
oxygen extraction to support
phagocytosis of sudden overload of
bacterial endotoxins.
 Late - Constricted splanchnic
vasculature due to septic shock.
 Dysregulation of physiologic hepatic
arterial buffer response.

Right heart failure
 Passive hepatic congestion due to CCF
causes little if any damage to liver.
 Prognosis depends on the severity of
underlying cardiac illness.
 Reversible after the cardiac function is
improved.

Anaesthetic Agents
 N20 – Higher prevalence of jaundice in
personnel chronically exposed to N2O.
 Propofol, midazolam, fentanyl have not
been shown to significantly alter hepatic
function.
 Very large doses (>750 mgs) of
thiopentone may cause hepatic
dysfunction.

Halothane hepatitis
 Incidence 1:7000-30,000
 It is even rarer in paediatric patients and
with the newer volatile agents.
 The risk is thought to be higher in
- women,
- middle aged,
- obese,
- repeated exposure within 4 weeks

Halothane hepatitis
 Possible immunological mechanism..
 Hepatic blood flow is decreased by
halothane in parallel with an overall
decrease in cardiac output.
 Avoid repeat exposure within 3 months.
 History of unexplained jaundice following
Halothane use is an absolute contraindication
for its further usage

Common Hepatotoxic drugs
 Isoniazid
 Oral contraceptives
 Androgens
 Chlorpromazine
 Erythromycin
 Acetaminophen
 Hydralazine
 Methyl dopa
 Halothane
 Alcohol
 Valproic acid
 Phenytoin
 Carbamazepine
 Statins
 Allopurinol
 Amiodarone

Drug induced liver damage
ANTIBIOTICS
 Tetracyclines - fatty infiltration
 Penicillins,Cephalosporins – hepatitis
 Sulphonamides - hypersensitivity
focal hepatocellular
necrosis

ANALGESICS
 Paracetamol - centrilobular necrosis
 Salicylates - focal hepatic necrosis
 Carbamazepine - cholestasis

 STEROIDS - cholestasis.
 HALOTHANE - hepatitis ,massive liver
cirrhosis.
 PHENYTOIN - hepatocellular necrosis

Statins
 HMG - CoA reductase inhibitors.
 Statins reduce cholesterol by blocking
an enzyme in the liver (HMG-CoA
reductase) that produces cholesterol.
 Statins cause abnormalities of liver
tests, and cause transient elevations in
liver enzymes.

Statins
 Therapy should be discontinued if > 3-
fold elevation in AST,ALT occurs.
 Enzyme levels return to normal within 2
weeks.
 Levels should be measured 6 weeks and
3 months after initiation of therapy and
every 6 months thereafter.
 Contraindicated in the presence of pre
existing hepatic dysfunction.

Aspirin
 Well documented cause of dose-related,
reversible form of hepatotoxicity.
 Within days to weeks after initiating
therapy.
 Increased aminotransferases.
 Hyperbilirubinemia uncommon.
 Resolves with discontinuation of
therapy.

Paracetamol
 Commonly used drug for post op pain.
 Large doses (3-8 gm/day) results in
chronic liver injury.
 In patients with poor nutritional status
even 2 gm/day may produce serious liver
injury.
 Whenever suspected , N-acetylcysteine
should be given without delay,

Post Pump Jaundice
 Hypotension
 Hypoxia
 Haemolysis
 Heart failure.
 Hypothermia ???

Post Cardiopulmonary bypass
 Neurohumoral response
 Non pulsatile perfusion
 High dose vasopressors

History
 H/O Blood transfusion
 H/O IV drug abuse
 Alcohol
 Hepatotoxic drugs, toxins,infections
 Family History
 Past Medical History
 Any Abdominal Surgery

Physical Examination
 Icterus
 Fever
 Abdominal mass/ tenderness
 Stigmata of Chronic Liver Disease
 Kayser-Fleischer ring
 Hyperpigmentation, Xanthomas

Lab investigations
 Liver function tests
 Blood culture
 USG/ CT
 ERCP/ PTC
 Liver biopsy

Aminotransferases
 Indicators of hepatocellular injury
 Normal levels:
AST- 5-35 IU/L
ALT- 5-35 IU/L

Aminotransferases
 Small increase (<3-fold) – steatosis,
chronic viral hepatitis
 Larger increases (3-20 fold) – suggest
acute hepatitis or exacerbation of
chronic hepatitis
 Largest increases (>20-fold) – indicates
massive hepatocellular necrosis (severe
viral hepatitis, septic shock, drug
toxicity)

Alkaline Phosaphatase
 Sensitive test for assessing the integrity
of the biliary system.
 Also elevated in hepatocellular jaundice,
Pajet’s disease, pregnancy.
 Normal level: 30-300 IU/L.

Bilirubin
 Assessment is central to the
evaluation of hepatobiliary disorders.
 Normal level- 0.25-1.0 mg/dl
 Estimation of direct, indirect and
total bilirubin.

Albumin
 Constitutes 60% of total protein
 Major determinant of C.O.P
 Best indicator of hepatic synthetic
function.
 Normal value: 3.5-5.0 gm/dl
 May be decreased in nutritional
deficiency
 Long half life -20 days- may not reflect
acute injury .

Glutathione -S- transferase
 Sensitive and specific marker for drug
induced liver damage.
 Aminotransferases are highly located in
zone 1 periportal region.
 GST is predominantly located in zone 2
centrilobular hepatocytes.
 Centrilobular hepatocytes are more
susceptible to injury from hypoxia,
hypotension and toxic products of drug
metabolism

Gamma glutamyl transpeptidase
 Specific marker for alcoholic liver
disease.
 Normal values:
Males: 11-51 IU/L.
Females: 7-33 IU/L.

5’ Nucleotidase
 Highly specific for hepatobiliary injury
 Also increased in cholestatic jaundice

LDH
 Serves as a marker for hepatic injury.
 Markedly increased in hepatocellular
necrosis, shock liver, hemolysis,
myocardial infarction.
 Normal level: 70-250 IU/L.

Serological Markers
Hepatitis A, B, C
Ferritin
Alpha-1 antitrypsin level
Ceruloplasmin
AMA
ANA & antismooth muscle antibody

Management of post op jaundice
 Determine the nature of jaundice by LFTs
and urine testing for bilirubin
 When suspected- screening tests for
hemolysis
 R/o sepsis – blood culture
 If jaundice is cholestatic,
- withdraw any offending drug
- USG,ERCP,PTC
- Percutaneous liver biopsy

Hemolytic jaundice
 Unconjugated hyperbilirubinemia
 Increased urobilinogen and urobilin in
urine.
 Increased LDH
 Increased reticulocyte count
 History S/O hemolysis.

Hepatocellular jaundice
 Grossly elevated serum transaminases.
 Conjugated hyperbilirubinemia.
 Increased GGT,5’ Nucleotidase
 Increased alkaline phosphatase
 History S/O hepatocellular injury.

Cholestatic jaundice
 Conjugated hyperbilirubinemia
 Increased GGT
 Increased 5’ Nucleotidase
 Increased Alkaline phosphatase
 Minimal or no elevation of transaminases
 Presence of bilirubin in urine.
 USG,CT,PTC.

Interpretation of LFTs
TESTS HEMOLYSIS PARENCHYMA CHOLESTASIS
AST,ALT N INCREASED N
ALP N N INCREASED
Sr.protein N DECREASED N
PT / INR N INCREASED N
Bilirubin UNCONJUGATED CONJUGATED CONJUGATED

 Patients with active liver disease, such
as hepatitis, are at high risk of
deterioration during surgery and this
should be avoided or delayed where
possible.

 Hypoperfusion, haemodilution and
other factors that reduce the delivery of
oxygen to the liver or increase the
bilirubin load are thought to cause
postoperative hyperbilirubinaemia and
should be avoided.

 Longer the operative time and the
larger the volume of blood transfused,
the higher the incidence of
postoperative hyperbilirubinaemia

Summary
 Distinguish whether jaundice is
prehepatic, hepatic or post hepatic.
 Identify reversible causes.
 Mainstay of treatment - supportive.
 Discontinue possible hepatotoxic drugs.
 Sepsis mandates aggressive therapy.
 Extrahepatic biliary obstruction may
prompt surgical treatment.

Postoperative jaundice - Dr PSN Raju

More Related Content

What's hot (20)

Viewers also liked (13)

Similar to Postoperative jaundice - Dr PSN Raju (20)

More from isakakinada (20)

Recently uploaded (20)

Postoperative jaundice - Dr PSN Raju