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Dr. Debjyoti Mandal
2nd Year PGT
Dept of Anaesthesiology
BSMCH
Definition-
Postoperative jaundice is defined as the elevation of
bilirubin that occurs after the completion of surgery and
has many possible causes, associated laboratory
findings, and implications.
It can, but not always, be associated with icterus.
Jaundice Factfile-
Approximately 1 out of 80 healthy patients who
undergo surgery under anaesthesia (mostly cardiac
surgery) may have clinically significant post
operative liver dysfunction that is totally unrelated
to surgery or anaesthesia
Increased Bilirubin Production Decreased Bilirubin Excretion
 Hemolysis
 Massive blood
transfusion
 Incompatible
transfusions
 Ineffective
erythropoiesis
 Large hematoma
absorption
***all leading to hemolytic
jaundice
 Inherited Liver
Disorders
1. Gilberts Syndrome
2. Criggler Najjar Type I,II
3. Dubin Johnson Syndrome
4. Rotors’ Syndrome
 Acute Liver Disease
1. Viral infections
2. Parasitic infections- Malaria,
Leptospirosis
3. Reye’s Syndrome
4. Alcoholism
 Chronic Liver
Disease
 Hemolytic Jaundice results in unconjugated
hyperbilirubinemia.
 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.
 Prosthetic cardiac valves known to cause the same.
Diagnosed by Biochemical tests
 Elevated LDH
 Ser. Unconjugated Bilirubin
 Reticulocyte count
 Urinary Haptoglobulin
 Mild self - limiting conjugated
hyperbilirubinemia
 Reactive hepatitis - multifactorial origin
- reduced hepatic blood flow
- hypoxia, hypercarbia
- breakdown of transfused cells
- temporary hepatocellular
dysfunction
 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
 Primary biliary tract problem
 Significant liver disease
 Severe 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.
 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
 There are essentially 3 types of
hepatobiliary disorders associated with
parenteral nutrition (PN) therapy: steatosis,
cholestasis, and gallbladder sludge/stones.
 Etiologic factors specifically related to the
PN formulation or nutrient intake have also
been evaluated, including excessive calorie
intake, dextrose-to-lipid ratio, amino acid
dose, taurine deficiency, IV fat emulsion
(IVFE) dose, carnitine deficiency, choline
deficiency, and continuous vs cyclic
infusion.
 Minor increases in serum aminotransferase
concentrations are relatively common in
patients receiving PN therapy and generally
require no intervention.
 The primary indicator of cholestasis is a
serum conjugated bilirubin >2 mg/dL.
 When a patient receiving PN develops liver
complications, it is necessary to rule out all
treatable causes and minimize other risk
factors.
 All potential hepatotoxic medications and
herbal supplements should be eliminated.
 Modifications to the PN regimen that may
be helpful include reduction of calories,
reduction of IVFE dose to <1 g/kg/d,
supplementation of taurine in the infant,
and use of cyclic infusion. Initiation of even
small amounts of enteral nutrition and use
of ursodiol may be beneficial in stimulating
bile flow.
 In the long-term PN patient with severe and
progressive liver disease, intestinal or liver
transplantation may be the only remaining
treatment option.
 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.
 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
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
 Isoniazid
 Oral Contraceptives
 Erythromycin
 Acetaminophen-
centrilobular necrosis
 Aspirin- dose-related,
reversible form of
hepatotoxicity
 Hydralazine
 Methyl dopa
 Cephaloporins-
hepatitis
 Alcohol
 Valproate
 Phenytoin-hepatocellular
necrosis
 Carbamazepine-
cholestasis
 Statins-transient elevation
of liver enzymes
 Amiodarone
 Neurohumoral response
 Non pulsatile perfusion
 High dose Vasopressors
Obtain following History
 H/O Blood transfusion
 H/O IV drug abuse
 Alcohol
 Hepatotoxic drugs, toxins,infections
 Family History
 Past Medical History
 Any Surgery
 Icterus
 Fever
 Abdominal mass/ tenderness
 Stigmata of chronic liver disease
 Liver function tests
 Blood culture
 USG/ CT
 ERCP/ PTC
 Liver biopsy
Distinguish whether jaundice is prehepatic, hepatic or
post hepatic.
Identify reversible causes.
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
Postoperative Jaundice

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Postoperative Jaundice

  • 1. Dr. Debjyoti Mandal 2nd Year PGT Dept of Anaesthesiology BSMCH
  • 2. Definition- Postoperative jaundice is defined as the elevation of bilirubin that occurs after the completion of surgery and has many possible causes, associated laboratory findings, and implications. It can, but not always, be associated with icterus.
  • 3. Jaundice Factfile- Approximately 1 out of 80 healthy patients who undergo surgery under anaesthesia (mostly cardiac surgery) may have clinically significant post operative liver dysfunction that is totally unrelated to surgery or anaesthesia
  • 4.
  • 5.
  • 6. Increased Bilirubin Production Decreased Bilirubin Excretion  Hemolysis  Massive blood transfusion  Incompatible transfusions  Ineffective erythropoiesis  Large hematoma absorption ***all leading to hemolytic jaundice  Inherited Liver Disorders 1. Gilberts Syndrome 2. Criggler Najjar Type I,II 3. Dubin Johnson Syndrome 4. Rotors’ Syndrome  Acute Liver Disease 1. Viral infections 2. Parasitic infections- Malaria, Leptospirosis 3. Reye’s Syndrome 4. Alcoholism  Chronic Liver Disease
  • 7.  Hemolytic Jaundice results in unconjugated hyperbilirubinemia.  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.  Prosthetic cardiac valves known to cause the same. Diagnosed by Biochemical tests  Elevated LDH  Ser. Unconjugated Bilirubin  Reticulocyte count  Urinary Haptoglobulin
  • 8.  Mild self - limiting conjugated hyperbilirubinemia  Reactive hepatitis - multifactorial origin - reduced hepatic blood flow - hypoxia, hypercarbia - breakdown of transfused cells - temporary hepatocellular dysfunction
  • 9.  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
  • 10.  Primary biliary tract problem  Significant liver disease  Severe sepsis
  • 11.  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.
  • 12.  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
  • 13.  There are essentially 3 types of hepatobiliary disorders associated with parenteral nutrition (PN) therapy: steatosis, cholestasis, and gallbladder sludge/stones.  Etiologic factors specifically related to the PN formulation or nutrient intake have also been evaluated, including excessive calorie intake, dextrose-to-lipid ratio, amino acid dose, taurine deficiency, IV fat emulsion (IVFE) dose, carnitine deficiency, choline deficiency, and continuous vs cyclic infusion.
  • 14.  Minor increases in serum aminotransferase concentrations are relatively common in patients receiving PN therapy and generally require no intervention.  The primary indicator of cholestasis is a serum conjugated bilirubin >2 mg/dL.  When a patient receiving PN develops liver complications, it is necessary to rule out all treatable causes and minimize other risk factors.  All potential hepatotoxic medications and herbal supplements should be eliminated.
  • 15.  Modifications to the PN regimen that may be helpful include reduction of calories, reduction of IVFE dose to <1 g/kg/d, supplementation of taurine in the infant, and use of cyclic infusion. Initiation of even small amounts of enteral nutrition and use of ursodiol may be beneficial in stimulating bile flow.  In the long-term PN patient with severe and progressive liver disease, intestinal or liver transplantation may be the only remaining treatment option.
  • 16.  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.
  • 17.  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
  • 18. 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
  • 19.  Isoniazid  Oral Contraceptives  Erythromycin  Acetaminophen- centrilobular necrosis  Aspirin- dose-related, reversible form of hepatotoxicity  Hydralazine  Methyl dopa  Cephaloporins- hepatitis  Alcohol  Valproate  Phenytoin-hepatocellular necrosis  Carbamazepine- cholestasis  Statins-transient elevation of liver enzymes  Amiodarone
  • 20.  Neurohumoral response  Non pulsatile perfusion  High dose Vasopressors
  • 21. Obtain following History  H/O Blood transfusion  H/O IV drug abuse  Alcohol  Hepatotoxic drugs, toxins,infections  Family History  Past Medical History  Any Surgery
  • 22.  Icterus  Fever  Abdominal mass/ tenderness  Stigmata of chronic liver disease
  • 23.  Liver function tests  Blood culture  USG/ CT  ERCP/ PTC  Liver biopsy
  • 24.
  • 25.
  • 26. Distinguish whether jaundice is prehepatic, hepatic or post hepatic. Identify reversible causes. 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