postoperative jaundice - dr psn raju
TRANSCRIPT
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Approach to Jaundice
Dr.Ashok.K.
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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
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Key Learning Objectives
What is jaundice? Bilirubin metabolism Implications of hyperbilirubinemia D/D of post operative jaundice Appropriate workup. Management
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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.
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Bilirubin metabolism
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PREHEPATIC - HAEMOLYTIC
HEPATOCELLULAR POST HEPATIC-OBSTRUCTIVE
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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.
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HYPERBILIRUBINEMIA
Production Clearance
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Increased Bilirubin production
Hemolysis Massive blood transfusion Incompatible transfusions Ineffective erythropoiesis Large hematoma absorption
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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
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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.
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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.
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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
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Acute Liver Diseases
Viral infections
Parasitic infections- Malaria, Leptospirosis
Reye’s Syndrome
Alcoholism
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Chronic Liver Diseases
Viral ( Hep B & C ) Alcohol Vinyl chloride, CCl 4 Metabolic Liver Diseases
- Wilson’s, - Hemochromatosis,
- Alpha-1antitrypsin deficiency.
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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
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Benign postoperative cholestasis
Mild self - limiting conjugated hyperbilirubinemia
Reactive hepatitis - multifactorial origin
- reduced HBF
- hypoxia, hypercarbia
- breakdown of transfused cells
- temporary hepatocellular dysfunction
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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
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Progressive severe jaundice
Primary biliary tract problem Significant liver disease Severe sepsis
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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.
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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.
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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.
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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
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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
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Common Hepatotoxic drugs
Isoniazid Oral contraceptives Androgens Chlorpromazine Erythromycin Acetaminophen Hydralazine Methyl dopa
Halothane Alcohol Valproic acid Phenytoin Carbamazepine Statins Allopurinol Amiodarone
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Drug induced liver damage
ANTIBIOTICS
Tetracyclines - fatty infiltration Penicillins,Cephalosporins – hepatitis Sulphonamides - hypersensitivity focal hepatocellular
necrosis
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Drug induced liver damage
ANALGESICS
Paracetamol - centrilobular necrosis Salicylates - focal hepatic necrosis Carbamazepine - cholestasis
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Drug induced liver damage
STEROIDS - cholestasis. HALOTHANE - hepatitis ,massive liver
cirrhosis. PHENYTOIN - hepatocellular necrosis
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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.
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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.
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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.
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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,
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Post Pump Jaundice
Hypotension Hypoxia Haemolysis Heart failure. Hypothermia ???
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Post Cardiopulmonary bypass
Neurohumoral response Non pulsatile perfusion High dose vasopressors
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History
H/O Blood transfusion H/O IV drug abuse Alcohol Hepatotoxic drugs, toxins,infections Family History Past Medical History Any Abdominal Surgery
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Physical Examination
Icterus Fever Abdominal mass/ tenderness Stigmata of Chronic Liver Disease Kayser-Fleischer ring Hyperpigmentation, Xanthomas
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Lab investigations
Liver function tests Blood culture USG/ CT ERCP/ PTC Liver biopsy
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Aminotransferases
Indicators of hepatocellular injury Normal levels:
AST- 5-35 IU/L
ALT- 5-35 IU/L
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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)
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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.
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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.
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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 .
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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
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Gamma glutamyl transpeptidase
Specific marker for alcoholic liver disease.
Normal values:
Males: 11-51 IU/L.
Females: 7-33 IU/L.
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5’ Nucleotidase
Highly specific for hepatobiliary injury Also increased in cholestatic jaundice
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LDH
Serves as a marker for hepatic injury. Markedly increased in hepatocellular
necrosis, shock liver, hemolysis, myocardial infarction.
Normal level: 70-250 IU/L.
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Serological Markers
Hepatitis A, B, C
Ferritin
Alpha-1 antitrypsin level
Ceruloplasmin
AMA
ANA & antismooth muscle antibody
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CLINICAL APPROACH
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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
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Hemolytic jaundice
Unconjugated hyperbilirubinemia Increased urobilinogen and urobilin in
urine. Increased LDH Increased reticulocyte count History S/O hemolysis.
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Hepatocellular jaundice
Grossly elevated serum transaminases. Conjugated hyperbilirubinemia. Increased GGT,5’ Nucleotidase Increased alkaline phosphatase History S/O hepatocellular injury.
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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.
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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
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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.
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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.
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Longer the operative time and the larger the volume of blood transfused, the higher the incidence of postoperative hyperbilirubinaemia
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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.
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