Postoperative Jaundice

Jaundice

1. Postoperative Jaundice Dr. Debjyoti Mandal 2 nd 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. HYPERBILIRUBINEMIA 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 Gilberts Syndrome Criggler Najjar Type I,II Dubin Johnson Syndrome Rotors’ Syndrome Acute Liver Disease Viral infections Parasitic infections- Malaria, Leptospirosis Reye’s Syndrome Alcoholism Chronic Liver Disease

5. 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 Hemolytic Jaundice

6. Mild self - limiting conjugated hyperbilirubinemia Reactive hepatitis - multifactorial origin reduced hepatic blood flow hypoxia, hypercarbia breakdown of transfused cells temporary hepatocellular dysfunction Benign postoperative cholestasis

7. 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

8. Primary biliary tract problem Significant liver disease Severe sepsis Progressive Severe Jaundice

9. 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. Sepsis

10. 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 Right Heart F ailure

11. 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. PN-associated liver disease (PNALD)

12. 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.

13. 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.

14. 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. Anaesthetic Agents

15. 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

16. 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

17. 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 Common Hepatotoxic drugs

18. Neurohumoral response Non pulsatile perfusion High dose Vasopressors Post Cardiopulmonary Bypass

19. Obtain following History H/O Blood transfusion H/O IV drug abuse Alcohol Hepatotoxic drugs, toxins,infections Family History Past Medical History Any Surgery Approach

20. Icterus Fever Abdominal mass/ tenderness Stigmata of chronic liver disease Physical Examination

21. Liver function tests Blood culture USG/ CT ERCP/ PTC Liver biopsy Laboratory Investigations

22. 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 Summary