Obstructive Jaundice – Whipple’s Operation Anesthetic Management

1. Obstructive Jaundice – Whipple’s OperationAnesthetic Management Munisha Agarwal Professor Deptt. of Anaesthesiology & Intensive Care L N Hospital & Maulana Azad Medical College Delhi Obs. J www.anaesthesia.co.inanaesthesia.co.in@gmail.com

2. Obstructive Jaundice Physiological functions of Liver ? Obs. J

3. Physiological functions of Liver • Glucose Homeostasis • Fat Metabolism • Protein Synthesis • Drug & Hormone Metabolism • Bilirubin formation &excretion • Anti bacterial action • Blood Reservoir Obst. J

4. Glucose homeostasis Glucose hepatocytes glycogen glucose lactate glycerol AA Obst. J

5. Glucose Homeostasis • Glycogen stores 75gm 24—48hrs • Anesthesia – gluconeogenesis • Provide ext. source of glucose Obst. J

6. Fat metabolism • Synthesis of lipo-proteins & cholesterol • Oxidation of FA to ketone bodies Obst. J

7. Protein Metabolism • Deamination of AA • Formation of urea • Plasma proteins - All except y globulin & factor VIII - Albumin daily prod. 10—15g/d (3.5-5.5gm%) - liver disease  alb  glob Albumin ? Obst. J

8. Protein synthesis • Plasma O. P. • Drug binding • Coagulation • Hydrolysis Obst. J

9. Drug binding • Drugs reversibly combine with Albumin •  albumin  binding sites  free drug • Albumin < 2.5gm% • Acute Hepatic dysfunction ? Coagulation ? Obst. J

10. Drug binding • Acute hepatic dysfunction - drug binding not affected • T ½ Albumin : 14 – 21 days • Coagulation : affected (2—6hrs) • Vitamin K dependent Coag. Factors? Obst. J

11. Coagulation • Prothrombin, fibrinogen • Factor V, VII, IX, X ( except VIII) Deranged Coagulation ? Obst. J

12. Coagulation Deranged coagulation • ed synthesis of Clotting factors • ed PT Vit. K deficiency d/t biliary obstruction absence of bile salts • Thrombocytopenia • ed Fibrinolysins Obst. J

13. Coagulation • Evaluate PT/ PTTK/ BT • LFT grossly deranged before coagulation abnormalities appear • 20%--30% activity required for normal coagulation • T1/2 of clotting factors produced in liver is very short (in hrs) • Ac. Hep dysfunction  Coag. Abn. Obst. J

14. Drug metabolism - Lipophilic →water soluble, less reactive Enzymatic reaction phase I - oxidation (Cyt P450) - reduction & hydrolysis (L.A) phase II - conjugation, glucuronidation, sulphation, methylation & acetylation - UDGT ( Bilirubin, morphine, aminophylline) Conjugation reaction? Obst. J

15. Drug metabolism Clearance of drugs from plasma High HE ratio ~ Hepatic Blood Flow (HBF) Lidocain, Pethidine, Fentanyl low HE ratio ~microsomal enzymes ~protein binding diazepam, thiop, pancuronium Obst. J

16. Drug metabolism Anesthetic implications • Chronic liver disease  drug metabolism d/t - ed no. of hepatocytes - HBF • Repeated injection  cumulative effect • Volatile anesth. Agents  ed clearance of drugs Obst. J

17. Bilirubin formation & excretion • Daily prod 250—350mg/d • Interpretation of plasma & urine bilirubin • Categories of liver dysfunction 1 unit BT ? Obst. J

18. Blood Reservoir • 10% of total blood volume • Available for Auto transfusion into central circulation Obst. J

19. Hepatic Blood Supply • Unique ? Obst. J

20. Hepatic Blood Supply • 25% to 30% of CO • Dual supply Portal V (75%) 85% saturated Hepatic A (25%) 95%saturated 2/3 of oxygen used by liver Obst. J

21. Control of Liver Blood Flow INTRINSIC • AUTOREGULATION - Hepatic artery-80 mmHg - Portal vein – flow from spleen, intestine - resistance to vascular bed • Hepatic Arterial Buffer response. Extrinsic ? Obst. J

22. Increase HBF Acute hepatitis Supine posture Hypercapnia Drugs βadrenostimulation Decrease HBF Hypoxia Hepatic cirrhosis Upright posture Hypocapnia/IPPV/PEEP Drugs βadrenoreceptor blockade/ α agonist Ganglion blockade Anaesthetic agent Control of Liver Blood FlowEXTRINSIC Obst. J

23. Liver Function Tests • Non specific • Large hepatic reserve LFT ? Obst. J

24. Liver Function Tests • S. Bilirubin (T) - 0.3—1.1mg% {(I) 0.2-0.7mg%, (D)0.1—0.4mg%) • Transaminases—SGOT/SGPT/LDH hepatocyte damage hypoxia/drugs/viruses Extrahepatic—heart/lungs/skeletal ms Marked (3x)-ac. Hep damage • Alkaline phoshphatase - bile duct cells slight obstruction (3x) bone –extrahep source • S. Albumin • 5- Nucleotidase • GGT Prehepatic / Hepatic / Posthepatic J ? Obst. J

25. Obst. J

26. SPECTRUM OF LIVER DISEASE • Parenchymal-Acute & Chronic Hepatitis -Hepatic Cirrhosis (+ portal hypertension) • Cholestatic -Intrahepatic – viral hepatitis – drug induced -Extrahepatic (Obstructive jaundice) – Calculi, stricture, growth. Parenchymal disease ultimately possesses an obstructive component & Obstructive disease produces cellular dysfunction. Clinical Hallmarks ? Obst. J

27. Signs &Symptoms • Prog sev jaundice • Dark urine • Clay coloured stools • Pruritis • High fever+ chills • Biochemical hallmarks Obst. J

28. Obstructive Jaundice • Primary mechanism- Obst. of E.H. bile duct. • Bile duct pressure - Normal – 10-15 cm H2O > 15 cm → bile flow decreases > 30 cm → bile flow stops Obst. J

29. Pathophysiological consequences Obst. J Bile Acids are potent toxins

30. Endotoxemia in obstructive jaundice Bile salts are surfactants----disrupt endotoxins Causes of endotoxemia • Absence of bile in intestine  intest.bact. Flora • Breakdown of GI mucos. barrier- bact. translocation • Hepatic RES function clearance of endotoxins Systemic Alterations – CVS ? Obst. J

31. Systemic alterations • Circulatory homeostasis CHOLEMIA ●vasodepressor effect on BVs ● cardiodepressor  LVF ● PVR   BP  sympath + renal & cerebral vasoconstriction ●redistribution of TBV  trapping of blood in splanc. Circulation  effective BV ● NO - insensitive to vasoconstrictors  Hypotension & circulatory collapse Obst. J

32. Renal system • Mild renal vasoconstriction • Renal hypoperfusion( hypovolemia) • Refractoriness of tubules to ADH • Endotoxemia Obst. J

33. Renal System • Acute Renal Failure • Hepatorenal Syndrome Obst. J

34. Renal system Hepatorenal Syndrome • Oliguria • Inability to excrete Na in urine( 10mmol/l) • Functional change • Normal renal blood flow • Treatment : Prevention-identify high risk patients Obst. J

35. Systemic alterations • Coagulopathy(low grade DIC) Impaired platelet function  FDP---inhibition of fibrinolysis  Endotoxins • Hm gastritis & stress ulcers • Impaired wound healing Obst. J

36. Anesthetic problems in Obstructive Jaundice ? Obst. J

37. PROBLEMS DUE TO DYSFUNCTION OF LIVER ITSELF : - Low serum proteins - Coagulopathy - Drug metabolism and disposition - Metabolic derangement - Hypoglycemia - Electrolyte imbalance - Haematological - Anaemia – Thrombocytopenia – Leucopenia – DIC - Deficiency of fat soluble vitamins (A, D, E, K) - Increased serum cholesterol (atheromatous changes) Obst. J

38. PROBLEMS DUE TO INVOLVEMENT OF OTHERSYSTEMS • CVS– TBV , PVR , Circulatory collapse • Renal - pre renal azotemia - Hepatorenal failure • GIT - Hm gastritis & stress ulcers • Resp.– Arterial Hypoxemia - vulnerability to pulmonary infection • CNS – Hepatic encephalopathy Problems related to surgery ? Obst. J

39. Problems related to surgery • Whipple’s procedure---Carc. Head of panc • Distal gastrectomy,PJ, HJ, GJ • Major surgery---long duration • Increased blood loss/fluid shifts • Wide incision---Roof top—warrants good postoperative analgesia • Extensive monitoring reqd for favourable outcome Obst. J

40. Risk Factors • Age > 60yrs • Albumin < 30gm% • Preop. renal dysfunction • Long standing biliary obstruction  infection  sepsis • Weight loss Serum creatinine & Sepsis—prognostic factors Periop CVS collapse & renal failure Obst. J

41. Preoperative Assessment OBJECTIVES • Assess the type and degree of liver dysfunction. • Assess effect on other system. • To ensure – post operative facilities (High risk patient). Obst. J

42. Preoperative Assessment • History • Clinical examination • Investigations ??? Unexplained jaundice of 4wks duration or longer will prove to be caused by obstruction in nearly 75% patients Blumgart L Obst. J

43. Preoperative Investigations To know the pattern of disease : ­ S. Bilirubin ­ SGOT, SGPT 90% predictive ­ alk. phosphatase Obst. J

44. Preoperative Investigations To judge the synthetic ability of liver • Serum albumin– < 2·5 gm% - severe damage • Albumin/globulin ratio – reversed. • Prothrombin time –> 1·5 sec. Over control – INR - > 1.3 (D/D – Par entral Vit. K – Obst. Jaundice) Obst. J

45. (i) Haematological · Hb TLC, DLC Platelet Count Clotting factors (PT, PTTK) BT (ii)Cardiorespiratory Chest X-ray ECG Blood gases (iii) Metabolic- Serum proteins Serum glucose Electrolyte Urea / Creatinine Urinary-Urea/ Creatinine -Electrolyte (iv) Hepatic imaging (v) Microbiological – - Culture -Hep. B marker - Viral antibodies To assess general condition of patient Obst. J

46. Preoperative management • Avoid prolonged hyperbilirubinemia • Treat infection –cholangitis • Use Aminoglycosides carefully • Avoid pre renal failure • Correct Anaemia/Coagulation/hypoalbuminemia • Avoid all NSAIDS • I/V saline & mannitol pre & postop Obst. J

47. Preoperative management No conclusive evidence for – • Preop percutaneous biliary drainage • Gut sterlization • Polymyxin B • Oral bile salts Pre medication ? Obst. J

48. Premedication • Anxiolytic – oral short acting BDZ • Oral H2 antagonist • Vit. K (Obst. J) – 10 mg B D X 3 day • If Bilirubin > 8 mg% – · I/V fluid – 1-2 ml/kg/hr. · Mannitol – 100 ml of 20% 2 hrs preop. • Order morning PT / S. Electrolyte • Preop urinary catheter & CVP Obst. J

49. Anaesthetic Management General Considerations Minimize physiological insult to liver & kidney • Maintain O2 supply – demand relationship in liver. →Adequate pulmonary ventilation and cardiovascular fn. • Maintain renal perfusion →Avoid Hypotension, hypoproteinemia & Hypoxia → meticulous fluid balance Choose appropriate anaesthetic agent Metabolism of drugs + Effect on HBF. Induction ? Obst. J

50. Anesthetic technique • General anesthesia • Preoxygenation • Induction - Thiopentone Propofol • Muscle relaxant – Suxamethonium Vecuronium 0.15mg/kg Rocuronium0.6mg/kg Atracurium(DOC) • Opioids ? Obst. J