Anaesthetic management of obstructive jaundice

1. Anaesthetic management of obstructive jaundice Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab.DCA, Dip. Software statistics PhD (physio) Mahatma Gandhi Medical college and research institute ,puducherry- India

2. Anatomy

3. Functions of liver • The liver is vital for • protein synthesis • glucose homeostasis • bilirubin excretion • toxin removal • the liver has a substantial functional reserve because of its dual blood supply: portal-venous (75%) and hepatic-arterial (25%).

4. The liver conjugates bilirubin, produced from the degradation of the haemoglobin of red cells that are at the end of their normal life span. • This now water-soluble form of bilirubin is then excreted into the bile ducts and thence into the small intestine

5. Physiology • Bile acids are derivatives of cholesterol synthesized in the hepatocyte. • Cholesterol, ingested as part of the diet or derived from hepatic synthesis is converted into the bile, which are then conjugated to an amino acid (glycine or taurine) to yield the conjugated form that is actively secreted into cannaliculi.

6. Pathophysiology of obstruction • As conjugated bilirubin is water-soluble it will be excreted in the urine which becomes dark. • Stools are pale as a result of poor lipid absorption. • the absorption of vitamin K is dependent on the excretion of bile salts into the small intestine.

7. Obstructive Jaundice – causes • extrahepaticcholestasis • choledocholithiasis, • tumors of the bile ducts and pancreas, postoperative strictures, • primary sclerosingcholangitis, • acute or chronic pancreatitis

8. Obstructive Jaundice – causes • intrahepaticcholestasis carcinomas of the intrahepatic ducts, primary sclerosing hepatitis bacterial cholangitis, • hepatic metastases,

9. Bile salts increase • so what ?? • Bile salts cause prolong steroid NMB ARF by ATN Cardiac arrhythmias

10. bilirubin increase • causes • ↓ SVR • Resistance to vasopressors • ↑ incidence of periop renal failure

11. What for - it comes to us ? • Surgery in these cases is to remove or bypass the obstruction or to drain infected obstructed bile. • i.e . CBD exploration • T tube insertion • Resection tumour • Choledochojejunostomy and bypass

12. Surgery?? • CTP class C, • high MELD score, • ASA class V, • acute hepatitis, • severe coagulopathy, • severe extrahepatic manifestations of liver disease (eg, acute renal failure, hypoxia, cardiomyopathy).

13. Bad cases • ERCP. • Percutaneous drainage • Come down on bilirubin, sepsis, • And try for major procedure

14. Obs. Jaundice different!! • Obstructive jaundice and hepatocellular disease may not go together • Only common thing • hyperbilirubinemia

15. Preop assessment • Routine assessment • Secretory function • Serum bilirubin1.25 mg = 20 µmol. • Jaundice can be prehepatic (haemolytic), hepatic (hepatocellular) or posthepatic (obstructive) in origin. Conj or unconj.

16. Synthetic function • Synthesis of many proteins takes place in the liver including most clotting factors and many carrier proteins, such as albumin, which to a varying degree bind drugs used during anaesthesia. How to assess?? • Serum albumin • Prothrombin time and INR

17. Metabolic function • AlanineTransaminase (ALT) and AspartateTransaminase (AST)-raised menashepatocellular damage • Alkaline Phosphatase (ALP) GammaglutamylTransferaseSignifies obstruction • Abnormal liver enzyme results -- 4% of normal individuals and up to 36% of psychiatric patients

18. coagulation • Prothrombin time and INR • Inj. Vit K as vit. K1 10-20 mg, 6-8hrly, 3 days • or FFP Correct coagulopathy with vitamin K and FFP to achieve prothrombin time within 3 seconds of normal. Sometimes DDAVP helpful

19. Decreased synthetic function • evidence of decreased protein synthesis, with oedema and ascites, • signs of delayed clotting only partly reversed by vitamin K administration, • and even encephalopathy • Alkalosis, hepatic encephalopathy more concerned in liver diseases

20. Child-Pugh score • Measure 1 point 2 points 3 points • Total bilirubin, • (mg/dl) (<2) (2-3) (>3) • Serum alb >35 28-35 <28 • INR <1.7 1.71-2.20 > 2.20 • Ascites None Mild Severe • Hepatic encep.None Grade I-II Grade III-IV

21. Ascites ; paracentesis , diuretics • Minimize ascites why? • decrease risk of abdominal-wall herniation, • wound dehiscence, problems with ventilation. • Encephalopathy – lactulose, • Avoid – azotemia, GI bleed, constipation, alkalosis , sedatives

22. Model For End-Stage Liver Disease • MELD = 3.8[Ln serum bilirubin (mg/dL)] + 11.2[Ln INR] + 9.6[Ln serum creatinine (mg/dL)] + 6.4where Ln is the natural logarithm • MELD score > 14 – high risk

23. Pre op investigations & assessment • Hb% • Edema, ascites. • Nutrition • SPO2 • Renal parameters. • Blood grouping typing

24. Pre op • Systolic and diastolic BP • Widened PP suggests CLD • The goal platelet count is >50-100 × 103/L • Correct preopHyponatremia Hypokalemia Hypomagnesemia Hypoglycemia More in liver disease

25. Pre op asssesssment • CxR • ECG --CMP • USG, CT scan • Drug history • Alcoholism • HbsAg

26. Infection more common • bacterial colonization of the biliary tree • impaired Kupffer cell function • defective neutrophil function • high rate of endotoxemia • Pre op antibiotics lactulose + • Rifaximin + broad spectrum antibiotics.

27. Perioperative mortality ranged from 8 to 28 percent • An initial hematocrit value <30 percent • An initial serum bilirubin level >11 mg/dL (200 µmol/L) • A malignant cause of obstruction (eg, pancreatic carcinoma or cholangiocarcinoma)

28. Respiratory system • Hepatopulmonary syndrome Pulmonary vascular dilatations, V A/Q mismatch Reduced DLCO • Shift in oxyhemoglobin dissociation curve, • Portopulmonaryanastomoses • Pulmonary hypertension

29. Respiratory system in obstruction alone ?? • Restrictive lung pattern due to ascites • Expiratory airflow obstruction • Chest wall deformity,Pleural effusions • Panacinar emphysema • Pleuritis, Bronchitis / bronchiectasis • Hepatic hydrothorax • Impaired hypoxic vasoconstriction • Respiratory alkalosis

30. Anaesthetics and liver disease • Nitrous oxide (N2O) produces decrease in portal blood flow, and mild vasoconstriction of the hepatic arterial system • But safe in the absence of hypoxemia • N2O - safe

31. Volatile anaesthetics • All volatile anesthetics decrease hepatic blood flow • but desflurane and sevofluranehave the least significant effect on total hepatic blood flow and hepatic oxygen delivery, • halothane induces the most profound reductions in hepatic blood flow. • Isoflurane ideal – in coagulation problems

32. halothane • Do not use after prior history or family history of unexplained jaundice after halothane? • Do not use unless indicated?

33. halothane : "exercise care if obese, pre-existing liver disease, hypoxia likely“, avoid if : over 40 years old, long operation, biliary surgery, female patient, obese, allergic, sepsis, exposure less than 3 months previously

34. Halothane and Jaundice • The incidence of this halothane hepatitis in adults is thought to be 1:7000-30,000 halothane anaesthetics. • rarer in paediatric patients and with the newer volatile agents. • The risk is higher in women, the middle aged and the obese.

35. IV anaesthetics

36. IV drugs • propofol, etomidate, and midazolam,- safe • Benzodiazepines in low doses acceptable • Thio in high doses ?? • Everything only in ??

37. Relaxants • Atracurium safe • Steroidal NMB s ?? • Suxa OK if renal parameters are normal

38. Narcotics • All opioids increase tone of the common bile duct and the sphincter of Oddi • But make patients pain free. • Use remifentanyl • Can use butrum or nalbuphine if peropcholangiogram is planned

39. peropcholangiogram is planned • If narcotic induced spasm is problematic • Options are • Use NTG, • naloxone • Or Inj glucagon 2 mg IM

40. Relaxants

41. Factors decrease liver blood flow • IPPV + PEEP • Hypocapnia & hypoxia • Upright Posture, abd. surgery • Cirrhosis, Alfa stimulants • Ganglion Blockers,H2 blockers • Vasopressin • Anaesthetics – Volatile & intravenous • Important in liver diseases

42. Monitoring • Simple chole or whipple s • If major , • add • CVP, IBP, temperature,NMJ,urine,ecg • Hyperbilirubinemic Vent. Tachycardia • Difib. Available

43. Renal protection • adequate hydration and a urine flow of at least 50ml/hr in the average adult patient. If bilirubin 20 mg% IV fluids 24 hours before surgery and for 36 hours, postop. IV mannitol 10% 0.5-1g/kg should be administered prior to surgery AND during surgery • Hydration and urine

44. Renal protection • Pre op albumin infusion decreased • Post op renal failure

45. Epidural and GA • If Coagulation parameters are ok • Post op and intraop analgesia • Epidural narcotics • Avoid hypoxemia, ETCO2 • Maintain hemodynamics, urine output

46. malignancy • Surgery – palliative or radical • Splanchnic plexus block with alcohol • Possibility of thrombosis

47. Post op • Pain • Hepatic flow , jaundice, encephalopathy • Renal protection • Oxygen and hemodynamics.

48. Summary of anaesthetic management of obstructive jaundice ??

49. Child reading ABCD • Child – child pugh criteria • A – antibiotics • B – blood, biliary spasm • C – coagulation • D – diuretics