1. Obstructive Jaundice (Long case-Exam oriented discussion) Dr Ramprasad Gorai Prof Dipasri Bhattacharya Dept of Anaesthesia, Critical Care & Pain. R.G.Kar Medical College

2. How to write long case? A. Patients particulars- B. History Proper- 1. Chief complaints 2. H/O Present illness 3. Past History 4. Family History 5. Personal History 6. Treatment History 7. Menstrual and Obstetric History C. Physical Examinations- 1. General Survey 2. Systemic Examination 1. GI 2.Hepato-biliary 3.CNS 4.CVS 5.Resp 6.Lymphoreticular 7.GU 3. Airway Assessment 4. Venous access D. Summary E. Provisional Diagnosis F. Differential Diagnosis G.Relevant Investigations

3. Patients particular 1.Name 2.Age 3.Sex 4.Address 5.Marital status 6.Occupation 7.Religion 8.Date of admission 9.Date of examination My patient Mr Robin Das is 56 year old Hindu married auto driver from Dumdum, North Kolkata admitted in R.G.Kar Medical college on 15th dec 2016 with chief complaints of- 1. Yellowish discoloration of eyes and urine-6 month 2. Swelling in right upper abdomen-5 month 3. Low grade fever-1 month Our Patient- Chief Complain 1. 2. 3.

4. H/O Present Illness Yellowish discolouration of eyes and urine Mass in abdomenFever 1. Gradual onset 2. Duration 6 month 3. Progressive 4. No prodromal symptom at onset 5. No abdominal pain 6. Associated with- -Pruritus -Clay coloured stool -Loss of appetite -Weight loss -Black liquid stool 7. No History of -Blood transfusion -Travel to endemic area -Upper abdominal surg. 1.Right upper abdomen 2.Duration 5 month 1.Low grade 2.No Chill & Rigor 3.No particular fever pattern 4.Can occur during day or night. 5. a/w -Loss of appetite, Weight loss, Easy fatigability 6.Duration 1 month.

5. Past History 1. Medical Illness (DM/HTN/IHD etc.) 2. Operative and Anaesthetic History 3. Hospitalization 4. Exposure 5. Contact (any contagious disease ) Personal History 1. Education 5. Income 2. Occupation 6. Life style 3. Marital status 7. Dietary Habit 4. Addiction 8. High Risk Behavior Family History 1. Similar illness in Family 2. HTN/DM/Asthma/IHD/Carcinoma 3. Consanguinous marriage 4. Bad anaesthetic history in relatives Treatment History 1. Treatment received so far for present illness. 2. Allergy / Blood transfusion 3. Daily medication Our Patient He is known Hypertensive which is well controlled with Amlodipine 5 mg once daily. No H/O DM, IHD, Asthma, COPD or any major illness Known smoker (10-15 bidi per day - 20 years) Non vegetarian, Auto driver by profession & denies any high risk behavior. Family history nothing significant. Visited local doctor for Jaundice and fever.

6. CONSENT OF PATIENT FOR EXAMINATION (including private part)

7. General Survey 1. Level of Consciousness (A/C/C) 2. Appearance 3. Build 4. Nutrition (BMI) 5. Decubitus 6. Facies 7. Anemia 12. Pulse 8. Jaundice 13. BP 9. Cyanosis 14. Respiration 10. Edema 15. Temparature 11. Clubbing 16. Saturation 17. Lymph nodes 18. Neck Vein and artery. 19. Nail/Skin/Hair 20. Dehydration 21. Obvious deformity 22. Bony tenderness 23. Thyroid gland Our Patient Nutrition poor Pallor ++ Deep jaundice present. No Cyanosis, Edema, Clubbing. Pulse 62/min, Regular, Volume normal,No Radio radial, Radio- femoral delay. All peripheral pulse are palpable. BP 140/80 mm of Hg in Right arm on sitting position. Scratch mark present on exposed body area. No Lymph node palpable.

8. Discussion with elaboration BMI Vital signs Pallor: Gastrointestinal bleeding Icterus Lemon yellow – Hemolytic Orange yellow – Hepatocellular Greenish yellow – Obstructive Pedal edema - hypoproteinemia Scratch marks - pruritis Xanthoma - hypercholesterolemia Bruises - Coagulopathy Fat Soluble vitamin deficiency Vitamin A deficiency – Bitot’s spot, hyperpigmentation Vitamin K deficiency - Ecchymoses GENERAL SURVEY

10. Syst Exam (GI & Hepato-biliary) INSPECTION Shape of the abdomen/Flanks/Umbilicus Movement with respiration Visible peristalsis/pulsation Engorged veins (direction of flow ) Striae/scar mark/Pigmentation Swelling or mass (tell the site) genitalia (with permission of the patient) PALPATION Organ-Liver/Spleen/Gall Bladder/Kidney/testes Mass-site/size/shape/consist/tender/Mobility) Fluid thrill Per-rectal & Per vaginal PERCUSSION Liver /Splenic dullness Shifting dullness (if ascites ). AUSCULTATION Bowel sounds Hepatic/Renal/Splenic - bruit or rub Our Patient Abdomen is scaphoid, Umbilicus normal, Flank are not full. No engorged vein or visible pulsation. Palpable mass in right subcostal region appear to be gall bladder, as its lower, lateral and medial border are palpable but upper border passes deep to costal margin and not palpable. Liver and spleen not palpable. No free fluid in abdomen.

11. Other System CNS CVS Respiratory Lympho-reticular Genito-urinary Our Patient CNS GCS 15/15. No asterixis. CVS Apex beat-5 th IC space inside midclavicular line.Heart sounds are normal.No murmur. Respiratory Resp rate 12/Min. Bilaterally normal vesicular breath sound. No added sound. Lympho-Reticular No lymphadenopathy Genito-urinary No abnormality

12. Airway Assessment 1. Mallampati Score 2. Mandibular Space -Thyro-mental distance -Hyo-mental distance 3. Neck Mobility 4. Neck Circumference 5. Inter incisor gap. 6. Upper lip bite test 7. Gross Anomaly/ Beard/ Artificial or loose tooth. Our patient Mallampati-2 Thyro-mental dist- 4 finger breadth Neck movement-Normal Inter incisor gap > 3 cm Mandibular teeth can be protruded beyond maxillary teeth.

13. Summary 56 years male hypertensive patient presented with Yellowish discolouration of eyes and urine for last 6 months, Mass in right upper abdomen for last 5 months and Low grade fever for last 1 month. Yellowish discolouration of urine and eyes is gradually onset, progressive, without any prodromal symptom at onset, and is associated with pruritus, clay colour stool but no abdominal pain although there is a mass in right upper abdomen. There is also history of passage of black tarry stool 2 months back, which lasted for about 7 days. No history of vomiting or hematemesis, or alteration of bowel habit. He also having low grade fever without chill and rigor. Fever occurs both day and night without any pattern and is associated with weight loss, anorexia, easy fatigability. No urinary complaint. Patient has no other systemic symptoms.

14. Summary cont.. On general examination, nutrition poor, pallor moderate and deeply jaundiced. No cervical lymphadenopathy. Abdominal examination-shape and contour of abdomen normal. Umbilicus normal. Liver and spleen not palpable. A lump palpable in the right hypochondriac region extending to the epigastric and right lumbar region. The lower, medial and the lateral margins are palpable and the upper margin passes deep to the right costal margin. The palpable swelling appears to be the palpable gall bladder. There is no free fluid in the abdomen. Bowel sounds are audible. Per rectal examination not done.

15. Provisional Diagnosis Obstructive jaundice probably due to periampullary carcinoma in a hypertensive patient posted for exploratory laparotomy followed by Whipple’s pancreatico-duodenectomy if operable. Why Obstructive Jaundice? Patient complains of- 1. Gradually progressive increase in yellowish discoloration of eyes and urine. 2. Patient is having itching all over the body and 3. He is passing clay coloured stool since the onset of jaundice. Why periampullary carcinoma ? 1. Patient is elderly. 2. History of painless progressive jaundice for last 6 months. 3. Patient had melena 2 months back. 4. Anorexia and weight loss for last 6 months. 5. Lump in his right side of upper abdomen for last 3 months. 6. No history of biliary colic 7. Gallbladder is palpable, which is tense cystic in feel and is non tender.

17. Differential Diagnosis 1.Cholangio-carcinoma 2.Carcinoma of gallbladder 3.Choledocho-lithiasis 4.Lymph node mass in the porta causing biliary obstruction (Metastatic, lymphoma, tuberculosis) 5.Bile duct stricture 6.Sclerosing cholangitis 7. Chronic pancreatitis

18. Management Plan Kausch – Whipple’s Procedure

19. DISCUSSION

20. Bacterial B glucuronidase 80- 90% 10- 20% MRP-2

21. Biliary system HeaptocytesCanaliculi Bile ductules, Duct Rt+Lt Hepatic duct =CHD CHD + CD = CBD CBD + PD = Ampulla Duodenum

22. Liver largest organ Weight 1-1.5 kg Most vascular organ 30% of CO 100 – 120 ml/100gm/min Synthetic, Storage, Excretion Endocrine

23. Anatomy Four Lobes – Right – Left – Caudate – Quadrate Four Ligaments – Rt/Lt Coronary – Rt/Lt Triangular – Falciform – Teres/Round

24. Physiologic Segments Considerable variability Couinaud system Eight Segments 1st segment is caudate CE-Spiral CT

25. Liver Lobule Anatomical unit 3mm in circumference 50k to 1lakh Hexagonal – portal canals Portal canal – Portal triad, nerve fibers, lymphatics, connective tissues

26. Liver Acinus Functional Microvascular Three Zones – Z I -> Periportal -> High pO2 – Z II -> Midzone – Z III -> Pericentral -> Low pO2 Zone I – Highest Mitochondria Synthetic fn, Urea cycle Zone III – High SER, Cyt P450 Xenobiotics

28. Hepatic Blood Supply 25% to 30% of CO Dual supply – Portal V (80%)-Nutrient rich – Hepatic A (20%)-Oxygen rich Oxygen delivery is 50% by both 2/3 of oxygen used by liver Sinusoids can accommodate 400 – 600 ml of blood Plasma clearance of indocyanine green--- most commonly used to assess hepatic blood flow

29. Control of Liver Blood Flow- Intrinsic AUTOREGULATION – Anaesthesia abolish HEPATIC ARTERIAL BUFFER RESPONSE (HABR) -- This physiologic adaptation, matches reductions in PBF with increases in HABF to maintain total hepatic blood flow (THBF) constant in the presence of profound hypovolemia, indirect effects of major abdominal surgery, or severe hemorrhage (Halothane disrupts this compensatory response, sevoflurane and isoflurane maintain HABR) – Max doubles the H.Art flow – Adenosine METABOLIC – O2 tension, pH of PV -> HABF

30. Control of Liver Blood Flow- Extrinsic Increase HBF  Acute hepatitis  Supine posture  β-adreno-stimulation  Glucagon Decrease HBF  Hypoxia, Hypotension  Hepatic cirrhosis  Upright posture  Hypercapnia/Hypocapnia  IPPV/PEEP  β-blocker/ α agonist  Angiotensin II, Vasopressin  Anaesthetic agent

31. NERVE SUPPLY Symphathetic (Splanchnic) – Celiac plexus T5 – T11 Parasymphathetic – Rt & Lt Vagus nerve – Rt phrenic nerve Importance in spinal/epidural anaesthesia – Fall in MAP  SBF/ PVBF  THBF – Impact of LA/Epinephrine – Unknown – Treat by IVF ; – avoid -agonistic Vasopressors

32. Receptors Portal vein – only α receptor Hep artery – α/β present Importance – Dopamine [DOC] – Dobutamine – Noradrenaline

33. Halothane Hepatitis Halothane causes vasoconstriction in the hepatic arterial vascular bed. Hepatic blood flow returned to normal 20 minutes after discontinuation. Causes Immune mediated hepatotoxicity in genetically susceptibles. Subclinical – Reversible ; LFT abnormal – May occur 20% of patient exposed to halothane – TriFluroEthyl (TFE) radical Fulminant Hepatitis – 1: 20,000, Fatal, 50 – 75% mortality – Rare in child – Repeated exposure – IgG autoantibody directed against microsomal protein on surface of hepatocytes----acetylation----Change from self to nonself protein--- autoantibody against this nonself protein---Autoimmune-hepatitis & Necrosis.

34. Postop Jaundice mild ( 4 mg/dL). APPROACH - 1 st –Benign postop intra hepatic Cholestasis(Prolong surgery, Hypotension, Hypoxia, Massive BT) 2 nd –Consider large occult Hematoma/Hemolysis/sepsis 3 rd –Consider Drug induced/Immune mediate hepatitis. StoeltingMiller

35. Physiological functions of Liver Blood Reservoir (10% of total Blood vol) Glucose Homeostasis (Glycogen stores 75gm; 12—24hrs) Fat Metabolism Protein Synthesis Drug & Hormone Metabolism Bilirubin formation &excretion Anti bacterial action Anest inhibits gluconeogenesis Provide ext. source of glucose in long duration surgeries

37. Liver Function Test Tests for liver functioning Based on detoxification & excretory function Enzymes indicating liver injury Measure biosynthetic function Damage to hepatocytes Cholestasis Serum bilirubin Urine bilirubin Blood ammonia Aspartate aminotransferase Alanine aminotransferase Alkaline phosphatase 5 nucleotidase GGT Serum albumin Serum globulin Coagulation factors

38. Jaundice Define Jaundice? Yellowish discolouration of skin & mucous membrane due to increased serum bilirubin. Values? Normal- 0.2-1mg/dl ( Direct 0.1-0.4mg/dl, Conjugated <15% ) Latent jaundice- 1-3mg/dl Clinical jaundice - >3 mg/dl Obstructive jn - Direct Bilirubin > 15% Where to look? Sclera, Under surface of tongue, Mucous membrane, Palm, Sole, Nail & Skin- in bright natural day light idealy infront of open window. Yellowing of sclera at 3 mg% Bilirubin has got high affinity for elastin, sclera has high elastin content Yellowing of skin and mucous membrane at 6 mg%

39. Important History of Jaundice Patient? 1.OnsetSudden / Gradual 2.DurationWeeks /Months 3.Prodromal SymptomViral hepatitis 4.Associated Symptom a)Abdominal pain1.Biliary colic (Severe, Intermittent, Colicy) 2.Pancreatic pain(Continuous, Dull, Radiate to back) b)FeverFever+ arthralgia- Viral hepatitis prodrome Fever +Rigor- Cholangitis Low grade fever- Malignancy c)Pruritus/Clay StoolSuggest Obstructive jaundice d)GI Bleeding1.Portal HTN (Ascites, Splenomegaly, Variceal bleeding) 2.Ampullary malignancy e)Anorexia/Weight loss 1.Alcohol/Drug induced hepatitis 2.Malignancy

40. Cont… 5.H/O-TravelHepatitis A,E 6.H/O Upper abd surgPost op Jaundice 7.H/O-Blood transfusionHep –B,C 8.H/O-MedicationCholestasis- OCP / Rifampicin / Erythomycin Fatty liver- Valproate / Tetracycline Hepatitis- INH /Halothane /Phenytoin / Methyl dopa / Acetaminophen 9.HepatomegallyDull continuous dragging pain d/t stretching of Glisons capsule Intermittent JaundiceProgressive Worsening Jaundice 1.Chole-docho-lithiasis 2.Ampullary Carcinoma 3.Relapsing Viral Hepatitis 1.Malignant Obstruction 2.Primary Sclerosing Cholangitis 3.End Stage Liver Disease

41. EFFECTS OF OBSTRUCTIVE JAUNDICE ON VARIOUS SYSTEMS

42. 1. CHANGES IN LIVER BLOOD FLOW Acute obstruction Increase in hepatic arterial blood flow (HABF) No change in portal venous blood flow (PVBF) Chronic obstruction Decrease in total liver blood flow, dilatation of sinusoids and elevation of portal pressure

43. 2. CARDIOVASCULAR EFFECTS Circulating Bile salts leads to--  Bradycardia due to direct effect on SA node.  Impaired cardiac contractability  Impaired response to beta agonist drugs  Decreased peripheral vascular resistance Net result Hypotensive patient prone for circulatory collapse Exaggerated hypotensive response to bleeding More prone to perioperative shock - therefore replace volume losses immediately in peri-operative period.

44. 3. EFFECT ON RENAL SYSTEM 10 % incidence of Renal involvement with 70 % mortality  Factors responsible are Effect of bile salts, Endotoxins, inflammatory mediators on kidney Decresed cardic function - Hypotension Refractoriness of tubules to ADH Increased levels of ANP resulting in hypovolemia  Resulting in Renal vasoconstriction, hypoperfusion Shunting of blood from cortex Activation of complement system leading to tubular and cortical necrosis

45. 4. IMMUNE SYSTEM  Defects in cellular immunity  Depressed function of RE system i.e Kuffer cells  Impaired T cell proliferation  Decreased neutophil chemotaxis  Defective bacterial phagocytosis  Can lead to Sepsis  Associated cholangitis and bactibilia  Escape of endotoxins from intestine into portal blood

46. 5. Deranged coagulation  ed synthesis of Clotting factors  Prolongation of Prothrombin time/INR Vit. K deficiency d/t biliary obstruction  Defective γ- carboxylation (Factor 2,7,9,10) Endotoxin, Hyperspleenism  Thrombocytopenia Endotoxin   ed Fibrinolysis, Low grade DIC Loss of calcium Decreased absroption of fat solube vitamins A,D,E,K

47. 6. WOUND HEALING  Delayed wound healing  High incidence of wound dehiscence  Decresed activity of enzyme Propyl hydroxylase in the skin  This helps in incorporation of proline in collagen  Defective synthesis of collagen

48. 7. ENDOTOXEMIA Bile salts are surfactants----disrupt endotoxins Absence of bile in intestine   intest.bact. Flora Breakdown of GI mucosal Barrier   bact. translocation  Hepatic RES function   clearance of endotoxins

49. Goals of investigations Determine level of obstruction Severity of jaundice & Pattern Ductal dilatation Establish jaundice Cause of obstruction

50. Harrison 19 TH p 281

52. How to approach in Surgical jaundice ? Site of Disease ? First Investigation? ? Malignancy Level ? CLUE- Elderly age Painless Progressive Jaundice Anorexia,Weight loss Low grade Fever Palpable GB

53. EVALUATION OF CHOLESTATIC JAUNDICE The first question -whether the cholestasis is from intrahepatic or extrahepatic process ? CLUES TO EXTRAHEPATIC OBSTRUCTIONS – 1.Abdominal pain, 2.Palpable GB or upper abdominal mass, 3.Evidence of cholangitis, 4.Past H/O- biliary surgery. CLUES TO INTRAHEPATIC CHOLESTASIS- 1.Pruritus, as in primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) patient

54. Why Pruritus? Central mechanism: ↑central opioido-ergic tone in patients with cholestasis Peripheral Mechanism: accumulation of numerous substances e.g. bile acids, histamine, serotonin & endogenous opoids in the systemic circulation subsequent to failure of elimination Treatment: Opioid antagonists, Cholestyramine, Rifampicin (Induce CP450 which inactivates pruritogen), Phenobarbitone, 5-HT antagonist, UDCA (Urso deoxy cholic acid), Propofol, Lidocaine, Charcoal hemofiltration, Plasmapheresis, Ileal diversion, Liver transplantation.

55. Extrahepatic causes of cholestatic jaundice Benign 1.Choledocholithiasis 2.Postoperative biliary strictures 3.Primary sclerosing cholangitis 4.Chronic Pancreatitis 5.AIDS cholangiopathy 6.Mirizzi’s Syndrome 7.Parasitic Disease (Ascariasis) Malignant 1.Cholangiocarcinoma 2.Pancreatic cancer 3.Gall Bladder Cancer 4.Ampullary Cancer 5.Malignant involvement of the porta hepatis lymph nodes Harrison Internal Medicine 19 th ed p 284

56. Intrahepatic causes of cholestatic jaundice 1)Viral Hepatitis A.Fibrosing cholestatic hepatitis – Hep. B &C B.Hep.A, EBV, CMV 2)Alcoholic Hepatitis 3)Drug toxicity A.Pure cholestasis- Anabolic & contraceptive steroids B.Cholestatic hepatitis- chlorpromazine, erythromycin, Amoxiclav C.Chronic cholestasis- chlorpromazine & prochloperazine 4)Primary Biliary cirrhosis 5)Primary Sclerosing cholangitis 6)Vanishing Bile duct Syndrome A.Chronic rejection of liver transplant B.Sarcoidosis C.Drugs 7)Non hepatobiliary Sepsis 8)Benign post-operative cholestasis 9)Para neoplastic Syndrome 10)Veno-occlusive disease 11)GVHD 12)Inherited A.Progressive familial intrahepatic cholestasis B.Benign recurrent cholestasis 13)Cholestasis of pregnancy 14)Total Parenteral Nutrition 15)Infiltrative diseases A.TB B.Lymphoma C.Amyloidosis 16)Infections A.Malaria B.Leptospirosis Harrison Int Medicine 19 th ed 284

57. Imaging  RUQ Ultrasound  CT scan  ERCP  PTC  Endoscopic Ultrasound  Endoscopic CT  MR cholangiography

58. USG 1.First-line imaging 2.Less expensive 3.No ionizing radiation 4.GB stones readily detected. 5.Absence of biliary dilatation suggests intrahepatic cholestasis. 6.Dilated in extrahepatic cholestasis. Limitations 1)Distal CBD, bowel gas, Obesity 2)False negative – Partial obstruction,cirrhosis, scarring d/t PSC 3)Except mass lesion in the head of the pancreas, USG usually does not identify the type of obstruction.

59. Gallbladder Dilated bile ducts Mass in head of the pancreas CT Scan 1)Localizes level of the obstruction, in about 90% cases. 2)First choice in lymphoma, for retroperitoneal lymph node involvement

60. When clinical suspicion is supported by CT or USG, 1)MRCP-  Noninvasive screening,rapid and comfortable.  Failed or incomplete conventional ERCP.  Variant biliary duct anatomy/ congenital duct abnormalities.  Post operative anatomy where ERCP would be difficult.  Evaluating changes of chronic pancreatitis or sclerosing cholangitis. Distal CBD Stone PSC

61. ERCP

62. Normal ERCP

65. Technique of PTC & corresponding Cholangiogram

66. PTC is preferred when obstructing lesion is high C/I- Marked ascites and coagulopathy. PTC and ERCP may be used together across a difficult obstruction. Sometimes hepatobiliary scintigraphy, may help in evaluating biliary leaks & congenital malformations. Endoscopic CT & MRCP – Biliary obstruction, specially in setting of liver transplantation.

67. Liver Biopsy Major indications – 1)Chronic hepatitis, 2)Cirrhosis (unknown etiology) 3)Unexplained abnormal LFT, 4)Hepatosplenomegaly of unknown etiology, 5)Suspected infiltrative / Granulomatous disease Complications 1)Minor – Prolonged RHC pain, (6%). 2)Major - Intra-abdominal bleeding, mortality ( 0.01%). Contraindications – 1)Bleeding tendencies, 2)INR>1.5 or PT >4 sec above the control, 3)Severe thrombocytopenia 4)Marked ascites.  Transjugular liver biopsy or no biopsy at all are alternatives.

68. Drug-induced cholestasis. Clinically mimic viral hepatitis or biliary tract disease. Serum-sickness-like features (rash, arthralgia,& eosinophilia) Only practical approach is to eliminate the drug and monitor. Antimicrobial agents Augmentin, cloxacillin, erythromycin, ethambutol, dapsone, fluconazole, griseofulvin, ketoconazole Antimicrobial agents Augmentin, cloxacillin, erythromycin, ethambutol, dapsone, fluconazole, griseofulvin, ketoconazole Cardiovascular agents Disopyramide β -blockers, ACE inhibitors, ticlopidine, warfarin, methyldopa Cardiovascular agents Disopyramide β -blockers, ACE inhibitors, ticlopidine, warfarin, methyldopa Endocrine agents Sulfonylureas, estrogens, tamoxifen, androgens, niacin, OCPs, anabolic steroids Endocrine agents Sulfonylureas, estrogens, tamoxifen, androgens, niacin, OCPs, anabolic steroids HAART- Zidovudine, Protease Inhibitors ( Indinavir, Ritonavir) HAART- Zidovudine, Protease Inhibitors ( Indinavir, Ritonavir) Immunosuppressive agents – Azathioprine, cyclosporine, gold salts, NSAIDs Immunosuppressive agents – Azathioprine, cyclosporine, gold salts, NSAIDs Psychopharmacologic agents Tricyclic antidepressants, BZDs, Phenothiazines, Phenytoin, halothane Psychopharmacologic agents Tricyclic antidepressants, BZDs, Phenothiazines, Phenytoin, halothane Direct hepato-toxic Idiosyncratic

69. Anaesthetic problems in Obstructive Jaundice ?

70. Anaesthetic Problems in Obstructive Jaundice ? DUE TO DYSFUNCTION OF LIVER ITSELF DUE TO INVOLVEMENT OF OTHER SYSTEMS PROBLEM RELATED TO SURGERY 1. Low serum proteins 2. Coagulopathy 3. Drug metabolism and disposition 4. Metabolic derangement Hypoglycemia Electrolyte imbalance 5. Haematological Anemia Thrombocytopenia Leucopenia DIC 6. Deficiency of fat soluble vitamins (A, D, E, K). 7. Increased serum cholesterol (atheromatous changes) 1. CVS– TBV , PVR ,  Circulatory collapse 2. Renal – Pre renal azotemia Hepatorenal failure 3. GIT Gastritis & Stress ulcers 4. Respiratory Arterial Hypoxemia Pulmonary infection 5. CNS Hepatic encephalopathy 1.Major surgery---long duration. 2.Increased blood loss/fluid shifts 3.Wide incision---Roof top— warrants good postoperative analgesia. 4.Extensive monitoring required for favourable outcome

71. PRE ANAESTHETIC CHECKUP (PAC) OBJECTIVES 1.Assess the type and degree of liver dysfunction. 2.Assess the effect on other system. 3.To ensure post operative facilities (High risk patient). REVIEW 1.History 2.Clinical examination 3.Investigations ??? Unexplained jaundice of 4wks duration or longer will prove to be caused by obstruction in nearly 75% patients

72. Preoperative Investigations To know the pattern of disease - ­ 1.S. Bilirubin 2.SGOT, SGPT 3.Alkaline phosphatase To judge the synthetic ability of liver- 1. Serum albumin – < 2·5 gm% - severe damage 2. Albumin/globulin ratio – reversed. 3. Prothrombin time – > 1·5 sec Over control – INR - > 1.5 (T/t -Parentral Vit. K – Obst. Jaundice) To assess general condition of patient- 1. Haematological- Hb, TC, DC, Platelet Count, Clotting factors (PT, aPTT) 2. Cardiorespiratory - Chest X-ray, ECG, Blood gases 3. Metabolic-Serum proteins, Glucose, Electrolyte, Urea / Creatinine 4. Urinary-RE/ME & C/S (?sepsis) 5. Hepatic imaging- Accordingly (USG/CT/ERCP/MRCP/PCT Cholangiography) 6. Microbiological – Culture, Hep- B,C marker, Viral antibodies, HIV Serology.

73. Preoperative risk factors associated with increased postoperative mortality (Garrison et al) 1.Serum albumin <3g/L 2.Presence of infection 3.White blood cell count > 10000/cmm 4.Treatment with more than two antibiotics 5.INR > 1.5 6.Serum bilirubin > 3mg/dl 7.Presence of ascites 8.Malnutrition 9.Emergency surgery Other Risk Assessment Score in patient wirh Cirrhosis are- 1.Child Turcotte Pugh Classification 2.Model for End Stage Liver Disease (MELD) Score 3.Integrated MELD (including Na & Age)

75. Android Application

76. Preoperative management 1. Avoid prolonged hyper-bilirubinemia 2. Treat infection –cholangitis 3. Use Aminoglycosides carefully 4. Avoid pre renal failure 5. Correct-Anaemia / Coagulation / Hypoalbuminemia 6. Avoid all NSAIDS 7. Adequate Hydration (pre & postop) 8. Percutaneous Trans Hepatic Biliary Drainage No conclusive evidence for 1.Preop percutaneous biliary drainage 2.Gut sterlization 3.Polymyxin B 3.Oral bile salts

77. Maintain Hepatic blood flow AVOID 1. Sympathetic stimulation, Hypotension, Hypoxia, Hypocapnea 2. Pressure effect-cause by surgical traction, tumour, laparoscopy 3. Hepatic venous congestion-by-Head down, IPPV, PEEP, Rt heart faliure Maintain Renal Function- PRE-OPERATIVELY- 1. Avoid NSAID,Aminoglucosides 2. Prophylactic antibiotics 3. Oral bile salt to normalize gut flora 4. Stenting to reduce hyperbilirubinemia INTRA-OPERATIVELY- 1. Avoid Dehydration, Hypotension, Hypoxemia 2. Mannitol / Frusemide (after ensuring adequate hydration) Choose appropriate anaesthetic agent. Considering Metabolism of drugs + Effect on HBF. Avoid Hypoglycemia,Hypothermia. Aggresive replacement of blood loss. Anaesthetic Goal

78. Ref- Wylie Churchill Davidson

79. Plan of Anaesthesia General anaesthesia Supplimental Epidural (if not contraindicated) for perioperative analgesia. Concern of Epidural- Hypotension & Coagulopathy

80. Anaesthetic technique PREMEDICATION- 1. Anxiolytic – oral short acting BDZ if neurological status normal. 2. Aspiration prophylaxis 3. Vit. K (Obst. J) – 10 mg Intramuscular OD X 3 days 4. If Bilirubin > 8 mg% – I/V fluid – 1-2 ml/kg/hr. Mannitol – 100 ml of 20% 2 hrs preoperatively (Controversy) 5. Order morning Coagulation profile (PT/INR), S. Electrolyte 6. Preop urinary catheter (maintain U.O. >1 ml/kg/hr) & CVP. PREOXYGENATION 100% Oxy, 20 deg Head end elevation. 3-5 min tidal ventilation / 8 VC breath over 60 sec/ CPAP 5-10 cm of H2O /PSV 5-15 cm

81. INDUCTION THIOPENTONE- Slow titrated dose to be given. Reduced dose required d/t decreased protein binding. Alcoholic patient require higher dose d/t cross tolerance. Total body clearance is unaffected in cirrhosis. PROPOFOL- 17% decrease in HBF (SVR and BP decrease) Care to be taken in CVS instability. AIRWAY MANAGEMENT SUXAMETHONIUM Pseudocholinesterase level reduced but action seldom prolonged (1mg/kg). RAPID SEQUENCE INDUCTION. Gentle intubation → avoid sympathetic stimulation

82. MAINTAINANCE Volatile Anesthetics Well tolerated Can be entirely eliminated Disadvantage- ---CVS instability  vasodilation   perf. press.   blood velocity  oxygen extraction   HBF & oxygen supply Isoflurane—best maintain of HBF & oxygen (AGENT OF CHOICE) Des/ Sevo-also maintain HBF ( use as alternative) IPPV Maintain eucapnia Liver low pr. tissue bed- --Avoid large TV & high airway pressures

83. ANALGESIA MORPHINE- Metabolism reduced d/t decrease hepatic blood flow( avoided ) REMIFENTANYL- DOC-Hydrolyse by Nonspecific tissue and plasma esterase(Clearance independent of liver and kidney). 2 nd choice Fentanyl. NSAIDS- avoided d/t ill effect on GIT/Kidney/Platelets MUSCLE RELAXANT CISATRACURIUM- (DOC) –If Not available ATRACURIUM is 2 nd choice. Hoffman degradation independent of hepatic metabolism Higher dose required (increased binding to raised globulin, Increased resistance, Shorter duration) VECURONIUM- alternative 0.15mg/ kg body weight ROCURONIUM- avoided Action is prolonged (as mainly eliminated by liver & clearance decrease)

84. MONITOING 1. ASA Standard Monitoring Oxygenation- Pulse oxymetry Ventilation- Capnography Circulation- NIBP, Cont ECG Core Temperature NM junction monitoring Urine output 2. Additional Monitor CVP IABP 3. Hematological (if prolong surgery) Hb/Hct TEG (Thromboelastography) Electrolyte (Na,K) CBG POST OP PAIN depends on Coagulation function If NORMAL- Lower thoracic/Upper lumbar Epidural (0.0625% Bupivacaine + Fentanyl 2microgram/ml) If ABNORMAL- IV Patient Controlled Analgesia(PCA)

85. References-

86. Thank You

87. PHYSIOLOGICAL FACTS BILE Total bile flow- 600 ml/day(500-1000ml/day) Hepatocyte component is - 450ml/day Bile salt dependent due to biliary glutathione and ductular bicarbonate secretion Cholangiocyte component- 150ml/day It depends on secretin stimulation With conjugated bilirubin <15 %

88. Bile Heterogenous – Bile acid, salts – Conj. Bilirubin – Cholesterol – Phospholipids – Electrolytes Bile Acid/salt – 200mg – 500mg/day – Primary / Secondary – Entero-hepatic circulation – Buffer system of the gut  Functions ‒ Absorption of Lipids, LCFA, FS Vitamins ‒ Excretion of lipid soluble wastes exogenous/endogenous ‒ Regulate plasma lipid levels

89. PHYSIOLOGY OF OBSTRUCTION  Normal secretory pressure of bile is 15-25 cm of water  At 35 cm of water there is suppression of bile flow  High pressure leads to cholangiovenous and cholangiolymphatic reflux of bile  Dilatation of bile duct and intra hepatic biliary radicals(IHBR)  IHBR dilatation may be absent if there is secondary hepatic fibrosis or cirrhosis

90. Patho-physiology Increase in biliary pressure leads to Disruption of tight junctions between hepatocytes and bile duct cells with increased permeability Reflux of bile contents in liver sinusoids Neutrophil infiltration,increased fibrinogenesis and deposition of reticulin fiberes in portal triad Reticulin fibers gets converted in to type 1 collagen Laying down of collagen fibers leads to hepatic fibrosis obstruction of sinusoids and secondary biliary cirrhosis and portal hypertension Fibrosis can also lead to atrophy of obstructed liver