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Ravinder Kumar Batra Professor Department of Anaesthesiology, AIIMS Obstructive Jaundice

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Presentation on theme: "Ravinder Kumar Batra Professor Department of Anaesthesiology, AIIMS Obstructive Jaundice"— Presentation transcript:

1 Ravinder Kumar Batra Professor Department of Anaesthesiology, AIIMS Obstructive Jaundice www.anaesthesia.co.inwww.anaesthesia.co.in anaesthesia.co.in@gmail.comanaesthesia.co.in@gmail.com

2 Chief Complaints 4O yr male presented with : Yellow coloration of Eye -8 months Yellow coloration of urine – 8 months

3 History of present illness Gradually progressive yellowish coloration eye Recurrent episode of itching White stools 4 months back, persisted for 2 months Abdominal pain- Right upper quadrant- 6 months Generalized weakness & fatigability- 6 months Weight loss 75-50 kg in 7 months Reduced appetite No fever

4 H/o past illness Typhoid fever – 9 months back No h/o DM, HT, TB, Chest pain No previous surgery Personal History Normal Bowel & bladder habits Smoker – 25 yrs Non-alcoholic Effort tolerance good

5 Important points in History Duration of Jaundice Progress & previous attacks of jaundice Prodrome Fever Abdominal pain: Biliary/pancreatic/Dull Pruritis, Colour of urine and stool Drug ingestion Manifestations of fat soluble Vit deficiency Weight loss

6 History suggestive of Normal colored urine/cola color in hemolysis Recurrent episodes Recurrent anaemia No prodrome Pain Chills, fever, systemic illness Biliary surgery Unconjugated hyperbilirubinemia/hemolysis Bile duct stones/cholangitis/obstructive jaundice

7 History suggestive of Contact with other jaundiced patient History of injections or blood transfusions Exposure to drugs Prodrome of anorexia, nausea, vomiting Pruritis Clay coloured stools VH/Drug induced Hepatitis Cholestasis

8 Examinations General Physical Examination: –Pulse 88/min,BP 110/70 Pallor +, Jaundice + –No Lymphadenopathy Per abdomen –Soft non-tender –Gall bladder palpable –Liver: 3cm below costal margin –No free fluid

9 Airway Examination MMP grade II Mouth opening: Adequate Teeth intact, no loose tooth

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14 General Examination Body mass index Vital signs: Pulse Pallor: GI bleeding, Hemolysis Icterus Pedal oedema: hypoproteinemia/cirrihosis Shiny nail & scratch marks (pruritis) Xanthoma Ecchymosis, Bitot spots (Vitamin deficiency)

15 Abdomial Examination Abdominal distension, distended veins, scar Hepatomegaly Splenomegaly Gall bladder or any mass, Free fluid

16 Define Jaundice and where all you will look for this?

17 Yellowish pigmentation of the sclera, skin, mucous membrane & other tissues: Jaune Excess plasma bilirubin Normal range < 1 mg/dl (I: 0.2-0.7mg/dl;D:0.1—0.4mg/ dl, <5% in Conjugated form) Clinically obvious 2-3 mg/dl Sites – Sclera, undersurface of the tongue, palms, nails, skin, hard-palate High Affinity for Collagenous tissue

18 Describe Bilirubin Formation & Excretion?

19 Bilirubin Metabolism Ret En System Plasma Liver Bile Heme oxygenase Biliverdin reductase Haem BVD UCB UCB UCB Albumin 70% 30% BMG BMG BMG & BDG Hb other BDG BDG haemoproteins Glomerulus Urine Bilirubin production: 250-350mg/day

20 Portal vein

21 How will you Differentiate the three types of Jaundice Biochemically?

22 FeaturesPrehepatic (hemolytic) Intrahepatic Heptocellular Post-hepatic (Obstructive) UCB ↑ Normal CBNormal ↑ ↑ AST or ALTNormal ↑↑Normal SAPNormal ↑↑ Urine Bilirubin AbsentPresentIncreased UrobilinogenIncreasedPresentAbsent

23 FeaturesPrehepatic (hemolytic) Intrahepatic Heptocellular Post-hepatic (Obstructive) Plasma Albumin NormalDecreasedNormal or decreased PTNormalIncreasedIncreased but correccted by Vitamin K

24 How will you Evaluate a Case of Jaundice?

25 HISTORY clinical evaluation Hemolysis Vs Cong Hyperbilirubinemia Normal Abnormal AST, ALT, ALP USG if biliary obstruction is suspected Non-dilated ducts Dilated ducts Hepatocellular jaundice Biliary Obstruction Evaluation for: Acute vs Chronic Etiology Evaluation for: Cause Extent GGT, Viral Markers, Autoimmune Markers Liver Biopsy ERCP, MRCP, PTC, CT

26 Investigations Bilirubin, Serum enzymes (SGOT, SGPT) SAP, GGT, 5-nucleotidase Proteins: Albumin, Globulins, INR or PT, markers Ultrasound, CT scan ERCP Percutaneous Transhepatic Cholangiography Magnetic resonance cholangiopancreaticography Liver Biopsy

27 What are the Pathophysiological consequences of Obstructive / Cholestatic Jaundice?

28 Consequences of Cholestasis Retention of bile salt in liver Decreased hepatocyte function Dysfunction of Cyto -450 Albumin & clotting factors synthesis decreased Decreased Kuffer cell activity Bile constituents in serum Jaundice, Pruritis CVS depression Nephrotoxicity Hypercholesterolemia, atheroma, Xanthoma

29 Consequences of Cholestasis Absence of bile in Intestine Escape of endotoxins into portal blood Malabsorption of fats, Vit A, D, E & K Clay colored stools Pruritis: Exact pathology is not known: Central mechanism: ↑ central opioidoergic tone Peripheral: accumulation of bile acids, histamine, serotonin & endogenous opioids

30 Anaesthetic Problems associated with Obstructive Jaundice

31 –Impaired myocardial contractility –Bradycardia –Vasodilatation  ↓ ability to mobilise blood from splanchnic vasculature during haemorrhage – ↓ sensitivity to vasopressors  Hypotension & circulatory collapse Small blood losses poorly tolerated Replace volume losses immediately in perioperative period Anaesthetic Problems: CVS

32 Anaesthetic Problems: Renal system Etiology Multifactorial Arterial hypotension-myocardial depression Reduction in intravascular volume Nephrotoxicity - bile salt, endotoxins & Inflammatory mediators –Incidence 5 -10%, mortality: 32 – 100% –Level of hyperbilirubinemia correlates with postoperative decrease in creatinine clearance

33 Anaesthetic Problems: Sepsis Associated cholangitis and bactibilia Escape of endotoxins from intestine  portal blood ↓ kuffer cell activity Prevention Perioperative antibiotics Preoperative oral bile salts

34 Anaesthetic Problems: Coagulopathy Vit. K malabsorption (Activation II,VII,IX,X )  ↑ PT Pre-op. Vit. K 10 mg OD × 3 days long lasting biliary obstruction  Sec. biliary cirrhosis  ↓ syn. of coag factors (poor prognosis)  transfusion of FFP

35 Anaesthetic Problems Multiple Vitamin Deficiency - A, D, E, K ( A - night blindness,D – osteoporosis and ms weakness, E- leg cramps,K- easy bruising ) Haemorrhagic gastritis and stress ulcer Impaired wound healing Altered drug handling due to cholestasis Long standing extrahepatic biliary obstruction > 1yr → biliary cirrhosis → problems of liver dysfunction

36 Investigations for Assessing Liver Functions?

37 Assessment for liver cell injury S. Bilirubin Transaminase SGOT/SGPT - 0 – 35 IU/L SGOT -extrahepatic- heart/sk ms/kidney/brain:less specific SGPT - primarily found in liver, more specific Alcoholic hepatitis SGOT/SGPT > 2 (deficiency of pyridoxine-5-PO 4 ) Alkaline phosphatase – 35 – 100 IU/L Extrahepatic- bone, intestine, liver, placenta 5- Nucleotidase - confirms hepatic origin of ALP Gamma Glutamyl Transpeptidase – most sensitive indicator of biliary tract disease

38 Aminotransferases Alk PO4 Diag. Likelihood Viral hep. Obstr. > X 6< X 2.5 90% 10% x 2..5 10% 80% Parenchymal diseases ultimately produce an obstructive component & Long standing Obstructive diseases cause cellular dysfunction

39 Assessment of Synthetic Ability of Liver Prothrombin time – factors II, VII, IX & X short t ½ 2 - 6hr Good Indicator of liver fn. in both Acute & Chronic Liver disease. D/D - Obst. jaundice parentral vit. K → PT normalises in 24 – 48 hrs Serum albumin – t ½ life - 14-20days Liver – substantial reserve for alb. syn. Not a good indicator for acute or mild liver damage Indicator of severity of chronic liver disease < 2·5 gm% - severe damage

40 What are the other Preoperative Investigations required ?

41 Preoperative Investigations Hb - ↓ in concealed blood loss, haemolysis, TLC, DLC - ↑ infection Platelet Count, clotting studies - PT, PTTK Urea, S. Creatinine, Electrolyte HBV, HCV Chest X-ray, ECG, blood gases

42 Investigations Hb-9.7, TLC-16200, PC-4.56 Lac LFT-S.Bil T-14.0/D11.3/2.7 SGOT/SGPT-183/81, SAP-1493 Urea/Creatinine: 15/1 PT : normal CxR: Normal CA-19-9: 10.6U/ml (1.9 -24 u/ml –male) Side View Endoscopy: Ampulla bulky friable, ulcerated Ampullary Biopsy: Few displasia & atypical cells

43 Investigations USG-Abd: solid mass in distal CBD, dilated CBD, Intrahepatic Biliary distension with distended GB with hepatomegaly Dual Phase CT: Mass at lower end of CBD with dilated upper stream Biliary system Endoscopy US: Mass in uncinate process likely malignant

44 CT imaging

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50 Case : Diagnosis Periampullary Carcinoma

51 What are Troisier’s sign and Courvoisier’s law?

52 Troisier’s sign Enlargement of Left Supraclavicular Lymph Node due to Secondary involvement seen in malignancies of G.I.T., Breast and Testis.

53 Courvoisier’s law If the CBD is obst. due to calculus, the GB is usually not distended owing to previous inflammatory fibrosis. In obstr. of the CBD due to growth, the GB becomes distended in order to reduce the press. in the biliary system.

54 What are the Surgical Procedures done for Obstructive Jaundice?

55 Ca GB: Radical Cholecystectomy with wedge ressection and CBD excision Choledocholithiasis: ERCP removal or CBD exploration/ bilio- enteric anastmosis Cholangio Ca: Liver resection and or local excision of the lesion or Whipple Biliary Stricture: Hepatico-jejunostomy/ liver resection

56 Periampullary Ca: Whipple’s Procedure Chronic Pancreatits with head Mass: Whipple/ bilio-enteric anastmosis

57 Whipple’s Procedure Pancreaticojejunostomy- end to end Hepatico-jejunostomy – end to side Gastrojejunostomy – end to side Feeding Jejunostomy

58 What are the Risk factors for Operative Mortality in these patients?

59 Dixon etal – GUT 1983 Hematocrit 12mg% Malignant cause of biliary obstruction Mortality 60% if above present, 5 % otherwise Blamey et al 1983 : Brit J of Surg 8 factors Age >60, Malignant D, S Bil> 6mg/dl, Hct 10000, S. alb 1.5, SALP >600 Preoperative Risk factors

60 Bose et al Ind J Surg 1990 Age >60, Associated DM, Previous Biliary tract surgery & prolonged surgery Friedman –Hepatology June1999 Azotemia, Hypoalbuminemia & Cholangitis Preoperative Risk factors

61 What are the anaestheic goals in surgery for an Obstructive Jaundice patient ?

62 Maintain Hepatic oxygen supply – demand relationship Renal function Anaesthetics Goals

63 MANTAINING HEPATIC BLOOD FLOW AVOID : Sympathetic stimulation Hypotension (decreased venous return / cardiac output) caused by : Haemorrhage Cardiac depressant drugs Regional anaesthesia e.g.; thoracic epidural analgesia Hypocapnia Pressure effects caused by Surgical retraction Tumors Ascites / Laparoscopy Hepatic venous congestion caused by Head down position, IPPV, Rt. side heart failure

64 Maintaining Renal function Preoperatively Avoid NSAIDs & nephrotoxic antibiotics e.g.; (aminoglycosides) Oral bile salts to normalize gut flora Prophylactic antibiotics to prevent sepsis Drainage stent - ↓ Hyperbilirubinaemia PTC, ERCP or papillotomy Intraoperatively Avoid hypotension & hypoxaemia Avoid dehydration Renal dose dopamine? mannitol/furosemide

65 Preoperative preparation Anxiolytic – oral short acting BDZ Oral H2 antagonist Vit. K (Obst. J) – 10 mg OD X 3 day, FFP Perioperative broad spectrum antibiotics Oral bile salts

66 Preoperative preparation for Anaesthesia Rehydration and adequate diuresis 1ml/kg/hr If Bilirubin > 8 mg% – I/V fluid – 1-2 ml/kg/hr. Furosemide/ Mannitol Catheterization & CVP monitoring

67 Choice of Anaesthesia?

68 Choosing appropriate anaesthetic agent No drug is contraindicated in Cholestatic liver disease per se Other considerations Coexisting hepatocellular disorder Renal dysfunction Drugs ↑ cholestasis e.g.; chlorpromazine Anaesthetic agent of choice Not dependent on hepatic metabolism Maintains hepatic O2 supply – demand relationship

69 General anesthesia Induction agent - Thiopentone/Propofol slow titrated dose → avoid hypotension → avoid symp. Stimulation during intubation Muscle relaxant Suxamethonium - RSI Atracurium (DOC) - Hoffman’s elimination Vecuronium

70 Anaesthetic technique Opioids fentanyl (DOC)- maintains hepatic oxygen supply – demand spasm of sphincter of Oddi – incidence < 3% Bil. colic, false + cholangiogram T/T naloxone, glucagon, atropine, nitroglycerine Volatile Anesthetics Isoflurane - maintains HBF & oxygen supply IPPV –- Maintain eucapnia Avoid high airway pressures

71 DrugDurationMetab.Eli. Kid. % Eli. Liv. % SchUltrashortButyrylcholinestras 99% <2None AtraIntermediateHoff & ester 60-90 % Urine & Bile 10-40None CisIntermediateHoff 77%16% VecIntermediateLiver 30-40% Urine & Bile 40-5050-60 RocLong10-208515 dTcLongNone80%?20% Metabolism & Elimination of Ms Relaxants

72 Regional anaesthesia as supplement to G.A. Epidural anaesthesia : Concerns –Coagulopathy –Hypotension

73 Intraoperative Monitoring

74 Intra Operative Monitoring Routine ECG, NIBP SaO2, EtCO2 Urine output Temperature NMJ monitoring Longer & extensive surgeries Intra arterial and CVP Biochemical: B.Sugar, ABG, Electrolytes Hematology: Hb, PT, PTTK, TEG

75 Post-operative Management?

76 Postoperative management Conscious, adequate NM recovery, vitals stable → extubate → oxygen - enriched air Else - Continue IPPV - Correct Fluid & Electrolyte imbalance - Correct hypothermia - Achieve CVS stability Adequate analgesia & chest physiotherapy Antibiotics + H2 receptor antagonist Maintain urine output Replace blood and blood products

77 What are the Causes of Cholestasis: Intrahepatic & Extrahepatic

78 Extrahepatic: Benign causes Choledocholithiasis Primary sclerosing cholangitis AIDS Cholangiopathy Post-surgical stricture Pancreatitis

79 Extrahepatic: Malignant Causes Carcinoma gall bladder Periampullary Carcinoma Cholangiocarcinoma Carcinoma of the head of pancreas Obstruction of the drug due to metastatic LN

80 Intrahepatic cholestasis Cholestasis phase of AVH Alcoholic H Drug induced liver D Primary biliary cirrhosis Primary sclerosing cholangitis TPN

81 Intrahepatic cholestasis Graft-versus-host D Cholestasis of pregnancy Sepsis Benign postoperative Cholestasis Fibrosing cholestatic hepatitis.

82 Name the Drugs that lead to Cholestasis Jaundice?

83 Estrogen Tamoxifen Anabolic steroid Azathioprine Chlorpromazine Carbamazepine Antibiotics- Erythromycin, Rifampicin Drugs that lead to Cholestasis Jaundice?

84 Name the Conditions where Family H/o of jaundice is present?

85 Family H/o Jaundice Progressive Familial Intrahepatic Cholestasis syndrome ( Dublin Johnson’s and Rotor’s syndrome) α- antitrypsin deficiency Wilson’s Disease ( Hepatolenticular degenertion- copper accumulation)

86 Describe the structural/ architectural and the functional units of liver.

87 Hepatic lobule: Str. Unit

88 Hepatic Acinus : Func. Unit - divided into zones that correspond to distance from the blood supply Zone 1-Richer in O2 and nutrients Zone 3-poorer in O2 and nutrients

89 Zone I – Periportal – ↑ mitochondria Oxidative and phase 2 metabolism, glycogen synthetase Zone 3 - Centrilobular ↑ SER, cyt-P-450, NADH Anaerobic & phase 1 metabolism Most sensitive to injury from circulatory disturbances and toxic byproducts

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91 Isolated elevation of S.Bilirubin Unconjugated hyperbilirubinemia Increased Bil Production (Hemolysis) Ineffective erythropoiesis, resorption of hematoma Decreased hepatocellular uptake (Rifampicin) Decreased conjugation (Gilbert & Crigler-Najjar) Conjugated hyperbilirubinemia Dubin Johnson Syndrome and Rotar syndrom

92 Hepatocellular Jaundice Acute or subacute hepatocellular injury VH, alcohol, drugs, ischemic hepatitis, Wilson’s disease, acute fatty liver of pregnancy Chronic hepatocellular disease VH, Alc liver D, autoimmune H, Wilson’s disease Non-alcoholic steatohepatitis, α-antitrypsin deficiency

93 Hepatocellular Jaundice Hepatic disorders with prominent cholestasis Diffuse infiltrative disorders: granulomatous D – myobacterial infestions, sarcoidosis, lymphoma, drugs, amyloidosis, malignancy Inflammation of the intrahepatic bile ductules &/or portal ducts (primary biliary cirrhosis), graft- vs host D, chlorpromazine

94 Hepatocellular Jaundice: Miscellaneous Benign recurrent intrahepatic cholestasis Use of oestrogens and steroids TPN, bacterial infections Paraneoplastic, syndromes Intrahepatic cholestasis of pregnancy postoperative cholestasis

95 DESCRIBE THE LIVER BLOOD SUPPLY ? and different factors affecting it?

96 1 2

97 30 % BLOOD 70 % BLOOD 40 – 50 % OXYGEN 50- 60% OXYGEN 25% of C.O.- 1500 ml/min, Dual Bld Supply

98 FACTORS AFFECTING LIVER BLD. SUPPLY Increased by: Supine position Food Hypercapnia Acute hepatitis Drugs: barbiturates, P450 enzyme inducers, b agonists Decreased by: Upright position IPPV/PEEP, Surgery Hypocapnia, hypoxia Cirrhosis Anaesthetics agents volatile, inhalational, b blockers, a agonists Surgical Manipulations

99 What are the Functions of Liver ?

100 Protein metabolism – synthesis of plasma pr( albumin & α-acid glcoprotein, C-reactive protein, haptaglobin, pseudocholinestrase, deamination of A.A, formation of urea, Glucose Homeostasis - gluconeogenesis, glycogenolysis( glucagon), glycogenesis (Insulin) Fat Metabolism - Synthesis of lipoproteins, cholesterol, triglycerides, oxidation of FA to ketone bodies Reservoir of Blood Endocrine Function: IGF1, Thrombopoitin, Angiotensinogen, Thyroid homeostasis, steroid hormone inactivation( Testesterone, estradiol, glucocorticoid, ald.)

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102 Functions of the Liver Bilirubin formation & excretion Drug & Hormone Metabolism Phase I & II reactions Hematological function – haematopoiesis in fetus, heme synthesis, Immunological function – largest RE organ, Kupffer cells - phagocytosis of Antigen from GIT. Synthesis of Coagulation factors:I,II,V,VII,IX, X,XI, XII,XIII, prekallikrein,kininogen- Anticoagulants: Antithrombin III, α1antitrypsin, α2 antiplasmin,protein C & S, plasminogen, plasminogen activator inhibitor


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