Presentation on theme: "Ravinder Kumar Batra Professor Department of Anaesthesiology, AIIMS Obstructive Jaundice"— Presentation transcript:
Ravinder Kumar Batra Professor Department of Anaesthesiology, AIIMS Obstructive Jaundice www.anaesthesia.co.inwww.anaesthesia.co.in firstname.lastname@example.org@gmail.com
Chief Complaints 4O yr male presented with : Yellow coloration of Eye -8 months Yellow coloration of urine – 8 months
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
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
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
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
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
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)
Abdomial Examination Abdominal distension, distended veins, scar Hepatomegaly Splenomegaly Gall bladder or any mass, Free fluid
Define Jaundice and where all you will look for this?
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
What are the Pathophysiological consequences of Obstructive / Cholestatic Jaundice?
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
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
Anaesthetic Problems associated with Obstructive Jaundice
–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
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
Anaesthetic Problems: Sepsis Associated cholangitis and bactibilia Escape of endotoxins from intestine portal blood ↓ kuffer cell activity Prevention Perioperative antibiotics Preoperative oral bile salts
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
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
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
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
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
What are the other Preoperative Investigations required ?
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
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
What are Troisier’s sign and Courvoisier’s law?
Troisier’s sign Enlargement of Left Supraclavicular Lymph Node due to Secondary involvement seen in malignancies of G.I.T., Breast and Testis.
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.
What are the Surgical Procedures done for Obstructive Jaundice?
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
Periampullary Ca: Whipple’s Procedure Chronic Pancreatits with head Mass: Whipple/ bilio-enteric anastmosis
Whipple’s Procedure Pancreaticojejunostomy- end to end Hepatico-jejunostomy – end to side Gastrojejunostomy – end to side Feeding Jejunostomy
What are the Risk factors for Operative Mortality in these patients?
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
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
What are the anaestheic goals in surgery for an Obstructive Jaundice patient ?
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
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
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
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