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Obstructive Jaundice

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Obstructive Jaundice Whipple s Operation Anesthetic Management Munisha Agarwal Professor Deptt. of Anaesthesiology & Intensive Care L N Hospital & Maulana – PowerPoint PPT presentation

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Title: Obstructive Jaundice


1
Obstructive Jaundice Whipples Operation
Anesthetic Management
  • Munisha Agarwal
  • Professor
  • Deptt. of Anaesthesiology
  • Intensive Care
  • L N Hospital Maulana
  • Azad Medical College Delhi

www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om
2
Obstructive Jaundice
  • Physiological functions of Liver ?

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

4
Glucose homeostasis
  • Glucose hepatocytes glycogen glucose
  • lactate
  • glycerol
  • AA

5
Glucose Homeostasis
  • Glycogen stores 75gm 2448hrs
  • Anesthesia gluconeogenesis
  • Provide ext. source of glucose

6
Fat metabolism
  • Synthesis of lipo-proteins cholesterol
  • Oxidation of FA to ketone bodies

7
Protein Metabolism
  • Deamination of AA
  • Formation of urea
  • Plasma proteins
  • - All except y globulin factor VIII
  • - Albumin daily prod. 1015g/d (3.5-5.5gm)
  • - liver disease ? alb ? glob
  • Albumin ?

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

9
Drug binding
  • Drugs reversibly combine with Albumin
  • ? albumin ? binding sites ? free drug
  • Albumin lt 2.5gm
  • Acute Hepatic dysfunction ?
  • Coagulation ?

10
Drug binding
  • Acute hepatic dysfunction - drug binding not
    affected
  • T ½ Albumin 14 21 days
  • Coagulation affected (26hrs)
  • Vitamin K dependent Coag. Factors?

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

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

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.

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?

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

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

17
Bilirubin formation excretion
  • Daily prod 250350mg/d
  • Interpretation of plasma urine bilirubin
  • Categories of liver dysfunction
  • 1 unit BT ?

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

19
Hepatic Blood Supply
  • Unique ?

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

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 ?

22
Control of Liver Blood Flow
EXTRINSIC
  • Decrease HBF
  • Hypoxia
  • Hepatic cirrhosis
  • Upright posture
  • Hypocapnia/IPPV/PEEP
  • Drugs
  • ßadrenoreceptor blockade/ a agonist
  • Ganglion blockade
  • Anaesthetic agent
  • Increase HBF
  • Acute hepatitis
  • Supine posture
  • Hypercapnia
  • Drugs
  • ßadrenostimulation

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

24
Liver Function Tests
  • S. Bilirubin (T) - 0.31.1mg
  • (I) 0.2-0.7mg, (D)0.10.4mg)
  • TransaminasesSGOT/SGPT/LDH
  • hepatocyte damage hypoxia/drugs/viruses
  • Extrahepaticheart/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 ?

25
Hepatic dysfunction Bilirubin Transaminase enzyme Alkalinephosph. Causes
Pre hepatic Unconjug ated (indirect) Normal Normal Hemolysis/ hematoma resorp./ bilirubin overload-BT
Intrahepatic(hepatocellular) Conjugated(direct) elevated Normal to Slightly ? Viral/drugs/sepsis/hypoxia/cirrhosis
Posthepatic (cholestatic) conjugated Nomal to slightly ?ed ? (2x) Stones, Sepsis, tumor
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 ?

27
Signs Symptoms
  • Prog sev jaundice
  • Dark urine
  • Clay coloured stools
  • Pruritis
  • High fever chills
  • Biochemical hallmarks

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

29
Pathophysiological consequences
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 ?

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

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

33
Renal System
  • Acute Renal Failure
  • Hepatorenal Syndrome

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

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

36
  • Anesthetic problems in Obstructive Jaundice ?

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)

38
PROBLEMS
  • DUE TO INVOLVEMENT OF OTHER SYSTEMS
  • 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 ?

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

40
Risk Factors
  • Age gt 60yrs
  • Albumin lt 30gm
  • Preop. renal dysfunction
  • Long standing biliary obstruction ? infection ?
    sepsis
  • Weight loss
  • ?Serum creatinine Sepsisprognostic factors
  • ?Periop CVS collapse renal failure

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).

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

43
Preoperative Investigations
  • To know the pattern of disease
  • S. Bilirubin
  • SGOT, SGPT 90 predictive
  • alk. phosphatase

44
Preoperative Investigations
  • To judge the synthetic ability of liver
  • Serum albumin lt 25 gm - severe damage
  • Albumin/globulin ratio reversed.
  • Prothrombin time gt 15 sec. Over control
  • INR - gt 1.3
  • (D/D Par entral Vit. K Obst. Jaundice)

45
To assess general condition of patient
  • (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

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

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

48
Premedication
  • Anxiolytic oral short acting BDZ
  • Oral H2 antagonist
  • Vit. K (Obst. J) 10 mg B D X 3 day
  • If Bilirubin gt 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

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 ?

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

51
Anesthetic technique
  • Opioids Well tolerated
  • smaller doses
  • Morphineph-II reac.
  • fentanyl(DOC)
  • spasm of sphincter of Oddi

52
Anesthetic technique
  • Spasm of sphincter of Oddi
  • Interpretation of operative cholangiography
    biliary pressures
  • All patients do not show this response
  • Incidence of spasm is very low
  • Intraop manipulation of BD system ? spasm
  • Treatment

53
Anesthetic technique
  • Volatile Anesthetics
  • Useful well tolerated
  • Can be entirely eliminated
  • Disadv- CVS instability ? vasodilation ? ?perf.
    Press. ? ? blood velocity ?? oxygen extraction ?
    ? HBF oxygen supply
  • Isofluranebest maint. of HBF oxygen
  • IPPV ?

54
Anesthetic technique
  • IPPV
  • - Maintain eucapnia
  • - Liver low pr.tissue bed
  • - Avoid large VT high airway pressures

55
Anesthetic technique
  • Maintenance of BV and Renal function
  • Mannitol
  • Frusemide
  • Dopamine
  • Adequate blood/component replacement

56
Monitoring
  • BP,HR,SpO2
  • EtCO2
  • CVP
  • Urine output
  • Core temp
  • NMJ monitoring
  • Blood loss

Biochemical B.Sugar,ABG S.Electrolytes Hematologi
cal Hb,PT,,PTTK,TEG
57
Postoperative management
  • All well ? Extubate
  • Unstable
  • - Continue IPPV in Post.op. period
  • - Fluid Electrolyte imbalance
  • corrected
  • - CVS stability achieved.
  • - Hypothermia corrected.
  • - Urine Output 1 ml/kg/hr.
  • Adequate analgesia (Small doses)
  • Blood / blood product replaced.
  • Antibiotics H2 receptor antagonist

58
Thank You
www.anaesthesia.co.in anaesthesia.co.in_at_gmail.c
om
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