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Obs. J
Obstructive Jaundice – Whipple’s Operation Anesthetic Management
Munisha Agarwal Professor Deptt. of Anaesthesiology & Intensive Care L N Hospital & Maulana Azad Medical College Delhi
www.anaesthesia.co.in [email protected]
Obs. J
Obstructive Jaundice
Physiological functions of Liver ?
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Physiological functions of Liver Glucose Homeostasis Fat Metabolism Protein Synthesis Drug & Hormone Metabolism Bilirubin formation &excretion Anti bacterial action Blood Reservoir
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Glucose homeostasis
Glucose hepatocytes glycogen glucose lactate glycerol AA
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Glucose Homeostasis
Glycogen stores 75gm 24—48hrs Anesthesia – gluconeogenesis Provide ext. source of glucose
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Fat metabolism
Synthesis of lipo-proteins & cholesterol Oxidation of FA to ketone bodies
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Protein Metabolism
Deamination of AA Formation of urea Plasma proteins - All except y globulin & factor VIII - Albumin daily prod. 10—15g/d (3.5-5.5gm%) - liver disease ↓ alb ↑ glob Albumin ?
Obst. J
Protein synthesis
Plasma O. P. Drug binding Coagulation Hydrolysis
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Drug binding
Drugs reversibly combine with Albumin ↓ albumin ↓ binding sites ↑ free drug Albumin < 2.5gm% Acute Hepatic dysfunction ?
Coagulation ?
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Drug binding
Acute hepatic dysfunction - drug binding not affected
T ½ Albumin : 14 – 21 days Coagulation : affected (2—6hrs)
Vitamin K dependent Coag. Factors?
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Coagulation
Prothrombin, fibrinogen Factor V, VII, IX, X ( except VIII)
Deranged Coagulation ?
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Coagulation
Deranged coagulation ↓ed synthesis of Clotting factors ↑ed PT Vit. K deficiency d/t biliary
obstruction absence of bile salts Thrombocytopenia ↑ed Fibrinolysins
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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.
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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?
Obst. J
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
Obst. J
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
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Bilirubin formation & excretion
Daily prod 250—350mg/d Interpretation of plasma &
urine bilirubin Categories of liver
dysfunction
1 unit BT ?
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Blood Reservoir
10% of total blood volume Available for Auto transfusion into central
circulation
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Hepatic Blood Supply
Unique ?
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Hepatic Blood Supply
25% to 30% of CO Dual supply Portal V (75%) 85% saturated Hepatic A (25%) 95%saturated 2/3 of oxygen used by liver
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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 ?
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Control of Liver Blood Flow EXTRINSIC
Increase HBF Acute hepatitis Supine posture Hypercapnia Drugs βadrenostimulation
Decrease HBF Hypoxia Hepatic cirrhosis Upright posture Hypocapnia/IPPV/PEEP Drugs βadrenoreceptor blockade/ α agonist
Ganglion blockade Anaesthetic agent
Obst. J
Liver Function Tests
Non specific Large hepatic reserve
LFT ?
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Liver Function Tests S. Bilirubin (T) - 0.3—1.1mg% {(I) 0.2-0.7mg%, (D)0.1—0.4mg%) Transaminases—SGOT/SGPT/LDH hepatocyte damage hypoxia/drugs/viruses Extrahepatic—heart/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 ?
Obst. J
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
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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 ?
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Signs &Symptoms
Prog sev jaundice Dark urine Clay coloured stools Pruritis High fever+ chills
Biochemical hallmarks
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Obstructive Jaundice
Primary mechanism- Obst. of E.H. bile duct.
Bile duct pressure - Normal – 10-15 cm H2O > 15 cm → bile flow decreases > 30 cm → bile flow stops
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Pathophysiological consequences
CHOLESTASIS
Retention of bile solutes
In liver Hepatocyte func ↓ Cyto-450 –metab
Protein synth-alb ↓ - clotting factors ↓
Bile constituents in serum ↑conju. Bilirubin
Serum bile acids—pruritus Hypercholesterolemia- Ahteromas, Xanthomas
Systemic effect-CVS/renal/ GIT
Absence of bile in intestine Malabsorp steatorrhoea ↓ Vitamin A,D, E, K
Escape of endotoxins into portal blood
Bile Acids are potent toxins
Obst. J
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 ?
Obst. J
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
Obst. J
Renal system
Mild renal vasoconstriction Renal hypoperfusion( hypovolemia) Refractoriness of tubules to ADH Endotoxemia
Obst. J
Renal System
Renal vasoconstriction
Arterial hypotension Nephrotoxic bile salt & pigments
Endotoxins & Inflammatory mediators
• Acute Renal Failure
• Hepatorenal Syndrome
Obst. J
Renal system
Oliguria Inability to excrete Na in urine( 10mmol/l) Functional change Normal renal blood flow
Treatment : Prevention-identify high risk
patients
Hepatorenal Syndrome
Obst. J
Systemic alterations
Coagulopathy(low grade DIC) Impaired platelet function ↑ FDP---inhibition of fibrinolysis ↑ Endotoxins Hm gastritis & stress ulcers Impaired wound healing
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Anesthetic problems in Obstructive Jaundice ?
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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)
Obst. J
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 ?
Obst. J
Problems related to surgery
Whipple’s procedure---Carc. Head of panc Distal gastrectomy,PJ, HJ, GJ Major surgery---long duration Increased blood loss/fluid shifts Wide incision---Roof top—warrants good
postoperative analgesia Extensive monitoring reqd for favourable
outcome
Obst. J
Risk Factors
Age > 60yrs Albumin < 30gm% Preop. renal dysfunction Long standing biliary obstruction → infection →
sepsis Weight loss ↑Serum creatinine & Sepsis—prognostic factors ↑Periop CVS collapse & renal failure
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Preoperative Assessment
OBJECTIVES Assess the type and degree of liver
dysfunction. Assess effect on other system. To ensure – post operative facilities (High risk
patient).
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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
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Preoperative Investigations
To know the pattern of disease : S. Bilirubin SGOT, SGPT 90% predictive alk. phosphatase
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Preoperative Investigations To judge the synthetic ability of liver Serum albumin– < 2·5 gm% - severe
damage Albumin/globulin ratio – reversed. Prothrombin time –> 1·5 sec. Over control – INR - > 1.3 (D/D – Par entral Vit. K – Obst. Jaundice)
Obst. J
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
Obst. J
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
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Preoperative management
No conclusive evidence for – Preop percutaneous biliary drainage Gut sterlization Polymyxin B Oral bile salts
Pre medication ?
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Premedication
Anxiolytic – oral short acting BDZ Oral H2 antagonist Vit. K (Obst. J) – 10 mg B D X 3 day If Bilirubin > 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
Obst. J
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 ?
Obst. J
Anesthetic technique
General anesthesia Preoxygenation Induction - Thiopentone Propofol Muscle relaxant – Suxamethonium Vecuronium 0.15mg/kg
Rocuronium0.6mg/kg Atracurium(DOC) Opioids ?
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Anesthetic technique
Opioids – Well tolerated smaller doses Morphine—ph-II reac. fentanyl(DOC) spasm of sphincter of Oddi
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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
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Anesthetic technique
Volatile Anesthetics Useful & well tolerated Can be entirely eliminated Disadv- CVS instability → vasodilation → ↓perf.
Press. → ↓ blood velocity →↑ oxygen extraction → ↓ HBF & oxygen supply
Isoflurane—best maint. of HBF & oxygen IPPV ?
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Anesthetic technique
IPPV – - Maintain eucapnia - Liver low pr.tissue bed - Avoid large VT & high airway
pressures
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Anesthetic technique
Maintenance of BV and Renal function Mannitol Frusemide Dopamine Adequate blood/component replacement
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Monitoring
BP,HR,SpO2 EtCO2 CVP Urine output Core temp NMJ monitoring Blood loss
Biochemical B.Sugar,ABG S.Electrolytes Hematological Hb,PT,,PTTK,TEG
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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
