Anesthetic implications or considerations in Obstructive jaundice

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 CVS:

  • Cardiac depression
    • Bile acid causes direct negative inotropic and chronotropic effect
      • SA node inhibition by ↓ spontaneous depolarisation 
      • ↓ Duration of the action potential by inhibiting calcium current 
      • The negative chronotropic impact is due to the binding of Bile acid with the Muscarinic M2 receptor that inhibits intracellular cAMP.
      • ↑ Vagal response 
      • ↑ Plasma ANP levels that inhibit sympathetic transmission and augment vagal response

  • Intravascular volume depletion
    • Due to the effect of Bile acid with Na/H antiport, ↓ Sodium absorption in proximal convoluted tubule and ↑ excretion is accompanied by ↓ water reabsorption. 
    • ↑ ANP and BNP  - diuretic and natriuretic effect 

  • Vascular hyporesponsiveness
    • Endotoxemia induced ↑ vascular Nitric oxide synthesis 
    • Bile acid-induced vascular potassium channel activation 
    • Downregulation of ⍺1 receptor
    • Impaired Baroreceptor sensitivity 
Renal:
High of acute renal failure due to - 
  • Endotoxemia induced renal vasoconstriction 
  • ↓ Intravascular volume 
  • ↓ Response to vasoactive substance 
  • Bile salt deposition in renal tubule 
Coagulation abnormality:
  • The predominant effect is hypocoagulabity due to malabsorption of Vitamin K, which causes the decreased formation of both Vit K dependent procoagulants and anticoagulants. 
  • A combination of hepatocyte dysfunction and endotoxemia may result in micro thrombosis and trigger an intrinsic cascade which may precipitate DIC.  
GIT:
  • Malnutrition is due to the malabsorption of fat.
  • Stress ulcer 
  • Barrier dysfunction 
Immunity:
  • Immunosuppression due to inhibition of cellular immunity.
Pharmacological:
  • Drug metabolism, extraction ratio, and bile duct excretions are altered. 
  • ↓ MAC of volatile anaesthetics.
  • ↑ sensitivity and duration of action of volatile anaesthetics.
  • Thiopental - ↓ plasma protein binding, ↑ free unbound drug concentration, exacerbated response 
  • Pharmacokinetics of Propofol is unchanged but exassarated cardiac depression in induction dose. 
  • ↓ Opioid dose requirement due to ↑ release of endogenous Encephaline.
  • Morphine - the risk of accumulation due to ↓ metabolism, hepatic blood flow, hepatic extraction 
  • Prolong duration of action and potency of Neuromuscular blocking agents (Rocuronium) due to ↓ metabolism and biliary excretion and protein binding.
  • Bradycardia or ventricular arrhythmia with Succinylcholine.
  • High risk of arrhythmia and cardiac arrest with Neostigmine.

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