Anesthetic implications or considerations in Obstructive jaundice

 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.