Anaesthesia in liver disease patient. Baharulhakim Said b Daliman Department of Anaesthesiology & Intensive Care Hospital Kuala Terengganu. www.anaesthesia.co.in firstname.lastname@example.org. Objectives. It is an important topic? Physiology Pharmacology ~ Phase I & II metabolism
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Anaesthesia in liver disease patient
Baharulhakim Said b Daliman
Department of Anaesthesiology & Intensive Care
Hospital Kuala Terengganu
albumin can be decreased with liver disease
colloid osmotic pressure will be reduced
fewer binding sites for drugs and the unbound, active portion of protein-bound drugs will be increased example : Thiopental.
Clotting factors V, VII, IX, X, prothrombin and fibrinogen are all dependent on the liver for synthesis ~ many of the factors require only 20-30% of normal levels to stop bleeding, significant impairment of liver function must occur before problems begin.
Plasma half-lives of clotting factors are measured in hours. Therefore, acute liver dysfunction can lead to coagulopathies.
Both severe parenchymal disease and biliary disease may lead to coagulopathy - the former due to impaired synthesis and the second by decreased vitamin K absorption due to the absence of bile salts secondary to biliary obstruction.
Divided into 2 phase:
Factor affecting drug metabolism:
Pharmacokinetic changes cause by liver disease:
Pharmacodynamic changes occur because:
Classic symptoms are:
Aberrations of physiology in chronic liver disease:
# clinical pearl is to decrease the drug dosage by half and modify as needed (Conn, 1991).
Extreme peripheral vasodilation ► extreme ↓ arterial blood volume & hypotension
Activates homeostatic mechanism ► vasoconstriction of renal vasculature
↓ GFR & plasma renin remains high with salt & water retention
Prognosis is poor
Most of us will never take part in a transplant but the lessons learned can be applied each time we administer anesthesia to a patient with hepatic disease
iii. Liver dialysis machine
(molecular adsorbent recirculating system)