Regarding regional citrate anticoagulation for continuous renal replacement therapy (CRRT):
a) What is the mechanism by which citrate provides anticoagulation? (20% marks)
b) What is the metabolic fate of the citrate? (20% marks)
c) What are the features of citrate toxicity? (20% marks)
d) What conditions may increase the risk of citrate toxicity? (20% marks)
e) What alternative(s) to citrate could you use in a patient with severe HITS? (20% marks)
Forms a calcium – citrate complex which drops the serum ionized calcium level. Calcium is necessary for IX → IXa, X → Xa and PT → thrombin.
Citrate complexed with calcium is partially removed by the filter, but some enters the circulation. Citrate is largely metabolized in the liver, entering the tricarboxylic acid pathway (Krebs cycle) generating NADH. Also generates bicarbonate (at a rate of 3 bicarb per 1 citrate).
2 sorts of problems.
First (most commonly described), due to inadequate calcium replac ement, are those of low ionized calcium, i.e. chilliness, anxiety, perioral paraesthesiae, carpopedal spasm, tetany, QT prolongation and arrhythmias. Associated with metabolic alkalosis from citrate metabolism, and possibly with sodium overload from the hy pertonic sodium citrate.
Secondly (less common), due to citrate load in excess of hepatic ability to metabolise it, i.e. accumulation of citrate - calcium complex. Metabolic acidosis with high anion gap from citrate; raised ratio of total to ionized calcium from complexed calcium in circulation (normal total:ionized ratio 1.9 - 2.2:1, toxic ratio > 2.5:1.
Low cardiac output (i.e. poor hepatic perfusion)
At least 3 classes or 4 drug names for full marks
Prostacyclin (PGI 2 )
This question is identical to Question 29 from the first paper of 2013.