1. calcium gluconate
2. dextrose
3. normal saline
4. sodium citrate
Citrate toxicity
Ans: 1
Cause: Citrate is the anticoagulant used in blood products. It is usually rapidly metabolised by the liver. Rapid administration of large quantities of stored blood may cause hypocalcaemia and hypomagnesaemia when citrate binds calcium and magnesium. This can result in myocardial depression or coagulopathy. Patients most at risk are those with liver dysfunction or neonates with immature liver function having rapid large volume transfusion.
Management: Slowing or temporarily stopping the transfusion allows citrate to be metabolised. Replacement therapy may be required for symptomatic hypocalcaemia or hypomagnesaemia.
Treatment: calcium (based on ECG changes-Hypocalcemia typically prolongs the Q-T interval on electrocardiograms and may lead to complete heart block).
90% of the citrate found in whole blood products is found in FFP and platelets (not PRBCs).
Signs and symptoms of hypocalcemia (whether or not caused by citrate) include hypotension, decreased pulse pressure, arrhythmias, increased LVEDP and CVP, mental status changes, tetany, laryngospasm, Chvostek (facial nerve) and Trousseau (brachial artery occlusion) signs.
Note, however, that citrate intoxication is very rare
Citrate intoxication may be more likely in the setting of hypothermia (metabolism is decreased 50% at 31C), liver disease/transplantation, hyperventilation (alkalemia, albumin releases protons which are replaced by Ca++, effectively lowering serum levels), and is more likely in pediatric patients.
Normally citrate is metabolized by the liver, and a reduction of such activity, ex. in the setting of liver disease/transplantation, contributes to hypocalcemia. Unmetabolized citrate is also excreted by the kidneys
6 units/hour (or 35 mL/min) of blood must be transfused before ionized calcium levels begin to decrease. Similarly, hyperkalemia requires an infusion of blood at 120 mL/min or more
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