Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis.

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Li K, Xu Y

Citrate metabolism in blood transfusions and its relationship due to metabolic alkalosis and respiratory acidosis.

Int J Clin Exp Med. 2015 Apr 15;8(4):6578-84. eCollection 2015.

PubMed ID
26131288 [ View in PubMed
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Abstract

Metabolic alkalosis commonly results from excessive hydrochloric acid (HCl), potassium (K(+)) and water (H2O) loss from the stomach or through the urine. The plasma anion gap increases in non-hypoproteinemic metabolic alkalosis due to an increased negative charge equivalent on albumin and the free ionized calcium (Ca(++)) content of plasma decreases. The mean citrate load in all patients was 8740+/-7027 mg from 6937+/-6603 mL of transfused blood products. The citrate load was significantly higher in patients with alkalosis (9164+/-4870 vs. 7809+/-3967, P < 0.05). The estimated mean total citrate administered via blood and blood products was calculated as 43.2+/-34.19 mg/kilogram/day. In non-massive and frequent blood transfusions, the elevated carbon dioxide output has been shown to occur. Due to citrate metabolism causes intracellular acidosis. As a result of intracellular acidosis compensation, decompensated metabolic alkalosis + respiratory acidosis and electrolyte imbalance may develop, blood transfusions may result in certain complications.

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