Metabolic Complications of Massive Transfusion
Description
Potential metabolic abnormalities secondary to massive transfusion include hypocalcemia, hypomagnesemia, metabolic alkalosis, hyperkalemia or hypokalemia.
Citrate Toxicity: hypocalcemia, hypomagnesemia, metabolic alkalosis
Blood components are anticoagulated with sodium citrate. It is rapidly metabolized by the liver, and a normothermic adult can tolerate the citrate in a unit of plasma or several units of red blood cells given every five minutes. When transfused, citrate may bind with circulating ionic calcium and magnesium. During massive transfusion, the capacity of the liver to metabolize citrate may be overwhelmed, and potentiated by hypothermia or hypotension, particularly in the presence of underlying liver disease, leading to hypocalcemia and/or hypomagnesemia. Metabolic alkalosis may also develop secondary to the accumulation of bicarbonate, the metabolic by-product of citrate.
Metabolic acidosis
Metabolic acidosis is rare. It may be caused from the acid pH of blood products, and aggravated by lactic acidosis seen in patients with tissue hypoxia.
Hyperkalemia or Hypokalemia
Potassium release from red cells increases during storage, and after irradiation. Levels of up to 80 mmol/L may be reached in a unit of red blood cells. Massive transfusion may lead to hyperkalemia, which can cause cardiac arrhythmias or myocardial depression. Young infants are the most susceptible patients, particularly if stored blood is transfused rapidly into a central line.
Paradoxically, hypokalemia has also been described with massive transfusion. Possible causes include metabolic alkalosis secondary to citrate metabolism and re-accumulation of potassium in transfused potassium-depleted RBCs.