Clinical Presentation - Metabolic Complications of Massive Transfusion
Metabolic complications of massive transfusion may cause multi-system, non-specific abnormalities in cardiac function, muscular function, and tissue oxygenation. Diagnosis is made by ongoing laboratory monitoring.
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 and particularly in the presence of diffuse liver disease and/or hypothermia and hypotension, the capacity of the liver to metabolize citrate may be overwhelmed. Citrate toxicity may lead to a functional hypocalcemia and hypomagnesemia. Metabolic alkalosis may develop secondary to the accumulation of bicarbonate, the metabolic by-product of citrate.
Potassium release from red cells increases during storage, and after irradiation. Levels of up to 80 mEq/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. Hypokalemia, possibly due to alkalosis, catecholamine effects, and intracellular influx, may also complicate massive transfusion.
Metabolic acidosis is rare. It may be caused from the acid pH of blood components and aggravated by lactic acidosis seen in patients with tissue hypoxia.
Clinical symptoms of electrolyte abnormalities include hypotension, decreased ventricular function, decreased pulse pressure, i.e., the difference between the systolic BP and the diastolic BP, increased pulmonary artery pressure, neuroexcitability, tetany (muscular irritability or spasms), paresthesia (abnormal sensation), and arrhythmias.