In addition to coagulopathy, other complications of MT include hypothermia, hypocalcemia, hyperkalemia, hypokalemia, acid-base imbalance, and impaired hemoglobin function.

• Hypothermia is a consequence of exposure, impaired thermoregulation, and the rapid transfusion of cold, banked blood. It is recommended that the room temperature be increased, and all fluids and blood pass through fluid warmers, in order to prevent hypothermia.

• Hypocalcemia can result from blood loss and inadequate citrate metabolism. Sodium citrate is present in stored blood to bind calcium and prevent clotting. With a high rate of transfusion, ionized calcium can be chelated by citrate, resulting in decreased levels of circulating free calcium. Consequences of hypocalcemia include bradycardia and ST segment prolongation, hypotension due to decreased myocardial contractility, and worsening coagulopathy from impaired coagulation (calcium is clotting factor IV). It is recommended to administer 1 to 2 gm of IV calcium chloride with every round of MTP.

• Hyperkalemia can occur in the massively transfused patient. Potassium concentrations in pRBCs can range from 7 to 77 mEq/L, in part due to inactivation of the red blood cell membrane Na, K-ATPase pump. Although the likelihood of life-threatening sequelae from hyperkalemia is low during MTP, in the shock state with hypoperfusion and acidemia, dangerous manifestations of hyperkalemia, such as cardiac arrhythmias, become more evident.

• Hypokalemia is also a possibility after MTP. Citrate is metabolized to bicarbonate by the liver, inducing a metabolic alkalosis that can lead to hypokalemia. Furthermore, transfused red blood cells take up potassium, with reactivation of the membrane Na, K-ATPase pump, which could potentiate hypokalemia.

• Acid-base imbalance is a problem during MTP. Donor blood pH has a low of 6.8 with prolonged storage. However, alkalosis rather than acidosis is more commonly seen during MTP due to the metabolism of citrate to bicarbonate. The presence of acidosis can usually be attributed to shock, which is often reversible with restoration of normal perfusion. In general, supplemental bicarbonate should not be given based on an arbitrary number of units transfused. Nevertheless, if metabolic acidosis persists, sodium bicarbonate might be warranted, especially in the setting of renal failure and severe muscle damage.

• Impaired hemoglobin function is possible after MTP. The 2,3-diphosphoglycerate levels are decreased in banked blood, shifting the oxygen-hemoglobin dissociation curve to the left. A leftward shift causes oxygen to be held onto more tightly by the hemoglobin molecule with a potential of limiting oxygen release to the tissues. However, no studies have documented any clinical adverse effects related to this phenomenon.

References

• Ditzel RM Jr, Anderson JL, Eisenhart WJ, et al. A review of transfusion- and trauma-induced hypocalcemia: is it time to change the lethal triad to the lethal diamond? J Trauma Acute Care Surg. 2020;88:434-439.
• Drummond JC, Petrovitch CT. The massively bleeding patient. Anesthesiol Clin North Am. 2001;19:633-649.
• Sihler KC, Napolitano LM. Complications of massive transfusion. Chest. 2010;137:209-220.