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Metabolic complications may occur when large volumes of blood products are transfused. The so-called lethal triad of massive transfusion, including acidosis, hypothermia, and coagulopathy will be discussed in this chapter. Other complications of massive transfusion will be reviewed, including hyperkalemia, hypoglycemia, hypocalcemia from citrate in transfused products, and other metabolic abnormalities associated with hypothermia. Hypotensive reactions and transfusion-associated dyspnea will also be discussed.
Metabolic complications of blood transfusion are most often seen in neonates or in circumstances in which large volumes of blood products are transfused, such as massive transfusion (see Chapter 58 ). The category of “metabolic complications” typically includes acidosis, citrate toxicity (hypocalcemia), hyperkalemia, hypokalemia, and hypothermia.
Metabolic complications are secondary to blood product storage in the cold (1–6°C), citrate within the anticoagulant/preservative solution, and the RBC storage lesion; together these three elements may result in hypothermia, hypocalcemia, acidosis, and hyperkalemia. Changes in RBCs during storage include a decrease in ATP and 2,3-DPG, and an increase in hemolysis. In the supernatant fluid, increases in potassium and decreases in pH, sodium, and glucose are observed. In addition, irradiation of RBC products increases the amount of potassium in the supernatant over time.
Hyperkalemia can result in cardiac arrhythmias and potentially death. Potassium levels increase during storage (27 mmol/L at day 0–78.5 mmol/L at day 35 in CPDA-1 and 45–50 mmol/L at day 42 in AS; Table 31.1 ); irradiation increases supernatant potassium levels (see Chapter 42 ).
Patients at particular risk for complications from hyperkalemia include infants and neonates who receive large volumes of irradiated and/or older units and those with higher pretransfusion potassium levels. Use of central lines increases the risk of cardiac arrhythmias. The Society for Pediatric Anesthesia released recommendations to reduce the incidence of transfusion-associated hyperkalemia and associated cardiovascular risks. These recommendations include use of fresh RBC products in cases where massive transfusion is anticipated and use as soon as possible after irradiation; and if RBCs with high potassium levels are the only readily available option, the unit can be washed. Other recommendations include use of AS units, supernatant removal, monitoring of potassium levels, transfusion through peripheral infusion line, and management of pretransfusion potassium levels. Potassium filters are in development and use of perioperative salvage technology to wash allogeneic RBCs has been reported.
Other patients at risk for clinical problems due to hyperkalemia include those with severe tissue injury or underlying renal insufficiency or failure. Rapid rates of blood transfusion (100–150 mL/minute or greater) commonly develop transient hyperkalemia, and rapid transfusion through a central venous catheter has been associated with hyperkalemic cardiac arrest, particularly in vulnerable populations of patients.
While hyperkalemia from blood transfusion is a well-recognized, hypokalemia may also occur in association with transfusion. This can occur after blood transfusion, because donor RBCs are often potassium-depleted. Citrate metabolism causes further movement of potassium into cells, particularly in those receiving large amounts of plasma. Patients at risk include pediatric liver transplant patients and massively transfused trauma patients receiving other potassium-poor solutions, such as crystalloid, platelets, and plasma. Metabolic alkalosis may occur when renal function is impaired due to the release of bicarbonate when citrate is metabolized, which results in a lower serum potassium level.
Hypothermia has a range of effects, including the following:
Decreases in tissue oxygenation due to increases in hemoglobin’s affinity for oxygen, which can result in a metabolic acidosis.
Increases in the metabolic rate, resulting in increased oxygen consumption.
Impairment of the metabolism of citrate and some medications.
Inhibition of coagulation factor enzymatic reactions and disruption of platelet function leading to a bleeding diathesis.
Induction of ventricular arrhythmias when large volumes of cold blood are infused through a central catheter in close proximity to the cardiac conducting system. This risk is exacerbated by coexisting hypocalcemia and hyperkalemia.
Hypothermia (cold toxicity) results in increased blood loss and transfusion requirements. Normothermia is defined as a core body temperature of 36–38°C. Severe hypothermia with temperatures <32°C is associated with significantly increased mortality, which has prompted the development of guidelines for maintaining normothermia during surgery. Management and prevention of hypothermia in the operative setting may include use of active warming (e.g., forced air warming both preoperatively and intraoperatively), minimizing heat loss through warming of IV fluids, irrigation fluids, and blood warmers for transfusion.
Hypocalcemia is a result of citrate toxicity (i.e., excess citric acid) in the anticoagulant solution, as citrate chelates calcium to prevent blood from clotting. Citrate (an acid) is metabolized primarily in the liver through the Krebs cycle, which results in the release of bicarbonate (a base), which is subsequently excreted by the kidneys. Recipients are at increased risk of hypocalcemia if the amount of citrate is large, such as in massive transfusion or apheresis, or if the recipient is unable to metabolize the citrate adequately secondary to hepatic impairment, which may be from hypothermia, or liver failure. In addition, metabolic alkalosis may result if the bicarbonate cannot be excreted, such as in renal failure.
Hypothermia causes increased oxygen requirements, impaired metabolism of citrate and lactate, release of potassium, increased affinity of hemoglobin for oxygen, and ventricular arrhythmias. Hypothermia commonly occurs in patients who require massive transfusion from hemorrhagic shock. Infusion of unwarmed blood products is a well-known contributing factor. The consequences of hypothermia include metabolic acidosis, coagulopathy, peripheral vasoconstriction, cardiac arrhythmias, and other associated morbidities.
Citrate toxicity results in hypocalcemia, which causes paresthesia, nausea, hyperventilation, and depressed cardiac function. Hyperkalemia may result in cardiac arrest.
Contributing to the hemostatic abnormalities, which often develop during massive transfusion, including dilutional and consumptive coagulopathy, hypothermia impacts platelet function and impairs the coagulation cascade with resultant decreased ability to form stable clots. This is due to reduction in coagulation factor activity for each 1°C drop in temperature, which underscores the importance of avoiding hypothermia in patients requiring massive transfusion.
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