Shock Syndromes II
Some metabolic complications are associated with massive transfusions that are notable for
pharmacotherapy considerations.
Potassium abnormalities may include hypokalemia or hyperkalemia.
Hyperkalemia:
| (a) | ATPase pumps become deactivated in stored blood, leading to elevations in potassium |
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concentrations from 7 mEq/L to 77 mEq/L.
| (b) | After transfusion, the ATPase pump is restored, and potassium is shifted intracellularly. |
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| (c) | Although this generally leads to minimal sequelae, hyperkalemia may develop in those |
with renal insufficiency or severe tissue injury and transfusion rates. Rapid transfusion
through a central venous catheter has been associated with hyperkalemia-induced cardiac
arrest.
| (d) | For patients at risk, the recommended management is to slow the infusion rate to less than |
|---|
100–150 mL/minute.
ii.
Hypokalemia: Secondary to restoration of the ATPase pump on transfusion, shifting potassium
intracellularly, metabolic alkalosis from citrate administration, release of hormones (e.g.,
aldosterone, antidiuretic hormone), and co-infusion of potassium-poor solutions (e.g., normal
saline)
iii.
Potassium should be closely monitored and managed during massive transfusion.
Complications secondary to citrate:
Each unit of stored blood is anticoagulated with around 3 g of citrate. The metabolic capacity
of the liver for citrate metabolism is around 3 g every 5 minutes, which is diminished with
underlying liver dysfunction or in shock states leading to citrate accumulation.
ii.
Accumulation of citrate after several transfusions may bind endogenous calcium, inducing
severe hypocalcemia, prolonged QT intervals, circulatory depression, hypotension, tremors,
and PEA.
iii.
Therefore, it is critically important to monitor ionized calcium concentrations and to administer
calcium chloride or calcium gluconate to maintain normal concentrations.
iv.
Evidence is currently lacking regarding optimal calcium dosing in a massive transfusion.
Calcium chloride 1–3 g is often the preferred dose and preparation in the setting of MTP due
to the higher potency of elemental calcium relative to calcium gluconate. The total elemental
calcium concentration in calcium chloride 10% and calcium gluconate 10% is 270 mg/10 mL
and 90 mg/10 mL, respectively.
Magnesium may also be bound by citrate, which can further increase the effects of
hypocalcemia, necessitating appropriate monitoring and management.
vi.
Although citrate is metabolized to bicarbonate, which may induce metabolic alkalosis, with
prolonged storage, PRBCs have a pH below 7.0, contributing to metabolic acidosis. Metabolic
acidosis is more common in patients requiring a massive transfusion, given hypoperfusion and
anaerobic metabolism in a shock state.
Antifibrinolytics
Tranexamic acid
An antifibrinolytic agent that binds plasminogen to prevent the dissolution of a fibrin clot.
Tranexamic acid is a competitive inhibitor of plasmin and plasminogen.
CRASH-2 trial:
Evaluated the effects of tranexamic acid in adult trauma patients with, or at risk of, significant
bleeding who were within 8 hours of injury compared with placebo (0.9% saline). Tranexamic
acid (loading dose of 1 g over 10 minutes, followed by a 1-g infusion over 8 hours) reduced
28-day mortality for all-cause trauma compared with placebo (relative risk [RR] 0.91; 95% CI,
0.85–0.97; p=0.0035).