Massive Blood Transfusion
Acceptable, most common definitions of massive blood transfusion
-10 units (2,500 mL) or more RBCs within 24 hours: this is about the same as the total blood volume of the avg. adult -4 units of RBCs in 1 hr with anticipation of continued need for blood product support -Replacement of 50% of a patient's total blood volume with blood products within 3 hrs
Because hypoCa is a result of massive transfusion, what might you expect to see in this patient?
-Chvostek's sign: facial muscle spasm -Trousseau sign: carpal spasm -Hyperreflexia (aka muscle spasms everywhere) -Lock jaw -Cramps -More bleeding since Ca contributes to the clotting cascade -Myocardial depression: leads to dysrhythmias
What can cause metabolic acidosis in a patient who got a massive transfusion
-Citrate: citrate is acidic. Loading the patient up with PRBCs = loading them up with citrate as well -Liver dysfx, causing lactic acidosis (inability of liver to convert lactate to HCO3) -Cellular hypoperfusion leading to lactic acidosis -PRBCs that have been sitting in the fridge for a while. After 2 wks of storage, PRBCs have a pH < 7.
Complications of hypothermia
-Decreased citrate metabolism -Decreased drug clearance -Hypothermic coagulopathy: when core temp < 34 C, platelet function and clotting cascade are impaired. This contributes to the bleeding risk that exists with massive transfusion -Potential for ventricular dysrhythmias: PVC, VTach, VFib
Because hypoMg (Mg < 1.5) is a result of massive transfusion, what might you expect to see in this patient?
-Musculoskeletal symptoms similar to hypoCa: hyperactive reflexes (spasms), muscular tetany, tremors, cramps -Potential for seizures -Dysrhythmias can developp: PVCs, VTach, VFib. Torsade de pointes is a dysrhythmia closely associated with Mg < 1.5.
Patients that are at risk for developing hyperK after receiving a massive transfusion
-Neonates -Patients with pre-existing cardiac and kidney diseases
If a patient is in hyperK after having gotten a massive transfusion, what might you expect to do?
-Potentially put them on continuous ECG: watch for peaked T waves, AV blocks (all 3 degrees), and worse enough VFib -Give insulin with D50 -Give Ca gluconate
Clinical scenarios that may require a massive blood transfusion
-Trauma (esp. in the Army) -Massive, uncontrollable intraoperative bleed -DIC
What does acidosis do to platelets
Acidosis directly reduces activity of both extrinsic and intrinsic coag pathways AND significantly reduces the activity of Factor VIIa and Factor VIIa/tissue factor
How does a massive blood transfusion lead to hypoMg
Because of citrate. Citrate binds with serum Mg. Additionally, infusion of Mg-poor IV fluids (isotonics - 0.9% NS, LR) that are given during hemorrhage contributes to this.
Why can massive blood tranfusion cause hypothermia
Because you're transfusing a massive amount of blood products RAPIDLY. Blood products are cold - they're kept in a fridge! For this reason, expect IV fluids and blood to be run through a warmer
How can a massive blood transfusion cause hypoK (K < 3.5)
D/T: -all of the serum K can shift into the transfused RBCs -Release of stress hormones -Metabolic alkalosis that causes transcellular shift of H+ ions out and K+ ions in Watch K level, ECG, expect to give IV K if critically low
What may decrease the risk of hyperkalemia occuring after a massive blood transfusion
Transfusin blood that is < 5-10 days old or irradiated < 24 hrs ago
How to treat the complications of massive transfusion
Treating the event that triggered the need for massive transfusion + obviously treating each individual complication
You're taking care of a patient who was in a motor vehicle accident and bleed out a lot. The patient was given 12 units of PRBCs within the past 24 hours. Would you be surprised if the patient's CBC showed low PLT (< 150) and deficiencies in certain clotting factors?
No. Massive blood transfusions can cause dilutional coagulopathy - the pt might end up bleeding after receiving massive amounts of blood transfusions. Coagulation factors are diluted out b/c: -PRBCs contain ONLY RBCs. There are no PLTs are clotting factors in PRBCs. You're overloading the serum with RBCs & leaving little room for coag factors -During hemorrhagic shock, fluid shifts from the interstitial to the intravascular compartment, reulsting in the dilution of coag factors
Why does critically low hypocalcemia occur in patients receiving massive blood transfusions?
The citrate (additive that prevents PRBCs from clotting in the bag) binds with the patient's serum calcium (free Ca - Ca that's unbound to albumin). Ca can get significantly lower than 9. Those at risk: neonates, patients w. pre-existing liver dysfx
How can a massive transfusion cause hyperK (K > 5.0)?
This particularly can occur if blood that has been in the fridge longer or is closer to its expiration date is transfused. The older the blood is, the more hemolyzed red blood cells it contains. Whenever RBCs are hemolyzed, they release their intracellular contents. K just happens to be in the cell. So now a ton of K is in the bag. Irradiation of blood can also cause hemolysis of RBCs and lead to hyperK Aciodosis 2/2 hypoperfusion (likely caused by the underlying cause) can also worsen hyperkalemia. During metabolic acidosis, a transcellular shift occurs: H+ ions are moving into the cell while K+ ions move out