Similar to LGIB transfusion prediction rules, the BLEED (ongoing bleeding, low systolic blood pressure, elevated prothrombin time [PT], erratic mental status, unstable comorbid disease) classification identified patients with UGIB most likely to require transfusion. High-risk patients had one or more of the following: ongoing bleeding, SBP <100 mm Hg, PT more than 1.2 times the control value, altered mental status, the presence of an unstable comorbid disease, or a disease process requiring management in the intensive care unit.18
Trauma
Within the first 48 hours of presentation, blood loss accounts for more than 50% of all trauma deaths.19,20 Posttraumatic bleeding is attributed to several factors, including vascular injury and coagulopathy. Hemodilution from large amounts of crystalloid infusion, hypothermia, and acidosis in early resuscitation adversely affect coagulation, platelet function, protein C consumption, and increases levels of tissue plasminogen activator inhibitor.21 A recent study comparing coagulation tests at the trauma scene and for 1 hour after injury, demonstrated significant activation and consumption of Factors V and XIII, fibrinogen, and proteins C and S.22 Patients with acute coagulopathy of trauma-shock (ACTS) were 4 times more likely to die than those without ACTS.22
In patients with evidence of hemorrhagic shock, hemodynamic instability, and inadequate oxygen (O2) delivery, a restrictive approach to transfusion is favored to maintain a goal hemoglobin of 7 to 9 g/dL. Generally, transfusion is considered when Hgb drops to <7 g/dL, especially in mechanically ventilated and other critically ill patients. Red blood cell transfusion should not be considered the singular or absolute method to improve tissue O2 consumption.23
Obstetric Hemorrhage
Postpartum hemorrhage (PPH) is a catastrophic maternal complication of delivery and a leading cause of maternal morbidity and mortality. Delayed hemorrhage may be seen in the ED days to weeks postpartum. Initial measures to control bleeding include uterine massage, uterotonic medications (ie, oxytocin), and blood-product components. Coagulopathy may be rapidly identified and FFP considered if a clot does not form within 7 minutes in a collection tube containing no anticoagulant (ie, red-top tube).12 During an ED delivery, uterine atony should be anticipated if the uterus is enlarged or the fundus is “doughy.” Atony is the most common cause of PPH within 24 hours and is managed with oxytocin 20 to 30 U/L at 200 mL/h. Alternatively, methylergonovine maleate 0.2 mg may be administered intramuscularly.24
Transfusion Complications
Several immediate complications may arise from transfusion, including intravascular hemolytic transfusion reactions, fever, urticaria, and transfusion-related lung injury (TRALI). Delayed complications include extravascular hemolytic reactions, and TA-GVHD. Other complications include acute bacteremia from contamination, viral infection, electrolyte derangements, cardiogenic pulmonary edema, and transfusion-associated circulatory overload (TACO).
Intravascular Hemolytic Reactions
Intravascular hemolytic reactions resulting from ABO incompatibility are the most severe transfusion complication. Immediate onset symptoms include fever, chills, headache, nausea, vomiting, chest discomfort, and severe back pain. Treatment involves immediate cessation of the transfusion, replacement of all tubing components, and aggressive IV crystalloid fluid therapy with diuretics to maintain a urine output of 1 to 2 mL/kg/h. All remaining blood, along with the patient’s blood and urine samples, should be sent to the laboratory to detect free Hgb. A positive Coombs test on the posttransfusion blood confirms the diagnosis.
The most common reaction is a 1°C temperature elevation with no other cause. Treatment for fever and urticaria consists of antihistamines and antipyretics. However, febrile patients receiving blood for the first time should be managed as an intravascular hemolytic transfusion reaction until proved otherwise by a negative Coombs test. Mild reactions may be due to an allergic response to donor plasma proteins, but in patients with genetic immunoglobulin A (IgA) deficiency can represent an afebrile life-threatening reaction characterized by hypotension and respiratory symptoms. An IgA deficiency should be considered in patients of European descent as a cause of transfusion-related anaphylactic reactions.25
The most common cause of mortality from transfusions is due to transfusion-related acute lung injury (TRALI), which presents within the first 6 hours of transfusion. Signs and symptoms of TRALI include noncardiogenic pulmonary edema, dyspnea, hypoxemia, fever, and hypotension. A portable chest X-ray may reveal bilateral infiltrates, and a complete blood count may demonstrate transient leukopenia. While the underlying mechanism is likely multifactorial, TRALI may be precipitated by a “leaky” pulmonary endothelium as a direct or indirect result of antibodies against the recipient. One strategy to reduce the incidence of TRALI is to use male donors for plasma to reduce the incidence of allotypic leukocyte antibodies that can occur in women who have had prior pregnancies. Management of TRALI includes immediately stopping the transfusion, notifying the blood bank, and providing respiratory support. Blood products may be transfused from a different donor. Unlike TACO or cardiogenic pulmonary edema, TRALI demonstrates no evidence of circulatory overload, and it does not respond to diuretic therapy.26 Circulatory overload may be avoided by infusing a single unit of PRBCs over 4 hours.