Approach

Patients should be transfused in clinical areas under direct observation of staff trained in administration of blood products and management of patients receiving blood transfusion, including emergency treatment of anaphylaxis.[1] If a patient develops new symptoms during a transfusion, the transfusion should be stopped. The identity of the patient and compatibility label of the blood product should be confirmed.[1] If the symptoms are mild, the patient can be monitored in line with standard monitoring regimens; if a more serious reaction is suspected, further medical assessment is warranted.[1]

Successful treatment of acute immune-mediated transfusion reactions relies on prompt recognition of onset with immediate cessation of the transfusion; recognition and immediate management should be incorporated into local transfusion policies and staff should receive mandatory training on the transfusion process.[1]

Initial treatment should be directed by signs and symptoms; delays to treatment should not occur while waiting for results of investigations.[1] Specific treatment of the various immune-mediated reactions is outlined.

Acute haemolytic transfusion reaction

Patients with a clinically significant haemolytic transfusion reaction should be managed in an intensive care unit.[3] Depending on the severity of the patient's condition, airway support with intubation and mechanical ventilation, haemodynamic invasive monitoring, vasopressor administration, and renal replacement therapy with dialysis may be warranted.[1] Prompt initiation of crystalloid resuscitation should be instituted to support the circulation and maintain renal cortical perfusion. Urine output goal is >0.5 to 1.0 mL/kg body weight per hour to prevent oliguric renal failure. Should fluid resuscitation fail to meet the urine output goal, forced diuresis should be considered, and renal dialysis may be needed.[3]​ Mannitol is often the diuretic of choice in this setting because it acts as a free radical scavenger, theoretically mitigating renal cellular injury, though it should be used with caution in patient with anaemia and cardiac comorbidities.​​[3][39]​​[40][41]​​ Prior to initiating a forced diuresis, intravascular volume depletion should be excluded by evidence of central venous pressure or pulmonary artery catheter monitoring.

Anaphylactic reaction or severe allergic reaction

Symptoms often occur within minutes of the initiation of transfusion, though reactions can present much later, even up to hours after finishing a transfusion.[1]​ Anaphylaxis may follow urticaria, and typically affects two or more body systems with features such as angio-oedema, hypotension, dyspnoea, wheezing, stridor, and collapse.[5][6] ​

Anaphylaxis requires immediate administration of intramuscular adrenaline (epinephrine) as soon as the diagnosis is suspected: emergency treatment should not be delayed to allow for formal confirmation of the diagnosis or until specific diagnostic criteria are met.[1][5]​​[6][42] Delayed administration has been implicated as a contributor to mortality and has also been linked to increased risk of biphasic reactions.[5][43]​​

Intramuscular adrenaline may be repeated every 5 minutes as necessary to alleviate stridor and improve blood pressure. Intravenous adrenaline infusion may be administered in the setting of cardiac arrest or profound hypotension refractory to intramuscular injection of adrenaline.[42]​​

The airway should be secured with intubation and initiation of mechanical ventilation if symptoms do not immediately respond to adrenaline injection. Supplemental oxygen should be considered for all patients with anaphylaxis regardless of their respiratory status, and must be administered to any patient with respiratory or cardiovascular compromise and to those who do not respond to initial treatment with adrenaline.[42] Bronchospasm may benefit from the adjunct use of an inhaled bronchodilator (e.g., salbutamol).​

Crystalloid administration should be performed to support circulation. Beta-blockers (and the underlying condition they are prescribed for, e.g., coronary artery disease [CAD]) may complicate the treatment of severe anaphylaxis.[5] Beta-blockers may cause resistance to adrenaline treatment, manifested by refractory bradycardia and hypotension.[5] Glucagon may be used to overcome beta blockade, but the resulting tachycardia can be detrimental in patients with severe CAD.[44] Therefore, early consultation of a cardiologist is warranted.​​​

Antihistamines may also be administered as an adjunct to adrenaline.[42] Corticosteroid administration (such as methylprednisolone) is not routinely recommended as evidence is lacking for clear benefit in anaphylaxis, however it may be considered after initial resuscitation.[42][45]​​​[46]​​ See Anaphylaxis (Management approach).

Urticarial reaction without anaphylaxis

When urticaria alone develops during transfusion, the transfusion should be temporarily discontinued and an antihistamine administered. Once symptoms have resolved, the transfusion may be resumed, and no further work-up is necessary. The patient should be closely monitored for onset of anaphylaxis, which may progress rapidly. In such severe cases, the transfusion should not be resumed.

Febrile non-haemolytic transfusion reaction

An antipyretic, such as paracetamol, may be administered for patient comfort, though efficacy has not been proven.[1][4] Aspirin should be avoided in the setting of thrombocytopenia. The transfusion should be discontinued until a haemolytic reaction has been ruled out (although often the fever first develops following completion of the transfusion). If no clinical concern for haemolysis exists, transfusion may be resumed. Alternatively, the patient may be transfused with a new component.[1]

Transfusion-related acute lung injury (TRALI)

Management is supportive, and may range from supplemental oxygen by mask for a brief period to mechanical ventilation for a period of days, depending on the severity of the patient's respiratory insufficiency. Resolution of the syndrome generally occurs rapidly, typically within fewer than 7 days following transfusion.

Delayed haemolytic transfusion reaction

Delayed haemolytic reactions can present days to weeks after a transfusion; if the reaction is manifested by a brisk haemolysis, treatment should be rendered as for an acute haemolytic reaction.[1]​ In the majority of cases, the haemolysis observed is extravascular and relatively mild. Some patients develop jaundice. The fact that haemolysis is primarily extravascular explains why acute renal failure and disseminated intravascular coagulation rarely occur. Delayed haemolysis often occurs in the absence of symptoms. The diagnosis may be made when a new positive direct antiglobulin test and/or positive antibody screen is identified during the preparation of a subsequent transfusion.[3]​ Usually no specific treatment is required.

Transfusion-associated graft-versus-host disease

Transfusion-associated graft-versus-host disease occurs rarely, typically in immunocompromised patients. It tends to lead to marrow aplasia, with rapid progress towards death. Many immunosuppressive regimens have been tried. Corticosteroids, antithymocyte globulin, methotrexate, cyclosporine, azathioprine, serine protease inhibitors, chloroquine, and OKT3 have all yielded poor results.[30] Treatment is supportive.

Post-transfusion purpura

Post-transfusion purpura is uncommon. High-dose intravenous immune globulin (immunoglobulin) is the therapy of choice and should correct the associated thrombocytopenia in a matter of days.[4][47][48]

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