Clinical Presentation - Acute Hemolytic Transfusion Reactions (immune)
Signs and symptoms usually appear within minutes after the transfusion is started but can occur anytime during the transfusion. They may include (but are not limited to):
- fever (temperature increase of more than 1oC)
- chills
- rigors
- nausea and vomiting
- anxiety
- malaise
- hypotension
- tachycardia
- burning along site of infusion
- skin flushing
- chest pain
- dyspnea, wheezing
- severe low back pain
- hemoglobinemia
- hemoglobinuria
- oliguria/anuria
- uncontrolled bleeding
In the anesthetized patient, the only signs may be unexplained bleeding due to disseminated intravascular coagulation (DIC), falling blood pressure, and/or fever.
The more severe transfusion reactions are characterized by shock, chills, fever, dyspnea, chest pain, back pain, headache and/or abnormal bleeding; these reactions may result in death. Hemoglobinemia, hemoglobinuria and subsequent hyperbilirubinemia are often detectable. Potentially life-threatening complications include:
- hypotension and shock
- disseminated intravascular coagulation
- renal failure
Mechanisms
The mechanisms involved in AHTR are complex and not fully understood. Following transfusion of ABO-incompatible red cells, the recipient's ABO antibodies bind to antigens on the transfused red cells triggering complement activation. IgM and IgG anti-A, anti-B, and anti-A,B are all excellent complement binders. As the classical complement pathway progresses, anaphylatoxins C3a and C5a are released into the recipient's plasma. Once C9 is bound, the recipient's cells are destroyed by IVH. Cytokines, such as interleukin-1, tumor necrosis factor, interleukin-6, and interleukin-8, are believed to play key roles in the immune hemolysis and its serious sequelae.
In brief, activation of the complement cascade may lead to:
- intravascular hemolysis with hemoglobinemia and hemoglobinuria
- release of vasoactive complement components resulting in hypotension and shock
- thrombin and platelet activation culminating in DIC
- renal failure due to glomerular deposition of immune complexes, DIC, and reduced renal blood flow due to hypotension