little amount of incompatible blood needs to be transfused to trigger the signs and symptoms of an impending IHTR. The first signs and symptoms may include fever, chills, general uneasiness, back pain, hemoglobinuria, dyspnea, hypotension, shock, uncontrollable bleeding, pain at the infusion site, nausea, flushing, lightheadness, substernal pain, hemoglobinemia and anemia. These reactions are the consequences of the various cytokines which are released including interleukin 1 (IL-1), tumor necrosis factor alpha (TNF-) and IL-6 and IL-8.6 These BMRs are all critical mediators of immune and inflammatory response and synergize with each other to precipitate the reactions and produce the major signs and symptoms of IHTR.
Many studies have expanded our knowledge of the pathophysiology of shock, inflammation and DIC, as they affect the outcome of HTRs. Rakic6 has shown in models of acute immunoglobulin M (IgM) mediated red cell incompatibility in experimental HTRs, that plasma TNF- levels rise sharply in a dose and time-dependent manner, peaking at 2 hours after the onset of the event. He also showed that the elevated rise in TNF- contributes to hyotension, fever, capillary permeability, and acute shock, which are associated with the HTRs. According to him, the levels of IL-8, monocyte chemotactic protein-1 (MCP-1), and neutrophil activators also rise after about 4 hours and remain elevated even after 48 hours. When the HTRs is IgG mediated, the concentrations of IL-1, IL-6, and IL-8 increase significantly within 6 hours, remain elevated for 24 hours and precipitate fever, hypotension, leukocytosis, shock, T cell proliferation and stimulation of immunoglobulin production. Increased BMRs also contribute to hemostatic dysfunction and precipitate a DIC. This may be attributed to the actions of IL-1 and TNF-, which produce changes in the hemostatic properties of endothelial cells surface, resulting in elevated tissue factor and a decrease in thrombomodulin expression and a suppression of the activity of protein C. Activation of thrombin, bradykinin, epinephrine and IL-1 may induce acute renal failure, leading to renal hypoperfusion and widespread fibrin deposit. Thus the cytokines are major contributors to the immune and inflammatory response from HTRs.6
The morbidity and mortality of an acute hemolytic transfusion reaction correlates with the amount of blood transfused. The signs and symptoms associated with extravascular IHTR are relatively mild compared to intravascular hemolysis and not as life threatening. In either type of hemolytic crisis, the patients must be provided with the care and support they need to prevent or reduce the risk of developing DIC, hypotension, and acute renal failure. The best treatment for IHTR is preventative. Most cases of IHTR are preventable because they are usually attributable to clerical errors. Error is ubiquitous whenever humans are involved in a process. Fortunately, most transfusion-related errors are benign however, the risk of death due to IHTR rivals that of HIV transmission and administration of the wrong blood or of blood component to the wrong recipient has occurred at many facilities.7 Most blood misadministration errors are caused by failure to identify the recipient and blood unit adequately, although phlebotomy errors and blood bank errors also contribute significantly. Many of the errors are multifactorial and may reflect underlying systems defects. Noncompliant specimen labels may be a cue to an increased risk of phlebotomy error. Autologous blood is not immune from error and poses infectious disease risks as well as the risk of hemolytic transfusion reaction as is perioperatively recovered blood which may pose a risk of air embolism if improperly handled.7
When all standard operating procedures (SOPs) are scrupulously followed and adhered to, to ensure proper patient identification, sample collection, labeling and identification of units, patient testing, and handling and correct transfusion at patient bedside, then the incidences of IHTR is minimized.2 Hemolytic transfusion reaction is considered a rare complication of platelet transfusion. If minor ABO incompatibility exists such as the presence of donor antibody directed against recipient's red cells in plasma-incompatible platelets, the antibodies present in the plasma of platelets might cause acute hemolysis.8
Delayed Hemolytic Transfusion Reaction Delayed hemolytic transfusion reaction (DHTR) is the destruction of transfused blood or blood components after an interval during which the recipient mounts a secondary immune response to the foreign antigens. This reaction might be seen along with delayed serologic transfusion reaction (DSTR) in which transfused red cells are sensitized by newly formed antibodies without clinical hemolysis. Various alloantibodies have