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Acute hemolytic ABO incompatibility reaction to RBC antigens.
Fever, chills, and flushing Low back pain Tachycardia and hypotension Vascular collapse Cardiac arrest http://two.xthost.info/wardclass1/BT%20Reactions.pdf
Prevention: Proper identification of the patient from sample collection through to blood administration, proper labelling of samples and products is essential. Prevention of nonimmune haemolysis requires adherence to proper handling, storage and administration of blood products.
http://www.rch.org.au/bloodtrans/adverse.cfm?doc_id=5323#Acute_Haemolytic
Acute hemolytic transfusion reaction

Acute hemolytic transfusion reactions occur within 24 hours of the transfusion and often occur during the transfusion. Ominously, the patient may report a "feeling of impending doom". They may also complain of a burning sensation at the site of the infusion, together with chills, fever, and pain in the back and flanks. The severity of the reaction depends upon: (1) how much incompatible antigen was transfusedhow much blood was given and the number of antigens per red blood cell; (2) the nature of the antigen - its size and location on the red blood cell membrane; and (3) the nature of the recipient's antibodies - the type (IgG or IgM) and subtype (IgG3) of antibody, the amount present in the circulation at the time of the transfusion, its avidity for binding to the antigen, and its ability to activate complement. Intravascular hemolysis The most severe reactions involve an intravascular hemolysis; the donor RBCs are destroyed by the recipient's antibodies while they are still inside blood vessels. Such reactions involve antibodies that strongly activate complement, which in turn lyses the donor RBCs. Hemoglobin is released into the plasma and excreted in urine (hemoglobinuria), turning the urine a dark brown color. Bilirubin, a metabolite of hemoglobin usually secreted into bile by the liver, instead accumulates in the blood causing jaundice. Massive activation of complement can cause
shock, as can the large amounts of tissue factor released by RBC debris that triggers an uncontrollable clotting cascade (disseminated intravascular coagulation). The most common cause of an acute intravascular hemolytic transfusion reaction is ABO incompatibility. The ABO blood group antigens are densely expressed on the RBC surface, and most people have adequate amounts of preformed antibodies that can not only bind to the RBCs but can also activate complement. Although routine typing and cross matching should prevent incompatible ABO blood group antigens from triggering this type of reaction, human error occasionally leads to the "wrong blood" being given during a transfusion. Apart from anti-A and anti-B, other antibodies capable of intravascular hemolysis of transfused RBCs include antiH produced in people with the Bombay blood group (see the H blood group), anti-Jka (see the Kidd blood group), and anti-P, P1, Pk (see the P blood group system). Extravascular hemolysis In extravascular hemolytic reactions, the donor RBCs are removed from the circulation by macrophages in the spleen and liver. The macrophages destroy the red blood cells inside these organs. The donor RBCs may still be coated with the recipient's antibodies, but these antibodies do not trigger an immediate intravascular hemolysis. Instead, their presence (specifically, the Fc component of the antibody) is recognized by IgG-Fc receptors of macrophages, which aids the phagocytosis of the cells. Antibodies directed at antigens of the Rh blood group mediate this type of RBC removal. Other types of antibody that bind to the donor RBCs may bind the complement component C3b without activating the entire cascade. This further aids the phagocytosis by macrophages that have C3b receptors. Such antibodies include those directed against antigens of the ABO, Duffy, and Kidd blood groups. Because the extravascular destruction of RBCs is slower and more controlled than intravascular hemolysis, very little free hemoglobin is released into the circulation or excreted in the urine. The liver can keep up with the increased production of bilirubin, and jaundice rarely occurs. Therefore, the main symptoms of this type of reaction are fever and chills.
Delayed hemolytic transfusion reaction

Delayed hemolytic transfusion reactions may occur as soon as 1 day or as late as 14 days after a blood transfusion. The donor RBCs are destroyed by the recipient's antibodies, but the hemolysis is "delayed" because the antibodies are only present in low amounts initially. The recipient's antibodies were formed during a previous sensitization (primary stimulation) with a particular antigen. However, by the time a cross match is done, the level of antibody in the recipient's plasma is too low to cause agglutination, making this type of reaction difficult to prevent. Likewise, during the blood transfusion the level of antibody is too low to cause an acute transfusion reaction. However, during the blood transfusion, as the patient re-encounters the antigen, his or her immune system is stimulated to rapidly produce more antibodies (secondary stimulation). Over the following days, the recipient's antibodies bind to the donor RBCs, which are subsequently removed from the circulation by macrophages (extravascular hemolysis). The clinical outcome depends upon the rate at which the patient can produce antibodies and hence destroy the donor RBCs. Usually, this type of reaction is much less severe than acute hemolytic reactions. This type of transfusion reaction is associated with antibodies that target the Kidd and Rh antigens.

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Acute hemolytic ABO incompatibility reaction to RBC antigens.

Acute hemolytic transfusion reaction

Delayed hemolytic transfusion reaction

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