Transfusion-associated immune and non immune-mediated hemolysis

INTRODUCTION

Hemolysis (or shortened red blood cell survival) in a patient receiving, or having recently received, a blood transfusion is more often than not an immune-mediated phenomenon, properly referred to as a hemolytic transfusion reaction (HTR). There are also a number of non-immune-mediated causes of RBC destruction associated with transfusion. These phenomena (sometimes referred to as "pseudo-hemolytic transfusion reactions") [1], include RBC lysis caused by thermal injury, osmotic injury, mechanical injury, infection, congenital hemolytic anemia, acquired hemolytic anemia, and drugs.

This review will highlight both hemolytic and "pseudo-hemolytic" transfusion reactions, with special emphasis on the mechanism of RBC destruction in each situation (table 1). The general subject of immunologic blood transfusion reactions, which also includes anaphylactic and urticarial reactions, is presented separately. (See "Immunologic blood transfusion reactions".)

IMMUNE MEDIATED HEMOLYSIS

A hemolytic transfusion reaction can occur either during or following a blood transfusion. (See "Immunologic blood transfusion reactions", section on 'Acute hemolytic reactions' and "Immunologic blood transfusion reactions", section on 'Delayed hemolytic reactions'.)

Acute hemolytic transfusion reaction — When a hemolytic transfusion reaction (HTR) occurs during or immediately after transfusion, it is labeled an acute HTR, is a medical emergency requiring immediate intervention, and is almost always a result of complement-mediated intravascular hemolysis caused by preformed antibodies in the recipient's plasma to the donor's red blood cells (RBCs). This medical emergency results from the rapid destruction of donor RBCs by preformed recipient antibodies, usually anti-A or anti-B but occasionally anti-Rh or anti-Jka, capable of fixing complement. Rapid intravascular hemolysis may lead to disseminated intravascular coagulation (DIC), shock, and acute renal failure due to acute tubular necrosis.

The classic presenting triad of fever, flank pain, and red or brown urine (ie, hemoglobinuria) is rarely seen; fever and chills may be the only manifestation, except in patients under anesthesia, or in coma, for whom DIC may be the presenting mode.

             

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Literature review current through: Apr 2013. | This topic last updated: Sep 7, 2012.
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