Transfusion-associated immune and non immune-mediated hemolysis

INTRODUCTION

Hemolysis (or shortened red blood cell [RBC] 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.

             

Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Nov 2014. | This topic last updated: Jan 20, 2014.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2014 UpToDate, Inc.
References
Top
  1. Beauregard P, Blajchman MA. Hemolytic and pseudo-hemolytic transfusion reactions: an overview of the hemolytic transfusion reactions and the clinical conditions that mimic them. Transfus Med Rev 1994; 8:184.
  2. Darabi K, Dzik S. Hyperhemolysis syndrome in anemia of chronic disease. Transfusion 2005; 45:1930.
  3. Utoh J, Harasaki H. Damage to erythrocytes from long-term heat stress. Clin Sci (Lond) 1992; 82:9.
  4. Mollison PL, Engelfriet CP, Contreras M. Blood transfusion in clinical medicine, Blackwell, London 1993. p.498.
  5. Sazama K. Reports of 355 transfusion-associated deaths: 1976 through 1985. Transfusion 1990; 30:583.
  6. Fridey JL. Standards for blood banks and transfusion services, 22nd ed, American Association of Blood Banks, Arlington, VA 2003.
  7. Ryden SE, Oberman HA. Compatibility of common intravenous solutions with CPD blood. Transfusion 1975; 15:250.
  8. Dubey A, Verma A, Sonker A, et al. Transfusion medicine illustrated. Sudden increased incidence of transfusion reactions reported from a ward: root cause analysis. Transfusion 2009; 49:409.
  9. Ismeno G, Renzulli A, Carozza A, et al. Intravascular hemolysis after mitral and aortic valve replacement with different types of mechanical prostheses. Int J Cardiol 1999; 69:179.
  10. Martin R, McKenty S, Thisdale Y, et al. Hemolysis during cardiopulmonary bypass. J Cardiothorac Anesth 1989; 3:737.
  11. Mair DC, Eastlund T, Rosen G, et al. Hemolysis during percutaneous mechanical thrombectomy can mimic a hemolytic transfusion reaction. Transfusion 2005; 45:1291.
  12. Kleinman S, Chan P, Robillard P. Risks associated with transfusion of cellular blood components in Canada. Transfus Med Rev 2003; 17:120.
  13. Holland PV. The diagnosis and management of transfusion reactions and other adverse effects of transfusion. In: Clinical practice of transfusion medicine, 2nd ed, Petz LD, Swisher SN (Eds), Churchill-Livingstone, New York 1989. p.713.
  14. McCurdy PR, Morse EE. Glucose-6-phosphate dehydrogenase deficiency and blood transfusion. Vox Sang 1975; 28:230.
  15. Krevans JR. In vivo behaviour of sickle trait erythrocytes when exposed to continuous hypoxia. Clin Res 1959; 7:203.
  16. Sirchia G, Zanella A. Transfusion of PNH patients. Transfusion 1990; 30:479.
  17. Valentine WN, Paglia DE, Fink K, Madokoro G. Lead poisoning: association with hemolytic anemia, basophilic stippling, erythrocyte pyrimidine 5'-nucleotidase deficiency, and intraerythrocytic accumulation of pyrimidines. J Clin Invest 1976; 58:926.
  18. Manzler AD, Schreiner AW. Copper-induced acute hemolytic anemia. A new complication of hemodialysis. Ann Intern Med 1970; 73:409.
  19. Wood L, Jacobs P. Cyclophosphamide-related intravascular haemolysis during continuous-flow plasma exchange. J Clin Apher 1985; 2:250.
  20. Sacchi S, Kantarjian H, O'Brien S, et al. Immune-mediated and unusual complications during interferon alfa therapy in chronic myelogenous leukemia. J Clin Oncol 1995; 13:2401.
  21. Brox AG, Cournoyer D, Sternbach M, Spurll G. Hemolytic anemia following intravenous gamma globulin administration. Am J Med 1987; 82:633.
  22. Hong F, Ruiz R, Price H, et al. Safety profile of WinRho anti-D. Semin Hematol 1998; 35:9.
  23. Brecher ME. Technical Manual 14th Edition. American Association of Blood Banks, Bethesda, MD 2002; 439-445.