Transfusion reaction: Difference between revisions
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===Transfusion-associated Microchimerism (TA-MC)=== | ===Transfusion-associated Microchimerism (TA-MC)=== | ||
Transfusion-associated [[Chimera (genetics)#Microchimerism|microchimerism]] is the stable persistence of donor's genetically distinct cells (usually <5%) in a recipient's circulation following fresh [[blood transfusion]], especially in the setting of [[Physical trauma|trauma]].<ref name="pmid18766299">{{cite journal| author=Kunadian V, Zorkun C, Gibson WJ, Nethala N, Harrigan C, Palmer AM et al.| title=Transfusion associated microchimerism: a heretofore little-recognized complication following transfusion. | journal=J Thromb Thrombolysis | year= 2009 | volume= 27 | issue= 1 | pages= 57-67 | pmid=18766299 | doi=10.1007/s11239-008-0268-0 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18766299 }} </ref> As a result of the current advancement in [[polymerase chain reaction]] techniques, TA-MC has been demonstrated among patients with [[Physical trauma|trauma]] following [[blood transfusion]], [[pregnancy]] and [[transplant|organ or stem cell transplantation]]. Several studies have implicated other forms of [[Chimera (genetics)#Microchimerism|microchimerism]], including [[Chimera (genetics)|fetomaternal microchimerism]], with acute and chronic illnesses such as [[congenital heart block]] in a patient with [[neonatal lupus erythematosus]]<ref name="pmid14996783">{{cite journal| author=Adams KM, Nelson JL| title=Microchimerism: an investigative frontier in autoimmunity and transplantation. | journal=JAMA | year= 2004 | volume= 291 | issue= 9 | pages= 1127-31 | pmid=14996783 | doi=10.1001/jama.291.9.1127 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14996783 }} </ref> and [[systemic sclerosis]].<ref name="pmid9492775">{{cite journal| author=Nelson JL, Furst DE, Maloney S, Gooley T, Evans PC, Smith A et al.| title=Microchimerism and HLA-compatible relationships of pregnancy in scleroderma. | journal=Lancet | year= 1998 | volume= 351 | issue= 9102 | pages= 559-62 | pmid=9492775 | doi=10.1016/S0140-6736(97)08357-8 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9492775}} </ref> | Transfusion-associated [[Chimera (genetics)#Microchimerism|microchimerism]] is the stable persistence of donor's genetically distinct cells (usually <5%) in a recipient's circulation following fresh [[blood transfusion]], especially in the setting of [[Physical trauma|trauma]].<ref name="pmid18766299">{{cite journal| author=Kunadian V, Zorkun C, Gibson WJ, Nethala N, Harrigan C, Palmer AM et al.| title=Transfusion associated microchimerism: a heretofore little-recognized complication following transfusion. | journal=J Thromb Thrombolysis | year= 2009 | volume= 27 | issue= 1 | pages= 57-67 | pmid=18766299 | doi=10.1007/s11239-008-0268-0 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18766299 }} </ref> As a result of the current advancement in [[polymerase chain reaction]] techniques, TA-MC has been demonstrated among patients with [[Physical trauma|trauma]] following [[blood transfusion]], [[pregnancy]] and [[transplant|organ or stem cell transplantation]]. Several studies have implicated other forms of [[Chimera (genetics)#Microchimerism|microchimerism]], including [[Chimera (genetics)|fetomaternal microchimerism]], with acute and chronic illnesses such as [[congenital heart block]] in a patient with [[neonatal lupus erythematosus]]<ref name="pmid14996783">{{cite journal| author=Adams KM, Nelson JL| title=Microchimerism: an investigative frontier in autoimmunity and transplantation. | journal=JAMA | year= 2004 | volume= 291 | issue= 9 | pages= 1127-31 | pmid=14996783 | doi=10.1001/jama.291.9.1127 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14996783 }} </ref> and [[systemic sclerosis]].<ref name="pmid9492775">{{cite journal| author=Nelson JL, Furst DE, Maloney S, Gooley T, Evans PC, Smith A et al.| title=Microchimerism and HLA-compatible relationships of pregnancy in scleroderma. | journal=Lancet | year= 1998 | volume= 351 | issue= 9102 | pages= 559-62 | pmid=9492775 | doi=10.1016/S0140-6736(97)08357-8 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9492775}} </ref> | ||
Genetic factors such as the [[Tumor necrosis factors|TNF]] (-308A) [[single nucleotide polymorphism]]s (SNP) have been implicated in the development of TA-MC such as the The risk of developing TA-MC is largely dependent on the clinical setting, i.e., it is rare in situations which do not involve massive trauma.<ref name="pmid21981710">{{cite journal| author=Sanchez R, Lee TH, Wen L, Montalvo L, Schechterly C, Colvin C et al.| title=Absence of transfusion-associated microchimerism in pediatric and adult recipients of leukoreduced and gamma-irradiated blood components. | journal=Transfusion | year= 2012 | volume= 52 | issue= 5 | pages= 936-45 | pmid=21981710 | doi=10.1111/j.1537-2995.2011.03366.x | pmc=PMC3257351 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21981710 }} </ref> Although leukoreduction removes > 99.9% of donor's [[white blood cell]]s, it has not been proven to prevent the development of TA-MC.<ref name="pmid17076839">{{cite journal| author=Utter GH, Nathens AB, Lee TH, Reed WF, Owings JT, Nester TA et al.| title=Leukoreduction of blood transfusions does not diminish transfusion-associated microchimerism in trauma patients. | journal=Transfusion | year= 2006 | volume= 46 | issue= 11 | pages= 1863-9 | pmid=17076839 | doi=10.1111/j.1537-2995.2006.00991.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17076839 }} </ref><ref name="pmid16078913">{{cite journal| author=Lee TH, Paglieroni T, Utter GH, Chafets D, Gosselin RC, Reed W et al.| title=High-level long-term white blood cell microchimerism after transfusion of leukoreduced blood components to patients resuscitated after severe traumatic injury. | journal=Transfusion | year= 2005 | volume= 45 | issue= 8 | pages= 1280-90 | pmid=16078913 | doi=10.1111/j.1537-2995.2005.00201.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16078913 }} </ref> | Genetic factors such as the [[Tumor necrosis factors|TNF]] (-308A) [[single nucleotide polymorphism]]s (SNP) have been implicated in the development of TA-MC such as the The risk of developing TA-MC is largely dependent on the clinical setting, i.e., it is rare in situations which do not involve massive trauma.<ref name="pmid21981710">{{cite journal| author=Sanchez R, Lee TH, Wen L, Montalvo L, Schechterly C, Colvin C et al.| title=Absence of transfusion-associated microchimerism in pediatric and adult recipients of leukoreduced and gamma-irradiated blood components. | journal=Transfusion | year= 2012 | volume= 52 | issue= 5 | pages= 936-45 | pmid=21981710 | doi=10.1111/j.1537-2995.2011.03366.x | pmc=PMC3257351 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21981710 }} </ref> Although leukoreduction removes > 99.9% of donor's [[white blood cell]]s, it has not been proven to prevent the development of TA-MC.<ref name="pmid17076839">{{cite journal| author=Utter GH, Nathens AB, Lee TH, Reed WF, Owings JT, Nester TA et al.| title=Leukoreduction of blood transfusions does not diminish transfusion-associated microchimerism in trauma patients. | journal=Transfusion | year= 2006 | volume= 46 | issue= 11 | pages= 1863-9 | pmid=17076839 | doi=10.1111/j.1537-2995.2006.00991.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17076839 }} </ref><ref name="pmid16078913">{{cite journal| author=Lee TH, Paglieroni T, Utter GH, Chafets D, Gosselin RC, Reed W et al.| title=High-level long-term white blood cell microchimerism after transfusion of leukoreduced blood components to patients resuscitated after severe traumatic injury. | journal=Transfusion | year= 2005 | volume= 45 | issue= 8 | pages= 1280-90 | pmid=16078913 | doi=10.1111/j.1537-2995.2005.00201.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16078913 }} </ref> | ||
Revision as of 17:46, 16 March 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
In medicine, a transfusion reaction is any adverse event which occurs because of a blood transfusion. These events can take the form of an allergic reaction, a transfusion-related infection, hemolysis related to an incompatible blood type, or an alteration of the immune system related to the transfusion. The risk of a transfusion reaction must always be balanced against the anticipated benefit of a blood transfusion.
Types of Transfusion Reactions
Febrile Non-hemolytic Transfusion Reaction
This is the most common adverse reaction to a blood transfusion. Symptoms include fever and dyspnea 1 to 6 hours after receiving the transfusion. Such reactions are clinically benign, causing no lasting side effects or problems, but are unpleasant via a blood transfusion is estimated, as of 2006, at 1 per 2 million units transfused. Bacterial infection is a much more common problem (see below).
Bacterial Infection
Blood products can provide an excellent medium for bacterial growth, and can become contaminated after collection while they are being stored. The risk is highest with platelet transfusion, since platelets must be stored near room temperature and cannot be refrigerated. The risk of severe bacterial infection and sepsis is estimated (as of 2001) at about 1 in 50,000 platelet transfusions, and 1 in 500,000 red blood cell transfusions.[1]
Acute Hemolytic Reaction
This is a medical emergency resulting from rapid destruction (hemolysis) of the donor red blood cells by host antibodies. The most common cause is clerical error (i.e. the wrong unit of blood being given to the wrong patient). The symptoms are fever and chills, sometimes with back pain and pink or red urine (hemoglobinuria). The major complication is that hemoglobin released by the destruction of red blood cells can cause acute renal failure.
Anaphylactic Reaction
An anaphylactic (or severe allergic) reaction can occur at a rate of 1 per 30,000-50,000 transfusions. These reactions are most common in people with selective IgA deficiency (although IgA deficiency is often asymptomatic, and people may not know they have it until an anaphylactic reaction occurs). An anaphylactic reaction is a medical emergency, requiring prompt treatment, and may be life-threatening. ===Transfusion-associated Acute Lung Injury (TRALI) TRALI is a syndrome of acute respiratory distress, often associated with fever, non-cardiogenic pulmonary edema, and hypotension. It may occur as often as 1 in 2000 transfusions.[2] Symptoms can range from mild to life-threatening, but most patients recover fully within 96 hours, and the mortality rate from this condition is less than 10%.[3]
Volume Overload
Patients with impaired cardiac function (eg congestive heart failure) can become volume-overloaded as a result of blood transfusion, leading to edema, dyspnea (shortness of breath), and orthopnea (shortness of breath while lying flat). This is sometimes called TACO, or Transfusion Associated Circulatory Overload.
Iron overload
Each transfused unit of red blood cells contains approximately 250 mg of elemental iron. Since elimination pathways for iron are limited, a person receiving numerous red blood cell transfusions can develop iron overload, which can in turn damage the liver, heart, kidneys, and pancreas. The threshold at which iron overload becomes significant is somewhat unclear, but is likely around 12-20 units of red blood cells transfused.
Transfusion-associated Graft-vs-Host Disease (GvHD)
GVHD refers to an immune attack by transfused cells against the recipient. This is a common complication of stem cell transplantation, but an exceedingly rare complication of blood transfusion. It occurs only in severely immunosuppressed patients, primarily those with congenital immune deficiencies or hematologic malignancies who are receiving intensive chemotherapy. When GVHD occurs in association with blood transfusion, it is almost uniformly fatal.[4] Transfusion-associated GVHD can be prevented by irradiating the blood products prior to transfusion.
Transfusion-associated Microchimerism (TA-MC)
Transfusion-associated microchimerism is the stable persistence of donor's genetically distinct cells (usually <5%) in a recipient's circulation following fresh blood transfusion, especially in the setting of trauma.[5] As a result of the current advancement in polymerase chain reaction techniques, TA-MC has been demonstrated among patients with trauma following blood transfusion, pregnancy and organ or stem cell transplantation. Several studies have implicated other forms of microchimerism, including fetomaternal microchimerism, with acute and chronic illnesses such as congenital heart block in a patient with neonatal lupus erythematosus[6] and systemic sclerosis.[7]
Genetic factors such as the TNF (-308A) single nucleotide polymorphisms (SNP) have been implicated in the development of TA-MC such as the The risk of developing TA-MC is largely dependent on the clinical setting, i.e., it is rare in situations which do not involve massive trauma.[8] Although leukoreduction removes > 99.9% of donor's white blood cells, it has not been proven to prevent the development of TA-MC.[9][10]
Treatment of Transfusion Reactions
The most important step in treating a presumed transfusion reaction is to stop the transfusion immediately (saving the remaining blood and IV tubing for testing) and to provide supportive care to the patient. More specific treatments depend on the nature and presumed cause of the transfusion reaction. Most hospitals and medical centers have transfusion reaction protocols, which specify testing of the blood product and patient for hemolysis, bacterial contamination, etc.
See also
External links
- ICD-10 Chapter T: World Health Organisation classification - Complications following infusion, transfusion and therapeutic injection
References
- ↑ Bacterial contamination of platelet concentrates: incidence, significance, and prevention. Blajchman MA; Goldman M. Semin Hematol 2001 Oct;38(4 Suppl 11):20-6.
- ↑ The association of biologically active lipids with the development of transfusion-related acute lung injury: a retrospective study. Silliman CC; Paterson AJ; Dickey WO; Stroneck DF; Popovsky MA; Caldwell SA; Ambruso DR. Transfusion 1997 Jul;37(7):719-26.
- ↑ Transfusion-related acute lung injury: a neglected, serious complication of hemotherapy. Popovsky MA; Chaplin HC Jr; Moore SB. Transfusion 1992 Jul-Aug;32(6):589-92.
- ↑ Transfusion-associated graft-versus-host disease and blood irradiation. Linden JV; Pisciotto PT. Transfus Med Rev 1992 Apr;6(2):116-23.
- ↑ Kunadian V, Zorkun C, Gibson WJ, Nethala N, Harrigan C, Palmer AM; et al. (2009). "Transfusion associated microchimerism: a heretofore little-recognized complication following transfusion". J Thromb Thrombolysis. 27 (1): 57–67. doi:10.1007/s11239-008-0268-0. PMID 18766299.
- ↑ Adams KM, Nelson JL (2004). "Microchimerism: an investigative frontier in autoimmunity and transplantation". JAMA. 291 (9): 1127–31. doi:10.1001/jama.291.9.1127. PMID 14996783.
- ↑ Nelson JL, Furst DE, Maloney S, Gooley T, Evans PC, Smith A; et al. (1998). "Microchimerism and HLA-compatible relationships of pregnancy in scleroderma". Lancet. 351 (9102): 559–62. doi:10.1016/S0140-6736(97)08357-8. PMID 9492775.
- ↑ Sanchez R, Lee TH, Wen L, Montalvo L, Schechterly C, Colvin C; et al. (2012). "Absence of transfusion-associated microchimerism in pediatric and adult recipients of leukoreduced and gamma-irradiated blood components". Transfusion. 52 (5): 936–45. doi:10.1111/j.1537-2995.2011.03366.x. PMC 3257351. PMID 21981710.
- ↑ Utter GH, Nathens AB, Lee TH, Reed WF, Owings JT, Nester TA; et al. (2006). "Leukoreduction of blood transfusions does not diminish transfusion-associated microchimerism in trauma patients". Transfusion. 46 (11): 1863–9. doi:10.1111/j.1537-2995.2006.00991.x. PMID 17076839.
- ↑ Lee TH, Paglieroni T, Utter GH, Chafets D, Gosselin RC, Reed W; et al. (2005). "High-level long-term white blood cell microchimerism after transfusion of leukoreduced blood components to patients resuscitated after severe traumatic injury". Transfusion. 45 (8): 1280–90. doi:10.1111/j.1537-2995.2005.00201.x. PMID 16078913.