Ostre poprzetoczeniowe uszkodzenie płuc – często nierozpoznawana reakcja po przetoczeniu składników krwi

• Authors: Jolanta Korsak , Anna Łata

Title variants

EN

Transfusion-related acute lung injury – a frequently undiagnosed reaction following transfusion of blood components

• Languages of publication: EN PL

Abstracts

EN

Transfusion-related acute lung injury is the leading cause of mortality following transfusion of blood components. Its characteristic feature is acute hypoxaemia during or 6 hours after transfusion. The syndrome should be differentiated from cardiogenic respiratory failure and transfusion-associated circulatory overload. This article presents: 1) The aetiology and pathomechanism of transfusion-related acute lung injury, which are still not fully understood despite numerous studies. The model currently accepted is the multi-event one which involves both factors related to the patient and to the transfused blood components. Transfusion-related acute lung injury may be either immunological, with anti-HLA/HNA antibodies in blood components, or non-immunological, with no antibodies. 2) The diagnosis of transfusion-related acute lung injury which is based on clinical signs, evidence of the relationship with blood component transfusion and detection of antibodies. 3) The treatment and prevention of transfusion-related acute lung injury. The most important element in the prevention of transfusion-related acute lung injury is a reduction in blood component transfusion, particularly of plasma and platelet concentrate. Yet, further studies on larger groups of patients are necessary to specify the limitations of blood component transfusion.

PL

Poprzetoczeniowe ostre uszkodzenie płuc jest jedną z najważniejszych przyczyn śmierci związanych z przetaczaniem składników krwi. Charakteryzuje się ostrym niedotlenieniem podczas przetaczania lub 6 godzin po nim i wymaga różnicowania z kardiogenną niewydolnością oddechową oraz poprzetoczeniowym przeciążeniem krążenia. W artykule przedstawiono: 1) Etiologię i patomechanizm poprzetoczeniowego ostrego uszkodzenia płuc, z podkreśleniem, że jest ona wciąż nie do końca poznana. Ostatnio zaakceptowano wielozdarzeniową patogenezę, która obejmuje czynniki pochodzące zarówno od chorego, jak i ze składników krwi. Poprzetoczeniowe ostre uszkodzenie płuc może być immunologiczne, z obecnością przeciwciał anty-HLA/HNA w przetoczonej krwi, lub nieimmunologiczne, bez wykrywanych przeciwciał. 2) Rozpoznanie poprzetoczeniowego ostrego uszkodzenia płuc – oparte jest na stwierdzanych objawach klinicznych i wykazaniu związku z przetoczeniem składników krwi oraz oznaczeniu obecności przeciwciał. 3) Leczenie i zapobieganie występowaniu poprzetoczeniowego ostrego uszkodzenia płuc – w profilaktyce poprzetoczeniowego ostrego uszkodzenia płuc największe znaczenie ma ograniczenie przetaczania składników krwi, szczególnie osocza i koncentratów krwinek płytkowych. Do sformułowania ostatecznych wniosków dotyczących ograniczenia przetoczeń konieczne są jednak badania przeprowadzone na dużej populacji chorych z różnymi chorobami.

Keywords

EN

DAMPs; anti-HLA antibodies; anti-HNA antibodies; blood components; poprzetoczeniowe ostre uszkodzenie płuc (TRALI); przeciwciała anty-HLA; przeciwciała anty-HNA; składniki krwi; transfusion-related acute lung injury (TRALI)

Discipline

• MEDICINE: MEDICINE

• Publisher: Medical Communications
• Journal: Pediatria i Medycyna Rodzinna
• Year: 2015
• Volume: 11
• Issue: 3
• Pages: 250–258

Contributors

author

Jolanta Korsak

• Zakład Transfuzjologii Klinicznej, Wojskowy Instytut Medyczny, Warszawa. Kierownik Zakładu: dr hab. n. med. Jolanta Korsak, prof. nadzw. WIM, ul. Szaserów 128, 04-141 Warszawa

author

Anna Łata

• Zakład Transfuzjologii Klinicznej, Wojskowy Instytut Medyczny, Warszawa. Kierownik Zakładu: dr hab. n. med. Jolanta Korsak, prof. nadzw. WIM

References

• 1. Toy P, Popovsky MA, Abraham E et al.; National Heart, Lung and Blood Institute Working Group on TRALI: Transfusion-related acute lung injury: definition and review. Crit Care Med 2005; 33: 721–726.
• 2. US Food and Drug Administration: Fatalities Reported to FDA Following Blood Collection and Transfusion: Annual Summary for Fiscal Year 2009. Updated December 18, 2012.
• 3. Barnard RD: Indiscriminate transfusion: a critique of case reports illustrating hypersensitivity reactions. NY State J Med 1951; 51: 2399–2402.
• 4. Popovsky MA, Moore SB: Diagnostic and pathogenetic consideration in transfusion-related acute lung injury. Transfusion 1985; 25: 573–577.
• 5. Toy P, Gajic O, Bacchetti P et al.: Transfusion-related acute lung injury: incidence and risk factors. Blood 2012; 119: 1757–1767.
• 6. US Food and Drug Administration: Fatalities Reported to FDA Following Blood Collection and Transfusion: Annual Summary for Fiscal Year 2010. Rockville (MD), Center for Biologics Evaluation and Research 2012.
• 7. US Food and Drug Administration: Fatalities Reported to FDA Following Blood Collection and Transfusion: Annual Summary for Fiscal Year 2012. Rockville (MD). Updated March 28, 2014.
• 8. Silliman CC: The two-event model of transfusion-related acute lung injury. Crit Care Med 2006; 34 (Suppl): S124–S131.
• 9. De Clippel D, Beaten M, Torfs A et al.: Screening for HLA antibodies in plateletpheresis donors with a history of transfusion or pregnancy. Transfusion 2014; 54: 3036–3042.
• 10. Kopko PM, Paglieroni TG, Popovsky MA et al.: TRALI: correlation of antigen-antibody and monocytes activation in donorrecipient pairs. Transfusion 2003; 43: 177–184.
• 11. Alam A, Huang M, Yi QL et al.: Perioperative transfusion-related acute lung injury: the Canadian Blood Services experience. Transfus Apher Sci 2014; 50: 392–398.
• 12. Sachs UJ, Wasel W, Bayat B et al.: Mechanism of transfusionrelated acute lung injury induced by HLA class II antibodies. Blood 2011; 117: 669–677.
• 13. Sayah DM, Leoney MR, Toy P: Transfusion reactions: newer concepts on the pathophysiology, incidence, treatment, and prevention of transfusion-related acute lung injury. Crit Care Clin 2012; 28: 363–372.
• 14. Fudala F, Krupa A, Stankowska D et al.: Does activation of the FcgRIIa play a role in the pathogenesis of the acute lung injury/acute respiratory distress syndrome? Clin Sci (Lond) 2010; 118: 519–526.
• 15. Reil A, Keller-Stanislawski B, Gunay S et al.: Specificities of leucocyte alloantibodies in transfusion-related acute lung injury and results of leucocyte antibody screening of blood donors. Vox Sang 2008; 95: 313–317.
• 16. Silliman CC, Ambruso DR, Boshkov LK: Transfusion-related acute lung injury. Blood 2005; 105: 2266–2273.
• 17. Bayat B, Tjakjono Y, Akylbek S et al.: Lung endothelial injury induced by HNA-3 alloantibodies in TRALI. Blood ASH Annual Meeting 2011; 118: 40.
• 18. Silliman CC, Paterson AJ, Dickey WO et al.: The association of biologically active lipids with the development of transfusion-related acute lung injury: a retrospective study. Transfusion 1997; 37: 719–726.
• 19. Silliman CC, McLaughlin NJ: Transfusion-related acute lung injury. Blood Rev 2006; 20: 139–159.
• 20. Saindenberg E, Petraszko T, Semple E et al.: Transfusion-related acute lung injury (TRALI): a Canadian blood services research and development symposium. Transfus Med Rev 2010; 24: 305–324.
• 21. Looney MR, Gilliss BM, Matthay MA: Pathophysiology of transfusion-related acute lung injury. Curr Opin Hematol 2010; 17: 418–423.
• 22. Land WG: Transfusion-related acute lung injury: the work of DAMPs. Transfus Med Hemother 2013; 40: 3–13.
• 23. Sachs UJ: Recent insights into the mechanism of transfusionrelated acute lung injury. Curr Opin Hematol 2011; 18: 436–442.
• 24. Kim-Shapiro DB, Lee J, Gladwin MT: Storage lesion: role of red blood cell breakdown. Transfusion 2011; 51: 844–851.
• 25. Kamel N, Goubran F, Ramsis N et al.: Effects of storage time and leucocyte burden of packed and buffy-coat depleted red blood cell units on red cell storage lesion. Blood Transfus 2010; 8: 260–266.
• 26. Gkoumassi E, Dijkstra-Tiekstra MJ, Hoentjen D et al.: Hemolysis of red blood cells during processing and storage. Transfusion 2012; 52: 489–492.
• 27. Donadee C, Raat NJ, Kanias T et al.: Nitric oxide scavenging by red blood cell microparticles and cell-free hemoglobin as a mechanism for the red cell storage lesion. Circulation 2011; 124: 465–476.
• 28. Mangalmurti NS, Chatterjee S, Cheng G et al.: Advanced glycation end products on stored red blood cells increase endothelial reactive oxygen species generation through interaction with receptor for advanced glycation end products. Transfusion 2010; 50: 2353–2361.
• 29. Peltz ED, Moore EE, Eckels PC et al.: HMGB1 is markedly elevated within 6 hours of mechanical trauma in humans. Shock 2009; 32: 17–22.
• 30. Sadallah S, Eken C, Martin PJ et al.: Microparticles (ectosomes) shed by stored human platelets downregulate macrophages and modify the development of dendritic cells. J Immunol 2011; 186: 6543–6552.
• 31. Rank A, Nieuwland R, Liebhardt S et al.: Apheresis platelet concentrates contain platelet-derived and endothelial cell-derived microparticles. Vox Sang 2011; 100: 179–186.
• 32. Matijevic N, Kostousov V, Wang YW et al.: Multiple levels of degradation diminish hemostatic potential of thawed plasma. J Trauma 2011; 70: 71–79.
• 33. Silliman CC, Voelkel NF, Allard JD et al.: Plasma and lipids from stored red blood cells cause acute lung injury in an animal model. J Clin Invest 1998; 101: 1458–1467.
• 34. Peters AL, van Hezel ME, Juffermans NP et al.: Pathogenesis of non-antibody mediated transfusion-related acute lung injury from bench to bedside. Blood Rev 2015; 29: 51–61.
• 35. Bux J, Sachs UJ: The pathogenesis of transfusion-related acute lung injury (TRALI). Br J Haematol 2007; 136: 788–799.
• 36. Maślanka K: Aktualny stan wiedzy na temat patofizjologii, diagnostyki i zapobiegania TRALI. Acta Haematol Pol 2013; 44: 274–283.
• 37. Żupańska B: Potransfuzyjna ostra niewydolność oddechowa (Transfusion-Related Acute Lung Injury – TRALI) – niebezpieczne i za rzadko rozpoznawane powikłanie poprzetoczeniowe. Acta Haematol Pol 2001; 32: 359–365.
• 38. Danielson C, Benjamin RJ, Mangano MM et al.: Pulmonary pathology of rapidly fatal transfusion-related acute lung injury reveals minimal evidence of diffuse alveolar damage or alveolar granulocyte infiltration. Transfusion 2008; 48: 2401–2408.
• 39. Gajic O, Gropper MA, Hubmayr RD: Pulmonary edema after transfusion: how to differentiate transfusion-associated circulatory overload from transfusion-related acute lung injury. Crit Care Med 2006; 34 (Suppl): S109–S113.
• 40. Vlaar AP, Hofstra JJ, Determann RM et al.: The incidence, risk factors, and outcome of transfusion-related acute lung injury in a cohort of cardiac surgery patients: a prospective nested casecontrol study. Blood 2011; 117: 4218–4225.
• 41. Triulzi DJ, Kleinman S, Kakaiya RM et al.: The effect of previous pregnancy and transfusion on HLA alloimmunization in blood donors: implications for a transfusion-related acute lung injury risk reduction strategy. Transfusion 2009; 49: 1825–1835.
• 42. Li G, Kojicic M, Reriani MK et al.: Long-term survival and quality of life after transfusion-associated pulmonary edema in critically ill medical patients. Chest 2010; 137: 783–789.

• Document Type: review