Recent advances – TRALI

1. Recent advances – TRALI Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab. DCA, Dip. Software statistics, PhD(physiology)

2. Definition • acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) (non cardiogenic pulmonary edema ) within 6 h of a blood product transfusion • Popovsky – father of TRALI Not necessarily massive

3. TRALI ( canadian consensus) • .a. New onset of acute lung injury (ALI) • b. Hypoxemia: PaO2/FiO2 < 300mm Hg or SPO2 90% • c. Bilateral infiltrates on frontal CXR • d. No evidence of left atrial hypertension (i.e., circulatory overload) • e. Symptoms occur during or within 6 hrs of transfusion • f. No preexisting ALI before transfusion • g. No temporal association to alternative risk factors for ALI

4. Possible TRALI • a. ALI occurring during or within 6 hours of transfusion • b. No preexisting ALI before transfusion • c. Clear temporal association for an alternative risk factor for ALI (pneumonia, drowning, burns etc)

5. As simple as such !! • TRALI primarily consist of hypoxia and bilateral pulmonary edema occurring during or within 6 h of a transfusion in the absence of cardiac failure or intravascular volume overload

6. Not clear incidence • Incidence : between 1/1,120 and 1/57,810 units transfused. • 0.02% per unit transfused and 0.16% per patient transfused • Mild tachypnea may get unnoticed

7. Pathogenesis

8. Setting or the first hit • surgery, sepsis, trauma, and massive transfusions ( but 15 ml has produced TRALI) • CPB, cancer chemo • Primed neutrophil pulmonary endothelium

9. Second hit – antibody • donor antibodies are transfused with the plasma-containing blood product. • These antibodies attach to specific antigens on primed neutrophils leading to the release of oxidative and non oxidative products that damages the pulmonary endothelium • increased permeability pulmonary edema

10. Second hit – lipid theory • Old blood cellular elements • Cell membrane breakdown • release of bioactive lipids (Lysophosphatidylcholines) • Prime neutrophil activation

11. Risk factors for second hit • parity of the blood donor, • relationship to the blood donor, • and the age of the blood products • can all be potential risk factors for the development of TRALI

12. Signs and symptoms • tachypnea, • frothy pulmonary secretions, • hypotension • fever, tachycardia and cyanosis. • Auscultation of the lung fields reveals diffuse rales.

13. Imaging • X ray show bilateral infiltrates • But no evidence of circulatory overload or frank CCF

14. Investigations • Arterial blood gas for hypoxemia • ECHO for cardiac cause and IVC status • CVP for volume status • Pulmonary edema fluid aspirates for transudate or exudate – compare plasma • Transient and dynamic leucopenia

15. Management • Inform blood bank • Re crossmatch • Donor especially female – granulocyte and HLA antigens testing • Multiparous females ?? - 74 donations – incidence TRALI high ??

16. Treatment • The first step in the treatment of TRALI is to make the correct diagnosis • Prevention • No multiparous • No old blood • No plasma from females in each first hit case

17. Treatment • Mortality due to TRALI is 5–10%, • Possible options • Oxygen • Mechanical ventilation with ARDS strategies • Vasopressors - ECMO • But usually settles in 96 hours No steroids No diuretics

18. Summary • Definition • Canadian criteria • Pathophysiology – (first and second hit) • Clinical signs • Investigations • Prevention • Treatment