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

2. Not necessarily massive
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 No steroids No diuretics 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