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

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

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

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)

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

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

Pathogenesis

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

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

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

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

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

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

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

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

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

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

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