Transfusion related acute lung injury (trali) - DIKIOHS DUHS

Transfusion related acute lung injury (trali) - DIKIOHS DUHS

1. Transfusion Related acute lung injury ( trali ) Presenter: Dr Shaharyar Hamid

2. introduction TRALI is a clinical diagnosis for which no diagnostic tests are available. The syndrome was initially regarded as the onset of respiratory distress due to antibody induced non-cardiogenic lung oedema.

3. Suspected trali Acute onset within 6 h of blood transfusion PaO2/FIO2<300 mm Hg, or worsening Bilateral infiltrative changes on chest radiograph No sign of hydrostatic pulmonary edema No other risk factor for acute lung injury

4. Possible trali Same as for suspected TRALI, but another risk factor present for acute lung injury. Same as for (possible) TRALI but onset within 6–72 h of blood transfusion . delayed trali

5. pathophysiology WBCs when bound by Antibodies, they gum up in the lung. Normally, WBC should roll through capillaries but now they are not because they are stuck. WBCs already hyped up during inflammatory response of surgery, So many WBCs choke alveolar walls and RBCs cant get through. Also WBCs have granules with proteases peroxide which damage endothelial tissue increase tissue permeability, and cause fluid accumulation in extravascular spaces such as pulmonary alveoli. Results in Pulmonary edema.

6. A study reported that, A significant decrease in the PaO2:FiO2 ratio was noted after the transfusion from the multiparous donor unit but not after the non-parous donor unit. M ultiparity is associated with an increased frequency of antibodies. O bservations suggest that the conditions required for TRALI are more complex than simply the presence of anti-leukocyte antibodies in transfused blood.

7. Silliman’s Two-Hit Model The first hit is a physiologic insult i.e sepsis, cardiac disease, trauma during surgery. Which activates pulmonary endothelium and promotes priming and adhesion of neutrophils. The second hit is an event such as exposure to biologically active agents from transfused blood that activates neutrophils, causing release of cytotoxic factors and endothelial damage with capillary leakage.

8. Age of stored blood correlates positively with transfusion reactions. Silliman demonstrated that stored blood components were capable of priming neutrophil in vitro. Plasma at the day of outdate or fresh plasma was added to primed neutrophils and respiratory burst was measured. Only day-of out date plasma primed Neutrophils, suggesting that substances present only in aging stored blood can activate neutrophils.

9. Recently, Kopko et al. in an attempt to explain cases of TRALI not related to known antibodies, and theorized that monocyte activation, with resultant cytokine production, occurs in TRALI. Although not proven, but the ultimate culprit may be monocytes, and not solely neutrophils.

10. Clinical presentation • Dyspnea • Fever • Usually hypotension • Hypoxia • Leukopenia • Pulmonary edema on chest x-ray • Normal left ventricular function • Normal pulmonary artery pressure

11. The original description of TRALI shows development of acute respiratory failure in patients 1 hour after a transfusion of a high-volume plasma product, with lungs having a white-out appearance on the radiograph. Laboratory testing in TRALI is not specific. The most prevalent symptom is a transient leukopenia, which arises in 5–35% of patients after transfusion with an antibody containing blood product, and is thought to be due to neutrophil-specific antibodies.

12. Treatment No treatment exists for this life-threatening syndrome. Management of TRALI is supportive. Patients need additional oxygen, and mechanical ventilation is unavoidable in 70–90% of cases. some case reports describe use of corticosteroids in patients with TRALI, but no evidence exists to show that these drugs should be applied. Diuretics might have a place in the treatment of TRALI, because a positive fluid balance is a risk factor for TRALI . Animal experiments show promising results for aspirin, But the effectiveness of these interventions has not been tested in patients .

13. Patient risk factors for onset of TRALi A retrospective study confirmed that the presence of mechanical ventilation predisposes to development of TRALI. Because the application of high peak airway pressures increases the risk for TRALI in patients. Assumption can be made that mechanical stretch of the lungs due to positive pressure ventilation results in priming of neutrophils.

14. What can attending physician do? Restrict transfusion policy. For patients on mechanical ventilation, airway pressures should be restricted before transfusion. Because ventilation with low tidal volumes decreases mortality in patients with acute lung injury. Instead of stored RBCs, fresh frozen plasma should be used or washed cell containing products. Suspected TRALI reactions should be reported to the blood bank for identification and exclusion of involved donors with antibodies to prevent future reactions

15. What can blood service do? Two groups of high-risk donors could be identified and excluded: multiparous donors and donors exposed to blood transfusion. An alternative approach is a proactive exclusion policy with exclusion of donors at risk for HLA or HNA antibodies.

16. Thank you