- What is TRALI?
- Noncardiogenic pulmonary edema, 5% mortality
- Plasma containing blood products (Plt and FFP >>> pRBCs)
- Reaction b/w donor anti-HLA or antileukocyte Ab’s & recipient leukocytes
- sequestration in microcirculation of lungs
- capillary endothelial damage/leak.
- Acute onset of hypoxemia (within 6 hrs of transfusion)
- Bilateral CXR infiltrates c/w ALI
- Normal LA pressures (<18mmHg)
- Absence of other causes of ALI
- Initial treatment similar to that of ARDS.
- Direct treatment at reversible processes such as sepsis or hypotension.
- Treat hypoxemia with oxygen. Avoid high peak inflation pressures >35cm H20 and high tidal volumes >8-10ml/kg because overdistension of alveli can induce iatrogenic lung injury as can a high Fi02 of greater than 0.5. Higher mortality with tidal volumes >10ml/Kg. Can also treat hypoxemia by increasing PEEP above the inflection point, using nitric oxide, inhaled prostacyclin, or prostaglandin E1(PGE2) and ventilating in the prone position. These techniques improve oxygenation but are not risk free and have not been associated with an improvement in survival.
- Steroids early in ARDS is associated with an increased mortality but are often used between days 4-10.
- Morbidity is usually secondary to the precipitating causes or to complications rather than the respiratory failure itself. Sepsis, renal failure, and GI hemorrhage top the list.
- Nosocomial pneumonia is particularly common in patients who have a protracted course. Renal failure is usually due to volume depletion, sepsis, or nephrotoxins and substantially increases the mortality rate (to > 60%). Prophylaxis for GI hemorrhage with sucralfate, antacids, H2 blockers, or proton pump inhibitors is recommended.