Hey Stalvl,
I actually had to take care of a patient in the MICU who had TRALI. The pateint was a 75 year old man with an extensive history of CAD. He was in a 10 hour spinal laminectomy operation and had received 6 units of blood and 2 units of FFP during the operation. The entire case was uneventful, until he was extubated (had his breathing tube pulled out at the end of the case). At this time, he became acutely hypoxic into the 80's, hypotensive into the 70's, and began coughing up pink frothy sputum (characteristic of pulmonary edema). He was immediately re-intubated and it was thought that he was in CHF with fulminant pulmonary edema. A stat transesophageal echo was ordered which showed a completely normal ejection fraction (basically ruling out CHF). He was started on 3 pressors (dobutamine, norepinephrine, and epinephrine) in order to maintain a reasonable blood pressure while we (MICU) were consulted to assume care for the patient. We ended up cutting the epi, but by day number 3 he was back up to 4 pressors (vasopressin, dobutamine, norepinephrine, and phenylephrine), plus we had him on Nitric Oxide because his Pulmonary artery pressures were over 50. Amazingly, this guy actually survived. We were able to wean him off his pressors over about a week and then finally extubated him about 10 days after the initial inslut. It was a great save, and I'll probably never forget it. Definitely one of the sickest guys I've had to take care of.
So, here's the uncomplicated way to think about TRALI... It's kind of like an allergic reaction to blood products which primarily affects the lung. Any blood products may cause it (pRBCs, platelets, FFP, or cryo). The key to diagnosis is proximity to blood product transfusion, pulmonary edema without evidence of congestive heart failure (normal ejection fraction), and excluding other possible causes for hypotension/ARDS (particularly sepsis or anaphylaxis to other medicines/contact exposures).
The reaction which occurs in the lungs is immunologic. Inflammation causes increased leukocyte infiltrates and release of toxic products. The result is increased vascular permeability in the lung capillary beds causing water to seep out into the lung tissue and alveolar air spaces where gas exchange occurs. Because water is filling the alveolar air spaces, gas exchange is very poor and blood cannot be oxygenated properly. This causes the patient to be hypoxic and the increased water filling the lungs causes the high pulmonary artery pressures often seen. Finally the patients can develop a right-sided heart failure from the increased pressure in the lungs.