They do however show the same morphologic alterations - endothelial cell vacuolation and focal necrosis, accompanied by interstitial and airspace edema. Fibrin microthrombi may be seen, and sloughing of alveolar pneumocytes is also common. The result of this injury is the formation of airspace hyaline membranes within days, which over the next week progressively organize and are incorporated into the pulmonary interstitium. This graft injury predisposes to infection, and may closely mimic acute rejection reactions, in that it is a diffuse process radiographically and is accompanied by hypoxemia. This contrasts with acute rejection which displays perivascular mononuclear infiltrates of small round, small cleaved, and large lymphoid cells.
Diagnostic confusion does occur in some instances when processes are superimposed.
This response manifested as diffuse pulmonary parenchymal opacification on chest radiographs, within a day or two of transplantation. Histologically, interstitial and airspace edema is noted with neutrophil margination. The etiology for this reaction is probably multiple. First, the interruption of the pulmonary lymphatics as part of the transplantation procedure impairs lymphatic drainage of the lung and predisposes to pulmonary edema. Finally mild cases of diffuse alveolar damage may manifest as pulmonary edema, and probably have been lumped into this category of lung injury.