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TRALI is due to pulmonary venule damage from leucocytes with cholesterol crystal formation
Author(s) -
Jensen H. M.,
Galante J. M.,
Kysar P. E.,
Tolstikov V. V.,
Reddy K. J.,
Holland P. V.
Publication year - 2010
Publication title -
vox sanguinis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.68
H-Index - 83
eISSN - 1423-0410
pISSN - 0042-9007
DOI - 10.1111/j.1423-0410.2009.01235.x
Subject(s) - pathology , lung , extravasation , endothelium , venule , cholesterol , pulmonary edema , medicine
Background There are two presumed mechanisms for the pulmonary oedema in transfusion‐related acute lung injury (TRALI). One is antibodies to leucocytes while the other is biologically active lipids. We evaluated the vascular injury due to the former. Methods The pulmonary vasculature was studied by light microscopy (LM) and scanning electron microscopy (SEM) in three fatal cases of TRALI and compared with that of two autopsied control patients. Lung tissue from two of the TRALI cases and both controls was studied by gas chromatography–mass spectroscopy (GC–MS) to identify crystals present in the former. Results All three TRALI cases exhibited massive pulmonary oedema by weight and light microscopy and extensive defects by SEM in the endothelium of venules of the lungs. Such endothelial defects were absent in controls. Thrombi, composed of crystals, were present in venules and small veins diffusely throughout the lungs in Case 1. Similar crystals were identified in Case 2. The crystals in the lung vessels were identified morphologically as cholesterol and were proximate to the cytoplasmic defects of the endothelial surfaces. By GC–MS, there were markedly elevated levels of cholesterol and fatty acids in the two TRALI lungs tested compared with the lungs of the two controls. Conclusions Pulmonary damage in TRALI is related to formation of cholesterol crystals that appear to pierce endothelial membranes of venules. The endothelial defects lead to plasma extravasation into the alveoli causing TRALI.