Pleural fluid and peripheral eosinophilia from hemothorax: hypothesis of the pathogenesis of EPE in hemothorax and pneumothorax.

Blood and air in the pleural space are the most common conditions associated with an eosinophilic pleural effusion. The recruitment of eosinophils is dependent upon stimulation by cytokines, specifically interleukin (IL)-3, IL-5, granulocyte-monocyte cell stimulating factor (GM-CSF), and RANTES (regulated upon activation, normal t-cell expressed and secreted), that cause eosinophil proliferation in the bone marrow, movement into the circulation, and adhesion and migration across endothelial barriers into tissues. There are several possible mechanisms that can explain eosinophilic pleural effusions. We report a case of an eosinophilic pleural effusion after spontaneous hemothorax that illustrates the course of pleural fluid and blood eosinophilia in following hemothorax and describe the different pathophysiology of eosinophil trafficking in the pleural space and serum following hemothorax and pneumothorax.