Exercise-induced Pulmonary Hemorrhage in Horses

The proposed pathophysiologic mechanism for pulmonary hemorrhage includes high pulmonary vascular pressures during maximal exercise, with resultant thickening of pulmonary vein walls and decreased luminal diameter and increased intravascular pressure at the level of the pulmonary capillaries.

Endoscopic observation of blood in the airways 30–90 min after exercise provides definitive evidence of EIPH. Other sources of hemorrhage in the upper airway, particularly guttural pouch mycosis (see Guttural Pouch Mycosis) and ethmoid hematoma (see Ethmoid Hematoma), must be excluded during endoscopic examination. If EIPH is suspected and the horse cannot be examined after exercise, cytologic examination of bronchoalveolar lavage fluid for semiquantitative assessment of hemosiderophages is diagnostic. Stains that highlight iron-containing pigments (Prussian blue) facilitate recognition of these cells. Thoracic radiography demonstrates alveolar or mixed alveolar-interstitial opacities in the caudodorsal lung fields; however, radiographic examination of the thorax has little impact on the diagnosis or management of EIPH.

Furosemide reduces the incidence and severity of EIPH in Thoroughbred racehorses. Horses with and without EIPH demonstrate equal improvements in race performance after administration of furosemide, indicating that the drug may enhance performance via mechanisms unrelated to EIPH. Application of nasal dilator bands reduces RBC counts in bronchoalveolar fluid from affected horses running on a treadmill by 33%. Alternative treatments, including procoagulant agents (eg, vitamin K, conjugated estrogens, aminocaproic acid), antihypertensive drugs, rheologic agents (pentoxyphylline), bronchodilators, prolonged rest, dietary supplements (hepseridin-citrus bioflavinoids), and anti-inflammatory drugs, have not demonstrated therapeutic benefit.