CHAPTER 71 Exercise-Induced Pulmonary Hemorrhage
Historically the use of epistaxis as the sole criterion for identifying horses with exercise-induced pulmonary hemorrhage (EIPH) resulted in repeated underestimation of the true prevalence of EIPH, with a reported range of 0.15% to 2.41% in Thoroughbred racehorses. Through the use of the flexible fiberoptic endoscope to examine the lower respiratory tract, more accurate estimates of EIPH prevalence by use of tracheobronchoscopy have been reported in Thoroughbred (42% to 75.4%) and Standardbred (26% to 87%) racehorses, racing Quarter Horses (62.3%), and Appaloosa horses (52.1%). In addition, the prevalence of EIPH has been documented in Chilean Criollo horses (60.8%), draft horses (0%), polo ponies (11.1%), cross-country ponies and mixed-breed horses (10%), mixed-breed endurance horses (0%), and Thoroughbreds competing in steeplechase racing (66.7%). EIPH also affects racing camels and Greyhounds.
The prevalence of EIPH is affected by age and speed. The condition develops more often in older horses and with increasing racing speed. Racing, rather than breezing, in Thoroughbred racehorses is associated with a higher prevalence of EIPH, whereas EIPH lesions are not observed in young Thoroughbred racehorses trained at speeds less than 7 m per second. Sex has no effect on EIPH prevalence. The prevalence and severity of EIPH in racehorses seem to be affected by altitude, as horses racing at sea level have EIPH more frequently and more severely.
Exercise-induced pulmonary hemorrhage commonly occurs in racehorses worldwide and should be considered the sole reason for poor performance if hemorrhage is severe. Cytologic examination of tracheobronchial aspirates and bronchoalveolar lavage fluid may yield evidence of EIPH, or blood may be detected during tracheobronchoscopy in underperforming racehorses. In a recent report, 43.9% of Thoroughbred racehorses that finished in the first three places had less severe tracheobronchoscopic evidence of EIPH than the 55.9% that finished in 4th to 14th place. Also, a cross-sectional study of Thoroughbred racehorses in Victoria, Australia, revealed a strong association between the presence and severity of EIPH and poor performance. This study showed that horses with grade 1 or lower EIPH were 4.03 times as likely to win and 1.78 times as likely to finish in the top three places than horses with grade 2 or higher EIPH and that horses with higher grades of EIPH finished significantly farther behind the winner.
Although EIPH is a ubiquitous condition, the precise etiopathogenesis is unclear. The most widely accepted hypothesis is that strenuous exercise causes increased transmural capillary pressures. This results in stress failure and rupture of the pulmonary capillaries when the transmural stress exceeds the tensile strength of the capillary. Stress failure is associated with reversible disruption of the capillary and alveolar epithelium, resulting in hemorrhage into the interstitial and alveolar spaces secondary to the increased permeability. Stress failure may be exacerbated in racehorses with upper airway obstruction because they generate greater capillary transmural pressures and more negative alveolar pressures that contribute to increased capillary transmural pressure. The origin of the hemorrhage may be from the pulmonary rather than from the bronchial circulation, as horses undergoing strenuous exercise have dramatic increases in pulmonary arterial pressure. The large increase in cardiac output raises pulmonary arterial pressure from 20 to 25 mmHg at rest to more than 90 mm Hg during exercise, and this increases pulmonary capillary pressure and alveolar wall stress.
Small-airway disease may impair respiratory mechanics by decreasing dynamic compliance and increasing respiratory resistance, and it also may cause airway hyperresponsiveness. Concurrent bronchiolitis is common in EIPH-affected horses and may predispose to bronchoconstriction, resulting in a decrease in alveolar pressure during inspiration and capillary rupture. Small-airway disease may be further exacerbated by concurrent viral infection, allergy, or air pollution. While preexisting airway inflammation has been implicated as a cause of EIPH, autologous intrapulmonary blood inoculation causes a prolonged local inflammatory reaction (as assessed by bronchoalveolar leukocyte concentration) and results in decreased dynamic compliance and increased respiratory resistance. Whether this inflammation is a direct consequence of EIPH or predisposes to EIPH remains unknown.
Locomotor impact-induced trauma was proposed as the underlying cause of EIPH through loading of the chest by the forelimbs, which produces shear forces within the lung that can either cause or worsen EIPH. Proponents of this hypothesis propose that, after locomotor impact of the forelimb, a pressure wave is generated that passes from the scapula through the body wall to the dorsocaudal lung lobes, causing tissue disruption, which may lead to EIPH. One report revealed that horses in steeplechase races were at increased risk of epistaxis compared with horses competing in flat racing, further suggesting that impact-induced trauma may play a role in EIPH. However, no direct evidence exists to support a locomotor-induced intrapulmonary or intrapleural pressure wave.
No defects in intrinsic and extrinsic coagulation pathways or enhanced fibrinolysis have been found in exercising horses or horses with EIPH. Thrombocytopenia and decreased clot retraction time were reported in horses with epistaxis, and exercise decreased adenosine diphosphate– induced platelet aggregation. In horses with EIPH, platelets are less responsive to agonists of platelet aggregation.