To discuss therapeutic approaches to this condition, both the pathology and how it relates to the proposed theories of pathogenesis must first be described in some detail. Although extensive descriptions of the clinical and pathologic features of EIPH exist in the literature, critical information detailing exact mechanisms of the condition is still lacking.

The first, and until recently the most comprehensive, review of EIPH pathology was performed more than 20 years ago. Specifically, grossly evident pleural discoloration (blue-black) of the caudodorsal lung regions was seen, and on histologic evaluation, extensive hemosiderosis, angiogenesis, pleural and septal fibrosis, and bronchiolitis (small airway inflammatory disease) were consistent findings. Authors of that study proposed that bronchiolitis played a causative role in EIPH. However, several lines of evidence exist that do not support this relationship.

First, in more recent studies, bronchiolitis was not found in association with the other histopathologic features of EIPH. Second, in an epidemiologic study performed in the United Kingdom, some association between inflammatory airway disease and EIPH was detected in Thoroughbreds in training. However, this association cannot be interpreted as a cause-and-effect relationship because both conditions have a high prevalence in that study population. Finally, if airway inflammation was a significant contributing factor, routine treatments for inflammatory airway disease, such as systemic or nebulized corticosteroids and nonsteroidal antiinflammatory drugs, with or without antimicrobial therapy, would be expected to control EIPH. Although the latter treatments have never been formally investigated, in a clinical setting at least, such therapeutic regimens are not perceived to affect EIPH incidence or severity.

A breakthrough study in 1993 demonstrated that pulmonary capillary rupture or disruption was commonly detected in lung tissue that had evidence of extravasation of red blood cells. These extravascular red cells were found both in the pulmonary interstitium and in surrounding alveolar airspaces. This work strongly implicated the pulmonary circulation as the source of hemorrhage in EIPH, and on the basis of these data, it was proposed that so-called stress failure of pulmonary capillaries secondary to transient but significant pulmonary circulation hypertension during exercise resulted in capillary disruption. This concept was strongly corroborated by studies that evaluated the magnitude of blood pressures in the horse’s pulmonary circulation during exercise. Pulmonary arterial pressures of approximately 100 mm Hg are reported, and from these measurements, pulmonary capillary pressures from 72.5 to 83.3 mm Hg can be calculated. Pressures of these magnitudes are unparalleled in any other mammalian species that has been investigated. This information, when considered in the context of a study that described the breaking strength of the horse’s pulmonary capillaries (75 mm Hg), makes pulmonary capillary stress failure a plausible theory of pathogenesis for EIPH. However, this theory does not account for the pathology seen in the lungs of horses with EIPH.

Diagnosis

The clinical evaluation of any horse with suspected EIPH, regardless of the breed, should involve careful cardiac auscultation. The rationale for this is that horses with atrial fibrillation have higher-than-normal pulmonary artery pressures during exercise and, with the reduced passive ventricular filling phase seen at high heart rates, pulmonary venous congestion and capillary rupture are likely to result. Epistaxis has been reported in association with atrial fibrillation in light-horse breeds. In draft horses with atrial fibrillation, severe EIPH is a common observation, in the author’s clinical experience.

Diagnosis of EIPH in the horse is performed relative easily with one or a combination of the following techniques: observation, tracheobronchoscopy, and bronchoalveolar lavage.