| Abstract: | New evidence confirmed that over 90% of Thoroughbreds have some degree of recurrent laryngeal neuropathy (RLN). This and the recognition that anything less than full extension of the atlanto-occipital joint in a racehorse implied a reduction in patency of the nasopharynx provided the basis of the hypothesis that exercise-induced pulmonary hemorrhage (EIPH) may be caused by an upper airway obstruction and that partial asphyxia could be the primary mechanism. EIPH was associated most frequently with the congenital (hereditary), left-sided, hemiparetic form of RLN. Other obstructive diseases, such as laryngeal chondritis and subepiglottic cysts, may be rare causes. Atlanto-occipital flexion on its own might also cause EIPH but more commonly was thought to be a factor which added to the upper airway obstruction resulting from RLN. Supporting evidence for this hypothesis was derived from retrospective and prospective studies of medical records; from necropsy findings on naturally occurring and experimentally produced cases of EIPH; from surveys on the prevalence of RLN; and from a literature review on asphyxia in man and animals.Clinical evidence which supported the hypothesis indicated that EIPH was a clinical sign of RLN. The epidemiology and prevalence of EIPH and congenital RLN appeared to be the same and both problems had a similar historical antiquity. It was already known that bilateral RLN caused asphyxia and EIPH and it appeared from this study that so also does untilateral RLN also does. Clinical signs of both EIPH and RLN were induced by exercise; both were capable of causing exercise intolerance; both were exacerbated by high ambient temperatures and humidity; both problems were permanent and incurable. EIPH was associated with neither the clinical signs nor the pathology of any other pulmonary disease, but was consistently associated with RLN. For it to be argued that EIPH was predominantly a clinical sign of RLN it was necessary that both problems should belong to the same etiological family. Once again, this condition seemed to be met, as EIPH and RLN both appeared more likely to be hereditary rather than environmental diseases.The pulmonary pathology of EIPH was compatible with asphyxia and similar to asphyxia in man. The bilateral symmetry of pulmonary hemorrhage in EIPH suggested an upper airway location for its causal mechanism. Secondary mechanisms might include such factors as increased upper airway resistance, increased pulmonary negative pressure, pulmonary congestion, hypoxemia, hypercapnia, pulmonary hypertension, increased capillary-alveolar pressure gradient, pulmonary edema, increased capillary permeability and microrupture of alveolar walls.Attempts to disprove the hypothesis failed. A prospective study of 201 Thoroughbreds showing EIPH revealed that all had an upper airway obstruction and 98% had RLN. The authors concluded that the hypothesis appeared to be viable. EIPH would seem to be not only a clinical sign of congenital RLN but possibly the most common sign of this common disease. In relation to RLN, the hypothesis could be restated as follows:a) A horse with laryngeal paraplegia, a rare form of RLN, may develop pulmonary hemorrhage with minimal exercise. b) A horse with laryngeal hemiplegia, a more common form of RLN, may develop pulmonary hemorrhage with severe exercise. c) A horse with laryngeal hemiparesis, the most common form of RLN, may develop pulmonary hemorrhage with maximal exercise. From this a maxim could be distilled regarding the conditions which may be needed for inducing pulmonary hemorrhage: The greater the airway obstruction, the smaller the exercise stress; the smaller the airway obstruction, the greater the exercise stress. The study drew attention to the importance of including in the routine necropsy protocol an examination of the intrinsic muscles of the larynx. Asphyxia has not in the past been considered as a possible explanation for sudden death in the horse but it became apparent that this represented an omission. |
