Exercise-induced pulmonary haemorrhage in the horses: results of a detailed clinical, post mortem and imaging study. VII. Ventilation/perfusion scintigraphy in horses with EIPH

Detailed post mortem examination of the lungs of horses with exercise-induced pulmonary haemorrhage (EIPH) has demonstrated significant small airway disease and intense bronchial arterial proliferation in the dorsocaudal lungfields. The purpose of this study was to investigate ventilation and perfusion distribution in the lungs of a similar group of horses to compare changes in the live animal with the previously reported post mortem findings. Thoracic radiography and ventilation/perfusion (V/Q) scintigraphy were performed on five racing Thoroughbreds with recent histories of EIPH. Parametric images of V/Q ratios for left and right lungfields were also generated from the scan images. In all horses, ventilation and perfusion deficits were demonstrated in the dorsocaudal areas of the lung corresponding closely to the observed radiographic lesions. In particular, the perfusion images and V/Q ratio displays indicated that, in affected areas of lung, pulmonary arterial perfusion was the more seriously impaired. This finding appears to confirm the post mortem evidence of reduced pulmonary arterial perfusion and bronchial arterial dominance in these areas. Ventilation deficits in the same areas also confirmed the likelihood of partial airway obstruction consistent with the small airway disease noted in previous post mortem observations. These results suggest that the vascular and airway lesions demonstrated in detailed post mortems of horses with EIPH are also functionally important in affected horses, even at rest. As a consequence of the apparent persistent, insidious and progressive nature of the lesions associated with EIPH there are serious long term implications for management of the condition.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. IV. Changes in the bronchial circulation demonstrated by C.T. scanning and microradiography

The purpose of this study was to use radiographic contrast techniques and special imaging methods to identify and high-light bronchial arterial involvement in lung lesions associated with exercise-induced pulmonary haemorrhage (EIPH) in horses. The lungs from four horses with histories of EIPH were prepared for computerised tomographic scanning and microradiography by perfusing the broncho-oesophageal artery with a mixture of red latex and either barium or iodine contrast materials while the pulmonary supply received only blue latex. Computerised tomographic scan slices of the prepared inflated lungs were obtained from the caudal tip of the lung to the hilus. Microradiography of selected lung slices was also performed on a Faxitron. Diffuse areas of increased density, with preferential bronchial arterial supply noted on the computerised tomographic scans were confirmed by microradiography. Dense focal and diffuse plexuses of markedly hypertrophied and highly branched bronchial arterial networks were identified, centred around certain small airways. The vascular supply to these plexuses was recruited predominantly from neighbouring bronchial vessels, and in some cases, from the enlarged vasa vasorum of pulmonary arteries sending anastomoses to the affected areas. The authors conclude that bronchial vascular lesions in EIPH cases are the likely origin of haemorrhage; that small airway disease is the probable initiating stimulus for bronchial vascular proliferation in these lesions; and that the morphology and nature of the neovascular tissue in these lesions provides the conditions leading to haemorrhage in the lungs of horses with EIPH.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. II. Gross lung pathology

Gross post mortem examinations were performed on the lungs of 26 Thoroughbred horses of known exercise-induced pulmonary haemorrhage (EIPH) status. The most consistent finding was a variable degree of bilaterally symmetrical, dark discolouration of the dorsocaudal regions of the caudal lung lobes. In more severely affected lungs, the stained areas extended cranially along the dorsal surfaces of the lungs, and in some cases affected approximately one third of the lung surface. Discoloured areas of lung were denser than normal, collapsed less readily, often contained trapped air and were slow to inflate. The subpleural bronchial arteries were more prominent in the discoloured regions. Pleural adhesions were noted in two horses but were not related to the discoloured lung regions. It was concluded that the discoloured lesions have a complex pathogenesis and were related directly to previous bouts of EIPH. Associated with them were signs indicating probable partial small airway obstruction, decreased tissue compliance and direct involvement of the bronchial arterial circulation.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. III. Subgross findings in lungs subjected to latex perfusions of the bronchial and pulmonary arteries

Latex was injected under pressure into bronchial and pulmonary arteries of the inflated lungs of Thoroughbreds and transverse sections taken to calculate the area of lesions resulting from exercise-induced pulmonary haemorrhage. Extensive areas of dense brown haemosiderin varying from 0 to 45 per cent of total lung volume were identified, predominantly in the dorsocaudal lungfields. Bronchial arterial proliferation appeared to have replaced the pulmonary supply in affected areas of the lung. Closely associated with the staining and bronchial arterialisation, there was widespread small airway disease. The most severely affected bronchioles contained thick gelatinous or mucous exudate or mucoid plugs and had grossly thickened walls. These lesions suggest that the source of haemorrhage in exercise-induced pulmonary haemorrhage is from alveolar capillaries anomalously supplied by the bronchial arterial circulation through the development of pathological shunts. Small airway disease is suggested as being of major importance in the pathogenesis of the disease and may have led to the initial proliferation of the bronchial circulation.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. VI. Radiological/pathological correlations

This study was initiated to determine if the extent and intensity of lung lesions associated with exercise-induced pulmonary haemorrhage (EIPH) in horses could be predicted from thoracic radiographs. Sets of thoracic radiographs from 24 horses with varied histories of EIPH were subjectively coded for radiographic quality, and perceived extent and intensity of diffuse interstitial opacity by three radiologists who had no knowledge of the corresponding autopsy results. Codes assigned from radiographs for the chosen parameters were compared with coded estimates of lung surface staining assigned at post mortem and volume measurements of haemosiderin deposits and bronchial arterial neovascularisation recorded from lung slices in separate studies. The non-parametric Spearman rank correlation test was used to test for statistical significance. All radiographically coded estimates of lesion severity were positively correlated with post mortem measurements of actual lesion involvement, but only the correlation between coded estimates of lesion opacity versus haemosiderin deposits and bronchial artery neovascularisation were statistically significant (P less than 0.05). Correlations between radiographic codes for lesion extent versus haemosiderin deposits and neovascularisation were just beyond the level of significance (P greater than 0.05 less than 0.1). These findings indicate that there are graded, radiographically discernible increases in interstitial opacity related to actual lesion severity. However, under the conditions of the study, accurate prediction of lung pathology in individual cases based on radiographic criteria was precluded by the wide variance of the coded values. The authors believe that with good radiographic technique and careful criteria selection, satisfactory prediction of lesion severity in EIPH cases could be achieved.     

A review of the pathophysiology of exercise-induced pulmonary haemorrhage in the equine athlete

In the United States, more than 75% of equine athletes are reported to suffer from exercise-related haemorrhage of the respiratory tract (Voynick and Sweeney, 1986; Sweeney et al., 1990). Fiberoptic endoscopy has traced the source of blood to beyond the bifurcation of the trachea. In 1981, the term exercise-induced pulmonary haemorrhage (EIPH) was introduced (Pascoe et al., 1981). Racehorses of all breeds, polo ponies and three-day event horses of mixed heritage, even foxhunters, may bleed (Voynick and Sweeney, 1986; Pascoe et al., 1981; Sweeney and Soma, 1983; Hillidge, 1986). Any horse working at speeds greater than 240 m/min is at risk (Voynick and Sweeney, 1986).The impact of exercise-induced pulmonary haemorrhage is difficult to assess. Most attempts to demonstrate statistically a negative correlation between EIPH and performance have been unrewarding, largely due to the number of uncontrollable variables (Pascoe et al., 1981; Raphel and Soma, 1982). In racing thoroughbreds (Mason et al., 1983) and standard breeds (MacNamara et al., 1990) approximately half as many EIPH-positive as EIPH-negative horses were placed in their races. Based on extensive intrapulmonary haemorrhage, a 3-year prospective study of sudden deaths in exercising thoroughbreds concluded that 9 out of 11 deaths were attributable to EIPH (Gunson et al., 1988).By correlation of clinical signs, thoracic radiographs, ventilation/perfusion scintigraphy, gross and subgross pathology and histopathology in 26 affected thoroughbreds, EIPH has been associated with chronic small airway inflammation, proliferation of subpleural, peribronchial and septal bronchial arterioles, interstitial connective tissue fibrosis and alveolar septal disruption in the dorsocaudal lung lobes (O'Callaghan et al., 1987). From this work it was proposed that the initial insult of EIPH started as focal, dorsocaudal pulmonary peribronchial inflammation which resulted in bronchial arterial neovascularization. Haemorrhage then occurred when, during exercise, bronchial blood pressure increased in fragile capillary buds. The incidence of bronchitis/bronchiolitis, regardless of aetiology, has been estimated to be 30% in non-racing equine athletes and close to 100% in one group of racing thoroughbreds (Sweeney et al., 1989). Histological study of lungs from horses with mild, moderate and severe chronic small airway disease consistently revealed a greater density of lesions in the diaphragmatic lobes (Winder and von Fellenberg, 1988).To understand further the aetiology and/or pathophysiology of EIPH, we will first explore some aspects of general mammalian and specific equine pulmonary and bronchial vascular anatomy and physiology. Exercise-related changes in these systems in normal and EIPH-positive horses will be briefly reviewed. Finally, a look at the types of therapies applied to bleeders may shed further light on the subject.     

Pulmonary response to airway instillation of autologous blood in horses

REASONS FOR PERFORMING STUDY: Exercise-induced pulmonary haemorrhage (EIPH) occurs in the majority of horses performing strenuous exercise. Associated pulmonary lesions include alveolar and airway wall fibrosis, which may enhance the severity of EIPH. Further work is required to understand the pulmonary response to blood in the equine airways. OBJECTIVES: To confirm that a single instillation of autologous blood into horse airways is associated with alveolar wall fibrosis, and to determine if blood in the airways is also associated with peribronchiolar fibrosis. METHODS: Paired regions of each lung were inoculated with blood or saline at 14 and 7 days, and 48, 24 and 6 h before euthanasia. Resulting lesions were described histologically and alveolar and airway wall collagen was quantified. RESULTS: The main lesion observed on histology was hypertrophy and hyperplasia of type II pneumocytes at 7 days after blood instillation. This lesion was no longer present at 14 days. There were no significant effects of lung region, treatment (saline or autologous blood instillation), nor significant treatment-time interactions in the amount of collagen in the interstitium or in the peribronchial regions. CONCLUSION: A single instillation of autologous blood in lung regions is not associated with pulmonary fibrosis. POTENTIAL RELEVANCE: Pulmonary fibrosis and lung remodelling, characteristic of EIPH, are important because these lesions may enhance the severity of bleeding during exercise. A single instillation of autologous blood in the airspaces of the lung is not associated with pulmonary fibrosis. Therefore the pulmonary fibrosis described in EIPH must have other causes, such as repetitive bleeds, or the presence of blood in the pulmonary interstitium in addition to the airspaces. Prevention of pulmonary fibrosis through therapeutic intervention requires a better understanding of these mechanisms.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. I. Clinical profile of horses

Detailed physical and clinical examinations were performed on 26 Thoroughbred racehorses which were used subsequently in a series of studies to investigate the contribution of the pulmonary and bronchial arterial circulations to the pathophysiology of exercise-induced pulmonary haemorrhage (EIPH). Twenty-five of the horses had been retired from race training in Hong Kong during the 1984-85 season, all but four raced that season; one horse had been retired the previous season. The average number of races for the group that season was 4.1 +/- 2 with an average distance of 1502 +/- 216 metres, mean racing speed 15.5 +/- 0.5 metres/sec. Time from last race to necropsy was 177 +/- 155 days, range 12 to 572 days. All but one horse had a known history of either EIPH or epistaxis. Time from last recorded incident of expistaxis (17 horses) to necropsy was 156 +/- 141 days, range 12 to 513 days, with a longer interval since last recorded endoscopic observation of EIPH. Focal abnormal lung sounds were detected in the dorsocaudal lungfields on auscultation during rebreathing in three horses and six had tracheobronchial cytology consistent with previous episodes of pulmonary haemorrhage (haemosiderophages). No other characteristics which might have allowed separation of this group of horses from other Thoroughbred horses recently in race training were identified.     

Exercise-induced pulmonary haemorrhage in the horse: results of a detailed clinical, post mortem and imaging study. V. Microscopic observations

Lungs from 19 Thoroughbred racehorses with a history of exercise-induced pulmonary haemorrhage (EIPH) were studied using several forms of microscopy. Light microscopy of paraffin sections revealed three lesions in the caudodorsal region of the lungs from each horse. These correspond with the location of blue to brown stains seen at necropsy. These lesions include sequelae of bronchiolitis, hemosiderophages and increased connective tissue. Much of each of the lungs appeared normal, especially the more cranial or ventral portions. Foci of eosinophil infiltration were found in seven of the 19 lungs examined. With two exceptions, these eosinophilic foci had a different distribution to the three lesions. In areas of severe bronchiolar changes and fibrosis, vascular lesions typical of hypertension were found occasionally. Transmission electron microscopy was used to confirm cell types seen by light microscopy and to examine arterioles for changes characteristic of neovascularisation. Areas of enlarged airspaces from the vascular injected right lungs were examined by scanning electron microscopy. The balance of fibrosis and destruction varied in these areas, but none were as extensive as those seen in chronic obstructive pulmonary disease. The authors hypothesise that bronchiolitis and related neovascularisation are essential components of the aetiology of EIPH.     

Upper airway obstruction (partial asphyxia) as the possible cause of exercise-induced pulmonary hemorrhage in the horse: An hypothesis

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.     

Bit‐induced asphyxia in the racehorse as a cause of sudden death

The prevention of sudden death requires removal of its cause and this is unknown. The author's hypothesis is that bit‐induced asphyxia, partial or complete, is a cause of sudden death. Antemortem data on bit‐induced asphyxia were compared with post mortem data on sudden deaths to explore a possible cause‐and‐effect relationship. Causal categories from sudden death necropsy data were reclassified. Those causing a horse to fall (cardiopulmonary failures) were considered primary effects and those resulting from a fall (CNS trauma and haemorrhagic shock) secondary effects. Cardiac failure from negative pressure pulmonary oedema caused by bit‐induced obstruction of the nasopharynx was consistent with the hypothesis. In 1988, asphyxia from recurrent laryngeal neuropathy was posited as a cause of exercise‐induced pulmonary haemorrhage (EIPH). It is now suggested that the bit is another cause of asphyxia; EIPH is a sign of negative pressure pulmonary oedema which, in turn, causes cardiac failure and sudden death. By breaking the airtight lip‐seal at exercise, a bit dissipates negative pressure in the oral compartments, destabilises the soft palate and obstructs the nasopharynx. Bitted rein pressure, kinking the airway and rendering parts of it flaccid, is a further cause of asphyxia. The data comparison supports a unifying hypothesis on 4 problems currently considered idiopathic; that the bit is an ultimate cause of palatal instability, dynamic collapse of the upper respiratory tract, EIPH and sudden death. Bitless training and racing trials are recommended as a means of demonstrating that bitless racing is possible, preferable and predicted to reduce the prevalence of all 4 problems.     

Analysis of Canadian and Irish forage,oats and commercially available equine concentrate feed for pathogenic fungi and mycotoxins

Respiratory infections, recurrent airway obstruction (RAO) and exercise induced pulmonary haemorrhage (EIPH) are major causes of poor performance in horses. Fungi and mycotoxins are now recognised as a major cause of these conditions. The most notable fungi are Aspergillus and Fusarium. Fungal spores can originate from forage, bedding and feed and, in turn, these fungal spores can produce a series of mycotoxins as secondary metabolites.This study set out to ascertain the degree of fungal and mycotoxin contamination in feed and fodder used in Irish racing yards over a one-year period. Weather conditions in forage producing areas were sampled by Met Eireann and the Canadian Meteorological Service.Fifty per cent of Irish hay, 37% of haylage and 13% of Canadian hay contained pathogenic fungi. Of the mycotoxins, T2 and zearalenone were most prominent. Twenty-one per cent of Irish hay and 16% of pelleted feed contained zearalenone. Forty per cent of oats and 54% of pelleted feed contained T2 toxins.     

Review of furosemide in horse racing: its effects and regulation

Furosemide has been used empirically and has been legally approved for many years by the US racing industry for the control of exercise-induced pulmonary haemorrhage (EIPH) or bleeding. Its use in horses for this purpose is highly controversial and has been criticized by organizations outside and inside of the racing industry. This review concentrates on its renal and extra-renal actions and the possible relationship of these actions to the modification of EIPH and changes in performance of horses. The existing literature references suggest that furosemide has the potential of increasing performance in horses without significantly changing the bleeding status. The pulmonary capillary transmural pressure in the exercising horse is estimated to be over 100 mmHg. The pressure reduction produced by the administration of furosemide is not of sufficient magnitude to reduce transmural pressures within the capillaries to a level where pressures resulting in rupture of the capillaries, and thus haemorrhage, would be completely prevented. This is substantiated by clinical observations that the administration of furosemide to horses with EIPH may reduce haemorrhage but does not completely stop it. The unanswered question is whether the improvement of racing times which have been shown in a number of studies are due to the reduction in bleeding or to other actions of furosemide. This review also discusses the difficulties encountered in furosemide regulation, in view of its diuretic actions and potential for the reduction in the ability of forensic laboratories to detect drugs and medications administered to a horse within days or hours before a race. Interactions between nonsteroidal anti-inflammatory drugs (NSAIDs) and furosemide have also been examined, and the results suggest that the effects of prior administration of NSAID may partially mitigate the renal and extra-renal effects which may contribute to the effects of furosemide on EIPH.     

Review of exercise induced pulmonary haemorrhage and its possible relationship with mechanical stress

Exercise induced pulmonary haemorrhage (EIPH) is a condition of uncertain aetiology. This article reviews the evidence relating to its incidence, clinical findings, radiological observations, histopathology and certain aspects of respiratory physiology. It is proposed that EIPH is primarily caused by mechanical stress in the dorsocaudal region of the lung.     

Oxidant injury,nitric oxide and pulmonary vascular function: implications for the exercising horse

The athletic ability of the horse is facilitated by vital physiological adaptations to high-intensity exercise, including a thin (but strong) pulmonary blood-gas barrier, a large pulmonary functional reserve capacity and a consequent maximum oxygen uptake (VO2max) far higher than in other species. A high pulmonary artery pressure also serves to enhance pulmonary function, although stress failure of lung capillaries at high pulmonary transmural pressures, and the contribution of other factors which act in the exercising horse to increase pulmonary vascular tone, may lead to pathological or pathophysiological sequelae, such as exercise-induced pulmonary haemorrhage (EIPH). Reactive oxygen species (ROS) are an important component of the mammalian inflammatory response. They are released during tissue injury and form a necessary component of cellular defences against pathogens and disease processes. The effects of ROS are normally limited or neutralized by a multifactorial system of antioxidant defences, although excessive production and/or deficient antioxidant defences may expose healthy tissue to oxidant damage. In the lung, ROS can damage pulmonary structures both directly and by initiating the release of other inflammatory mediators, including proteases and eicosanoids. Vascular endothelial cells are particularly susceptible to ROS-induced oxidant injury in the lung, and both the destruction of the pulmonary blood-gas barrier and the action of vasoactive substances will increase pulmonary vascular resistance. Moreover, ROS can degrade endothelium-derived nitric oxide (NO), a major pulmonary vasodilator, thereby, with exercise, synergistically increasing the likelihood of stress failure of pulmonary capillaries, a contributing factor to EIPH. This review considers the implications for the exercising horse of oxidant injury, pulmonary vascular function and NO and the contribution of these factors to the pathogenesis of equine respiratory diseases.     

Regional pulmonary veno-occlusion: a newly identified lesion of equine exercise-induced pulmonary hemorrhage

Exercise-induced pulmonary hemorrhage (EIPH) is common in horses following intense exertion, occurring in up to 75% of racing Thoroughbreds and Standardbreds. In spite of this, the pathogenesis of EIPH is poorly understood. In 7 racing Thoroughbred horses with EIPH, 6 sections were collected from the left and right lung, representing the cranial, middle, and caudal region of the dorsal and ventral lung (84 sites total). Grossly, both right and left lungs had numerous dark brown to blue-black foci along the caudodorsal visceral pleura. Tissue sections were stained with hematoxylin-eosin, Masson's trichrome, and Prussian blue. Verhoeff Van Gieson and immunohistochemistry for alpha-smooth muscle actin were used to assess the pulmonary vasculature. Histologic scores (HS = 0-3) were assigned to each region/slide for the presence and severity of 5 findings: interstitial fibrosis, hemosiderin accumulation, pleural/interlobular septal thickness, arterial and venous wall thickness, and evidence of angiogenesis (maximum cumulative HS = 15). Thirty-nine of the 84 (46%) sections were histologically normal (HS = 0); 33/84 (39%) were mildly to moderately affected, with small amounts of hemosiderin and fibrosis (HS = 1-9) while 12/84 (14%), primarily from the dorsocaudal lung, had severe vascular remodeling, fibrosis, and hemosiderin accumulation (HS = 10-15). In the latter, veno-occlusive remodeling of the intralobular veins colocalized with hemosiderosis, fibrosis, hypertrophy of vessels within the pleura, and interlobular septa and bronchial neovascularization. We propose that regional veno-occlusive remodeling, especially within the caudodorsal lung fields, contributes to the pathogenesis of EIPH, with the venous remodeling leading to regional vascular congestion and hemorrhage, hemosiderin accumulation, fibrosis, and bronchial angiogenesis.     

Bronchoalveolar lavage fluid in Standardbred racehorses: Influence of unilateral/bilateral profiles and cut-off values on lower airway disease diagnosis

The aim of this study was to determine whether the lung side being sampled would significantly influence bronchoalveolar lavage (BAL) cytological profiles and subsequent diagnosis in Standardbred racehorses. One hundred and thirty-eight French Trotters in active training and racing were included in a prospective observational study. BAL was performed using videoendoscopy in both right and left lungs during summer meetings in 2011 (64 horses) and 2012 (74 horses). Cytological data performed 24 h later from right and left lungs were compared and specifically used to classify horses as affected with exercise-induced pulmonary haemorrhage (EIPH), inflammatory airway disease (IAD), or were ‘controls’. For IAD, cytological definition was based on two different cut off values.Neutrophil percentages, haemosiderophage percentages and the haemosiderophage/macrophage (H/M) ratios were significantly higher in the right compared to the left lung. Measures of intra-class correlation coefficients revealed a fair agreement between left and right lungs for percentages of mast cells, eosinophils, and for the H/M ratio, and a moderate agreement for neutrophil percentages. Fair to moderate agreements were observed between left and right lungs for the diagnosis of IAD and/or EIPH based on kappa coefficients. When sampling one lung only, the risk of incorrectly classifying a horse as a ‘control’ increased with the use of the restraint cut-off values for IAD. As BAL from one lung is not representative of the other lung in the same horse, both lungs should be sampled for a better assessment of lung cellularity and for a precise diagnosis of lower airway diseases.     

Sex variation in the prevalence of exercise-induced pulmonary haemorrhage in racing quarter horses

Post race endoscopy was carried out on 255 two-year-old quarter horses and exercise-induced pulmonary haemorrhage (EIPH) was diagnosed in 166 (65 per cent) of them. Visible epistaxis was seen in a higher proportion of geldings than in either mares or stallions. The prevalence of EIPH was similar in mares (73 per cent) and in geldings (74 per cent). A significantly lower prevalence (49 per cent) was noted in stallions (P less than 0.01). It was concluded that a sex variation in the prevalence of EIPH exists in two-year-old quarter horses.     

Bronchoalveolar lavage findings in horses with exercise intolerance.

Significant differences were detected by bronchoalveolar lavage (BAL) between horses racing successfully and those showing exercise intolerance. Neutrophil percentage, haemosiderophage percentage and total bacterial numbers were significantly elevated in horses with exercise intolerance. BAL provided a more accurate indication of the incidence and extent of exercise induced pulmonary haemorrhage (EIPH) than visual inspection.