OBJECTIVE To identify risk factors associated with fatal injuries in Thoroughbred racehorses in the United States and Canada.
DESIGN Retrospective study.
ANIMALS 1,891,483 race starts by 154,527 Thoroughbred racehorses at 89 racetracks in the United States and Canada from 2009 to 2013.
PROCEDURES Data were extracted from the Equine Injury Database, which contained information for 93.9% of all official flat racing events in the United States and Canada during the 5-year observation period. Forty-four possible risk factors were evaluated by univariate then multivariable logistic regression to identify those that were significantly associated with fatal injury (death or euthanasia of a horse within 3 days after sustaining an injury during a race).
RESULTS 3,572 race starts ended with a fatal injury, resulting in a period incidence rate of 1.9 fatal injuries/1,000 race starts. Twenty-two risk factors were significantly associated with fatal injury. Risk of fatal injury was greater for stallions than for mares and geldings and increased as the number of previous nonfatal injuries and race withdrawals and level of competitiveness (eg, horse's winning percentage and race purse) of the horse or race increased.
CONCLUSIONS AND CLINICAL RELEVANCE Results identified several risk factors associated with fatal injuries in Thoroughbred racehorses. This information can be used as a guideline for the identification of racehorses at high risk of sustaining a fatal injury and in the design and implementation of preventative measures to minimize the number of fatal injuries sustained by horses competing in flat racing in the United States and Canada.
To identify risk factors associated with race-related sudden death in Thoroughbred racehorses in the US and Canada.
4,198,073 race starts made by 284,387 Thoroughbred horses at 144 racetracks in the US and Canada between 2009 and 2021.
Study data were extracted from the Equine Injury Database, which contains detailed records of 92.2% of all official race starts made in the US and Canada during the study period. Forty-nine potential risk factors were analyzed using univariable and multivariable logistic regression. Cases were defined as race starts that resulted in fatality within 3 days of racing, in which at least 1 of 5 codes relating to sudden death was recorded. Fatalities due to catastrophic musculoskeletal injury were omitted from the study cohort.
536 race starts resulted in sudden death, an incidence rate of 0.13/1,000 starts. Fifteen risk factors were significantly associated with sudden death, including horse age and sex, season and purse of race, race distance, and horses’ recent history of injury and lay-up. Horses racing while on furosemide medication were at 62% increased odds of sudden death.
Associations found between previous injury and sudden death suggests preexisting pathology could contribute in some cases. The association between furosemide and sudden death prompts further study to understand which biological processes could contribute to this result.
OBJECTIVE To evaluate ex vivo cyclooxygenase (COX) inhibition and compare in vitro and ex vivo COX-1 inhibition by flunixin meglumine and firocoxib in horses.
ANIMALS 4 healthy horses for in vitro experiments and 12 healthy horses (6 males and 6 females; 5 Thoroughbreds, 5 Warmbloods, and 2 ponies) undergoing elective surgery for ex vivo experiments.
PROCEDURES 12 horses received flunixin meglumine (1.1 mg/kg, IV, q 12 h) or firocoxib (0.09 mg/kg, IV, q 24 h). Blood samples were collected before (baseline) and 2 and 24 hours after NSAID administration. Prostanoids (thromboxane B2, prostaglandin E2, and prostaglandin E metabolites) served as indicators of COX activity, and serum drug concentrations were measured by use of high-performance liquid chromatography. An in vitro coagulation-induced thromboxane B2 assay was used to calculate drug concentration-COX-1 inhibition curves. Effect of time and treatment on COX activity was determined. Agreement between in vitro and ex vivo measurement of COX activity was assessed with Bland-Altman analysis.
RESULTS At 2 and 24 hours after NSAID administration, COX-1 activity was reduced, compared with baseline activity, for the flunixin meglumine group only and relative COX-1 activity was significantly greater for the firocoxib group, compared with that for the flunixin meglumine group. There was no significant change in COX-2 activity after surgery for either group. Bland-Altman analysis revealed poor agreement between in vitro and ex vivo measurement of COX-1 activity.
CONCLUSIONS AND CLINICAL RELEVANCE Compared with flunixin meglumine, firocoxib had COX-1-sparing effects ex vivo in equine patients that underwent elective surgery.
Objective—To investigate effects of exercise on hyaline cartilage (HC), calcified cartilage (CC), and subchondral bone (SCB) thickness patterns of equine tarsi.
Sample Population—30 tarsi from cadavers of horses with known exercise history.
Procedures—Tarsi were assigned to 3 groups according to known exercise history as follows: pasture exercise only (PE tarsi), low-intensity general-purpose riding exercise (LE tarsi), and high-intensity elite competition riding exercise (EE tarsi). Osteochondral tissue from distal tarsal joints underwent histologic preparation. Hyaline cartilage, CC, and SCB thickness were measured at standard sites at medial, midline, and lateral locations across joints with a histomorphometric technique.
Results—HC, CC, and SCB thickness were significantly greater at all sites in EE tarsi, compared with PE tarsi; this was also true when LE tarsi were compared with PE tarsi. At specific sites, HC, CC, and SCB were significantly thicker in EE tarsi, compared with LE tarsi. Along the articular surface of the proximal aspect of the third metatarsal bone, SCB was thickest in EE tarsi and thinnest in LE tarsi; increases were greatest at sites previously reported to undergo peak strains and osteochondral damage.
Conclusions and Clinical Relevance—Increased exercise was associated with increased HC, CC, and SCB thickness in mature horses. At sites that undergo high compressive strains, with a reported predisposition to osteoarthritic change, there was increased CC and SCB thickness. These results may provide insight into the interaction between adaptive response to exercise and pathological change.
To investigate equine squamous gastric disease (ESGD) and equine glandular gastric disease (EGGD) in Icelandic horses moving from pasture into training.
81 horses (median age, 3 years; interquartile range, 1 year) from 10 farms representing 4 different Icelandic regions.
Initial gastroscopy was undertaken within 2 weeks of moving from pasture into a training establishment. A total of 71 horses underwent endoscopic examination again 8 weeks later. Various management and behavioral factors were assessed through face-to-face questionnaires with the owners or trainers. Multivariable logistic regression was used to determine factors contributing to any change in ESGD and EGGD severity score during the 8-week training period.
Incidence of EGGD and ESGD in this feral population was similar to that found in domesticated horses. ESGD incidence (severity score, ≥ 2; score range, 0 to 4) reduced from an initial 71.6% (58/81) to 25.4% (18/71). On multivariable analysis, sex (ie, being a stallion or a female vs gelding) increased the likelihood of ulcer grade reduction. Being fed preserved forage 3 or more times a day also improved the likelihood of ESGD reduction (odds ratio, 17.95; 95% CI, 1.67 to 193.40; P = .017). Overall, the farm explained 35% of the variance, confirming the importance of management factors. Incidence of EGGD (severity score, ≥ 1; score range, 0 to 2) reduced from 47% (38/81) to 40.8% (29/71) during the same period. No measured variables were associated significantly with EGGD incidence or reduction.
Pasture provision (without supplementary feed or forage) does not result automatically in a low incidence of gastric ulcers. Regular provision of preserved forage is a key factor in reducing ESGD incidence.
To examine the association between prerace administration of phenylbutazone and the risk of musculoskeletal injury (MSI) and fatal injury in Thoroughbred racehorses that raced between 2006 and 2015 at 2 of the 4 official racetracks in Argentina.
Data from racetrack databases and veterinary reports on 283,193 race starts.
Data were collected relating to race performance and injury outcomes for starts at these tracks. The incidence of MSI and fatal injury was calculated for each year, stratified by the declared prerace administration of phenylbutazone. Univariable logistic regression, followed by multivariable logistic regression, was used to identify significant risk factors for both MSI and fatal injury.
Analyses identified associations between the declared prerace administration of phenylbutazone and the risk of MSI and fatal injury during racing. Horses with declared prerace phenylbutazone administration had greater odds of MSI (OR, 1.45 [95% CI, 1.03 to 2.04]) and fatal injury (OR, 1.59 [95% CI, 1.1 to 2.27]) than did horses racing without prerace phenylbutazone administration. These associations remained significant when other risk factors were accounted for in both multivariable models.
CONCLUSIONS AND CLINICAL RELEVANCE
Results suggested an association between the prerace administration of phenylbutazone and the risk of MSI and fatal injury in Thoroughbred racehorses during racing. Although these results did not imply a direct causal relationship between prerace phenylbutazone administration and injury, they may be considered in the development of more conservative medication policies to optimize racehorse welfare in North and Latin America.
Objective—To identify the risk factors for premature retirement because of tendon injury in a Thoroughbred racehorse population.
Animals—175 Thoroughbred racehorses (cases) at the Hong Kong Jockey Club that were retired from racing because of tendon injury between 1997 and 2004 and for which the last preretirement exercise was at a fast pace were each matched with 3 control horses that were randomly selected from all uninjured horses that had galloped on the same date as that last exercise episode.
Procedures—Training data for all horses were examined. Conditional logistic regression analyses were performed to identify risk factors for retirement from racing attributable to tendon injury. Two multivariable conditional logistic regression models were created; each contained 8 explanatory variables.
Results—Compared with control horses, case horses were older at the time of import, accumulated more race distance soon after import, were more likely to have had previous official veterinary or ultrasonographic examinations, raced fewer times during their career, and were in training for a longer period and had exercised at a reduced intensity during the 180-day period preceding the last fast-paced work date.
Conclusions and Clinical Relevance—In addition to identification of risk factors for tendon injury among racing Thoroughbreds, results have suggested that resources focused on obtaining accurate training data may be misdirected in the absence of internationally agreed criteria for incident tendon injury among racehorses. Nevertheless, changes in training intensity and findings of previous clinical examinations could be used to identify horses at risk of tendon injury–associated retirement.
Objective—To investigate effects of age on thickness and morphologic characteristics of hyaline cartilage, calcified cartilage, total cartilage, and subchondral bone (SCB) in the equine tarsometatarsal joint.
Sample Population—23 tarsal joints from cadavers of 23 ponies (11 days to 25 years old); ponies were limited to pasture exercise and euthanatized for reasons not related to this study.
Procedures—Tarsi were allocated into several age groups (11 days old [n = 3], 6 to 9 months old , 2 to 3 years old , 6 to 8 years old , 11 to 17 years old , and 20 to 25 years old ). Histologic examination and histomorphometric measurement of hyaline cartilage, calcified cartilage, total cartilage, and SCB were performed at medial and lateral sites.
Results—A significant decrease was detected in thickness of hyaline cartilage and total cartilage with increasing age, but there was a significant increase in thickness of calcified cartilage and SCB with increasing age. Differences in chondrocyte and collagen fiber arrangement, tidemark, and osteochondral junction morphology were evident among age groups.
Conclusions and Clinical Relevance—These findings suggested that the various tissues of the osteochondral unit change in different ways with age. The response of each tissue may be related to relative response of the tissues to strains induced by pasture exercise but could have an influence on how the overall properties of the osteochondral unit change with age. The findings may also be suggestive of changes that develop prior to the onset of osteoarthritis.
Objective—To determine whether histopathologic characteristics of the osteochondral units of equine distal tarsal joints were associated with exercise history in horses without lameness.
Sample Population—30 cadaver tarsi from horses without lameness and with known exercise history were separated into 3 groups: nonridden, pasture exercise (group P); low-intensity, ridden exercise (group L); and high-intensity, elite competition exercise (group E).
Procedures—Standardized sites from the centrodistal and tarsometatarsal joints under went histologic preparation. A grading system was adapted to describe location, depth, and shape of lesions; cellular arrangement; organization at cartilage and subchondral bone (SCB) junctions; and organization of SCB. A high score signified a more severe pathological change than a low score. Exercise groups were compared by calculation of Spearman rank correlations.
Results—In the centrodistal joint, lesions were present in groups L and E but only medially. Cellular arrangement scores were higher at the dorsomedial location in group P than in groups L and E. Groups L and E had higher scores than group P for the organization of the cartilage, SCB junctions, and SCB, with higher scores at the dorsomedial location. In the tarsometatarsal joint, lesions were evident across the whole joint surface, with more severe lesions located laterally in all 3 groups. Overall, group E had higher scores for cellular arrangement and SCB organization than groups P and L.
Conclusions and Clinical Relevance—Ridden exercise may increase the risk of osteochondral lesions at distal tarsal sites predisposed to osteoarthritis relative to the risk with nonridden exercise.