Exertional heat illness: a review of the syndrome affecting racing Thoroughbreds in hot and humid climates

Metabolic heat produced by Thoroughbred racehorses during racing can rapidly elevate core body temperature (1°C/min). When environmental conditions are hot and humid, the normal physiological cooling mechanisms become ineffective. The heat accumulated may exceed a critical thermal maximum (estimated to be 42°C), which may trigger a complex pathophysiological cascade with potentially lethal consequences. This syndrome has been labelled exertional heat illness (EHI). EHI is described in humans, but has not been well documented in Thoroughbred racehorses. The clinical signs described in racehorses would suggest that the pathophysiological events affecting the central nervous (CNS) and gastrointestinal systems are similar to those described in humans. Clinical signs are progressive and include signs of endotoxaemia and increasing levels of CNS dysfunction. Initially, horses that may be mildly irritable (agitated, randomly kicking out) may progress to unmanageable (disorientation, severe ataxia, falling) and ultimately convulsions, coma and death. Currently, the approach to treatment is largely empirical and involves rapid and effective cooling, administration of drugs to provide sedation, administration of non‐steroidal anti‐inflammatory drugs to ameliorate the effects of endotoxaemia and glucocorticoids to stabilise cell membranes and reduce the effects of inflammation on the CNS. This review provides an overview of the current knowledge about EHI in Thoroughbred racehorses, suggests a likely pathophysiology of the syndrome in horses based on the current literature on heat illness in humans and horses, and outlines current treatment strategies being used to treat racehorses with clinical signs of EHI.     

Anti‐Müllerian Hormone in the Domestic Dog during the Anestrus to Oestrous Transition

The reproductive cycle of the domestic dog features a long period of relative ovarian inactivity or anestrus. The mechanism of anestrous termination/oestrous resumption is not yet fully understood, which presents a challenge to the development of oestrous induction protocols. In this study, we assess the possibility that anti‐Müllerian hormone (AMH) might play a role in this transition by characterizing its patterns of expression in the circulation during the transition from anestrus to oestrous and in all stages of ovarian follicular growth. Serum samples from five beagles (2.0–4.5 years) were collected three times per week at least 30 days prior to the onset of oestrous and assessed for AMH concentrations. Serum AMH concentration increased significantly during the transition from anestrus to proestrus and then declined back to the anestrous baseline beginning on day ?4 before the luteinizing hormone surge, which was determined by changes in serum progesterone concentrations. Cortical sections of ovaries from females undergoing routine ovariohysterectomy (aged 8 months–5 years, n = 4) were evaluated for AMH by immunohistochemistry. Pre‐antral and small antral follicles were most strongly immunoreactive for AMH. These data suggest that the increase in the number of antral follicles is associated with the rise in serum AMH as the anestrous period comes to an end. The rise in AMH might be useful in predicting the onset of oestrus and therefore assist with the optimization of oestrous induction protocols and possibly other assisted reproductive technologies.     

Nonsurgical management of type II fractures of the distal phalanx in 48 Standardbred horses

OBJECTIVE: To evaluate nonsurgical management of type II fractures of the distal phalanx in Standardbred horses. DESIGN: Retrospective study of 48 affected horses. RESULTS: Most fractures occurred on the lateral palmar process of the left forelimb or the medial palmar process of the right forelimb; 81% of horses were considered sound enough to return to training and 63% raced. Of those returning to racing, 41% competed in > 10 races, 37% in 2 to 10 races and 22% in only 1 race. There was no difference in performance before and after fracture. Twenty-four of 25 horses had a bar shoe fitted for > 50% of the treatment phase. Of those horses returning to training without a bar shoe, 89% refractured at the same site. Sixty percent of horses returning to training with a bar shoe raced successfully. The total convalescent time, the time rested in a box and the time spelled in a paddock were similar for horses returning to racing and those that did not. The age of the horse had no effect on the ability to return to racing. CONCLUSION: The prognosis for type II fractures of the distal phalanx is guarded. It is advisable to fit a bar shoe on the horse during convalescence. Horses returning to training and racing with a bar shoe appear less likely to refracture the distal phalanx. Those horses that return to racing can perform at a level similar to that prior to fracture.