The combination of extreme heat, humidity and strenuous exercise is potentially challenging to the thermoregulatory system of a Thoroughbred racehorse, and under certain circumstances can cause a condition called exertional heat illness (EHI). It is difficult to predict its occurrence in an individual animal due to the combination on race day of extrinsic and intrinsic risk factors. Education regarding EHI is essential to its prevention, and lack of understanding amongst those responsible for the horse's care may in fact be the most important risk factor. The pathophysiology of EHI is similar across elite athletic species and is directly related to an elevation in core body temperature that exceeds the 'critical thermal maximum', causing widespread destruction of cells. It is not only the high core temperature but also its duration that will dictate outcome. Treatment strategies should decrease the hyperthermia to near normal levels within 30 min of onset, which will minimise adverse consequences.This review article outlines the pathophysiological changes as EHI progresses, and the case definition at each emergent level. Pharmacological treatment strategies and their rationale are presented. Aggressive cooling, however, is the key treatment and requires a technique which is both practical and effective in rapidly reducing core body temperature. The treatment paradigm is early detection, rapid assessment enabling prioritisation of individuals and aggressive cooling. Each stage is critically discussed.
Summary When racehorses fail to thermoregulate effectively, whether due to intrinsic or extrinsic factors, a condition called exertional heat illness (EHI) may occur, which can be life‐threatening and represents a significant welfare issue. Horses usually become affected in the recovery phase soon after racing, so that a knowledge of the ‘normal’ thermoregulatory processes which operate at this time and their variations is essential to enable early detection of EHI. Racing in hot or warm and humid weather conditions represents the upper extreme of thermoregulatory variations, and observations on how horses normally recover at the racetrack may provide a clearer perspective on the physiology of that process for all sports horses. This review focuses on the post‐exercise thermoregulatory capacity of the Thoroughbred racehorse, with a view to understanding the physiological mechanisms that should efficiently dissipate excess heat. The clinical manifestations of exertional heat illness are due to inadequate or harmful physiological responses, and if recognised and treated early can be effectively curtailed.
A simple epidemiological model of disease causation is proposed for exertional heat illness (EHI) in Thoroughbred racehorses. The agent of disease causation that must be present for the condition to occur is strenuous exercise, producing substantial quantities of metabolic heat. This is stored during racing but must be dissipated rapidly in the post-race period to prevent core body temperature rising to a critical level and causing the clinical manifestations of EHI. Environmental factors are next in the epidemiological triad, and it is a common misconception that these are the direct cause of EHI. In fact, environmental conditions enable EHI by either diminishing the evaporative capacity of the environment or promoting internal heat gain. This article deals with the specific effects of the four thermal elements, separately and in combination, on individual thermo-effector mechanisms. The final component in the epidemiological triad is individual host factors. A critical premise of epidemiology is that conditions such as EHI may not occur randomly in a population but may be more likely to occur in some individuals due to the presence of certain factors that predispose them to the condition. For the purpose of assessing risk, it is not feasible to examine the balance between metabolic heat production and the intrinsic and extrinsic factors, which collectively determine each individual's heat stress response. Therefore, the measurement of environmental factors remains the only practical way of obtaining a credible risk assessment for EHI, so that effective countermeasures can be instigated and the welfare of our racehorses ensured.
Exertional heat illness (EHI) is a complex medical disease. The thoroughbred (TB) racehorse is at considerable risk because of the intensity of its exercise activity and its high rate of metabolic heat production. The pathophysiology of EHI can combine aspects of both the heat toxicity pathway and the heat sepsis or endotoxemic pathway. Treatment regimes depend upon the detection of earliest clinical signs, rapid assessment, aggressive cooling and judicious use of ancillary medications. Ice-cold water provides the most rapid cooling, consistent with the need to lower core body temperature before tissue damage occurs. Research into EHI/HS by inducing the condition experimentally is ethically unjustifiable. Consequently, leading researchers in the human field have conceded that “most of our knowledge has been gained from anecdotal incidents, gathered from military personnel and athletes who have collapsed during or following physical activity, and that retrospective and case studies have provided important evidence regarding recognition and treatment of EHI”. The authors’ review into EHI shares that perspective, and the recommendations made herein are based on observations of heat-affected racehorses at the racetrack and their response, or lack of response, to treatment. From 2014 to 2018, 73 race meetings were attended, and of the 4809 individual starters, signs of EHI were recorded in 457. That observational study formed the basis for a series of articles which have been published under the title, ‘EHI in Thoroughbred racehorses in eastern Australia’, and forms the background for this review.
The traditional approach to exertional heat illness (EHI) is based on the premise that external heat is the trigger and sole driver of the condition. During the last few decades, many researchers have suggested that climatic heat alone does not fully explain the pathophysiology of EHI, and a second pathway has been proposed which focuses How to cite this article: Brownlow, M.A. & Mizzi, J.X. (2023) Pathophysiology of exertional heat illness in the Thoroughbred racehorse: Broadening perspective to include an exercise-induced gastrointestinal syndrome in which endotoxaemia and systemic inflammation may contribute to the condition.
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