Another view on bleeding

Asphyxia is suggested as cause of pulmonary edemaBrent Keley, D.V.M., provided a good answer to the interesting question from Frederick Spohn, M.D., about the effectiveness of Lasix as a treatment for exercise-induced pulmonary hemorrhage (EIPH) in the horse (Thoroughbred Times, October 26, 1996). There is, however, one item in his answer upon which I would like to comment: Kelley correctly points out that Lasix is a well-recognized treatment for pulmonary edema in man but adds that pulmonary edema ... has nothing to do with EIPH in the horse.
With all due respect to Kelley, whose articles I read with pleasure and instruction, I must disagree. My research indicates horses that bleed from the lungs during exercise are, in fact, suffering from exactly this problempulmonary edema.
If a post-mortem examination is carried out immediately on a horse that has died from EIPH (within, say, 30 minutes), acute pulmonary edema will be found. On the other hand, ifas is more usualthe post-mortem is delayed several hours, the edema will have dispersed or been masked by congestive lung changes that occur after death in any horse, regardless of the cause of death. The ephemeral quality of pulmonary edema probably explains why the true nature of EIPH has not been recognized.
The condition we refer to as EIPH is, I believe, a misnomer. Instead, I propose the more accurate name asphyxia-induced pulmonary edema (AIPE). My reasons are as follows:

1. The nasal discharge that we have called a hemorrhage is not, in fact, blood, but heavily blood-stained pulmonary edema fluid. It does not, for example, have the ability to clot.
   
2. The post-mortem lesions found in the lung that we have called exercise-induced are not specific to exercise alone, for they can also be seen in a horse that has not been recently exercised.
   
3. The factor common to both is not exercise, but asphyxia. Clinical signs and post-mortem findings characteristic of so-called EIPH occur in horses that have experienced an obstruction to the upper airway (an obstruction at any point between the nostrils and the windpipe at the level of the first rib). The same post-mortem findings are present regardless of whether the airway obstruction occurs in the standing or the galloping horse. Asphyxia (generally, partial deprivation of air rather than complete) sets in motion a cascade of events, and the pulmonary effects, serious though they are, are secondary.
   

Pulmonary edema is secondary to upper-airway obstruction. In a galloping horse with an airflow problem, the thin walls of the air sacs of the lung (which are 15 times thinner than a standard sheet of airmail paper) are exposed, at each breath, to a greater than normal suction pressure. The result is that fluid and red blood cells are sucked out of the lungs into the small airways. Some of this blood-like fluid may appear at the nostril when the horse lowers its head.

Partial asphyxia
It is true, as Kelley cites, that as many as 95% of horses in training show evidence of EIPH on endoscopic evidence. Sadly, it is my belief that over 95% of racehorses also suffer from varying degrees of asphyxia during a race. Most of these episodes of asphyxia are slight and partial, but a few are severe and fatal.
Upper-airway obstruction in racehorses is common enough to explain the high prevalence of AIPE. For example, any bit pressure that results in head flexion of the slightest degree causes airway obstruction at the level of the throat. Furthermore, there are many conformational defects that are sufficiently prevalent to represent common sources of asphyxia.
Two examples will suffice. First, there is the narrow jaw defect, and, therefore, the narrow throat and voice-box (larynx) that this implies. Secondly, there is the much-commoner-than-realized deformity of a collapsed windpipe. In addition to head flexion and conformation defects, upper-airway diseases are yet another source of asphyxia. Whether inherited or acquired, a feature of almost every disease of the upper airway is that it obstructs airflow.
One disease that occurs, to varying degrees, in over 95% of horses is the inherited form of recurrent laryngeal neuropathy (RLN). In the live animal this can be shown to be present by an objective measurement of laryngeal nerve function, using an instrument that I developed six years ago and call an electro-laryngeograph.
The subjective assessment of laryngeal movement by endoscopy (especially so in the unsedated horse) is, in my opinion, not accurate enough to detect the true prevalence of the disease or to grade its severity. It is, I believe, precisely this limitation of endoscopy that results in our failure to recognize the universal prevalence of this potentially fatal, performance-limiting disease, RLN.
In the dead animal, RLN can be shown to be present by a microscopic examination of the laryngeal muscles and nerves. The reason that this neurological disease is not more frequently discovered is that it is not being looked for. If a proper examination of the larynx were made part of the regular post-mortem, the presence of neurogenic muscle atrophy would be found. Examination of the larynx is time-consuming but possible.

An insoluble problem
Let me now refer to Spohns request for scientific evidence on whether EIPH affects performance and whether Lasix moves a horse up. There are so many variables involved that, even if a factor under test were measurable (and most are not), the influence of any one factor is probably impossible to show. How to measure degrees of asphyxia, bleeding, or pulmonary edema at racing exercise may well be an insoluble problem.
Treadmill stress tests, unfortunately, do not simulate the stress of racing. On the treadmill, horses do not have a standing start, gallop as fast, turn corners, carry a whip-armed jockey, have their heads flexed, run on a soft, clinging, or wet surface, battle against a wall of air equivalent to a headwind of not less than 37 miles per hour and often stronger, experience high ambient temperatures and humidity, get jostled by other horses, or have mud and dirt thrown in their faces.
In short, they do less physical work. Proof of this comes from the fact that few, if any, of treadmill horses bleed. Even the measuring of racing performance itself is nothing like as easy a problem as it may at first appear, especially so in a sport where the difference between success and failure can be as little as one-fifth of a second. How would one introduce correction factors for such variables as wind, weather, jockeys, and state of the ground, quite apart from any day-to-day variations in a horses will to win? My conclusion is that the measuring of racing performance is an insoluble problem.
But absence of evidence is not evidence of absence. Just because there is no proven evidence that Lasix improves performance, we cannot assume that it does not. Similarly, just because there is no evidence of a correlation between nonfatal episodes of AIPE and racing performance, we are not entitled to conclude that pulmonary edema does not affect performance.
There is proof enough that AIPE can affect performance when a horse dies from this condition on a racetrack. We should certainly not comfort ourselves with the notion that it is normal for a racehorse to bleed (develop pulmonary edema).
It is true to say that, within the racing Thoroughbred population, pulmonary edema is statistically common and might therefore be considered statistically to be the norm, or average for this particular population, but it is not true to say that it is biologically normal for the horse as a species to develop pulmonary edema at exercise.
The presence of blood-stained edema fluid in the airway is not physiological. The air sacs of the mammalian lung should be filled with air, not fluid. Whether human or equine, any athlete that develops pulmonary edema is likely to be a less successful performer than one with a healthy pair of lungs. This argument from first principles surely justifies us in assuming that pulmonary edema does affect performance.
Kelley characterizes EIPH (AIPE) as an unavoidable consequence of competitive training and racing, and, with regret, I agree. I see no possibility of ever eliminating AIPE when Thoroughbreds are raced. What I think is possible, however, is a reduction in its prevalence and severity. This will take time, care, and effort on the part of breeders, owners, trainers, jockeys, and veterinarians.
The first step in improving the welfare of the horse in this respect, and in initiating damage limitation for the racing industry in general, will be a willingness on the part of everyone concerned to consider the possibility that many instances of poor performances, some racetrack breakdowns (fractures, strained tendons, and ligaments), and some deaths are caused by asphyxia.

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W. Robert Cook, Ph.D., is emeritus professor of surgery at Tufts Universitys School of Veterinary Medicine in North Grafton, Massachusetts. He has written extensively on upper-airway obstructions.