A trail of blood. . .

The evidential cause of exercise-induced pulmonary hemorrhage leads to questions about the use of LasixDocuments related to the training and racing of horses make it obvious that exercise-induced pulmonary hemorrhage (EIPH) syndrome was experienced early on, and the drawing of horses the limitation of their hay consumption in the 6-to-12 hours prior to racingwas deemed necessary to a good effort and to avoid bleeding.

1. In my own experience over the last 50 years in racing, I have observed that:
   
2. Speed over short distances seems to occasion a higher number of patent bleeders.
   
3. Reports from veterinarians who practice among racing Quarter horses and Thoroughbreds suggest that patent bleeders are more numerous among Quarter horses.
   
4. EIPH is rare in heavy draft horses, but it is observed most frequently in pulling contests, stump removal, and other endeavors which require the animals to repeatedly jerk their load forward in a to-and-fro rocking motion.
   
5. Grand Prix jumpers at the highest levels of competition rarely bleed but, when they do, it is most often over a lengthy course and after one or more jump-offs; Conversely:
   
6. Rated contests over a distance of ground occasioned fewer patent bleeders.
   
7. The incidence of patent bleeding in steeplechasers and hunt meet horses is less than in horses racing on the flat.
   
8. Thoroughbreds, even those winnowed out of racing because of bleeding, rarely bleed overtly when recycled in hunting, eventing, and other non-racing pursuits, including the Olympics. (My experience with polo ponies is limited, so I have no cogent observation to report.)
   
9. The incidence of patent bleeders in Standardbred racehorses is less than in Thoroughbred racehorses.
   
10. Patent bleeding is unknown in endurance horse competitions.
    

An examination of the above criteria and our experience in practice and in training indicates that bleeding is often related to the character of the use to which the horse is put.
The question is, why?
Studies of motion and respiration show us that when a horse gallops, the respiratory cycle is related to the galloping action. Inhalation, lung filling, and chest expansion takes place when the front feet hit the ground and the skeletal frame extends. Exhalation takes place when the front feet leave the ground and the skeletal frame contracts. The parts of the body related to motion and respiration are active and synchronized. In that motion/respiration cycle, horses will sometimes vary the relationship of respiration to motion, but the action appears to remain synchronized. A respiration-to-motion ratio of 1:1, 1:2, and sometimes 1:3 has been observed.
There is, however, within the horses abdomen a passive, free-floating intestinal mass suspended from the roof of the abdomen by suspensory ligaments (mesenteric, colic, etc.). At the relaxed canter (lope) and slow hand gallop from a fluid transition from the walk or trot, the mass is seen to move in relative synchronism with the skeletal motion and respiratory sequence.
In the contests which require a crouch, a quick spring from the stall starting gate and all-out speed from the start, a to-and-fro tugging motion, as in the heavy draft horse, or the back, up, and over of the Grand Prix jumper, the synchronization of the frame and respiration with the free surging motion of the intestinal mass is sometimes lost. The intestinal mass moves to and fro in a piston-like surging movement, forcing the flexible diaphragm repeatedly forward, laterad, and upward into the chest cavity.
The diaphragm is a pliable, thin wall of muscle which separates the chest (thoracic) cavitywhich contains the heart and lungsfrom the abdominal cavity, which contains the visceral mass. The caudal and dorso-caudal areas of the lungs are in intimate free contact with the thoracic side of the diaphragm and the chest wall.
When the unsynchronized action of the intestinal mass surges repeatedly against the flexible diaphragm, it momentarily forces the diaphragm to extend further into the chest cavity in a forward, somewhat laterad, and upward thrust just as the chest wall contracts inward, slightly forward, and upward on expiration. At that instant, the thoracic-phrenic angle narrows so that the caudal portions of the lungs are impinged momentarily between the diaphragm and chest wall, irritating and bruising these caudal outer reaches of the lungs.
In those remote caudal (posterior) portions of the lungs, the alveoli (air sacs) are much smaller and the parenchyma (tissue between the alveoli) are more dense than in the central and anterior portions of the lungs, where the alveoli are many times larger and the parenchyma correspondingly less dense. It is in those anterior and central portions of the lungs where most of the ventilation and perfusion (gaseous exchange) takes place, which has been estimated at about 94% of total exchange. This indicates that the insulted caudal portions of the lungs are of relatively little or of no physiologic importance to the normal respiration of the racing horse.
It appears that the histologically different caudal portions of the lungs are able to cope to a degree with the natural trauma of certain racing efforts, but those areas do suffer inflammation, bruising, and rupture of the minor blood vessels in the parenchyma and in those surrounding the thin-walled alveoli, causing small amounts of blood to seep into the alveoli. In some cases, the bleeding is so slight that it is confined to the alveoli and, in others, some traces of blood ascend from the alveoli into the bronchial treeand sometimes to the trachea and upper respiratory passages. In cases which do not show patent blood, the microscopic evaluations of washings from the tract indicate the presence of blood, confirming that all racehorses bleed. Only the degree of bleeding is different.
The gross post-mortem findings reflect the area and extent of the insult to the lung and, in most cases, the blue discoloration which is indicative of bruising can be observed on both the inner phrenic side and the outer thoracic side of the lung, suggesting impingement in the repeatedly narrowed thoracic-phrenic angle. The much milder discoloration on the hilum (dorsal side) of the lung may result from referred upward pressure, and in that area the microscopic lesions are commensurate with repeated trauma. The observed enlargement of the subpleural vasculature would seem to be the predictable response to recurrent inflammation and tissue damage in the areas of insult. We have much to learn about the histological (tissue) changes which take place in the area of insult in order to have a better understanding of the problem and, to that end, steps have been taken.

Observations on- and off-track

This sequence of events explains many of the things we witness on and off the track.

1. It suggests why most horses do not show any external bleeding at all. The site of the bleeding is remote and the bleeding inconsequential.
   
2. It also suggests why some horses do not show any blood until an hour or two after the race. It is a long journey from the most remote alveoli in the caudal lung to the nostrils.
   
3. It explains why so many horses treated with Lasix continue to show blood on scoping post-race. Lasix cannot prevent or control the trauma which is believed to be the source of EIPH. Dr. John Pascoe, a very capable investigator and professor of surgery at the University of California, states that, At least 50% of furosemide-treated horses continue to experience EIPH and, while furosemide may decrease the amount of bleeding, it is not effective in preventing EIPH in most horses.
   
4. It explains why so many horses which showed patent blood post-race had been able to race wellto in some cases winand were otherwise clinically asymptomatic.
   
5. It explains why EIPH was never a problem in American racing (and has never been a concern abroad) until the bronchoscope came into broad use and the enhancing effects of Lasix needed the appearance of legitimacy.
   
6. It suggests the circumstances under which the heavy draft horses and the Grand Prix jumpers sometimes demonstrate EIPH.
   
7. It explains why very few horses bleed when recast in strenuous nonracing roles.
   
8. It explains why withdrawing hay for 6-to-12 hours or longer prerace, thereby decreasing the size and weight of the intestinal mass, helps to decrease the severity of the insult and the incidence of patent EIPH.
   
9. It explains why mild exercise on the track on race day, wherein the horse might blow out one-sixteenth or one-eighth of a mile, may assist in two ways. Exercise usually stimulates defecation, thereby reducing the weight and volume of the intestinal mass. The outing might also serve to lessen hypertension, both physical and psychological, for it helps to preserve the stable routine of a non-racing day in those horses which fret and are otherwise adversely affected by changes in their daily routine.
   

In considering EIPH, there is a wide variation in the incidence quoted and observed. This is understandable for three reasons; namely, the degree of EIPH is commensurate with the degree of insult, the relative degree of lost synchronization, and the weight, volume, and frequency of the insulting intestinal mass. The second factor is that endoscopic evaluation is, in many instances, more subjective than objective and all too often reflects not the fact but the feeling which the observer chooses to impart. Thirdly, only a segment of the horses racing have been scoped either prerace or post-race, and there are no comprehensive records. In truth, we do not know the incidence of EIPH because clinical symptoms are dependent upon the degree of insult and, in some instances, the degree of insult is so minor that no clinical symptoms are observed. As previously stated, good evidence indicates that all racehorses bleed; only the degree is different.
In reports on EIPH, figures are often quoted. Realistically, the only figures which have had any relevancy come from the patent bleeders which are observed and recorded on-track as part of the regulatory and chart-making processes. They may, however, not be as meaningful as we once thought, for the simple reason that some horses which were thought to suffer respiratory disease are, in fact, experiencing only EIPH.
As we further investigate this whole matter, it becomes obvious that we have three individual circumstances:

1. Simple exercise-induced pulmonary hemorrhage (EIPH), which, as we have suggested, is a natural, circumstantial response to all racing efforts. It is traumatic in nature, self-limiting, and heals spontaneously without the need for treatment. Time is the best ally. The growing bulk of evidence substantiates the fact that all racehorses experience some alveolar bleeding.
   
2. Patent pulmonary hemorrhage (PPH), which reveals patent blood from the nostrils initiated by any one or a multiple of causes hereinafter outlined. It requires definitive diagnosis and rational treatment.
   
3. Composite bleeding in which the horse may be experiencing both EIPH and some form of PPH.
   

Among the many other circumstances which may precipitate the appearance of blood in the respiratory tract are: hypertension, allergy, clinical and subclinical bronchiolitis previously mentioned; infections in the respiratory tract and/or gutteral pouches; erosions of the nasal, laryngeal, tracheal, and/or bronchial mucosa; neoplasms, both malignant and benign, in the lungs and/or thoracic cavity; and trauma, etc. Each and all require definitive diagnosis, rational treatment, and comprehensive management.
Early in my appearance in racing, horses were drawn as a regular routine, and virtually all horses went out on the track early on race day for light exercise and were often blown out. It was those experiences, coupled with racings pernicious drug culture, which have fueled my continuing personal interest. The spark came in the summer of 1993 when I witnessed a weight-pulling contest in which the wheeler of the struggling team bled and the owner told me, The only time he bleeds is when I compete with him or pull stumps. It doesnt seem to bother him in his other work. And we dont do anything to treat it because it takes care of itself. Other guys have the same problem, if it is a problem.
These observations will, I hope, prompt further investigation. In the meantime, we must be guided by objective management, good training practices, and rational treatment, which means definitive treatment predicated on sound diagnosis.
The continued administration of Lasix for performance enhancement in the guise of definitive treatment is without merit, ethically questionable, and a major destructive force in American racing.
The very variable nature of the insult which causes EIPH explains why an understanding of the pathogenesis has been so elusive. It should be obvious to all, however, that the sequence and intensity of the insult and the resultant inflammation, trauma, and bleeding vary from horse to horse, and within the same horse from outing to outing. The severity of the hemorrhage appears to be related to the degree of lost synchronization, the size and weight of the offending intestinal mass, the frequency and intensity of the insult, and other less obvious contributing factors which, in all likelihood, include body type, level of conditioning, athletic quality of the individuals natural galloping motion, etc.
The empirical use of Lasix is not only without merit but may be dangerous, for it lulls the patients principles into complacency while the true nature of the horses complaint is left undetected and unresolved, his racing potential unachieved.
We must bear uppermost in mind that:

1. Lasix does not prevent trauma, inflammation, or contusion.
   
2. It is not an anticoagulant as some have suggested.
   
3. The amount of blood lost in most uncomplicated EIPH episodes is inconsequential.
   
4. The diuresis initiated by prerace Lasix does cause some loss of electrolytes and total body fluid at the time of the race when those factors are most needed.
   
5. All body processes function on the system of osmosisthe passage of a less dense fluid through a more dense fluid or membrane. Osmosis can only operate efficiently when the fluid and electrolytic balances in the blood are at optimum levels.
   
6. The diuresis caused by Lasix upsets those delicate balances. The body tries to respond in order to reestablish the optimum levels in the blood and to achieve equistasis by calling on contributions from other body tissues, thereby leaving the donor tissues depleted in whole or in part.
   
7. It is this tampering with the horses normal body function which adversely affects the racing performance of many horses to which Lasix has been administered prerace. This is especially true in the finely tuned stakes horse. The saddest part of the whole problem is that there has been very little comprehensive, clinical monitoring of the Lasix-treated horses in racing. Some get the one- or two-race enhancing effect of Lasix, while others suffer serious challenges to their physiologic balances and racing performance. The untoward physiologic changes sometimes effected by Lasix are most often subtlevery subtlebut very insidious. So far as performance is concerned, Lasix has proven to be a double-edged sword, for it often diminishes performance.
   

There is also some less known research that suggests that Lasix may release any one of several different prostaglandins from the kidney, varying from horse to horse, which suggests a variability in the responses elicited by Lasix in different horses.

Quality of the evidence adduced
Diagnosis is an adventure in discovery and is based on the clinical evidence adduced and supported by laboratory finding and, when possible, by post-mortem findings in horses similarly afflicted, and the attitudes and physical performance of the patient itself.
The field evidence which we have adduced herein to show the sequence of events which cause EIPH are:

1. Prima facie.
   
2. Clear and compelling.
   
3. Consistent with the published findings of the major investigators.
   
4. Consistent with our total experience and records on-track and off.
   

Investigation needed
My hope in revealing these observations and conclusions is to stimulate additional investigation within the research community, the profession in the field, and the objective elements in racing so that we can put this whole matter of EIPH and race-day medication into proper perspective to the future best interests of racing, the horse which makes it possible, and the veterinary profession. I will be the first to recognize that my own thesis outlined herein begs additional investigation.
This has been a solo endeavor based on personal experience and the gnawing need to know.

Racing Retreat
In the coming weeks and months, we will assemble the best and most experienced minds to consider EIPH as the variable response to a racing effort. It will be the opening challenge of an investigative endeavor which we have named Racing Retreat. Racing Retreat is not another organization in racing. We have too many organizations in racing which spend too much time and too much money in their administration, empire-building advertising, and self-aggrandizement in pursuit of selfish goals.
At this writing, we are in the process of incorporating, which provides for the statutory executive positions only, which will be served on a pro bono basis. In pursuit of its investigative goals, Racing Retreat will seek the input and cooperation of persons from major organizations in the sport, including, but not limited to, the Jockey Club, state commissions, American Association of Equine Practitioners, American Horse Council, and other service groups within racing which have demonstrated active altruism for the sport. The desired objective of Racing Retreat cannot be achieved by persons and organizations which are motivated by selfish interests.
Following the investigation of EIPH and race-day medication, Racing Retreat will examine the lost image of racing and its causes (both intrinsic and extrinsic), which will be followed by the formulation of doable recommendations for its restoration. Next will come racing officials. Then the use of the regulatory tools held by the commissions and racing associations, and other questions will be considered as the need arises.
In the course of our invitations to participants, the number will, of necessity, be limited to proven performers in the particular field under investigation. These will be intensive think tank sessions to investigate the question at hand to the ultimate benefit of the racing sport and the Thoroughbred.

Recognition
In presenting these personal observations, I would be amiss if I did not recognize the fine research work on motion, the piston effect, respiration, and/or EIPH which has been conducted and documented by Drs. Lawrence Soma, Corinne R. Sweeney, and Jill Beech at the University of Pennsylvania; Dr. John Pascoe, Dr. John B. West, and their coworkers at the University of California; Dr. Jim Rooney at the University of Kentucky; and a score of other dedicated investigators here and abroad, and the equally dedicated practitioners in the field who have supported their research efforts.

---

Dr. Joseph C. ODea, DVM, a former president of the American Association of Equine Practitioners, is a state steward at Finger Lakes in upstate New York.