Equine exertional rhabdomyolysis
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Equine exertional rhabdomyolysis (ER, also known as tying up, azoturia, or Monday morning disease) is a syndrome that damages the muscle tissue in horses. It is usually due to overfeeding a horse carbohydrates and appears to have a genetic link.
Causes and process of EREdit
Beyond a highly probable hereditary factor, there does not seem to be a single cause that triggers ER in horses. Exercise is seen in every case, but exercise is always accompanied by another factor. It is likely that several factors must act together in order to cause an ER attack.
Other possible factors include:
- The overfeeding of non-structural carbohydrates (grain and pellets, for example)
- Poor conditioning or fitness, sudden increase of workload
- The work of a horse after a period of rest, if the concentrate ration was not reduced
- Electrolyte or mineral imbalances, especially seen with potassium
- A deficiency in selenium or vitamin E
- Imbalance of hormones, including the reproductive hormones in nervous fillies and mares and thyroid hormones in horses with hypothyroidism
- Wet, cold, or windy weather conditions
The more factors that are present, the greater the likelihood that the horse will develop ER. However, the most common cause of ER is an imbalance between the animal's diet and his workload, especially when he has a high-grain diet.
ER occurs when there is an inadequate flow of blood to the muscles of an exercising horse. The muscle cells, lacking in oxygen, begin to function anaerobically to produce the needed ATP. The anaerobic work creates a buildup of waste products, acid, and heat. This subsequently alters the cell by preventing the cell's enzymes from functioning and the myofilaments from efficiently contracting. The cell membranes may then be damaged if the horse is forced to continue work, which allows muscle enzymes and myoglobin to leak into the bloodstream.
The body builds up a store of glycogen from converted carbohydrates in muscle cells. Glycogen, a fuel used by muscles for energy, is depleted during work and restocked when a horse rests. Oxygen-carrying blood metabolizes glycogen, but the blood can not flow fast enough to metabolise the excess stored glycogen. The glycogen that is not metabolized aerobically (by the oxygenated blood) must then be metabolized anaerobically, which then creates the cell waste products and heat, and ER has begun. A horse on a high-grain diet with little work collects more glycogen in its muscles than it can use efficiently when exercise begins, which is why horses on a high-grain diet are more likely to develop ER.
Proper conditioning can help prevent ER, as it promotes the growth of capillaries in muscles and the number of enzymes used for energy production in muscle cells. However, improvement in these areas can take several weeks. Thus, ER is more common in horses that are only worked sporadically or lightly, and in horses just beginning an exercise regimen.
A common misconception is that ER is caused by the buildup of lactic acid. Lactate is not a waste product for a cell, but a fuel, used when the cell's oxygen supply is insufficient. Lactate does not damage a cell, but is rather a byproduct of the true cause of cell damage: inadequate blood supply and altered cell function. Lactate naturally builds up in an exercising horse without harming the muscle cells, and is metabolized within an hour afterward.
The pain is caused by the inadequate blood flow to the muscle tissue, the inflammation from the resulting cell damage, and the release of cell contents. Muscle spasms, caused by the lack of blood to the muscle tissue, are also painful.
A horse developing ER will usually begin showing signs right after the beginning of exercise, although for mild cases, signs may not be seen until after the horse is cooled out. Signs include reluctance to move, stiffness or shortened gait when the animal is forced to move, and muscle spasms or cramps, with hard, painful muscles (especially the hindquarters) when palpated. If an observer is unfamiliar with ER, initial symptoms may appear to be tiredness or perhaps lameness but the condition is far more complex.
Signs of a severe bout of ER may include: reluctance to move, sweating, elevated heart and respiratory rates as a result of the pain, anxious expression, shifting of weight from side to side, standing hunched and tense, passing reddish-brown urine, dehydration, shock, and inability to rise. Usually there is a correlation between how long it takes the signs to be seen and how severe the bout of ER is, with the more severe bouts of ER displaying signs right after work has begun.
If signs of ER are seen, the horse should not be moved. Movement can cause further muscle damage. If the animal is far from the barn, it is best to trailer him back rather than move him.
Mild or moderate casesEdit
The horse should receive several days of NSAIDs, rest, and grain or pellets should be withheld. To improve blood flow to the muscles and help to with muscle spasms, heat therapy and Equine Massage may be beneficial, as well as hand-walking if the horse is comfortable walking. Turn-out in a pasture or paddock will encourage movement. A horse should be moving normally within 12–36 hours after the attack.
A horse may need fluids, especially if his urine is colored, the horse is receiving NSAIDs, or if he is dehydrated. Fluids will increase the production of urine that will in turn help flush out the excess, and potentially damaging, myoglobin from the kidneys and will reduce NSAID-produced kidney damage. Fluids should be administered until the urine is clear, which usually takes from a few hours to a few days.
Vasodilators, such as acepromazine, can help improve blood flow to the muscles. However, the owner should only give acepromazine if it is prescribed by the horse's veterinarian, as it can lower the animal's blood pressure and can cause collapse in a severely dehydrated horse. The human drug dantrolene is sometimes given to alleviate the muscle spasms and prevent further degeneration of muscle tissue.
Except to get a horse to his stall, a horse showing signs of severe ER should not be moved until he is comfortable enough to do so eagerly. This may take several days. After this point, it is important to either hand-walk the horse a few times each day, or provide him with a few hours of turnout in a pasture or paddock.
Returning the animal to workEdit
A horse may be returned to work after it is no longer showing signs of ER, and is no longer on NSAIDs—which can hide signs of another bout of ER. If NSAIDs are needed to keep the horse comfortable, or if the horse is reluctant to continue work, the animal is not yet ready for a return to his regular training program. Blood tests should reveal that the horse's CPK concentration and AST levels are normal before the horse is returned to work.
To begin bringing the horse back, he should be exercised at the walk and trot for 10–15 minutes at least once every day. This regimen will gradually be increased as the horse becomes more willing. For a moderate or severe bout of ER, it may take 4–6 weeks to return to the regular program. It is important not to push the horse more than he is ready or a relapse may occur. A second bout of ER is usually more severe than the first, not only taking the horse out of training for a longer time, but possibly causing permanent muscle damage.
Grain is gradually reintroduced as exercise resumes, but grain can contribute to the development of ER.
For mild to moderate cases of ER, the prognosis is excellent, with the horse successfully returning to its former level of competition. However, if the vet's recommendations for preventing ER are not followed, ER may likely recur.
Horses who experience a severe case of ER (the muscle degeneration is significant) are less likely to return to their previous level of competition, as fibrosis may have occurred, which would result in loss of muscle function. The prognosis is guarded for these horses.
Reducing any extra energy in a horse's diet is essential to maintaining a horse that has experienced ER. Decreasing carbohydrates and increasing the daily intake of hay or pasture can usually accomplish this. Grain may need to be cut out altogether and replaced by a substitute, such as vegetable oil, to meet the individual energy needs of the horse.
Grain should be reduced or removed from a horse's ration on days when he cannot be worked.
Proper conditioning is very important in preventing ER. Beginning with a base of long, slow distance work will ensure that the horse has a foundation before proceeding on to more strenuous work. The horse should always have a 10-minute warm-up at the walk and trot before more strenuous work is begun, and should always have a proper cool down of 10 minutes.
It is best that a horse receive exercise every day, or possibly twice a day, to prevent the recurrence of ER. If possible, avoid breaks in the horse's exercise schedule. Training, riding, driving, longeing, or turnout are all suitable.
Daily pasture turnout is ideal for horses likely to suffer from ER, as it provides exercise and adds roughage to the animal's diet.
Supplements and drugsEdit
As with any supplements and drugs, it is best to confer with a veterinarian as to the recommended dosages. Some drugs are not allowed in competition and may need to be withheld a few days before.
Adding potassium and salt to the diet may be beneficial to horses that suffer from recurrent bouts of ER. Horses in hard training may need a vitamin E supplement, as their requirements are higher than horses in more moderate work. The horse may also be deficient in selenium, and need a feed in supplement. Selenium can be dangerous if overfed, so it is best to have a blood test to confirm that the horse is in need of supplemental selenium.
Thyroid hormone supplementation is often beneficial for horses with low thyroid activity (only do so if the horse has been diagnosed with hypothyroidism).
Other drugs that have been used with success include phenytoin, dantrolene, and dimetyl glycine.
Bicarbonate and NSAIDs are of no use in preventing ER.
- King, Christine & Mansmann, Richard, VMD, PhD. Equine Lameness. Copyright Equine Research (1997). Pages 357–368.