Azoturia, or Equine Rhabdomyelosis, is a condition that affects the muscles of horses, ranging from stiffness and mild cramps to the horse becoming unable to stand with discoloured urine. Terminology for the disease is variable and includes Monday Morning Disease, Tying-Up, Azoturia, Paralytic Myoglobinuria, Myositis and Setfast. It is unlikely that a single process can explain all the clinical types, but the term rhabdomyelosis is often though to be the more accurate description and it is this term that shall be used for this discussion.

Equine Rhabdomyelosis can affect any horse of any age but is much more common in fillies and mares than geldings and stallions. Young animals tend to have one or two episodes and then no further problems, which can lead to unfounded claims of successful treatment. It can affect just one individual in a group which are all under the same management regime and severity and frequency are highly variable.

What Causes It?
The basic mechanism of the disease is poorly understood and it is likely that the predisposing and triggering factor(s) are slightly different for each animal. Possible predisposing factors include:

Carbohydrate Overloading -The classical presentation is the draught horse in work that is rested or the weekend on full feed, then when the horse returns to work several days later it suffers an attack of the disease. It is thought that muscle glycogen accumulates during the rest period and when used during exercise it produces excessive lactic acid. This causes local tissue damage and constriction of the blood vessels, resulting in decreased blood flow to the tissues and further reduction in lactic acid removal.
Local Hypoxia - Certain types of muscle fibres are larger, have greater glycogen stores and fewer surrounding blood vessels than others. Local hypoxia (lack of oxygen supplied by the blood) may increase the lactic acid production in these fibres. However equine rhabdomyelosis normally occurs at the start of exercise, when these fibres would not yet be working and the condition is not usually seen in horses with other conditions causing impaired circulation
Thiamine Deficiency - Thiamine (one of the B Group of Vitamins) acts in the metabolism of waste products from muscle activity. A deficiency, therefore, could lead to a build up of these waste products and hence, lactic acid.
Vitamin E and Selenium Deficiency - This theory is based on reports of success at preventing further episodes following supplementation. Clinical trials have failed to confirm this.
Hormonal Disturbances - Reproductive hormones, thyroid hormones and cortisol have all been implicated in equine rhabdomyelosis, but there is still considerable debate.
Electrolyte Imbalances - Studies from UK racing stables have indicated that chronic sodium and/or potassium deficiencies may be involved in chronic equine rhabdomyelosis. This is difficult to detect routinely so a special urine test is used to assess levels.
Viral Causes - Muscle involvement following viral disease (e.g. influenza) has been investigated but the associated muscle pain (myalgia) is generally considered to be a separate and distinct disease process.
History and Clinical Signs
Signs vary widely depending on the extent of muscle damage.

Mild cases simply involve stiffness and shuffling hindlimb gait. There may be pain over the gluteal muscles (hindquarters). This form is more common in horses receiving only small amounts of exercise.
Some cases are a result of stressful triggering factors. This is common in younger horses and will often have a behavioural component.
In some very mild cases, poor performance is the only manifestation of the disease.
Severe cases may include signs of severe pain with sweating, increased pulse rate, increased respiration rate and reluctance to move. There may be hard and painful locomotor muscles, red urine (due to the presence of muscle breakdown products) and even recumbency. This often transpires in horses during endurance training where significant fluid and electrolyte alterations occur.
Diagnostic Tests
Diagnosis is sometimes based on clinical signs alone but with mild cases it is important to carry out further tests. These may include:

Serum Muscle Enzymes - the blood can be tested to look for abnormal values of these substances, which are produced when muscle has been damaged. 
Urinary Electrolyte Testing - Can be used to detect electrolyte abnormalities, which can predispose to the disease and it can also be used to monitor management and treatment. 
Urinary Testing - like the blood, the urine can be tested for products associated with the breakdown of muscle tissue.
Muscle biopsy - this involves a small sample of muscle which is removed under local anaesthesia and sedation and examined under the microscope for abnormalities.
The aims of treatment are to limit further muscle damage, to reduce pain and anxiety, to maintain fluid and electrolyte balance, and to prevent kidney failure. Of all the treatment options, few have been examined critically for their effectiveness but the following are a broad outline of the treatments vets can use.


Thiamine, vitamin E and selenium have been used widely in practice, and some evidence suggests they are useful in improving recovery.
Non-steroidal anti-inflammatory drugs (NSAIDs) such as flunixin and phenylbutazone may be used to control the pain
Some drugs, such as Acepromazine (ACP) can be used to increase blood flow and alleviate muscle spasm. 
3-4 days box rest is indicated, followed by a gradual return to exercise.
Walking mildly affected horses is sometimes effective, and most will recover without further treatment.
Lowering the training intensity and decreasing the grain in the diet is also very useful.

Fluid therapy is vital to relieve shock and to prevent renal failure. This can be oral, but in very severe cases, will be used intravenously.
Steroids may be used during initial acute stages
NSAIDs may once again be indicated to relieve pain.
If there is severe pain, other, stronger painkillers may be used.

Substances which alter the metabolism of minerals in the blood may be used.
If urine electrolyte tests indicate very low values of Sodium or Potassium, supplementation may be required.
Since equine rhabdomyelosis is usually associated with periods of exercise followed by rest and then exercise again, it is sensible to investigate the horse’s management. The first stage of any preventative regime is to ensure a well-balanced and controlled exercise and feeding programme. A balanced diet should be fed according to the workload, and during periods of inactivity feed intake should be reduced. Regular exercise appears to be of benefit, prolonged turnout to grass can also be of value and some benefit is gained from being ridden whilst out at grass. Anecdotally, a blanket over the lumbar area in cold weather has been recommended.

Preventative agents have been suggested and are broadly based on whatever is thought to be the underlying cause of the problem. Some are based on a few clinical successes. However, few effective clinical trials have been carried out. These include sodium bicarbonate, vitamin E and selenium, Dantrolene, thyroxine, thiamine, acepromazine, phenytoin, diazepam and electrolytes.

 From Equine Hospital

it is so often difficult to determine why a horse becomes suddenly susceptible to muscle damage. However, the first thing to note is that your horse was ill or off colour before the attack of azoturia. It is possible that he had a mild virus problem, causing the anaemia and lack of energy. It is known, for example, that herpes virus infection can predispose horses to azoturia, and so it would seem possible that a virus of some type might have been involved here in the past.

I would therefore recommend that, as well as supplementing with iron, you give an immune stimulating mix of herbs containing, for example, echinacea, or tropical herbs. For anaemia you should also consider a course of iron which is chelated, making it easier for the body to absorb.

As for the azoturia attack, it is often difficult to know whether it is the damage that has already been done that is predisposing your horse to further problems, or whether it is the root cause of the first attack that is still present. It would seems to me that the latter is true.

Some azoturia is congenital, meaning that there is a natural tendency in the horse's genes to always get the disease.

In such situations there are drugs which can help stabilise the cell membranes in the muscle which is getting damaged.

Your own vet can discuss these matters with you. However, I think it is likely that other alternatives may be more useful. You should consider the use of chelated mineral supplements that increase the supply of magnesium, potassium and calcium for your horse. In addition a supply of fenugreek seeds can help to protect muscles and prevent further damage and a supply of vitamin E and selenium could be important.  Some herbs have potent antioxidant action and can also be extremely useful.

Prevention of Azoturia
Regular exercise with warming up and cooling down periods together with only the necessary amount of feed will help to prevent Azoturia.

The Equine

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