- Pets and Animals
HORSE HEALTH; Tying-up and Azoturia
An Introduction to Equine Metabolic Disorders
Tying-Up Syndrome and Azoturia are Complex Metabolic Disorders called Exertional Myopathy or Myositis. Myopathies, like Exertional Myopathy, are disorders that affect the muscles of the horse. Myositis is inflammation of muscle. Metabolic diseases are typically acquired by the horse but may be inherited. Metabolic diseases affect energy production and/or create tissue damage in tissues necessary for survival. Azoturia and Tying-Up Syndrome are specifically referred to as Exertional Rhabdomyolysis because they affect the skeletal muscles (rhabdomyo-) and these skeletal muscles are being broke down (-lysis). Exertional Rhabdomyolysys is the most common muscle problem in horses.
Other Myopathies include Muscle Atrophy, a myogenic (muscle, genetic) type such as Cushing’s Disease (also known as PPID or Pituitary Pars Intermedia Dysfunction) or a neurogenic (nerve) type such as Equine Protozoal Myelitis (EPM), and Muscle Fasciculation (muscle twitch) such as Hyperkalemic Periodic Paralysis (HyPP) (also known as Hyperkalemic Periodic Paresis) associated with Quarter Horses of the Impressive line. Another Complex Metabolic Disorder is Insulin Resistance.
Other Equine Metabolic Disorders:
- Cushing's Disease (PPID)
- Insulin Resistance
- Exertional Rhabdomyolysis
Names and Forms Associated with Tying-up and Azoturia
Tying-Up is a less severe form of Exertional Rhabdomyolysis and is milder than Azoturia. It may also be known as:
- Monday Morning Sickness (may be used interchangeably with Azoturia)
- Monday Morning Disease (may be used interchangeably with Azoturia)
- Cording Up
Azoturia is a more severe form of Exertional Rhabodomyolysis. It may also be referred to as:
- Paralytic Myoglobinuria
- Black Water Disease
- Set Fast
Exertional Rhabdomyolysis in general is categorized as being either Sporadic or Chronic:
- Sporadic Exertional Rhabdomyolysis (sporadic meaning single or infrequent episodes)
- Chronic Exertional Rhabdomyolysis (chronic meaning repeated episodes)
Chronic Exertional Rhabdomyolysis can be sub-categorized into the following forms:
- Polysaccharide Storage Myopathy (PSSM) or Equine Polysaccharide Storage Myopathy (EPSM)
- Recurrent Exertional Rhabdomyolysis (RER)
Anatomical Systems Involved with Exertional Rhabdomyolysis
Digestive as a causative tract, nutritionally and possibly toxically
Circulatory as a carrier of both between the digestive to muscle and the muscle to urinary
Urinary as being possibly affected in the process of the disease and symptoms noticed
Possible Symptoms of a Horse that is Tying-Up or is Developing Azoturia
In any case the horse is in distress.
During Tying-Up, the milder form, the horse may show signs early on during a workout or may appear to move normal during this phase but then may begin to develop symptoms, possibly in the cooling out period after a vigorous exercise routine:
- Becoming sluggish
- Movement is not free with motion becoming stilted, especially behind
- Developing a stiff back, especially over the loin and croup
- Profuse sweating, dripping sweat even while standing still, may feel thick and sticky and smell sweet (but the horse may not sweat)
Horse may show symptoms similar to or that may even be thought to have the following:
- Lameness (unsoundness)
- Colic (belly pain)
- Laminitis (inflammation of the lamina, the sensitive structures of hoof, pain and heat in the feet)
- Tetanus (Lockjaw, a neurological disease causing paralysis)
Episodes of Azoturia are quicker to onset; hence the name Set Fast, usually within 15 minutes from the beginning of exercise and may mimic signs in Tying-Up or continue into:
- Very firm and hard muscles (femoral, gluteal, and iliopsoas) over the loin (lumbar) and croup (sacral) that may be painful when palpated or during movement
- Weakness in the hind limbs leading to un-coordinated action
- Reluctance to move, only moves when forced to
- Elevated pulse rate
- Elevated respiratory rate
- Urinating stance but unsuccessfully urinating
- Dehydrated (the pinch test on the neck indicates this, by the skin remaining tented)
Severe Azoturia may progress into a horse that:
- Has Myoglobinuria, dark red or brown colored urine; this is how it acquired the name Black Water Disease
- May lay down, unwilling or unable to rise
- May sit in a stance similar to a dog
- Has permanent lameness – due to muscle atrophy
Predisposing Factors in Horses that Develop Exertional Rhabdomyolysis
A horse that has had an episode of Tying-Up or Azoturia before is prone to it reoccurring. It is most prevalent after a rest period of a day or a few days.
Sporadic Exertional Rhabdomyolysis: (as Tying-up or Azoturia)
- Any breed, sex or age
- Exercised beyond conditioned level
- Overexerted into exhaustion, dehydration, or hyperthermia (overheating)
- Worked during environmental extremes of hot, hot and humid, cold or cold and damp
- Worked while recovering from a respiratory infection (bacterial like Strangles or viral like Influenza or possibly even herpes)
- Trauma or struggle, like an accident or trying to free self from being caught
Polysaccharide Storage Myopathy form of Chronic Exertional Rhabdomyolysis: (usually as Azoturia)
- Easy keeping, typically calmer, well muscled breeds such as Quarter Horses, Drafts like Belgian or Percheron and Warmbloods
- During retraining initiated after an extended idle period
- At the initial state of being put into training
- Parentage passes on genetic mutation
Recurrent Exertional Rhabdomyolysis form of Chronic Exertional Rhabdomyolysis: (usually as Tying-up)
- Hard keeping, usually hotter, lighter breeds like Arabians, Standardbreds and Thoroughbreds
- High-strung nervous temperament
- Mares and fillies, especially if hormonal
- Fit horses, like endurance, polo and racing
- Excessive mental or physical stress
- Parentage passes on genetic abnormalities
An Introduction to Carbohydrates and Normal Energy Processes
Carbohydrates are found in an abundance of horse feeds like hays, grains, and pasture grasses. Carbohydrates serve as the major source of energy and are necessary for the metabolism of fats. They are formed in plants during photosynthesis. In photosynthesis, chlorophyll in the plant utilizes solar energy (from the sun) to produce carbohydrates. Carbohydrates can either be simple or complex.
The carbohydrates are primarily digested and absorbed in the small intestine. During the initial phase of digestion the catabolism of the plant carbohydrates begins. This process breaks down the plant sugars, plant starches, plant cellulose and lignin. Then during anabolism (building process) the plant materials are converted to utilizable and absorbable animal sugars and animal starches and into separated out waste products. Carbohydrates must be broken down into monosaccharides for absorption from the digestive system. During this process carbohydrate molecules become oxidized. This oxidization creates energy and Pyruvic Acid. The Pyruvic Acid formed continues on to help digest fat molecules. The energy is used or stored by the horse. Most of the fuel to create energy for the horse comes from carbohydrates.
Simple (soluble, hydrolysable, or non-structural) carbohydrates are in abundance in the concentrate portion of a horse’s diet. Concentrates are grains and pelleted or processed feeds. Simple starches and sugars are referred to as Nitrogen-Free Extracts. They are readily and highly digestible. Simple sugars include monosaccharides, disaccharides and trisaccharides, along with starch and dextrin. The animal sugar glucose is created in the digestive process. It is a monosachharide; it is absorbed from the digestive system and transported in the bloodstream. This is energy that is immediately available for the horse to use. The animal starch glycogen is a polysaccharide. It is a storable form of energy created in the digestive process. Glycogen is stored in the liver, kidneys and muscles. Glycogen is able to converts to glucose when the work load or blood sugar level requires it. Muscle cell glycogen is an immediate reserve for glucose to the muscle cells. The hormone insulin acts as a glucose regulator in the bloodstream. When the insulin level lowers, glycogen converts to glucose being released into the bloodstream. In intense exercise, energy is derived from anaerobic metabolism (energy production that does not use oxygen). Glucose is the only fuel that can be used in anaerobic metabolism.
Complex (fermentable, crude, or structural) carbohydrates are found in hays and forages. They include hemicelluloses, cellulose and lignin. They form the cell wall in the plants and provide fiber in the horse’s diet. Complex carbohydrates are poorly digestible.
Understanding this whole process makes the simple carbohydrates contained in grains seem to be a convenient and readily available source of extra energy for a horse. However, a horse on a high grain diet collects more glucose than it can efficiently use therefore storing glycogen in abundance.
The oxidative pathways explain energy production. The aerobic oxidative pathway is the Krebs cycle. It is also known as the TCA or tricarboxylic acid cycle and the Citric Acid Cycle. The end result of the Krebs cycle is the oxidation of carbon and hydrogen to form carbon dioxide, water, energy stored as adenosine triphosphate (ATP) and heat. Adenosine triphosphate is used to drive energy required processes such as muscle contraction. It is important in the transfer of energy at the cellular level. Carbon dioxide is eventually exhaled by the lungs. The horse dissipates the heat resulting from oxidation.
Myocytes are muscle cells. Myocytes contain proteins and molecules in the extracellular space. The cell membrane is configured of larger particles of the myocyte. Normally the intracellular and extracellular distribution of ions is in balance. Ions are predominantly intracellular or extracellular. Sodium, calcium, chloride, and bicarbonate ions are mainly extracellular while potassium, magnesium, and phosphate remain chiefly intracellular. This electrolyte distribution is preserved by the sodium-potassium (ion) pump. This pump is energy dependant, fueled by adenosine triphosphate. Oxygen produced adenosine triphophate is sufficient but anaerobically a breakdown of the pump and cell membrane may occur. Damage the mycocyte membrane allows intracellular content to escape and extracellular content to enter. Heat can destroy myocytes, damaging the cell membrane structure. Myoglobin supplies oxygen to the myocytes.
The energy for muscle contraction is provided by high-energy phosphate bonds in adenosine triphosphate. At exercise the main source of energy is from that stored in creatine phosphate. It serves to rephosphorylate adenosine diphosphate to adenosine triphosphate. Adenosine triphosphate is generated from two other sources that serve as the main source form muscle contractions. One source of energy is from aerobic energy production. Sources of its fuel are glucose, fatty acids, and protein. Glucose is fragmented into Pyruvate via this aerobic pathway of glycolysis (The Embden-Myerhoff pathway). In aerobic cellular respiration Pyruvate eventually enters the Krebs cycle as acetyl-CoA. Advantages of energy formed from aerobic oxidation are: a high adenosine triphosphate yield, the absence of toxic waste (carbon dioxide and water are the waste products), and the energy can be produces for long periods of time. Disadvantages to forming energy this way are the need from oxygen and the amount of time before adenosine triphosphate can be produced in substantial amounts. The increased oxygen demand must be met by a series of cardio-vascular and respiratory system changes. If these are inadequate to meet energy demands during strenuous exercise, anaerobic sources are called upon. Glucose is metabolized in the absence of oxygen to yield adenosine by having Pyruvate do the oxidation converting it to Lactate. This anaerobic cellular respiration form of energy production has a low yield of adenosine triphosphate, but it can be turned on very rapidly, and will form adenosine triphosphate at a high rate. Lactic Acid is a toxic end product of anaerobic glycolysis.
Endurance type training requires staying within the aerobic metabolism of energy production so a horse can exercise for an extended period of time. This is done by slowly modifying intensity and duration of training. This training increases mitochondria in the muscle cell so more oxygen can be utilized and increase the oxygen delivery system to the muscles.
Strength type training, or quick bursts of high-intensity, involves increasing muscle mass. Anaerobic energy sources then predominate. Training is done to promote tolerance of very high levels of plasma lactate accumulated from anaerobic muscle use training.
The muscle fibers used by the horse are according to gait, speed, and duration of exercise. The various muscle fibers are either Type I or Type II. Type I are slow-twitch, high-oxidative fibers or fast-twitch high-oxidative fibers. Type II are fast-twitch, low oxidative fibers. Slow twitch muscles fibers are suited for aerobic metabolism. Fast twitch are energized by anaerobic alactic (without lactate) metabolism or anaerobic lactic metabolism.
Cause and Process of the Disease Exertional Rhabdomyolysis
In many cases the cause of Tying-Up and Azoturia is never established. Typically it is exercise accompanied by another factor, hence the partial name phrase “Exertional”. It is related to nutrition, conditioning and sometimes genetically as a mutation or as an abnormality. In short, it is a metabolic disorder, or a feeding problem that is systemically involved. There are many possible causes just as there are different levels of intensity and forms of Exertional Rhabdomyolysis. There is continuous research being done to understand more about this complex disorder.
Sporadic Exertional Rhabdomyolysis, (may also contribute to chronic forms):
- Having a full feed, especially concentrates, for the simple carbohydrates, on day(s) off produces more energy in the form of glucose than the horse can use. This extra energy is then stored as glycogen creating an excessive accumulation in the muscles. Shortly after going back into work, the stored muscle glycogen is rapidly converted to glucose for usable energy. There may be a dangerous overabundance of glycogen in the muscles.
- The glycogen that is not metabolized aerobically, by oxygenated blood, must be metabolized anaerobically, which creates the cell waste products and heat. Excess heat may damage the mycocyte membrane. Damage disrupts the balance of electrolytes that it once maintained since extracellular fluids can flow in freely as well as intracellular fluids flow out.
- The ion pumps (sodium-potassium, calcium-magnesium, and calcium-ATPase) in the membrane of the mycocyte (muscle cell) which moves electrolytes in and out of the cell are disrupted. The mycocyte is unable to function. The muscle cell shuts down in a contracted position, similar to rigor mortis. The muscle tissue surrounding and enclosing the muscle cell (sarcolemma) is disrupted, releasing the contents of the muscle into the bloodstream. The content includes myoglobin and muscle cell enzymes.
- Untrained muscles making contractions beyond conditioning tears the muscle bundles creating myopathy
- Electrolyte imbalance from the loss of body fluids or nutritionally. This can possibly effect muscle contractions.
- Vitamin imbalance (Vitamin E deficiency may contribute to muscle cell damage)
- Mineral imbalance (Deficiencies of sodium and calcium may also contribute to muscle cell damage, selenium deficiency may also but usually in conjunction with a Vitamin E deficiency)
- Hormonal imbalance
- Hypothyroidism, low thyroid creating imbalance of insulin
Myoglobin (hemoglobin of the muscle) is a red pigmented protein that supplies oxygen to mycocytes (muscle cells). The bloodstream picks up myglobin as it is released from the breakdown of the damaged muscle tissues. Blood is not easily cleansed of myoglobin. Nephrons are microscopic tube-like structures in the kidneys which filter the blood and cause waste to be removed. Kidneys are not designed to cleanse the blood of myoglobin. Myoglobin is a red pigmented protein. The nephrons become blocked by the myoglobin. The pigment from the myoglobin turns the urine dark, hence the name black water disease. The kidney blockage can lead to renal (kidney) failure, permanent damage, and may be fatal.
Chronic Exertional Rhabdomyolysis - Polysaccharide Storage Myopathy (PSSM)
- A horse with PSSM has a genetic predisposition to store excess amounts of glycogen (storage form of sugar, glucose) and abnormal polysaccharide (sugar) complexes in muscles because insulin tells them too
- Combined with a rest period allows for even more excess of glycogen to be accumulated and stored. Normally this fuels the muscles during work. But with PSSM there is an abnormal regulation of glycogen synthesis. This may create a deficit of energy generation in muscles.
Chronic Exertional Rhabdomyolysis - Recurrent Exertional Rhabdomyolosis (RER)
- A horse with RER has abnormal muscle contractions from muscles cells abnormally regulating intracellular calcium during a muscle contraction. This abnormality is not related to dietary calcium intake.
- Stress and stimuli creating excitement
- Electrolyte and hormonal imbalances, deficiencies of Vitamin E and mineral selenium
- Typically seen in a horse put back into work after a couple to few days off. Normally they would be in an intense exercise program and being fed grain. The grain ration will not be adjusted for the days off. This is how it developed its name, Monday Morning Sickness. Horses would be worked during the week with Sunday or the weekend off. But now horses may be used in performances on the weekend and have Monday off. But the fit horse is used to a high rate of metabolism of energy feed but is unable to utilize them without work.
The ingestion of blister beetles and Day Blooming Jasmine can cause signs of Exertional Rhabdomyolysis. For example, the blister beetle toxin is cantharidin; ingested it causes severe gastrointestinal disturbances. This toxin in the system causes nephritis (inflammation of the kidneys). The toxin is excreted in the urine causing irritation. In small doses signs may be sweating, muscle rigidity and a gait of shortened stride. Ingestion of toxins like ionophores, creates cellular permeability and inflammation of the heart muscle, from an item like monensin sodium (Rumensin) found commonly in cattle supplements. Reactions to certain drugs can cause muscle damage and the horse may display of symptoms of Exertional Rhabdomyolysis.
Immediate Owner/Handler Care Essential to be Given to a Horse Displaying Symptoms of Exertional Rhabdomyolysis
Once symptoms are noticed, or you are suspect that your horse may be tying-up or beginning a bout of Azoturia, stop; allow the horse to stay still. Attempts to walk a horse with myositis can result in permanent damage. Call your veterinarian. If you are a long way out, try to get a trailer to your horse and haul the horse back to a stall area. Do not move the horse more than necessary to get the horse into confinement; if possible leave the horse motionless and have the veterinarian travel to the horse. Once these initial precautions are taken:
- Keep the horse quiet and calm.
- Offer water to the horse, a water electrolyte mix may be better
- Rub the horse dry. The horse is probably sweaty. Rubbing will help to dry, massage and promote circulation.
- Keep the horse warm and comfortable. Blanket accordingly with the weather. Do not blanket in hot weather.
- Apply cold packs to the effected hindquarters area at the onset. This may help reduce inflammation if applied shortly after myositis becomes apparent.
- Apply warm compresses secondarily. This increases circulation and may encourage relaxation.
- Massage the effected hindquarters area unless this causes apprehension.
- Watch the horse for anaphylactic shock. Signs may include lengthened capillary refill time along with cool and pale mucus membrane.
- Do not feed the horse unless there is an extended time prior to your veterinarian’s instructions. Limit feed intake to hay in small amounts. Give no concentrates.
- If the horse is down create a deep soft bed. Turn the horse from side to side to help prevent bedsores and internal problems.
In the mild case of Tying-Up with only back pain shown, a slow walk of 30-45 minutes may be enough to relieve pain and help the horse return to normal. There is little muscle damage and there will not be any scarring. The horse may be put on medication. The horse is still prone to reoccurrence so management needs to be done accordingly. This treatment should be done with veterinary recommendation and support.
Diagnosis of Exertional Rhabdomyolysis
Exertional Rhabdomyolysis should be accurately diagnosed and treated as to rule out the possibility of it or be properly treated in accordance with it rather than for a problem with similar signs (like colic, lameness, laminitis, tetanus, or mild toxin ingestion from blister beetle).
Since there are many possible causes that may need to be treated differently, a veterinarian will make a diagnoses and give a treatment regimen based on the specific horses case. Along with the clinical signs, the enzymes levels can be used in diagnosing Exertional Rhabdomyolysis. The enzymes tested for are:
- Creatine kinase (CK)
- Lactate dehydrogenase (LDH)
- Aspartate amino transferase (AST)
Creatine kinase is also known as creatine phosphokinase (CPK) or phoshocreatine kinase (PCK). This muscle enzyme catalyses the conversion of creatine and consumes adenosine triphosphate (ATP) to create phosphocreatine and adenosine diphosphate (ADP). In tissue and cells that consume adenosine triphosphate (ATP) rapidly, especially skeletal muscles, phophocreatine serves as an energy reservoir for the rapid buffering and regeneration of adenosine triphosphate (ATP) as well as for intracellular energy transport by the phosphocreatine shuttle or circuit. It is a marker for the rhabdomyolysis (severe muscle breakdown). Serum levels of creatine kinase are elevated when muscle cells are damaged.
Lactate dehydrogenase (LDH or LD) is a marker of tissue breakdown. It is abundant in red blood cells and can function as a marker for hemolysis (the breaking open of red blood cells and release of hemoglobin).
Aspartate amino transferase (AST) is also called apartate transaminase (AST) or serum glutamic oxalacetic transiminase (SGOT). Aspartate amino tranferase is raised in acute liver damage. It is present in red blood cells and cardiac muscle, skeletal muscle, and kidney and brain tissue. It may elevate due to damage of these as well; so serum levels of aspartate amino transferase are also elevated when muscle cells are damaged.
Although a blood test of these enzymes may diagnose that a horse has or has had the disorder, it still might not diagnose the underlying cause. A muscle biopsy could be taken for more information.
Possible Veterinary Treatment of Exertional Rhabdomyolysis
Treatment should be administered by a veterinarian based on individual analysis. Possible treatments may include one or more of the following or a different remedy:
- It may be advised to give the horse a sedative or tranquilizer, like Acepromazine (Ace), especially if the horse is nervous or thrashing.
- Drugs such as Phenylbutazone (Butazolidin or “Bute”), or other non-steroidal anti-inflammatory (NSAID) agents, like Flunixin meglumine (Banamine), Naproxen (Equiproxen), and Ketoprofen, may help to relieve pain (as an analgesic). Phenylbutazone acts directly on the muscoskeletal muscles controlling inflammation and may help treat problems within the muscles by reducing secondary inflammation damage. But, be careful of its damaging effect on the kidneys from prolonged use, especially since the kidneys may already be damaged from this disease. NSAID’s are non-narcotic.
- If used corticosteroids (cortisone), should be administered during the first few hours. They have powerful anti-inflammatory agents. They should not be used thereafter or for longer periods as steroids have been implicated in causing attacks (or inflammation of the muscle of the heart), increasing healing time, and can contribute to other health issues including laminitis.
- A narcotic analgesic (pain reliever) like Demerol may be given. Demerol is a synthetic drug. Narcotics depress the pain sensitive cells. However, they need to be used wisely as their effect is somewhat unpredictable. Narcotics could produce excitation, apprehension, and increase muscular activity rather than analgesia and sedation.
- Used topically, Dimethyl sulfoxide (DMSO) removes byproducts of inflammation. If used wear gloves as a precautionary measure.
- A Vitamin E or a Vitamin E and Selenium injection may be helpful. This tends to create a response of relaxation and pain relief.
- May give intravenous fluids, like Lactated Ringer’s solution, along with an oral electrolyte solution, like calcium gluconate, to the horse to restore fluid balance, promote urine flow, and protect the kidneys from myoglobin damage by aiding the kidneys in flushing out. Fluids are given until the urine has cleared of pigmentation.
- Urinating may be difficult; a diuretic may be administered or a catheter may be passed.
- Anti-histamines are sometimes given in the case of a reaction to a drug.
- Stomach tubing the horse with an oily laxative like mineral oil may help keep the intestinal content moving in a case where the horse is lying down without the ability to rise.
Prognosis of Horses with Exertional Rhabdomyolysis
Prognosis depends on the destruction of muscle tissue and the amount of scarring that has occurred during muscle damage.
- It is better for horses that stay up, or that do not need to continue to lie down.
- It is better for horses that remain quiet or that do not need to be moved as they are not creating further muscle damage with movement.
- It is better for horses that appear normal within 24 hours after the occurrence.
- Myositis horses may suffer lameness from prolonged or permanent atrophy of involved muscles.
Recovering from Exertional Rhabdomyolysis
Blood tests determining the levels of enzymes from the muscle that is in the serum, will be the most accurate determining factor for allowing a horse to return to work. These levels or concentrations should be or remain normal before returning to work. Muscle tissue may begin regenerating after about three months.
- CK or creatine kinase concentration
- AST or aspartate transaminase levels
- LDH or lactate dehydrogenase
Long term high levels of creatine kinase may show continual muscle atrophy.
Long Term Care with Veterinary Support:
- Rest the horse several days or even weeks even after signs disappear. Allow turn-out after the initial symptoms subside. Gradually bring the horse back into training with hand walking initially.
- Gradually increase the horses feed intake.
- Test for plasma enzyme levels before making a decision regarding the start of re-conditioning. Visual analysis may not be enough. The horse should be off all drugs that may mask any soreness.
- Do not push the horse as a relapse may occur; a second bout could potentially be more severe than the first, although the horse handler may be better informed as to what is happening and what to do which may help to lessen the severity.
Maintenance of Horses that have had Episodes of Exertional Rhabdomyolysis
Maintenance should be done according to the veterinarian instruction. Possible general maintenance schemes are as follows.
- Cut the concentrates in half 24 hours before the horse is used in performances
- Keep the horse on a feeding routine that varies little from day to day
- The ration should be well balanced and should be done so the horse is possibly a bit on the leaner side
- Carefully measure hay and grain to ensure proper dietary intake
- Adjust the grain accordingly to exercise, especially if exercise varies from day to day.
- Ideally the exercise level should be similar day to day and the horse should receive some exercise every day
- Provide turnout
- Provide grazing opportunity. The green leafy parts in the forage contain Vitamin E.
- A vitamin E and selenium injection may be given every month or three or six or low doses may be added to the horses feed. Most diets are sufficient in Vitamin E and Selenium unless the area selenium levels are low. Balance the ration first.
- Thyroid hormone supplementation may be beneficial for horses with low thyroid activity, if the horse has been diagnosed with hypothyroidism.
- Alfalfa hay contains more calcium than grass; this may be taken into account when developing a balanced ration
- In chronic cases the veterinarian may prescribe a maintenance administration of medicine. This could be a daily low dose of Acepromazine or feeding Dantrolene sodium (Dantrium) prior to exercise, relaxing skeletal muscles by inhibiting intracellular calcium release
- A daily oral dose of Phenytoin sodium (Dilatin) as an anticonvulsant (anti-seizure) may help prevent a reoccurrence but could also cause drowsiness
- If the horse is only ridden or worked on the weekend and is prone to Exertional Rhabdomyolysis it may be kinder to get a horse that is not since the weekend use lifestyle sets the horse up for another episode
For Sporadic Exertional Rhabdomyolysis
- Diet should include good quality hay
- Feed only a little grain
- Have salt available always
- Supplement with a vitamin and mineral mix
For Chronic Exertional Rhabdomyolysis – PSSM – Polysaccharide Storage Myopathy
- Feed roughages or a complex carbohydrate diet
- Avoid concentrates for the simple carbohydrates (starches and sugars) in order to maintain a low blood sugar level and insulin concentrations
- Provide constant turnout and consistent exercise
For Chronic Exertional Rhabdomyolysis – RER – Recurrent Exertional Rhabdomyolysis
- Minimize excitement and stress
- Teach susceptible horses to react calmly to excitable stimuli.
- Provide horses with turn-out
- Unlike PSSM grains and sweet feeds do not need to be completely removed from the diet with RER, but limiting them in the diet may help to decrease excitability and nervousness
- Daily progesterone might improve a nervous mare by suppressing estrus , controlling heat cycles
Preventive Measures to Reduce the Likeliness of Exertional Rhabdomyolysis
This is a health problem that could typically be avoided through proper care and management. A well thought out careful conditioning and nutritional program may help prevent Tying-Up and Azoturia. Cut concentrates, or the grain portion of the ration, in half, or reduce the amount of feed fed, prior to when the horse is idle and on rest day. Do this especially if the horse is stall kept. Feed a well balanced ration. Balance the ration for minerals (electrolytes) and vitamins. Supplement if necessary with deficient minerals (like possibly potassium). Also check for excesses. A horse should have access to salt and an adequate water supply. Withhold feed for 24 hours prior to surgery that a horse needs to be laid down for, if your veterinarian requests. Feed little and often rather than in one or two large meals. This is true for both roughages and concentrates. Dividing the concentrates into portions reduces a hit of glucose on the system and also reduces other feeding problems like cecal acidosis.
Use proper training techniques. Slowly warm up the horse before continuing onto the workout. Thoroughly and slowly cool down after work/exercise. Conditioning can help promote oxygen’s ability to be used for energy production in muscle cells. Condition the horse for the specific activities being performed. Thoroughly care for and allow horses with infections of the immune system to completely recover before exercising the horse again.
Disease Spread of Exertional Rhabdomyolysis
Exertional Rhabdomyolysis is non-contagious. Horses are affected so differently by nutrition it may or may not be noticed throughout a barn of horses fed the same or similar ration or that are on a similar exercise program. Genetic mutations and abnormalities are inherited giving Chronic Exertional Rhabdomyolysis some degree of spreading through a breeding program. Genetic testing can be performed by licensed laboratories so owners can make informed decisions about breeding.
Historical Theories Behind the Cause and Treatment of Typing-Up or Azoturia
It used to be thought that all forms of Tying-Up and Azoturia were the same. Now the various forms have been properly categorized and realized separately as having different causes. It was once thought that Lactic Acid was the cause of muscle cramping during an episode of Exertional Rhabdomyolysis. It was felt to be exclusive in horses having a day of rest that developed an excess amount of glycogen. This glycogen over-supply was rapidly metabolized creating Lactic Acid as an end product of anaerobic energy metabolism. It was theorized that this Lactic Acid build up created the muscle damage. Bicarbonates were used as an oral treatment to reduce the acidity from the Lactic Acid. Now there is a better understanding of Azoturia and research developments that prove otherwise.
Terminology Used and Glossary of Terms
Adenosine Triphosphate: compound required for energy transfer and the phosphorylation of compounds
Anabolism: constructive metabolism in which simple substances are converted into more complex substances by living cells
Anaphylactic: involving extreme sensitivity
Anticonvulsant: a drug that prevents or reduces seizures
Antihistamine: a drug which counteracts the effects of histamine, especially useful in allergic reactions
Anti-inflammatory: an agent that counteracts or suppresses the inflammatory response
Aspartate amino transferase: an enzyme present in red blood cells and cardiac muscle, skeletal muscle, and kidney and brain tissue that is elevated due to damage to these sources as well as in acute liver damage
Carbohydrates: sugars and starches
Catabolism: the breaking down of complex substances into more simple compounds by living cells, destructive metabolism.
Complex: made up of many interrelated parts; difficult to analyze, understand, or solve
Corticosteroids: hormones of the adrenal cortex or other natural or synthetic compound having a similar activity, having an effect on glucose utilization like Dexamethazone and inhibits the inflammatory process and having
Creatine Kinase: an enzyme that catalyzes the conversion of creatine and consumes adenosine triphosphate to create phosphocreatine and adenosine diphosphate
Disease: a medical condition resulting in pathological symptoms and not a direct result of physical injury; a disorder with recognizable signs and having a known cause
Disorder: an illness disturbing the usual function of the mind or body
Diuretic: an agent that increases the production of urine
Electrolyte: a substance present in body fluids which is capable of conducting electricity in various body functions such as nerve impulses, oxygen and carbon dioxide transport, and muscle contraction
Enzyme: organic compound which produces or accelerated changes in a substance without being consumed in the process
Glucose: a crystalline monosaccharide occurring naturally in fruits, honey and blood
Glycogen: transformed plant sugar into animal sugar, a polysaccharide, produced and stored in animal tissue, especially in the liver and muscles, and changed into glucose as the body needs it
Glycolysis:from glucose, glucose degredation
Histamine: a chemical compound which dilates capillaries, constricts the smooth muscle of the lungs and increases secretions of the stomach; substance released in anaphylactic reactions and shock
Hypothyroidism: a deficiency of thyroid activity
Inflammation: a condition of tissues characterized by pain, heat, redness, swelling and various exudations as a reaction to injury. It serves to eliminate harmful substances and damaged tissue.
Intravenous: within a vein
-itis: denotes inflammation of a given part
Krebs Cycle: the major series of pathways through which carbohydrates are oxidized to produce energy in animal cells
Lactate deydrogenase: an enzyme abundant in red blood cells and functions as a marker for hemolysis or tissue breakdown
Lactic Acid: an organic normally present in muscle tissue, produced by anaerobic muscle metabolism. (It may also be produced in carbohydrate material by bacterial fermentation.)
Metabolic: relating to metabolism
Metabolism: life-sustaining chemical activity of converting food into energy and products utilized by the body
Monosaccharide: simple sugar, carbohydrate that cannot be decomposed by hydrolysis
Muscle relaxant: an agent that specifically aids in reducing muscle tension
Myocyte: muscle cell
Myoglobin: a ferrous complex pigment which gives muscle its characteristic color and acts as a store of oxygen, hemoglobin of muscle
Myopathy: any disease of a muscle
Myositis / Myocitis: inflammation of a voluntary muscle
Non-steroidal anti-inflammatory: medicines that relieve pain, swelling, stiffness, and inflammation other than corticosteroids like Bute and Banamine
Pathological: uncontrollable; relating to disease or arising from disease
Photosynthesis: the production of organic substances, chiefly sugars, from carbon dioxide and water occurring in green plant cells supplied with enough light to allow chlorophyll to aid in the transformation of the radiant energy into a chemical form
Polysaccharide: one of a group of carbohydrates which contain more than four molecules of simple carbohydrates combined with each other, many sugar molecules
Progesterone: hormone which prepares uterus for reception and development of fertilized egg
Prophylactic: an agent that tends to prevent disease
Pyruvic Acid: an organic acid that is formed as an intermediate compound during the aerobic metabolism of carbohydrates and proteins.
Recurrent: regular or periodic
Renal: pertaining to the kidney
Rhabdomyo-: skeletal muscle
Rhabdomyolysis: destruction of skeletal muscle cells
Sedative: an agent that reduces and controls excitement
Sporadic: occurring irregularly, at intervals that have no apparent pattern
Syndrome: a set of signs which occur together usually indicating a particular type of disease process
Thyroid Gland: organ that secretes the hormone thyroxin, which increases the rate of metabolism
Tranquilizer: an agent that produces a quieting or calming effect, without changing the level of consciousness
-uria: a condition of the urine, typically by the presence of a substance in it
Tying-Up and Azoturia Quiz
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Summary of Equine Exertional Rhabdomyolysis
Tying-up and Azoturia are correctly referred to as Exertional Rhabdomyolysis. It is the most common muscle problem in horses and surfaces as being either being sporadic or chronic. The genetically inherited chronic forms are Polysaccharide Storage Myopathy or Recurrent Exertional Rhabdomyolysis. If a horse displays symptoms immediately stop from working and call the veterinarian. Signs include a reluctance to move, profuse sweating, and hard muscles in the hindquarters. There are many possible causes. An excessive amount of glycogen stored in the skeletal muscles from high grain diets being continually fed on days off or a genetic predisposition to store extra glycogen may disrupt the metabolic energy development once work is reestablished. A genetic abnormality causing muscle contractions could also be the culprit. Proper diagnosis and treatment protocol will be based individually. Typically a change in diet and continual exercise with turn-out will eliminate or reduce Chronic Exertional Rhabodmyolysis. A well followed conditioning and feeding program could prevent an attack. This would include reducing the sugar and starches on days off.
Links to Resources on Exertional Rhabdomyolysis and other Metabolic Disorders
Disclaimer and Warning
Every effort has been made to make this article as complete and as accurate as possible for the level indicated, but no warranty is implied. The information provided is on an “as is” basis. The author and publisher shall have neither liability nor responsibility to any person or entity with respect to any loss or damages arising from the information contained in this article or from use of the links and files accompanying it. This is an informational piece only; consult your veterinarian.