Diagnosis and Treatment of Rhabdomyolysis in Foals
We hear a lot about a horse experiencing rhabdomyolysis (tying-up) during or after exercise. However, foals are also susceptible to muscle damage. Stephanie Valberg, DVM, PhD, of the University of Minnesota, presented "A Review of the Diagnosis and Treatment of Rhabdomyolysis in Foals" at the 2002 American Association of Equine Practitioner's Convention. She began her presentation with a discussion of what a practitioner might do when presented with a possible case of tying-up.
To assess the damage to the muscles, a practitioner might indicate that a serum chemistry profile is necessary, said Valberg. The activity of specific enzymes such as creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate transaminase (AST) provide information about muscle damage. Serum CK values will peak about four to six hours after muscle damage, and they will return to normal between three to seven days after the muscle damage stops occurring. "Thus, high serum CK activity indicates acute muscle degeneration, and persistently elevated serum CK activity over time indicates ongoing rhabdomyolysis," she said.
Increases in LDH and AST activity can also indicate tying-up, but they can also point to liver damage. LDH peaks 12 hours after muscle damage, with values returning to normal seven to 10 days after damage. AST peaks one to two days after muscle damage and won't return to normal for five to 14 days. To rule out liver disease, a biochemistry profile will also measure glutamyl transferase (GGT) and sorbitol dehydrogenase (SDH).
In addition, if extensive muscle damage occurs, a blood profile might indicate less sodium, chloride, and calcium in the bloodstream as it seeps into the damaged tissue, and more potassium, phosphorus, and myoglobin in blood samples as those chemicals move from damaged muscles into the bloodstream.
Valberg said that the serum chemistry profile will tell the practitioner how severe the episode was and when it possibly occurred, but other diagnostic tests are needed to determine the underlying cause of the tying-up. These tests include:
- Complete blood count (CBC) to identify associated infections;
- Thoracic radiographs or ultrasound to identify bronchopneumonia or aspiration pneumonia;
- Arterial blood gas analysis in neonates to identify asphyxia (inadequate intake of oxygen) and hypoxia (reduction of oxygen in the tissues);
- Whole blood selenium concentrations and serum vitamin E concentrations;
- Evaluation of pastures for the presence of toxic plants; and
- Muscle biopsy and histopathological evaluation.
These tests can help determine if the muscle damage is a result of birth hypoxia, fulminant (sudden) sepsis, clostridial myositis (muscle inflammation), nutritional muscular degeneration, pasture myopathies (toxic plants that damage muscle), polysaccharide storage myopathy (PSSM), or glycogen branching enzyme deficiency (GBED) in Quarter Horse-related foals. PSSM and GBED are two different types of causes of muscle damage in foals.
If an affected foal is so ill that he cannot stand on his own, he needs intensive care provided by a veterinary clinic. With this intensive care, the foal can be given assistance nursing every hour, or if he is unable to nurse, he might receive nutrition via another route.
Treatment can be labor-intensive since the foal needs to be repositioned every hour. Non-steroidal anti-inflammatory drugs such as ketoprofen and flunixin might be prescribed for pain and inflammation. Pneumonia is a possibility due to inhalation of pathogens while the foal is lying down, weakness of respiratory muscles, and a compromised immune system. If the foal does get pneumonia, then antibiotics might be prescribed.
Correction of fluid and electrolyte imbalances is necessary. Intravenous dextrose, bicarbonate, and insulin can be used to treat elevated potassium levels, except in severe tying-up cases, in which mineralocorticoids (a group of hormones) can be used. For the decrease in blood sodium levels, hypertonic saline might be administered.
Calcium levels can be corrected with a calcium borogluconate and saline mixture. If serum creatinine is elevated, it indicates decreased blood flow to the kidneys and potentially kidney damage. Drugs such as dobutamine or dopamine might increase blood flow to the kidneys, and sodium bicarbonate might prevent proteins from blocking tubules within the kidney.
Nutritional myodegeneration (NMD), also known as white muscle disease, is a common problem associated with muscle stiffness and elevation of CK and AST activities. Foals will show signs of painful hind limb, back, or neck muscles with increasing weakness, stiffness, trembling, and recumbency, according to Valberg. Pneumonia is also a worry with NMD. However, sometimes foals might only have difficulty in swallowing without other signs. When the heart is involved, the practitioner will hear an irregular heartbeat, and the foal will be really weak and not be able to stand. Sudden death is possible.
NMD results from a dietary deficiency of selenium and/or vitamin E in gestating mares. Affected foals are treated with the same supportive care as foals with other causes for muscle damage. However, supplementation to correct the nutritional deficiency is necessary. For a selenium deficiency, foals might receive an injection of selenium.
"Absorption and distribution of injectable selenium occurs rapidly and may account for the rapid improvement in clinical signs seen in reversible cases," said Valberg. "Injection site reactions are common, so dilution with sterile saline and injecting the pectoral muscles in two sites is recommended. Injection of cervical (neck) muscles is not recommended because injection reactions in the neck will decrease the foal's ability to suckle.
"Foals that remain recumbent for three to five days without significant clinical improvement have a poor prognosis. If myocardial involvement is present it is usually extensive and invariably fatal."
If horses are fed properly prepared and stored feeds and high-quality forage, then this should eliminate the risk of a vitamin E deficiency. Testing of blood for selenium deficiencies every 60-90 days for those animals at risk and every six to 12 months to monitor supplementation might be necessary.
Polysaccharide Storage Myopathy (PSSM)
Polysaccharide storage myopathy is found only in Quarter Horse-related breeds, and it has been found to be a heritable trait characterized by enhanced insulin sensitivity and accumulation of glycogen and abnormal polysaccharide in skeletal muscle fibers, said Valberg. Young foals can develop severe muscle damage with PSSM, often in association with an infection. A muscle biopsy is used to diagnose PSSM. Biopsies show excessive accumulation of sugar stored as glycogen and as an abnormal sugar structure called polysaccharide. The accumulation occurs slowly over time so in some cases, accumulation of abnormal polysaccharide might not occur until seven to 18 months of age. One study confirmed the genetic link. "Breeding horses with PSSM is not recommended because of the evidence supporting inheritance of the trait, the severity of clinical signs in foals, and the high likelihood of recurrence of rhabdomyolysis in affected animals," said Valberg.
Management of affected foals included daily pasture turnout, eliminating sweet feed, providing a low-starch concentrate with 20% fat, a balanced vitamin/mineral supplement, and grass hay. A study showed that providing complete turnout of foals onto pasture resulted in foals with normal CK responses to exercise, while foals that were confined to stalls had elevated CK levels in response to treadmill exercise.
Glycogen Branching Enzyme Deficiency (GBED)
GBED is a newly recognized cause of death in foals of Quarter Horse-related breeds. Foals with GBED can display a variety of signs, such as weakness and hypothermia at birth, intermittent hypoglycemia, weakness, seizures, flexural deformities, difficulty moving, recumbency, lack of energy, and even sudden collapse. Muscle damage is not as severe as with PSSM and NMD, and muscles are not firm or sore when palpated. Although foals respond initially to supportive treatment, they eventually die from persistent weakness or sudden collapse due to the heart stopping. This disease is inherited as a recessive trait where both the sire and dam are thought to carry the trait.
Diagnosis is made by staining for glycogen in skeletal and cardiac muscles using Periodic acid Schiff's (PAS) stains. Abnormalities include low background staining for normal sugar and globules of abnormally structured sugar scattered throughout the heart and skeletal muscle. This newly recognized disorder has been known to be fatal in all cases by the time the foal reaches eight weeks of age.
About the Author
Sarah Evers Conrad has a bachelor’s of arts in journalism and equine science from Western Kentucky University. As a lifelong horse lover and equestrian, Conrad started her career at The Horse: Your Guide to Equine Health Care magazine. She has also worked for the United States Equestrian Federation as the managing editor of Equestrian magazine and director of e-communications and served as content manager/travel writer for a Caribbean travel agency. When she isn’t freelancing, Conrad spends her free time enjoying her family, reading, practicing photography, traveling, crocheting, and being around animals in her Lexington, Kentucky, home.
POLL: Rehabbing the Injured Horse