Page 420 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Musculoskeletal system: 1.9 Muscle disorders of the horse 395

VetBooks.ir leading to cell membrane damage and degeneration Diagnosis
Clinical signs, including myoglobinuria, are strongly
in both skeletal and cardiac muscles. Rapidly growing
foals (birth to 1 year old), born to dams on selenium
samples. Low selenium may be detected in whole
deficient pastures (<0.05 ppm), are most frequently suspicious. Increased plasma CK and AST on blood
affected, although the condition has been reported blood samples and vitamin E measured from serum
in older horses. Other factors include the level of or plasma may also be low. Post-mortem examina-
succinoxidase inhibitors in grass or hay, which inter- tion reveals the skeletal muscles as typically pale,
fere with vitamin E levels, plus the increased intake with or without white streaks. Subcutaneous oedema
of unsaturated fats in milk or diet and strenuous and brown fatty tissue are observed.
exercise.
Management
Clinical presentation Selenium and vitamin E supplementation should be
The clinical signs can vary with age but can be split administered but these are rarely effective in acute
into two forms: cases. D-α-tocopherol is the most biologically active
form of vitamin E in the horse. Antibiotics may be
• Cardiac form. Sudden death, respiratory required to treat secondary complications, such as
difficulty, pulmonary oedema, weakness, pneumonia, if present. Nursing care to ensure ade-
recumbency, depression and irregular heart quate fluid and nutritional intake may be necessary.
rhythm may all be present. Systemic NSAIDs are useful to control pain and
• Skeletal form. Slower in onset, difficulty stiffness. A daily dietary intake of 10 µg/kg selenium
moving, stiffness, stilted gait, muscle and 2–5 mg/kg vitamin E is recommended for pre-
fasciculations and weakness. Animals may vention, usually in last trimester pregnant or lactat-
become recumbent. Muscles are often firm on ing mares, or in milder chronic cases for treatment.
palpation.
Prognosis
Young foals often present with weakness, recum- Good in the skeletal form but poor if there is cardiac
bency and possibly dysphagia. Older foals often involvement, particularly in acute cases.
present after periods of brisk exercise with acute or
subacute signs. Milder signs are of stiffness in gait CLOSTRIDIAL MYOSITIS
and neck carriage sometimes progressing to recum-
bency. Swollen firm muscles may be accompanied Definition/overview
by subcutaneous oedema over the rump, neck and Clostridial myositis is an acute to peracute condi-
ventral thorax/abdomen. There may be myoglobin- tion, characterised by rapid muscle necrosis due to
uria. In the acute form there may be sudden col- infection by Clostridium spp. and associated with
lapse after exercise, with death in some cases within severe systemic disturbances (toxic shock). It is also
4–5 hours due to heart failure and pulmonary referred to as ‘clostridial myonecrosis’, ‘malignant
oedema. In adult horses the condition may present oedema’, ‘gangrene’ or ‘clostridial cellulitis’.
as colic, muscle stiffness/soreness and oedema of
the head and neck. Aetiology/pathophysiology
Clostridial organisms are ubiquitous in the environ-
Differential diagnosis ment, where they can survive for long periods of
Other causes of heart failure must be differentiated time. Contamination of an open or puncture wound,
from the cardiac form. The skeletal form must be necrotic area or haematoma with various clostridial
differentiated from cerebellar disease, colic, spinal organisms, such as C. perfringens, C. septicum and
cord compression, tetanus, trauma, meningitis or C. chauvoei, can lead to an acute myonecrosis.
toxin ingestion (e.g. organophosphates) and exer- Intramuscular or perivascular injections, especially
tional rhabdomyolysis. of irritant substances (e.g. NSAIDs, thiopentone),