Page 415 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition
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390 CHAPTER 1
VetBooks.ir • A high lipid diet may increase the requirement and lower and upper airway disease should all be
for antioxidants, therefore a feed balancer
excluded.
containing vitamin E may be beneficial.
• These recommendations are based on studies of Diagnosis
horses with PSSM1. It is presumed that similar Mitochondrial myopathies are diagnosed on the
recommendations apply to horses with PSSM2, basis of mitochondrial staining patterns in muscle
although further investigation of this is required. biopsy samples, or measuring pyruvate and lac-
tate following exercise. Reduced aerobic metabo-
Prognosis lism leads to alterations in the ratio of pyruvate to
The prognosis is favourable in cases where dietary lactate.
and exercise recommendations are followed. These
horses are significantly more likely to have an Management
improvement in the severity and frequency of clini- There are no specific treatments available for horses
cal signs relative to those cases where only one with mitochondrial myopathies.
(exercise or dietary) recommendation is followed.
A clinical improvement may be observed within Prognosis
6 weeks, although complete adaptation to these diets The prognosis is generally poor.
often takes several months.
MUSCLE TEARS AND STRAINS
Acquired causes of exertional
rhabdomyolysis Definition/overview
Muscle injuries are a common but poorly understood
There are several early studies that suggested cause of lameness and poor performance. They
acquired causes of rhabdomyolysis, such as varia- may occur in any muscle group within the fore- or
tions in female sex hormones, hypothyroidism and hindlimbs and the axial skeleton, including the lum-
electrolyte imbalances. Most of these suggested risk bar and gluteal regions.
factors are yet to be corroborated, with different
studies yielding conflicting results. It remains pos- Aetiology/pathophysiology
sible that these risk factors may increase the chances Injuries most commonly occur in equine athletes
of clinical disease in an already genetically suscep- such as racehorses, showjumpers, eventers and
tible animal. Western horses. They may be caused by direct
trauma, excessive or unusual exercise, secondary to
MITOCHONDRIAL MYOPATHIES other sources of lameness (especially hindlimb) or
a poorly fitting saddle. Varying degrees of muscle
Aetiology/pathophysiology damage may lead to pain and muscle fibre strain or
In humans, there are several mitochondrial defects even tearing.
that lead to rhabdomyolysis with profound exercise
intolerance, and there are a few reports of similar Clinical presentation
pathology in the horse. This will vary with the degree of damage and the site
of the muscle. Acute muscle damage and subsequent
Clinical presentation haemorrhage/inflammation may lead to acute-onset
Horses present with a marked exercise intolerance. moderate to severe lameness and palpable swelling/
heat/pain in affected muscles (Fig. 1.760), if super-
Differential diagnosis ficial. Deeper muscle injuries will not be palpable.
Other causes of exercise intolerance such as systemic Later, on palpation the muscle may be firm if there
infection, musculoskeletal pain, cardiac disease is fibrosis, atrophied with muscle loss, or reveal a