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complications (Votion et al. 2007; van Galen et al. 2011a). Subclinical disease
has been described and is sometimes encountered in seemingly healthy
cograzers of clinically affected horses (Delguste et al. 2002; Votion et al.
2007).
1.4. Diagnosis
Diagnosis of AM can be challenging, amongst others due to the rapid
clinical evolution of cases. The history of the horse is important for the
diagnosis of AM. A prerequisite is that the horse has to be at pasture at the
onset of clinical signs, or at least within several days preceding. The diagnosis
of AM becomes more likely if the case occurs during autumn and during an
outbreak. A diagnosis of AM should be questioned when severe
rhabdomyolysis develops following general anaesthesia or intensive exercise
(suspicion of post-anaesthetic myopathy or exertional myopathy, respectively).
A suspicion of AM can be further strengthened based on clinical signs,
blood and urine analysis (explosive increase of serum levels of CK and
presence of myoglobinuria (Votion et al. 2007; van Galen et al. 2011b),
histology on muscle samples, and in fatal cases a full post-mortem
examination (Cassart et al. 2007).
1.5. Treatment and Prognosis
Unfortunately, treatment of affected horses is often unrewarding. Specific
therapies directed against the hypothetical causative agents are unavailable,
and thus practitioners rely solely on supportive care. Nevertheless 24% of
affected horses survive AM (van Galen et al. 2011a,b) and supportive therapy
should be tempted when horses have none or only a few of negative prognostic
factors or if the horse improves following treatment. Negative prognostic
factors were described to be recumbence, sweating, myoglobinuria,
hypothermia, anorexia, congestive or cyanotic mucous membranes, dyspnoea,
tachypnoea and/or tachycardia (van Galen et al. 2011a).
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