Perform clinical examination(including rectal examination if safe), take blood (haematology, biochemistry and Cardiac Troponin I as a minimum; venous blood gas including lactate if available) and urine sample (catheterised or free catch) and make provisional diagnosis in context of history.

There may only be one affected case but all horses and ponies in the field could have been exposed to hypoglycin A and have the potential to develop clinical signs.

a. All horses: Remove all horses from the affected field to stables. Keep them warm, minimise stress and do not transport. Feed adlib forage with carbohydrate based feed if additional calories are required. Supplement with anti-oxidants (Vitamin B, C, E and selenium). Monitor muscle enzymes (CK and AST) sequentially for early evidence of disease. If there are no concerns within five days the horse is unlikely then to develop clinical signs.

b. The affected horse/s: In the early stages most affected horses even if recumbent can be encouraged to rise to move to a stable. On yard management is favoured over referral due to the physical effort and stress of transport (exacerbate myopathy; cause negative energy imbalance and respiratory alkalosis) but this should be balanced with the level of care that can be provided. Discuss with the owner the commitment and estimated costs entailed and the expected prognosis.

Atypical myopathy has a high fatality rate (74%) the majority of non-survivors are euthanized or die within 72 hours of the onset of clinical signs and the remainder within 10 days (van Gelsen et al 2012a). Positive prognostic indicators are normal defaecation, remaining standing, normal mucous membrane colour and temperature. Horses that recover usually regain muscle mass overtime and return to former level of activity. Negative prognostic indicators include recumbency, sweating, anorexia, tachycardia, tachypnoea and dysnpnoea (which can progress to respiratory failure).