Page 419 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

394 CHAPTER 1

VetBooks.ir MYOTONIC DISORDERS results in characteristic abnormalities. Between
episodes horses may appear clinically normal.
Aetiology/pathophysiology
Abnormal excitability of muscle cell membranes Homozygous animals appear to be more severely
affected than heterozygous carriers. DNA test-
leads to delayed relaxation of muscle following con- ing can confirm the gene mutation. The American
traction or stimulation. The most common form is Quarter Horse Association accepts tests performed
hyperkalaemic periodic paralysis (HYPP), which in certain licensed laboratories including: Veterinary
is associated with a defect in sodium channel pro- Genetics Lab at University of California at Davis;
teins, causing altered sodium/potassium exchange Shelterwood Laboratory at Carthage, Texas; Vita-
through the skeletal muscle membrane. Abnormal Tech Canada Inc., Markham, Ontario; NSW
sodium influx and leakage of potassium increase Agriculture in Australia; Veterinary Diagnostics
muscle fibre excitability, initially causing spontane- Center, Fairfield, Ohio; Stormont Labs, Woodland,
ous twitching and myotonia, eventually followed by California; Gene Check, Inc., Ft. Collins, Colorado;
flaccid paralysis. The blood potassium concentration and Maxxam Laboratory at Guelph, Ontario.
consequently increases.
This is an inherited defect (autosomal dominant) Management
in the Quarter horse in animals descended from In mild cases feeding grain or a sugar solution may
the prolific sire “Impressive”. Other breeds such as be helpful. Other treatments include: epineph-
the Appaloosa and American Paint and associated rine (3 ml of 1:1000 per 500 kg i/m); acetazolamide
crosses are also affected. Myotonia congenita is a (3 mg/kg p/o q12 h); intravenous calcium gluconate
less common condition, associated with a defect in (0.2–0.4 ml/kg of 23% in 1 litre of 5% dextrose) given
chloride channels, that has been described in a num- over 10 minutes helps to decrease muscle hyperexcit-
ber of New Forest ponies. ability; and dextrose (6 ml/kg of a 5% solution with
or without 1–2 mEq/kg sodium bicarbonate) will
Clinical presentation help to decrease the hyperkalaemia.
Episodes of HYPP may be triggered by fasting,
anaesthesia, stress or diets high in potassium, or may Long-term management
occur apparently spontaneously. Clinical signs vary Clinical episodes are minimised by reducing dietary
between individuals and tend to decrease with age. potassium (stop alfalfa, molasses and bran intake)
Affected animals often present with bouts of sweat- and increasing potassium excretion using acetazol-
ing, weakness, muscle fasciculations and prolapse of amide. Fasting or sudden changes in diet should be
the third eyelid, which may last for minutes to sev- avoided. Regular graduated exercise is beneficial.
eral hours. Dimpling of the muscles is often detected
and this may be exacerbated by percussion. In severe Prognosis
cases, animals may become recumbent, develop Overall the prognosis is fair and mild episodes are
respiratory distress (laryngeal paralysis) and can die. often self-resolving. Severe episodes are emergen-
cies, but death in these cases is rare. In most cases
Differential diagnosis the condition can be managed, although recurrent
Other causes of severe rhabdomyolysis should be bouts may occur. Affected horses should not be used
considered; renal failure should be considered as a for breeding.
cause of hyperkalaemia in horses with HYPP; colic;
tetanus; viral myeloencephalopathies. NUTRITIONAL MYODEGENERATION
(‘WHITE MUSCLE DISEASE’)
Diagnosis
History and clinical signs are essential. Aetiology/pathophysiology
Hyperkalaemia in blood samples occurs in most A rare condition caused by a dietary deficiency of
cases during episodes but not between them. EMG selenium +/− vitamin E, plus as yet unknown factors,