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polysaccharide storage myopathy. The fact that muscle fibre
necrosis was ongoing 4 days following resolution of the
clinical signs is consistent with previous studies of horses with
polysaccharide storage myopathy (Valberg et al. 1997).
Follow-up
Analysis of the concentrate portion of the mare?s diet 7
indicated that she had been consuming approximately 0.6 kg
starch and 0.06 kg fat per day. A recommendation was made
for a change to a high fat-high fibre diet with low starch and
sugar with as much exercise as possible. The initial diet
employed was 0.9 kg of a commercially available high fat feed
(Empower) 6and provided approximately 0.2 kg fat and 0.2 kg
starch per day. Medium quality grass hay was fed ad libitum .
Analysis of serum CK and AST 4 months later indicated
persistent mild increase in CK (519 u/l); AST was normal
(364 u/l). The diet was changed to a commercial pelleted feed
(Strategy) 1that the mare would accept with 480 ml added
corn oil, to provide approximately 0.4 kg starch and 0.52 kg
fat per day, along with ad libitum grass hay. Analysis of serum
CK and AST 5 months later indicated reduction in serum CK
(399 u/l); AST was within the normal range (410 u/l). The
mare?s body condition was markedly improved (estimated
weight 435 kg; Fig 3 ). The mare remained on the prescribed
high fat, low soluble carbohydrate diet for 30 months, and
there were no further episodes of rhabdomyolysis either on
pasture or while being ridden.
Discussion
Exertional rhabdomyolysis is recognised to occur in Arabians
(Hildebrand et al. 1990; Freestone and Carlson 1991; Harris
1991; Valentine et al. 1998a, 2000). Although no reports of
incidence within the breed were found, Harris (1991) reported
48 affected Arabians in a survey of 628 horses with exertional
rhabdomyolysis and Valentine et al. (1998a) reported one
Arabian in a group of 19 horses with exertional rhabdomyolysis.
Equine polysaccharide storage myopathy (EPSSM, also
called PSSM and EPSM) is recognised to be a cause of
exertional rhabdomyolysis in Quarter Horse, Paint, Appaloosa,
draught and Warmblood related breeds (Valberg et al. 1992,
1999; Valentine et al. 1998a; McGowan et al. 2003; Valentine
2003; McLeay 2004). Other clinical signs related to muscle
dysfunction, including muscle atrophy, are also common
(Valentine et al. 1998b, 2001a; Valentine 2003). Although the
exact pathogenesis of this metabolic myopathy is still unclear,
the abnormality appears to involve abnormal muscle cell
carbohydrate metabolism, which may lead to an ?energy crisis?
(Annandale et al. 2004). The diagnosis of EPSSM is based on
finding characteristic aggregates of abnormal polysaccharide,
particularly amylase resistant material, in myofibres (Valberg et
al. 1992, 1999; Valentine et al. 1998b, 2001b; McGowen et
al. 2003; Annandale et al. 2004; MacLeay 2004). Findings
consistent with EPSSM can be found in muscle samples of
many horses of various breeds, indicating that this underlying
myopathy is not uncommon (Valentine et al. 2001b; Valentine
and Cooper 2005). Affected horses can be successfully treated
with a combination of dietary change (high fat, high fibre, low
starch and sugar) and exercise (Valentine et al. 1998a, 2001a;
Ribeiro et al. 2004). The most effective diets are those that
provide at least 0.45 kg fat per 450 kg of horse per day and
as much reduction in starch and sugar as the horse will accept
(Valentine et al. 1998a, 2001a).
Based on in vitro studies, exertional rhabdomyolysis in
Thoroughbreds has been reported to be related to abnormal
myofibre calcium handling (Lentz et al. 1999; Valberg et al.
1999; MacLeay 2004). Rhabdomyolysis in Arabians has been
attributed to a similar mechanism (Valberg et al. 2001)
although previous in vitro studies of muscle from affected
Arabians found no abnormalities (Hildebrand et al. 1990).
The mare in the current report was treated at the farm on an
after-hours emergency basis as part of the university?s rural
practice service. Practical and financial concerns limited testing
and therapy. Serial evaluation of serum CK and AST soon after
examination would have aided in determination of the degree
and time course of the muscle injury. Evaluation of renal
parameters to rule out myoglobin-induced renal damage would
also have been useful. Blood levels of selenium and vitamin E
were not analysed in this case. However, dietary vitamin E
deficiency is unlikely given the diet of alfalfa hay and spring
pasture grass, and the mare was on a selenium-supplemented
concentrated feed. Although treatment of acute rhabdomyolysis
with vitamin E and selenium may reduce free radical-induced
muscle membrane injury, deficiency of dietary vitamin E or
selenium is considered unlikely to be a cause of rhabdomyolysis
in horses on a good nutritional programme (Beech 2000). Given
the history, a diagnosis of sporadic exertional rhabdomyolysis
might have been considered (Beech 2000). The persistent high
serum CK detected prior to institution of sufficient dietary fat is
Fig 3: 12-year-old Arabian mare 8 months after instituting ahigh fat, high fibre, and low starch and sugar diet. Despitehaving only recently weaned a foal, body condition isimproved, with increased muscling, particularly in the dorsalmusculature of the rump.
EQUINE VETERINARY EDUCATION / AE / APRIL 2007