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Equine practice

Diagnosis and management of

equine rhabdomyolysis

John Keen

Our knowledge of rhabdomyolysis has increased greatly in the past 10

years. Detailed clinical and molecular investigations are starting to uncover
and identify more diverse disorders that lead to a clinical end-point that
John Keen graduated from represents signs of muscle disease. In equine practice, despite the fact that
the Royal Veterinary College in cases of acute sporadic rhabdomyolysis (ie, ‘tying up’) are quite common,
1996, after which he spent four the pathophysiology of this disease is still poorly understood. The astute
years in mixed and subsequently clinician can, however, recognise chronic cases that may have an underlying
predominantly equine practice. In metabolic defect that predisposes to muscle disease even when management
2000, he was appointed the RCVS practices are optimal. This article describes the most commonly seen types of
Clarke and Sparrow resident in rhabdomyolysis in horses, discusses the approach to diagnosis and highlights
equine studies at Edinburgh, where the options for treatment in affected cases.
he is currently a senior clinician in
the equine hospital. He holds the
RCVS certificate and European
diploma in equine internal Terminology and causes of equine The term myopathy is a generic term that simply
medicine, an MSc and a PhD for rhabdomyolysis refers to muscle disease. Rhabdomyolysis more spe-
studies on the role of microvascular cifically refers to the breakdown of muscle. However,
disease in laminitis. He is an RCVS The terminology used in descriptions of muscle dis- both terms are often used interchangeably. A useful
and European specialist in equine ease has become confusing with a variety of terms still classification scheme for rhabdomyolysis in adult hors-
internal medicine. in common usage. Clinical or descriptive terms such es is shown in Box 1. Some of the disorders included
as ‘Monday morning disease’, ‘tying up’, ‘set fast’ and may have limited histopathology consistent with mus-
‘azoturia’ have become replaced by terms that reflect cle cell lysis, while others show spectacular damage.
both the pathology found in muscle and our current The most common and clinically important rhab-
understanding of molecular disorders leading to that domyolyses are described below, while others, includ-
pathology. The terminology is likely to adapt further ing some that are encountered in foals, are listed in
as other specific disorders become known. Table 1.

Box 1: Classification of rhabdomyolysis in adult horses

Exertional rhabdomyolyses are the most common type seen. Sporadic exertional rhabdomyolysis represents the
classic acute case of ‘tying up’, while chronic exertional rhabdomyolysis should be suspected if patients present
with repeated episodes.
Rhabdomyolysis

Non-exertional
Exertional rhabdomyolysis
rhabdomyolysis

Sporadic exertional Chronic exertional

Atypical myopathy Other myopathies
rhabdomyolysis rhabdomyolysis

Recurrent exertional
Toxic (eg, ionophore)
rhabdomyolysis

Infectious (bacterial/
Idiopathic chronic
viral)
exertional
rhabdomyolysis
Immune-mediated
Polysaccharide storage
myopathy Post-anaesthetic/
recumbency
doi:10.1136/inp.d454

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Equine practice

Sporadic exertional rhabdomyolysis Table 1: Less common or poorly described myopathies often
Sporadic exertional rhabdomyolysis is generally characterised by rhabdomyolysis
associated with over-training or over-exertion above
Disorder Key features
the animal’s level of fitness. Alternatively, the condi-
Glycogen branching enzyme disease Affects young quarterhorse foals. Is 100 per cent fatal
tion may be seen in some horses that have been laid
off for a period of time (one or more days) without Hyperkalaemic periodic paralysis Is an inherited skeletal muscle defect of the sodium
channel. Only affects quarterhorse breeds. Is episodic.
a concomitant reduction in feeding. Although this is Animals will have high potassium levels during an
the most commonly encountered muscle disorder in episode
practice, it is one of the most poorly understood. It has Immune-mediated myositis History of Streptococcus equi infection affecting
been suggested that excessive glycogen accumulates in either the individual or the farm. Animals will have
muscles when horses are rested on a full ration, thus concurrent signs of vasculitis
impairing aerobic metabolism when they subsequently Ionophore toxicity History. Affected horses also have cardiovascular signs
exercise, which leads to lactic acid build-up. Various Bacterial myositis Is focal. Affected animals may have a history of recent
other pathophysiological processes, including oxida- intramuscular injection
tive stress-mediated damage, have been implicated. Viral myositis Poorly described in horses. Is possibly due to influenza
However, the specific evidence for such mechanisms is virus or herpesvirus
lacking and the aetiology is undoubtedly complex and Post-anaesthetic/recumbency myopathy Affected animals have a history of recent anaesthesia
multifactorial. It is possible that some horses affected with or without hypotension
by sporadic exertional rhabdomyolysis have an under- White muscle disease Is due to vitamin E deficiency. Affects foals and young
lying genetic defect that is less severe than the chronic horses. Is rare
forms (see below) and therefore more easily managed. Myotonia congenita/dystrophy Affects foals and young horses. Is very rare
Most cases of sporadic exertional rhabdomyolysis are
easily resolved with appropriate treatment (see later),
and are unlikely to recur if appropriate attention is thermia, but this is very unlikely to be the cause of
paid to feeding and training regimens. recurrent exertional rhabdomyolysis. Another protein
involved in the excitation–contraction coupling mech-
Recurrent exertional rhabdomyolysis anisms in muscle is likely to be a factor. Inheritance
In the UK, recurrent exertional rhabdomyolysis dis- (autosomal dominant) has been shown to be present
order is especially noted in thoroughbreds in race in a university breeding herd of thoroughbreds with
training, but other breeds such as Arabs or standard- recurrent exertional rhabdomyolysis. Definitive diag-
breds may also be affected. Younger animals and fillies nosis in these horses comprised in vitro contracture
appear predisposed to the condition. Vitamin defi- tests using caffeine, but these must be performed on
ciencies, electrolyte derangements and environmental fresh tissue and this facility is not commercially avail-
temperature changes may be risk factors, although the able. No large scale studies have been carried out to
mechanism for this is unclear. As electrolyte disor- determine if this caffeine hypersensitivity in muscle
ders have been noted in the UK in a small population is true of recurrent exertional rhabdomyolysis in the
of training thoroughbreds with recurrent exertional UK thoroughbred population, although this seems
rhabdomyolysis, it may be worthwhile investigating very probable. Histopathology in cases of recurrent
electrolyte clearance in these horses. exertional rhabdomyolysis is not specific but shows
The aetiopathogenesis of recurrent exertional chronic myopathic changes consisting of internalised
rhabdomyolysis is thought to involve a defect in the nuclei, increased fibre size variation and inflammatory
ability of skeletal muscle to control intracellular cal- cell infiltrates (Fig 1).
cium levels. The ryanodine receptor, one of the trans-
porters that sequesters calcium from the cytoplasm Polysaccharide storage myopathy
into the sarcoplasmic reticulum is dysfunctional in Polysaccharide storage myopathy predominantly
pigs and (very rarely) horses with malignant hyper- affects quarterhorses, draughthorses and warmbloods,
and should be suspected in chronic cases of rhabdo­
myolysis of these breeds. However, the condition has
also been described in a wide variety of other breeds.
Clinical signs are highly variable (see later). Creatine
kinase (CK) and aspartate transaminase (AST) levels
are usually markedly raised in some horses for the
amount of work they have performed and may remain
so for a considerable period of time. In other horses,
especially draughthorses and warmbloods, CK and
AST levels may be minimally elevated despite clinical
signs of rhabdomyolysis.
The aetiopathogenesis involves intracellular accu-
mulation of abnormally high levels of the polysac-
charide glycogen and its intermediary compound
glucose-6-phosphate. It was previously thought that
Fig 1: Photomicrograph of skeletal muscle from a animals with this condition had an impaired ability
case of recurrent exertional rhabdomyolysis. Note the
to break down glycogen, leading to anaerobic respira-
variation in fibre size, internal nuclei and macrophage
cell infiltrate (arrow). (Haematoxylin and eosin stain, tion and lactate accumulation. However, the reverse
magnification x20) (Picture, Caroline Hahn) appears to be the case in many patients; affected ani-

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Equine practice

recumbency and respiratory difficulty in many cases.

Animals that spend long periods of time recumbent
have a grave prognosis. Horses are generally afebrile
and have normal appetite and thirst. Some horses may
Fig 2: Photomicrograph of have dysphagia, possibly due to weakness of mastica-
skeletal muscle from a case
of polysaccharide storage tory muscles and/or smooth muscle of the oesophagus.
myopathy. (Periodic acid-Schiff Cases of atypical myopathy may be confused with colic
stain, magnification x40). or grass sickness. The urine is characteristically dark
There are subsarcolemmal
or chocolate-coloured due to severe muscle break-
accumulations of glycogen
(black arrow) that were down and myoglobin accumulation, and many horses
resistant to amylase digestion. have difficulty in posturing to urinate. CK and AST
Internal nuclei can also be seen levels are markedly raised, although the levels reached
(red arrow). (Picture, Caroline
Hahn)
do not necessarily indicate the severity or prognosis.
The aetiology of atypical myopathy is unknown
but epidemiological studies suggest a pasture-borne
mals often have enhanced insulin sensitivity causing toxin, and a clostridial toxin has been implicated
greater glucose uptake and increased glycogen synthe- (Unger-Torroledo and others 2010). Environmental
sis. Characteristic histopathological changes are seen factors may be important in triggering toxin produc-
in cases of polysaccharide storage myopathy, which tion, thus explaining the seasonal occurrence of most
consist of abnormally high accumulations of glycogen cases (autumn and occasionally spring). Many cases
with or without amylase-resistant inclusion granules seem to occur following a sharp decline in ambient
(Fig 2). A specific genetic defect (point mutation) temperature and/or are associated with high winds or
has recently been detected in the glycogen synthase excessive rainfall. Histopathology of muscles, espe-
1 (GYS1) gene, which causes this enzyme to be over- cially those with a high proportion of oxidative (type
productive. Horses positive for the GYS1 mutation are I) fibres such as the diaphragm, heart (Fig 3) or inter-
referred to as having type 1 polysaccharide storage costal muscles, shows marked fragmentation, swelling
myopathy. Type 2 polysaccharide storage myopathy and macrophage infiltration of muscle fibres (Fig 4).
includes all horses that are positive for the condition Lipid stains such as Oil Red O have shown lipid accu-
on clinical and histopathological grounds, but with- mulation in type I fibres, while ultrastructural studies
out the specific genetic defect. It is probable that other have shown mitochondrial injury; both of these find-
specific defects in glycogen metabolism will become ings are consistent with the impaired fatty acid oxida-
apparent in these type 2 cases.

Atypical myoglobinuria/atypical myopathy

Atypical myoglobinuria/atypical myopathy of unknown
aetiology was first described fully in 1984 in the UK
and still occurs sporadically. The autumn of 2009 saw a
huge surge in the number of cases diagnosed, with over
350 highly suspicious or confirmed cases throughout
Europe, of which 42 were in the UK. Although rare, it
carries a high mortality. Mortality was originally esti-
mated to be 90 per cent although more recent Europe-
wide estimates suggest figures of around 75 per cent.
Subclinical cases occur in cograzers and their recogni-
tion may partially account for the apparently improved
prognosis recently. Fig 4: Photomicrograph of skeletal muscle from a
Atypical myopathy mainly occurs in young horses severe case of rhabdomyolysis. Fig 4a (above): Cross-
and ponies at grass and is not related to exercise. It section showing normal muscle bundles interspersed
with swollen fibres (black arrow) and degenerating
may affect one or more animals in a group. Clinical fibres (red arrows). Fig 4b (below): Longitudinal
signs are sudden-onset muscle weakness and stiffness. section showing profound muscle fibre degeneration
This quickly (within about 48 hours) progresses to and oedematous endomysium. (Haematoxylin and
eosin stain, magnification x20)

Fig 3: Postmortem appearance

of the left ventricular wall of
a case of atypical myopathy,
showing areas of pallor that
are consistent with severe
myopathy affecting the
myocardium

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tion that occurs in cases of atypical myopathy. Further Table 2: Differential diagnoses for primary myopathy/
studies are in progress to investigate whether there is a rhabdomyolysis
deficiency in several mitochondrial enzymes involved Differential diagnosis Differentiating factors/comments
in fatty acid oxidation that may play a significant part
Laminitis Increased digital pulses, laminitic stance, foot pain,
in the pathophysiology of atypical myopathy. radiographic signs
Colic Other signs of gastrointestinal tract dysfunction

General approach to a suspected Aortoiliac thrombosis Hindlimb weakness rather than stiffness, sudden-onset
at exercise, cool limbs, quickly reversible
case of rhabdomyolysis
Pleuritis Other signs of respiratory dysfunction

History and clinical signs Musculoskeletal injuries, especially Localising factors, scintigraphy. Can look very similar
relating to the sacroiliac and to sporadic exertional rhabdomyolysis
A marked variation in the severity of clinical signs is
pelvic regions
seen in horses with rhabdomyolysis. These can range
Hypocalcaemia Periparturient mares, exhausted endurance horses,
from a slight change in gait, a reluctance or inability to
synchronous diaphragmatic flutter. Measure the
move through to recumbency and death in rare cases. concentration of ionised calcium
The severity of clinical signs does not necessarily reflect Neuromuscular diseases
the degree of muscle damage. Most cases of myopa- Botulism Generalised neuromuscular weakness, especially
thy are exercise related – that is, signs occur during bulbar musculature, silage feeding
or immediately following exercise. In some patients, Tetanus Spastic paralysis, non-vaccination
Equine motor neurone disease Predominantly weakness, muscle wastage. Biopsy
signs may even occur following minimal exercise, of the sacrocaudalis dorsalis can aid diagnosis
which suggests chronic myopathy. Exercise probably
serves as a trigger, having a compounding effect on
primed abnormal muscle metabolism. Occasionally, Ancillary diagnostic techniques
non-exercise-related myopathies may be seen in which Blood biochemistry
signs are not associated with exercise at all. Biochemical analysis of muscle-derived enzymes with-
Sporadic exertional rhabdomyolysis usually affects in serum samples can help to confirm muscle dam-
the muscles of both hindlimbs, especially the gluteal, age. The three enzymes that are of most use are CK,
femoral and lumbar muscles. Affected horses develop AST and lactate dehydrogenase (LDH), although the
a stiff gait and may refuse to move. Palpation reveals former two are the most commonly measured.
affected muscle groups to be painful, hard and swollen In cases of rhabdomyolysis, the degree of increase
(Fig 5). The animal is frequently distressed, sweating, in concentration of these enzymes reflects the degree
with a moderately increased temperature, and raised of muscle damage but does not always equate to the
heart and respiratory rates. Signs often associated with severity of clinical signs. CK is the most specific for
colic, such as pawing at the ground, are relatively com- skeletal muscle damage. A more accurate diagnosis
mon. If forced to move and in severe cases, the animal and prognosis may be possible if all three enzymes are
may show obvious muscle fasciculation and may quickly measured and this practice allows the determination
become recumbent due to muscular weakness. of acute versus chronic muscle damage (Fig 6). CK
Other more subtle signs that owners may describe rises and falls first, followed by LDH, and then AST.
and may indicate muscle disease, particularly with CK peaks at two to 12 hours after onset, may reach
regard to the chronic forms of rhabdomyolysis, are 100,000 IU/litre or more, and may return to near nor-
poor performance, difficulty lifting limbs, a ‘shiver- mal levels after 24 to 36 hours (depending on the extent
ing’ gait and muscle atrophy. of the peak). LDH peaks at approximately 15 hours
Differential diagnoses for primary muscle disease and may reach several thousand IU/litre. AST peaks at
are listed in Table 2. 24 hours and may reach many thousand IU/litre and
can remain high in the blood for up to three weeks.
Mild increases in these enzymes may occur after mod-

100,000 Creatine kinase

Lactate dehydrogenase
10,000
International units/litre (log)

Aspartate transaminase

1000

100

10

Fig 5: Appearance of caudal thigh muscles in a

thoroughbred racehorse with sporadic exertional 1
rhabdomyolysis. This horse developed a slow and
0 100 200 300 400
stiff gait while returning from the gallops. Note the
increased definition caused by swelling of the muscles Time (hours)
(arrows). The thigh muscles on both limbs were firm Fig 6: Schematic representation of muscle enzyme kinetics in a case of acute
and painful on palpation rhabdomyolysis

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erate work in unfit horses, or strenuous exercise in fit,

normal horses. Some chronic cases of rhabdomyolysis
may present with much smaller elevations in the serum
concentration of these enzymes.

Exercise tests and plasma muscle enzymes

Exercise tests and plasma muscle enzymes allow the
clinician to detect whether muscles’ response to exer-
cise is ‘normal’. It can be used diagnostically for chron-
ic exertional rhabdomyolysis, or as a training aid when
it is used approximately three days after a return to
exercise or following any increase in workload in sus- Fig 8: Clipped sites for muscle biopsy to evaluate
chronic rhabdomyolysis. The needle technique is best
ceptible horses. The tests involve taking blood samples carried out at the dorsal lumbar and gluteal sites,
two to six hours and 24 hours following exercise. The while the excision technique should be performed
level of exercise should be appropriate for the level of at the semitendinosus/semimembranosus muscles.
Horses should be sedated with an alpha-2 agonist and
fitness. The results may be interpreted as follows:
butorphanol. Penicillin and phenylbutazone should be
■■ Levels of CK and AST should be normal or near administered 30 minutes before surgery
normal pre-exercise;
■■ There should be no more than doubling of CK at
two to six hours; diseases. A needle (eg, Bergstrom) or excision technique
■■ Levels of CK should return to the baseline at 24 may be used (see Fig 8 and Boxes 2, 3). For the evalua-
hours; tion of chronic myopathy, muscles with a high percent-
■■ There should be no more than a 50 per cent increase age of type II fibres (eg, semitendinosus, gluteal, dorsal
in the level of AST at any point; lumbar) should be biopsied. Histopathology in cases of
■■ There should be no clinical signs of stiffness. polysaccharide storage myopathy is highly character-
istic, consisting of abnormally high levels of intracel-
Urinalysis lular glycogen and, in some patients, amylase-resistant
Severe rhabdomyolysis leads to the presence of myoglob- granular accumulations of glycogen.
in in the urine, which consequently takes on a reddish-
brown colour (Fig 7). Commercial urine dipsticks cross Fractional electrolyte excretion test
react on the ‘blood’ tab with both myoglobin and hae- Measurement of fractional electrolyte excretion is
moglobin – ie, the stick detects general haem (iron and a means of evaluating a horse’s electrolyte balance.
porphyrin) pigments. Few laboratories offer a service to Some studies have shown abnormal electrolyte clear-
distinguish between these two proteins but the distinc- ance in horses with recurrent bouts of rhabdomyolysis.
tion is academic in the presence of other clinical signs Excretion of a particular electrolyte in the urine should
and biochemical findings consistent with muscle dis- be compared to that of creatinine (which reflects glomer-
ease. Very dark brown to red urine in a horse showing ular filtration rate) by collecting a free catch urine sam-
signs of weakness or recumbency at pasture is strongly ple before exercise and feeding. A blood sample should
suggestive of atypical myopathy. be collected soon after the urine catch and the following
calculation used to measure the fractional excretion:
Muscle biopsy
Fig 7: Chocolate brown Muscle biopsy is easy to perform and provides very Fractional [e]urine [Cr]plasma
urine, which is characteristic useful information in cases of recurrent myopathy. The electrolyte = x x 100 (units %)
[e]plasma [Cr]urine
of severe rhabdomyolysis. excretion
technique is particularly useful in horses with polysac-
Dipstick analysis in this [e]urine Electrolyte in urine, [e]plasma Electrolyte in plasma,
case was strongly positive charide storage myopathy, but can also be helpful in
for haem pigments patients with other chronic muscle and neuromuscular [Cr]urine Creatinine in urine, [Cr]plasma Creatinine in plasma

Box 2: Technique for needle biopsy of muscle

Skeletal muscle needle biopsy instruments The biopsy area should be prepared and a small bleb of local anaesthetic injected
(eg, Bergstrom needle) consist of a needle subcutaneously. The biopsy instrument should be directed through a stab incision deep into
(A), cutting cannula (B) and probe (C). The the muscle (left) and at the required depth should be angled (right), which causes muscle
probe is used to remove any muscle sections tissue to enter into the instrument. The cutting cannula is then driven home to excise a thin
left in the cannula section of muscle

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Box 3: Technique for excision biopsy of muscle

(A) After surgical preparation, carry out line

infiltration of the skin and subcutaneous tissue using
a local anaesthetic (eg, mepivacaine). Care must be
taken not to enter the muscle as this will distort
A histopathological analysis of the sample obtained

B C

(B) Make a bold incision through the skin to reveal subcutaneous tissue. There may be a considerable depth of
fat before the epimysium is encountered (C)

D E

(D and E) Make two parallel incisions in the muscle and use mosquito forceps to undermine a strip of
muscle. Close the forceps over one end and cut the muscle, after which cut the other end to remove
the strip of muscle

(F) The strip of muscle should be placed on card

and sent for histological analysis. Most laboratories
prefer the section to be placed in a damp (not wet)
G
saline soaked swab and packed with a cool pack in
bubble wrap or similar material for transport (see (G) Muscle and subcutaneous tissue should be sutured
further information). As a back-up, in case of postal using absorbable sutures and the skin apposed as
mishaps, a small section of the sample should be normal. An adhesive dressing (eg, Primapore; Smith
placed directly into formalin & Nephew) may be placed over the incision site

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Interpretation of findings can be difficult because lysis (ie, recurrent exertional rhabdomyolysis and
they can be highly variable and also due to the influ- polysaccharide storage myopathy).
ence of diet on results. Any electrolyte supplementa- ■■ Diet. Reduced carbohydrate (<10 per cent starch)
tion should be stopped before the test is performed. rations appear to be beneficial for the management
The author has rarely found this technique to be useful of both types of chronic disease. If a horse is on
in the evaluation of muscle disease in horses, but finds minimal exercise, probably only forage is required.
it considerably more helpful for the evaluation of renal If extra energy is needed for increased work, oils
disease. may be substituted for carbohydrate. Proprietary
feeds are available from various feed companies
(eg, Dodson and Horrell, and Waltham in the
Treatment UK). Horses should not be fed in anticipation of
an increase in workload; instead, increased calorie
Sporadic exertional rhabdomyolysis intake should follow increased workload.
■■ Rest. Further muscular activity is likely to exacer- ■■ Exercise. All cases of chronic rhabdomyolysis
bate the disease. Therefore, if possible, the horse benefit from continual daily exercise (ie, no rest
should not be moved. Some very mild cases may days), with adequate warm-up periods and without
respond to walking out after the initial signs have breaks in routine. Turnout is also very beneficial.
subsided but, if in doubt, do not move the horse. ■■ Stress avoidance. This is especially important in
The rest period adopted will depend on the sever- horses with recurrent exertional rhabdomyolysis,
ity of muscle damage and response to therapy. as these animals are often of a nervous disposi-
Monitoring muscle enzyme levels until they return tion. Providing company (eg, a pony or goat) or
to within the normal reference range is best prac- a stimulating environment (eg, stable toys) can
tice but can often be impractical. help. Ideally, affected horses should be fed first at
■■ Analgesics. Non-steroidal anti-inflammatory feeding times. Turnout is also beneficial for these
drugs (NSAIDs), such as flunixin meglumine and cases.
phenyl­butazone, are useful for their analgesic and ■■ Drugs.
anti-inflammatory properties. In severe cases with ●● Acepromazine (8 to 15 mg/450 kg) has been

myoglobinuria, there is a risk that NSAIDs may used to reduce the stress of training in horses with
exacerbate renal failure. However, horses that are recurrent exertional rhabdomyolysis, but is unlikely
severely affected should also receive intravenous to be of use in animals with polysaccharide storage
fluid therapy, which will reduce the risks of NSAID- myopathy.
induced renal toxicity. Intravenous opioids may also ●● Dantrolene has anecdotally been found to be

be indicated in severe cases. useful for a number of years. More recently, studies
■■ Fluids. Oral fluids may be considered in mild cases, have shown this drug to be useful in reducing post-
although this is usually not necessary. Intravenous exercise levels of CK, and preventing myopathy
balanced isotonic fluids are indicated for more severe (approximately 2 to 4 mg/kg, 60 to 90 minutes
cases (see section on the treatment of severe rhab- before exercise) (Edwards and others 2003,
domyolysis/atypical myopathy). Acid–base status is McKenzie and others 2004).
rarely abnormal in horses with sporadic exertional ●● Phenytoin has also been used in chronic cases of

rhabdomyolysis, so the injudicious use of bicarbo- rhabdomyolysis, but reports of efficacy are only
nate is contraindicated. Diuretics are usually con- anecdotal. It is very unlikely to be of use in cases of
traindicated unless, despite vigorous fluid therapy, polysaccharide storage myopathy.
the horse is oliguric. ■■ Other.
■■ Sedatives. Acepromazine (8 to 15 mg/450 kg) may ●● Salt. Horses that are undergoing intense exercise

help to alleviate anxiety and muscle spasm. It may may sweat profusely, resulting in a loss of sodium
also promote peripheral vasodilatation. Alpha and chloride. Common salt can be added to the diet
adrenergic agonists (eg, romifidine, detomidine) (20 to 50 g per day, depending on time of year, and
may be useful in very distressed animals. work and sweating rates).
■■ Corticosteroids. Short-acting corticosteroids are ●● Vitamin E and selenium. Although vitamin E and

purported to play a useful role in ‘stabilising cellu- selenium deficiency is unlikely to be involved in
lar membranes’. The risks of laminitis following the the pathogenesis of most types of rhabdomyolysis,
use of high doses of potent corticosteroids are rare, supplementation may be beneficial in severe cases to
but should always be discussed with the owner. ‘soak up’ free radicals (at a dose of 3000 mg/5000
■■ Calcium carbonate and calcium gluconate. These IU per day). More importantly, animals on high-fat
products may be useful in severe cases as calcium, diets should be given additional vitamin E (at a dose
which is often depleted, is necessary for the normal of 100 IU of vitamin E to 100 ml of oil) in their diet,
function of muscles (see section on the treatment of although proprietary feeds should have accounted
atypical myopathy). for this requirement. Occasionally, young foals with
white muscle disease may be encountered, for which
Chronic cases of rhabdomyolysis this therapy is very important.
Presumptive or, preferably, definitive diagnosis is
important in cases of chronic rhabdomyolysis, as this Severe rhabdomyolysis or
will govern the treatment to some extent. However, atypical myopathy
much of the recommended dietary and management Cases of atypical myopathy are generally character-
advice is similar for both types of chronic rhabdomyo­ ised by severe rhabdomyolysis that requires intensive

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Equine practice

therapy. Despite this, many affected horses (70 to 90 Summary

per cent) will die within three to five days.
■■ Bedding and protection. Ensuring that affected Sporadic exertional rhabdomyolysis, the classic ‘tying
horses are in a well-bedded or preferably padded up’ case, still remains the most common presentation
stall is paramount, as most horses will spend pro- of muscle disease in horses and, despite our lack of Further information
longed periods recumbent. Head masks and distal knowledge about exactly how it occurs, it is generally ■■ Neuromuscular Laboratory.
limb bandages will help to minimise trauma in easily treated. However, more severe cases of rhab- Royal (Dick) School of Veterinary
these areas. domyolysis, including the atypical pasture associated Studies, Edinburgh. www.
neurolab.vet.ed.ac.uk
■■ Fluids. Isotonic balanced salt solutions (eg, lactated form, can be problematic to treat and often carry a
■■ Comparative Neuromuscular
Ringer’s solution, given at twice to three times the poor prognosis. Furthermore, recurrent cases of rhab-
Disease Laboratory. Royal
maintenance flow rates) are warranted to mini- domyolysis should be investigated fully to evaluate Veterinary College, London.
mise myoglobin-induced renal toxicity. Urination whether the horse has underlying metabolic abnor- www.rvc.ac.uk/Research/Labs/
should be monitored carefully; horses may not malities that have led to a chronic myopathy. NeuroLab/Index.cfm
urinate if they find it difficult to adopt the cor-
rect posture or if they are suffering from oliguric References and further reading
acute renal failure. Periodic catheterisation is very EDWARDS, J. G., NEWTONT, J. R., RAMZAN, P. H., PILSWORTH, R. C. & SHEPHERD,
useful in case of the former situation, while diu- M. C. (2003) The efficacy of dantrolene sodium in controlling exertional rhabdomyolysis in the
retics (eg, furosemide) may be considered in the thoroughbred racehorse. Equine Veterinary Journal 35, 707-711
latter. MACLEAY, J. M. (2004) Diseases of the musculoskeletal system. In Equine Internal Medicine,
2nd edn. Eds S. M. Reed, W. M. Bayly and D. C. Sellon. Saunders. pp 461-522
■■ Analgesia. NSAIDs are beneficial on both analgesic
MCKENZIE, E. C., VALBERG, S. J., GODDEN, S. M., FINNO, C. J. & MURPHY, M. J. (2004)
and anti-inflammatory grounds. Opioids, such as Effect of oral administration of dantrolene sodium on serum creatine kinase activity after exercise in
morphine sulphate, have also been found to be use- horses with recurrent exertional rhabdomyolysis. American Journal of Veterinary Research 65, 74-79
ful in the author’s clinic. MCKENZIE, E. C., VALBERG, S. J. & PAGAN, J. D. (2003) Nutritional management of exertional
■■ Electrolyte supplementation. Any electrolyte sup- rhabdomyolysis. In Current Therapy in Equine Medicine 5. Ed N. E. Robinson. W. B. Saunders.
plementation should ideally be given based on pp 727-734
PIERCY, R. J. & RIVERSO, J. L. L. (2004) Muscle disorders of equine athletes. In Equine Sports
measured serum levels. Calcium is the electrolyte
Medicine and Surgery. Eds K. W. Hinchcliff, A. J. Kaneps and R. J. Geor. Saunders. pp 77-110
most likely to be deranged. In the absence of cal-
UNGER-TORROLEDO, L., STRAUB, R., LEHMANN, A. D., GRABER, F., STAHL, C., FREY, J.,
cium measurement, supplementation at 50 ml of GERBER, V., HOPPELER, H. & BAUM, O. (2010) Lethal toxin of Clostridium sordellii is associated
40 per cent calcium borogluconate per 5 litre bag with fatal equine atypical myopathy. Veterinary Microbiology 144, 487-492
of lactated Ringer’s solution is safe as long as the VALBERG, S. J. (2009) Heritable muscle diseases. In Current Therapy in Equine Medicine 6.
fluid rate remains at twice that of the maintenance Eds N. E. Robinson and K. A. Sprayberry. Saunders. pp 461-468
level. VOTION, D. M. & SERTEYN, D. (2008) Equine atypical myopathy: a review. Veterinary Journal
178, 185-190
■■ Antioxidant therapy. Vitamin E (3000 mg/5000 IU
per day) and selenium (10 mg/day) may be given
in an effort to minimise free-radical mediated
damage.
■■ Nutritional and glycaemic status. Providing carbo-
hydrate-based feeds has been suggested to be useful
in affected animals, as fat metabolism is deranged
in cases of atypical myopathy. Oral and/or intrave-
nous glucose solutions are also thought to be ben-
eficial based on this finding. In the field situation,
carbohydrate cereal foods that are easily adminis-
tered by stomach tube (eg, finely milled oat cereals)
with added glucose (0·5 mg/kg) may be the most
practical solution. Insulin (40 IU by subcutaneous
injection) may be helpful to promote normoglycae-
mia and lower triglyceride levels, but must be used
with care in case of inadvertent hypoglycaemia.
There may also be some rationale in administering
vitamins and nutrients that may support fatty acid
oxidation (eg, carnitine, riboflavin).
■■ Metronidazole. This can be given at 15 mg/kg orally
three times daily. Although definitive evidence link-
ing cause and effect is lacking, Clostridium species
have been implicated in the pathogenesis of atypi-
cal myopathy by workers in Switzerland (Unger-
Torroledo and others 2010).
■■ Oxygen. This may be warranted in some cases to
maintain an adequate partial pressure for oxygen.
It is best administered through a soft thin tube
into the nares, but some horses will not tolerate
this. Studies have suggested that a partial pres-
sure for oxygen of <60 mmHg affords a very grave
prognosis.

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Diagnosis and management of equine

rhabdomyolysis
John Keen

In Practice 2011 33: 68-77

doi: 10.1136/inp.d454

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