MSK Flashcards
3 types of equine muscle disorders
primary - traumatic/metabolic/infectious - diffuse or focal pain
secondary - using muscles differently because of pain - localised, muscle enzymes often normal
neuromuscular - muscle atrophy - myogenic or neurogenic
muscle strain - equine
acute pain
localised pain and swelling
hard to isolate - large muscle mass
risk factors -
type of activity
surface terrain
poor warm up
mildly elevated muscle enzymes
Ultrasound - fluid accumulation and disrupted fibre pattern
treatment -
cold hosing/icing
NSAIDs
rest
gentle mobilisation and exercises
exertional myopathies - equine
very prevalent
signs -
poor exercise tolerance
muscle stiffness
shortened hind limb stride
reluctance to move
firm, painful, hindquarter muscles
anxiety
pain
sweating
increased resp rate
colic type signs - pawing, trying to lie down
myoglobinuria
elevated CK and AST
sporadic or recurrant
sporadic - one off extrinsic factors - overexercising, dietary imbalance, exhausted horse syndrome
recurrant - intrinsic factors - heritable factos, breed related, recurrent exertional rhabdomyolysis, polysaccharide storage myopathy
recurrent exertional rhabdomyolysis (RER) - equine
abnormal regulation of muscle contraction
issue in calcium kinetics
light or hot breeds - thoroughbreds
suggested heritability
more often in nervous females
risk factor - high grain diet
diagnosis -
signs and history
serum CK and AST increase
muscle histology - used to rule out concurrent conditions
polysaccharide storage myopathy (PSSM) - equine
accumulation of glycogen in muscle fibres
type 1 - mutation in glycogen synthesis gene
can test for mutation
type 2 - looks similar on biopsy but no gene identified
mutation most common in draft breeds, warmbloods, appaloosas, cobs, and ponies
diagnosis -
signs
muscle enzymes
muscle biopsies - only see changes over 2yo
genetic testing - on blood or hair roots
myofibrillar myopathy - equine
exercise intolerance
intermittent RER
warmbloods and arabs
warmbloods can have normal muscle enzymes - confirm on biopsy
arabs - high enzymes after exercise, myoglobinuria - tend to be less painful
exertional myopathies - treatment - equine
relieve pain
correct fluids
protect kidneys from effects of NSAIDs
stabling for acute stages then keep them working - days off can make it worse
diet -
low starch, high fat
adequate electrolytes
vitamin E supplementation
amino acid supplementation - less evidence
medications - dantrolene sodium (muscle relaxant)
clostridial myositis - equine
rare but nasty
usually iatrogenic - recent IM injection
necrotising infection of muscle
systemic illness - severe toxemia
swollen, painful muscle at injection site
subcutaneous emphysema
antimicrobials
multiple surgical debridements
delayed onset muscle soreness - equine
poor performance
diffuse pain
couple of days after unusual exercise
eccentric muscle contractions - contraction when muscle under tension
equine motor neurone disease
not common
generalised atrophy
oxidative damage to motor neurons
risk factors -
vitamin E/selenium deficiency
prolonged pasture access with high CHO diet
signs -
happy enough
normal appetitie
muscle weakness and atrophy
trembling
weight shifting on standing
walk better than they stand
low head carriage
exercise intolerance
“elephant on tub” stance
retinal changes - pigmentation at back of retina
diagnosis -
low vitamin E in plasma
elevated muscle enzymes
muscle biopsy of tailhead - definitive
usually need euthanising
vitamin E deficiency - equine
presents similar to motor neuron disease
responsive to treatment
immune mediated myositis - equine
rapid atrophy
moderate muscle enzymes elevation
usually quarter horses
MYH1 mutation - homozygous horses more affected
triggered by exposure to episode of strangles or other respiratory disease
diagnosis -
biopsy - epxial or gluteal muscles
genetic testing
treatment - steroids, antibiotics if concurrent infection
hip dysplasia - risk factors
weight
types of exercise
overexercising when young
breed - big dogs
ddx - hip dysplasia
arthritis
legg-calves perthes - avascular necrosis of femoral head
psoas injury
elbow dysplasia
cruiciate injury
luxated patella
nervous conditions - sciatic pathology
neoplasia - bone or joint
sepsis
hip dysplasia - pathophysiology
joint laxity –> femoral head subluxation
osteoarthritis changes - wear, cartilage thinning, fluid, osteophytes
most crucial time for hip development - before 8 weeks
hip scoring
each hip scored between 0-52 (overall out of 106)
lower score better
VD radiograph under GA
very straight
both limbs straight out and tied together
labelled
ID number and kennel club number
reviewed by 2 experts
patellar luxation - pathophysiology
bad conformation - muscle action pulls patellar ligament and displaces patella
not congenital - born normal, other abnormalities/deformities in limb causing them to turn inwards
grading 1-4
hip dysplasia - signs
difficulty rising
abnormal gait
bunny hopping
pelvic limb lameness
clicking of hips
assymetric muscle mass
sensitivity on hind quarters - esp on extension and abduction
reduced range of motion
crepitus
asymmetric pad wear
all non specific
hip dysplasia - testing
ortolani test
barden test
radiography - VD legs extended, VD frogleg, lateral (hip series) - measures of dorsal acetabular cover, norberg angle, distraction index
hip dysplasia - management
pain management
exercises - range of motion, muscle mass, strength
controlled activity level
weight management
nutraceuticals
physiotherapy
surgery - excision arthroplasty (joint fills with soft tissue to create false joint), total hip replacement, joint fusion (not hips but other joints)
cruciate injury - signs
frog sitting - external rotation of opposing stifle
sit test
loss of muscle mass
cranial draw
meniscal injury
seen secondary to cranial cruciate rupture (in most cases)
usually medial meniscus
heals poorly - usually needs taken out
if taken out - always end up with degenerative joint disease
cruciate injury - management
suture - loop round to create rotating force and hold in place
osteotomy - TPLO, TTA - good outcomes, expensive
cruciate injury
cruciate function - prevents cranial translation and internal rotation of tibia and prevents hyperextension of stifle
most common cause of hindlimb lameness
often eventually bilateral
changes can exist before ruptures
partial tears common
usually not a contact injury - different from in people