Transcript Musculoskeletal Disorders

Musculoskeletal
Disorders
INAG 120 – Equine
Health Management
November 14, 2011
Musculoskeletal Disorders
Normal muscle physiology
Muscle response to injury
Muscle problems
Tendon disorders
Ligament problems
Normal Muscle Physiology
Type 1 – Slow Twitch
High oxidative
capacity, lots of
mitochondria
Aerobic metabolism
Low glycogen storage
capacity
Narrow muscle, slim
Normal Muscle Physiology
Type 2a & 2b – Fast
Twitch
Well-developed glycolytic
pathway, few
mitochondria
Anaerobic metabolism
High glycogen storage
capacity
Quarter horses, big
muscles
Muscle Tissue Response to Injury
Muscle can repair well if the supporting
structures remain intact
Atrophy = decrease in volume due to a
decrease in size of the individual muscle
cells
– Generalized = symmetrical; may be due to ↓
nutritional status, old age
– Localized = due to paralysis, area of damage
– Neurogenic = deprivation of nerve supply
Classification of Muscle Diseases
in Horses
1. Muscle damage
–
Non-exertional
Inflammatory, nutritional, toxic or metabolic
–
Exertional
Sporadic or chronic
2. Muscle atrophy
–
Neurogenic
EMND, EPM, focal nerve damage
–
Myogenic
Immune-mediated, chronic disease, malnutrition,
disuse, Cushing’s disease, PSSM
Classification of Muscle Diseases
in Horses
3. Abnormal muscle twitching
– Myogenic
Myotonia, HYPP, electrolyte imbalance,
botulism
– Neurogenic
Shivers, myoclonus, focal nerve damage,
ear ticks
4. Muscle weakness and exercise
intolerance
– Metabolic disorders
Exertional Rhabdomyolysis
Most Affected Muscles
Exercise-related
myopathy
Monday Morning
Disease
Exercise-induced
myositis
Tying-up
Azoturia
Tying Up
Equine Exertional Rhabdomyolysis
Clinical signs varied, depending on
severity:
– Mild – somewhat stiff after exercise
– Severe – incapacitation; horse unable to
stand or bear weight
– Muscles of hindquarters most severely
affected
Tying Up
Pain persists for several hours
Exhausted Horse Syndrome 
common in endurance horses
– Depression
– Severe dehydration
– Hyperthermia
– “Thumps” (fluttering of the diaphragm)
– Extensive muscle damage with or
without cramping
Tying Up
Severe cases  dark red-brown colored urine
– Myoglobinuria
© Knottenbelt DC,
Pascoe RR,
Diseases and
Disorders of the
Horse,
Saunders, 2003
© IVIS Reviews in Veterinary Medicine
Diagnosis = presence of creatine kinase (CK)
and aspartate aminotransferase (AST) in the
blood, muscle biopsy, genetic testing
Tying Up – Causes
Two broad categories:
Sporadic exertional rhabdomyolysis
– Horses which, on rare occasion,
experience tying up
Chronic exertional rhabdomyolysis
– Horse experiences repeated episodes
with the first usually occurring at a
young age
Sporadic ER
Exercise exceeds the horse’s fitness
level
– Horse competing after a lay-off and only
minimal training before the event
Electrolyte imbalance
Deficiencies of vitamin E and/or
selenium
Horses with concurrent illness
– Respiratory viral infections
Chronic ER
Animals prone to relapse  limit athletic career!
Many different breeds affected (Thoroughbreds,
Arabians, Standardbreds, QH, drafts and
warmbloods)
Possible causes:
– Hormonal imbalances (low thyroid)
– Lactic acidosis within muscle
– Diet
High grain diet
Vitamin E and/or selenium deficiency
Electrolyte imbalances
– Calcium?
– Genetics
Chronic ER
Study by Valberg et al. (1999) uncovered
two specific causes of Chronic ER:
– Polysaccharide storage myopathy (PSSM)
– Recurrent Exertional Rhabdomyolysis (RER)
PSSM
Polysaccharide Storage Myopathy
– Storage of excess carbohydrate in the
muscle
Muscle glycogen concentrations are 1.5 – 4
times higher
– Affects drafts, Quarter Horses,
warmbloods and a few Thoroughbreds
– Clinical signs often develop at a young
age when horse begins training
– Hereditary?
PSSM
40% of the type II muscle fibers have
been found to have an acid
mucopolysaccharide inclusion
– Abnormal metabolism  increased uptake of
glucose from the blood and quicker storage as
glycogen
CK and AST levels are elevated
– CK may remain high weeks after event (esp. in
QH)
Seen in calm, sedate horses that are
heavily muscled
Heredity of PSSM
Genetic mutation occurred early on
– Present in many different horse breeds
– Accounts for over 90% of PSSM cases in some
horse breeds
– P = horse carries mutant gene
– N = normal gene
P/P = more severely affected, harder to manage
(rare)
P/N = affected with PSSM, clinical signs vary
N/N = unaffected w/ PSSM type 1
Second mutation (MH) intensifies the
clinical signs in Quarter Horses and related
breeds
Treatment PSSM attack
Treatment:
– Oral or IV fluids to correct dehydration
– Physical therapy
24 hours after episode = large box stall to move
around
Few minutes of hand-walking ok, but best to
allow horse to move on its own
Small paddock turnout with quiet horse
Duration and frequency of walking bouts should
be increased over a week
– Massage therapy
– Detailed diagnostic exam if chronic
RER
Recurrent Exertional Rhabdomyolysis
– Defect in the mechanism of muscle
contraction
Increased sensitivity to contraction when exposed to
certain stimuli
Abnormal location of nuclei in muscle biopsies
Abnormal regulation of calcium movement within
cells
– Common in Thoroughbred, Arabian and
Standardbred horses
– May be hereditary in Thoroughbreds
– Increased levels of CK after exercise
Predispositions for RER
Age
– 2 year old >> 3 year old > 4 year old, etc.
Gender
– 65% are fillies
Temperament
– Nearly half characterized as “nervous”
Lameness
– Lameness is more common in horses that tie up
Diet
– Fed >10lbs of grain/sweet feed per day
Exercise intensity
– Tie up more often when gallop training than breezing or racing
– Three-day-event horses tie-up after the steeplechase, prior to
cross-country phase
– Racing Standardbreds tie-up after 15 minutes of jogging.
Management of horses with RER
Keep horse in quiet area of the barn
Train first rather than last
Turn-out
Avoid training regimes like holding back at a
gallop or intervals that excite the horse
Tranquilize before exercise to prevent excitement
Attention to and treatment of lameness
Avoid stall rest or lay-up
Use medications that affect intracellular calcium
regulation
– dantrolene 4mg/kg orally 1 hour before exercise
Tying Up – Prevention of attacks
Feeding:
– Fat supplemented diets
Diets high in carbohydrates can cause
excitement (RER)
In horses with PSSM, problem is one of excess
carbohydrate storage in muscle, so
elimination of grain is a must
20-25% of calorie requirements from fat!
– Balanced electrolytes, water and Ca:P
ratio, Vitamin E and Selenium
– High quality forage (alfalfa or grass)
Muscle Cramping
Due to overactivity
– Endurance horses
– Exertional rhabdomyolysis
– Hypocalcemia (not enough Ca)
Stiffness, pain, periodic spasms
Increase in muscle enzymes
Endurance Horse Muscle
Cramping
Clinical Signs
– Elevated temperature, pulse, respiration
– May be seen with “Thumps”
– Stiffness, pain, periodic spasms
– NO increase in muscle enzymes
Treatment
– Rest
– Rehydration with appropriate
electrolytes
Thumps
Synchronous Diaphragmatic Flutter
– Diaphragm contracts synchronously
with the heart
– Seen as a flank twitch coincident with
heart rate
Causes
– Endurance exercise during hot weather
– Hypocalcemia, digestive disturbances,
some medications
Post-anesthetic Related
Myopathies
Localized
– Found in individual muscle groups which
are in contact with hard surface for
prolonged periods
– Musculature starved of blood
Generalized
– Involves multiple muscle groups,
increased heart & respiratory rate,
sweating and myoglobinuria
– Reaction to anesthetic used
Equine Sports Massage Therapy
Equine Sports Massage Therapy
differs from other forms of massage:
– Focuses on the cause of the muscle
injury
– Relieves pain
– PREVENTION of future injuries to those
muscles
Involves a full body massage at
every session
When and Why to Massage
Pre-Event:
– Supple muscles
– Enhance range of
motion
– Positive effect on the
contraction and release
process of the muscles
Post-Event:
– Reduce postperformance anxiety
and stress
– Prevents soreness
– Release tension so the
horse's muscles can
relax
When and Why to Massage
Post-Injury:
– Reduce inflammation and
swelling in joints
Stall Bound:
– Stimulate circulation of
blood and lymph
throughout the body
– Increase production of
vital fluids in joints
Maintenance:
– Maintain fitness by
enhancing the muscle tone
Benefits of Massage
1. Increased blood flow to tissues
 More nutrients to cells  quicker removal of
waste products
2. Increased lymphatic flow
 Reduction in swelling and removal of waste
products
3. Relief from muscle spasms
 Stretching and warming of muscle tissues
allows for relaxation
4. Fibrosis and scar tissue inhibited
5. Pain relief through release of endorphins
Tendon Properties
Tendons connect muscle to bone
Tough, inelastic band of fibers
Shock absorbers in locomotion
Change with age: become more
prone to damage
Poor at functional adaptation
Original tendon strength after
damage is not as high
Tendon Injury
Catastrophic failure
– Massive overload  exceeds
strength of tendon (VERY
unusual)
Apparent catastrophic
failure
– Weakening of structure due
to accumulated microdamage
Partial failure
– Micro-damage limited to
portion of tendon (tendonitis)
(most common)
Equine
Emergency!
Tendon Injuries
Treatment
– Ice/cold therapy
20 minutes every hour for 1st 24 hours
– NSAIDs
High doses; watch for ulcers, toxicosis
– Wrap legs
No heating agents or liniments; keep well-wrapped
for first few months
– PSGAG’s (e.g., Adequan)
Controversial; may be injected into lesion
Tendon injuries…
Controlled exercise program/ rehabilitation
Therapeutic ultrasound?
Stem Cell Therapy?
Treatments losing favor:
– Tendon splitting
– Blistering/pin-firing
– BAPN – “bapten” – plant derived substance
that is injected into lesion to prevent formation
of collagen during healing
Equine
Emergency!
Tendon Lacerations
Require IMMEDIATE specialist attention
May prove fatal
(may involve damage
and subsequent
infection of joint
capsule)
Septic tenosynovitis
– Difficult to treat if left
for more than a few hours
Ligament Properties
Connect bone to bone
Prevent displacement of tendons and
joints
Ligament that has been damaged
loses elasticity and can obstruct
movement
Annular Ligament
Constriction
Clinical signs
– Non-specific lameness
– Possible history of
trauma to fetlock
– Lameness worsens with
exercise/ doesn’t
improve with rest
Treatment:
– Surgical resection
– Good prognosis if only
ligament involved
– If damage to tendon 
guarded
Suspensory
Ligament Rupture
Complete rupture
Partial rupture
POOR PROGNOSIS
Racing injury
May occur with
fractures of sesamoids
Treatment = humane
euthanasia
May immobilize joint
for breeding stock
Suspensory Desmitis
Inflammation of suspensory ligament
– Runs along the back of the cannon bone
– Splits to become a medial and lateral branch
– Attach to the proximal sesamoid bones and the
proximal phalanx
Similar to tendonitis – less well diagnosed
Severe damage usually means the
sesamoid bone has been cracked
Treatment = same as for tendonitis
Sususpensory Ligament Desmitis