Equine Myopathies Flashcards
what anatomic components do most myopathies affect?
most myopathies on the level of the muscle fiber (cellular level / group of cells)
Musculoskeletal exam components
- Distance examination
◦ Posture & stance
◦ Muscle mass
◦ Muscle symmetry - Palpation
◦ Muscle tone - Presence of fasciculations
- Motion exam
◦ Lameness
◦ Ataxia
◦ Weakness
◦ Stiffness
◦ Spasticity
◦ Exercise intolerance
myopathies diagnostic tests, generally
- Biochemical analysis
◦ Creatine Kinase (CK) > acute
◦ Aspartate transamine (AST) > slower to rise and fall
◦ Lactate dehydrogenase (LDH)
◦ Creatinine
◦ BUN
> renal values relevant to pigment nephropathy - Urinalysis
- Vitamin E and selenium
- Exercise-Response Testing
- Imaging
◦ Thermography
◦ Nuclear Scintigraphy > r/o bony lesions
◦ Ultrasonography - Electromyography
- Muscle biopsy > common in field
◦ Semimembranosus
◦ Gluteus medius
◦ Epaxial
◦ Sacrocaudalis dorsalis - Genetic testing
Non-exertional Myopathies - infectious casues
◦ Viral
◦ Clostridium spp.
◦ Streptococcus equi
◦ Anaplasma phagocytophilum
◦ Sarcocystis fayeri
Non-exertional Myopathies - toxin causes
◦ Ionophores
◦ Hypoglycin A
Non-exertional Myopathies - nutritional causes
◦ Vitamin E deficiency
◦ Selenium deficiency
Non-exertional Myopathies - traumatic causes
◦ Compressive
◦ Postanesthetic
◦ Trauma
Non-exertional Myopathies - genetic causes
◦ Glycogen branching enzyme deficiency
◦ Hyperkalemic periodic paralysis
◦ Malignant hyperthermia
◦ Myosin heavy chain myopathy
Non-exertional Myopathies - immune-related causes?
Immune mediated
Sporadic Exertional Myopathies - causes
◦ Overexertion
◦ Exhaustion
◦ Dietary Imbalance
Chronic Exertional Myopathies - causes
◦ Polysaccharide storage myopathy type 1
◦ Polysaccharide storage myopathy type 2
◦ Myofibrillar myopathy
◦ Recurrent exertional rhabdomyolysis
◦ Idiopathic exertional rhabdomyolysis
Hypoglycin A myopathy
- what is it? etiology?
- signs
- dx
- prognosis
- Highly fatal lipid storage myopathy
- Ingestion of seeds from Acer sp. trees (boxelder maple)
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Clinical signs
◦ Weakness/ stiffness
◦ Sweating
◦ Fasciculations
◦ Tachycardia/ tachypnea
◦ Myoglobinuria
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Diagnosis – measurement of serum acylcarnitines and urine organic acids
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Prognosis - <75% of horses survive
Vitamin E and Selenium deficiency - myopathy
- what is it?
- forms, signs, prognosis?
Nutritional myodegeneration
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* Cardiac form
◦ Weakness, respiratory distress, tachycardia, arrythmias
◦ Poor prognosis, residual myocardial damage if survive
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* Skeletal form > far more common
◦ Slower onset
◦ Weakness, stiffness, trembling, and recumbency
◦ Painful, firm muscles on palpation
◦ Dysphagia > may be the only sign: foals with weak swallowing muscles
◦ Favorable prognosis with Vitamin E/Se supplementation
Glycogen Branching Enzyme Deficiency
- etiology of myopathy
- signs
- bloodwork
- dx?
Fatal autosomal recessive mutation in GBE1 gene
> way less GBE protein (enzyme) in these foals
> foals cant form branched glycogen
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Clinical signs
◦ Hypothermia
◦ Weakness & intermittent collapse
◦ Flexural deformities
◦ Ventilatory failure & cardiac arrhythmias
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Bloodwork
◦ Recurrent hypoglycemia
◦ Increased CK, AST and GGT
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Genetic testing
> these foals cannot go far - euthanize
Malignant Hyperthermia
- etiology of myopathy
- triggers
- clinical signs
- dx
- tx
Autosomal dominant mutation in RYR1 gene
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Triggers
◦ Halogenated anesthetics
◦ Depolarizing muscle relaxants
◦ Stress
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Clinical signs
◦ Hyperthermia (> 43 C)
◦ Tachycardia
◦ Muscle rigidity and rhabdomyolysis
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Genetic testing
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Treatment and prevention
◦ Dantrolene
Hyperkalemic periodic paralysis
- myopathy etiology
- clinical signs
- dx
- tx
Autosomal dominant mutation > incomplete penetrance, will have different degrees of clinical signs
◦ Voltage-dependent skeletal muscle Na channel
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Clinical signs
◦ Sporadic attacks of muscle tremors (“worms crawling under skin”), weakness, and collapse
◦ 3rd eyelid protrusion
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Serum hyperkalemia
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Diagnosis
◦ Genetic testing
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Treatment
◦ Oral &/or IV dextrose > insulin will drive K into cells
◦ IV calcium
◦ Acetazolamide
Myosin Heavy Chain Myopathy
- old name?
- who gets it?
- etiology, progression
- signs
Previously: Immune-mediated myositis
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Quarter horses and related breeds
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Autosomal co-dominant MYH1 mutation
* Rapid onset muscle atrophy > can be triggered by vaccine
◦ 30-40% of muscle mass in days
* Nonexertional rhabdomyolysis
◦ Muscle stiffness
◦ Pain
◦ Inability to rise
* 40% of heterozygous horses no clinical signs
- can have recurrence, especially with two copies of gene
Polysaccharide Storage Myopathy type 1
- prevalence
- etiology
- what is it?
- who gets it?
- triggers?
Autosomal dominant genetic mutation
◦ GYS1 gene
> can cause episodes of muscle stiffness and pain after exercise, also known as “tying up” or exertional rhabdomyolysis
* Prevalence:
◦ European continental drafts (Belgians & Percherons)
◦ Quarter horses & related breeds
- very common
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Most common trigger of clinical signs
* Less than 20min of exercise at one time
◦ Walk and trot
◦ Several days of rest prior
Polysaccharide Storage Myopathy type 1
- Acute clinical signs
- dx
- Acute clinical signs
◦ Muscle fasciculations
◦ Muscle stiffness
◦ Tucked up, camped out stance
◦ Sweating
◦ Reluctance to move forward - CK > 35,000 U/L
- Myoglobinuria
Polysaccharide Storage Myopathy type 1
- Chronic clinical signs: light horses
- biochem?
◦ Lack of energy
◦ Reluctance to move forward
◦ Frequently stopping and stretching out
◦ Poor performance
◦ Repeated episodes of exertional rhabdomyolysis
◦ Chronic back pain
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Persistent elevation in CK and AST
Polysaccharide Storage Myopathy type 1
- Chronic clinical signs: drafts and draft crosses
◦ Many are asymptomatic
◦ Progressive weakness and muscle loss
> Difficulty rising
> Normal CK level
◦ Severe rhabdomyolysis and myoglobinuria
> Recumbency and death
Polysaccharide Storage Myopathy Type 1
Diagnosis
Gold standard
◦ Genetic testing
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Muscle biopsy
◦ PAS+ & amylase-resistant inclusions
◦ False negatives
> Small samples
> Horses < 1 year of age
Polysaccharide Storage Myopathy type 2
- etiology?
- prevalence and who gets it?
No known genetic mutation
◦ Prevalence:
◦ Warmbloods (Dutch, Swedish, Selle Francois, Hanoveraian)
◦ Quarter horses and related breeds
◦ Morgans, Thoroughbreds & Standardbreds
Polysaccharide Storage Myopathy type 2
Acute and chronic clinical signs, who is affected
Acute clinical signs
◦ Most common in QHs, TB, STDB and Arabians
◦ Exertional rhabdomyolysis
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Chronic clinical signs
◦ Poor performance
◦ Gait abnormalities
◦ Sore muscles
◦ Unwillingness to work/ low energy
Polysaccharide Storage Myopathy type 2
- diagnosis?
No glycogenolytic enzyme defects
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Diagnosed by muscle biopsy
◦ Abnormal glycogen aggregates
◦ Amylase-sensitive
◦ PAS +
◦ Increase in normal beta glycogen particles
Management of PSSM type 1 & 2
- Exercise
◦ Limit stall rest to <48 hours
◦ Pasture turnout
◦ Regular daily exercise - Genetics
- Diet > lower sugar, higher fat
Exertional Rhabdomyolysis
- prevalence
- clinical signs
Most common muscle disease of the horse
◦ Sporadic or recurrent
◦ Associated with other muscle diseases
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Clinical signs
◦ Stiff, stilted gait
◦ Excessive sweating
◦ Tachypnea
◦ Reluctance to move/walk
◦ Painful, firm muscles on palpation
◦ Myoglobinuria
◦ Colic
◦ Recumbency
Exertional Rhabdomyolysis
Causes
- Overexertion
- Exhaustion
- Dietary imbalances
◦ High NSC
◦ Electrolyte deficiencies
◦ Selenium/ vitamin E deficiency - Genetics?
◦ Recurrent exertional rhabdomyolysis
Exertional Rhabdomyolysis
Diagnosis, treatment
Diagnosis
◦ History and exam
◦ Elevated CK and AST
◦ +/- myoglobinuria
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Treatment
◦ Fluid therapy > for pigment nephropathy, and if they are painful they dont drink
◦ Correct electrolytes
◦ Pain management > Use caution with NSAIDs
◦ Rest
