LA Myopathies, Mechanical Lameness, and Neurologic Lameness Flashcards
describe pathophysiology of muscle damage
- cell damage allows Ca2+ to enter cytoplasm, which activates destructive cellular processes and inhibits mitochondrial respiration
- results in necrotic cell death and inflammatory response
what is required for muscle healing? possibly not revelant
- ruptured mofibers contract, forming gaps between stumps; allowing access for inflam cells from capillaries
- contraction bands (cytoskeletal and sarcomeric material) plug myofiber stumps, reventing further damage
- satellite cells (adult skeletal muscle stem cells) get activated; migrate to area of damage over a period of 5 days and fuse to form multinucleated myotubes
- myotubes differentiate into myofibers over several months
- if basement menbrane damage occurs, more extensive fibrosis can occur
what are 6 clinical signs of myopathies?
- stiffness
- muscle hypertonicity/swelling
- pain on muscle palpation
- reduction in performance
- unwillingness to work
- urinary effects
describe testing for myopathies (ON EXAM!!!!!!!!!)
- bloodwork:
-CK (creatinine kinase): peaks 4-6 hours following muscle damage; half life of 12 hours
-aspartate aminotransferase (AST): peaks 24 hours after muscle damage and remains elevated for days to weeks - exercise testing:
-baseline CK
-light exercise for 20 minutes
-check CK 4 hours later
-a 2-3 fold increase in CK suggests underlying myopathy - muscle biopsy
- genetic testing
describe exertional rhabdomyolysis; include clinical signs, diagnosis confirmation, and treatment (WILL BE ON EXAM!!!)
- often history of recent and sudden increase in exercise, change in training
- also called tying up, weekend warrior syndrome, capture myopathy
- due to lack of muscle conditioning, increased anaerobic metabolism
clinical signs:
-mild stilted gait to severe stiffness, sweating, and recumbency
-achycardia
-firm, painful muscles (esp in hindlimbs, pelvis, and back)
-in horses: may present with colic signs or posturing to urinate
diagnosis confirmation:
1. bloodwork: elevated muscle enzymes
2. check kidney values!
-horses may have or develop pigmenturia due to myoglobin release from muscles that will damage the kidneys; creatinine will be elevated in these cases
treatment:
1. NSAIDs: caution if kidney values elevated
2. acepromazine: vasodilator, improve blood flow in muscle to increase comfort
3. rest with light exercise (hand walking or paddock turnout)
4. fluids may be necessary if kidneys affected (solution to pollution is dilution)
describe polysaccahride storage myopathy (PSSM)
formation of polysaccharide with abnormal structure that accumulates as HORSES age and cause deficits in energy when exercised, resulting in stiffness, mild exertional rhabdomyolysis signs
what are the 2 types of PSSM?
Type I:
1. seen in QH and draft breeds
2. hereditary; mutation in skeletal muscle
3. diagnose with genetic testing of hair sample
4. homozygotes more severe clinically
Type II:
1. in QH and warmbloods
2. no documented gene mutation or hereditary link
3. signs can be vague performance issues
4. may not have elevated CK/AST
5. diagnosis only with muscle biopsy!!
describe treatment of PSSM
- diet chance: reduced carbohydrate intake, increase calories from fat
- consistent exercise routine
describe hyperkalemic periodic paralysis (HYPP)
- genetic disorder in QH descended from the stallion Impressive
- autosomal dominant mutation in alpha subunit of skeletal muscle SODIUM channel!!!!
- sodium channels normally closed during rest and open during depol, but in HYPP, some Na+ channels stay open, allowing Na+ to enter cell and have a resting potential closer to threshold than normal cells; hyperkalemia occurs due to voltage-gated K+ channels remaining open, allowing continual K+ efflux; cell never turns off and deactivates
- episodes triggered by: cold, exercise, stress
- clinical signs:
-myotonia
-3rd eyelid protrusion (often 1st sign)
-muscle fasciculations/muscle spasms, esp facial
-paresis: swaying or buckling, stilted gait, dog sitting, collapse/recumbency
-laryngeal/pharyngeal spasm: pharyngitis, dysphagia, dyspnea
-cardiac arrhythmias, respiratory distress can be fatal
describe clinical signs and diagnosis of HYPP
diagnosis:
1. during an episode:
-electrocardiography consistent with hyperkalemia
-serum biochemistry: hyperkalemia, total protein elevated, CK/AST normal to mod elevated
- electromyography: myotonic changes between and during episodes
- muscle biopsy: often norma
- definitive diagnosis: genetic testing
describe treatment and prevention of HYPP
during an episode:
1. feed sweet feed or oral corn syrup
2. IV dextrose: stimulates insulin which moves glucose and potassium into cells
3. calcium gluconate: raises membrane threshold potentials
prevention:
1. avoid high potassium feeds: brome, alfalfa hay, canola, soybean oil, molasses, K+ supplements
2. acetazolamide:
-carbonic anhydrase inhibitor
-promotes K+ excretion in kidneys
describe white muscle disease
- nutritional myodegeneration that affects cattle and small ruminants; affects calves
- DUE TO SELENIUM OR VITAMIN E DEFICIENCY
-increased oxidative damage
-selenium involved in calcium homeostasis (muscle contraction) - occurs with cattle turned out on pasture deficient in selenium/vitamin E
- muscle is pale, discolored with white streaks; indicatvie of aclfication, WBC infiltration
describe clinical signs of white muscle disease
- stiff gait, unable to ruse
- respiratory distress: can affect heart, diaphragm, tongue
- increase in retained placentas during calving season
describe diagnosis and treatment/prevention of white muscle disease
diagnosis:
1. serum biochemistry: elevated CK
2. blood selenium, vitamin E levels
3.plasma glutathione peroxidase concentration, faster and less expensive than selenium
treatment/prevention: supplement selenium and itamin E
describe fibrotic myopathy
occurs when scar tissue forms within the hindlimb caudal thigh muscles after injury: semitendi, semimembi, gracilis
- scar tissue causes reduced protraction of limb
- cahracteristic tin soldier gait: shortened cranial phase of stride and slapping motion of limb before impact
- usually palpate scar tissue in hamstring muscles but can verify with ultrasound
treatment:
1. tenotomy of affected muscle, cut out scar tissue but it often comes back!
prevention: iskey!
treat muscle tears aggressively: acute icing, anti-inflam, LASER then in remodeling phase: heating and passive ROM
describe upward fixation of the patella
- fixation of the stifle part of passive stay apparatus
- normally disengaged by contraction of quads lifitng the medial patella ligament off trochelar ridge; when cannot engage = upward fixation
- can be due to:
-weakness of quads (stall rest, young unfit horses)
-pathology within stifle
-inflam of femeropatella joint - appears as horse leaving limb in extension caudally, often followed by sudden unlocking of stifle
- can be intermittent, persistent, uni or bilateral
diagnosis: gait observation
treatment:
1. exercises to strengthen quads
2. inject femeropatellar joint if effusion to break inflam cycle
3. estrogen to soften MPL
4. surgery: desmoplasty, desmotomy of MPL
describe stringhalt
- exaggerated flexion of hindlimb towards the horse’s belly
- may be unilat (idiopathic) or bilat (idiopathic, ingestion of dandelions or cheeseweed in australia)
- treatment:
-if mild: not performance imiting
-if mod to severe: myotenectomy of lateral digital extensor tendon can resolve
-botox of long and lat digital extensors
describe suprascapular nerve paralysis
- also known as Sweeney; blunt force trauma to suprascapular nerve, lack of innervation to supraspinatious and infraspinatous results in lateral deviation/instability of the shoulder region
- will be acutely painful but no chronic pain
treatment:
acutely:
1. anti-imflammatories!
2. nerve stimulation (electroacupuncture)
3. physiotherapy exercises to prevent muscle atrophy
chronic:
1. nerve stimulation (electroacupuncture, NMES)
2. physiotherapy exercises to regain muscle/prevent further atrophy
3. scapular notch surgery (scap nerve decompression)
describe post-anesthetic myopathy
- ischemic muscle damage during an anesthetic event leads to impairments during the recovery phase- one of the top anesthetic complications in horses!
- impairments range from mild lameness to incoordination to inability to stand
- often occurs due to decreased microperfusion to muscle groups
- treatment: based on severity
-assistance to stand
-supportive care: IV fluid therapy, pain meds - affected by:
-type of drug protocol: inhalants more likely to cause hypotension compared to total IV protocols (hypotension decreases bloodflow decreases oxygenation/perfusion)
-positioning: standing anesthetic procedures do not cause compression of muscles so should not cause this!
–for field anesthesia, avoid anesthetizing large patients on hard surfaces
–for general anesthesia: place on appropriately padded large animal tables
–when in lateral recumbency, offset some compression of dependent forelimb by pulling the down leg forward; also helps prevent radial nerve compression
-duration of anesthesia: increased risk of muscle damage the longer the patient in anesthetized
-size of patient: the large the patient, the higher the risk of muscle damage
what are 4 other causes of inability to stand during recovery from anesthesia?
- radial or femoral nerve paralysis
- fracture
- electrolyte imbalances
- exhaustion
