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Flashcards in Large animal muscle disease Deck (86)
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List muscle diseases causing muscle pain/cramping

- Equine rhabdomyolysis syndrome (sporadic or chronic)
- Atypical myoglobinuria
- Malignant hyperthermia


List the muscle diseases causing muscle weakness in horses

- Muscle atrophy (disuse, neurogenic, cachexia)
- Equine motor neurone disease


List the muscle diseases causing collapse in horses

- Myotonia
- Hyperkalaemic periodic paralysis


List muscle disease in horses other than those causing weakness, collapse, or muscle pain/cramping

- Fibrotic myopahty
- Muscle rupture
- Aorto-iliac thrombosis
- Spastic paralysis
- Stringhalt


List the possible clinical signs of muscle disease in large animals

- Muscle atrophy
- Muscle stiffness/pain
- Myoglobinuria
- Recumbency/collapse
- Hyperthermia
- Exercise intolerance
- Abnormal contraction
- Non-specific signs


What are the differentials for myoglobinuria in the horse?

- Muscle disease
- Haematuria
- Haemoglobinuria


Explain why hyperthermia may occur with muscle disease

- Inflammation leading to pyrexia
- May also increase heart production from contracting muscles


What aspects of the history are particularly relevant for investigation of muscle disease in horses

- Temperament, diet
- Occurrence: acute, recurrent, chronic
- Progression of signs
- Other diseases


Which parameters may be raised on biochemistry, indicating muscle disease in a large animal?

- Creatine kinase
- Aspartate aminotransferase (AST)
- Lactate dehydrogenase 5 (skeletal muscle isoenzyme)
- +/- urea


Explain the interpretation of creatine kinase in an animal with suspected muscle disease

- Can be cardiac or skeletal, where there are clinical signs of muscle disease can decide whether MSK
- Short half life, good for identification of acute conditions or ongoing pathology


Explain the interpretation of AST in an animal with suspected muscle disease

- Produced in skeletal muscle, bone, liver
- If both CK and AST are elevated can be fairly certain is due to muscle pathology
- If CK normal but AST high, may be due to longer half life (7-8days vs 2hrs) of AST but need to rule liver disease


Explain the interpretation of myoglobinuria in an animal with suspected muscle disease

- Suggestive of significant disease
- Is toxic to renal tubules
- In all cases need to administer fluids


Why might urea be elevated in muscle disease?

Concurrent renal disease


Outline the exercise test used where muscle disease is suspected

- Used to determine chronic recurrent pathology
- Biochemistry following 15mins mild exercise e.g. trot lung
- Normal: CK<200% increase between 2-6 hours, and AST <50% increase at 24 hours


Which parameters are assessed in the diagnosis of muscle disease on urinalysis?

- Myoglobinuria (urine dipstick)
- Fraction excretion of electrolyte


Explain the significance of fractional excretion of electrolytes in muscle disease in the horse

- May increase with recurrent rhabdomyolysis due to myoglobinuria causing damage to the renal tubules
- Generally more indicative of intracellular ions than serum measurement


Where are muscle biopsy samples taken from in the horse for the investigation of the different muscle disease in the horse?

- RER, PSSM: semitendinosus
- EMND: sacrodorsalis caudalis medialis
- RER: gluteal


Outline the assessment of muscle biopsies for the diagnosis of muscle diseases

- Confirmation of disease by assessing degeneration, necrosis and regeneration vs lysis or oedema
- Identify underlying mechanisms
- Estimate % of fibres affected


What advise should be given to a horse owner following a muscle biopsy?

- Likely to be uncomfortable, esp. gluteal biopsy
- Box rest will reduce use of this muscle and thus reduce discomfort perceived by the horse


List the diagnostic tools used in the diagnosis of equine muscle disease

- Physical examination and palpation
- Blood biochemistry
- Urinalysis
- Exercise test
- Muscle biopsy


What is equine rhabdomyolysis syndrome also known as?

Tying up


What is equine rhabdomyolysis syndrome usually precipitated by?

Exercising beyond their level of fitness


What are the different presentations of equine rhabdomyolysis syndrome?

- Sporadic: exertional rhabdomyolysis (exhausted horse syndrome)
- Chronic: Recurrent equine rhabdomyolysis (RER), Polysaccharide storage myopathy (PSSM)


Outline the clinical signs of equine rhabdomyolysis syndrome and when might these occur?

- May occur before, during or after exercise
- Exercise intolerance
- Stiff gait
- Reluctance to move
- Recumbency
- Muscle pain, hard muscles
- Myoglobinuria
- Pain - sweating, tachycardia, tachypnoea
- Hyperthermia


what are the potential consequences of myoglobinuria in thehorse?

- Pre-renal azotaemia: often hypovolvaemic (dehydration from intense exercise)
- Renal azotaemia: pigmenturia, damage to kidney, can be life threatening


When does recurrent/chronic equine rhabdomyolysis syndrome commonly occur?

- Before, during or after only light exercise
- Agitation prior to exercising


Describe the pathology that occurs with equine rhabdomyolysis syndrome

Lysis of muscle fibres esp type II (fast twitch) fibres


List the trigger factors for sporadic exertional rhabdomyolysis in the horse

- Overexertion
- Heat exhaustion
- Dietary imbalance (high non-structural carb feeding, vit E/selenium deficiency)
- Electrolyte imbalance
- Viral, immune mediated (rare - viral myositis)


Describe the signalment for sporadic exertional rhabdomyolysis in the horse

- No underlying muscle defect
- Any age, breed, sex


Outline the problems related to sporadic exertional rhabdomyolysis in the horse

- Hypovolaemia
- Hyperthermia
- Low muscle pH (high speed exercise)
- Depleted glycogen (endurance exercise)
- Impaired membrane pump function leading to electrolyte imbalances and ATP deficiency
- Increased sarcoplasmic Ca2+
- Ileus, cardiac dysrhyhmias
- Synchronous diaphragmatic flutter (thumps)


Explain why thumps may develop as a result of sporadic exertional rhabdomyolysis in the horse

Most commonly a sign of dehydration and electrolyte depletion among horses performing in endurance races


Outline the treatment of sporadic exertional rhabdomyolysis/exhausted horse syndrom

- Rapid cooling
- REhydration with isotonic solution via NG tube or IV
- NSAIDs (once dehdration corrected)
- Correciton of electrolyte imbalances


How can exhausted horse syndrome be prevented?

- Training, heat acclimation
- Free access to water and food
- High roughage diet
- Veterinary check throughout ride (esp. for endurance races)


Outline the signalment for recurrent exertional rhabdomyolysis in the horse

- Mares predisposed
- TB
- Nervous temperament
- High grain diet
- Other concurrent MSK disorders


When do episodes of recurrent exertional rhabdomyolysis in the horse generally occur?

- When the animal is fit
- Episodes when training, not racing


Outline the pathogenesis of recurrent exertional rhabdomyolysis in the horse

- Underlying muscle condition
- Autosomal dominant gene
- Abnormal regulation of muscle contraction


Outline the clinical signs of recurrent exertional rhabdomyolysis in the horse

- Predisposition for typing up, repeat episodes
- Can be subclinical


Outline the diagnosis of recurrent exertional rhabdomyolysis in the horse

- Raised CK and AST post exercise
- Gluteal/semitendinosus muscle biopsy demonstrating increase in mature muscle fibres with centrally displaced nuclei, no amylase resistant polysaccharide


Outline type I polysacchardide storage myopathy in the horse

- Quarter horses
- GYS1 mutation
- Abnormal enzyme function results in inappropriate storage of glycogen in muscle cells so there is little energy available


Outline type II polysaccharide storage myopathy in the horse

- Warmbloods, Draft horses
- Histopath evidence of disease without GYS1 mutation


Outline the pathogenesis of type I PSSM in the horse

- GYS1 mutation
- Causes abnormal glycogen branching in muscle cells with increased glycogen storage, enhanced sensitivity to insulin
- Reduced ability to use that glycogen
- Leads to muscle necrosis due to abnormal energy metabolism
- Leads to exercise intolerance, muscle atrophy/weakness


Describe the clinical signs of PSSM in the horse

- Onset at 5yo
- Onset of exercise intolerance 20 ins after start exercise
- Worse after period of rest
- Variable severity
- HL more affected than FL


Outline the diagnosis of PSSM in the horse

- Persistently increased CK, 3x increase after exercise
- Semimembranosus muscle biopsy shows amylase resistant inclusion
- Blood test for GYS1 mutation


Outline the generic treatment for all forms of equine rhabdomyolysis

- Rest essential
- Analgesia: NSAIDs (care - high risk of azotaemia, hypovolaemia), opioids (pethidine), detomidine/ACP, lidocaine infusion (no VPL)
- DMSO, vit E, dantrolene suggested, little evidence
- Fluid therapy and electrolytes via NG tube (isotonic soln) if mildly affected, IV if severely affected


Outline the management of a case with exercise induced sporadic equine rhabdomyolysis

- Box rest then pasture turnout
- Reassess CK and AST 3 days after starting exercise, should be normal if sporadic


Outline the management of chronic exerise induced equine rhabdomyolysis

- PSSM: pasture rest asap, no more than 48hours stabled, gradual return to exercise, once in exercise no days off
- RER: limited rest, once in full exercise no days off
- Reduce stress, turnout with others
- Prolonged warmup and rest periods during training (interval training)
- Diet
- Medical management


Outline the dietary management of a case of chronic exercise induce equine rhabdomyolysis syndrome

- <20% of diet should be structural cardbohydrates
- Oil 10% of energy
- No excessive protein
- 1% BWT minimum fibre, ideally 2%
- Supplementation of Ca, Mg, Phos, Na, K, Vit E and selenium


Which drugs may be used in the managment of chronic exercise induced equine rhabdomyolysis syndrome?

- Sedation prior to exercise e.g. ACP (CARE)
- Dantrolene (800mg/day 1hr pre exercise not in food, reduces effect of exercise on CK rises)
- Phenytoin (affects ion channels and increases threshold for Ca release from SR)


Justify the use of sedatives in the management of equine rhabdomyolysos

- Anxiolytic
- May improve muscle perfusion
- Reduce use/contraction of muscles
- In chronic cases may be used prior to exercise with care


Describe the clinical signs of atypical myopathy/seasonal pasture myopathy in the horse

- Sudden onset myoglobinura
- Severe stiffness (recumbent, not moving)


What causes atypical myopathy/seasonal pasture myopathy in the horse?

- Plat toxin hyperglycin A, found in sycamore tree seeds in the UK (Box Elder in USA)
- Sudden onset exertion


Outline the pathogenesis of atypical myopathy/seasonal pasture myopathy in the horse

- Plant toxin
- Results in severe myoglobinuria
- Muscle fibre structure disruption and degeneration of fibres


Outline the management of atypical myopathy/seasonal pasture myopathy

- Supportive therapy - v high rates IVFT
- Glucose, insulin, carnitine and vit C
- Very high mortality - regardless of treatment likely to be fatal


Discuss the prevention of atypical myopathy in the horse

- Prevention of access to sycamore seeds e.g. hoovering/picking up sycamore seeds, fencing off areas, reducing stocking density in pastures, short turnout periods (<6hrs)
- Supply extra forage where pasture is poor


In which species does malignant hyperthermia occur?

Pigs and horses


Outline the pathogenesis of malignant hyperthermia

- Autosomal dominant mutation of ryanodine receptor (RYR)
- Results in increased [Ca2+] within the cell
- Heat from Ca2+/ATPase
- Depletion of ATP


Outline the treatment of malignant hyperthermia

Ryanodine receptor antagonist e.g. dantrolene


Briefly describe post anaesthetic myopathy in the horse (appearance, key ddx, causes)

- Prolonged recumbency following anaesthesia, muscles may be swollen, v firm, v sore
- DDx: neuropathy, myelopathy (in these limbs will be paralysed, in PAM are just too weak to stand on limbs), spinal cord malacia
- Causes: heavy horses, reduced perfusion of muscles, prolonged surgery, low BP, poor positioning


Describe the typical presentation for equine motor neurone disease

- Elephant stance
- Weak when standing, normal during movement
- Muscle fasciculation, weight loss


Explain the development of equine motor neurone disease

- Related to restricted pasture access, poor quality hay without balancers esp. vit E deficiency
- Selenium deficiency
- Oxidative daamge to type 1 fibres


Describe the typical laboratory findings for EMND

- CK and AST occasionally change
- CSF inflammatory
- Pigment retinopathy (line)
- Vit E <1ug/ml
- Muscle biopsy of tail head muscle (sacrocaudalis dorsalis medialis)


Outline the treatment of EMDN and the prognosis

- Vit E supplementation (hydrosoluble forms), up to 3mg/kg selenium supplementation
- Poor prognosis


Briefly outline the various presentations of nutritional muscle disease in large animals

- Peracute to subacute myodegeneration
- Very acute: sudden muscle necrosis
- Cardiac and skeletal muscle forms


Briefly describe cardiac and skeletal nutritional muscle disease in horses (cause, signalment, diagnosis)

- Selenium or vit E
- Often young, rapidly growing LA (<1yr), often Se deficient dams, also in utero form
- Dx: blood sample showing low Se and GSHPx
- Histopath showing inflammatory myositis


Describe the clinical presentation of cardiac nutritional myodegeneration in the horse

- Sudden onset
- Death
- Depression, resp. distress
- Rhythm disturbances


Describe the clinical presentation of skeletal myodegeneration

- Slower onset vs cardiac
- Weakness and stiffness
- Recumbency
- Muscle pain
- Can affect resp. muscles e.g. diaphragm and therefore affect resp.


Give alternative names for clostridial myonecrosis in the large animal

- Black leg
- Malignant oedema
- Gangrene


Describe the presentation of clostrial myonecrosis in large animals

- Rapidly progressive, high mortality
- Pyrexia
- Depression
- Pain
- Lameness


Describe the common causes of clostrial myonecrosis in horses, cattle and sheep

- Horse: injection site/puncture wounds
- Cattle: blunt trauma
- Sheep: shearing/dipping


Outline the treatment of clostridal myonecrosis in large animals

- Debridement and fasciotomy (introduce oxygen)
- Antibiotics: high dose penicillin q2h IV, metronidazole for non-food animals only
- Generally supportive management


Outline the prevention of clostridial myonecrosis in large animals

- Vaccination from 3-4 months q6m (BUT may cause more outbreaks -IM injection may facilitate introduction of bacteria into anaerobic environment)
- Remove all dead bodies


Describe the pathology that occurs with clostridial myonecrosis in large animals

- Swelling and autolysis of site (rancid odour)
- Blood stained fluid at orifices
- Swelling and crepitus (gas in tissues) of muscles
- Haemorrhagic dark muscles


Give examples of infectious agents that may cause muscle disease in large animals

- Clostridia
- S equi var equi (rare complication)
- Parasites e.g. sarcocystis
- Viral myopathy: equine flu, FMDV, MCF, BVD, bluetongue


Give examples of toxicities that may cause muscle disease in large animals

- Gossypol (cotton seed) in pigs
- Ionophores
- Organophosphates
- Trematone containing plants
- Cassia spp. and white snake root


Outline strangles as a cause of muscle disease in large animals (cause and Tx)

- Rare complication
- Immune mediate myositis 4 weeks post infection
- Tx corticosteroids (infection usually already cleared)


What is the importance of sarcocyctosis in large animal muscle disease?

Not clinically significant but important VPH implications


What is myotonia in goats and horses?

- Delayed relaxation of skeletal muscle
- In goats related to chloride channel, but not in horses


Describe the presentation, diagnosis and treatment of myotonia in goats and horses

- Atrophy weakness
- Horses: quarter horse, proximal limbs
- Goats: fainting goats
- Diagnosis: EMG (specialist)
- Tx: phenytoin (human drug)


Briefly outline the pathophysiology of hyperkalaemic periodic paralysis in horses

- Genetic disease, point mutation
- Normal between episodes, high potassium between episodes
- Caused by voltage gated sodium channels - remain open when triggered and do not inactivate
- Initially hyperexcitable then unexcitable


Describe the appearance of a horse with hyperkalaemic periodic paralysis (HYPP)

Muscle hypertrophy, esp. quarters, neck and shoulders


Outline the trigger factors for an episode in a horse with HYPP

- High K+ intake (alfalfa, molasses)
- Increased mobilisation (fasting, stress, anaesthesia, vigorous exercise)


Describe the clinical signs in a horse with mild HYPP

- Pronounced muscle development
- Prolapse of third eyelid
- Muscle fasciculations and weakness
- Onset at 2-3yo
- Normal after episodes


Describe the clinical signs in a horse with severe HYPP

- Muscle weakness
- Recumbency, dog sitting
- Dysphagia, pharyngeal collapse, laryngeal paralysis
- Can be fatal
- Normal after episode


Outline the diagnosis of HYPP in the horse

- Serum biochem: normal CK, increased K+ during episodes, normal before and after episodes
- EMG between episodes shows abnormal fibrillation potentials. complex repetitive discahrges, myotonic potentials
- DNA testing


Describe the treatment of acute hyperkalaemic periodic paralysis in the horse

- Calcium borogluconate IV (0.2-0.4ml/kg of 20% soln in 1L saline, raises membrane threshold potential)
- Glucose IV (6ml/kg as 5% soln, stimulates insulin secretion)
- Tracheostomy


Describe the ongoing treatment of hyperkalaemic periodic paralysis in the horse

- Acetazolamide (3mg/kg BID PO)
- Carbonic anhydrase inhibitor (increase renal loss of potassium)
- Dietary management to reduce potassium (can control episodes completely)