Large animal muscle disease Flashcards
(86 cards)
1
Q
List muscle diseases causing muscle pain/cramping
A
- Equine rhabdomyolysis syndrome (sporadic or chronic)
- Atypical myoglobinuria
- Malignant hyperthermia
2
Q
List the muscle diseases causing muscle weakness in horses
A
- Muscle atrophy (disuse, neurogenic, cachexia)
- Equine motor neurone disease
3
Q
List the muscle diseases causing collapse in horses
A
- Myotonia
- Hyperkalaemic periodic paralysis
4
Q
List muscle disease in horses other than those causing weakness, collapse, or muscle pain/cramping
A
- Fibrotic myopahty
- Muscle rupture
- Aorto-iliac thrombosis
- Spastic paralysis
- Stringhalt
- PPID
5
Q
List the possible clinical signs of muscle disease in large animals
A
- Muscle atrophy
- Muscle stiffness/pain
- Myoglobinuria
- Recumbency/collapse
- Hyperthermia
- Exercise intolerance
- Abnormal contraction
- Non-specific signs
6
Q
What are the differentials for myoglobinuria in the horse?
A
- Muscle disease
- Haematuria
- Haemoglobinuria
7
Q
Explain why hyperthermia may occur with muscle disease
A
- Inflammation leading to pyrexia
- May also increase heart production from contracting muscles
8
Q
What aspects of the history are particularly relevant for investigation of muscle disease in horses
A
- Temperament, diet
- Occurrence: acute, recurrent, chronic
- Progression of signs
- Other diseases
9
Q
Which parameters may be raised on biochemistry, indicating muscle disease in a large animal?
A
- Creatine kinase
- Aspartate aminotransferase (AST)
- Lactate dehydrogenase 5 (skeletal muscle isoenzyme)
- +/- urea
10
Q
Explain the interpretation of creatine kinase in an animal with suspected muscle disease
A
- 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
11
Q
Explain the interpretation of AST in an animal with suspected muscle disease
A
- 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
12
Q
Explain the interpretation of myoglobinuria in an animal with suspected muscle disease
A
- Suggestive of significant disease
- Is toxic to renal tubules
- In all cases need to administer fluids
13
Q
Why might urea be elevated in muscle disease?
A
Concurrent renal disease
14
Q
Outline the exercise test used where muscle disease is suspected
A
- 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
15
Q
Which parameters are assessed in the diagnosis of muscle disease on urinalysis?
A
- Myoglobinuria (urine dipstick)
- Fraction excretion of electrolyte
16
Q
Explain the significance of fractional excretion of electrolytes in muscle disease in the horse
A
- May increase with recurrent rhabdomyolysis due to myoglobinuria causing damage to the renal tubules
- Generally more indicative of intracellular ions than serum measurement
17
Q
Where are muscle biopsy samples taken from in the horse for the investigation of the different muscle disease in the horse?
A
- RER, PSSM: semitendinosus
- EMND: sacrodorsalis caudalis medialis
- RER: gluteal
18
Q
Outline the assessment of muscle biopsies for the diagnosis of muscle diseases
A
- Confirmation of disease by assessing degeneration, necrosis and regeneration vs lysis or oedema
- Identify underlying mechanisms
- Estimate % of fibres affected
19
Q
What advise should be given to a horse owner following a muscle biopsy?
A
- Likely to be uncomfortable, esp. gluteal biopsy
- Box rest will reduce use of this muscle and thus reduce discomfort perceived by the horse
20
Q
List the diagnostic tools used in the diagnosis of equine muscle disease
A
- Physical examination and palpation
- Blood biochemistry
- Urinalysis
- Exercise test
- Muscle biopsy
21
Q
What is equine rhabdomyolysis syndrome also known as?
A
Tying up
22
Q
What is equine rhabdomyolysis syndrome usually precipitated by?
A
Exercising beyond their level of fitness
23
Q
What are the different presentations of equine rhabdomyolysis syndrome?
A
- Sporadic: exertional rhabdomyolysis (exhausted horse syndrome)
- Chronic: Recurrent equine rhabdomyolysis (RER), Polysaccharide storage myopathy (PSSM)
24
Q
Outline the clinical signs of equine rhabdomyolysis syndrome and when might these occur?
A
- 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
25
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
26
When does recurrent/chronic equine rhabdomyolysis syndrome commonly occur?
- Before, during or after only light exercise
| - Agitation prior to exercising
27
Describe the pathology that occurs with equine rhabdomyolysis syndrome
Lysis of muscle fibres esp type II (fast twitch) fibres
28
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)
29
Describe the signalment for sporadic exertional rhabdomyolysis in the horse
- No underlying muscle defect
| - Any age, breed, sex
30
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)
31
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
32
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
33
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)
34
Outline the signalment for recurrent exertional rhabdomyolysis in the horse
- Mares predisposed
- TB
- Nervous temperament
- High grain diet
- Other concurrent MSK disorders
35
When do episodes of recurrent exertional rhabdomyolysis in the horse generally occur?
- When the animal is fit
| - Episodes when training, not racing
36
Outline the pathogenesis of recurrent exertional rhabdomyolysis in the horse
- Underlying muscle condition
- Autosomal dominant gene
- Abnormal regulation of muscle contraction
37
Outline the clinical signs of recurrent exertional rhabdomyolysis in the horse
- Predisposition for typing up, repeat episodes
| - Can be subclinical
38
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
39
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
40
Outline type II polysaccharide storage myopathy in the horse
- Warmbloods, Draft horses
| - Histopath evidence of disease without GYS1 mutation
41
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
42
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
43
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
44
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
45
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
46
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
47
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
48
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)
49
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
50
Describe the clinical signs of atypical myopathy/seasonal pasture myopathy in the horse
- Sudden onset myoglobinura
| - Severe stiffness (recumbent, not moving)
51
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
52
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
53
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
54
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
55
In which species does malignant hyperthermia occur?
Pigs and horses
56
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
57
Outline the treatment of malignant hyperthermia
Ryanodine receptor antagonist e.g. dantrolene
58
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
59
Describe the typical presentation for equine motor neurone disease
- Elephant stance
- Weak when standing, normal during movement
- Muscle fasciculation, weight loss
60
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
61
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)
62
Outline the treatment of EMDN and the prognosis
- Vit E supplementation (hydrosoluble forms), up to 3mg/kg selenium supplementation
- Poor prognosis
63
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
64
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
65
Describe the clinical presentation of cardiac nutritional myodegeneration in the horse
- Sudden onset
- Death
- Depression, resp. distress
- Rhythm disturbances
66
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.
67
Give alternative names for clostridial myonecrosis in the large animal
- Black leg
- Malignant oedema
- Gangrene
68
Describe the presentation of clostrial myonecrosis in large animals
- Rapidly progressive, high mortality
- Pyrexia
- Depression
- Pain
- Lameness
69
Describe the common causes of clostrial myonecrosis in horses, cattle and sheep
- Horse: injection site/puncture wounds
- Cattle: blunt trauma
- Sheep: shearing/dipping
70
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
71
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
72
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
73
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
74
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
75
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)
76
What is the importance of sarcocyctosis in large animal muscle disease?
Not clinically significant but important VPH implications
77
What is myotonia in goats and horses?
- Delayed relaxation of skeletal muscle
| - In goats related to chloride channel, but not in horses
78
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)
79
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
80
Describe the appearance of a horse with hyperkalaemic periodic paralysis (HYPP)
Muscle hypertrophy, esp. quarters, neck and shoulders
81
Outline the trigger factors for an episode in a horse with HYPP
- High K+ intake (alfalfa, molasses)
| - Increased mobilisation (fasting, stress, anaesthesia, vigorous exercise)
82
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
83
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
84
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
85
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
86
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)
