Treatment of muscle disease Flashcards

1
Q

General considerations

A

▪Severity of episode: clinical signs, muscle enzymes and kidney function
▪Pain
▪Suspected aetiology
▪Exercise return speed
▪Nutrition: electrolytes, starch and proteins

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2
Q

Acute-severe rhabdomyolysis tx (but applies to any myopathy)

A

Analgesia & anti-inflammatories
➢ NSAIDs for 3-6 days:
– be careful with kidneys
– Always monitor plasma creatinine and water intake
– flunixin, bute or meloxicam
➢ Acepromazine: Tranquilizer and vasodilation (increase blood supply in affected muscles)
➢ Alpha-2+ butorphanol q 4h IM (CRIs ?)
– for a short period in extreme cases

Muscle relaxants
➢ Methocarbamol 5-22mg/kg IV or PO
– excellent muscle relaxant with some analgesic effects
➢ Dantrium Na 2-4mg/kg PO
– is a regulator of the calcium entrance into the muscle fibres
➢ FEI controlled substances

Anti-oxidants
➢ Vit E
➢ Vit B group
➢ Vit c

Rest/exercise
➢ Stable rest for 48h, then start walking 5 min 2-3 times a day for 3 days, increase progressively
➢ Be careful with AM cases: Longer resting periods
➢ Rest important to give enough time for the muscle fibres to recover

Moderate-severe cases - myoglobinuria:
➢ IV fluids (isotonic)
– flush the kidneys
– to prevent pigment nephropathy

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3
Q

Sporadic rhabdomyolysis tx - management

A

➢ Re-think training program: slow-down 15 min exercise/day
– Gradual exercise program: 10 min walk and trot/day for 7d, then increase 5 min load weekly
– Canter can be included on the 3rd week
– days/week of exercise and increase in intensity depends on the intended activity of the horse

➢ Maintain diet with Ca:P ratio 2:1

➢ Keep access to good quality hay: be careful with haylage (high starch content)

➢ Provide 30-50g day NaCL + 15-25g K-CL either with water or feed
– helps replenish electrolytes stored in the muscles fibres and maintain the horse with correct hydration as encourages drinking

➢ Do not feed concentrates/grains with more than 15-20% NSC

➢ Feed 4-8% fat
– adding fat helps provide healthy fuel stores for the muscles

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4
Q

RER tx

A

➢ Manage the environment: reduce stress ➢ pasture with other horses
➢ barn with fewer horses
➢ Do not hold them back during galloping: race horses
➢ Daily exercise: min 15 min a day
➢ Commercial feed: 8-12% NSC and 10-13% fat
➢ Medication: Be careful with withdrawal times in performance horses
– Dantrium sodium: 4mg/kg PO 1 hour before exercise
-> helps with the regulation of calcium entry into muscle fibres
-> 2w withdrawal before any FEI competition
– Acepromazine 20 min before exercise to reduce stress

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5
Q

PSSM-1 tx

A

➢Moderate starch and sugar content diet (<12%) with slightly higher protein content (20%). If higher calorie intake is necessary for performance, energy should be supplemented as fat»> vegetable oil
– Commercial product called relieve that already has these % adjusted
➢Avoid sweet feed, corn, wheat, oats, barley, and molasses
➢Ration balancer with vitamins and minerals (check starch content)
➢Consistent exercise, avoid resting (for long periods): regular exercise enhances glycogen utilization, increases turnover of structural proteins in the muscle and builds mitochondrial enzymes needed to burn energy as fuel.

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6
Q

Myofibrillar myopathy tx

A

➢Moderate starch and sugar content diet (<15%), fat (4-8%) and protein protein content (15%)
➢Antioxidants: Vit E and Coenzyme Q
➢Branched-amino acids (in the form of a supplement)
➢Consistent exercise: Particularly important in WB ➢Long warm-up with stretching exercise ➢30-50 min training max
➢3 days work and 2 days rest

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7
Q

HYPP tx

A

➢ Limit K intake (max 1%)
– Test hay (regular quality 1-2% K)
– Avoid alfalfa and clover hay (high K)
– Plain oats»> BE CAREFUL WITH STARCH content

➢ Consistent exercise, avoid resting: exercise increments over 5-7 days

➢ Moderate cases: no paresis
– Karosyrup: insulin mediated K removal
– 2nd or more cut of hay/haylage (less K)
– Small meals of oats/beet pulp over 2 weeks
– Gentle walking

➢ Acute/severe crisis ± paresis
– Epinephrine
– 23% Calcium gluconate
– 5% dextrose

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8
Q

Atypical myopathy tx

A

➢ Limit pigmented nephropathy
– IV-fluids

➢ Replenish Vitamin B2 stores

➢ Accumulation of partially-metabolized FAs (acyl-carnitines)
– Antioxidants very important: Vit E, Vit B12

➢ Toxin Binders : charcoal or bio-sponge NGT 1-2 doses

➢ Correct electrolyte abnormalities: K + Ca +Mg» check electrolytes

➢ Analgesia: headache?, myalgia?> NSAID, Paracetamol, CRIs (with xylazine & butorphanol), Morphine

➢ Be careful with feeding:
–25% dysphagia, 90% reduced gut sounds
–Damage of masseters, tongue and oesophagus , prolonged recumbency
–Use of glycogen as main energy source:
-> Maintain glucose availability
-> Provide glucose sources

➢ Monitor cardiac function: frequent auscultation, daily ECG?
– these horses

➢ Provide thick bedding (ideally straw) in large stable
– some will go through periods of recumbency so try to avoid pressure sores and damage

➢ Urinary catheterization
– necessary for those with bladder atony

➢ Keep the stable warm (air heaters)
– most AM cases occur during autumn and winter in the UK, therefore need to keep the stable warm
– also avoids further muscle crampin

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9
Q

IMM tx

A
  • IV-fluids if muscle enzymes too high
  • Antibiotics: controversial
    –For those with concurrent streptococcal infection the use of antibiotics is good
  • Steroids (anti-inflammatory/immunosuppressive)
    – Dexamethasone 0.05mg/kg IM/IV for 3 days
    – Followed by 1mg/kg prednisolone PO for 10 days,
    – then tapered over 1 month
    – Use of steroids appears to immediately improve CS and prevent further progression of muscle atrophy
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10
Q

Myonecrosis tx (& clostridial infections)

A
  • Drain the abscess (fenestration)
  • Antibiotics: broad spectrum but
    – High dose Penicillin 44 000IU q 12h for 4 days
    – Metronidazole whilst getting results from culture
  • Control Pain
    – Flunixin Meglumine
    – Phenylbutazone
    – CRI of alpha2 and butorphanol necessary for severe and extensive cases
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11
Q

Why is rest so important for atypical myopathy cases?

A
  • we don’t have an antidote for Hypoglycin-A, therefore the damage this toxin produces into the dehydrogenases within the mitochondria cannot be counteracted
  • Therefore, the body needs enough time and resources to regenerate those enzymes
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12
Q

Why is vitamin B2 important for atypical myopathy cases?

A
  • It will provide the cofactors necessary to regenerate the dehydrogenase
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13
Q

Role of antioxidants in the tx of atypical myopathy

A
  • they help reduce the damage produced by acyl-carnitine that accumulate because of malfunction of the dehydrogenase
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14
Q

Role of toxin binders in the tx of atypical myopathy

A
  • use is a bit controversial BUT is recommended in all cases
  • as we don’t know when the animal has ingested the sycamore plant material, we don’t know if they still have some plant material in their GIT
  • so the binders would minimise the absorption of the toxin that is still within the GIT
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15
Q

Role of electrolytes in the tx of atypical myopathy

A
  • breaking of the muscle fibres not only releases myoglobin (-> pigment nephropathy) but the stores of electrolytes
  • so these should be replenished
  • but care taken with K as can trigger cardiac arrhythmias in horses with atypical myopathy
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16
Q

Why do you need to closely monitor the cardiac function of horses with atypical myopathy?

A
  • These horses are at risk of having cardiac dysfunction, could be related to the release of electrolytes from the broken muscle fibres but also due to their muscle weakness and myocyte rupture that’s also occurring at the level of the heart muscle
17
Q

Why do you need to be careful with feeding horses with atypical myopathy?

A
  • Dysphagia, reduced gut sounds and recumbency make digestion of fibre difficult
  • Fat metabolism is impaired by the action of the toxin
  • Therefore, glucose and glycogen are the only fuel possible to cover the energetic needs in these horses
  • BUT don’t want to encourage gluconeogenesis in these horses
  • We know that gluconeogenesis in horses is mainly driven by the branch amino acid metabolism, and it’s believed that this is the main route of conversion of hypoglycin-A into its toxic metabolite
  • Therefore, provide these horse with readily available glucose - could be through the use of oral Karosyrup or an infusion of dextrose CRI.