Equine myopathies Flashcards
(39 cards)
Name 3 Non-exertional rhabdomyolyses seen in horses.
- Vitamin E deficency
- Selenium deficiency
- Equine Anesthetic-Associated Myopathy
Which biochemical parameter from blood will give you insight in case of rhabdomyolysis?
creatine kinase, muscle enzyme
- Muscle specific
- Peak in 4-6 h, normalises in 72h
- Is Evidence of rhabdomyolysis and assess response to treatment and resolution.
- Controlled exercise tests consisting of 15 minutes of walk and trot exercise may provoke abnormal
increases in serum CK of 2 to 3 times baseline in horses with specific disorders (such as PSSM1). - Can increase in endurance horses, without a muscle disorder.
Polysaccharide Storage Myopathy (PSSM1)
Which biochemical parameter after CK, will give you insight in case of rhabdomyolysis?
- AST
- Non-specific, also liver
- Increases within 18 to 24 hours, elevations can persist for 10 to 14 days.
- Very large increases (>4000 U/L) are a strong indicator of diffuse severe rhabdomyolysis.
Urine analysis findigns in rhabdomyolysis. (4)
Myoglobinuria
* CK ≥ 25000 U/L
* Ongoing muscle loss
* Nephrotoxic
Pigmenturia
* Bilirubin
* Myoglobin
* Hemoglobin
Hematuria
* RBC
Iatrogenic
* Medication (rifampin)
EXERTIONAL RHABDOMYOLYSIS is a Syndrome of
muscle pain and cramping associated with exercise.
„tying up“
- 2% to 3% of horses
- 81% of cases of ER in Polo horses are attributed to overexertion, with 30% of cases occurring after a day of rest.
“Tying up” is a common lay term used for a group of muscle disorders that cause muscle cramping and stiffness during or after exercise. It describes how the horse’s muscles seem to seize up—they “tie up” and the horse may be reluctant or unable to move, often with rock-hard hindquarter muscles.
A diagnosis of exertional rhabdomyolysis (ER) requires establishing that
serum creatine kinase (CK) activity is elevated in association with clinical signs of muscle pain and stiffness
Exertional rhabdomyolysis has several different causes. Sporadic ER occurs from extrinsic factors.
Chronic Exertional rhabdomyolysis occurs from intrinsic abnormalities that cause muscle dysfunction.
Causes of chronic ER include: (5)
- malignant hyperthermia (MH)
- recurrent exertional rhabdomyolysis (RER)
- type 1 polysaccharide storage myopathy (PSSM1)
- type 2 polysaccharide storage myopathy-ER (PSSM2-ER)
- myofibrillar myopathy (MFM-ER)
Causes of Acute exertional rhabdomyolysis. (3)
Exercise performed beyond training adaptation or to the point of exhaustion.
Dietary imbalances of electrolytes, antioxidants, or
nonstructural carbohydrates (NSCs).
* Deficiency of electrolytes
* Inadequate in selenium and vitamin E
* High nonstructural carbohydrate content and low forage diet.
Exercising in the face of underlying respiratory viral disease.
Clinical signs of acute exertional rhabdomyolysis.
Mild cases
* stiffness during exercise
* decrease in willingness to work
Moderate to severe
* A short stride
* Shifting lameness
* Stiffness
* Sweating
* Reluctance to go forward
* Firm muscles particularly in the hindquarters
* Inappropriately rapid respiratory and heart rates
* Pawing
* Recumbent and unwilling to rise
Heat exhaustion
* High fever of 40-42°C
* Weakness
* Ataxia
* Tachypnoe
* Muscle fasciculation
* Collapse
* Myoglobinuria
* Muscle stiffness ±
Diagnosis of acute exertional rhabdomyolysis. (3)
Damage of muscle cells release muscle enzymes into serum
* CK Increases quickly
* AST increases
* LDH (lactate dehydrogenase) increases
Tx of acute exertional rhabdomyolysis. (4)
Rest
* No walking
* Long distance transportation not recommended for 24-48h
* Treat and manage on competition site
Pain management- until effect (18-24h)
* NSAIDS (Flunixin meglumine)
* Tranquilizers (Acepromazine (alpha-adrenergic antagonist))
* Alpha 2 agonists (Detomidine)
* Opioids (Butorphanol)
* CRI some of these if needed (e.g. Lidocaine, detomidine, butorphanol)
Fluid therapy
* For Dehydration, myoglobinuria, NSAIDs
nefrotoxicity
* Mild hydration with an NG tube
* Moderate to severe with IV fluids
Offer both Fresh water and 2nd bucket of electrolyte
solution.
- If Ca is low, add 100-200ml 23% calcium
borogluconate into 5l Ringer, Monitor Ca levels.
Muscle relaxants
* Methocarbamol
* Dantrolene (Also prevents further rhabdomyolysis, note Increases K+ level)
rest, analgesia, fluids, muscle relaxants
Management after acute exertional rhabdomyolysis. (3)
Rest+ paddock:
* After stiffness resolved
* Consider Free movement vs handwalks
Feeding:
* Hay/grass 10%–17% NonStructuralCarbs by weight
* Concentrates providing moderate levels of soluble carbohydrate (20%–30% NSC by weight), fat (4%–
8%), and fiber (20%–30% NDF).
* A salt block or 30 to 50 g (1–3 tablespoons) of salt per day.
Weekly measurements of CK:
* When normal (usually 2-3 weeks) start regular exercise with <20min, then increase gradually.
Chronic exertional rhabdomyolysis is
An intrinsic abnormality in muscle function.
All of the following conditions umbrelled under the term:
* Malignant hyperthermia (MH)
* Recurrent exertional rhabdomyolysis (RER)
* Type 1 polysaccharide storage myopathy (PSSM1)
* Type 2 polysaccharide storage myopathy-ER (PSSM2-ER)
* Myofibrillar myopathy (MFM-ER)
What is Recurrent Exertional Rhabdomyolysis and name 3 Risk factors.
Recurrent Exertional Rhabdomyolysis is a Form of chronic ER.
* Affects 5% to 7% of Thoroughbreds and 6% of Standardbreds
* Likely also occurs in Arabians, Warmbloods, racing Quarter Horses, and other breeds.
Risk factors:
* Nervous horses
* Young mares
* High grain diet
Clinical signs of Recurrent Exertional Rhabdomyolysis.
- Clinically normal when unfit or exercising in low-stress environments.
- Signs appear when fit and heavy training/competion. Within 30 min or less of exercising or after finishing.
- Risk increases when day or more rest before exercise.
- In Standardbreds Occurs while jogging.
- In Thoroughbreds, 3-day event horses and Arabians. When horses are held back by the rider.
- ER rarely occurs when horses are allowed to achieve maximal exercise speeds.
Pathogenesis of Recurrent Exertional Rhabdomyolysis.
- Intermittent prolonged opening of RYR1 (Calcium release channel)
- Excessive release of calcium into the myoplasm
- Persistent muscle contracture
- Excessive mitochondrial calcium uptake
- Uncoupling of the mitochondrial electron transfer system
- Mitochondrial degeneration
- Activation of proteases and loss of myofiber
integrity
Diagnosis of Recurrent Exertional Rhabdomyolysis involves: (4)
- Clinical signs
- Presence of risk factors such as Nervousness & High grain diet
- Elevations in serum CK and AST in association with exercise (Samples obtained 4 to 6 hours after an episode when Serum CK peaks)
- Muscle histopathology is unrewarding except to Evaluate forms of ER and you need to Biopsy from specific muscles.
Can be heritable but No tests available to test for it.
Management of Recurrent Exertional Rhabdomyolysis. (7)
- Reduce stress/exitement
- NO box rest cause >2days rest increases the risk.
- Back to training CK <3000 U/l
- With Standardbreds, you should Avoid fighting to hold horses at a slower pace. Interval training and reduction of jog miles to no more than 15 minutes per session.
- Event horses should get Calm exposure to speeds achieved during the crosscountry phase.
- Arabian endurance horses should be Delayed start until most horses have left cause it makes it a Calmer start.
- A nutritionally balanced diet with appropriate caloric intake and adequate vitamin and mineral
intake.
Management of Recurrent Exertional Rhabdomyolysis using medication. (3)
Dantrolene
* Decreases release of calcium from the ryanodine receptor in skeletal muscle and lowers elevated myoplasmic calcium concentrations.
* 1 to 2 mg/kg PO 60 minutes before exercise
Acepromazine
* 7 mg IV 20 minutes before exercise is reported to make horses more relaxed and manageable
* Use When horses are in their initial phase of training and during accommodation to a new environment.
Progesterone
* Supresses estrus in mares
NB but you can’t use these competing cause it counts as Doping, check withdrawal period.
Myofibrillar myopathy is an
- Independent disease
- Previously grouped under type 2 polysaccharide myopathy
- Is Not a glycogen storage disease
Diagnosed by biopsy
* Gluteal or semimembranosus muscles
* Presence of desmin aggregates
Seen in Arabians and warmbloods but they have Different presentations.
Clinical signs of Myofibrillar myopathy in arabians vs in warmbloods.
Arabians
* Increased CK and AST (CK>10 000-300 000 U/L)
* Exertional rhabdomyolysis
* Signs appear after off-work period (Muscle stiffness
& Muscle pain)
Warmbloods
* 6-8y olds
* Exercise intolerance seen as a Lack of stamina, Unwillingness to go forward, Abnormal canter transitions and inability to sustain a normal canter.
* Mild to moderate atrophy at the Topline & Hindquarters.
* Stiffness
* Moderate muscle pain
* Mild hindlimb shifting lameness
* NB normal CK and AST!
Management with Diet
of Myofibrillar myopathy in arabians vs warmbloods.
Management with exercsie
of Myofibrillar myopathy in arabians vs warmbloods.
Vitamin E deficiency Develops in horses who
who don’t have access to grass or only receive Hay rations and do not receive additional supplementation.
- Vit E requirement 1 IU/kg (500kg horse 500 IU)
- Grass provides 30 to 100 IU/kg dry matter (DM)
