Equine Myopathies Flashcards
(26 cards)
How are equine myopathies classified
-Primary or secondary
-Primary myopathies can be further classified as non-exertional or exertional, and with rhabdomyolysis or without rhabdomyolysis
What are causes of nonexertional myopathies with rhabdomyolysis and without rhabdomyolysis
-Rhabdomyolysis:Nutritional (VitE/selenium deficiency), Metabolic (glycogen branching enzyme deficiency), Drug (anesthesia), toxic (drug, pasture), trauma, inflammatory (Infectious), Immune mediated (strep equi equi)
-Without rhabdomyolysis: PPID, drug, disuse
What are causes of exertional myopathies with and without rhabdomyolysis
-Rhabdomyolysis: traumatic (strains or tears), sporadic/acute (lack of fitness, overexertion, heat exhaustion, electrolyte imbalance), chronic (dietary, PSSM, RER, idiopathic)
-No rhabdomyolysis (due to mitochondrial defects/metabolic):Complex I respiratory chain enzyme deficiency, PPID
-No rhabdomyolysis (altered muscle membrane conduction aka ion channel diseases): hyperkalemia periodic paralysis, myotonia, myotonic dystrophy
What should you look for in the signalment and physical exam when checking for equine myopathies
-Signalment: intermittent disorder triggered by certain stimuli, check training, use, duration and frequency of issues
-Physical exam: complete examination of all systems, lameness and neuro evaluation, assess symmetry of muscle mass, signs of pain, atrophy, fasciculations (pain, fear,weakness, electrolyte disorder, ear tick, shivers), differences between neurogenic and myotonic muscle atrophy
What values on hematology, serum biochem, and urinalysis are important to look at in a horse with suspected myopathy
-Combined CK and AST elevations support ongoing myonecrosis
-Ongoing CK reduction with elevated AST supports resolving myonecrosis
-Assess color, specific gravity, protein content, cast formation, RBC/hemoglobin/myoglobin, fractional excretion of electrolytes
What are some other tests you should run on a horse with suspected myopathy
-Vitamin E, glutathione peroxidase, selenium concentrations
-Exercise response test to induce clin signs
-US, electromyography
-Muscle biopsy
-DNA testing: HYPP, Glycogen branching enzyme deficiency,type 1 polysaccharide storage myopathy, malignant hyperthermia
What are signs of exertional rhabdomyolysis in a horse
-clin signs usually occur shortly after onset of exercise: firm an painful muscles most commonly involving lumbar and sacral gluteal region, excessive sweating, tachycardia, tachypnea, reluctance to move, discolored urine
-Confirm with elevations in serum CK, AST, LDH, screen for PSSM defect, take muscle biopsy
What are some causes of nutritional myodegeneration
-White muscle disease (selenium), nutritional muscular dystrophy
-Myodegenerative disease due to selenium or vit E deficiency
-Associated with selenium or Vit E deficient soil resulting in deficient grains and forages
What are clinical signs and lab abnormalities of nutritional myodegeneration
-Weakness, recumbency, tachypnea, dyspnea, dysphasia, sudden death
-Elevated CK/AST, decreased blood Se or GPX, electrolyte disturbances due to myodegeneration (Na and K) myoglobinuria, azotemia
What is atypical myopathy in horses also known as
Acquired equine multiple acyl-CoA dehydrogenase deficiency, seasonal pasture myopathy, sycamore myopathy
What are the clinical signs associated with atypical myopathy and what causes it in horses
-Diffuse and extensive rhabdomyolysis, sudden stiffness, muscle tremors, collapse, colic signs, hypothermia, dark urine
-Caused by ingestion of hypoglycin A toxin from seeds, seedlings, and flowers from trees of the genus Acer, most commonly sycamore trees
What clinical signs will you see with traumatic rhabdomyolysis in horses
-Site of damage will dictate type of clinical signs
-May exhibit lameness, unwillingness to jump to turn sharply, may be focal area of pain/swelling, hematoma, scarring, mild elevations in serum muscle enzymes
What are the clinical signs of sporadic/acute exertional rhabdomyolysis in horses and what is the treatment
-Horse with single or infrequent episodes presenting with overexertion, muscle strain, heat exhaustion
-Clin signs include stilted gait, stiffness, sweating, myoglobinuria, elevations in serum muscle enzymes, aztoemia
-Treatment: for acute episode treat with rest, fluids, pain relief, anti-inflammatories. For long term management monitor neutrino and exercise, have access to water and electrolytes
What are the two types of chronic exertional rhabdomyolysis in horses and how are they different
-Acquired: Over-exertion, metabolic exhaustion, oxidative injury (“weekend warriors” but every weekend)
-Inherited: recurrent exertional rhabdomyolysis, polysaccharide storage myopathy
What clinical signs and presentation are associated with recurrent exertional rhabdomyolysis in horses
-Intermittent or chronic muscle stiffness, cramping, pain, exercise intolerance
-Acute cases present with discolored brown urine and signs of discomfort
-Commonly presentation: nervous young Tb fillies in training on high carb diet, more frequent with more fitness
What is the most prevalent muscle disease in Thoroughbreds
Recurrent exertional rhabdomyolysis
What is the management of Recurrent exertional rhabdomyolysis (RER) in horses
-Initially treat with rest, analgesia, antiinflammatories, fluids
-Manage through controlled exercise, reduction in stress and diet (high fat, reduced carbs in small frequent meals), give dantrolene prior to morning feed
What breeds of horses are mostly affected by polysaccharide storage myopathy (PSSM)
Predominantly seen in quarter horses, also drafts and warm bloods
What is the breed relationship between horses getting RER and PSSM
-You could see RER in “heavy” breeds (QH, drafts, paints, Appaloosa, warm bloods) but you wont see PSSM in “light” breeds (Tbs, Standardbreds, Arabians)
What are the triggers, characteristics, and genetic components of PSSM in horses
-Triggers: lack of regular exercise or prolonged rest between exercise
-Characterized by excessive/abnormal muscle storage of sugar (glycogen and polysaccharide)
-Genetics: inherited disease (autosomal dominant), type 1 mutation in the glycogen syntheses 1 gene, account for >90% of PSSM (type 2 possible in other forms with abnormal straining for muscle glycogen)
What is the management for PSSM in horses
-Managed though controlled exercise and diet
-Same diet as RER (high fat reduced carbs) can gradually add 2-3 cups of corn oil per day
-ideal diet contains >10% fat, <20% carbs
-daily exercise extremely important, helps to decrease muscle glycogen stores through utilization
What is the genetic component of hyperkalemia periodic paralysis (HYPP) in horse
-Genetic disorders in “impressive” line of horses
-Caused by mutation in alpha subunit of skeletal muscle Na channel
-Excessive inward flux of Na and outward flux of K occurs
-Autosomal dominant inheritance, mandatory testing for HYPP for foals descending from Impressive
What are the clinical signs of hyperkalemia periodic paralysis of horses
-exertional myopathy without rhabdomyolysis
Asymptomatic to daily muscle fasciculations and weakness usually by 2-3 years of age
-Muscle hyper-excited an then flaccid
-Life threatening complications including arrhythmias, asphyxiation
-Respiratory strider, obstruction, distress
-Episodes of myotonia, spasms of facial muscles, and weakness, episode duration varies
-Death due to dysnoea, cardiac arrhythmias
What are the risk factors and diagnosis of HYPP in horses
-More common in foals and young adults
-Ingestion of diets high in K trigger episodes
-Other triggers include fasting, anesthesia, sedation, sedation, trailer rides, stress, exposure to cold, concurrent disease
Diagnosed by: hyperkalemia, mild hyponatremia, hemoconcentration, endoscopy changes in upper airway
