Equine Muscular Diseases

type I (slow twitch): aerobic metabolism (endurance)
type II (fast twitch): anaerobic metabolism (speed & strength)

skin vasodilation
sweat
-prolonged sweating --> dehydration, electrolyte abnormalities
extrinsic water

importance
excitation contraction coupling: Na, K, Cl
-resting membrane potential
-action potential/depolarization
contraction (sliding filament): Ca, Mg, ATP
relaxation

causes of electrolyte imbalances
electrolyte loss: sweating, GI dz, renal dz
membrane abnormalities: Na channels, excitation contraction coupling

PE for muscle problems: TPR, mm, CRT, sweating?, gait abnormalities, distribution of lesions, evaluation of muscles

clin path
-CK (good for acute problems), LDH, AST
-electrolytes: Na, K, Cl, Ca, Mg
-acid-base status
-serum lactate:ammonia ratio

exercise test: not done very often
-measure CK before & 4-6 hrs & 24 hrs after exercise
-exercise could be lunging, treadmill, or normal exercise routine
-however CK may not change at all w/ exercise

muscle bx: histopath, biochemical analysis, histochemical analysis, caffeine, halothane reactivity

electromyography nerve conduction velocity (not commonly done): electrical silence, insertional activity, motor unit APs, miniature end plate potentials, fibrillation potentials, positive sharp waves

a.defect in muscle membrane ion channel conductance
-autosomal dominant w/ incomplete penetrance
-episodic: may occur rarely to daily; episodes can last minutes to hours
b. recurrent episodes of muscle fasciculations & weakness
exercise intolerance: less willing to work; greater lactic acid production for a given amt. of work
+/- 3rd eyelid prolapse, recumbency, laryngeal swelling/paralysis
c. colic, tetanus, seizure, choke, rhabdomyolysis, hypocalcemia, neurologic, resp. distress

a. clinical signs, ↑ serum K, pedigree, genetic testing, electromyogram, KCl provocation test
-CK, AST remain normal, or nearly so
b. drive K+ into cells w/ calcium, bicarb, dextrose, (insulin)
c. avoid high K feeds (alfalfa hay, molasses), regular exercise, acetazolamide

a. monensin, salinomycin, lasalocid, narasin
-coccidiostats: poultry, ruminants
-growth promoters: ruminants
b. acute: anorexia, colic, weakness, ↑ muscle enzymes, ataxia, shock, death
-chronic: CV dysfunction, exercise intolerance
c. clinical signs, muscle enzymes, ID drug in feed, necropsy, multiple horses affected
d. if acute, try to prevent further absorption
-supportive care

a. type II muscle fibers affected: ischemia, build up of lactic acid, damage to cell mems
↑ cytosolic Ca --> ↑ uptake into sarcoplasmic reticulum & mitochondria, damage to cell mems & organelles
disruption of cell mems --> leakage of myoglobin, K, CK, LDH, AST, etc. into extracellular space --> muscle inflammation & necrosis w/ heat, pain, swelling, loss of function
b. 1º: polysaccharide storage myopathy, glycogen branching deficiency, malignant hyperthermia, defect in excitation contraction coupling
2º: poor management, training errors, carbohydrate loading, vitamin E/Se deficiency, K deficiency, estrous cycle, hypothyroidism, nervous horses, post anesthesia

a. mild: may be confused w/ lameness
-stiff gait, dragging toes, pain over croup, loin, thigh musculature, “back sore”
severe: reluctance to move, anxiety, tachycardia, tachypnea, sweating, pyrexia, tense swollen painful muscles, myoglobinuria, recumbency
b. ↑ muscle enzymes (CK: 2-6 hrs, LDH: 12 hrs, AST: 12-24 hrs)
electrolyte abnormalities
+/- azotemia
c. b’twn episodes: hx, exercise test, clin path (muscle enzymes, electrolytes, U/A, thyroid status, vitamin E/Se), scintigraphy, thermography, muscle bx
-during acute episode: clinical signs, muscle enzymes, +/- myoglobinuria

limit further muscle damage
control pain: NSAIDs safe to give if making urine, else Torb
control anxiety: xylazine
combat inflammation
flush kidneys
↑ blood flow to muscles: fluids, vasodilators (ex. ace)
restore electrolyte, acid-base balance
supportive care

a. inappropriate release of Ca for sarcoplasmic reticulum in anesthetized horses
-halothane & succinylcholine are common inciting agents
-probably a genetic predisposition
b. sudden ↑ in body temp, muscle cramping & fasciculations, sweating, tachycardia, irregular breathing, acute ↑ in serum K
c. turn off inhalation anesthetic
-↓ body temp w/ ice
-↑ IV fluids
-dantrolene
-symptomatic: restore electrolyte & acid-base status, etc.
d. no grain prior to elective sx
-keep anesthesia time short
-don’t use halothane or succinylcholine
-pre-treat horses prone to myositis w/ dantrolene (not commonly used in horses) or phenytoin

a. probably inherited, esp. in quarterhorse related & draft breeds
-accumulation of glycogen & unavailable mucopolysaccharide in type II muscle fibers
-↑ insulin sensitivity
b. calm demeanor, low exercise tolerance, signs of recurrent rhabdomyolysis at a young age (vary in duration & severity)
c. clinical signs, muscle bx
d. regular daily exercise
-dietary adjustment: low carb, ↑ fat

a. familial abnormality in excitation contraction coupling
-signs may be mild
b. young nervous fillies, lame horses more likely to develop dz
c. exercise test, muscle bx
d. consistent daily exercise
-dietary adjustments +/- electrolyte supplementation
-vasodilator sedatives
-control of estrus behavior
-dantrolene
-phenytoin

a. Clostridium spp. present in environment & on skin surface --> invade at site of injection or puncture --> proliferate in bruised (anaerobic) muscle --> release of necrotizing & hemolyzing toxins
b. swelling, pain, & crepitus (Clostridia --> gas production) at site, depression, fever, tachycardia, progression to severe toxemia & death
c. clinical signs, suggestive hx, ↑ muscle enzymes, CBC (toxemia, inflammation), U/S or rads: gas w/in muscle planes, anaerobic culture of tissue aspirate
d. must be rapid & aggressive
-IV penicillin +/- metronidazole
-surgical debridement or fenestration: must let O2 into wound
-specific antitoxin if available
-supportive care