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equine muscle
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Question | Answer |
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Many muscle diseases have intermittent clinical signs or | are triggered by certain environmental stimuli |
Observe size, shape, and symmetry | of all muscle groups |
Are fasciculations | present |
Note symmetry | of gait |
Gait abnormalities | may result from pain, muscle weakness, stiffness, muscle cramping, spasticity, decreased range of joint motion,dysfunction of motor neurons and ataxia |
Palpation of all major muscle groups | for evidence of pain, cramping, fibrosis |
Muscle percussion | may be performed |
Running a needle cap or pen over the lumbar and gluteal muscles | should elicit a normal extension (swayback) followed by flexion (hogback) |
Horses that guard against running a needle cap or pen over the lumbar and gluteal muscles | may have pelvic or thoracolumbar muscular pain |
Creatine Kinase (CK) | Enzyme responsible for breaking down creatine phosphate to creatine and phosphate, releasing energy for muscular contraction |
Found predominantly in skeletal and heart muscle | CK |
Short plasma half-life (2 hours) | CK |
Remarkable sensitivity as an indicator of muscle injury | CK |
Serum CK activity | increases within hours of insult |
Training, transport, and recumbency can cause mild elevations that quickly return | CK to normal (< 8,000 IU/L) |
Intramuscular injection | may elevate CK |
With muscle injury | CK elevation is typically > 100,000 IU/L |
Aspartate Aminotransferase (AST) | Previously known as SGOT (serum glutamic-oxaloacetic transaminase) |
High activity level in skeletal/cardiac muscle cells, hepatocytes, RBCs | AST |
Elevations in AST | are not specific for muscle injury |
Plasma half-life longer than CK 7–10 days | AST |
AST activity rises more slowly in response to muscle injury | than does CK peaks 12-24 hr after insult |
Rule(s) of thumb Increased CK and AST | reflect recent or active muscle injury |
Persistently elevated CK | ongoing muscle injury |
Elevated AST with decreasing or normal CK | resolving myositis |
Lactate Dehydrogenase (LDH) | Elevations occur because of damage to various organs in body composed of muscle and heart subunits |
Not specific for muscle disease | LDH |
Myoglobin | needed for transport of oxygen into and within muscle cells |
Urine dipstick positive for blood in the absence of hemolysis or RBCs in urine | is hightly suggestive of myoglobinuria |
Evaluation of muscle disorders precipitated by exercise | may require an exercise challenge test |
Evaluation of muscle disorders precipitated by exercise by induce subclinical elevations in serum CK | Requires 15 minutes walking/trotting (lunge line/treadmill) |
Pre-exercise blood sample | followed by second blood sample taken 4–6 hours following exercise |
In normal horses, rarely see > 3-fold increase | in CK with exercise |
Greater than 5-fold increase | indicative of rhabdomyolysis |
Not recommended for horses with overt signs of rhabdomyolysis | evaluation of muscle disorders by exercise |
Electromyography | Useful to evaluate muscle tone |
In electromyography Normal muscle should produce a burst of electrical activity | followed by quiescence |
Scintigraphy | May be useful for diagnosing deep muscle disease not evident by palpation |
Ultrasonography | Useful for identification of muscle trauma, crepitus, fibrosis, atrophy |
Acute injury | areas of hypoechogenicity due to loss of normal muscle fiber striation |
Tears in muscle fascia may be identified | US |
Hematomas may be observed | US |
Hyperechoic regions may indicated increased connective tissue or loss of muscle cell mass | US |
Gas echoes and mineralization may also be observed | US |
Muscle Biopsy Typical sites for percutaneous biopsy in cases of generalized muscle disease | Semimembranosus, biceps femoris, middle gluteal |
Can use specific muscle if it can be isolated | muscle biopsy |
Care should be taken to inject anesthetic only into subcutaneous tissue and caution used when handling muscle | so as to avoid crush of the sample |
Rhabdomyolysis | A syndrome of muscle cramping that occurs during physical exertion or exercise |
Recurrent Exertional Rhabdomyolysis | Common in Thoroughbred linebreeding,Autosomal dominant trait |
Recurrent exertional rhabdomyolysis Predisposing environmental triggers | Gender (67pct females)Temperature,Diet,Excitement,Exercise duration and intensity,Lameness |
Clinical signs and laboratory findings of recurrent exertional rhabdomyolysis | Mild to moderate signs of muscle cramping of gluteals, semimembranosus, semitendinosis, biceps femoris, & quads |
Mild to severe pain,Anxiety, profuse sweating, refusal to move, increased HR & RR,Affected muscles firm and painful on palpation,May have areas of muscle tearing and edema | recurrent exertional rhabdomyolysis |
Most cases recover in several hours severe cases may be recumbent | recurrent exertional rhabdomyolysis |
Recurrent exertional rhabdomyolysis | CK, AST, LDH, and myoglobin released into circulation |
Systemic acidosis and dehydration promote acute tubular necrosis from pigment nephropathy (ARF) | recurrent exertional rhabdomyolysis |
Recurrent rhabdomyolysis Possible | defect in dihydropyridine or ryanodine receptor and affects calcium regulation |
Recurrent Exertional rhabdomyolysis Diagnosis | Muscle biopsy suggests disease is similar to malignant hyperthermia in pigs,Caffeine or Halothane muscle contracture test,Biopsy from intercostals muscle Not readily available so diagnose based on history, lab findings, and histopath of muscle |
Histopath increased number of central nuclei without evidence of PSSM (glycogen PAS staining) | |
Treatment for rhabdomyolysis | Dietary (decrease carbs, increase fat)Add corn oil / rice bran for additional calories,Manage stress (nervous horses),Dantrolene |
Decrease the rate of calcium release from the sarcoplasmic reticulum | dantrolene |
Used for prevention with success – given orally prior to exercise | dantrolene |
No data on long-term use / efficacy of drug | dantrolene |
Polysaccharide Storage Myopathy | Common in Quarter horses, Paint horses, Drafts, Warmbloods |
Repeated bouts of exertional rhabdomyolysis that in some cases may be induced with little exercise | PSSM |
Most distinctive characteristic is mild to severe accumulation of abnormal polysaccharide within the myoplasm | PSSM |
clinical signs and Laboratory findings of PSSM | Frequent episodes of muscle cramping and rhabdomyolysis |
Increased CK, AST, myoglobinuria | PSSM |
Mild episodes Stiff gait, anxiety, stretching out | PSSM |
Severe episodes Anxiety, painful behavior, sweating, reluctance to move, recumbency | PSSM |
Definitive diagnosis of PSSM | from muscle biopsy,abnormal PAS staining of glycogen |
PSSM horses | often have a calm and sedate demeanor |
Classic signs include a posture that resembles a urination stance, a tucked-up abdomen, muscle fasciculations and pawing in the stall post-exercise | PSSM |
PSSM | Elevations of muscle enzymes are usually present and may remain elevated for long periods even when rested |
Glycogen accumulation due to increased ability to synthesize glycogen | PSSM |
PSSM horses | have enhanced insulin sensitivity, enhanced glucose clearance, and enhanced synthesis of glycogen |
Defect related to deficiency of glycogen synthase 1 | PSSM |
Treatment of PSSM includes | decreasing starch,concentrate from diet,> 13pct fat in digestible energy requirements,Use fat supplementation to provide additional calories,Rice bran,corn oil,alfalfa pellets,Gradual training program to reduce risk of triggering episode |
Nutritional Rhabdomyolysis White Muscle Disease | Peracute to subacute myodegenerative disease of cardiac and skeletal muscle caused by a dietary deficiency of selenium or vitamin E |
one distinct form of white muscle disease | Cardiac has sudden onset,severe debilitation,may be found dead,Lesions in heart,diaphragm,intercostal muscles |
Skeletal form of nutritional rhabdomyolysis | has a slower onset characterized by muscular weakness or stiffness, recumbency possible |
Muscles of tongue may be involved, leads to dysphagia | skeletal form |
Intercostal muscle involvement may lead to respiratory distress | skeletal form |
Cardiomyopathy may be present,Elevated CK, AST during acute phase,Myoglobinuria | white muscle disease |
Diagnosis of white muscle disease | Measure selenium,Vitamin E,Tissue,whole blood,Measure GSH-Px |
Se-dependent glutathione peroxidase | Formed in RBCs |
Selenium deficient soil in | areas across the United States, may predispose |
Poor quality hay/lack of green forage | leads to Vitamin E deficiency |
Necropsy findings | Bilaterally symmetrical myodegeneration,Pale discoloration,White streaks in muscle bundles Represent coagulative necrosis,Calcification,intramuscular edema |
Cardiac form | poor prognosis |
Usually not compatible with life | cardiac form |
Skeletal muscle form | may be treatable |
Prognosis remains guarded | skeletal muscle form |
Selenium,Vitamin E supplementation,Injectable selenium/Vit E compounds | critical |
Additional oral α-tocopherol (Vit E) | recommended |
Prevention of nutritional rhabdomyolysis white muscle disease | supplement mares during gestation,allow access to green forage |
Inflammatory Rhabdomyolysis,Clostridial Myonecrosis | Infections are characterized by a rapid clinical course, fever, systemic toxemia, and high mortality |
Development following IM injection or deep penetrating wound may be the result of direct spore deposition into the tissue | inflammatory rhabdomyolysis,clostridial myonecrosis |
The spores | undergo a conversion into the vegetative, toxin-producing form of the organism |
Also, can gain access to the body through the | alimentary tract and are present in liver and muscle in the dormant spore form |
Proliferation of clostridial agents in devitalized tissues is associated with the release of powerful exotoxins, responsible for the local necrotizing myositis and systemic toxemia | Lecithinase and hemolysin |
Aggressive treatment with high dose penicillin and muscle fasciotomy | inflammatory rhabdomyolysis clostridial myonecrosis |
Poor to guarded prognosis for life,very high mortality | IRCM |
No equine vaccine preventative | IRCM |
Use good IM injection technique to prevent | IRCM |
Use muscle groups with effective drainage for injection to prevent | IRCM |
Monitor IM injection sites CAREFULLY – good client education is a must | IRCM |
Specific Disorders of Muscle Tone,Hyperkalemic Periodic Paralysis | Inherited autosomal dominant trait commonly seen in Quarter Horse, Paints, and Appaloosas |
All related to QH stallion Impressive | HYPP |
Horses may be carriers (heterozygous) and be asymptomatic or be affected with varying degrees of severity | HYPP |
Homozygous individuals | have clinical signs of HyPP |
HYPP | is due to a point mutation causing a phenylalanine to leucine substitution in a key part of the skeletal muscle sodium channel |
This voltage-dependent channel permits rapid membrane depolarization during the initial phase of the action potential | skeletal muscle channel |
In horses with HYPP, the resting membrane potential | is closer to threshold than normal horses |
The resting membrane potential is closer to threshold and results in | an excessive inward flux of sodium and outward flux of potassium, resulting in persistent depolarization of muscle cells |
Clinically, this myopathy manifests as abnormal skeletal muscle membrane excitability leading to episodes of myotonia, sustained muscle contraction and/or paralysis | HYPP |
During episodes in HYPP | serum potassium is generally elevated |
Sweating and muscle fasciculations in flank, neck and shoulders may be seen | in episodes of HYPP |
Stimulation and attempts to move may exacerbate muscular fasciculations | during episodes of HYPP |
Muscular weakness during HYPP episodes | is very common |
Respiratory distress from paralysis of muscles of URT / larynx | occurs during HYPP episodes |
Tracheostomy | may be required in some HYPP individuals |
HYPP Definitive test is | the demonstration of the base-pair sequence substitution in the abnormal segment of the DNA encoding for the alpha subunit of the sodium channel |
HYPP Submission samples include | hair roots or whole blood in EDTA tubes |
EMG may reveal abnormal fibrillation potentials, complex repetitive discharges with occasional myotonic potentials, and trains of doublets even between episodes | HYPP |
Oral potassium chloride challenge test | frequently produces clinical signs within 1-4 hours, but is not recommended |
Treatment for HYPP | Mild cases may respond with mild exercise (hand-walking) which stimulates epinephrine, which stimulates sodium-potassium ATPase activity to mobilize potassium (drive it intracellularly) |
Feeding grain or corn (KARO) syrup to stimulate insulin-mediated movement of potassium across cell membranes may also be helpful | treating HYPP |
Why should you Avoid molasses in HYPP cases | high K+ level |
IV dextrose +/- bicarbonate | can be used to enhance intracellular movement of potassium |
Control HYPP by | Decrease dietary potassium and increase renal urinary excretion of potassium |
Avoid alfalfa, molasses, canola and soybean oil | to help control HYPP |
Feed several times a day and Regular exercise | In HYPP horses |
Acetazolamide (K+ wasting diuretic) | causes increased renal potassium ATPase activity and has been shown to stabilize blood glucose and potassium by stimulating insulin secretion |
Specific Disorders of Muscle Cramping Synchronous Diaphragmatic Flutter | Also known as thumps |
Typically occurs in horses suffering from fluid and electrolyte imbalances | thumps |
Contraction or twitch in the flank region in synchrony with the heart | SDF or thumps |
Most consistent metabolic derangement reported in horses is | low serum ionized calcium associated with hypochloremic metabolic alkalosis |
Metabolic alkalosis | may alter the ratio of free to bound calcium (increasing calcium binding to protein and decreasing ionized calcium) |
Occurs in association with atrial depolarization in horses | SDF or thumps |
May disrupt the normal membrane potential of the phrenic nerve, which passes directly over the atrium, resulting in nerve discharges in response to atrial depolarization | SDF thumps |