Muscle Disease Flashcards
What are the three ways that muscle can respond to injury?
- Hypertrophy
- Necrosis
- Atrophy
Muscle necrosis causes (3)
- calcium metabolism
- Free radical damage
- Release of enzymes
Muscle atrophy causes (4)
- Disuse
- Neurogenic
- Cachexia
- Myositis
Muscle hypertrophy causes (3)
- Condition
- Compensatory (on the “good” side)
- Muscle damage
What questions should you get for your history?
- Recent exercise
- Recurrent
- Genetic factors
Signalment
- VERY IMPORTANT TO GET
- Many muscular diseases are very breed specific
Physical Examination Factors to focus on
- Visual assessment
- Palpation (do the muscles look tight?)
- Lameness/reluctance to walk
What values on the chemistry panel are most helpful for muscle disease?
- Creatinine Kinase (CK)
- Aspartate aminotransferase (AST)
CK
- Normal <300 IU/L
- You want to know exactly how high it is because that helps you with treatment
- Mild elevations due to trailer ride, lying down, IM shots
- Severe muscle damage >10,000 IU/L
Urinalysis
- Breakdown of muscle will end up in the urine
- Really gross brown color
- Will see pigmenturia
- Likely myoglobinuria
What two organs is AST release from?
- Muscle and liver damage (NOT cholestasis)
Which half life is longer: AST or CK?
- AST
- CK will go up for about 4-6 hrs
How long can AST stay elevated vs CK?
- Can take many many days for AST to come down (20+)
- CK meanwhile can take like a day to come down
Urinalysis changes
- Pigmenturia
- Myoglobinuria
Is myoglobinuria harmful to kidneys?
- Yes
Other diagnostic tests for muscle disease
- Muscle biopsy
- Exercise tests
- Electromyography
Muscle biopsy
- If you don’t want to do a muscle biopsy can do an exercise test
- Immune mediated disease
- Sites: gluteal muscles (esp for immune-mediated); semimembranosus; semitenindosus
Exercise tests
- Presample CK (measure after trailer ride)
- Exercise for 20 minutes
- Wait 4-6 hours and measure CK again
- If concentration doubles or above 1000, then that’s indicative of genetic predisposition or muscle injury
Electromyography
- Have to have someone who knows how to read it
Clinical signs with muscle disease
- Quite variable
- Hind limb cramping, stiff gait
- Reluctant to move
- Anxious, sweating, tachycardia, tachypnea
- Pain on palpation of affected muscles
- Especially deep palpation of back and hind limbs
- Firm to palpation
- Gross or microscopic myoglobinuria
Exhausted horse
- Depressed, +/- stiff gait, dehydration
- Variable electrolyte abnormalities
- Gross myoglobinuria
Chemistry panel changes
- CK (rise most quickly)
- AST, LDH more slowly
- +/- plasma potassium concentrations (go up due to release of potassium from cells)
- BUN/creatinine if myoglobin induces pigment nephropathy
CBC panel changes
- Hemoconcentration, splenic contraction, inflammation
Rhabdomyolysis typical history
- Hasn’t been ridden for awhile before 25 mile trail ride
- Horse now has an abnormal gait
Physical exam for Tying up for Rhabdomyolysis (case in class)
- QAR, sweating
- muscles of hind end are “rock hard”
- normothermic, slightly tachycardic, slightly tachypneic
- Tacky mm
- urinating a dark brown stream
How quickly does sporadic exertional rhabdomyolysis happen? How quickly do you need to treat it?
- Very acute
- Emergency therapy required
Why does exertional rhabdomyolysis happen?
- Sudden change in exercise pattern
- Performing beyond conditioning
- Trauma
- Surgery/anesthesia
- Electrolyte imbalances
- Hormonal influences
- Genetic influences
- Infections (respiratory)
Classic clinical signs for exertional rhabdomyolysis (acute form)
- Stiff gait, reluctant to move
- Anxious, sweating
- Tachycardia, tachypnea
- Pain on deep muscle palpation
- Hard, hot swollen muscles
- “red” or “dark” urine
Most common clinical signs for exertional rhabdomyolysis
- Mobility (slight stiffness, shortened stride)
- May be reluctant to move
- Muscle often has no abnormality detected
- Urine usually not discolored (could also be discolored)
- Maybe increased sweating
- Maybe tachycardia
Diagnosis of Sporadic ER
- History
- Physical exam (variable depending on severity)
- Laboratory abnormalities
Treatment of sporadic ER
- Decrease muscle damage (REST, REST, REST)
- Non Steroidal anti-inflammatories (may need to wait until urinating clearly)
- Fluids, fluids, fluids!!!! (regulate electrolyte and acid base)
- Goal is normal urination (monitor color and analysis)
- Supportive care (Pain management with Flunixin or phenylbutazone; muscle relaxants like methocarbamol or dantrolene sodium; Acepromazine; Vitamin E as antioxidant)
What is the feature of exhausted horse syndrome?
- Prolonged, submaximal exercise
- Endurance or race horses
Clinical signs of exhausted horse syndrome
- Variable muscle cramping
- Poor perfusion
- Depressed, profuse sweating, elevated temperature
- Colic, tucked up abdomen
- Cannot perform further
Lab data for exhausted horse syndrome
- Dehydration
- Profound sweat loss
What electrolytes are lost in sweat?
- Sodium, potassium and chloride primarily!
- Regardless of serum concentrations
- Moderate loss of calcium and magnesium
Sweat loss fluid depletion per hour of riding
- About 1 gallon/hr
- Depends on heat and humidity
What is the acid base status of the exhausted horse?
- metabolic alkalosis
Cardiovascular response to exercise
- Increase in blood flow
Heat stress cardiovascular response
- Divert blood flow from visceral circulation
- Colic in endurance horses
- Decreased blood volume due to fluid loss in sweat and transduction of fluid into tissues
- Higher heart rate needed to maintain cardiac output
Respiratory response to exercise
- Prolonged exercise
- Hot humid environments
- Sweating cannot be maintained
- Respiratory system serves an important role in thermoregulation
- Exhausted horses pant
Fluid and electrolyte abnormalities with exhausted horses
- sweat losses partially replaced by water consumption
Desire to drink and eat in exhausted horses
- Desire to drink is decreased or eliminated by a change in volume of blood and its concentration of salts and minerals
- Anorexia or hyporexia
Behavior changes in horses that have fluid and electrolyte abnormalities
- Obtunded
Muscle pathology that occurs in horses that have fluid and electrolyte abnormalities
- Muscle cramps and spasms including synchronous diaphragmatic flutter
What electrolyte abnormality causes diaphragmatic flutter?
- Calcium
Treatment for exhausted horses
- Restore fluid volume (oral or IV depending on severity)
- Correct electrolyte disturbances (LRS or plasmalyte are fine)
- Provide readily available energy source
- Reduce hyperthermia
Post anesthetic myopathy history
- Horse on the table for a long time
- Very large horse (often 1500 lbs +)
Reasons for a horse not being able to get up after surgery
- Myopathy
- Neuropathy
- Fracture
- Metabolic disturbances
- Cerebral swelling, myelopathy
- Endotoxemia
Risk factors for post anesthetic myopathy
- Duration of anesthesia
- Hypotension
- Hypoxia
- Acidosis
- Poor perfusion of dependent muscles
- Insufficient padding
- Weight of patient
Clinical findings of post anesthetic myopathy
- Localized painful swollen muscle
- Non weight bearing on affected limbs
- Sweating
- Tachycardia, tachypnea
Treatment for post-anesthetic myopathy
- Fluid therapy especially if low calcium or other electrolyte derangements
- Also fluids help dilute myoglobin in the kidneys
- Acepromazine
- Methocarbamol (muscle relaxant)
- Rest (often have to sling)
Recurrent rhabdomyolysis Causes
- Genetic most commonly!
Genetic causes of Recurrent rhabdomyolysis
- Polysaccharide storage myopathy (PSSM) Type I
- Polysaccharide storage myopathy (PSSM) Type 2
- Recurrent Exertional Rhabdomyolysis
- Mitochondrial myopathy
Breeds Associated with PSSM Type I
- Quarter Horses (Appaloosas/Paints
Breeds Associated with PSSM Type II
- Quarter Horses
- Warmbloods
- Draft breeds
- Arabians- endurance rides (4%)
Breeds Associated with Recurrent Exertional Rhabdomyolysis
- Thoroughbreds and Standardbreds
Breeds Associated with Mitochondrial myopathy
- Arabians
Uncommon causes of recurrent rhabdomyolysis
- Concurrent illness
- Hormonal imbalances
- Electrolyte imbalances
- Vitamin E/Selenium deficiency
Important aspects to diagnosing RR
- History and signalment
- CBC/Chemistry/UA
- Exercise Test
- Muscle biopsy
Changes seen on CBC/Chem/UA with RR
- CK/AST/creatinine
- Myoglobinuria
- Usually no evidence of inflammation
Muscles used for muscle biopsy in RR
- Semimembranosus and semitendinosus
Type I PSSM (“classic”) Pattern of Inheritance
- Autosomal dominant (maybe incomplete)
Type I PSSM chance that a foal will be affected if sire or dam has the disease
- 50% chance
What % of quarter horses are affected by PSSM?
- ~10%
- Also related breeds, Morgans, some draft and Warmblood (Belgian, Percheron, and other European)
- Less common in Shires, Clydesdales (British origin breeds)
- Advantage in horses working hard daily
What type of Quarter Horses are most affected by PSSM?
- Paint
- Western Pleasure
- Cutting
Typical presentation of horses with PSSM Type I
- Quite variable
- Often a complaint of poor performance
- Mild rhabdomyolysis
- Muscle wasting
- Usually quite subtle
Pathogenesis of PSSM Type 1
- Mutation in glycogen synthase 1 (GYS1)
- Muscles cannot generate adequate energy
- Enhanced insulin sensitivity and uptake of glucose
- Enzyme imbalances
- Increased synthesis of less branched glycogen
Appearance of PSSM Type I on biopsy
- PAS positive inclusion on biopsy
PSSM Type II Clinical signs
- share same signs as Type I
PSSM II underlying pathogenesis
- Excessive glycogen in their muscles
- Unclear of mutation causing defect
PSSM Type II in other breeds
- Warmbloods
- Unknown prevalence
- Draft Breeds
- > 36% of Belgians
- Marked muscle weakness and atrophy
- Not the same as “Shivers”
Definitive diagnosis of PSSM Type I
- Genetic test available for glycogen synthase 1 gene (GYS1)
Type of sample needed for GYS1 test
- Hair or whole blood
Sensitivity for GYS1 test
- 75%
Muscle biopsy sample for PSSM
- Semimembranosus
Sensitivity of muscle biopsy for PSSM Type I
- 100% sensitivity
RYR 1 mutation gene
- Modifying gene in Quarter Horses for malignant hyperthermia ???
Chance of cure for PSSM
- No cure
- 80% improve and return to function
- Acute episodes
management of PSSM
- Exercise must be consistent
- Diet
Diet changes for PSSM
- Decrease soluble carbohydrates
- Grass hay
- If more calories needed, add fat only
Recurrent Exertional Rhabdomyolysis example history
- Very nervous filly
- Ties up when gallop training but not on race day
- Diet is sweet feed significantly
- Off and on lameness issues due to thin soles
Breed for Recurrent Exertional Rhabdomyolysis
- Thoroughbreds and Standardbreds
Inheritance pattern for Recurrent Exertional Rhabdomyolysis
- Autosomal dominant
% of thoroughbreds affected by Recurrent Exertional Rhabdomyolysis
- ~5% of TB
Sex predilection for Recurrent Exertional Rhabdomyolysis
- Females more affected than males
Other clinical features of Recurrent Exertional Rhabdomyolysis
- Concurrent lameness often
- Exacerbated in cold weather
- Signs of ER
- Triggered by stressful events
- In Standardbred, may have enhanced performance
Recurrent Exertional Rhabdomyolysis underlying pathogenesis
- Excitation-contraction coupling defect
- Defect in intracellular Calcium regulation
- Possibly related to malignant hyperthermia
Diagnostics for Recurrent Exertional Rhabdomyolysis
- Caffeine Halothane contracture test
- Muscle biopsy
- Biopsy bathed in fluid containing caffeine and observed for contracture
- if it contracts, it’s RER
Management of RER
- No stress!
- Regular exercise
- Turn out is best
- Diet is same as PSSM (low carb, high fat)
- Balanced electrolytes are important
Medications used for management of RER
- Dantrolene: alters calcium release in the muscle
- PO one hour before exercise
Cause of shivers
- Unknown cause
- Neurologic, myopathic, genetic, infectious
- All postulated on necropsy of 2 affected horses where muscle biopsy revealed a decreased carbohydrate content in a horse
- Maybe infectious cause
Clinical signs of “Shivers”
- Variable
- Difficult to detect in early stages of disease
- Involuntary spasms of the muscles in the pelvic region, limbs, and tails
Mild cases of “Shivers” clinical signs
- Trembling tenseness in pelvic limbs and jerky extensor movement of tail
Severely affected clinical signs of “Shivers”
- Hind limb suddenly raised poised in spastic state for seconds to minutes
- Tail elevated and tremulous
Diagnosis of “Shivers”
- Diagnosis of Rule out
- Clinical signs
Treatment for “Shivers”
- No really good treatment
- Adequate Vitamin E and Selenium is important
- Massage and acupuncture may help
- Consistent exercise
DfDx for “Shivers”
- Stringhalt
- Upward fixation of the patella
- Fibrotic myopathy
- Equine Motor Neuron Disease
- EPM
Stringhalt Clinical Features
- hocks flex violently toward abdomen
- Bunny hopping
- May be caused by a mustard
Upward fixation of the patella Clinical Features
- Medial patellar ligament momentarily caught
- Can mimic stringhalt
- Mini horses tend to get this
- Bunny hops out of the stall
Fibrotic myopathy Clinical Features
- Scar tissue formation due to injury of semimembranosus/tendinosus
Equine Motor Neuron Disease Clinical Features
- Weight loss, symmetrical muscle wasting
- Muscle fasciculations
- Bizarre hind limb gait in chronic cases
- Vitamin E deficiency
EPM
- Rule out via titers
- Looks like anything
Treatment for “Shivers”
- No cure
- Low carbohydrate diet
- +/- fat
- Vitamin E 1000 IU/day (Alpha tocopherol)
Mitochondrial myopathy clinical features
- Started into light work
- Stiff, short strides, profuse sweating
- Metabolic acidosis
- Marked lactic acidemia
Mitochondrial myopathy overview
- Severe exercise intolerance
- Rare overall
- Usually unable to exercise for more than 6 minutes
- Prolonged recovery
Breeds with mitochondrial myopathy
- Quarter Horses, Arabians, Thoroughbreds
Pathogenesis of mitochondrial myopathy
- Mutations in mtDNA occur spontaneously
- Inherited from mother (maternally derived; become evident when mutated mtDNA predominate)
- Defective oxidative phosphorylation (results in greater emphasis on anaerobic glycolysis for energy production)
- Rise in lactate due to anaerobic metabolism
Diagnosis of mitochondrial myopathy
- Muscle biopsy
- Normal CK
- Marked plasma lactate levels (10-30)
- EMG Dive Bomber
Biochemical analysis of Muscle biopsy in mitochondrial myopathy
- mitochondrial electron transport system enzyme activity
- Analyzed in mitochondrial preparations from affected muscle
Treatment and prognosis for mitochondrial myopathy
- Depends upon degree of respiratory chain involvement
- Likely prognosis is poor
- No treatment
- Animals very unlikely to be athletic
Differentials for a 5 day old Quarter horse foal unable to rise, weak, and unable to control body temperature with elevated CK (12-15,000), elevated AST, Elevated GGT, and leukopenia
- Myodegeneration (Selenium deficiency)
- Glycogen branching enzyme deficiency
- Sepsis
Importance of glycogen for the fetus
- Important energy source for the fetus and neonate
- Synthesized by two enzymes (glycogen synthase and glycogen branching enzyme)
Glycogen synthase
- Creates straight chains of glucose
Glycogen branching enzyme
- With 1,4-glycosidic linkages, glycogen branching enzyme creates branches of glucose through alpha 1,6-linkages
Importance of GBE
- Glycogen becomes a compact, highly branched, and energy dense molecule
- Without it, you are unable to form normally branched glycogen
-
GBED foals GBE Enzyme activity
- No measurable GBE enzyme activity
- No immuno detectable GBE
Which tissues require an ability to store and mobilize glycogen to maintain normal glucose homeostasis?
- Cardiac and skeletal muscle
- Liver
- Brain
GBED prognosis
- Always fatal - most foals die before 8 weeks of age
GBED inheritance pattern
- Autosomal recessive
GBED Breeds affected
- Quarter horses and similar breed (Paint, Appaloosa)
Carriers of GBED chance of passing to offspring
- 50% of time
- Do not breed with another carrier horse
What breed is most commonly affected by hyperkalemic periodic paralysis?
- Quarter Horses
What is the pattern of inheritance for hyperkalemic periodic paralysis?
- Autosomal dominant
What does the mutation in hyperkalemic periodic paralysis actually do?
- Mutation in voltage-gated Na channels
- ultimately leads to hyperexcitable muscles
Pathogenesis of paralysis in hyperkalemic periodic paralysis?
- K+ intake or exercise followed by rest
- Small increase of extracellular K+
- Slight membrane depolarization
- Opening of Na+ channels with failure of abnormal Na+ channels to activate
- Persistent inward Na+ current increases intracellular Na+
- Sustained depolarization of cell membranes
- Combined efflux of intracellular K+ and inactivation of normal Na+ channels
- Loss of electrical excitability
- Paralysis
Clinical signs of HYPP
- Variable severity and duration
- Weakness, muscle fasciculations
- Anxious but alert and responsive
- Prolapse of the third eyelid, facial muscle spasms
- Respiratory stridor, dyspnea
- Can progress to recumbency
- Episodes last 15-60 minutes
- rarely, acute death
- Increased respiratory paralysis
- Generally not painful
- Normal between episodes
What two diseases can cause prolapse of the third eyelid?
- Tetanus and HYPP
Presumptive diagnosis of HYPP
- Acute episode
- History/signalment (any Impressive blood)
- Clinical signs
- Plasma K+ levels
- Other lab work
Definitive diagnosis of HYPP
- After an episode
- DNA blood or hair test
- Results as normal horse, heterozygote, or homozygote
Which horse is responsible for the introduction of HYPP gene into so many Quarter Horses?
- Impressive
What is the goal of treatment for HYPP?
- Decrease K+ levels in plasma
How can you achieve a decreased potassium level in plasma with HYPP mild attacks?
- Karo syrup, grain
How can you achieve a decreased potassium level in plasma with HYPP severe attacks?
- Intravenous bicarbonate (pushes potassium back in)
- IV dextrose (same)
- Calcium gluconate (decreases excitability of potassium)
- Insulin
Management of HYPP horses
- Diets low in potassium
- No alfalfa, bran, molasses based feeds
- Avoid rapid feed changes
- Regular exercise or turn out
- Acetazolamide
What diets should you avoid in HYPP horses?
- Alfalfa, molasses, bran based feeds
Acetazolamide action
- Increases K+ excretion in urine
- Diuretic that is potassium wasting
Breeding HYPP horses?
- This is the big question
- It’s a problem
- Should be discouraged, but these horses often are winning at shows
Which ionophores cause a problem with antibiotic toxicity?
- Monensin
- Lasalocid
- Salinomycin
Acute signs of ionophore toxicity
- Hypovolemic shock
- Colic
- Cardiovascular dysfunction
- Ataxia
- Sudden death
- Increased muscle enzymes
Chronic signs of ionophore toxicity
- weeks to months of exposure
- Cardiovascular dysfunction
- Atrial fibrillation
- Exercise intolerance
Diagnosis of ionophore toxicity
- History of exposure
- Mixing error at the feed mill (most common*)
- Clinical signs
- Pathology
Treatment of ionophore toxicity
- No known antidote
- Mineral oil
- Activated charcoal
- Supportive care
- Vitamin E/Selenium
What is Fibrotic myopathy?
- Fibrosis or ossification of the semimembranosus, semitendinosus, Biceps femoris, or Gracilis muscle
- Usually result of trauma
- Congenital form has been described
Clinical signs of fibrotic myopathy
- History
- Characteristic gait
- Muscle palpation
DfDx for fibrotic myopathy
- Shivers
Treatment of fibrotic myopathy
- Surgical excision of affected muscles
- Tenotomy
Nutritional myodegeneration synonyms
- White muscle disease
- Nutritional muscular dystrophy
What causes nutritional myodegeneration?
- Deficiency of selenium and/or vitamin E, which are antioxidants
Nutritional myodegeneration - what is it?
- Non-inflammatory degenerative disease of skeletal and/or cardiac muscle
What diseases are associated with Vitamin E/Selenium deficiency?
- Nutritional myodegeneration
- masseter myonecrosis
- Tongue myopathy
- Adult exertional rhabdomyolysis
- Equine Motor Neuron Disease
- Equine Degenerative Myelopathy
- Predisposition to post-anesthetic myopathy (?)
Nutritional myodegeneration cardiac form - what age is affected?
- Usually very young foals
Clinical signs of nutritional myodegeneration cardiac form
- Recumbent, unable to rise
- Pulmonary edema, dyspnea, heart murmurs
- Death within 24 hours or found dead
Nutritional myodegeneration subacute skeletal form - what age is affected?
- Foals and weanlings
Clinical signs of nutritional myodegeneration subacute skeletal form
- Profound weakness
- Stiff, spastic gait
- Tense and painful muscles
- Dysphagia, poor suckle reflex
- Bright and alert or depressed
Nutritional myodegeneration chronic myopathy - what age?
- Often weanlings, but maybe adult horses too
Clinical signs of nutritional myodegeneration chronic myopathy
- Masseter muscle atrophy and degeneration
- Dysphagia, inability to eat
- Weight loss
- Limited range of jaw motion
- Occasional tongue movement
Diagnosis of nutritional myodegeneration
- Increased CK and AST
- +/- myoglobinuria
- Whole blood selenium/serum concentration
- Glutathione peroxidase activity***
- Serum vitamin E?
- Muscle biopsy
- Response to therapy
Glutathione peroxidase activity in horses with nutritional myodegeneration
- Tend to be lower than normal
Treatment for subacute and chronic forms
- Vitamin E/Selenium injections given IM
- Have been linked to severe reactions
- Oral supplementation
- Rest and supportive care; restrict exercise
- Feeding NSAIDs, fluid
What will selenium levels be in a horse with selenium deficiency who got a recent dose of selenium?
- It will show them as normal, so don’t necessarily trust this
Prevention of selenium deficiency
- Have feed analyzed in a selenium deficient area
- Selenium supplementation with organic formulations
- Especially important for pregnant mares because the foal needs
- Selenium injections at birth
- Check selenium and glutathione peroxidase levels
Seasonal pasture associated myopathy - geographic location and timing
- Seen in the fall in the mid-west
- Can be seen in spring and summer
- Not when snow is present
What causes seasonal pasture associated myopathy?
- Ingestion of seed pods of box elder tree
What is the toxic principle in the box elder tree sed pods?
- Hypoglycin A leads to multiple acyl CoA dehydrogenase deficiency MADD)
Clinical signs of seasonal pasture myopathy
- Acute severe rhabdomyolysis of skeletal, cardiac, and respiratory muscles
- SUDDEN DEATH
Treatment for seasonal pasture myopathy
- None
- Supportive only
Mortality rates of seasonal pasture myopathy
- 75%-90%
Prevention of seasonal pasture myopathy
- Other feeds accessible on pasture, especially if overgrazed
- Rotate pastures
- Minimize number of box elder trees and seeds accessible
What are dfdx for a painful, swollen neck?
- Clostridial myonecrosis
- Injection site abscess
- Perforated esophagus
- Trauma
- Fracture
- Snake bite/spider bite
- Hypersensitivity reaction
Dfdx for SC emphysema
- Clostridial myonecrosis
- Other anaerobic infection
- Perforated esophagus
- Perforated trachea
- Puncture wound, axilla, groin
Etiology of Clostridial myonecrosis
- Clostridial perfringens most common
Most common predisposing factor for clostridial myonecrosis
- usually follows IM injection or puncture wound (banamine especially)
- can also be post castration, parturition injuries, puncture wounds, and particularly intramuscular injections
Pathogenesis of clostridial myonecrosis
- necrotizing and hemolyzing toxins
- May invade GIT
- Germination of spores and vegetative growth occur when suitable local anaerobic conditions exist
- Toxin production results in destruction of cellular defense mechanisms and significant tissue necrosis
Suitable anaerobic conditions
- Alkaline pH, low oxidative reduction potential
Clinical findings of clostridial myonecrosis
- Sudden death
- Obtundation, pyrexia, tachypnea
- swelling, pain, crepitus
- Malodorous serosanguinous discharge
- Rapidly progressive, high mortality rate
Diagnosis of Clostridial myonecrosis
- Clinical signs and history
- Increased muscle enzymes
- Gram positive rods in tissue aspirate
- Culture of aspirates
Treatment of clostridial myonecrosis
- AGGRESSIVE
- Includes initial administration of doses of potassium penicillin
- Surgical debridement
- Metronidazole can be added (she has NOT had good luck with this)
- Fenestration +/- oxygen therapy
- Essential to remove necrotic tissue and disrupt anaerobic environment
Length of treatment for clostridial myonecrosis
- SHould be long-term antibiotics and nursing care
- Antibiotics should continue until wound is resolved and for a minimum of 7 days after
- Many times diffuse cellulitis following muscle planes occurs
- Necessitates therapy for at least several weeks
Supportive therapy in clostridial myonecrosis
- Fluid therapy and analgesics often necessary in initial stages due to systemic toxemia
Corticosteroid use in clostridial myonecrosis
- often controversial
- Use cautiously
- may be beneficial initially in horses with evidence of shock
Prognosis of horses with clostridial myonecrosis
- Guarded
- Can survive
- Extensive skin and muscle sloughing may occur, which can necessitate euthanasia
With which etiology is clostridial myonecrosis most survivable?
- C. perfringens infections
