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Equine Medicine Final > Muscle Disease > Flashcards

Muscle Disease Flashcards

1
Q

What are the three ways that muscle can respond to injury?

A
  1. Hypertrophy
  2. Necrosis
  3. Atrophy
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2
Q

Muscle necrosis causes (3)

A
  • calcium metabolism
  • Free radical damage
  • Release of enzymes
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3
Q

Muscle atrophy causes (4)

A
  • Disuse
  • Neurogenic
  • Cachexia
  • Myositis
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4
Q

Muscle hypertrophy causes (3)

A
  • Condition
  • Compensatory (on the “good” side)
  • Muscle damage
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5
Q

What questions should you get for your history?

A
  • Recent exercise
  • Recurrent
  • Genetic factors
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6
Q

Signalment

A
  • VERY IMPORTANT TO GET

- Many muscular diseases are very breed specific

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7
Q

Physical Examination Factors to focus on

A
  • Visual assessment
  • Palpation (do the muscles look tight?)
  • Lameness/reluctance to walk
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8
Q

What values on the chemistry panel are most helpful for muscle disease?

A
  • Creatinine Kinase (CK)

- Aspartate aminotransferase (AST)

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9
Q

CK

A
  • 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
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10
Q

Urinalysis

A
  • Breakdown of muscle will end up in the urine
  • Really gross brown color
  • Will see pigmenturia
  • Likely myoglobinuria
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11
Q

What two organs is AST release from?

A
  • Muscle and liver damage (NOT cholestasis)
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12
Q

Which half life is longer: AST or CK?

A
  • AST

- CK will go up for about 4-6 hrs

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13
Q

How long can AST stay elevated vs CK?

A
  • Can take many many days for AST to come down (20+)

- CK meanwhile can take like a day to come down

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14
Q

Urinalysis changes

A
  • Pigmenturia

- Myoglobinuria

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15
Q

Is myoglobinuria harmful to kidneys?

A
  • Yes
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16
Q

Other diagnostic tests for muscle disease

A
  • Muscle biopsy
  • Exercise tests
  • Electromyography
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17
Q

Muscle biopsy

A
  • 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
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18
Q

Exercise tests

A
  • 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
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19
Q

Electromyography

A
  • Have to have someone who knows how to read it
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20
Q

Clinical signs with muscle disease

A
  • 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
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21
Q

Exhausted horse

A
  • Depressed, +/- stiff gait, dehydration
  • Variable electrolyte abnormalities
  • Gross myoglobinuria
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22
Q

Chemistry panel changes

A
  • 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
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23
Q

CBC panel changes

A
  • Hemoconcentration, splenic contraction, inflammation
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24
Q

Rhabdomyolysis typical history

A
  • Hasn’t been ridden for awhile before 25 mile trail ride

- Horse now has an abnormal gait

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25
Q

Physical exam for Tying up for Rhabdomyolysis (case in class)

A
  • QAR, sweating
  • muscles of hind end are “rock hard”
  • normothermic, slightly tachycardic, slightly tachypneic
  • Tacky mm
  • urinating a dark brown stream
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26
Q

How quickly does sporadic exertional rhabdomyolysis happen? How quickly do you need to treat it?

A
  • Very acute

- Emergency therapy required

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27
Q

Why does exertional rhabdomyolysis happen?

A
  • Sudden change in exercise pattern
  • Performing beyond conditioning
  • Trauma
  • Surgery/anesthesia
  • Electrolyte imbalances
  • Hormonal influences
  • Genetic influences
  • Infections (respiratory)
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28
Q

Classic clinical signs for exertional rhabdomyolysis (acute form)

A
  • Stiff gait, reluctant to move
  • Anxious, sweating
  • Tachycardia, tachypnea
  • Pain on deep muscle palpation
  • Hard, hot swollen muscles
  • “red” or “dark” urine
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29
Q

Most common clinical signs for exertional rhabdomyolysis

A
  • 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
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30
Q

Diagnosis of Sporadic ER

A
  • History
  • Physical exam (variable depending on severity)
  • Laboratory abnormalities
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31
Q

Treatment of sporadic ER

A
  • 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)
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32
Q

What is the feature of exhausted horse syndrome?

A
  • Prolonged, submaximal exercise

- Endurance or race horses

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33
Q

Clinical signs of exhausted horse syndrome

A
  • Variable muscle cramping
  • Poor perfusion
  • Depressed, profuse sweating, elevated temperature
  • Colic, tucked up abdomen
  • Cannot perform further
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34
Q

Lab data for exhausted horse syndrome

A
  • Dehydration

- Profound sweat loss

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35
Q

What electrolytes are lost in sweat?

A
  • Sodium, potassium and chloride primarily!
  • Regardless of serum concentrations
  • Moderate loss of calcium and magnesium
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36
Q

Sweat loss fluid depletion per hour of riding

A
  • About 1 gallon/hr

- Depends on heat and humidity

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37
Q

What is the acid base status of the exhausted horse?

A
  • metabolic alkalosis
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38
Q

Cardiovascular response to exercise

A
  • Increase in blood flow
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39
Q

Heat stress cardiovascular response

A
  • 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
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40
Q

Respiratory response to exercise

A
  • Prolonged exercise
  • Hot humid environments
  • Sweating cannot be maintained
  • Respiratory system serves an important role in thermoregulation
  • Exhausted horses pant
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41
Q

Fluid and electrolyte abnormalities with exhausted horses

A
  • sweat losses partially replaced by water consumption
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42
Q

Desire to drink and eat in exhausted horses

A
  • Desire to drink is decreased or eliminated by a change in volume of blood and its concentration of salts and minerals
  • Anorexia or hyporexia
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43
Q

Behavior changes in horses that have fluid and electrolyte abnormalities

A
  • Obtunded
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44
Q

Muscle pathology that occurs in horses that have fluid and electrolyte abnormalities

A
  • Muscle cramps and spasms including synchronous diaphragmatic flutter
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45
Q

What electrolyte abnormality causes diaphragmatic flutter?

A
  • Calcium
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46
Q

Treatment for exhausted horses

A
  • Restore fluid volume (oral or IV depending on severity)
  • Correct electrolyte disturbances (LRS or plasmalyte are fine)
  • Provide readily available energy source
  • Reduce hyperthermia
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47
Q

Post anesthetic myopathy history

A
  • Horse on the table for a long time

- Very large horse (often 1500 lbs +)

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48
Q

Reasons for a horse not being able to get up after surgery

A
  • Myopathy
  • Neuropathy
  • Fracture
  • Metabolic disturbances
  • Cerebral swelling, myelopathy
  • Endotoxemia
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49
Q

Risk factors for post anesthetic myopathy

A
  • Duration of anesthesia
  • Hypotension
  • Hypoxia
  • Acidosis
  • Poor perfusion of dependent muscles
  • Insufficient padding
  • Weight of patient
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50
Q

Clinical findings of post anesthetic myopathy

A
  • Localized painful swollen muscle
  • Non weight bearing on affected limbs
  • Sweating
  • Tachycardia, tachypnea
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51
Q

Treatment for post-anesthetic myopathy

A
  • 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)
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52
Q

Recurrent rhabdomyolysis Causes

A
  • Genetic most commonly!
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53
Q

Genetic causes of Recurrent rhabdomyolysis

A
  • Polysaccharide storage myopathy (PSSM) Type I
  • Polysaccharide storage myopathy (PSSM) Type 2
  • Recurrent Exertional Rhabdomyolysis
  • Mitochondrial myopathy
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54
Q

Breeds Associated with PSSM Type I

A
  • Quarter Horses (Appaloosas/Paints
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55
Q

Breeds Associated with PSSM Type II

A
  • Quarter Horses
  • Warmbloods
  • Draft breeds
  • Arabians- endurance rides (4%)
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56
Q

Breeds Associated with Recurrent Exertional Rhabdomyolysis

A
  • Thoroughbreds and Standardbreds
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57
Q

Breeds Associated with Mitochondrial myopathy

A
  • Arabians
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58
Q

Uncommon causes of recurrent rhabdomyolysis

A
  • Concurrent illness
  • Hormonal imbalances
  • Electrolyte imbalances
  • Vitamin E/Selenium deficiency
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59
Q

Important aspects to diagnosing RR

A
  • History and signalment
  • CBC/Chemistry/UA
  • Exercise Test
  • Muscle biopsy
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60
Q

Changes seen on CBC/Chem/UA with RR

A
  • CK/AST/creatinine
  • Myoglobinuria
  • Usually no evidence of inflammation
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61
Q

Muscles used for muscle biopsy in RR

A
  • Semimembranosus and semitendinosus
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62
Q

Type I PSSM (“classic”) Pattern of Inheritance

A
  • Autosomal dominant (maybe incomplete)
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63
Q

Type I PSSM chance that a foal will be affected if sire or dam has the disease

A
  • 50% chance
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64
Q

What % of quarter horses are affected by PSSM?

A
  • ~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
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65
Q

What type of Quarter Horses are most affected by PSSM?

A
  • Paint
  • Western Pleasure
  • Cutting
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66
Q

Typical presentation of horses with PSSM Type I

A
  • Quite variable
  • Often a complaint of poor performance
  • Mild rhabdomyolysis
  • Muscle wasting
  • Usually quite subtle
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67
Q

Pathogenesis of PSSM Type 1

A
  • 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
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68
Q

Appearance of PSSM Type I on biopsy

A
  • PAS positive inclusion on biopsy
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69
Q

PSSM Type II Clinical signs

A
  • share same signs as Type I
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70
Q

PSSM II underlying pathogenesis

A
  • Excessive glycogen in their muscles

- Unclear of mutation causing defect

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71
Q

PSSM Type II in other breeds

A
  • Warmbloods
  • Unknown prevalence
  • Draft Breeds
  • > 36% of Belgians
  • Marked muscle weakness and atrophy
  • Not the same as “Shivers”
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72
Q

Definitive diagnosis of PSSM Type I

A
  • Genetic test available for glycogen synthase 1 gene (GYS1)
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73
Q

Type of sample needed for GYS1 test

A
  • Hair or whole blood
74
Q

Sensitivity for GYS1 test

A
  • 75%
75
Q

Muscle biopsy sample for PSSM

A
  • Semimembranosus
76
Q

Sensitivity of muscle biopsy for PSSM Type I

A
  • 100% sensitivity
77
Q

RYR 1 mutation gene

A
  • Modifying gene in Quarter Horses for malignant hyperthermia ???
78
Q

Chance of cure for PSSM

A
  • No cure
  • 80% improve and return to function
  • Acute episodes
79
Q

management of PSSM

A
  • Exercise must be consistent

- Diet

80
Q

Diet changes for PSSM

A
  • Decrease soluble carbohydrates
  • Grass hay
  • If more calories needed, add fat only
81
Q

Recurrent Exertional Rhabdomyolysis example history

A
  • 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
82
Q

Breed for Recurrent Exertional Rhabdomyolysis

A
  • Thoroughbreds and Standardbreds
83
Q

Inheritance pattern for Recurrent Exertional Rhabdomyolysis

A
  • Autosomal dominant
84
Q

% of thoroughbreds affected by Recurrent Exertional Rhabdomyolysis

A
  • ~5% of TB
85
Q

Sex predilection for Recurrent Exertional Rhabdomyolysis

A
  • Females more affected than males
86
Q

Other clinical features of Recurrent Exertional Rhabdomyolysis

A
  • Concurrent lameness often
  • Exacerbated in cold weather
  • Signs of ER
  • Triggered by stressful events
  • In Standardbred, may have enhanced performance
87
Q

Recurrent Exertional Rhabdomyolysis underlying pathogenesis

A
  • Excitation-contraction coupling defect
  • Defect in intracellular Calcium regulation
  • Possibly related to malignant hyperthermia
88
Q

Diagnostics for Recurrent Exertional Rhabdomyolysis

A
  • Caffeine Halothane contracture test
  • Muscle biopsy
  • Biopsy bathed in fluid containing caffeine and observed for contracture
  • if it contracts, it’s RER
89
Q

Management of RER

A
  • No stress!
  • Regular exercise
  • Turn out is best
  • Diet is same as PSSM (low carb, high fat)
  • Balanced electrolytes are important
90
Q

Medications used for management of RER

A
  • Dantrolene: alters calcium release in the muscle

- PO one hour before exercise

91
Q

Cause of shivers

A
  • 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
92
Q

Clinical signs of “Shivers”

A
  • Variable
  • Difficult to detect in early stages of disease
  • Involuntary spasms of the muscles in the pelvic region, limbs, and tails
93
Q

Mild cases of “Shivers” clinical signs

A
  • Trembling tenseness in pelvic limbs and jerky extensor movement of tail
94
Q

Severely affected clinical signs of “Shivers”

A
  • Hind limb suddenly raised poised in spastic state for seconds to minutes
  • Tail elevated and tremulous
95
Q

Diagnosis of “Shivers”

A
  • Diagnosis of Rule out

- Clinical signs

96
Q

Treatment for “Shivers”

A
  • No really good treatment
  • Adequate Vitamin E and Selenium is important
  • Massage and acupuncture may help
  • Consistent exercise
97
Q

DfDx for “Shivers”

A
  • Stringhalt
  • Upward fixation of the patella
  • Fibrotic myopathy
  • Equine Motor Neuron Disease
  • EPM
98
Q

Stringhalt Clinical Features

A
  • hocks flex violently toward abdomen
  • Bunny hopping
  • May be caused by a mustard
99
Q

Upward fixation of the patella Clinical Features

A
  • Medial patellar ligament momentarily caught
  • Can mimic stringhalt
  • Mini horses tend to get this
  • Bunny hops out of the stall
100
Q

Fibrotic myopathy Clinical Features

A
  • Scar tissue formation due to injury of semimembranosus/tendinosus
101
Q

Equine Motor Neuron Disease Clinical Features

A
  • Weight loss, symmetrical muscle wasting
  • Muscle fasciculations
  • Bizarre hind limb gait in chronic cases
  • Vitamin E deficiency
102
Q

EPM

A
  • Rule out via titers

- Looks like anything

103
Q

Treatment for “Shivers”

A
  • No cure
  • Low carbohydrate diet
  • +/- fat
  • Vitamin E 1000 IU/day (Alpha tocopherol)
104
Q

Mitochondrial myopathy clinical features

A
  • Started into light work
  • Stiff, short strides, profuse sweating
  • Metabolic acidosis
  • Marked lactic acidemia
105
Q

Mitochondrial myopathy overview

A
  • Severe exercise intolerance
  • Rare overall
  • Usually unable to exercise for more than 6 minutes
  • Prolonged recovery
106
Q

Breeds with mitochondrial myopathy

A
  • Quarter Horses, Arabians, Thoroughbreds
107
Q

Pathogenesis of mitochondrial myopathy

A
  • 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
108
Q

Diagnosis of mitochondrial myopathy

A
  • Muscle biopsy
  • Normal CK
  • Marked plasma lactate levels (10-30)
  • EMG Dive Bomber
109
Q

Biochemical analysis of Muscle biopsy in mitochondrial myopathy

A
  • mitochondrial electron transport system enzyme activity

- Analyzed in mitochondrial preparations from affected muscle

110
Q

Treatment and prognosis for mitochondrial myopathy

A
  • Depends upon degree of respiratory chain involvement
  • Likely prognosis is poor
  • No treatment
  • Animals very unlikely to be athletic
111
Q

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

A
  • Myodegeneration (Selenium deficiency)
  • Glycogen branching enzyme deficiency
  • Sepsis
112
Q

Importance of glycogen for the fetus

A
  • Important energy source for the fetus and neonate

- Synthesized by two enzymes (glycogen synthase and glycogen branching enzyme)

113
Q

Glycogen synthase

A
  • Creates straight chains of glucose
114
Q

Glycogen branching enzyme

A
  • With 1,4-glycosidic linkages, glycogen branching enzyme creates branches of glucose through alpha 1,6-linkages
115
Q

Importance of GBE

A
  • Glycogen becomes a compact, highly branched, and energy dense molecule
  • Without it, you are unable to form normally branched glycogen

-

116
Q

GBED foals GBE Enzyme activity

A
  • No measurable GBE enzyme activity

- No immuno detectable GBE

117
Q

Which tissues require an ability to store and mobilize glycogen to maintain normal glucose homeostasis?

A
  • Cardiac and skeletal muscle
  • Liver
  • Brain
118
Q

GBED prognosis

A
  • Always fatal - most foals die before 8 weeks of age
119
Q

GBED inheritance pattern

A
  • Autosomal recessive
120
Q

GBED Breeds affected

A
  • Quarter horses and similar breed (Paint, Appaloosa)
121
Q

Carriers of GBED chance of passing to offspring

A
  • 50% of time

- Do not breed with another carrier horse

122
Q

What breed is most commonly affected by hyperkalemic periodic paralysis?

A
  • Quarter Horses
123
Q

What is the pattern of inheritance for hyperkalemic periodic paralysis?

A
  • Autosomal dominant
124
Q

What does the mutation in hyperkalemic periodic paralysis actually do?

A
  • Mutation in voltage-gated Na channels

- ultimately leads to hyperexcitable muscles

125
Q

Pathogenesis of paralysis in hyperkalemic periodic paralysis?

A
  1. K+ intake or exercise followed by rest
  2. Small increase of extracellular K+
  3. Slight membrane depolarization
  4. Opening of Na+ channels with failure of abnormal Na+ channels to activate
  5. Persistent inward Na+ current increases intracellular Na+
  6. Sustained depolarization of cell membranes
  7. Combined efflux of intracellular K+ and inactivation of normal Na+ channels
  8. Loss of electrical excitability
  9. Paralysis
126
Q

Clinical signs of HYPP

A
  • 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
127
Q

What two diseases can cause prolapse of the third eyelid?

A
  • Tetanus and HYPP
128
Q

Presumptive diagnosis of HYPP

A
  • Acute episode
  • History/signalment (any Impressive blood)
  • Clinical signs
  • Plasma K+ levels
  • Other lab work
129
Q

Definitive diagnosis of HYPP

A
  • After an episode
  • DNA blood or hair test
  • Results as normal horse, heterozygote, or homozygote
130
Q

Which horse is responsible for the introduction of HYPP gene into so many Quarter Horses?

A
  • Impressive
131
Q

What is the goal of treatment for HYPP?

A
  • Decrease K+ levels in plasma
132
Q

How can you achieve a decreased potassium level in plasma with HYPP mild attacks?

A
  • Karo syrup, grain
133
Q

How can you achieve a decreased potassium level in plasma with HYPP severe attacks?

A
  • Intravenous bicarbonate (pushes potassium back in)
  • IV dextrose (same)
  • Calcium gluconate (decreases excitability of potassium)
  • Insulin
134
Q

Management of HYPP horses

A
  • Diets low in potassium
  • No alfalfa, bran, molasses based feeds
  • Avoid rapid feed changes
  • Regular exercise or turn out
  • Acetazolamide
135
Q

What diets should you avoid in HYPP horses?

A
  • Alfalfa, molasses, bran based feeds
136
Q

Acetazolamide action

A
  • Increases K+ excretion in urine

- Diuretic that is potassium wasting

137
Q

Breeding HYPP horses?

A
  • This is the big question
  • It’s a problem
  • Should be discouraged, but these horses often are winning at shows
138
Q

Which ionophores cause a problem with antibiotic toxicity?

A
  • Monensin
  • Lasalocid
  • Salinomycin
139
Q

Acute signs of ionophore toxicity

A
  • Hypovolemic shock
  • Colic
  • Cardiovascular dysfunction
  • Ataxia
  • Sudden death
  • Increased muscle enzymes
140
Q

Chronic signs of ionophore toxicity

A
  • weeks to months of exposure
  • Cardiovascular dysfunction
  • Atrial fibrillation
  • Exercise intolerance
141
Q

Diagnosis of ionophore toxicity

A
  • History of exposure
  • Mixing error at the feed mill (most common*)
  • Clinical signs
  • Pathology
142
Q

Treatment of ionophore toxicity

A
  • No known antidote
  • Mineral oil
  • Activated charcoal
  • Supportive care
  • Vitamin E/Selenium
143
Q

What is Fibrotic myopathy?

A
  • Fibrosis or ossification of the semimembranosus, semitendinosus, Biceps femoris, or Gracilis muscle
  • Usually result of trauma
  • Congenital form has been described
144
Q

Clinical signs of fibrotic myopathy

A
  • History
  • Characteristic gait
  • Muscle palpation
145
Q

DfDx for fibrotic myopathy

A
  • Shivers
146
Q

Treatment of fibrotic myopathy

A
  • Surgical excision of affected muscles

- Tenotomy

147
Q

Nutritional myodegeneration synonyms

A
  • White muscle disease

- Nutritional muscular dystrophy

148
Q

What causes nutritional myodegeneration?

A
  • Deficiency of selenium and/or vitamin E, which are antioxidants
149
Q

Nutritional myodegeneration - what is it?

A
  • Non-inflammatory degenerative disease of skeletal and/or cardiac muscle
150
Q

What diseases are associated with Vitamin E/Selenium deficiency?

A
  • Nutritional myodegeneration
  • masseter myonecrosis
  • Tongue myopathy
  • Adult exertional rhabdomyolysis
  • Equine Motor Neuron Disease
  • Equine Degenerative Myelopathy
  • Predisposition to post-anesthetic myopathy (?)
151
Q

Nutritional myodegeneration cardiac form - what age is affected?

A
  • Usually very young foals
152
Q

Clinical signs of nutritional myodegeneration cardiac form

A
  • Recumbent, unable to rise
  • Pulmonary edema, dyspnea, heart murmurs
  • Death within 24 hours or found dead
153
Q

Nutritional myodegeneration subacute skeletal form - what age is affected?

A
  • Foals and weanlings
154
Q

Clinical signs of nutritional myodegeneration subacute skeletal form

A
  • Profound weakness
  • Stiff, spastic gait
  • Tense and painful muscles
  • Dysphagia, poor suckle reflex
  • Bright and alert or depressed
155
Q

Nutritional myodegeneration chronic myopathy - what age?

A
  • Often weanlings, but maybe adult horses too
156
Q

Clinical signs of nutritional myodegeneration chronic myopathy

A
  • Masseter muscle atrophy and degeneration
  • Dysphagia, inability to eat
  • Weight loss
  • Limited range of jaw motion
  • Occasional tongue movement
157
Q

Diagnosis of nutritional myodegeneration

A
  • Increased CK and AST
  • +/- myoglobinuria
  • Whole blood selenium/serum concentration
  • Glutathione peroxidase activity***
  • Serum vitamin E?
  • Muscle biopsy
  • Response to therapy
158
Q

Glutathione peroxidase activity in horses with nutritional myodegeneration

A
  • Tend to be lower than normal
159
Q

Treatment for subacute and chronic forms

A
  • Vitamin E/Selenium injections given IM
  • Have been linked to severe reactions
  • Oral supplementation
  • Rest and supportive care; restrict exercise
  • Feeding NSAIDs, fluid
160
Q

What will selenium levels be in a horse with selenium deficiency who got a recent dose of selenium?

A
  • It will show them as normal, so don’t necessarily trust this
161
Q

Prevention of selenium deficiency

A
  • 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
162
Q

Seasonal pasture associated myopathy - geographic location and timing

A
  • Seen in the fall in the mid-west
  • Can be seen in spring and summer
  • Not when snow is present
163
Q

What causes seasonal pasture associated myopathy?

A
  • Ingestion of seed pods of box elder tree
164
Q

What is the toxic principle in the box elder tree sed pods?

A
  • Hypoglycin A leads to multiple acyl CoA dehydrogenase deficiency MADD)
165
Q

Clinical signs of seasonal pasture myopathy

A
  • Acute severe rhabdomyolysis of skeletal, cardiac, and respiratory muscles
  • SUDDEN DEATH
166
Q

Treatment for seasonal pasture myopathy

A
  • None

- Supportive only

167
Q

Mortality rates of seasonal pasture myopathy

A
  • 75%-90%
168
Q

Prevention of seasonal pasture myopathy

A
  • Other feeds accessible on pasture, especially if overgrazed
  • Rotate pastures
  • Minimize number of box elder trees and seeds accessible
169
Q

What are dfdx for a painful, swollen neck?

A
  • Clostridial myonecrosis
  • Injection site abscess
  • Perforated esophagus
  • Trauma
  • Fracture
  • Snake bite/spider bite
  • Hypersensitivity reaction
170
Q

Dfdx for SC emphysema

A
  • Clostridial myonecrosis
  • Other anaerobic infection
  • Perforated esophagus
  • Perforated trachea
  • Puncture wound, axilla, groin
171
Q

Etiology of Clostridial myonecrosis

A
  • Clostridial perfringens most common
172
Q

Most common predisposing factor for clostridial myonecrosis

A
  • usually follows IM injection or puncture wound (banamine especially)
  • can also be post castration, parturition injuries, puncture wounds, and particularly intramuscular injections
173
Q

Pathogenesis of clostridial myonecrosis

A
  • 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
174
Q

Suitable anaerobic conditions

A
  • Alkaline pH, low oxidative reduction potential
175
Q

Clinical findings of clostridial myonecrosis

A
  • Sudden death
  • Obtundation, pyrexia, tachypnea
  • swelling, pain, crepitus
  • Malodorous serosanguinous discharge
  • Rapidly progressive, high mortality rate
176
Q

Diagnosis of Clostridial myonecrosis

A
  • Clinical signs and history
  • Increased muscle enzymes
  • Gram positive rods in tissue aspirate
  • Culture of aspirates
177
Q

Treatment of clostridial myonecrosis

A
  • 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
178
Q

Length of treatment for clostridial myonecrosis

A
  • 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
179
Q

Supportive therapy in clostridial myonecrosis

A
  • Fluid therapy and analgesics often necessary in initial stages due to systemic toxemia
180
Q

Corticosteroid use in clostridial myonecrosis

A
  • often controversial
  • Use cautiously
  • may be beneficial initially in horses with evidence of shock
181
Q

Prognosis of horses with clostridial myonecrosis

A
  • Guarded
  • Can survive
  • Extensive skin and muscle sloughing may occur, which can necessitate euthanasia
182
Q

With which etiology is clostridial myonecrosis most survivable?

A
  • C. perfringens infections

Equine Medicine Final (10 decks)

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