Equine MidSem 2 Exam Flashcards
(148 cards)
List the 5 standard radiographs for the distal extremity.
Standing on a block:
- Lateromedial
- Dorsopalmar / dorsoplantar (zero degree)
Standing on a tunnerl (or special block):
- Dorsal 65 degree proximal palmarodistal oblique (distal phalanx / “upright pedal”)
- Dorsal 65 degree proximal palmarodistal oblique (navicular bone)
- Palmaroproximal palmarodistal oblique (navicular skyline)
List the 5 standard radiographic view for the fetlock.
Standing:
- Lateromedial (LM)
- Dorsopalmar / plantar (DP) & dorsal 15 degree proximal-palmarodistal oblique
- Dorsolateral palmaromedial oblique (DLPMO)
- Dorsomedial palmarolateral oblique (DMPLO)
Flexed:
- Lateromedial (LM)
List the standard views for carpus radiographs.
- Dorsopalmar (DP)
- Lateromedial (LM)
- DMPLO 45
- DLPMO 30
- Flexed lateral
- Skyline distal row
Define Lameness.
Any gait abnormality including:
- Limping, hobbling
- Incapacity of properly using one or multiple legs
- Generally caused by pain in horses - eviction strategy
- But can be of mechanic or neurologic origin
What are the 10 steps of a lameness exam?
- History
- Examination from a distance
- Palpation
- Movement
- Selected tests - manipulation, flexion, direct pressure, wedge
- Diagnostic analgesia
- Imaging
- Diagnosis
- Management
- Follow up examination
What are the 4 main stages / questions of a lameness examination?
- Is it lameness?
- Which leg(s) is it? Notions of primary, secondary & compensatory
- Which part of the leg(s) is affected?
- What is the nature of the lesion?
What is the difference between primary, secondary & compensatory lameness?
Primary lameness = the leg that hurts the most (real intense lameness)
Secondary lameness = real lameness but intensity is lower than primary
Compensatory lameness = compensatory by other areas / legs due to primary lameness (without the primary lameness the compensatory goes away)
What are some of the most common lameness findings?
- 60:40 ratio of FL to HL
- FL up to 95% distal to carpus
- In the foot until proven otherwise
- Owners often think it is behind when it is actually in front & vice versa
What does the concept “down on the sound” mean in terms of lameness?
- Head & neck elevate when the lame limb is weight bearing
- Head & neck nod down when the sound limb is weight bearing (“down on the sound”)
If the front & hind diagonal limbs (contralateral sides) appear lame / affected - where is primary lameness coming from?
If it is the front & hind limbs on the same side that both appear lame - where is primary lameness coming from?
- If it is front & hind diagonal limbs (contralateral sides) that both appear lame / affected – primary lameness is more likely to come from the front leg
- If it is front & hind limbs on the same side that both appear lame / affected – primary lameness is more likely to come from the hind leg
What are the 5 AAEP grades of lameness?
- Grade 0 = not perceptible under any circumstances
- Grade 1 = difficult to observe & not consistently apparent regardless of the circumstances
- Grade 2 = difficult to observe at a walk or when trotting on straight line but consistently apparent under certain circumstances
- Grade 3 = consistently observable at a trot under all circumstances
- Grade 4 = obvious at a walk
- Grade 5 = minimal weight bearing in motion or at rest / complete inability to move
Define valgus & varus & possible causes for it.
Valgus = limb deviates laterally distal to a reference point (+/- supernation of carpus / fetlock)
Varus = limb deviates medially distal to a reference point (+/- pronation of carpus / fetlock)
Aetiology:
- Perinatal factors - malposition, placentitis, nutrition, premature or dysmature foals
- Developmental factors - poor nutrition, excessive exercise & trauma
- Most commonly: disproportionate growth of metaphyseal growth plates
Prognosis:
- The more deviation there is the less chance of spontaneous correction
Discuss incomplete ossification of carpal / tarsal bones.
- Cuboidal bones have rounded edges
- Common congenital induced angular limb deformity - prematurity or dysmaturity
- Can also occur in normal foals
- Failure to diagnose & treat in 1st few days of life > wedge shaped cuboidal bones > permanent damage
- Diagnosis: radiographs
Treatment:
- Can be manually corrected early on
- Restrict exercise and/or provide external support
- Typically 2-4 weeks to allow for ossification
Discuss assymetric growth of metaphysis & epiphysis.
- From birth or develops in 1st weeks / months of life
- Trauma likely major cause of asymmetric growth (asymmetric compression on physis)
Diagnosis:
- Radiographs – asymmetric longitudinal growth of metaphysis or epiphysis
Treatment:
- Physeal growth rates determine rate of correction by modifying chondral growth patterns
- Total amount of growth remaining determines amount of correction achievable
- Chondral growth patterns are modified with: exercise control, farriery (trimming, shoeing), surgery (growth retardation > transphyseal bridging / screws), (growth acceleration > periosteal elevation & transection)
- Treatment method depends on: joint involved, degree of deformity, amount of growth remaining
Treatment for young foals with mild to moderate ALD:
- Stall rest 2 weeks (fetlock), 8 weeks (carpus) > autocorrection possible
- Resolution before end of rapid growth phase - if no resolution > surgery
Discuss hyperextension deformity (laxity).
- Toe does not touch the ground
- Congenital or acquired
- Mostly occurs in immature & dysmature foals
- Occurs in hindlimbs > front limbs
- Lack of flexor tone
Aetiology:
- Idiopathic
- Bandaging / casting
- Lack of exercise
- Overgrown hooves
Mild deformities:
- Respond to time & controlled exercise
Moderate & non-responsive deformities:
- Glue on extended heel shoe
- May need to bandage foot & fetlock
- Thick bandages contraindicated > more soft tissue relaxation
*Most foals correct in 2-6 weeks
Discuss flexural deformities (“contracted tendons”).
- Length disparity between tendons & bones
- Occurs in forelimbs > hindlimbs
- Structures affected: fetlock, coffin join (DIP), carpus (worse prognosis), determine if SDFT, DDFT, SL
Congenital flexural deformities aetiology:
- Uterine malpositioning
- Teratogens (locoweed, sudan grass, influenza)
- Hypothyroidism
- Neuromuscular disorder
- Genetic factors
- Nutritional imbalances in pregnant mare
Congenital flexural deformities - treatment:
- Begin ASAP
- Younger foals respond better to treatment
- Combine medical & physical therapy
- Farrier - toe extensions
- Oxytetracycline - chelation of calcium ion
We need to increase exercise in angular limb deformities or flexural deformities to improve outcome?
- Angular limb deformities we need to decrease exercise
- Vs. Flexural deformities we need to increase exercise
Tendonitis / Desmitis - list the different phases of healing.
Inflammatory phase:
- Vascular & cellular
Repair phase:
- Fibroblasts
- Intrinsic & extrinsic repair
Remodelling phase - end result:
- Decreased tensile strength
- Decreased elasticity
Discuss the pathogenesis of flexor tendinitis.
- Gradual accumulation of fatigue & progressive impact on collagen – main cause high intensity exercise / training for young horses
- Progressive degeneration of the SDFT
- Excessive stress overstretches & ruptures the collagen fibre bundles
- Low-grade tendon fibre disruption results in an accelerating cycle of inflammation, degeneration & further tendon disruption
- Acute mechanical failure results in partial (usually) tendon rupture
- Muscle is fatigued > prevents it from relaxing > injury
Discuss SDFT (Superficial Digital Flexor Tendon) Tendinitis.
Racehorses:
- Up to 30% suffer from tendon injury
- 4% fatal injuries in flat racing
- 11% of fatal injuries in races with jumps
Risk factors:
- Track design, surface type & condition
- Fitness, hoof trimming & shoeing
- Re-injury is common
- Forelimbs most commonly affected
Clinical signs:
- Moderate to severe injury – heat, swelling of SDFT & lameness
- Mild cases – slight pain on firm palpation
- Chronic cases – very large & thickened
- ‘Low bows’ – digital sheath swelling
Diagnosis:
- Clinical signs
- Thermography - low specificity
- Ultrasonography - transverse & longitudinal (must use both)
- Reduced echogenicity - anechoic
- Disruption of linear fibril pattern
Essential / most effective therapy:
- Physiotherapy - cold water hydrotherapy & padded support bandage
- Anti-inflammatory drugs - NSAIDs (or corticosteroids) +/- topical DMSO (Dimethyl Sulfoxide)
- Exercise - stall rest & controlled walking only
- Controlled rehabilitation program - low impact exercise (water walking)
Surgical treatment:
- Tendon splitting - now outdated.
- Superior check ligament desmotomy - transection of superior check ligament (SCL) alters functional length of SDFT & mechanics. Concept = cutting the limiting fibres > longer function of the tendon > transfers centre of pressure / force to whole tendon & muscle (rather than in scar tissue)
- Annular ligament desmotomy
How long does it take to recover from a tendon injury vs. a ligament injury?
Tendon injury = ~6 months (“tendon” has 6 letters)
Ligament injury = ~8 months (“ligament” has 8 letters)
Descibre how to examine the muscular system.
- History
- Physical exam - inspection (asymmetry), palpation (of several muscles) & percussion (with a hammer), gait analysis
Biochemical parameters:
- CK - increased CK related to cell lysis. >100,000 IU/L, peak at 4-6h, T1/2 12h, abnormal is >2-4 fold increase from baseling
- AST - peak 12-24h, T1/2 7-8 days
- LDH - extra analysis but not essential
- Urinalysis - myoglobinuria
Advanced diagnostic testing:
- Plasma Vit E & selenium
- Muscle biopsy - epaxial, gluteal or semimembranosus
- Genetic testing
- Exercise testing - rule out other diseases (e.g. colic due to severe water loss via sweating). Demonstrate mild increase of muscle enzyme activity by provoke test.
- Ultrasonography - depth of muscle
- Electromyography (EMG) - evaluation of muscle tone
Define myotonia vs. myopathy vs. muscle atrophy.
Mytonia = something wrong with the muscle tone.
Myopathy = something wrong with the muscle fibre e.g. muscle necrosis (rhabdomyolysis / “tying up”), non-exertional
Muscle atrophy = no muscle present due to a neurogenic or myogenic problem e.g. denervation / dis-use
Discuss exertional rhabdomyolysis (“tying up”) syndrome.
History:
- Episodes of post-exercise muscle stiffness
- Changes in training or management
Clinical signs:
- Muscle cramping and/or stiffness
- Muscle pain especially of lumbar & sacral regions
- Sweating, tachycardia, tachypnoea
- Reluctance to move
- Myoglobinuria
Diagnosis:
- Myoglobinuria
- Plasma CK & AST activities
Treatment - supportive:
- IV or oral fluids - maintain urine output to prevent or minimise the nephrotoxic effects of myoglobin & maintain circulation to muscle tissue
- Analgesics - NSAIDs (be careful - kidney insult), opiates
- Keep warm
- Acepromazine
- Vit E / Selenium
- Stall rest
Treatment - long term:
- Rest & regular (daily) turn-out
- Regular daily exercise
- Diet - fat based diet (rice bran, oils) instead of easily digestible carbs, Vit E / Selenium, electrolytes