neuro and muskuloskeletal Flashcards
Muscle strain type injuries in horses
Presentation: Acutely painful with localised lameness +/- swelling
Likely under recognised, challenging to diagnose. Palpable swelling. Asymmetry.
Risk factors: Type of activity, surface terrain, poor warm up.
May lead to ossifying / fibrotic myopathy.
Muscle enzymes may be mildly elevated but can be normal ( depends on timing and amount of muscle injured)
Ultrasound: may see fluid accumulation and disrupted fibre pattern.
treatment-
Cold hosing, icing, analgesia NSAID’s
Rest
Gentle stretching and hand walking
Range of motion exercises
Exertional Myopathies in horses
The most important and prevalent muscular disorder of performance horses
Acute clinical signs of EM are very similar across the spectrum of causes.
Associated with exercise although this may be low intensity.
Muscle stiffness, shortened hind limb stride, reluctance to move.
Firm, painful hindquarter muscles
Anxiety, pain, sweating, increased respiratory rate
Can show “Colic” type symptoms. Pawing, attempting to lie down.
Dark urine (myoglobinuria)
Elevations of muscle enzymes CK/AST
Sporadic (one off) (extrinsic factors)-
Exercise that exceeds training
Dietary Imbalance (high NSC low forage, electrolyte imbalances, low Vit E/selenium)
Exhausted Horse Syndrome (may not have firm muscles on palpation)
Recurrent / heritable (intrinsic factors)-
Recurent Equine Rabdomyalisis
Polysaccharide storage myopathy
Breed related myopathies – uncommon in UK
HYPP (QH) Malignant Hyperthermia (QH)
Myofibrillar myopathy ( Arab/ WB)
Recurrent exertional rhabdomyolysis: RER
Abnormal regulation of muscle contraction
Defect in intracellular calcium kinetics (currently unknown)
Light or hot breeds (TB/ standardbred predominate)
Prevalence 4.9-6.7%
Heritability suggested but not proven
Females> Males
Nervous horses’ higher incidence.
Horses fed more than 2.5kg of grain feed more likely to show signs
Diagnosis:
Based on clinical signs and the presence of risk factors/breed
Serum CK and AST elevations
Muscle histopathology is nonspecific – used to rule out other conditions in recurrent cases.
cause of recurrent muskuloskeletl disease
cause of er
Polysaccharide storage myopathy
Characterised by accumulations of abnormal polysaccharide in muscle.
Two types:
Type 1(PSSM1) mutation in the glycogen synthase 1 gene (GYS1)
Type 2 (PSSM2) – origins as yet unknown but do not have
GYS1 mutation.
Type 1 mutation is autosomal dominant – if you get the gene from only one parent you can develop the disease ( 50% chance)
Prevalence: More than 20 breeds possess the GYS1 mutation (PSSM1)
Highest prevalence in draft breeds, QH’s, Warmbloods, draft breed crosses, Appaloosa’s cobs and ponies.
Low to non-existent in light horse breeds, such as Arabians, Standardbreds and Thoroughbreds.
Diagnosis:
Based on clinical signs, muscle enzymes, muscle biopsies of horses greater than 2 years of age.
Genetic testing for PSSM1 blood or hair root samples.
cause of recurrent muskuloskeletl disease
cause of er
Myofibrillar myopathy
Causes of recurrent muskuloskeletal disease
Recently identified disorder in horses presenting with exercise intolerance or intermittent ER.
Defined by specific histopathology
Seen in WB’s and Arabs but seem to get different presentations of this disease.
Warmbloods
Muscle enzymes may be normal
Poor performance, “muscle” lameness, unwillingness to go forward
Arabs
Less painful but very high muscle enzymes after exercise
Myoglobinuria and mild muscle stiffness
cause of er
Treatment of Acute Exertional Rhabdomyolysis
Aims
Relieve muscle pain and anxiety
Correct fluid deficits
Protect kidneys from nephrotoxic effects of myoglobinuria, dehydration, and NSAIDs
Often stabled in the acute stages but prolonged box rest not recommended.
Reduce known risk factors (excessive grain/ CHO in diet)
management-
Low starch, high fat diet: RER and PSSM1 & 2
Ensure adequate electrolyte and vitamin E intake ( especially if restricted pasture access)
Regular/frequent exercise
RER, MFM, PSSM
Amino acid supplementation?
MFM/Type 2 PSSM
Benefits unclear and unproven
medication-
Dantrolene Sodium (muscle relaxant)
Prevents ER in Thoroughbreds
Normalized contracture of RER muscle in vitro
Normalized CK with exercise in RER horses
medication for Acute Exertional Rhabdomyolysis
Dantrolene Sodium (muscle relaxant)
Prevents ER in Thoroughbreds
Normalized contracture of RER muscle in vitro
Normalized CK with exercise in RER horses
Infectious Myopathies in Horses
Virus-associated Myositis (EIV, EIA, EHV1)
Clostridial myositis-
Necrotizing infection of muscle related to Clostridium sp.
Can have accompanying severe toxaemia ( mortality 15-70%)
Typically, Cl. perfringens A
80% of equine cases arise at IM injection sites (12h – 1 week later)
Diffuse, rapidly spreading areas of subcutaneous emphysema and crepitation.
Require rapid aggressive treatment, surgical
debridement and antimicrobials.
differentails for the horse with unexplained elevation in muscle enzymes and poor performance
Horses with recurrent causes of exertional myopathies can also present with more chronic clinical signs:
lack of energy under saddle, reluctance to move forward
stopping and stretching out as if to urinate
chronic back pain, failure to round over fences
fasciculations or pain upon palpation of lumbar muscles.
Warmblood horses with PSSM2 or Myofibrillar myopathy often have normal muscle enzymes
DOMS (delayed onset muscle soreness)
Overtraining can also be a problem
DOMS (delayed onset muscle soreness in horses
Presentation: Poor performance and diffuse pain:
Delayed onset muscle soreness (DOMS) following unusual or unaccustomed exercise (especially eccentric contractions)
Think about how you feel 24- 48 hours after a new sport!
Eccentric contraction: Contraction when muscle is under tension (lengthened
Mild to moderate elevations in serum AST in racehorses may be associated with cumulative muscle damage from training or trauma associated with unaccustomed exercise.
overtrianing as a differentail for The horse with unexplained elevation in muscle enzymes and poor performance
Overtraining can also be a problem
This is different from acute muscle injury
Imbalance between training and recovery manifesting as a syndrome of chronic fatigue and poor performance
AST showed a significant linear increase
with cumulative training days
Muscle Atrophy in horses
Loss of muscle mass, can be focal or generalised.
Neurogenic: Damage to the motor nerve supplying the muscle
Myogenic: Direct damage or atrophy of muscle fibres (myogenic)
could also be secondary- malabsorbtion, catchexia, ppid, chronic disease
causes of generalised primary neurogenic muscle atrophy in horses
equine motor neurone disease
vitimeine e related deficiency
immune- mediated myositis
PSSM1 homozygotes
Equine motor neurone disease
Oxidative damage to motor neurons, associated with vitamin E/selenium deficiency.
Denervation of the muscle results in atrophy
Horses with prolonged restricted pasture access but high CHO diet are predisposed
cs-
Normal appetite.
Muscle weakness and atrophy
Trembling.
Weight shifting when standing.
“Walk better than they stand”
Raised tail head
Abnormally low head carriage.
Exercise intolerance.
“Elephant on tub” stance
Retinal changes
Diagnosis -
Low plasma Vitamin E (alpha-tocopherol): <1 microg/ml in >90% of cases.
Muscle enzymes elevated in acute case but may be normal in more chronic stable cases
Muscle biopsy of tailhead muscle - denervation atrophy
Prognosis-
May stabilise but recurrence can occur. 30% will require euthanasia
Treatment: none proven, vitamin E therapy used.
The sacrocaudalis is often the only muscle that will show lesions of vitamin E–deficient myopathy (VitEM) or equine motor neuron disease (EMND).2 The site for biopsy of the SC muscle is within 1.5 inches of the tail head and 0.25 inches off of midline
Vitamin E deficiency in horses
Chronic vitamin E deficiency can result in EMND
Some horses with vitamin E deficiency develop a myopathy which is similar but more subtle
Unlike EMND, is remarkably responsive to treatment
The sacrocaudalis is often the only muscle that will show lesions of vitamin E–deficient myopathy (VitEM) or equine motor neuron disease (EMND).2 The site for biopsy of the SC muscle is within 1.5 inches of the tail head and 0.25 inches off of midline
Immune-mediated myositis in horses
Rapid atrophy of topline muscles
CK/AST moderately to marked elevation
Primarily occurs in Quarter Horse–related breeds (less common in UK)
Associated with carrying heterozygous or homozygous genotypes for a mutation in MYH1
Homozygous horses more affected
A triggering factor appears to be exposure to S equi or a respiratory disease
Diagnosis Muscle biopsy ( epaxial and gluteal muscles)/ genetic testing
Treatment: Corticosteroids ( abx if concurrent infection)
PSSM type 1 homozygotes in horses
Horses which are homozygous for PSSM type 1 (less common that heterozygous)
Clinical signs are often more profound an may be associated with generalised muscle atrophy.
that encodes the fast-twitch type 2X myosin heavy chain
diagnosis-
History, clinical signs
Acute diffuse pain
Acute focal pain
Unexplained muscle enzyme increases with poor performance
Atrophy
Focal pain/lameness - Ultrasound or other imaging
Muscle atrophy – systematic approach
Vit E/ alpha-tocopherol concentrations
Muscle biopsy (SCDM)
+/- Genetic testing for PSSM1
- Metabolic disease. Sporadic or recurrent?
Muscle enzymes (CK and AST)
If mild signs or muscle enzymes not elevated on resting sample but you suspect a myopathy you can perform an exercise test - Exercise test: 15 minutes lunge
Useful to detect elevations in CK in subclinical cases
Elevation of CK 4 hours after exercise test from pre-exercise values
More than double or >1000 U/l indicative of recurrent/ metabolic muscle disorder
** Remember WB’s with PSSM2 or Myofibrillar myopathy often have normal muscle enzymes and will require a biopsy for diagnosis
Kinetics of plasma CK and AST in horses
Plasma CK peaks at 4–6 hours following muscle damage and (unless the damage continues) starts to decline, with a half-life of approximately 12 hours (Fig. 7.7).28 AST activity peaks about 24 hours after an episode and can remain elevated for several days to weeks
high ast but normal ck indicates chronic problem
high ck low ast indicates acute problem
genetic testing for conditions that causte metabolic myopathy in horses
Test for PSSM1 if:
Appaloosa
Quarterhorse (Can also test for MH / HYPP/ MYH1)
Cold bloods (cobs and ponies) and Warmbloods
Confirmed recurrent disease in non-Thoroughbred/Standardbred
But remember 30% of horse with PSSM will be PSSM2 and
will be negative on the basis of genetic testing
approch to diagnonis of metabolic myopathy in horses
So, what if I do have evidence of a metabolic myopathy?
Genetic testing
Test for PSSM1
Appaloosa
Quarterhorse (Can also test for MH / HYPP/ MYH1)
Cold bloods (cobs and ponies) and Warmbloods
Confirmed recurrent disease in non-Thoroughbred/Standardbred
But remember 30% of horse with PSSM will be PSSM2 and
will be negative on the basis of genetic testing
Muscle Biopsy
Indicated if genetic testing is negative (Gluteal or semimembranosus biopsies are preferred)
For diagnosis of Myofibrillar myopathy
In cases of muscle atrophy (EMND and VitEM use tailhead muscle for IMM use epaxial and gluteal muscles )
Laxity versus Dysplasia in cases of hip dysplasia
Hip dysplasia is a hereditary condition, but
Puppies are born with normal hips
Many dogs will have laxity early in life, but this does not predict dysplastic changes later
Multiple factors have been implicated as risks for HD, including
Diet
Exercise
laxity as a puppy progresses into significant pathology in adulthood- Hip Dysplasia at 10 months of age and severe arthritis at 3 years of age
causes abnomal bone load and remodling
clinical presentation of hip dysplasia
Common breeds include Labradors, GSDs, Rotties, Goldens and (increasingly) cross-breeds
Typically, 6-7 months at first presentation, but may be older (DJD)
Presenting signs may include difficulty rising, abnormal gait, bunny hopping, pelvic limb lameness or clicking/clunking of the hips
ortho exam-
Asymmetric muscle mass, esp. quads and gluteals
Sensitivity over hind quarters
Pain on hip extension, abduction
Reduced range of motion, crepitus (DJD)
Asymmetric pad wear
Be cautious about over-inferring…these are not specific signs
dx-
Avascular necrosis of the femoral head (Legg-Calve Perthes)
Fracture (pelvis, proximal femur)
Luxation
Psoas injury
Sciatic pathology
Neoplasia (bone or joint)
Sepsis
ortolani test for hip dysplasia
dog under ga and dorsa recumbrancy
put dorsal pressure on stifle
abduct to detect reduction
adduct to deted subluxation
barden test for hip dysplasia
dog in lateral recumbrancy
proximal femur is plapated
apply dorsal lift to femur
then reduce with thumb
palpable movement indicated laxity
questionable value
Radiography – “Hip Series”
includes VD extended
VD flexed (frogleg)
and lateral
what is looked for in a Hip Assessment on Radiographs
Hip subluxation
Dorsal acetabular cover
Norberg angle
Distraction index- DI < 0.3 – good prognosis
DI > 0.7 – poor prognosis- not gennarally used in uk but usefull. involved radiograph exposure however- limb must be positioned in a way to measure how much femoral head is moved out of joint
Management and treatment of Joint Disease (hip dysplasia ect)
Start with identifying the treatment goals
Know the current therapies and the evidence for/against them
Understand the client’s expectations- Age of dog, intended use, stage of disease
Consider the financial implications of treatment selections
goals- Pain
Joint ROM
Limb function
Muscle mass and strength
Activity level
Quality of life
treatment-
Conservative management (see CAM seminar for more details)- Weight management, exercise control, nutraceuticals, physio, medication
Surgical management:
Pain reduction, mechanical realignment
Excision arthroplasty
Joint replacement
Excision Arthroplasty
Joint Fusion (Arthrodesis)
Joint Replacement (Arthroplasty)- good results
Cruciate Ligament Disease
functions of the ccl- Prevents cranial translation, internal rotation of the tibia
Prevents hyperextension of the stifle
clinical presentation-
Very common injury in the dog
Usually a “non-contact” injury (cf. human)
Often bilateral (10% at presentation/50% within 2yrs)
Breed predispositions
Changes often exist before the rupture
Partial tears are common
Meniscal Injury
Identified in up to 75% of dogs with CCLR
Medial meniscus typically affected
Most often evident at surgery, but can also occur later as a complication
Poor residual healing capacity, so partial or complete removal indicated
sugrigal managemtn of ccl injury
meniscal injury- Identified in up to 75% of dogs with CCLR
Medial meniscus typically affected
Most often evident at surgery, but can also occur later as a complication
Poor residual healing capacity, so partial or complete removal indicated
surture-
Externally rotates and limits cranial tibial translation
Suture will fail but ideally after fibrosis has stabilised the joint
Inexpensive and simple to do
Low risk of complications
will eventaally fail but goal is to encorage fiborous tissue growth to reduce draw and reduce pain
osteotomy-
Tibial Plateau Levelling Osteotomy- rotaits tibia to flatten it and loading is straight down, improving patient pain
or tibial tuberosity advancment- tibial crest teperated and wedged forwart
Canine Elbow Dysplasia
Most common cause of FL lameness in medium- and large-breed dogs
Young dogs (primary disease) to older dogs (DJD)
Commonly bilateral (80%) so always check both legs
Genetic component – IEWG scheme
Osteochondrosis of the humeral condyle
Ununited anconeal process
Fragmented coronoid process
Radi-ulnar incongruity
Can occur concurrently
cs-
Lameness
Often shortened (“choppy”) FL gait
Commonly bilateral, often asymmetric
Effusion (best detected on the lateral aspect of the joint between the lateral epicondyle and olecranon)
Pain +/- crepitus, reduced ROM
Ununited Anconeal Process (UAP)-
Growth plate normally fuses by 5 mths
GSDs, BMDs, Wolfhounds, M>F
Surgery offers best prognosis
Reattachment if possible
Fragment removal if not
Fragmented Coronoid Process
Labradors, GSDs, BMDs 6-14 months
Medial coronoid fragments due to sub-surface fissuring
Hard to see on X-ray - CT preferred
Arthroscopy is definitive- not generally done, refferal
Untreated, will lead to DJD…but benefits of surgery not clear
Osteochondrosis
Medial humeral condyle
Failure of endochondral ossification
Subsurface failure and cartilage lifts
Inflammation, pain, DJD
Surgical management - arthroscopic debridement +/- osteoarticular graft
Similar approach for shoulder OCD
Elbow joint incongruency
Step between the radius and ulna
Short radius > short ulna
Hard to diagnose on X-ray, CT better
Surgical management usually involves ulnar osteotomy to allow the ulna to “find a new position”
Patellar Luxation
Heritable condition
Developmental but not congenital
Several theories, none proven
Abnormal hip development
Hormones (estradiol)
Abnormal muscle growth (quadriceps)
Muscle imbalance leads to bone deformity
signalment-
Small breed dogs: terriers, Chihuahua (medial)
Medium breeds: Spaniel, SBT (medial)
Large breeds: flat coat retriever (lateral),
Labrador (medial)
Cats: unusual (British short hair)
cf-
Pelvic limb lameness
If intermittent, owner may report a ”skipping gait”
May be unable Inability to fix the stifle when weight-bearing
May be bilateral (50-64%)
small breed dogs generally medial luxation- percentage shifts to lateral as dog gets bgger
Management of Patellar Luxation
Surgical vs. conservative care
Medial or lateral release and/or imbrication
Wedge recession
Block recession
Abrasion
Tibial tubercle transposition (TTT)
grade 1 and 2 often managed with conservative care
Classifying Fractures
Cause of fracture – intrinsic vs. extrinsic, muscle action, etc.
Communication with external environment (open vs. closed)
Extent of bone damage
Number and position of fragments
Direction of fracture lines
Location
Forces acting on the fracture/displacement Stability
Degree of complexity and involvement of other tissues
Age of fracture (recent, old)
Femoral Fractures
Most common appendicular
fractures in small animals
Surgical access from lateral
IM pin, plates and ILNs are all good options
Avoid ESFs (large muscle mass) except when used as pin tie
Radius-Ulna Fractures
Distal diaphyseal fractures most common
Plate + screw repair cranially and/or medially recommended
Can consider repairing repairing both the radius and ulna in select cases
External coaptation only for simple transverse fractures with stability and good apposition – case selection very important!
Tibial Fractures
Dependent on fracture assessment, all options for fixation can be considered.
Remember to assess whether fibula is intact when assessing fracture
Medial side is tension side of bone and gives best surgical access for plate fixation
ESF excellent for comminuted and/or open fractures
Salter Classification of Physeal Fractures
method used to grade fractures that occur in young animals and involve the growth plate, which is also known as the physis or physial plate
type I-
slipped
5-7%
fracture plane passes all the way through the growth plate, not involving bone
cannot occur if the growth plate is fused cit
good prognosis
type II- above ~75% (by far the most common)fracture passes across most of the growth plate and up through the metaphysis good prognosis
type III-
lower
7-10%
fracture plane passes some distance along with the growth plate and down through the epiphysis
poorer prognosis as the proliferative and reserve zones are interrupted
type IV-
through or transverse or together
intra-articular
10%
fracture plane passes directly through the metaphysis, growth plate and down through the epiphysis
poor prognosis as the proliferative and reserve zones are interrupted
type V- ruined or rammed uncommon <1% crushing type injury does not displace the growth plate but damages it by direct compression worst prognosis
Location of Physeal Fractures
Femur - 46.5%
Humerus - 19.8%
Tibia - 13.5%
Radius - 11.8%
Fractures are 4 x more common in the distal physis
compared to the proximal physis
Repair of Physeal Fractures
Early management is recommended
Always warn the owner about the risk of complications due to GP compromise
Avoid devices that compress/restrict bone lengthening at the physis
Recognise difference between tension and compression GPs
Smooth K-wires, typically <10% the width of the physis, are preferred whenever feasible
femoral head growth plate fracture
Operate early - delayed management worsens prognosis
Generally heal quickly
FHNE or THR for chronic cases or in cases with non-union
Proximal Tibia growth plate fracture
tension groth plate- patellar ligamebt
Mandibular Symphyseal Separation
Very common, particularly in cats
Not usually a challenging diagnosis – can range from minimal displacement to a gaping chasm!
Repair technique involves simple materials – hypodermic needles (16-21G) and cerclage wire (18-24G)
Tweak the repair to get perfect occlusion
Be careful not to overtighten wire and crush tissues
Straightforward and often no need for post-operative X-rays as reduction and stability are apparent
Wire is removed after 4-6 weeks under sedation or GA
Heavy-gauge PDS can be an alternative to wire and avoids the need for repeat sedation/GA
If there is caudal instability or comminution, consider intraoral splinting
Pelvic Fractures
conserns- diaphramatic hernea, heamoragge, nerve damage
Box shape, so usually >1 fracture
Abundant soft tissues
Rarely open fractures
Good healing potential
Surgical access can be tricky
Indications for Surgery-
Fractures along the weight-bearing axis- SI joint (not always), ilial body and acetabulum
Articular fractures (acetabulum)
Significant (>30%) narrowing of the pelvic canal
Severe pain
Nerve entrapment
Concomitant ipsilateral fractures
Working/athletic/breeding dogs where function must be optimal
Treatment of SI Luxation
Manage conservatively if unilateral and <50% displacement
Lag screw repair (>60% sacral width) or trans-ilial bolt or pin (easier)
Ilial Body Fractures
Usually result in pelvic canal narrowing
On the weight-bearing axis
Lateral approach with lateral plating (can do dorsal
Post-op Management-
Repeat neuro exam post-op to confirm integrity
Stool softeners, plenty of water or fluids
Crate confinement
Lead exercise only for bathroom
Re-evaluate at 4-6 weeks (X-ray)
primary tumours of bone
osteosarcoma- makes bone
myeloma
lymphoma
chondrosarcoma
secondary tumours of bone
locally invasive- squamous cell carcinoma
metastisis to bone- metastatic tumour
Osteosarcoma
Osteosarcoma is the most common primary bone malignancy in the dog
Middle aged - older dogs (but not exclusively)
Large & giant breeds (> 30kg)
Males > females
Distal radius
Proximal humerus
Proximal tibia
Distal femur
(distal tibia)
Away from the elbow, towards the knee
managment-
amputation + cisplatin/ carboplatin/ doxorubin (some sort of chemo)
amputation alone gives dogs 3 months- ok for pain releif but not atdiquate alone
diagnosis-
Usually, metaphyseal location
Bone destruction
Poorly defined margin
Cortical destruction
May see periosteal new bone
disorganised / sunburst
Pathological fracture
BONE BIOPSY
at diagnosis- 90% will have micro-metastasis
if metastasis seen in lung there is no reason to treat
Ligaments and Tendons
Highly specialised connective tissues
Both are composites of collagen type I (98%) in a proteoglycan matrix produced by fibroblasts
Mechanical and biological properties defined by their composition, structure and blood supply
Tendon blood supply is more resilient as it comes from multiple sources, not just the insertion sites
Healing of Tendon and Ligament
Poor blood supply
Heal by formation of scar tissue
Requires initial protection (3 weeks)
Followed by controlled mobilisation
Regain around 60% strength by 6 weeks
Susceptible to re-injury
Orthotics can be invaluable in managing these injuries
Common Ligament Injuries
Cruciate ligaments
Collateral ligaments
Round ligament of the femoral head (luxation)
Plantar ligament injuries
Carpal ligament injuries
Collateral Ligament Injuries
These injuries are usually traumatic, commonly road traffic accident
May be open or closed
Collateral ligament ruptures are seen in the shoulder (glenohumeral ligaments), elbow, carpus, stifle, hock and interphalangeal joints
May attempt primary repair of the ligament but usually reinforced with a prosthetic repair
Suture, fibre wire or tape
Suture anchors
Open Injuries to Ligaments
Commonly major trauma – e.g. dragged by car
Soft tissue management critical, not just repair or replacement of collaterals
Post-operative focus needs to be on protecting soft tissue cover over the ligaments and any associated implants
May not be possible to repair these, and stabilisation by arthrodesis may be indicated
Shearing Injuries to ligamnets
Commonly major trauma – e.g. dragged by car
Soft tissue management critical, not just repair or replacement of collaterals
Protect soft tissue cover over the ligaments and any associated implants
If impossible, may need to stabilise by arthrodesis
Principles of Arthrodesis
Remove residual cartilage (saw, burr, curette)
Placement of cancellous bone graft
Direct compression of bone surfaces
Rigid stabilisation at at functional angle
Indications for Arthrodesis-
Chronic pain from DJD that is not treatable
Untreatable fractures, esp. comminuted, intra-articular
Chronic joint luxation
Partial neurological injuries
Ligament injuries or instability that cannot be surgically stabilised
outcomes-
Carpus: Good to excellent function
Hock: Good to excellent
Shoulder: Fair to good
Elbow: Poor
Stifle: Poor
Digits: Unpredictable
Causes of Luxation
Congenital
Developmental (e.g. patellar luxation )
Traumatic (motor vehicle, fall)
Hip Luxation
Usually traumatic (RTA or fall) - 60% are craniodorsal
Can be ventral too
managment-
Acute cases may be closed reduced
Immobilisation with Ehmer sling
Open reduction may be required
Luxations that cannot be closed reduced
Luxations that recur following initial
closed reduction
open tratment-
Prosthetic capsule
Toggle pin
Transarticular pin
Causes of Tendon Injury
(Developmental)
Acquired
Trauma
Iatrogenic
Degenerative
Drug related: corticosteroids, fluroquinolones
Muscle Contracture
Infraspinatus
Supraspinatus
Quadriceps
Gracilis/ST
Panosteitis
Shifting leg lameness
Severe cases can be systemically ill
Typically 5-8 months
Breeds - large especially GSDs
Male > female
Pain on direct bone palpation
Aetiopathogenesis
Viral, excess nutrition, genetic?
Histopathology
Degeneration of medullary adipocytes
Stromal cell proliferation,
Intramembranous ossification
Management
Analgesics
Usually self-limiting
Avascular Necrosis (AVN)
Ischaemic necrosis
Small breeds
From 5 months of age
Pain on hip extension & flexion
Muscle wastage
Radiographic Features of AVN-
Lucent areas initially
Distinct from OA
Collapse & mushrooming
Articular surface is then destroyed
Craniomandibular Osteopathy
Signalment
Breeds – Terriers, esp. WHW, Scotties, Bostons and
Cairns
Age 3-8 months
Male = Female
Genetic basis – autosomal recessive in WHWT
Viral?
Nutritional?
Physical examination
Palpably enlarged mandibles
Limited mouth opening
Pain on opening mouth or palpation
Radiography
Proliferative new bone on mandibles
Sometimes on TMJs
On bullae
describe what can be assesed on a dosolateral medopalmar view of a horses limb
hilights the sorsomedial aspect and the l ateral palmar aspect
why do you pack the hoof when x reaying horses feet
to prevent the natural clefts and ridges from appearing as fractures (and artefacts) on radiograph
Forebrain function
pecial
senses- e.g. vision,
hearing,
taste, smell (processing not collection- crainial nerves
Behaviour
Brain Stem function
Midbrain, and hindbrain (pons and medulla)
Cranial nerves
Autonomic activity - Parasympathetic outflow cranial nerves III (eye), VII (lacrimal, mandibular and submandibular glands), IX (parotid and mucosal glands), X (vagus – to cardiorespiratory,
gastrointestinal systems)
Reticular activating formation/system (RAS)-
Controlling and activating centreMaintains central processing areas in state of activity
Cerebellum function
Abnormality causes loss of fine control Exaggerated, coarse, abrupt movement Worse for voluntary
MUST be intact for normal menace response- Complex response NOT simple reflex
indicators fo forebrain disease
Behaviour - may indicate forebrain disease
e.g. seizures in foals, head pressing,
compulsive wandering, circling, changes in
voice
depression/obtundation
+/- coma, +/- seizures, +/- circling, +/-blindness (central)
gaiut- mild ataxia
no crainil nerve involvment
indicaors for brainstem/ RAS disease
Mental Status - RAS and forebrain= level of awareness of consciousness
Depression/obtundation +/- circling, +/- head tilt (if caudal
lesion)
ataxia?- None
ataxia/weakness +/-quadruparesis
crainial nerve involvment?- Yes
Rostral lesion CN II; mid-brain CN IIIIV; caudal lesion V-XII
Vestibular disease - peripheral or central
-Basisphenoid fracture
Facial nerve paralysis (vii&viii may occur
together)
Ocular abnormalities e.g. horner’s
Pharyngeal/laryngeal deficits – dysphagia
Trigeminal neuritis - headshaking
indicators for cerebellar disease
Head posture- however could also be peripheral vestibular,
central, musculoskeletal,
neuromuscular
Intention tremor, +/- menace reflex
gait?- Dysmetria/spasticityNo weakness
no crainial nerve involvment
Neuro Exam: Cranial Nerves assesment steps
The three step cranial nerve exam:
I - olfactory – smell (can’t test for unilateral
lesions – ignore)
STEP 1. THE EYE: II, III, IV, VI, (plus V+VII
with palpebral)
Menace, eye position & movement
including different head positions, normal
positional nystagmus, PLR and palpebral
reflex
parasympathetic innervation to the eye
Step 2. “ears” Vestibular VIII - head posture,
induced eyeball movement/normal
vestibular nystagmus, normal gait,
blindfold, hearing
Step 3. “mouth” Swallowing and tongue IX, X,
XI, XII
Pull out tongue, assess for tone and
symmetry, replace and observe swallow
Neuro. Exam: Cranial Nerves
I - olfactory - smell
II - optic - sight, menace (note neonates), PLR, swinging light test, cerebellum
III - occulomotor - PLR & eye position & movement
IV, VI - trochlear and abducens - eye
position & movement
-note normal responses
-sympathetic & parasympathetic innervation to the eye
V - trigeminal - sensation to face, motor
to muscles of mastication
-facial reflex vs. sensation - look for
behavioural response
VII - facial - muscles of facial expression
- may be subtle asymmetry
-palpation may be useful
VIII - vestibulocochlear - head posture, induced
eyeball movement, normal vestibular
nystagmus, normal gait, blindfold, hearing
IX, X, XI - glossopharyngeal, vagus &
accessory - sensory & motor to pharynx &
larynx -
swallowing, endoscopy
- XI motor to trapezius, cranial part of
sternocephalicus
XII - hypoglossal - tongue size, tone &
symmetry
Neuro. Exam: Gait and Posture
Assessment of spinal cord and
peripheral nerve and muscle function
Which limbs are abnormal?
What are the abnormalities?
Grade (1-4)?
Is there concurrent or primary
lameness?
Ataxia -
General body
Conscious proprioception deficits
Weakness -
paresis, hypometria, postural deficits, recumbency (tetraparesis)
Hyper-reflexia/increased muscle tone-Hypermetria
Hypo- reflexia/decreased muscle tone-Hypometria (note spasticity can also appear hypometric)
atophy
Upper motor neurones
Cell bodies in motor centre of brain-
series of synapses from cortex through brainstem
(NB motor cortex itself
Afferent fibres travel down spinal cord-
inhibitory or modulating function
Synapse with lower motor neurone
Lower motor neurones
Cell bodies in ventral horn (grey matter) of
spinal cord - cervical and lumbosacral intumescence
(thickening)
LMN final common pathway whether
voluntary or reflex motor response (and also
sensory in efferent fibres)
Spinal Cord Disease: UMN
With increasing compression more
functional deficits occur:
loss of proprioception- ataxia- wide based stance
motor weakness- narrow based stance
loss of sensory perception - touch
loss of pain- very rare and only with sever traumatic leasions
UMN vs. LMN in disease
UMN – spinal cord and
brainstem-
Increased muscle tone
Increased reflexes
No atrophy
Variable weakness and
sensory loss depending
on depth of lesion
LMN – spinal cord Grey
matter and peripheral nerves
Decreased muscle tone
Decreased reflexes
Muscle atrophy
Weakness
Sensory loss
Specific tests for ataxia in the horse:
proprioceptive deficits
Whole body or limb
look for poor co-ordination, swaying, limb moving excessively during swing phase - weaving,
abduction, adduction, crossing of limbs, stepping on themselves-
exaggerated by tight circles - pivoting, circumduction, serpentine, sudden stopping, backing, hills, raising the head visual compensation
Concurrently observe for reflexia and muscle tone
Specific tests for weakness
(paresis) in the horse:
look for hoof wear - dragging toes, low arc of flight of the hoof (hypometria)
tail pull - at rest (LMN) and during walking (UMN able to reflexly resist while standing still)
hopping, circling, slope - trembling, buckling of weak limb, knuckling over
generalised weakness ‘walk better than they
stand
Weakness vs. different neuroanatomical locations in the horse
generalised weakness, no ataxia -
neuromuscular disease
localised weakness - LMN or peripheral nerve
disease
weakness and ataxia - UMN - descending
motor pathway ipsilateral and caudal to the
site of the lesion
weakness’ associated with vestibular disease
- tend to fall towards the side of the lesion
Deficits vs. lesion localisation – which limbs are
affected when there is a problem with c1-6
UMN signs in both fore and hindlimbs
Deficits vs. lesion localisation – which limbs are
affected when there is a problem with C7-T2
lower motor neurone signs in forelimbs
upper motor neuron signs in hindlimbs
Deficits vs. lesion localisation – which limbs are
affected when there is a problem with T3-L3
normal neurone signs in forelimbs
upper motor neuron signs in hindlimbs
Deficits vs. lesion localisation – which limbs are
affected when there is a problem with L4-S3
normal neurone signs in forelimbs
lower motor neuron signs in hindlimbs
Deficits vs. lesion localisation – which limbs are
affected when there is a problem with S3-Ca…
normal in all limbs
Spinal Cord Disease: Classification of deficits
1 (+) subtle- deficits just barely detected at normal gait, occur during backing, stopping, turning, swaying, neck extension etc.
2 (++) mild)- detected at normal gait, exaggerated by above manoeuvres
3 (+++) moderate- prominent at normal gait, tend to buckle and fall with above techniques
4 (++++) severe- tripping falling spontaneously at normal gait to complete paralysis
Forelimbs may be a grade less than the hind limbs with focal cervical spinal cord and brainstem lesions
Neuro. Exam in the horse: Neck and
forelimbs
For horses with signs localised cranial to T2 -
confirmation and localisation
Observation and palpation of neck- muscle atrophy, asymmetry, sweating
Range of movement of the neck
sensory perception - two-step technique
local cervical and cervicofacial reflexes
sway reaction
Neuro. Exam in the horse: trunk, hindlimbs, tail, anus
Observation and palpation- muscle atrophy, asymmetry, sweating
Sensory perception
Tail - voluntary movement, tone
Perineal reflex/tail clamp
Male external genitalia
Rectal examination - assess lumbar, sacral or coccygeal vertebrae, bladder volume, tone
Neuro. Exam in the horse: the recumbent
patient
Decide on anatomical location-
good use of thoracic limbs? - caudal to T2
weak use of thoracic limbs? - caudal cervical
lifts head only? - cranial cervical
Reflexes, tone, voluntary effort can be used- as with small animals
Reflexes, tone, voluntary effort can be used -as with small animals
Often awkward, emergency situation,
insufficient info. or time
adrenaline/autonomic domination for
first 1-2 hours after trauma
make every effort to make the animal
stand after this time (unless fracture is
suspected)
best to delay final decision 24 hours
Equine Forebrain Diseases
Brain disease in Adults:
Trauma (meningitis)
Hepatic encephalopathy
Uncommon -
Abscess
Cholesterol granuloma
Verminous
Infectiousmeninigitis and meningoencephalomyelitis
Neoplasia
Toxins (mouldy corn etc)
DDx: Other e.g.
Intracarotid injection
Sleep Disorders – hypersomnia- occurs when horses cannot coplete full sleep cyle by lying down- muskuloskeletal? fear fo being cast?
Previous term ‘narcolepsy’ less
accurate
Rapid raising of head old horses- carrotid bareoreceptor- dx for seasures
Metabolic e.g. hypoCa/Mg,
ammonia
Perinatal asphyxia syndrome
(dummy foals, hypoxia ischaemic encephalopathy)
Ischaemia, oedema and reperfusion
injury to foal’s brain, kidneys, intestine
and other organs due to lack of oxygen
In utero hypoxia
Interruption of oxygen supply during birth
May not be apparent until the foal is 12-
24 hours old
Severe cases may have central
respiratory depression
Mild
- Unable to attach to mare, poor suck reflex
Moderate
-Aimless wandering
Abnormal phonation (barkers)
Blind
Severe- Seizures, coma
HIE/PAS Treatment and Prognosi
Prognosis good if sepsis score
<11 (not septic) with good nursing
Can take up to 2 weeks
Expensive
Rare long term effects e.g.
cerebellar injury
Still need basic care for neonate
Antibiotics (short term), +/- gastric
ulcer meds, nutrition, care of eyes,
stop damage to self
Oxygen
Neonatal Seizures and
Epilepsy
Trauma
Sepsis- less common manifestation
Secondary neurologic
disorders-
ANAEMIA
Hypoglycemia
Metabolic - e.g. hypo Na+
Developmental
abnormalities &
malformations
Cerebellar ‘fits’
Portocaval shunt
Benign epilepsy of foals
esp. Arabs, up to 12 months
of age
low seizure threshold during
development
Cerebellar Hypoplasia in foals
Signs usually at birth, may develop in 1st 6 mths
Developmental abnormality Arabian foals
intention tremors
loss of fine motor control
ataxia, basewide stance
no treatment
Vestibular disease in horses
trauma and otitis media/interna are the
Otitis media/interna in horses
temporohyoid/stylohyoid osteoarthropathy
predominantly peripheral VIII
rarely an extension from otitis externa- usually haematogenous infection of middle ear
low-grade infectious process- rarely results in rupture of tympanic membrane
DDx
idiopathic
neoplasia
Parasitic (including EPM in USA)
diagnosis-
clinical signs, lesion localisation
Radiography/Computed tomography
guttural pouch endoscopy - for evidence of
stylohyoid bones changes or rarely drainage
from middle ear, NOT for guttural pouch disease
Dysphagia in horses
uttural pouch mycosis and empyema
disease is more common than neurological presentation
CN’s IX, X, XI, and XII and internal carotid artery are in
the dorsomedial aspect of the medial compartment
Lead poisoning
Facial Nerve paralysis in horses
Facial nerve paralysis is commonly iatrogenic due to halters left on during field anaesthesia
injury- Prolonged/permanent deficits
Eye injury, keratitis, dry eye
Dysphagia, feed pouching
Poor performance - nostril
collapse
Horner’s Syndrome in horses
Note most common cause of Horner’s syndrome is iatrogenic
due to extra vascular injection of irritant.
Miosis, enophthalmus, and protruding nictitating membrane as for other spp.
Hyperaemic mm of head & face, sweating of the head & face due to interruption of sympathetic supply to blood vessels & sweat glands of the head
trigeminal neuritits in horses
Headshaking
Abnormal rapid usually vertical
flicking of the head e.g. “bee up the
nose
May rub the nose on objects or on the
ground- nostril clamping during exercise
Horses may seek shady areas, or put
his face right under the tail of other
horses (photic)
Severe cases strike at face
grading system in horses
Abnormal trigeminal nerve function – reduced threshold for stimulation-
No pathology or abnormal potentials once triggered
Similarities to human trigeminal neuralgia
Diagnosis by exclusion of other causes
Treatment – trial in order of:
nose nets, medical therapy, percutaneous electrical nerve stimulation (PENS)
Headshaking: grades in horses
0/3 = no headshaking
1/3 = headshaking at exercise but insufficiently severe as to interfere with ridden exercise
2/3 = headshaking at exercise, of a severity sufficient to make riding impossible or
dangerous
3/3 = headshaking even at rest, in the stable and/or field
Spinal Cord Diseases in the horse
Spinal cord trauma
Cervical Vertebral Malformation (CVM)*
>90% equine spine lesions are trauma and CVM (nonEPM areas)
Others include neoplasia, osteomyelitis, AO malformation
in Arabian foals
Spinal Trauma in the horse
History of sudden onset of ataxia or
recumbency, sometimes an
observed incident
No progression, frequently
improvement, although later
progression due to callus formation
may occur
Trauma may play a role in the acute
exacerbation of CVM
Sites of predilection:
1. Occipitoatlantoaxial region
2. caudal cervical
3. mid-back, but requires considerable force - usually u
Signs - vary from ataxia and paresis to recumbency
no or short-lived spinal shock / Schiff-Sherrington
may be focal of diffuse sweating with C1-T2 lesions
horses may panic
Cervical Vertebral Malformation in horses
Aetiology is multifactorial
but includes congenital,
familial esp. TB’s and
Warmbloods, dietary and
managemental (including
exercise) factors
mares that produce a lot ofmilk might predispose their foals
Is related to developmental
orthopaedic disease (DOD)
Assessment:
Lesion localisation
Note: neck pain is rarely seen in CVM versus trauma
Radiography, CT +/- contrast
Plain radiography may be all that is required
Minimum sagittal diameters etc. can aid in diagnosis
MSD: the narrowest diameter form the dorsal aspect of the vertebral body to the ventral border of the dorsal laminae
Types of lesions:
a) stenosis of vertebral canal - dynamic or static
b) abnormal articular processes (incl. OC lesions)
c) subluxation of vertebrae on flexion (C2-C6) or extension (C6-T1) of the neck
d) enlarged vertebral physeal growth regions
e) overriding of the vertebral arch and next caudal vertebral body causing dynamic stenosis during flexion or extension
f) proliferation of articular and periarticular soft tissuesm
managment of cervical vertebral malformation
In the horse surgery can be performed but is costly and may only improve the horse on average one grade
An ataxic horse should not be ridden
Early detection in young foals (6 m) and dietary restrictions have resulted in resolution of ataxia and successful racing careers
Once disease is advanced, prognosis for suitable riding animal is poor
Cauda Equina Syndrome
Sacrococcygeal spinal cord segments, cauda equina, sacral plexus and peripheral nerves to the bladder, rectum, anus, tail and perineum
May or may not involve lumbosacral nerve roots to the lumbosacral plexus - gait
abnormalities
Clinical signs:
degrees of hypotonia, hyporeflexia and
hypalgesia of the tail, anus and perineal region, urinary bladder paresis, rectal dilation, penile prolapse
may also see LMN weakness and paresis of pelvic limbs
can be difficult to distinguish UMN disease with urinary retention and 20 contusion of tail, anus from recumbency
causes-
Trauma: sacrocccygeal fracture and luxation,
avulsion of the cauda equina
Infectious, inflammatory, immune
inflammatory e.g. polyneuritis equi
viral/immune? e.g. EHV-1
verminous e.g. EPM
Toxic:
cystitis and ataxia associated with Sorghum spp. ingestion
Miscellaneous congenital anomalies
Neoplasia
EHV1 myeloencephalopathy
Cauda equina signs are a
result of vasculitis and
thrombosis of arterioles in
brain and spinal cord (viral
endotheliotrophism)
Can occur in outbreaks –
biosecurity essential!
diagnosis:
lesion localisation
r/o other causes
look for history of respiratory inf. or abortion
CSF - xanthochromic, +/- antibodies to EHV1
isolate virus from affected or in-contacts
(nasopharyngeal swabs or buffy coat)
high antibody titres (rising titres may not be
demonstrated)
EHV1 myeloencephalopathy
management:
isolation should be employed
prognosis reasonable with good nursing care
better if not recumbent - rapid recovery over days to
weeks, although full recovery may take > 1 year
if recumbent > 24 hours, poor prognosis (but not
hopeless)
recurrence of neurological disease in recovered
horses has not been documented
Peripheral nerve and neuromuscular disease in horses :
Localised weakness:
- Peripheral nerve injuries
Diffuse weakness:
Equine motor neurone disease
-others including botulism, grass sickness, VitE/Se def, post anaesthetic
myoneuropath
Abnormal hind limb gait:
Shivering and stringhalt
Generalised tetany
tetanus
prognosis-
neuropraxia (loss of function only)
may resolve within 14 days
axonotomesis (severance of axons)
6 months for recovery
should be the worse scenario for closed lesions to the side of the face (i.e. iatrogenic)
neurotmesis (severance of entire nerve fibre)
prolonged to permanent loss of function
scarring, fibrous tissue or callus formation may lead to (permanent) worsening of nerve injury
Hindlimb:
sciatic, femoral & obturator
forelimb- brahceal plexis, radial nerve paralysis
Peripheral Nerve Injury treatment
Treatment:
initial stages: anti-inflammatories
support other limb
surgery?
physiotherapy
not > 12 inches of nerve re-growth
EMG may help in monitoring
Neuromuscular Disorders causing diffuse weakness in the horse
Equine Motor Neuron Disease
(EMND)
Botulism: Clostridium botulinum
Abnormal hindlimb gait: stringhalt
Tetanus
Equine Motor Neuron Disease
(EMND)
EMND Clinical signs:
acute onset of trembling,
excessive recumbency,
shifting of weight, reluctance
to stand still/confined and
muscle atrophy (esp.
hindquarters), elevation of
tail head
appetite normal to ravenous
no ataxia
Diagnosis:
clinical signs and history
mild increases in muscle enzymes
low serum vitamin E
muscle biopsy of the tail head muscle
retinal lipopigment deposits
Treatment
Vit E supplementation
Physiotherapy
prognosis poor
Botulism: Clostridium botulinum in the horse
ingest preformed toxin (8 types - B, C, D):
toxin source:
contaminated feed (Big Bales), grass/corn silage
water (dead waterfowl)
UK: associated with poultry litter & carcasses
toxicoinfectious route (horse)
type B grows in ingesta of suckling foals, Kentucky,
eastern USA
infected wounds (gastric ulcers) (rare)
blocks acetylcholine exocytosis at presynaptic membrane of neuromuscular junction-
failure of muscle contraction => weak
abrupt progressive onset flaccid paralysis of skeletal muscle (tetraplegia)
Abnormal hindlimb gait: stringhalt in the horse
Another peripheral neuropathy
Uni (classical- biomechanical problem secondary ot injury) or bilateral (pasture associated, toxic condition occuring in australia and new zealand- pature assosiated)
Generalised tetany
poor prognisis
Clostridium tetani (soil, gi flora)
wounds, metritis, omphalitis, tooth loss spores may remain dormant for months
anaerobic: sporulate, releases toxins
tetanospasmin
inhibits presynaptic inhibitory neurons (Renshaw cells) in intermediate grey column
inhibits release of glycine
disinhibition of gamma motor neurons
muscles continuously contract (tetany)
tetany elicited by sound, light, touch
toxin only circulates and is able to be bound by antitixin for a window of time
Problems associated with Head and Neck in Farm animals
Wooden tongue
Lumpy jaw
Mandibular fractures
Tooth root abscesses
Obstructions
Oral lesions/stomatitis
Calf diptheria
Laryngeal Chondritis
Diseases involving the mouth and jaws will often share clinical picture
Unable to eat
Weight loss (through lack of food intake or disease process)
Pain
Excess salivation
Visible/palpable lumps
Conditions of the throat will often present with other symptoms
Increased respiratory noise and effort
Exercise intolerance
Inappetence
Malodourous breath
Wooden Tongue; Actinobacillosis
Common disease of cattle
Worldwide distribution
Caused by Actinobacillus lignieresii
Gram-negative bacteria
Commensal of URT and alimentary tract
Gains entry through breaks in buccal muscosa
Wooden tongue is most common clinical presentation of infection-
Can see intestinal and cutaneous forms
Most commonly seen as individual animal
Clinical Signs;
Sudden onset salivation
Dysphagia
Protrusion of tongue
Enlarged LNs
Submandibular swelling
Firm, swollen and painful tongue
Discrete yellow lesions visible beneath tongue mucosa
Differentials;
Stomatitis
Lumpy jaw
Dental disease
Oral foreign bodies
Pharyngeal trauma
Diagnosis;
Based on clinical signs
Bacterial culture (and sensitivity) can be used if appropriate
managmetn and treatment of wooden tongue
Management;
Isolate
Ensure adequate food and water
Treatment;
5-7 days streptomycin/dihydrostreptomycin or TMPS
Commonly penicillin/dihydrostreptomycin combination used
Oral potassium iodide or IV sodium iodide have been used historically
Neither treatment licensed in food animals in the UK
Lumpy jaw; Actinomycosis
Causes pyogranulomatous osteitis/osteomyelitis in adult cattle
Can be seen in young cattle when teeth erupting
Worldwide distribution
Caused by Actinomyces bovis
Gram-positive bacteria
Commensal of oral cavity
Gains access to bony structures via lymphatic system from the oral cavity through breaks in muscosa
Clinical Signs;
Affected generally BAR
Enlargement of horizontal ramus
Soft tissue swelling present and painful
Swelling is irregular and involves fibrous tissue and bone remodelling- Can lead to tooth displacement or pathological fracture
May see discharging sinus tracts
Enlargement of ipsilateral subman. LN
Pain and physical deformity lead to dysphagia- Results in weight loss
Differentials;
Tooth root abscess
Fracture of mandible
Neoplasia
Foreign body
Feed impaction
Diagnosis;
Based on clinical signs
Impression smears of pus from sinus will demonstrate gram-positive filamentous rods
Radiography can be used to analyse extent of bone lysis and remodelling
managment and treatment od actinomycosis
Management;
Ensure adequate food and water
Treatment;
As per wooden tongue
5-7 days streptomycin/dihydrostreptomycin or TMPS
Commonly penicillin/dihydrostreptomycin combination used
Long term abx treatment can lead to cessation of lesion growth
Mandibular fracture in farm animals
Can occur due to trauma-
Hit by tractor wheel when head through feed space
Kick from adult bovine (more likely in calf)
Excessive traction at parturition
Clinical Signs;
Dysphagia
Weight loss
Excess salivation
Swelling at site of fracture
Protruding tongue
Differentials;
Lumpy jaw
Wooden tongue
Dental disease
Diagnosis;
Jaw misalignment at fracture site can typically be palpated
Radiography can demonstrate extent of fracture
treatmet of mandibular disease in farm animals
Treatment;
Slight displacement treated conservatively
Fracture repair- Wire placement, External fixators
Euthanasia/Emergency slaughter
Prognosis;
Depends on site of lesion ramus vs mandibular symphysis
Depends on compromise of local tissues
Aftercare is key
dental disease in farm animals
Dental disease uncommonly reported in farm animals
Inefficient mastication (and rumination) can have dramatic effect on feed intakes and therefore productivity
Most frequent diseases include loss of incisors, abnormal occlusal surfaces, diastemata with food impaction between cheek teeth, and third molar overgrowth
Tooth root abscess can occur due to infection
May originate from periodontal disease or penetration of the crown by oral bacteria
Clinical signs;
Swelling of jaw
Excessive salivation
Malodourous breath
Discharging sinus tracts
Inappetence
Weight loss
Diagnosis;
Examination of the oral cavity
External palpation
Radiography- multiple views
Tooth root abscess in farm animals
Treatment;
Removal of infected tooth
Flush?
Suture?
Implication?
Antibiotics?
Conservative treatment-
NSAIDS?
Antibiotics?
Dietary changes?
Oesophageal obstructions (Choke) in farm animals
Common occurrence in cattle
Can occur in proximal cervical oesophagus, thoracic inlet on within thoracic oesophagus
Most commonly described due to access to root crops ie. potatoes
Can also occur with accidental access to fruits such as apples
Clinical Signs;
Cattle are distressed
Characteristic stance with neck extended and head lowered
Profuse salivation
Repeated attempts to swallow
If obstruction is lower than large quantities of clear, viscous saliva accumulate in cervical oesophagus
Ruminal bloat occurs over several hours
Differentials;
Frothy bloat
Gassy bloat
Tetanus
(Rabies)
Diagnosis;
History of access
Cervical oesophageal obstructions may be palpable
Visual/manual examination of proximal part of oesophagus
Passage of stomach tube to confirm blockage
treatment of choke in farm animasl
Treatment;
Relieve bloat by trocar/needle if needed (respiratory distress)
Hyoscine butylbromide 4.0mg IV to relax oesophagus
Manually remove obstruction (first 20-30cm of oesophagus)
Massage obstruction cranially
Pass stomach tube (Selekt pump tube) to dislodge and push into rumen
Use of Probang to dislodge or slice obstruction
