neuro and muskuloskeletal

Question 1

Muscle strain type injuries in horses

Answer 1

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

Question 2

Exertional Myopathies in horses

Answer 2

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)

Question 3

Recurrent exertional rhabdomyolysis: RER

Answer 3

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

Question 4

Polysaccharide storage myopathy

Answer 4

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

Question 5

Myofibrillar myopathy

Answer 5

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

Question 6

Treatment of Acute Exertional Rhabdomyolysis

Answer 6

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

Question 7

medication for Acute Exertional Rhabdomyolysis

Answer 7

Dantrolene Sodium (muscle relaxant)
Prevents ER in Thoroughbreds
Normalized contracture of RER muscle in vitro
Normalized CK with exercise in RER horses

Question 8

Infectious Myopathies in Horses

Answer 8

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.

Question 9

differentails for the horse with unexplained elevation in muscle enzymes and poor performance

Answer 9

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

Question 10

DOMS (delayed onset muscle soreness in horses

Answer 10

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.

Question 11

overtrianing as a differentail for The horse with unexplained elevation in muscle enzymes and poor performance

Answer 11

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

Question 12

Muscle Atrophy in horses

Answer 12

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

Question 13

causes of generalised primary neurogenic muscle atrophy in horses

Answer 13

equine motor neurone disease
vitimeine e related deficiency
immune- mediated myositis
PSSM1 homozygotes

Question 14

Equine motor neurone disease

Answer 14

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

Question 15

Vitamin E deficiency in horses

Answer 15

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

Question 16

Immune-mediated myositis in horses

Answer 16

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)

Question 17

PSSM type 1 homozygotes in horses

Answer 17

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

4. 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
5. 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

Question 18

Kinetics of plasma CK and AST in horses

Answer 18

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

Question 19

genetic testing for conditions that causte metabolic myopathy in horses

Answer 19

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

Question 20

approch to diagnonis of metabolic myopathy in horses

Answer 20

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 )

Question 21

Laxity versus Dysplasia in cases of hip dysplasia

Answer 21

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

Question 22

clinical presentation of hip dysplasia

Answer 22

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

Question 23

ortolani test for hip dysplasia

Answer 23

dog under ga and dorsa recumbrancy

put dorsal pressure on stifle
abduct to detect reduction
adduct to deted subluxation

Question 24

barden test for hip dysplasia

Answer 24

dog in lateral recumbrancy
proximal femur is plapated
apply dorsal lift to femur
then reduce with thumb

palpable movement indicated laxity

questionable value

Question 25

Radiography – “Hip Series”

Answer 25

includes VD extended
VD flexed (frogleg)
and lateral

Question 26

what is looked for in a Hip Assessment on Radiographs

Answer 26

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

Question 27

Management and treatment of Joint Disease (hip dysplasia ect)

Answer 27

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

Question 28

Cruciate Ligament Disease

Answer 28

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

Question 29

Meniscal Injury

Answer 29

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

Question 30

sugrigal managemtn of ccl injury

Answer 30

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

Question 31

Canine Elbow Dysplasia

Answer 31

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

Question 32

Ununited Anconeal Process (UAP)-

Answer 32

Growth plate normally fuses by 5 mths
GSDs, BMDs, Wolfhounds, M>F
Surgery offers best prognosis
Reattachment if possible
Fragment removal if not

Question 33

Fragmented Coronoid Process

Answer 33

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

Question 34

Osteochondrosis

Answer 34

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

Question 35

Elbow joint incongruency

Answer 35

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”

Question 36

Patellar Luxation

Answer 36

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

Question 37

Management of Patellar Luxation

Answer 37

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

Question 38

Classifying Fractures

Answer 38

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)

Question 39

Femoral Fractures

Answer 39

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

Question 40

Radius-Ulna Fractures

Answer 40

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!

Question 41

Tibial Fractures

Answer 41

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

Question 42

Salter Classification of Physeal Fractures

Answer 42

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

Question 43

Location of Physeal Fractures

Answer 43

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

Question 44

Repair of Physeal Fractures

Answer 44

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

Question 45

femoral head growth plate fracture

Answer 45

Operate early - delayed management worsens prognosis
Generally heal quickly
FHNE or THR for chronic cases or in cases with non-union

Question 46

Proximal Tibia growth plate fracture

Answer 46

tension groth plate- patellar ligamebt

Question 47

Mandibular Symphyseal Separation

Answer 47

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

Question 48

Pelvic Fractures

Answer 48

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

Question 49

Treatment of SI Luxation

Answer 49

Manage conservatively if unilateral and <50% displacement
Lag screw repair (>60% sacral width) or trans-ilial bolt or pin (easier)

Question 50

Ilial Body Fractures

Answer 50

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)

Question 51

primary tumours of bone

Answer 51

osteosarcoma- makes bone

myeloma
lymphoma
chondrosarcoma

Question 52

secondary tumours of bone

Answer 52

locally invasive- squamous cell carcinoma

metastisis to bone- metastatic tumour

Question 53

Osteosarcoma

Answer 53

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

Question 54

Ligaments and Tendons

Answer 54

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

Question 55

Healing of Tendon and Ligament

Answer 55

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

Question 56

Common Ligament Injuries

Answer 56

Cruciate ligaments
Collateral ligaments
Round ligament of the femoral head (luxation)
Plantar ligament injuries
Carpal ligament injuries

Question 57

Collateral Ligament Injuries

Answer 57

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

Question 58

Open Injuries to Ligaments

Answer 58

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

Question 59

Shearing Injuries to ligamnets

Answer 59

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

Question 60

Principles of Arthrodesis

Answer 60

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

Question 61

Causes of Luxation

Answer 61

Congenital
Developmental (e.g. patellar luxation )
Traumatic (motor vehicle, fall)

Question 62

Hip Luxation

Answer 62

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

Question 63

Causes of Tendon Injury

Answer 63

(Developmental)
Acquired
Trauma
Iatrogenic
Degenerative
Drug related: corticosteroids, fluroquinolones

Question 64

Muscle Contracture

Answer 64

Infraspinatus
Supraspinatus
Quadriceps
Gracilis/ST

Question 65

Panosteitis

Answer 65

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

Question 66

Avascular Necrosis (AVN)

Answer 66

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

Question 67

Craniomandibular Osteopathy

Answer 67

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

Question 69

describe what can be assesed on a dosolateral medopalmar view of a horses limb

Answer 69

hilights the sorsomedial aspect and the l ateral palmar aspect

Question 70

why do you pack the hoof when x reaying horses feet

Answer 70

to prevent the natural clefts and ridges from appearing as fractures (and artefacts) on radiograph

Question 71

Forebrain function

Answer 71

pecial
senses- e.g. vision,
hearing,
taste, smell (processing not collection- crainial nerves

Behaviour

Question 72

Brain Stem function

Answer 72

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 centreMaintains central processing areas in state of activity

Question 73

Cerebellum function

Answer 73

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

Question 74

indicators fo forebrain disease

Answer 74

 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

Question 75

indicaors for brainstem/ RAS disease

Answer 75

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

Question 76

indicators for cerebellar disease

Answer 76

Head posture- however could also be peripheral vestibular,
central, musculoskeletal,
neuromuscular

Intention tremor, +/- menace reflex

gait?- Dysmetria/spasticityNo weakness

no crainial nerve involvment

Question 77

Neuro Exam: Cranial Nerves assesment steps

Answer 77

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

Question 78

Neuro. Exam: Cranial Nerves

Answer 78

 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

Question 79

Neuro. Exam: Gait and Posture

Answer 79

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

Question 80

Upper motor neurones

Answer 80

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

Question 81

Lower motor neurones

Answer 81

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)

Question 82

Spinal Cord Disease: UMN

Answer 82

 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

Question 83

UMN vs. LMN in disease

Answer 83

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

Question 84

Specific tests for ataxia in the horse:
proprioceptive deficits

Answer 84

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

Question 85

Specific tests for weakness
(paresis) in the horse:

Answer 85

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

Question 86

Weakness vs. different neuroanatomical locations in the horse

Answer 86

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

Question 87

Deficits vs. lesion localisation – which limbs are
affected when there is a problem with c1-6

Answer 87

UMN signs in both fore and hindlimbs

Question 88

Deficits vs. lesion localisation – which limbs are
affected when there is a problem with C7-T2

Answer 88

lower motor neurone signs in forelimbs

upper motor neuron signs in hindlimbs

Question 89

Deficits vs. lesion localisation – which limbs are
affected when there is a problem with T3-L3

Answer 89

normal neurone signs in forelimbs

upper motor neuron signs in hindlimbs

Question 90

Deficits vs. lesion localisation – which limbs are
affected when there is a problem with L4-S3

Answer 90

normal neurone signs in forelimbs

lower motor neuron signs in hindlimbs

Question 91

Deficits vs. lesion localisation – which limbs are
affected when there is a problem with S3-Ca…

Answer 91

normal in all limbs

Question 92

Spinal Cord Disease: Classification of deficits

Answer 92

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

Question 93

Neuro. Exam in the horse: Neck and
forelimbs

Answer 93

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

Question 94

Neuro. Exam in the horse: trunk, hindlimbs, tail, anus

Answer 94

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

Question 95

Neuro. Exam in the horse: the recumbent
patient

Answer 95

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

Question 96

Equine Forebrain Diseases

Answer 96

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

Question 97

Perinatal asphyxia syndrome

Answer 97

(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

Question 98

HIE/PAS Treatment and Prognosi

Answer 98

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

Question 99

Neonatal Seizures and
Epilepsy

Answer 99

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

Question 100

Cerebellar Hypoplasia in foals

Answer 100

 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

Question 101

Vestibular disease in horses

Answer 101

trauma and otitis media/interna are the

Question 102

Otitis media/interna in horses

Answer 102

 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

Question 103

Dysphagia in horses

Answer 103

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

Question 104

Facial Nerve paralysis in horses

Answer 104

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

Question 105

Horner’s Syndrome in horses

Answer 105

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

Question 106

trigeminal neuritits in horses

Answer 106

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)

Question 107

Headshaking: grades in horses

Answer 107

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

Question 108

Spinal Cord Diseases in the horse

Answer 108

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

Question 109

Spinal Trauma in the horse

Answer 109

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

Question 110

Cervical Vertebral Malformation in horses

Answer 110

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

Question 111

managment of cervical vertebral malformation

Answer 111

 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

Question 112

Cauda Equina Syndrome

Answer 112

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

Question 113

EHV1 myeloencephalopathy

Answer 113

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)

Question 114

EHV1 myeloencephalopathy
management:

Answer 114

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

Question 115

Peripheral nerve and neuromuscular disease in horses :

Answer 115

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

Question 116

Peripheral Nerve Injury treatment

Answer 116

Treatment:
initial stages: anti-inflammatories
support other limb
surgery?
physiotherapy
not > 12 inches of nerve re-growth
EMG may help in monitoring

Question 117

Neuromuscular Disorders causing diffuse weakness in the horse

Answer 117

Equine Motor Neuron Disease
(EMND)
Botulism: Clostridium botulinum
Abnormal hindlimb gait: stringhalt
Tetanus

Question 118

Equine Motor Neuron Disease
(EMND)

Answer 118

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

Question 119

Botulism: Clostridium botulinum in the horse

Answer 119

 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)

Question 120

Abnormal hindlimb gait: stringhalt in the horse

Answer 120

Another peripheral neuropathy
Uni (classical- biomechanical problem secondary ot injury) or bilateral (pasture associated, toxic condition occuring in australia and new zealand- pature assosiated)

Question 121

Generalised tetany

Answer 121

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

Question 122

Problems associated with Head and Neck in Farm animals

Answer 122

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

Question 123

Wooden Tongue; Actinobacillosis

Answer 123

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

Question 124

managmetn and treatment of wooden tongue

Answer 124

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

Question 125

Lumpy jaw; Actinomycosis

Answer 125

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

Question 126

managment and treatment od actinomycosis

Answer 126

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

Question 127

Mandibular fracture in farm animals

Answer 127

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

Question 128

treatmet of mandibular disease in farm animals

Answer 128

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

Question 129

dental disease in farm animals

Answer 129

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

Question 130

Tooth root abscess in farm animals

Answer 130

Treatment;
Removal of infected tooth
Flush?
Suture?
Implication?
Antibiotics?

Conservative treatment-
NSAIDS?
Antibiotics?
Dietary changes?

Question 131

Oesophageal obstructions (Choke) in farm animals

Answer 131

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

Question 132

treatment of choke in farm animasl

Answer 132

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

Question 133

Oral lesions in farm animals

Answer 133

Stomatitis is a common clinical sign of several diseases
Some are zoonotic (Bovine Papular stomatitis) some are notifiable (FMDV)
Can be caused by trauma or contact with chemical irritants

Question 134

Bovine Papular Stomatitis

Answer 134

Caused by parapoxvirus virus
Worldwide condition
Zoonotic
Spread by direct contact, entry through mucosal abrasions

Clinical Signs;
Most common in calves 1-12m old
Anorexia
Salivation
Mild pyrexia
Expanding popular lesions on muzzle, nostrils and buccal mucosa
Severe form can lead to raised lesions and sloughing of mucosa

Differentials;
FMDV
BVDV
Vesicular stomatitis
BHV
BTV

Clinical Signs;
Most common in calves 1-12m old
Anorexia
Salivation
Mild pyrexia
Expanding popular lesions on muzzle, nostrils and buccal mucosa
Severe form can lead to raised lesions and sloughing of mucosa

Question 135

Foot and Mouth disease

Answer 135

Caused by picornavirus
Endemic in many parts of world
Most of Europe, North America, Australia and New Zealand are free from disease.
Notifiable in the UK; can affect most farmed species (cloven hoofstock)
Extremely contagious

Clinical Signs;
Incubation 2-10 days
Anorexia
Depression
Pyrexia
Excessive salivation
Milk drop

Vesicles develop on tongue, dental pad and hard palate
Quickly rupture to from shallow ulcers
Submucosa hyperaemic

Question 136

Calf diptheria

Answer 136

Caused by Fusobacterium necrophorum
Causes a necrotic stomatitis
Often seen as outbreak in young calves in unhygienic conditions
Lesions can be caused by trauma to buccal mucosa
Clinical signs;
Lower jaw wet due to excess saliva
Infections of cheek lead to large firm swellings
May see/feel loss of mucosa within mouth- Advanced cases develop necrotic plug in centre of lesion
Malodourous breath
Swelling of submand. LN
May have pyrexia

Clinical signs;
If infection involves larynx can lead to;
Anorexia
Pyrexia
Coughing
Inspiratory stridor
Dyspnoea

Death due to asphyxia can occur

Question 137

treatment of calf diptheria

Answer 137

Daily procaine penicillin
7-10 consecutive days
Can use TMPS and oxytetracycline

Corticosteroids during acute stage
NSAIDs thereafter

Tracheotomy can be performed in severe cases

Question 138

Laryngeal chondritis (Texel throat)

Answer 138

Upper respiratory tract disease of sheep
Unknown aetiology but certain breeds are predisposed
Health and welfare implications
Can have economic implications for flock
Infection of mucosal abrasions leads to abscesses forming in larynx- Texel breed may be predisposed due to short head and neck affecting laryngeal anatomy

Clinical Signs;
Severe dyspnoea
Acute onset respiratory distress
Marked inspiratory effort and stertor
Animals stand with neck extended, head lowered and nostrils flared
Often show open mouth breathing

Diagnosis;
Based on clinical signs
Breed predisposition
Can evaluate with endoscope, ultrasound or radiographs

Due to oedema of cartilages -> narrowing of airway

Question 139

treatment of Laryngeal chondritis (Texel throat)

Answer 139

Treatment;
Steroids in acute case to reduce swelling
NSAIDs longer term
Long term antibitoics to prevent abscess formation
Often recurs after ‘successful’ treatment
Unlikely to fully resolve so euthanasia often preferred
Tracheotomy can be used in severe cases

Question 140

when is the best time to refer an injury for physio

Answer 140

a week to 2 weeks after it was caued

during the remodling phase of healing

Question 141

Physiotherapy Tools and Techniques

Answer 141

Manual therapies
Massage
Passive Range of Motion (PROM)
Stretching

Electrotherapies and
Electrotherapeutic Agents

Remedial Exercise
Prescription

Question 142

What are manual therapies

Answer 142

Joint mobilisation
Massage
Myofascial release
Trigger Point release
Stretching

importance-
Biofeedback – use in assessment and for treatment
Availability- everyone has hands

Owner action and involvement- Little and often yields better results

Evidence based results- Decades of published scientific results to
explain how and when techniques work

Following the palpation element of the clinical work-up
Tissues and areas within the tissues that require treatment are identified
These will feel ‘abnormal’ as a result of the stress cycle in the muscle
This starts as muscle shortening

Manual techniques positively affects the following muscle components;
Golgi Tendon Organs
Muscle Spindles
Joint mechanoreceptors

Question 143

Why do we get muscle shortening

Answer 143

Pain causing muscle spasm / guarding
Altered joint mechanics
Conformation
Overuse or inappropriate repetitive
patterning - irreversible changes can
occur after just 8 weeks
Disuse e.g. immobilisation of a fractured limb (splinting or plaster casts), box / cage rest etc.

Question 144

massage as a treatment for muscle shortening

Answer 144

Use within sub-acute and chronic phases of tissue repair
Improves circulation to muscle
Improves lymphatic drainage
Desensitises facilitated areas
Release of endorphins = pain relief and reduction in muscle hypertonicity / spasm
Facilitates normal interchange of fluid and gases between tissues
Bonding

Effleurage massage-
Reduces muscle spasm that is secondary to pain
Increases circulatory flow
Reduces oedema
Calming effect
Before exercise = warms muscles
After exercise = removes metabolic waste

hacking and cupping-
Increases circulation
Relieves muscle spasm
Removes lung secretions

Question 145

Joint Mobilisation

Answer 145

Range of motion (ROM);
active (AROM),
active assisted (AAROM),
active resisted (ARROM),
passive (PROM),
joint accessory mobilisation techniques

Essential for the maintenance of synovial joint nourishment in the recumbent patient, or the patient with reduced physical activity (chronic pain management)

Focal or local : global approach

Question 146

Stretching as a treatment for muscle shortening

Answer 146

Elongates pathologically shortened tissues
sarcomeres are added to lengthen muscle tissue
increased resting length

Increases flexibility and joint ROM and reduces tightness in normal & abnormal tissues

Question 147

What are electrotherapies

Answer 147

Or more specifically – Electro Physical Agents (EPAs)
Electrical stimulation modalities
Thermal agents
Non-thermal agents

H-Wave
TENS
NMES
LASER
Therapeutic Ultrasound
Pulsed Electromagnetic Field Therapy

In combination with other therapies, there is a strong evidence base that these therapies effect a positive physiological change in cells / tissues.

Right choice
Right time
Right level
Right frequency

The ability to influence the tissue healing process to effect a better or quicker repair is a fundamental interest to Vet Physios

Select the best agent to use-
Determine nature of the pathology
Decide on the desired physiological response or outcome
Select a modality that can effect those changes

Arndt-Shultz Law-
Therapeutic window – will move
as patient’s condition alters- healing

Apply-
Introduce slowly
Build intensity
Reduce / remove if necessary

do not push if not well tolerated

Question 148

how do electrotherapies work

Answer 148

We transfer / confer energy on the cell, in various forms and at various levels
Sound
Heat
Light

This encourages cellular activity either by;
Delivering so much energy the cell membrane is forced to change activity
Delivering a smaller amount of energy and exciting the cell membrane; this leads to upregulation – doing more of what they normally do, harder and faster
The latest evidence points to the latter approach as being more effectiv

So, it’s the cells themselves that effect the change, not the therapy.

Question 149

What is remedial exercise

Answer 149

Active
Targeted
Tailored

Improves strength and endurance- Injury prevention
Improves range of motion of joints
Corrects gait patterning
Improves proprioception
Mood enhancing

Immediate effects of exercise-
Muscle contraction
Increased blood flow to muscles
Rise in muscle temperature

Long-term effects of exercise -
Increased bone density
Stronger muscle, tendon and ligament tissue
Increased joint stability
Increased joint ROM
Muscular hypertrophy
Higher fatigue threshold

Plus correct gait patterning
Improve proprioception

no exersise results in-
Bone density and modelling
Joint capsule and soft tissue contracture
Muscle mass and strength
Cardiovascular fitness
Proprioceptive capability

Question 150

Dynamic Assessment in physio (step 1)

Answer 150

Relates to how the animal moves. This informs the active rehab. plan
Observe in a straight line, and on small circles
Observe from cranial, caudal and lateral views
In walk and trot
On firm and soft surfaces

Consider-
Gait pattern- breed?- paso fino
Limb placement
Joint flexion
Harmonious use of the body

To develop an effective rehabilitation programme we need to fully understand the animal’s functional anatomy, locomotion and biomechanics-
Muscle antagonists, synergists
Joint ROM, and bones as levers
Gait patterning

And most importantly
Understand what Normal looks like, so we know when and where something isn’t right and how to develop effective exercises to restore function….. plus recognise when this has been achieved

Question 151

Choosing exercises that will work in physio (step 2)

Answer 151

Baited stretches
Poles
Labrynths
Proprioceptive tracks
Inclines, declines and steps
Gadgets and gismos

Question 152

Canine Specific Active Exercises

Answer 152

Sit to stand
Wobble cushion / board
Peanut and gym ball

Question 153

Deciding on Frequency and Repetitions in physio (step 3)

Answer 153

Balance

Increased muscle tone and strength

Improved ROM

Better limb loading

Increased stride length

reduced-
Muscle fatigue

Painful joints

Soft tissue injury

Muscle soreness

Tailor to the individual
Little and often
Start small and build

Question 154

Distance Assessment for neuro exam

Answer 154

Behaviour – circling/headpressing/blind?
Consciousness – Overexcited/ response to stimuli / depressed/ stupor / comatose?
Stance
Tremors – rapid contractions of muscle groups and their antagonists
Spasms – sudden intense contraction of muscle groups
Spasticity – Increased muscle tone; occurs from brain stem/ spinal cord lesions (spastic paresis)
Locomotion
Reduced coordination / ataxia
Weakness (dysmetria) – Paresis or paralysis, uni/bi-lateral
Orthopaedic or Neurological? – is the limb being carried or dragged? Is the step shorter or longer than normal?

Question 155

The Neuro Exam in farm animals

Answer 155

Percussion – Tap the face with your fingertips, use your fist over neck vertebrae and percussion hammer over vertebrae/pelvis

Test the reflexes - to localise the lesion
Cerebrum, cerebellum and vestibular labyrinth
Brain stem
Spinal reflexes

Coordination – Cerebrum Cerebellum and v labyrinth; can it correct?
Eye movement
Head movement
Cross one leg over the other
Walk towards obstacle on floor i.e. conscious proprioception
Repeat obstacle test but blindfolded i.e unconscious proprioception
Can the animal rise normally? (Cattle HL first!)

Brain stem-
Optical nerve. Blindness (no menace response): defect in retina, optical nerve, or cortex? First look at retina; then iris reflex (if blindness in cortex then reflex normal)
Trigeminal nerve. Jaw drop. Palate reflex – press palate and mouth should open
Facial nerve. Cannot close eyelid, lower lip hanging off (one-sided failure to close mouth)
Vagal nerve – animal not able to swallow (tube) or cough (pinch larynx/trachea); disturbed rumen contraction patterns (‘vagal indigestion’)
Hypoglossal nerve – tongue cannot be retracted and hangs out of mouth

Spinal reflexes -
Pinch the withers
Tail reflex (touch perineum or perineal side of tail)
Anus reflex (thermometer – contraction sphincter)
Scrotal reflex (wrinkling of the scrotal skin when it is touched)
Patella reflex (calves)
Radio-carpal extensor reflex (calves)
Pinch skin between claws – animal will bend leg

Question 156

diagnostoc tests for neuro disease in farm animals

Answer 156

Haematology - Differential WBC

Biochemistry
Hepatic Enzymes -(GLDH GGT), BHB, NEFAs (nervous ketosis/fatty liver)
Mg, Calcium in blood, Lead (post mortem)

ZST assess colostrum transfer
CSF – protein, WBC, bacterial growth

Question 157

cortical signs in farm animals

Answer 157

Ataxia, proprioceptive deficit, blindness, circling, nystagmus, changes in behaviour/ conciousness, head pressing
Acute or chronic?
forebrain disease

Acute-
Meningitis
Cerebro-Cortical Necrosis (CCN)
Lead poisoning - APHA
Nervous ketosis
Hypomagnesemia (Grass staggers)
Salt poisoning
IBR / MCF (sporadic)
Pseudorabies (Aujesky’s) - APHA/DVM
Rabies - APHA/DVM

Chronic-
Brain abscess
Bovine Spongiform Ecephalopathy (BSE) AHVLA/DVM
Hypovitaminosis A
Brain tumour (very rare)

Question 158

Cerebellar disease signs in farm animals

Answer 158

imbalanced, wide based stance, head tilt, dysmetria, nystagmus, tremors, hyperaesthesia

Question 159

Meningitis in farm animals

Answer 159

Extension of local infection (sinusitis) or haematogenous – Look for another lesion (septic arthritis, E. coli and Salmonellae in calves, Pseudomonas mastitis in adult cattle, liver abcess, endocarditis etc.)

Calves ~ 1 week of age which have not had enough colostrum

Diarrhoea, fever, anorexia, stiff neck, hyperaesthesia; spasmodic extension of limbs (when stimulated), muscle fasciculations; depression or ‘mania’, signs of pain when neck extended, tetraparesis, hyperflexia, circling, falling over; cranial nerves may be involved (nystagmus, facial palsy, blindness etc.); coma/fitting.
May present like hypomagnesemia (‘staggers’)
Early treatment essential; poor prognosis

Blindness and
‘Star gazing’

Seizure (shortly before death)

Question 160

Antibiotics - meningitis

Answer 160

Permeability- inflammation
Preferably IV
Preferably bactericidal
Penicillin (on its own) no activity against gram negatives so not a good choice
Continue for 10-14 days
Concomitant Dexamethasone

GOOD (NORMAL & INFLAMED)-
Trimethoprim/sulfonamide chloramphenicol, metronidazole, doxycycline, fluoroquinolones

POOR (NORMAL)-
Tetracyclin, penicillin, streptomycin

GOOD (INFLAMED)-
cephalosporins, penicillin

Question 161

CerebroCortical Necrosis (CCN)

Answer 161

‘Necrosis of the grey matter’ caused by Thiamine (Vit B1) deficiency.
absolute deficiency in preruminant calves
relative deficiency – large amount of bacterial thiaminases produced when overindulging on concentrates; bracken?
Most common in cattle 6-18 months old.
Early signs: head up in the air and appear blind; diarrhoea (concentrates?); hyperesthesia and muscle tremors also possible.
Late signs: opisthotonus, headpressing, strabismus, miosis, excitement, repetitive chewing, facial twitching, nystagmus, head tilt, convulsions.
Good response to treatment if diagnosed early.

Blindness and star gazing

High head carriage
Head pressing

Diagnosis:
History, Clinical Signs + Response to Treatment
Blood thiaminase assay
PME - Brain Pale and Swollen; patchy yellow discolouration (accumulation of lipofuscin pigments in lipophages) fluoresce under U.V light

Question 162

treatment of CerebroCortical Necrosis (CCN)

Answer 162

10-15mg/kg thiamine vit B1repeated every 4 hours for 24hrs
Respond in 3-6 hours
Corticosteroids and mannitol
Identify and rectify underlying cause
Thiamine-supplemented ration; introduce concentrates slowly

Question 163

Lead Poisoning in farm animals

Answer 163

Any age of cattle but especially young cattle due to curious nature
Access to old car batteries, engine oil, old lead paint, asphalt roofing, environmental pollution from industrial works
Acute encephalopathy (as opposed to horses). Cerebral and GI signs
Clinical signs:
First stages: stand alone and depressed; hyperaesthesia, muscular fasciculations
Progresses to ataxia, blindness (pupillary reflexes present), head pressing, episodic manic behaviour, convulsions, coma
Also abdominal pain, rumen atony (bloat), diarrhoea, frothing at the mouth
Severe will die 12-24 hrs; sudden death may also occur

Question 164

Lead Poisoning in farm animals Treatment

Answer 164

Control fits with I.v pentobarbitone (dose to effect)
Chelate lead CaEDTA slow drip 110mg/kg I.v every 2nd day for 3 treatments
Thiamine 20-100mg/kg subcut daily (mobilises intracellular lead into blood)
Oral magnesium sulphate 500-100g to precipitate lead from GI tract
Prognosis poor!!
Consider whether meat or milk is suitable for human consumption estimated 6-7 months for blood and milk levels to return to normal – Get APHA involved

Question 165

Nervous Ketosis

Answer 165

Aetiology as ketosis (acetonaemia itself a chronic disease; ‘slow fever’)
Acute onset of obsessive licking, circling, staggering, head pressing, pica, aggression
Signs last 1-2 hours; recur at ~ 10-hourly intervals
Diagnosis – clinical signs or ketones in blood
Treatment - 40% dextrose i.v, propylene glycol BID, corticosteroids - examine management

NEB > FAT MOBILISATION FROM ADIPOSE TISSUE > FFA
FFA + ALBUMIN > LIVER > GLUCOSE OR TRIGLYCERIDES
TG XS ACCUMULATE IN LIVER FATTY LIVER SYNDROME IMPAIR LIVER FUNCTION

Question 166

Hypomagnesemia

Answer 166

Especially in pastured lactating beef cows in first months after calving (but also non-lactating animals); Occasionally in 3-6 month old ruminants (on poor diet; little Mg in milk, less able to resorb from bones > 3 m)
Classically in spring but also autumn/winter
Mg stored in body not readily available
If uptake disturbed (Na:K ratio in rumen, stressors, not enough in diet or) levels rapidly dangerously low
Adverse weather conditions may predispose
Excretion of Mg in milk; - fresh cows most at risk

cs-
Hyperexcitable, may charge
Erect ears, ear twitching, hyperaethesia
Muscle fasciculations / tremors
Frenzied running turning into staggering
Lateral recumbency with violent episodes of ophistotonus and convulsions (can be triggered by any stimulus… also by vet!)
Dead within an hour of the seizure episodes

Question 167

Salt poisoning in farm animals

Answer 167

Either water containing too much salt or water deprivation.
Sodium deposition in the brain blocks anaerobic glycolytic pathways; increased intracranial pressure may also occur (attracts water)
Mostly during summer; normally a clear clue in the history
Dehydrated, depression, diarrhoea and colic, star-gazing, blindness, aggressiveness, hyperexcitability, vocalisation, head pressing, teeth grinding .
Poor prognosis; rehydrate first then hypertonic saline
(otherwise intracranial pressure increased).

Question 168

(Pseudo) Rabies

Answer 168

Pseudorabies (Aujesky’s disease, Mad Itch) Depression, ataxia, conscious prioprioceptive deficit, circling, nystagmus, strabismus, aggression, pruritus (of the head), dead within 2 days. Contact with pigs. APHA/ DVM

Rabies Hyperexcitability, fear, rage, depression, flaccid paralysis. APHA / DVM

Question 169

‘Occasional acute cortical disease’: Hydrocephalus

Answer 169

Holstein, Jersey, Friesan, Guernsey
Result from failure of drainage of CSF and therefore increased intracranial pressure
Domed cranium
Diffuse cerebral signs mania head pressing muscle tremor, convulsions blindness weakness
Increase in intracranial pressure defect drainage of CSF holsteins hereford ayrshie jersey
Sometimes domed cranium
Diffuse cerebral signs, Mania, head pressing, muscle tremor convulsions blindness weakness

Question 170

Brain abscess in farm animals

Answer 170

Normally Arcanobacterium pyogenes, often extension of sinus infection (so initially in front cortex); slower onset and more asymmetric signs than meningitis.
Initially vision loss/mydriasis in contralateral eye, may progress to compulsive walking, head pressing, circling, head tilt (towards lesion), depression or mania, coma.
When extending to base of the brain may give ‘cranial nerve signs’. Later stages: hypertonicity, hyperflexia, opisthotonus, coma, convulsions.
Treatment antibiotics (see meningitis); Prognosis poor.

Question 171

BSE

Answer 171

Agent unknown
Current theory Prion Hypothesis infectivity caused by a struturally modified form of the host protein PrP. Normal membrane associated protein found in the CNS . Modified PrP promotes the conversion of other PrP molecules which accumulate within the affected neurones.
Virino –core of nucleic acid and host proteins
Filamentous virus
Epidemiology points to extended common source epidemic.
No evidence of cattle to cattle transmission
Only common feature use of commercially produced compound feed containing meat and bone meal
Offspring of infected cows 10% more likely to develop BSE

Infectivity is caused by a struturally modified form of the host protein PrP . This is a normal membrane associated protein found in the CNS . The modified PrP promotes the conversion of other PrP molecules which accumulate within the cells

Multiple individual disease outbreaks which can be traced back to a common source

First recorded 1986
Outbreak peaked 1992
Total over 180,000 cases in U.K so far
2003 approx. 600 cases detected either from clinical cases on farm or compulsory testing of 1) fallen stock (over 24 months) 2) casualty animals over 30 months 3) sample of OTM 4) cattle over 30 months for HC (v few) 5) all cattle born after 31 July 1996 aged over 42 months
Recent case! – March 2023
Now virtually zero cases

cs-
3-6 years
Initial signs often subtle but always progressive, rate of progression variable 2-3 weeks to several months
Weight loss
Hyperaesthesia, fine fasciculations of head and neck shoulder flank, teeth grinding,
Apprehensive when approached, reluctant to be milked or moved through gate ways
Ataxia
Aggression

Differential Diagnosis :
Nervous ketosis
Focal abscessation
(Listeria encephalitis)
(Hypomagnesaemia)
(CCN)

Notifiable Disease
Inform DEFRA
VO visit inspect animal decide whether to PTS as BSE suspect or not
Farmer will be compensated and trace put out on the offspring of animal
If disease confirmed offspring will also be culled
Long incubation Period of BSE makes diagnostic and screening tests difficult
Current tests for PM. No test for live animals.
Histopathology
Western Blotting (PrPSC)
Immunocytochemistry (PrPSC)

Contact DEFRA, VO slaughter suspects
Confirmed cases offspring cull
Feed ban no mammalian protein in feed for food producing animals , fishmeal is allowed for pigs/poultry but strict production/ storage/ to prevent cross contamination with ruminant feed. Regular inspections of animal feeds carried out by DEFRA

Question 172

Hypovitaminosis A in farm animals

Answer 172

Deficiency VitA or precursor carotene
Plenty in green feeds and forages
Deficiency seen usually straw/ cereal based diet in housed animals
Clinical Signs: caused by thickening dura mater/ abnormal bony growth in the brain cavity, increase CSF pressure Congenital or acquired
Also retina degeneration - absent pupillary light reflex important diagnostic tool
Calves born to deficient dams – blindness, weakness, domed forehead, thickened carpal joints
Deficient calves – blindness, anorexia, diarrhoea, pneumonia (‘ill thrift’)
Older cattle – blindness, star gazing, nystagmus, ataxia (hind limbs first), convulsions; also diarrhoea and occasionally thickening and whitening of cornea.
Treatment = 400iu/kg vitamin A daily
Response even in fitting animals often good (48hrs)
Older cattle with ocular form often do not respond
Check diet 40iu/kg BW per day (green feed)

Ophthalmoscopic photograph of the fundus of
a steer with hypovitaminosis A. Optic disc is pale and
enlarged, with indistinct edges (papilledema).

Question 173

Cerebellar diseases -Hypoplasia in farm animals

Answer 173

Inherited Hereford, guernsey, holstein, shorthorn, ayrshire)
Acquired (BVD) – infection dam 90-170 days gestation
Severity varies
Balance (ataxia, falling backward) or unable to stand, tremor, hypermetria, nystagmus
Severe opisthotonus

Question 174

Intervertebral Disc Disease

Answer 174

Hansen Type 1(bursting) and Type 2 (bulging) intervertebral disc disease (IVDD)

Cervical myelopathy (Wobbler’s disease)

IVD degenerates with age but chondrodystrophoid breeds are at higher risk

Dachshund
Bassett hound
Pekingese
French Bulldog
Beagle
Shih Tzus
Cocker Spaniel

IVD degeneration occurs earlier in CD breeds than NCD breeds

In CD breeds, pathological changes seen in >75% of Ce, T and L discs by 12 months of age

Degeneration of the NP is followed by changes in the AF (dorsal&raquo_space; ventral AF)

more symptomatic in thoratic vertebra as less room in vertebral collum

Type 1 are more explosive and cause concussive damage to the SC, rather than compressive and chronic with Type 2

Pain (neck pain may be more obvious than lower back pain)

Reduced proprioception (check knuckling)

Weakness or paralysis - Ce lesions can affect all four legs, TL lesions affect hind limbs, bladder

pathophysiology-
SC concussion – acute haemorrhage, necrosis, infarction

SC compression

Nerve root compression

Irritation and inflammatory changes

For Grade 1 and 2, medical management is recommended

Grade 3 – transitional

Grade 4 and Grade 5 – outcome with surgery are certainly superior to those with medical management

Slow and unpredictable return of function – critically important to provide nursing support (e.g. bladder) and rehab

Question 175

Hansen Type l ivdd

Answer 175

Usually acute and explosive in onset

Ce or TL spine in CD breeds

Typically, young dogs (2 yrs of age)

Often multiple sites affected – 75%
cases involve T12 to L2

Can be accompanied by calcification of
the IVD

Question 176

Hansen Type 2

Answer 176

Much more common in NCD breeds (Terriers, Dalmatians, GSDs)

More usually caudal Ce and LS spine

Older dogs (>5 yrs)

Single level more common

Question 177

ivdd clinical grading

Answer 177

1-Painful but no neurological deficits
2-Painful, wobbly but ambulatory
3-Non-ambulatory but intact motor
4-No motor function, but intact deep pain
5-No motor function and deep pain gone

Question 178

Conservative (Medical) Management for ivdd

Answer 178

Usually grades 1 and 2

Strict cage rest for 3-4 weeks

Anti-inflammatories plus analgesics

Urinary bladder management

Question 179

Surgical Management for ivdd

Answer 179

Fenestration - no penetration of vertebral canal

Decompressive surgery
Removal of extruded material
Relief of compression
Prevention of further damage

May be hemilaminectomy (TL) or ventral slot (Ce)

Question 180

Disc Fenestration

Answer 180

Removal of the nucleus pulposus

Performed through one or more annulotomy incisions

Does not decompress the canal

Prophylactic (Ce or TL junction)

Question 181

Ventral Slot for ivdd

Answer 181

Ventral midline approach

Remove bone from one vertebral
body to the other (across the disc)

Does enter the canal, so removal of
extruded material is possible

Take care to avoid venous sinuses

Question 182

Wobbler Syndrome

Answer 182

Cervical spondylomyelopathy

Cervical vertebral instability

Cervical vertebral malformation-malarticulation

Cervical spondylopathy

Seen in humans, dogs and in horses

Cervical spondylomyelopathy

Cervical vertebral instability

Cervical vertebral malformation-malarticulation

Cervical spondylopathy

Seen in humans, dogs and in horses

Pathophysiology-

Disc- associated; Middle-aged Dobermanns
Dorsal annulus hypertrophy and protrusion
Dorsal ligamentum flavum hypertrophy
Ce5/6 and Ce6/7

Bone- associated: More likely in young Gt Danes
Bone malformation and OA of the articular facets
Multiple levels affected, most often cranial Ce spine

Question 183

managemtn of wobblers syndrome

Answer 183

Medical and surgical management have been described

Approximately 50% improve with medical management, 30% stay the same and 20% get worse

> 20 different surgical procedures have been described!

Most focus on a combination of decompression and stabilisation

Question 184

Fibrocartilaginous Embolism

Answer 184

Giant and large breed dogs but also common in Min Schnauzers and Shetland Sheepdogs

Vocalization (acute pain often subsides quickly)

Knuckling, weakness or collapse of one or more limbs (lateralised)

Lameness

Usually not progressive beyond 24 hours

Question 185

managment of Fibrocartilaginous Embolism

Answer 185

Conservative/supportive care
Non-steroidal anti-inflammatory drugs (NSAIDs) and steroids

Prognosis can be variable, even with aggressive treatment

Absence of deep pain is considered a poor prognostic sign

Question 186

Chronic Degenerative Radiculomyelopathy

Answer 186

Chronic, progressive myelopathy that has both UMN and LMN involvement

Most common in older dogs (> 8 yo) from breeds such as GSD, Boxer, Chesapeake and Ridgeback

Similar to ALS in humans (Lou-Gehrig’s Disease)

Veriable signs – wobbling, loss of proprioception, scuffed toes

Important to rule out other important causes of spinal disease
Disc disease
LS disease
Spinal tumours
Discospondylitis

X-rays, CT and MRI

Genetic testing available – SOD1 as a risk factor only

manangment- Supportive care only

Hydrotherapy and regular exercise can be helpful to keep animals moving and maximise QoL

Progression to non-ambulatory within 12 months is common

May well end up being a PM diagnosis

Question 187

Atlanto-Axial Instability

Answer 187

Diseases of the Vertebral Body

Toy or small-breed dogs <2 yo

Cervical pain – if you suspect it, take care not to flex the neck

Neurologic deficits map the lesion to C1-C5 UMN

Highly variable clinical picture ranging from mild pain through to tetraplegia/respiratory distress

diagnosis-
Major differential is Ce trauma so take care of the neck!

Radiography, CT and/or MRI

Congenital hypoplasia or complete absence of the dens

Question 188

Management of AA Instability

Answer 188

Conservative- Good option for mild casesAt least 6-8 weeks of neck bracing, strict rest

Surgical- Best outcomes with mild disease
Risky surgery – respiratory 20% risk of death in first 48 hours

Question 189

Spinal Neoplasia

Answer 189

Primary
Meningioma
Glioma
Nerve sheet tumour
Lymphoma
Neuroepithelioma

Secondary (metastatic)

Question 190

Hypervitaminosis A as a differential fro spinal disease of small animals

Answer 190

Seen most often with excessive intake of liver or cod liver oil

Acute toxicity can cause nausea/vomiting, but chronic exposure is more common

Clinical signs include lethargy, poor hair coat, constipation, anorexia, stiffness/reluctance to move

May see neurological deficits in the forelimb

First priority is to manage pain and stiffness

Change diet immediately to remove Vitamin A source

Prognosis depends on degree of involvemenet

Question 191

Discospondylitis

Answer 191

Infection of the disc and vertebral endplates
Most often Staph.pseudintermediusorStaph. aureus

Haematogenous, bite wounds, FBs, surgical site infection

Most often middle-aged dogs of large breeds – rare in cats

May be multifocal

Typically, gradual onset

Spinal pain, stiffness, ataxia and sometimes paresis

Pyrexia

In chronic cases, may see muscle atrophy

Question 192

managment of Discospondylitis

Answer 192

Risk of fracture – so rest the animal (confine to cage or room)

Antibiotics (based on C&S) for >8 weeks (check – FUNGAL?)

Anti-inflammatories (NSAIDs) and analgesia

Surgery to decompress, debride and collect samples for culture

Prognosis is fair to good (guarded to poor if fungal)

Question 193

Listeriosis IN CATTLE

Answer 193

(Listeria monocytogenes)
Environmental pathogen, infections sporadic and usually associated with feeding poor quality silage, fermentation and soil contamination
Infection travels up to brainstem from conjunctiva, face/mouth via trigeminal nerve. Forms microabscesses in brain stem/cerebellum/spinal cord; may progress to meningoencephalitis

Clinical Signs:
Febrile
Dull; loss of lip and cheek muscle tone: difficulty in eating chewing, accumulation cud in cheek, salivation, tongue protrude
Ptosis, drooping of ear on the deviant side, circling
Headpressing, propulsive walking

Question 194

treatment of listeriosos

Answer 194

Aim is stop disease getting worse as neurological deficits may not resolve.
High doses of penicillin 44,000iu/kg BID 7-14 days followed by 22,000iu/kg BID 7-14 days
High doses of oxytet.
Remove underlying cause ie silage

Question 195

Spinal fractures in farm animals

Answer 195

Spinal fractures – 3-6 month old calves: investigate underlying cause; VitD, calcium or copper deficiency?

Question 196

Spinal abscess in farm animals

Answer 196

– normally secondary to osteomyelitis (vertebrae); often cervical; haematogenous or injections;
A. pyogenes, Staph. aureus, P. haemolitica, F. necrophorum
Pain, heat, swelling; animals stiff, reluctant to eat from the ground; if close to brain hyperaesthesia, spasmic muscle contractions, recurrent profuse sweating.
Treatment: antibiotics (see meningitis).

Question 197

Spastic Paresis

Answer 197

Asymmetric spasticity and hypertonia of the extensor muscles of the rear limbs
Continuous when the animal stands but not when it lays down
Most breeds
A few weeks to 6 months
Genetic predisposition ? Do not breed from affected animals

Clinical signs
Excessive Tone of Gastrocnemius Muscle
Hyperextended hock
Unilateral or Bilateral
If unilateral the affected leg is thrust out behind during walking and advanced with a swinging motion without touching ground
Often spend longer lying down

Question 198

treatment of spastic paresis

Answer 198

Neurectomy of the tibial nerve rootlets innervating the gastrocnemius muscle
high epidural or GA
If bilateral then leave 6-10 weeks inbetween
Success rate ~ 60%

Inability to flex the hock
when walking, the limb is circumducted; ‘pendulum-like motion

Question 199

Tetanus in farm animals

Answer 199

Clostridium botulinum
Ensiled poultry waste (as food) (illegal), poultry litter applied to pasture or used as bedding, accidentally contain carcasses
Poor quality BBS
Carcasses in pasture or feed
Incubation period variable, normally 2-4 weeks Progression of disease 4-5 days
Stiffness, reluctance to move, muscle tremors
Prolapse 3rd eyelid, RUMEN TYMPANY, elevation tail
Progression to generalized muscular tetany and “rocking horse” position
Recumbancy, convulsions, death.

Extended head posture, extensive tone in facial musculature, stiff, raised tail,
legs held rigidly extended

No test; no characteristic PM signs; identify site of infection and attempt to culture.
Full blown tetanus prognosis poor PTS
Animal well bedded kept in dark and quiet
Antitoxin not much help unless very early.
2. Penicillin high doses.
3. Irrigation of infection site penicillin, antitoxin.
4. Muscle relaxants like ACP administer till signs resolve
Vaccination

Question 200

Botulism

Answer 200

Clostridium botulinum
Ensiled poultry waste (as food) (illegal), poultry litter applied to pasture or used as bedding, accidentally contain carcasses
Poor quality BBS
Carcasses in pasture or feed

Clinical Signs
Characterised by muscle weakness, progressing to ataxia and then paralysis
Anorexia, dilated pupils
Excessive drooling
Droopy expression, tongue may hang out of mouth
Decreased rumen motility, bloat, constipation
Respiratory failure leading to death

Diagnosis
History Clinical Signs
No specific PM findings
Toxin in serum ELISA (not always)
Samples of feed or bedding may help consult with lab.

Treatment
Supportive, purgatives to remove toxins. Fluids. Prognosis poor but if caught in early stages and source of infection removed the animal may recover

Question 201

Peripheral Neuropathies in farm animals

Answer 201

Obturator
Peroneal
Sciatic
Radial Nerve / Brachial Plexus

Question 202

Peripheral Neuropathies in farm animals -Obturator

Answer 202

Following dystocia
esp heifers
Obturator nerve damaged by foetal pressure
Unable to adduct limb (splits)
Diff Dx pelvic fracture
Treatment: chain between hind limbs (hobbles), soft bedding, coricosteroids

Question 203

Peripheral Neuropathies in farm animals -Peroneal

Answer 203

Branch of sciatic nerve damaged as it runs course over lateral aspect stifle joint esp recumbant cow or fall
Hyperextension of hock fetlock and digits flexed (knuckled over)
Loss skin sensation below fetlock dorsal surface
Self cure can bandage or cast to fetlock to prevent self trauma

Question 204

Peripheral Neuropathies in farm animals -Sciatic

Answer 204

Damage occurs when cow recumbant and struggling to rise
Non weight bearing, no sensation distal to stifle (medial mid tarsal region o.k)
Diff diagnosis femoral fracture
Prognosis guarded

Question 205

Peripheral Neuropathies in farm animals - Brachial plexus

Answer 205

Excessive traction of a large calf in anterior presentation
Inability to extend the elbow, carpus and fetlock and bear weight on the affected limb in severe cases
Treatment: Anti-inflammatories + time (guarded prognosis)
Prevention/control:
Avoid excessive traction during calf delivery.
Do not calve cows in a crush

There is a loss of muscle over the shoulder with resultant prominent spine of the shoulder blade. There is a dropped elbow, flexion of the distal limb joints and scuffing of the hooves as the leg is moved forward. The foot is knuckled over at rest.

Question 206

Common neuro problems in young lambs at birth

Answer 206

• Border Disease (tremors, hairy shakers)
• Congenital Swayback (ataxia)
• Drunken Lamb Disease (ataxia, depression star gazing)- treatment see lamb lecture
• Bacterial meningitis (collapsed)– Try high doses penicillin
• Tetanus

Question 207

Swayback

Answer 207

Congenital OR Delayed form (2-4m of age)
Ewes were deficient in copper during pregnancy (usually mid – late trimester)
Soil issue!
Breed pre-disposition in Scottish blackface
Stillbirth / weak lambs/ characteristic weakness of pelvic limbs
Confirm with a copper assay (blood and liver samples)
Congenital form – treatment is hopeless PTS on welfare grounds
Delayed form – some evidence that supplementation slows progression of disease, restrict exercise and feed high proportion of concentrates to achieve market weights

Swayback is a congenital condition affecting new- born lambs; delayed swayback (enzootic ataxia) most commonly affects lambs aged 2–4 months.
The incidence depends upon geographical area, soil type, land and pasture improvements through drainage and lime application, breed and weather conditions during the period corresponding to mid-trimester.

Question 208

Lamb Nephrosis- ‘Drunken Lamb’

Answer 208

1-3weeks of age
Acute onset ataxia and incoordination tending to recumbency
Death usually within 24-48 hours after clinical signs appear
Biochemistry shows weak azotaemia, hyperphosphataemic, and all have metabolic acidosis (very high D-lactate)
PME – Nephrosis observed, relevance to clin signs??

Treatment successful in one study-
50ml of solution of sodium bicarbonate dissolved in tap water (35g sodium bicarbonate in 400ml water to make a stock solution of 8 doses) was given orally
Parenteral long acting amoxycillin also given
Rapid clinical recovery- Resolution of clinical signs within hours, Lambs return to suckling mothers

Question 209

Common neuro problems in young lambs 7 days – 3 months of Age

Answer 209

spinal abscess
– Treat 1mg/kg dexamethasone
– Penicillin
* Lamb nephrosis
– “drunken lamb”
* D lactic acidosis
* Delayed swayback
– ataxia/recumbency
* Bacterial meningitis
* Listeriosis
– circling
– facial nerve paralysis)
* Louping ill
* Tetanus

Question 210

Louping ILL (Flavivirus)

Answer 210

Tick borne
* most infections are slight
and give immunity
* clinical disease in all ages
depending on immunity
– colostral antibody
– think of exposure periods
* can get outbreaks of disease
Important in Grouse (80% mortality)
* Vaccine available
* Variable signs
– head pressing
– trembling & tremors
– nystagmus
– lip twitching etc
– “louping gait”

Question 211

Common neuro problems in young lambs 3m to Adult

Answer 211

CCN
* Listeriosis
* Gid
* Louping ill (tick area)

Question 212

GID

Answer 212

Younger ewes
* Taenia multiceps
– Eggs picked up by sheep cysts develop
in brain cerebral, cerebellar (Coenoris
cerebralis)

Gradual onset
– circling
– unilateral blindness
* opposite side to lesion

head tilt
– skull softening
* Precise signs depend on site of lesion
– cerebral – good prognosis
– cerebellar – poor

• Control
  – worm dogs every 6-8 weeks (praziquantel)
  – keep away from sheep carcasses

Question 213

CCN

Answer 213

Vitamin B1 deficiency (thiamine)
* acute onset in growing lambs (2 –6 months)
* sporadic but can get outbreaks
* history of diet change or worming
– thiaminase production in rumen
– PME – brain

Clinical signs vary depending on
progression of disease
– Dull
– Disorientated
– Blind
– Tremors
– Recumbency
– Opisthotonos
– Convulsions

Question 214

treatment of cnn in sheep

Answer 214

– Vitamin B1 iv (slow
10mg/kg))
– Vit B1 i/m every 12 hours
– For 3 days
– House quietly
– Vision should return 5-7days

• Prevention ?
  – diet changes
  – Thiamine in food ??

Question 215

Listeria IN SHEEP

Answer 215

Common!!
* Listeria monocytogenes
* Associated with feeding poorly preserved silage soil contaminated (mouldy)
* 18-24 months old common, but not exclusive changing molar teeth allowing infection of buccal tissues
* Ascending infection to brainstem

Anorexia, depression
* Unilateral hemiparesis
* trigeminal nerve paralysis
- Salivation, food impacted in cheek
* Facial nerve paralysis (drooped ear, lowered eyelid, deviated muzzle, loss of blink)

Question 216

treatment of listeria in sheep

Answer 216

Diagnosis
– Clinical signs
– CSF tap
– PM
* Treatment
– Good if caught early
– 75kg ewe
– 6g benzylpenicillin (Crystapen x 2 vials) i.v
– 20ml procaine peniciliin i.m (divided sites)
– 1mg/kg dexamethasone i.v

– 5ml procaine penicillin daily for 5 days
– Supportive care
* Remove silage!!

Question 217

Common neuro Problems in Adult sheep

Answer 217

Cervical sub-luxation
(paresis, rams fighting)
* Gid cyst
* Listeriosis
* Brain abscess
* Louping Ill (tick areas, abnormal gait)

Metabolic disease (pregnancy)
– Pregnancy toxaemia-
* blind, dull
– Hypocalcaemia
* Collapsed, bloated, flaccid paralysis
– Hypomagnesaemia
* staggers, hyperaesthesia
* Wobbler Texels
* Scrapie

Question 218

Nervous Disease at Lambing- (collapsed recumbent ewe)

Answer 218

• Pregnancy toxaemia
  – diagnosis – History, clinical signs, ketones in urine, nasal secretion (PME)
  – treatment – poor prognosis unless very early
• Oral propylene glycol + IV glucose
• Hypocalcaemia
  – before lambing
  – stress factors
  – treat with 20 – 40 ml Ca Borogluconate I/V – instant and complete response ( 80 ml s/c slower response)
• Septicaemic listeriosis – hopeless prognosis - PTS

Question 219

Troubleshooting Preg Tox + Hypocalcaemia in sheep

Answer 219

Diet fed
– Energy
– Fibre (SARA)
– Trough space

• Stressors:
  – movement,
  – weather,
  – over-crowding
  – vaccination
  – Other disease:
• Lameness, pneumonia etc
• Housing
• Diagnostics
  – Response to Ca
  – Ketostix
  – BOHB
  
  • last 3 weeks – group of ewes

Question 220

Recurrent abscess in the foot – Ddx in the horse

Answer 220

Inadequate drainage initially
Foreign body
Sequestrum
Keratoma
Laminitis
Quittor

A non resolving draining tract MUST BE investigated

Question 221

Sequestrum and foreign body in the horse

Answer 221

History
Trauma?
Twisted shoe, stepped on nail?
Injury to hoof/ solar penetration

Clinical signs
Persistent foot abscess
Recurrent draining tract at coronary band

diagnostics- RADIOGRAPHS!!

Radiographs have a classic appearance- bone surrounded by involuprim (black area) (infection of bone,- treat with
Debride and follow the draining tract
Surgical debridement

dont resolve via antibiotis as cause still presednt

Sequalae…pedal osteitis

Question 222

Keratoma
in the horse

Answer 222

Benign tumour of keratinised tissue

diagnosis- radiographs-

Solar keratoma shows circular ‘onion like’ appearance on the sole sat within the white line
Radiographs!! Classic appearance – circular radiolucent area in P3.
(Care – Crena solar marginalis)

Treatment- Surgical removal under GA

Prognosis-
Good
Potential for recurrence

Question 223

Quitto in the horse

Answer 223

Necrosis of the collateral cartilages- infection
Secondary to trauma or infection
Uncommon- seen in draft breeds

Diagnosis-
Non healing wound
Draining tract is above the coronary band not from the coronary band!
Radiographs insignificant abnormalities – irregular active bone?
Probe or contrast material to define- put into draining tract and see where it communicates

Treatment-
Surgical debridement
Local and systemic antibiotic therapy

Question 224

White line disease in the horse

Answer 224

Poor quality hoof horn
Separation in the Stratum medium at the junction of the non-pigmented and laminar horn

Aetiology-
Unknown…BUT
Multifactorial: environmental/ nutritional/ mechanical/ infectious

Clinical signs-
Lameness
Hoof wall crumbling

Diagnosis-
Appearance
Radiography

Treatment-
Debride the affected tissue, stabilise the hoof wall
consider trigger factors- shoeing, dampness of enviroment, laminitis? (esspecially when it effects the hoof horn), nutrition effecting hoof quality

Question 225

Canker in the horse

Answer 225

Chronic hypertrophic pododermatitis

Hypertrophy of the dermis horn

Cause-
Anaerobic bacteria
Fusibacterium necrophorum
Bacteroides

Aetiology-
Infects stratum germinativum
Intertubular horn
Causes dyskeratosis

Causes dyskeratosis

Diagnosis-
Vegetative, moist, white mass
Rarely lame
Biopsy?

Treatment-
Surgical debridement- requires lots of packing post surgery
Topical metronidazole and astringents
RECURS

manage enviroment

Question 226

foot pain in the horse

Answer 226

Most common cause of forelimb lameness
80% of all FL lameness
Multiple structures can be affected
Requires a systematic approach

causes-
Foot balance
Hoof wall/capsule
DIP joint
Collateral ligament of the DIP joint
Digital cushion
Collateral cartilages
Navicular bone
Navicular bursa
DDFT
Distal sesamoidean ligament
Impar ligament
Sidebone

Unilateral vs bilateral!

Question 227

bilateral lameness in the horse

Answer 227

Lameness – chronic and intermittent
Inconsistent performance
Loss of suppleness
Stumbling
Unwilling to go forwards
Temporary improvement with rest
Worse on hard surface
Exacerbated with circling
Mild to moderate lameness
One limb more severely affected
Decreased cranial phase of the stride

Question 228

unilateral lameness in the horse

Answer 228

Minimal to no external signs:
Digital pulse
Swelling

Insiduous or acute onset
Improves with rest

The order of differential DDx is different between unilateral vs bilateral!!

Clinical examination
Look at static and dynamic foot balance

Diagnostic tests
Hoof testers
Distal limb flexion
Diagnostic analgesia

Diagnostic imaging
Radiography
US
Nuclear scintigraphy
MRI

Question 229

Poor foot balance in the horse

Answer 229

Likely contributing factor for all FL lameness
Needs addressing before evaluating for other DDx’s
Easily identified on clinical examination + radiography

Question 230

Navicular syndrome

Answer 230

A collection of clinical signs or diagnostic results which together constitute the picture of disease.

Our understanding of what we used to call ‘navicular disease’ has massively changed to the development of advanced imaging techniques which can identify specific structures as the cause of lameness.

Middle aged horses
Hunters/ showjumpers/ eventers/ dressage horses

Presentation-
Often bilateral shortened stride
Worse on a hard surface
Intermittent
Insidious onset

Contributing factors-
Upright confirmation
Poor foot balance: long toe, low heel
Repetitive concussion

Etiology-
Biomechanical forces
Repetitive trauma to the navicular bone causing bursitis
Movement between the DDFT and the navicular bone
Bone remodelling occurs due to load and pressure (flexor cortex)

Pathological changes-
Alteration of palmar fibrocartilage
Increase force on the subchondral bone causing sclerosis
Adhesions of navicular fibrocartilage to the DDFT

Radiographic abnormalities-

Synovial fossae- lollypop leasions
Enlarged
Abnormal shape
Abnormal location
7-8 normal in middle aged horses

Cyst formation

Enthesiophytes-
Collateral sesamoidean
ligament and impar
ligament

Osteophytes

Flexor cortex abnormalities

Medullary abnormalities-
sclerosis
decreased
corticomedullary definition
Synovial invaginations

Progressive disease
Not curable
Aim: manage pain and progression

Prognosis
Good in the early stages
Poor if lameness persists

Question 231

treatment of navicular syndrome

Answer 231

Farriery-
Balance foot
Decrease pressure on heels
Maximise weightbearing surface
Bar shoe

Medical-
NSAIDs- not licensed for long term but often used long term for this syndrome
Corticosteroids into bursa- wont reduced bony change but relieves inflamationn
Stem cells?

Polyacrymide hydrogel?
Bisphosphonates

Surgical-
Palmar digital neurectomy (SALVAGE)
Navicular bursocopy

Question 232

Deep digital flexor tendon tears in the horse

Answer 232

Presentation-
Unilateral forelimb lameness
Acute onset
No other abnormalities detected

Diagnostic analgesia-
PDNB?
Navicular bursa block?
DIP block?
ASNB positive

Diagnostic imaging-
No radiographic abnormalities
+/- US abnormalities
MRI!!

Question 233

Impar ligament desmitis in the horse

Answer 233

Presentation-
DDx for DDFT tear

Diagnostic analgesia-
As for DDFT tear

Diagnostic imaging-
No radiographic abnormalities
+/- US abnormalities
MRI!!

Remember impar = distal sesamoidean ligament that attaches the NB to P3

Question 234

Articular pain: synovitis/ osteoarthritis in the horse

Answer 234

Joints?
DIP and PIP

Presentation-
DDx for foot pain
Mild lameness/loss of performance

Diagnostic analgesia=
Block lameness to articular structure depending on severity and subchondral bone involvement

Diagnostic imaging
+/- radiographic abnormalities

Acute joint damage will lead to synovitis developing rapidly. Osteoarthritis is usually a consequence of ongoing damage

Question 235

DIP joint – Collateral ligament in the horse

Answer 235

Presentation-
Worse on a circle
Differential for foot pain

Diagnostic analgesia-
Variable blocking pattern

Diagnostic imaging-
Minimal to no radiographic abnormalities
+/- US abnormalities
MRI!

Question 236

Side bone in the horse

Answer 236

Presentation-
Rarely causes lameness
Can be lame if fractured

Diagnostic imaging-
Radiography – variation in radiographic appearance
Often incidental finding.

Question 237

medications for eqiune foot pathologies

Answer 237

NSAIDs
Bisphosphonates

Intra-articular therapies-
Corticosteroids
HA
Polyacrylamide gel

Regenerative therapies

Question 238

NSAIDs for equine foot pain

Answer 238

Commonly used
Analgesic and anti-inflammatory
Only effective in the face of an inflammatory process
Clinically used for myositis, tendonitis, laminitis, osteoarthritis, and surgically induced trauma
Timing important!

carprofen
firocoxib
phenylbutazone- main one due to low cost and ease of administration
flunixon magluminate ect

Question 239

Phenylbutazone for foot pain in horses

Answer 239

NSAIDs
Most widely used
Low cost
Safe at low doses
Orally or IV
More effective than flunixin in musculoskeletal disease?
4mg/kg lasts 12hours
Effective for synovitis

Side effects?
Renal
Hypoproteinamia
GI ulceration

Reduces inflammation, central analgesic mechanism by decreasing hypersensitivity to pain caused by inflammation

Question 240

Flunixin meglumine
for foot pain in horses

Answer 240

NSAID
More effective for visceral pain + anti-endotoxic properties
IV/orally – 1.1mg/kg

Question 241

Firocoxib for foot pain in horses

Answer 241

COX 2 preferential NSAID
Indications: alleviation of pain and inflammation associated with OA and reduction of associated lameness in horses
0.1mg/kg once daily
Now available in paste and tablet form
More expensive than phenylbutazone so most owners will use bute but htis is techniqally more suted to chronic cases due to reduced side effects
Licensed

Question 242

paracetamol for foot pain in horses

Answer 242

Mechanism of action still not fully understood
20mg/kg orally twice daily adjunctive analgesic for laminitis
Not licensed- use human tablets so large quantity
effective in lamnitis

Question 243

Bisphosphonates for foot pain in horses

Answer 243

Regulate bone activity by inhibiting osteoclastic metabolism without affecting osteoblastic action.
Notable side effects- large proportion of horses given this wil colic- NSAIDs contraindicated
Licensed for use in spavin (Tiludronate) and navicular disease (Clodronate).
Can be tested for in doping tests – detection time 28days FEI/ 30days BHA.

Weak evidence for use when navicular bone is primary cause of discomfort and where clinical signs are recent in onset.

Statistically significant results to support use in horses with tarsal OA.

Question 244

Intra articular steroids for foot pain in horses

Answer 244

Intra-articular medications can be a more targeted approach to joint pathology.

Their use remain controversial.

However we will cover the most common steroids used in practice and the indications and contraindications for each.

The action of corticosteroids is exerted through steroid-specific receptors in the cytoplasm of steroid-responsive tissues. This interaction results in the altered transcription of genes, leading to a wide variety of antiinflammatory effects, as well as other effects on the biology of articular cells that are of variable benefit. Corticosteroids are able to suppress inflammation at virtually all levels.
The humeral effects of corticosteroids are due to the inhibition of phospholipase A and the decrease in production of pro-inflammatory mediators by both the cyclooxygenase and lipoxygenase pathways. They also inhibit many of the other inflammatory effects, such as capillary dilation, migration of inflammatory cells and the production and release of degradative enzymes; however, such drugs may have a negative effect on the joint environment, as they can cause suppression of cartilage matrix synthesis, as well as, in rare cases, widespread joint mineralisation1,2

when to use them-
When we have made a diagnosis of synovitis
Reduce the risk of development of osteoarthritis
Reduces inflammation within the joint

Two main options:
Shorter acting Triamcinolone Acetonide (NOT LICENSED)
Longer acting Methylprednisolone acetate (LICENSED)

Return to work? Gradual 1-2weeks
Be conscious of detection times!- sport horses

risks-
Iatrogenic synovial sepsis
Laminitis

Mitigate risk?
Intra-articular antibiotics?

Must warn owners of the risks!
can gie ia antibiotics at same time but not necessary if in clean enviroment and follow ropper hygien

Question 245

Triamcinolone acetonidefor foot pain in horses

Answer 245

DOSE: 6mg to 18mg per joint.
Max total dose 20mg

steriod

Widely used in joint disease therapy
High motion joints: carpus/ fetlock and DIP joints
One off vs regularly in the face of clinical signs of joint disease
Effective in acute cases of synovitis
BUT rule out treatable primary cause prior to treatment
Shorter detection time

risks-
Iatrogenic synovial sepsis
Laminitis

Mitigate risk?
Intra-articular antibiotics?

Must warn owners of the risks!

Question 246

Methylprednisolone for foot pain in horses

Answer 246

20mg/kg to 40mg/kg
Max total dose 200mg
Longer acting
More detrimental to articular cartilage – therefore low motion joint such as tarsus
Longer detection time

steriod

risks-
Iatrogenic synovial sepsis
Laminitis

Mitigate risk?
Intra-articular antibiotics?

Must warn owners of the risks!

Question 247

Hyaluronic Acid for foot pain in horses

Answer 247

Improves viscosity of synovial fluid – better lubrication
Anti-inflammatory effects
Reduced pain

no scientific evidence that it is better than steriods alone

can be iv but often intrarticularly

Question 248

Polyacrymide hydrogel for foot pain in horses

Answer 248

Similar action to HA – improves lubrication of the joint
Studies in horses showed that intra-articular injection of PAAG supported cellular growth and integration.
Further studies needed to explore potential effects on synovial inflammation and pain are needed
100% synthetic, non-soluble – acts a substitute for synovial fluid
MCP/MTP and DIP commonly treated

Reduced risk of IA infection vs steroids
Slower improvement seen vs steroids
No proven risk of doping

Question 249

Regenerative therapies for foot pain in horses

Answer 249

Aim is to aid tissue healing
Restore normal structural architecture and biomechanical function to injured tissue.
Not cause harm?
Limitations?

Inflammation and Osteoarthritis-
IL-1 and TNF pro-inflammatory cytokines  Erosion of cartilage and osteoarthritis
OA has increased expression of IL-1 receptors
IL-1ra protein prevents IL-1 from interacting
Provide IL-1ra by conditioning of serum

ACS or IRAP

Question 250

ACS or IRAP for foot pain in horses

Answer 250

Regenerative therapies
lacks evidence

Autologous conditioned serum
It may contain Interleukin receptor antagonist protein.
Plus other things.
Theory of action: Interleukin-1 is a major driver of OA and thus blocking it is an objective in the treatment of OA.

when?-
Most commonly sports horses
If identified soft tissue pathology (MRI/arthroscopy)
Increasingly used early, often before a definitive diagnosis.- more efffective
Mainly coffin joints and fetlocks
If IA steroid fail
Cost- steriods much cheaper

in human case-
376 cases of knee arthritis
ACS significantly superior to HA and saline placebo

Carpal fracture model
16 horses
Significantly improved lameness grade
Significantly decreased synovial membrane hyperplasia
No adverse effects

Ongoing concerns with method of action
Low risk
Seems to be beneficial- lack control studies
Lack of controlled studies and high quality of evidence based medicine.
Repeated injections

Question 251

Allogenic stem cells for foot pain in horses

Answer 251

Arti-cell Forte
Allogenic stem cells
Authorised by VMD for ‘reduction of mild to moderate degenerative joint disease (osteoarthritis) in horses.
Contains chondrogenic induced mesenchymal stem cells that target cartilage

evidence?-
Assessment of short term effect on a limited number of horses, using an OA model
Declaration of interest that one author declares competing financial interests as a shareholder in Global Stem cell Technology - owners of Arti-cell Forte.

Question 252

Superficial digital flexor tendon (SDFT) injury

Answer 252

Supports the MCP joint
Flexes the MCP joint
Elastic energy store
16% strain at gallop (rupture at 12-20% in lab)
Loads in excess of 1tonne on a structure less than 1cmsq in cross-sectional area

Tendon operating close to its functional limit
Low tolerance = low safety margin
Suggests:
Any small degeneration in matrix/structural properties will dramatically increase the risk of tendinopathy
Prevention of any such change will dramatically reduce the risk of tendinopathy

prognosis-
Most treatment suggest 60% BUT re-injury rates lowest with stem cells
Re-injury is the primary reason for treatment failure
Older horses = poorer prognosis
Lesion present in tendon or carpal sheath carry worse prognosis – poorer blood supply.

Question 253

Tendinopathy in the horse

Answer 253

Types
Intrinsic (strain)
Extrinsic (percutaneous injury)
Displacement

Very common!
30-40% of NH horses in training suffer tendonitis
46% of limb injuries on racecourses involved flexor tendons/suspensory ligament
SDF tendonitis most common injury in event horses

Predisposing/causal factors-
Biomechanical reasons-
Previous tendonitis
Uneven or deep track surfaces
Muscular exhaustion
Foot imbalance
Long sloping pasterns

Anatomical reasons-
Certain reasons have reduced blood supply (mid SDFT)
Decreased cross-sectional area in certain areas of the tendon

Question 254

mechanical overload of tendons i the horse

Answer 254

Hyperthermia in the centre of the tendon at gallop (45deg)
Acute overload of the entire tendon
Protein and cellular damage (collagen fibre disruption)
Classical ‘core lesions’ – loss of fibre integrity in central region

Question 255

Degeneration
of tendons in the horse

Answer 255

Tendon accumulates microdamage with age (>3yrs)
May manifest as acute overload incident
Often may get more generalised severe tendonitis

Stages of tendon damage - clinical
Tendon matrix degradation
- cumulative
- ageing
Fibrillar slippage
- breakage of crosslinks
Fibril rupture
Complete rupture

Question 256

Diagnosis of tendon and ligament injuries in the horse

Answer 256

History:
Acute onset
Exercise?
Peak performance

Clinical evaluation:
!Stance? Fetlock sinking
!Gait – lameness (mild to moderate)
Palpation: whilst weightbearing and with limb lifted
Swelling
Thickening
Pain on palpation
Oedema
Heat

Ultrasonography
Diagnosis
normal and affected limb
Timing
4-7days post injury
TRANSVERSE AND LONGITUDINAL
Examine for:
Cross sectional area – 0-15% mild/ 15-25% moderate/ >25% severe
Peritendinous oedema
Echogenicity
Margination – subtle indicator of changes
Fibre alignment – indicates quality of scar tissue
Examination too acutely may underestimate true damage

Question 257

Acute tendon injury in the horse – inflammatory phase (days)

Answer 257

Clinical signs -
Lameness
Severe -> mild

Pain on palpation- palpate weightbearing and non weightbearing

Inflammation
heat
oedema
loss of definition

Pathology-
Haemorrhage
!Inflammation
-! neutrophils
- macrophages and monocytes
- increased bloodflow
- oedema
- proteolytic enzymes

Question 258

Acute tendon injury in the horse – inflammatory phase (days)- treatment

Answer 258

Aims:
Limit inflammation:
Cold water hosing/ ice packs
NSAIDs/ Corticosteroids
Bandage – reduce oedema
Protect from further damage
Firm supportive bandage
BOX REST!!!

Many treatments have been advocated in the past:
Most have no effect
Some are deleterious
‘above all do no harm’

Question 259

Subacute tendon injury in the horse – reparative phase (weeks)

Answer 259

Clinical signs-
Reduction in lameness
Resolution of signs of inflammation
Tendon still palpably enlarged and soft
Signs of reinjury if exercised too early (usually worse!)
Ultrasound: hypoechoic

Pathogenesis-
Angiogenesis

Fibroplasia-
- ++fibroblasts
- collagen type 3 (normal type 2)
- small collagen fibrils formed

Question 260

Subacute tendon injury in the horse – reparative phase (weeks)- treatment

Answer 260

Aims:
Prevent re-injury
BOX REST + mobilisation – controlled!!

Promote angiogenesis- Stem cells

Promote better quality repair- Intralesional injection of mesenchymal stem cells, platelet rich plasma etc

Physiotherapy
Therapeutic US
Low level laser therapy
Hydrotherapy
Reduce oedema

Question 261

Mesenchymal stem cells as a treatment of tendon njury in the horse

Answer 261

Expensive and time consuming - autologous
Pluripotent progenitor cells capable of forming tendon tissue rather than scar tissue
Re-implantation of mesenchymal stem cells (MSCs) into lesion
Expanded in vitro
Bone marrow from sternum most commonly
SDFT core lesions provide natural enclosure for implantation
At the time of implantation the granulation tissue provides a vascularised scaffold
After the initial inflammatory phase before fibrous tissue had formed
Reduced re-injury rate from 56% to 18% (small study)

Question 262

Platelet rich plasma as a treatment of tendon njury in the horse

Answer 262

Stall side treatment
Cheaper than MSC’s
Produced and implanted same day
Blood plasma with concentrated platelet count
Activated growth factors
Injected under US guidance
Long term results lacking

Question 263

Chronic tendon injury in the horse – remodelling phase (months)

Answer 263

Clinical signs-
Tendon size decreases
Tendon is less pliable
Reduced fetlock extension
Ultrasound: hypoechoic to hyperechoic (heterogenous)

Pathology-
Collagen type 3 -> type 1
Crosslinking
Thicker collagen fibrils

Question 264

Chronic tendon injury in the horse – remodelling phase (months)- treatment

Answer 264

Aims:
Promote re-orientation and modelling of fibrils
Begin loading –controlled exercise
Timing and progress monitored by US
- Increased fibre density and improved alignment indicated
- Further increase in exercise if appropriate

controlled exersise program

Question 265

Controlled exercise programme as a treatment for tendon injury in the horse

Answer 265

Most important aspect of rehabilitation of SDFT tendonitis
Initially box rest and limb support for 2-4weeks
Followed by small amounts of in-hand walking out
Progressively increase over 9-12months
Rescan every 2-3 months: before and after a change in exercise level

Question 266

Prognostic indicators- SDFT injury

Answer 266

Initial severity – lameness
Longitudinal pattern when returns to full work
Duration of rehabilitation
Nature of work
Recurrence
Treatment

Question 267

DDFT Tendonitis

Answer 267

Usually pastern/foot – P2/navicular level
If within the DFTS – usually distended sheath
Linear tears seen more commonly in the forelimb- Treated by tenoscopic debridement
MRI to diagnose in the foot
50-60% success rate with conservative or surgery

Question 268

ALDDFT – inferior check ligament desmitis->(Check ligament) injury

Answer 268

Clinical signs-
Swelling proximal 1/3 of the metacarpal region
Palmar to the suspensory ligament
Lameness can be variable

ultrasound-
Generalised enlargement
Focal abnormalities
Fibre pattern disruption
Concurrent SDFT tendonitis

Check ligament often vestigial in the hindlimb
Similar signs to forelimb when present

Question 269

ALDDFT – inferior check ligament desmitis->(Check ligament) injury treatment

Answer 269

Acute:
Box rest! (2-3 weeks then controlled exercise)
NSAIDs
Cold hosing/bandaging

Chronic:
Controlled exercise program
NSAIDs
Corrective farriery- foot can make a big difference in how tendon heals
become contracted/ DIP flexural deformity
Shockwave?

Prognosis
Acute – fair good
Chronic + SDFT involvement = poor

Question 270

Proximal suspensory desmitis - forelimb

Answer 270

Unilateral (can be bilateral –less common)
Lameness
Palpation – enlargement/pain deep palpation – care!

Ultrasound:
Focal or generalised lesions
Loss of striated pattern
Peri ligamentous fibrosis
Entheseopathy

Radiography-
Sclerosis of proximal MC3
Avulsion fractures

Prognosis generally good – (60-80%)

Question 271

Treatment + Prognosis

Answer 271

Controlled exercise (6-9months)
Stem cells/intra-lesional injection if core
Shockwave

Question 272

Shockwave as a treatment for Proximal suspensory desmitis

Answer 272

Electrohydraulic extracorporeal shock wave therapy (ESWT)
Control inflammation, angiogenesis and stimulate cytokine production.
Provides immediate pain relief – up to 4days

Question 273

Proximal suspensory desmitis - hindlimb

Answer 273

Usually chronic, bilateral hindlimb lameness (rarely acute/unilateral)
Clinical examination often unremarkable

BUT..
Associated with conformation- straight hindlimbs
Usually worse on soft surface
Worsens with exercise

Diagnosis-
Diagnostic analgesia: deep branch of the lateral plantar nerve.
Rule out tarsal joint pain with IA anaesthesia

Ultrasonography-
DIFFICULT!!
Enlargement and irregular margin
Poor fibre pattern – reduction in echogenicity
Irregular bone surface/fibrosis
Compare limbs

Radiography-
Sclerosis MT3

Question 274

Proximal suspensory desmitis - hindlimb- treatment

Answer 274

Controlled exercise (20-30%)
Shockwave (50%)

Surgery (70%)-
Neurectomy/fasciotomy
FEI implications…

Question 275

Body suspensory demitis

Answer 275

Older racehorses/event horses
Lameness variable
May be associated with splint bone exostosis

Diagnosis:
Based on palpation + ultrasound

Treatment:
Controlled exercise
Shockwave
HA?

Prognosis-
Fair – recurrence common
Some horses are managed in work with low grade chronic changes.

Question 276

Suspensory branch desmitis

Answer 276

Both forelimbs and hindlimbs
Conformation  abnormal loading
Variable lameness

Diagnosis
Palpation of branches
Occasional fetlock effusion

Ultrasonography:
Enlarged – reduced echogenicity
Occasionally core lesion exists
Entheseopathy
Periligamentous thickening

Prognosis:
Poor-fair

Question 277

Suspensory branch desmitis Treatment

Answer 277

Controlled exercise
Intra-lesional stem cells/PRP
Shockwave?

Question 278

Capped hock

Answer 278

Synovial fluid within the calcaneal bursa (point of the hock)
Cosmetic (lameness rare)

Question 279

Thoroughpin

Answer 279

Synovial distension of the tarsal sheath proximal to the hock
Cosmetic usually

Is the sheath of the larger lateral flexor tendon (DDFT) in the hindlimb
Swelling is often clinically insignificant
If the horse is lame, look elsewhere first!

Question 280

Windgalls

Answer 280

Synovial distension of the fetlock or tendonsheath
May or may not be related to lameness

may or may not be related to lameness

Question 281

Causes – DFTS tenosynovitis

Answer 281

Acute tenosynovitis: over extension of the fetlock region/trauma to sheath

Tendon lesion in DFTS:
DDFT tear in forelimb and manica flexoria tear hindlimb

Palmar annular ligament desmitis
May be idiopathic

PAL desmitis Causes constriction of the DFTS
Can be primary or occur secondary chronic tenosynovitis

Diagnosis-

Clinical exam
Lameness assessment:
Mild to moderate lameness
Minimal response to rest

Intrasynovial anaesthesia to confirm
Ultrasonography – CARE – see next slide!!
Radiography…manica tears…contrast studies
Tenoscopy

Question 282

Manica flexoria

Answer 282

Manica flexoria: a tendinous ring inserting on the medial and lateral borders of the SDFT at the palmar aspect of MCP region that holds the flexor tendons in position

Question 283

treatment of Acute tenosynovitis in horses

Answer 283

rule out sepsis
Rest
Ice/cold hosing
Systemic NSAIDs
Intrathecal medication: corticosteroids/ HA

Tenoscopy-
Indications:
Intrathecal pathology diagnosed or suspected
Lack of response to conservative management/medical therapy
Flush out inflammatory mediators
Lesion ID on MRI or US

Chronic tenosynovitis-
Many cases respond to rest and controlled exercise + medical therapy as described.

Tenoscopy:
As for acute tenosynovitis:
Remove damaged tendon fibres
Chronic cases PAL desmotomy
Remove synovial masses/adhesions

Early exercise postsurgery helps reduce post-operative adhesions

Question 284

DDFT tendonitis within the sheath treatment

Answer 284

Treatment:
box rest and controlled exercise
raised heel to reduce load on DDFT
PAL desmotomy?

Prognosis:
Guarded to poor

Question 285

Marginal tears of the DDFT or the manica flexoria

Answer 285

Aetiology:
Compression of the tendon during overextension of the fetlock

Treatment:
Tenoscopic debridement –removing loose fibres reduces tenosynovitis
Removal of chronic adhesions

Question 286

Palmar annular ligament desmotomy

Answer 286

Desmitis causes mechanical constriction of the smooth movement of the tendon sheath
Desmotomy – divide the ligament
Good prognosis if the cause of the desmitis has been controlled.

Question 287

carpal canal syndrome

Answer 287

Constriction known as carpal canal syndrome
Secondary to tendonitis of the SDFT and DDFT, intra-thecal trauma/haemorrhage, ALSDFT desmitis, fracture of the ACB or osteochondroma of the caudodistal radius.
Removal of any osseous impingement is important resolve clinical signs

Question 288

Tenosynovitis of the extensor sheaths

Answer 288

Over the carpus most commonly affected
Commonly aseptic tenosynovitis in jumping horses that suffer blunt trauma their knees.

Congenital condition in foals where the CDE ruptures with the extensor tendon sheath causing tenosynovitis
Resolved by box rest
Address associated flexural deformity

Question 289

Tendon lacerations- Extensor tendons

Answer 289

Subsequent to lacerations to the dorsal aspect of the limb
Horse unable to extend joints covered by the affected tendon:
Commonly: Common Digital and Long Digital extensor tendon

Standard wound care/splint if knuckling forward

Do not need to suture:
Tendon can be removed without long term sequalae
Toe extension on shoe to prevent knuckling during first few weeks

Prognosis:
Good to excellent
Horses adapt well!

Question 290

Tendon lacerations- Flexor tendons

Answer 290

Potentially serious and life threatening – major part of the support structure for the distal limb.
Over reach injury or sharp/blunt trauma
Risk of synovial sepsis if digital sheath, carpal/tarsal sheath involved.

Usually severe lameness
Attitude of the limb indicative which ligament/tendon is involved
Watch horse weight bear, walk a short distance or briefly pick up limb
Careful digital examination +/- US exam

site of laceration may differ from the site of the cutaneous wound
Synoviocentesis of the DFTS

SDFT
Fetlock drops on weightbearing

DDFT
Toe of the foot comes off the ground on weight bearing

SDFT, DDFT and SL
Toe comes off the ground, and fetlock drops to the ground

Question 291

Tendon lacerations- Flexor tendons TREATMENT

Answer 291

First aid: immobilise limb/splint cast
Debride wound under GA
Treat any synovial sepsis

Repair:
- Suture if tendon ends aren’t too macerated
-If there is a tendon gap leave by secondary intention or use prosthetic material

Immobilise limb in distal limb cast for 8-12weeks

Question 292

neuro test- olfaction

Answer 292

Pass a cotton swab soaked in spirit or a strong smelling treat under the nose and assess for a response

Olfactory nerve

Question 293

Menace response

Answer 293

making a menacing gesture (moving the hand quickly toward the eye) and assessing for the normal blinking response

Optic nerve Facial nerve

Question 294

Pupillary light reflex

Answer 294

Shine a light in one eye to elicit pupil constriction in the contralateral eye

Optic nerve Occulomotor

Question 295

Palpebral reflex

Answer 295

Touch the medial or lateral canthus of the eye to elicit a blink reflex
Trigeminal nerve – ophthalmic branch Trigeminal nerve – maxillary branch Facial nerve

Question 296

Corneal reflex

Answer 296

Touch the cornea to elicit blink and globe retraction

Trigeminal nerve – ophthalmic branch Facial nerve Abducent nerve

Question 297

Vestibulo-ocular reflex

Answer 297

Move the head to induce nystagmus

Vestibulocochlear nerve
Oculomotor nerve
Trochlear nerve
Abducent nerve

Question 298

Nasal mucosa response

Answer 298

Touch the nasal mucosa with the animals eyes covered to elicit head movement away from the sensation

Trigeminal nerve – ophthalmic branch Trigeminal nerve – maxillary branch

Question 299

Gag reflex

Answer 299

Touch the pharynx to elicit contraction/gaging behaviour

Glossopharyngeal nerve
Vagus nerve

Question 300

cranial nerve involed in hearing

Answer 300

Vestibulocochlear nerve

Question 301

Carpus extension reflex

Answer 301

Percussion of the extensor carpi radialis
Radial nerve Spinal cord segments C7-T2

Question 302

Elbow extension reflex

Answer 302

Percussion of the muscle belly of the triceps muscle

Radial nerve Spinal cord segments C7-T1

Question 303

Elbow flexion reflex

Answer 303

Percussion of the muscle belly of the biceps muscle

Musculocutaneous nerve Spinal cord segments C6-C8

Question 304

Thoracic limb withdrawal

Answer 304

Pinch a digit or part of the interdigital web on the front foot to elicit limb withdrawal

Thoracic limb nerves Spinal cord segments C6-T2

Question 305

Stifle extension reflex

Answer 305

Percussion of the straight patellar ligament overlying the stifle

Femoral nerve Spinal cord segments L4-L6

Question 306

Hock flexion reflex

Answer 306

Percussion of the muscle belly of the cranial tibial muscle

Sciatic nerve (peroneal branch) Spinal cord segments L6-S1

Question 307

Hock extension reflex

Answer 307

Percussion of the muscle belly of the gastrocnemius muscle

Sciatic nerve (tibial branch) Spinal cord segments L7-S1

Question 308

Pelvic limb withdrawal

Answer 308

Pinch a digit or part of the interdigital web on the hind foot to elicit limb withdrawal

Femoral nerve Sciatic nerve Spinal cord segments L4-S2

Question 309

Anal reflex

Answer 309

Stimulation of the perianal region to elicit contraction of the anus
Pudenal nerve Spinal cord segments S1-S3

Question 310

Cutaneous trunci reflexes

Answer 310

Use a pair of forceps to pinch the skin of the dorsal trunk and elicit a twitch.

The spinal cord segment approximately two vertebrae cranial to the area tested.

Question 311

Conscious proprioception

Answer 311

The paw is placed in an abnormal position and the animal is observed to see how quickly they correct to normal.

Non-specific indicator of nervous system disease

Question 312

Proprioceptive and postural tests - Hopping

Answer 312

Non-specific indicator of nervous system disease

The animal’s weight is placed exclusively on one limb and the animal’s body is forced in one direction.

Question 313

Proprioceptive and postural tests - Wheelbarrowing

Answer 313

Non-specific indicator of nervous system disease
The front or rear of the animal is raised so that the animal’s weight is placed on either both pelvic or both thoracic limbs. The animal is then forced by the examiner to move the body forward (when testing the thoracic limbs) and backward (when testing the pelvic limbs).

Question 314

Proprioceptive and postural tests - Hemiwalking

Answer 314

Non-specific indicator of nervous system disease

A thoracic and pelvic limb on one side are held up by the examiner and the animal is forced laterally in the opposite direction, making the limbs contacting the ground move laterally to accommodate this new body position.

Question 315

Proprioceptive and postural tests - Extensor postural thrust

Answer 315

Non-specific indicator of nervous system disease

The animal is suspended in the air by picking it up under the thoracic limbs and then lowering it toward the ground. As the animal is lowered, the pelvic limbs will extend prior to touching the ground, and the animal will begin to walk backwards as it touches the ground.

Question 316

Proprioceptive and postural tests -

Non-visual, tactile placing

Answer 316

Non-specific indicator of nervous system disease

The animal is held in the examiners arms suspended off the ground with its eyes covered, then moved toward the edge of a table or other edged surface until the dorsal aspect of the animal’s paw touches the table. The animal should bring the limb forward to rest on the table-top.

Question 317

Encephalitozoon cuniculi infection

Answer 317

Head tilt Positional nystagmus which can be horizontal, vertical or rotatory Abnormal proprioceptive responses

Paired IgM and IgG PCR

Question 318

Otitis media

Answer 318

Head tilt Horizontal or rotatory spontaneous nystagmus Facial nerve paralysis Horner’s syndrome

Clinical exam
Radiographs
CT scan

Question 319

Cerebellar hypoplasia

Answer 319

Intention tremors Ataxia Hypermetria Menace deficits Head tilt/nystagmus

MRI

Question 320

Steroid responsive meningitis

Answer 320

Neck pain Depression

Clinical signs
Haematology and biochemistry
CSF tap

Question 321

Epilepsy

Answer 321

Generalised seizures Agitation Lethargy/depression Intermittent blindness

Clinical signs and history Exclusion of other differentials via bloods, urinalysis, CSF tap, serology, imaging etc.

Question 322

Myasthenia gravis

Answer 322

Generalised weakness Dysphagia Regurgtation/megoesophagus

Clinical signs Serum acetylcholine receptor antibody titre Edrophonium chloride challenge test Electromyelography

Question 323

Idiopathic Horner’s syndrome

Answer 323

Miosis Enophthalmos Ptosis (drooping) of the upper and lower eyelids Narrowed palpebral fissure Protrusion of the third eyelid

Miosis Enophthalmos Ptosis (drooping) of the upper and lower eyelids Narrowed palpebral fissure Protrusion of the third eyelid

Question 324

Hepatic encephalopathy

Answer 324

Abnormal behaviour (depression, disorientation, wandering, phantom chewing) Head pressing Ataxia

Clinical signs Haematology and biochemistry testing Coagulation tests Radiography (contrast venography).

Ultrasonography Scintigraphy MRI of abdomen

Question 325

Intervertebral disc disease (typeI)

Answer 325

Schiff-Sherrington, spinal shock, or kyphosis posture Spinal hyperaesthesia Paraplegia Limb withdrawal may be absent

Clinical signs Radiography Myelography

Question 326

Intervertebral disc disease (type II)

Answer 326

Progressive pelvic limb weakness and ataxia Abnormal pelvic limb proprioceptive responses Behavioural changes (reluctance to jump or climb stairs)

Clinical signs Radiography Myelography

Question 327

Chiari-like malformation and

syringomyelia

Answer 327

Cervical pain (including intolerance of neck collars) Sensory abnormalities (face rubbing, foot chewing) Phantom scratching Tetraparesis Sensory ataxia Abnormal proprioceptive responses

Clinical signs Radiography MRI

Question 328

Wobbler syndrome

Answer 328

Progressive ataxia Tetraparesis (pelvic limbs more severely affected then thoracic limbs) Neck pain

Clinical signs Radiography Myelography CT/MRI

Question 329

Tail pull injury

Answer 329

Tail paralysis Tail anaesthesia Urinary incontinence (flaccid bladder with overflow vs distended bladder which is difficult to empty) Faecal incontinence Plantigrade stance

Clinical signs Radiography MRI

Question 330

Toxoplasmosis

Answer 330

Seizures Behavioural changes (depression, hyperexcitability) Hyperesthesia Tremors +/- ataxia Paresis/paralysis

Clinical signs Serology CSF PCR