Equine orthopaedics Flashcards
0
Q
What is the hoof growth rate?
A
7-10mm/month. 6-12 months for full cycle. Constant wear and exfoliation.
1
Q
What factors affect hoof growth and quality?
A
Hereditary
Diet - feed supplements containing methionine, biotin etc have been show to increase hoof growth rates.
Environment - wet horn is weaker than dry horn. ammonia rots horn. some hoof hardeners can damage the hoof wall as they contain formalin.
Farriery. (or lack of farriery) - may cause imbalance, nail placement affects function. Imbalance predisposes to cracks.
2
Q
DEscribe the ideal scenario of hoof balance in a horses foot?
A
All parts in proportion, geomatrical axial symmetry. The toe angle equals pastern angle, toe angle equals heel angle, heels asme length and height. Equal distributio of weight.
3
Q
Define cranial to caudal imbalance and mediolateral balance?
A
Cranial to caudal imbalance has been defined as a deviation in the hoof alignment or as problems with heel support.
Medio lateral balance defined as equal medial to lateral distribution of weight weight as more weight is normally placed on the caudal half of the hoof.
4
Q
Describe a good foot examination?
A
Always :
Use hoof testers, palpate digital pulses, palpate coronary band, manipulate the foot. Assess quality of farriery - horses normally shod every 6 weeks. If shoes are ill fitting or loose this can cause lameness. The shoe should fit the foot not the reverse. 7 nails usually.
5
Q
What is nail bind?
A
nail has penetrated sensitive tissues of the foot at the time of shoeing.
6
Q
Which diagnostic injections can be used in the horse foot?
A
Palmar digital nerve block,
abaxial sesamoid nerve block,
distal interphalangeal joint block,
navicular bursal block.
7
Q
Define farriery?
A
Farriery is defined as any work in connection with the preparation or treatment of the foot of a horse for the immediate reception of a shoe thereon, the fitting by nailing or otherwise of a shoe to the fit or the finishing off of such work to the foot. In the UK only qualified farriers are allowed to shoe a horse. only exemption to this is qualified veterinary surgeons.
8
Q
What is the aim of shoeing horses?
A
to protect the hoof wall against wear & tear, improve performance, additional support on slippery surfaces but they add weight , they restrict expansion of foot during loading, & they cause problems when incorrect.
9
Q
What are the commonly used therapeutic shoes?
A
Egg bar shoe, wedge shoe, rim shoe, heart bar shoe, frog support shoe.
10
Q
What is navicular syndrome?
A
The cliniical manifestation of different pathological processes in the navicular boe, the flexor surface of the NB, the DIP joiint, the DDFT, the navicular suspensory ligaments, impar ligament. (one theory is utrient arteries occlude > causes necrosis and bone resorption) - more accepted theory is increased pressure between the DDFt and NB - flat foot with long toe and low heel, leading to remodelling of the NB (scllerosis, marginal osteophytes, thickening of sc bone and inflammation of the NB - surface defects). Analogous to degenerative joint disease. Clinical findings include insidious onset - frequent stumbles, reluctant to work on circle, may point one foot, short strided at the trot, often bilateral lameness which is accentuated on the hard circle, diagnostic analgesia will improve to PDNB, DIP and NB block
11
Q
What is the treatment of navicular disease?
A
Foot care - support the heel relax the DDFT.
NSAIDS, vasodilators, intra bursal corticosteroids (contraindicated if DDFT lesion present). repeated injections less effective.
Tiludronate - reduces osteoclast activity.
Surgical - desmotomy of the suspensory ligaments (50%), decompression of the navicular medullary cavity (rarely performed), neurectomy.
12
Q
Describe hoof abscesses in the horse?
A
most common cause of lameness, typically acute lameness, typically increases in digital pulse. any insult to the sole can create an ideal medium for bacterial growth. chronic cases may present with cellulitis and systemic infection. variable clinical signs; infection can be misdiagnosed. Diagnosis by increase of digital pulse, hoof testers, warm poultice, radiographs (gas shadow), antibiotics and anti inflammatory can be contraindicated.
13
Q
What is the treatment for a hoof abscess?
A
Release infection & adequate drainage. drainage through the sole, debridement of necrotic tissue. Poultice until the infection is controlled. Warm bath with povidine and magnesium salt, antibiotics and anti inflammatory can be cotraindicated. Give tetanus prophylaxis.
14
Q
What is solar bruising or aseptic pododermatitis?
A
A single episode of trauma or due to repeated excess weight bearing due to poor foot balance. diagnosis by inspection & hoof testers. Deep solar bruising difficult to diagnose. treatment is rest, nsaids, solar pads r glue on shoes.
15
Q
What are corns?
A
Bruise of sole at specific location: medial angle - seat of corn much more common than lateral. Usually due to pressure from heel of shoe, either shod too short, shoe left on too long, dorsopalmar foot imbalance. Excessive heel loading leads to buises/subsolar abscesses. Corrective trimming and shoeing, extended heel support needed. Remove offending shoe, remove damaged horn, bandage or poultice and re shoe with wide webbed shoe, 3/4 shoe, silicone pad (only if defect is ready), bar shoe in case of dorsopalmar imbalance and bilateral corns.
16
Q
Describe puncture wounds of the sole and how they can be diagnosed and treated?
A
Common emergency in equine practice. important too rule out sepsis of synovial structures. commonly result in Sub solar abscesses. early treatment is essential. Diagnosis- radiographs, synooviocentesis, navicular bursa contrast study, MRI. Treatment - subsolar abscess localised using hoof testers. Pare tract to release pus. explore tract - warm bath with povidone/magnesium salt. poultice until the infection is controlled e.g animalintex. antibiotics required depending on the involvement of structures.
17
Q
What is seedy toe or white line disease?
A
White line is the sole - wall junction and a weak region due to the soft horn. combination of bacteria & fungi produce separation of the white line. Occasionally this produces lameness. Diagnosis; typically an incidental finding at the time of trimming. the white line becmes filled with poor quality infected tissue. characteristic hollow sound when the hoof capsule is perfussed. Often secondary to laminitis. Advanced cases cause instability of the pedal bone or infection into the sensitive laminae. Treatment; pare regions of abnormal horn and debridement of all crack and fissures. expose and removal of all diseased hoof wall. pack with iodine or metronidazole optional. Severe resections: bar shoe is indicated for stabilising the hoof. when the disease is eliminated reconstruction of the hoof with acrylics material is needed. Treat laminitis if this is involved in the aetiology
18
Q
What are hoof wall cracks?
A
Anywhere from the toe to the heels. superficial or full thickness. vertical cracks from coronary distally are sand cracks or from ground proximally grass gracks. result of chronic foot imbalance, lack of trimming, trauma, nutrition or poor hoof quality. May be sound or severely lame, depending on location & depth of crack. If in doubt as to significance, apply hoof testers. Assess hoof capsule and conformation and treat any underlying causes. debridement of any infected tissue, hoof balance, stabilise hoof wall adjacent to crack. if possible, reduce weight bearing in affected region. consider supplements to improve hoof wall quality & growth rate. Bridge crack using metal or fibreglass plate. use bar shoe, clips ad silicone, cast acrylic & wire or combination of all. Debridement of the crack, antiseptic, stabilisation with metal staples, silicone pad and corrective shoeing to release the pressure over affected area.
19
Q
What is a keratoma?
A
Benign hyperplastic keratin masses. Arise from the epidermal keratin producing cells and originate at any point in the hoof wall and sole, space occupying tumours, often causes recurrent hoof abscess.Diagnosis - disruption of the hoof architecture allow bacteria infection and recurrent abscess. may cause pressure necrosis an resorption of pedal bone margin leading to characteristic radiographic lucency, deformation of the white line. Surgical removal standing or under GA. combination of tools needed including hoof knifes, trephine, oscillating saw and motorised rotor. good prognosis after surgical removal.
20
Q
What is thrush?
A
An infection of the frog caused by wet environment, similar to ovine foot rot - fusobacterium necrophorum. Causes black sticky discharge and terrible smell. ca result in under run sole & limb oedema. Contracted heels may predispose to the condition (defined a a frog width less than 67% of the frog length). Treatment is to trim affected parts of the frog, move to dry environment and give antiseptic foot baths with povidone iodine.
21
Q
What is septic pedal osteitis??
A
Due to a A penetrating injury to the sole involving P3, chronic sub solar abscess or blunt trauma. Diagnosis - peel sole and localised necrotic track, radiographs, placement of a probe to confirm communication with distal phalanx. Treatment - surgical debridement standing or under GA, curettage of infected pedal bone, packing the area with antibiotic impregnated swab, regional perfusion with antibiotics, systemic antibiotics and anti inflammatory. medical grade maggots. Treatment - solar support, hooof bandage, good prognosis if small area is infected.
22
Q
What is canker?
A
Chronic Pododermatitis of the germinal layers. Gram negative bacterial infection of the stratum germinatum of the frogs epidermis. Hypertrophic dermatitis of the frog and the bulbs of the heels. Mainly affects draft horses. Horn of heels, bars and frog degenerates into strands of soft tissue with cheesy white discharge. Lame & frequently stamp feet. Treatment - radical surgical debridement of the affected tissue. topical treatment with metronidazole and bandages.
23
Q
What is quittor?
A
Collateral cartilage infection as a result of a hoof wall crack, puncture wound, chronic abscess or heel laceration. severe degree of lameness until adequate drainage is established. difficult to treat due to the avascular nature of cartilage. Chronic sepsis with intermittent purulent discharge above coronary bad. treatment - surgical excision of infected cartilage and surrounding tissue. opening of a ventral drainage portal is essential to allow resolution of infection.
24
Describe treatment of coronary band laceration?
This is an emergency in equine practice. it is important to rule out sepsis of synovial structures. Debridement and primary or delayed primary closure, with non absorbable sutures, GA or standing & immobilisation with a cast.
25
Which structures should you assess when looking at a heel bulb laceration/
Vital structures can be affected. important to rule out sepsis of synovial structures. Required GA to assess structures. Assess DDFt, collateral cartilages, navicular bursa, impar ligamet, DFTS, involvement of above structures decreases prognosis. Arthroscopic lavage and debridement of the area, immobilisation with cast
26
What are sheared heels?
Defined as a disparity between the medial and lateral heel legnths of 5cm or more. associated with dynamic lateromedial imbalance. one heel usually the medal one strikes ground before the other. proximal displacement of this heel. the wall on the side becomes short and upright. the opposite wall expands and flares outwards. continuous tearing and bruising of the sensitive laminae the compressed heel and breakdown of tissues that connect the heels result in lameess. treat - bar shoe floating the displaced heel.
27
What is bone spavin?
Bone spavin is a bony growth within the lower hock joint of horse or cattle. It is caused by osteoarthritis, and the degree of lameness that results can be serious enough to end a horse's competitive career.
28
What is bog spavin?
Bog spavin is a swelling of the tibiotarsal joint of the horse's hock which, in itself, does not cause lameness. The joint becomes distended by excess synovial fluid and/or thickened synovial tissue bringing about a soft, fluctuant swelling on the front of the joint, as well as in the medial and lateral plantar pouches. Bog spavin is generally an indication of underlying pathology within the joint.
29
Describe how to spot a forelimb lameness in a horse?
A horse with a unilateral forelimb lameness will trot with its head nodding Down when the sound limb lands, as it tries to shift the weight off the painful limb. This is best seen when the horse trots towards you, or on the lunge. Watch for the head nod first then look at which limb is being plcaed as head nodes down.
30
Describe how to spot a hindlimb lameness in a horse?
A horse with a unilateral hindlimb lameness will show an increase excursion ( up and down movement) of the gluteal region on the lame side at the trot (the hip hike). This is best seen as the horse trots away from you. Placing markers over the tubera coxae will make subtle movements easier to see. If severe, a hindlimb lameness will result in a head nod mimicking lameness of the ipsilateral forelimb.
31
Describe the different grades of lameness
0- sound, 1 - subtle head nod/gluteal movement, not at every stride, 2 - obvious and consistent head nod or gluteal movement, 3 - pronounced head nod or gluteal movement, 4 - horse so lame it can barely trot. 5- non weight bearing.
32
How do local anaesthetic agents woork and which ones are most commonly used?
Act by blocking sodium channels within the neurones preventing initiation and propagation of action potentials. two most commonly used = mepivicaine (rapid onset 5-10 minutes) duration 2-3 hours, and Bupivicaine moderate onset (upto 30 mins) , duration 4-6 hours.
33
What perineural nerve blocks ca be used in the horse?
Palmar/plantar digital, abaxial sesamoid, low 4 point (6 oint in hind), high 4 point, median/ulnar, tibial/peroneal
34
Describe the palmar /plantar digital nerve block technique and what it blocks?
Limb psition - limb held up, digit in partial felion. Landmark: axial to the neurovascular bundle at the level of the ungular cartilages. PDB can alleviate pain from most of the sole. IF performed distally, unlikely to alleviate pain from the proximal interphalangeal joint, but will do so if the needle is inserted mid pastern.
35
Describe the abaxial sesamoid nerve block technique and what it blocks?
forelimb - limb held up in partial flexion or in hind limb - limb weight bearing or held up. Landmarks - palmar t the medial and lateral neurovascular bundle at the level of the distal aspect of the proximal sesamoid bones. It blocks all of the hoof cpaulse, proximal interphalangeal joint, palmar pastern region including sesamoidean ligaments, DDFT, SDFT, distal part of tendon sheath. In the hindlimb, perineural analgesia of the dorsal branches in the pastern region is required for complete desensitisation.
36
How should a fracture be bandaged?
Robert jones bandage. must be 3xwidth of limb and 7-10 thin layers. Most common fault is that it is too loose, thereby achieving nothing.
37
Which tendon lacerations carry a good or bad prognosis?
Extensor tendon laceration - common and carry good prognosis. unable to extend digit if complete - recover well. bandage and fix in extension initially.
Flexor tendon laceration potentially life threatening - assess distal limb position. RJB, dorsal splint and heel wedge. must prevent hyperextension.. use kimzey splint. surgical repair possible.
38
What should you lavage a traumatic wound with?
Early lavage very important. presence of foreign bodies and bacteria can be significantly reduced. Infection >10^5 bacteria/gram tissue. Fluids - sterile saline optimal lavage. or 1 tbsp table salt + 600ml water. or 0.05% chlorhexiine or povidone iodine. always lavage with saline afterwards. Pressure 10-15PSI (30ml syringe, 19G needle).
39
Why is debridement of traumatic wounds important?
Aims: remove contaminated/infected tissue, remove devitalised/crushed tissue, preservation of the skin important where possible. Techiques: lavage, surgical (sharp,hydrosurgical), autolytic, enzymatic (maggots). Do not use wet to dry dressings to debride. non selective & remove healing factors.
40
Describe the different types of wound closure?
Primary closure - requirements for primary closure: perform promptly, minimise contamination first, tension relieving suture patterns/technique, not if infected, drains if dead space, always try to perform primary closure of eyelid/distal limb wounds.
Second intention healing - large tissue defects, heavily contaminated, infected.
Delayed primary - allow 2nd intention healing then trim and close primarily when healthy/sufficient tissue.
41
What are the aims of dressings & supportive bandage? describe the three layers needed.
Aims: minimise oedema with firm, even pressure, absorb exudate, maintain temperature & moisture, allow gaseous exchange, immobilise the wound, protect from further contamination and trauma.
Primary dressing - choose non adherent ressings. eg cotton cellophane (melolin) for non exudative. hydrophilic polyurethane foams (allevyn) for exudative, calcium alginates for healing by second intention, collagen dressings for healing by second intention, hydrogels for contaminated wounds hydrocolloids, manuka honey once granulation has begun, amnion, bovine /porcine intestinal mucosa, collagen dressings. Do not use poulticing material on wounds - contains boric acid.
2. Secondary layer - cotton wool/gamgee. Absorbs exudate, secures primary layer, supports and protects.
3. tertiary layer - vvetrap, secures, provides support & Pressure.
42
What are the BEVA guidelines for humane destruction for a horse with a severe injury?
If in doubt, do not destroy the horse, particularly if owner not present or horse is i nsured. it is always wise to seek a second opinion from colleague or referral centre.
BEVA: horse sustains an injury or illness or disease that is so severe as to warrant immediate destruction to relieve incurable and excessive pain that no options of treatment are available to that horse at that time. IF a vet is not present, a police officer can Euthanase a horse if required. Is the horse a hazard to itself or handlers - eg violent or uncntrollable, self destructive, thrashing behaviour in traffic or crowds. does the immediate condition carry a hopeless prognosis for life?
Hopeless prognosis includes;
Complete fracture of radius or humerus if horse >300kg, Log bone fractures with severe soft tissue damage, complete femoral or tibial fractures in adult, severely contaminated fractures.
Guarded prognosis (may be used for breeding or pasture pet) - joint luxation, flexor tendon lacerations, closed fractures).
43
How can long bone fractures be stabilised?
Aims are to prevent further soft tissue injury, further displacement of fracture, conversion to a compoundd fracture splints, bandages oor casts are used. the type of coaptation applie epends on the biochemical forces acting on that region. the wrong bandage or splint can make a bad situation worse, so again if i doubt ask a referral centre for advice before travelling the horse. Splinting materials include PCV half pipe, plank of wood, broom handle, bandage cast. DO NOT USE KIMZEY SPLINT IF YOU SUSPECT FRACTURE
44
List the different factors which can affect wound healing?
Haemorrhage/anaemia, malnutrition, NSAID administration, corticosteroids, concurrent disease cachexia, cytotoxic drugs (AW4- LUDES, cisplatin)
Local - trauma, infection, temperature, oxygen, movement, foreign material, transformation
45
What are the causes of delayed healing?
Infection - prolonged, less effective inflammatory phase. bacteria produce collagenases. factors predisposing to infection include devitalised tissue, foreign bodies, dead space/haematoma formation, excessive movement.
Exuberant granulation tissue - maturation of fibroblasts to collagen producing type. Prevention - treat/prevent infection, prepare wound well at first visit, ensure all FB /devitalised tissue removed, remove devitalised tendons/bony sequestrae as soon as they become apparent, immobilise lmb, apply pressure to wound - bandage, use a skin graft to promote epithelisation. Surgically excise granulation tissue to below epithelial margin, freshen edges of wound, does not require local anaesthetic. Topical therapies generally not necessary and often contraindicated as they delay healing.
46
Describe the uses of skin grafing in horses?
Used where skin loss is extensive. Improved cosmetic results. requires good early wound management leading too a healthy granulation bed. Infeciton/movement is the main cause of failure. Expensive. common graft techniques in horses include: pinch and punch grafts, mesh grafts, line grafts.
47
Describe why wounds to the hoof wall and coronary band are differet
Although in principle the same rules of wound healing apply, this region is specialised; lower healing rate due to constant movement in this region, proximity to the ground and therefor contamination, little scope for wound contraction due to rigid hoof wall. Preservation of the germinal layer of the coronary corium is essential for future hoof wall growth. if this is seriously damaged this may result in permanent hoof wall defect. A partially avulsed hoof wall will not heal back into place and should be debrided.
48
What is the most commonly affected joint with septic arthritis?
The tarsocrural joint is most frequently involved, followed by the fetlock, carpus, stifle and pastern joints.
49
How do synovial infections occur?
Septic arthritis/tenosynovitis/bursitis results form the inoculation of microorganisms into a synovial structure resulting in an inflammatory response which fails to prevent proliferation of the micro organisms. A rapid influx of leucocytes occurs which are capable of phagocytosing the bacteria and releasing destructive enzymes. disruption of the blood synovium barrier results in release of multiple inflammatory mediators into the joint and amplification of the inflammatory response. Release of inflammatory mediators stimulates chondrocytes within the joint to release enzymes causing disruption of the proteoglycan hyaluronan complex in the articular cartilage. The protection oft he articular cartilage is further compromised by changes in the synovial fluid due to changes in viscosity and fibrin and pus acucmmulation. accumulation of debris within the joint also facilitates adherence of the bacteria and impedes normal joint metabolism. Leakage of fluid into the synovial compartment results in joint or tenon sheath distension and increased intra articular pressure. this reduces blood flow to the synovium and impairs normal exchange across the synovial membrane. in joints this can further compromise the viability of the articular cartilage.
50
What is the aetiology of synovial joint infections?
Joint bursa and tendon sheath infections occur most frequently from direct contamination by a penetrating wound and much less commonly through idiopathic inoculation during intra articular medication. Haematogenous infection is unusual in adult animals but common in foals resulting in multiple joint infection.
51
What bacteria are most commonly isolated from synovial sepsis?
Gram positive isolates more commo in adults with staph aureus having the highest incidence and non haemoolytic staphyloccocus, B haemolytic and non B haemolytic streptococci, rhoodococcus equi, and corynebacterium have also been isolated. Multiple and gram negative infections are more frequent in foals with E. coli being most frequent isolate and pseudomoas, enterobacter, actinobacillus, proteus, klebsiella, salmonella have all been isolated.
52
What are the clinical signs of synovial sepsis?
Clinical signs of synovitis include pain, heat and swelling, and are similar for joint and tendo sheath infectioons. pyrexia is often absent and is a poor indicator of synovial infections in adults. pain may appear to be sudden in onset and lameness may ooften be almost non weight bearing. clear yellow viscous fluid exuding from a wound may suggest leakage of synovial fluid but could also be serum. common signs; severe lameness, wound nearby, joint effusio. Not useful; pyrexia, peripheral blood analysis, local skin temperature, radiography.
53
What gross changes may indicate synovial fluid abnormality?
Increase in turbidity, red or dark yellow colour and reduced viscosity. total protein values are indicative of synovitis, however iatrogenic haemorrhage may result in slightly elevated levels. leukocyte counts in synovial fluid rise quickly in infection, with most clinical cases having count of >30x10^9 and most cases having >80% neutrophils.
54
What is synovial distension?
Large patent wounds allowing free drainage of synovial fluid may render aspiration of a sample impossible. distension of the joint or tendon sheath with sterile polyionic fluid from an aseptically prepared site, distant to the wound may produce drainage through the wound, thereby demonstrating communication with the wound.
55
Describe infectious arthritis in foals?
Septic arthritis in foals is usually haematogenous in origin and should be considered as part of a more generalised disease e.g septicaemia or failure of passive transfer of immunity. foals with rhodococcus equi infections can develop an immune mediated synovitis or a septic physitis affecting multiple joints. all foals with signs of septicaemia are at risk of developing arthritis, and in the cuboidal carpal and tarsal bones. Foals of any age from a few days to four months may be affected, and multiple joints are frequently involves, especially in younger foals. Epiphyseal infectins may present with hot swollen joints, whereas physeal infections may display more subtle swellings at the physis, accompanied by severe lameness or recumbency. aspiration at the physis may yield positive culture. radiographic changes may be very subtle initially and radiography can be repeated after 7 days.
56
What is the treatment for Synovial sepsis?
Arthroscopic lavage is gold standard and debridement followed by closed suctiondrainage. athroscopy allows visual assessmet of the synovium and articular cartilage lavage and surgical debridement of fibrin, inflamed synovium, which may contain adhered bacteria and damaged articular cartilage. Lavage through needles is ineffective for removal of solid fibrin or pus but through and through lavage needles and catheters can be useful in foals. Systemic antibiotics - base on culture and sensitivity, or use Gentamicin combined with sodium benzyl penicillin. Intra articular medication also possibl with gentamycin, amikacin and cephazolin (empirical). Regional limb perfusion - into a peripheral vein after tourniquet application. Antibiotic impregnated polymethylmethacrylate or gelatin sponges - PMMA beads impregnated with gentamycin or collagen sponges impregnated with gentamicin. give higher levels of antibiotic than can be achieved by safe systemic administration. NSAIDs frequently withheld until after arthroscopically debriding a septic joint as return of lmeeness is good indicator of recurrence.
57
Describe long bone fractures in foals and how these should be treated?
Not uncommon (metacarpal/metatarsal three diaphysis, proximal tibial pysis) should be considered in ay severely lame foal. long bone fracture fixation is a more realistic option in a foal compared to an adult due to their lower body weight.
58
How may a fracture of the proximal sesamoid bone occur?
May be uniaxial or biaxial, single limb or multi limb. believed to be excessive exercise running after the mare commonly occurs between 2 weeks and 2 months. can be basilar or apex, commonly comminuted, conservative management possible or wire cerclage, may develop elongated bone.
59
What are subchondral bone cysts?
Characterised radiographically by radiolucent areas of bone often accompanied by a thin well d emarcated rim of sclerotic bone. usually occur in the subchondral boone underlying a weight bearing surface of the articular cartilage e.g medial femoral condyle, phalanges. Clinical signs include lameness & joint effusion. lameness in young horses (1-3 years) usually occurs at onset of training. diagnosis confirmed with radiography & ultrasound. treatment involves arthroscopically guided disruption of cyst lining and injection with corticosteroids. good prognosis in young horses.
60
What are angular limb deformities?
This is a common condition in foals and refers to when the limb has a deviation in the frontal plane i.e the leg will bend either inwards or outwards (valgus more common) . congenital and acquired forms are recognised.
61
What are congenital angular limb deformities?
Periarticular ligamentar laxity or hypoplasia of the cuboidal bones of the carpus or tarsus. malformation of the diaphysis of the long bones (rare). intrauterine malpositioning, mare nutrition (iodine deficiency in canada).
62
What is acquired angular limb deformity?
Only apparent as growth accelerates, asymmetrical growth at the physis. If deviation due to periarticular laxity or cuboidal bone collapse, limb should be straightened using padded bandage/cast. leave out foot to correctly load limb. restrict exercise. care with bandaging as foals skin very delicate. Older foal: deviation due to growth asymmtery. partially restrict exercise, monitor diet to avoid overweight/rapid growth, check Cu, Zn, Ca, P levels in diet. check for lameness. for valgus deformities use medial extension shoes ad for varus use lateral extension shoes.
63
What are the two different surgical techiques used to treat angular limb deformities?
Periosteal transection and elevation;
Performed on the short side of the bone, i.e the side towards which the limb is bent. the periosteum is stripped from the physis on one side of the bone and then replaced. using this procedure it is not possible to over correct the lesion.
Growth retardation - transphyseal bridging - surgical implants can be placed across the physis on the side that is growing too rapidly. used only in severe cases as it is possible to over correct. take implants out before limb is totally straight.
64
How do congenital flexural deformities occur?
Uterine malpositioning, toxic/viral insults during embryonic life. limbs held in permanent flexion. wide range of severity. evaluate which joints involved. could be arthrogryposis. may improve with weight bearing, intravenous oxytetracycline in first 48 hourus, physiotherapy, corrective foot trimming, reduce heels, consider toe etensions. bandaging will induce muscle laxity and prevent skin damage.
65
How do acquired flexural deformities occur?
Rapid growth, imbalance between growth of between bones and tendinous unit. excessive calorific intake /nutritional imbalances. reduced weight bearing in the limb, often associated with lameness/physitis.
66
What is club foot?
Usually develops 6w--6m of age. boxy upright foot, broken back hoof pastern axis. can develop very rapidly. type 1 dorsal hoof wall still slopes cranially, type 2 hoof wall past the upright i.e slopes caudally. Can be unilateral or bilateral. Conservative management in mild cases, dietary restriction, nsaids, controlled exercise, rasp down heels and place toe in extension. can try bandaging but usually successful in early cases only. surgical treatment in severe or progressive cases. Type 1: desmotomy of the accessory ligament of the deep digital flexor tendon
Type 2 - deep digital flexor tenotomy, usually viewed as a salvage proocedure.
67
What is fleor deformity of the metacarphophalangeal joint?
can be very rapid in onset and very variable in degree of flexion. can be unilateral or bilateral. forelimb or hindlimb. conservative as for DIPJ coondition,except raised heel shoes.
Tx - surgery. must perform careful palpation to see which tendons under most tension as can involve SDFT and DDFT. Desmotomy of ALDDFT or ALSDFT or both. often unsuccessful. SDFT tenotomy is a salvage procedure.
68
What is physitis?
Inflammation and disruption of growth in the physeal rgions. causes; overload, over exercise, rapid growth. firm, often paiful swelling of the physeal areas. often in distal radius and tibia also distal MT/C3. flaring of the growth plates gives the long bones a typical hour glass shape. This commonly occurs around the time of growth plate closure. rapidly growing, heavy animals are most commonly affected. Associated lameness is usually mild in degree and may be intermittent and in multiple limbs. osteochondrosis may be associated. radiographically the physis is widened and irregular. Most cases are self limiting. Treatment is required if condition is painful or is suspected to be causing secondary growth disturbance leading to angular or flexural limb deformities. Treatment is aimed at eliminating the inflammation of the physis. exercise reduction is important. the dietary energy intake of these foals should be reduced to slow the growth rate.
69
What are cuboidal bone abnormalities?
Commonly seen in premature or dysmature foals, presenting clinically with various angular limb deformities following uneven loading of a dysmature skeleton. identified radiographically as incomplete ossification of the carpal or tarsal bones .if less than 30% of the cartilage skeleton has ossified then prognosis for athletic activity is hopeless. Management consists of sleeve cast application and stall rest until skeleton matures sufficiently to tolerate normal weight bearing forces.
70
Describe infectious orthopaedic disease in the foal?
Sepsis is an important common potentially catastrophic cause of lameness in young foals, characteristically less than 4 months of age. In adults direct inoculation is far more common, Haematogenous spread is common in the foal. it is believed that synovial membrane and the physeal regions are common sites for bacterial precipitation due to their extensive capillary networks. bacteria from the bloodstream (remember to look for and treat the inciting cause) settle in one of these sites and provoke a profound inflammatory response. these inflammatory enzymes initiate the degradation of cartilage, proteoglycan, collagen.
71
What is osteochondrosis?
Osteochondrosis represents a disturbance in the process of endochodral ossification without a clearly understood aetiology. this disturbance can eventually lead to the formation of semi lose or even completely loose fragments within a joint.
72
What is endochondral ossification?
Endochondral ossification is the process of transformatio from the primordial cartilaginous skeleton into the bone coupled with simultaneous growth. ossification of the primary centres of ossification in the diaphysis of long bones occurs early in foetal life, however, ossification of the secondary centres of ossification at the epiphysis continues after birth. The cartilage cells of the physis and epiphysis proliferate and hypertrophy then undergo apoptosis followed by calcification of the cartilage and deposition of primary bone which is subsequently modelled into trabeculae.
73
What are the etiological factors involved in Osteochondrosis?
Biomehanical - loading plays a role.
Failures of vascularisation - blood supply to growth cartilage is provided by the cartilage canals. it has been suggested that disruption of this blood supply can lead to cartilage necrosis where vessels traverse the ossification front.
Exercise - this is known to steer the functional adaptation of cartilage to its topographically heterogenous character during the first year of life. exercised foals have lower incidence of OC. may have effect on final appearance of lesions but does not seem to be important in the primary pathogenesis.
Nutrition - hormonal factors & growth rate, dietary copper thought to have an effect on final outcome. High calcium did not increase levels of OC but high levels of phosphorous results in more esions.
Genetics - lesions rarely found in ponies and feral horses. has a polygenetic trait with a complex method of inheritance.
74
Where is OC most commonly seen?
In the tarsus, stifle and metocarpophalangeal joints. Tarsocrural in warmbloods more common, femoropatellar joint more common in thoroughbred. ALWAYS occur at certain predilection sites within a joint.
Tarsal - cranial end of the Distal intermediate ridge of the tibia (DIRT), distal end of the latral trochlear ridge of the talus, medial malleolus, medial trochlear ridge of the talus.
Stifle - lateral trochlear ridge of the femur, trochlear grooove, distal ed of patella.
Metacarpophalangeal - dorsal edge of sagittal ridge of metacarpus.
75
What are the clinical signs and diagnosis for OC?
clinical signs include lameness and synovial effusion usually in yearlings. sometimes in less severe cases clinical signs coincide with the onset of training. lameness can var from subtle to obvious with owners sometimes reporting that the horse has difficulties getting up. diagnosis is usually based on clinical signs and radiography. Lesios of the intermediate ridge of the tibia are best visualised on the DMPLO. lesions of the lateral trochlear ridge of the talus are best visualised on the DMPLO. Femeropatellar OC can be identified o the lateromedial and CaLCrMO projections. ultrasound is more sensitive for identifying the less common OC of the medial trochlear ridge of the femur.
76
What is the treatment of osteochonrosis?
Non surgical management consists of rest and controlled exercise. administration of NSAIDS ad intra articular medications have not been shown to be of benefit for OC cases. given the nature of the disease process conservative management can only be expected to be successful in very young animals or where lesions are mild. Surgical management is the treatment of choice in most cases. arthroscopic fragment removal is superior to arthrotomy as soft tissue trauma is reduced. the convalescent period is shorter and the functional an cosmetic recovery is better. additionally arthroscopy is associated with significantly fewer post operative infections.
77
What is the cause of laminitis?
Carbohydrate overload (grass, cereals)
Septicaemia/endotoxaemia (due to endometritis, colitis etc)
Mechanical (excess weigh bearing, severe prolonged lameness contralateral limb, galloping on cobbled streets),
Cortcosteroid administration
Cushings disease, hypothyroidism
Fat ponies and horses especially at risk, peak incidence at times of lush pasture growth.
78
Describe the pathogenesis of laminitis
Acute laminitis is the result of systemic disease (exception being mechanical). laminitis can be experimentally iduced. After noxious stimulus (eg stomach tube with excess carbohydrate) the development period lasts 2-3 days before clinical signs appear. During the development phase various inflammatory mediators act on the laminae. Excess carbohydrate in caecum causes increase in lactic acid producing bacteria, drop in caecal pH damage gram negative bacteria. endotoxin release into circulation. Peripheral vasoconstriction and activation of a-v shunts, decreases laminar perfusion, exacerbated by microthrombi. Laminar ischaemia causes necrosis and loss of pedal bone support. the dorsal laminae are vascularised last within the foot so they are most affected. oce the lamine are damaged the pull of the DDFT is no longer resisted and the bone rotates. if all laminae are affected at the same time as can occur in acute and very severe laminitis, then complete laminar separation may result and the peal bone will sink ventrally without rotation or the whole hoof capsule can even be shed. A more recent theory postulates that systemic disease activates proteolytic enzymes (mainly matrix metalloproteinases) which unravel type IV collagen that connects the hoof wall laminae to those of the pedal bone with the same sequence of events thereafter.
79
What are the clinical signs with acute laminitis?
Typical cases adopt a saw horse stance, with the fore feet placed forwards and the hind limbs under the body. this is because boh frot feet are painful, especially the toes. This is a condition affecting primarily the front feet but severe cases have all 4 feet affected, although the fore feet are usually worse than the hinds. Depressed, iappetant, increased HR and RR. Markedly increased digital pulsation, heat in feet, painful across sole to pressure from hoof testerss (if rotation has occurred then pain will be worst just dorsal to frog and sole may become convex at this point), coroary band depression.
80
What are the clinical signs in chronic laminitis?
Intermittent bouts of lameness, flat or convex sole, seedy toe and abscesses comoon. prominent hoof wall rings, narrowing at dorsal hoof wall (ddx form nutritional rings)
81
What should you do when presented with acute laminitis?
Remove the potential causes eg placenta, pasture, give liquid paraffin if appropriate. Support the feet by using styrofoam support pads, very deep bedding (sand or peat is better than shavings), once lameness improves, use glue on plastic shoes. Give analgesia, ACP QI for vasodilation effect. Feed hay only & farriers formula & methionine to promote hoof growth. many other treatments used but oof dubious efficacy: glyceryl nitrate, isoxsuprine, ice or cold water, hot water, aspirin or heparin for anticoagulation. Take radiographs to establish severity of the condition and provide baseline for monitoring progress. lateromedial views with markers to indicate position of coronary band and point of frog. measure angle of rotation ad founder istace. prognosis worse with increasing values as well with severity of lameness, solar prolapse and increasing number of feet affected.
82
What should you do in chronic laminitis?
Trim the feet - they are often overgrown. Use a shoe - egg bar, reverse, heart bar or wide webbed normal shoes. consider surgery - dorsal hoof wall resection or ALDDFT or DDFT transectionn.
83
What are your differentials when presented with acute severe lameness in the horse?
```
Subsoolar abscess/solar penetration
Septic joint/bursa /sheath
Subluxation/luxatio
Severe tendon or ligament strain/rupture
Radial paralysis
upward fixation of the patella
Cellulitis
Rhabdomyolysis
```
84
Describe your initial assessment of acute severe lameness
Horse may be recumbent because exhausted/winded. Lameness may improve rapidly if fracture is non displaced. look for wounds. in large animals, crepitus is only evident if the fracture is displaced. can take several days for fracture to be evident radiographically. Avoid local anaesthetic techniques. Take sufficient radiographic views.
85
What are the different types of fractures?
Incomplete/ complete (displaced/ no displaced), avulsion fracture, chip (one joint surface involved), slab (two joints involved), stress fractures, salter harris fractures.
86
What are stress fractures?
Microcrack formation with fatigue . during process of remodelling bone is weakened > micro fractures occur. During fatigue, muscles relax tendons which provide support to joints relax, abnormal range of movement > increased strains > microcracks coalesce and cause fractures.
87
What is direct bone healing?
Stable in constant bone with a gap <11mm heals by osteoclasts remove damaged bone. Osteoblasts create new haversian systems directly across fracture lines.
88
What is indirect bone healing?
Gap or movement between bone ends. Periosteal callus forms to stabilise. Gap haematoma > fibrous tissue > mineralisation, intense remodelling.
89
Describe impaired bone healing types delayed union, oon union and mal union
Delayed union - healing is progressive but at a lower rate - 4 months in adults, 3 months in foals.
Non union - healing/repair process has stopped but bone continuity has not been restored. Vascular non union: capable of biologic repair but displacement, instability. Avascular non union: loss of fragments, aseptic necrosis. Infected non union
Mal union - healing of bone in an abnormal position (functional or non functional).
90
What are the most common fractures in horses?
In 1st opinion/mixed -- splint bone, distal phalanx, skull fractures
Common in racehorse practice: cervical fractures, distal third metacarpal, carpal, proximal phalanx, pelvis and many more..
91
What factors determine whether a fracture can successfully be treated?
How much weight does the bone normally bear, is a joint involved, degree of comminution & displcaement, contamination, chronicity
92
Describe how proximal phalanx fractures present and hoow to treat them
Common racehorse injury - Saggital ridge of distal MC screws into proximal p1 at speed. sudden onset severe lameness. lameness may improve within days if non displaced. Swelling, pain on passive manipulation and fetlock effusion. crepitus only evident if very commiuted. Treatment options rage from fixation using one or several lag screws to arthroscopic fragment removal or half limb cast. Prognosis depends on fracture type and quality of repair but many horses will return to racing and repair is usually undertaken with that aim, not just salvage. Prerequisite for successful surgical repair is at least one strut of bone which extends from fetlock to pastern.
93
Describe how pedal bone fractures occur and the clinical signs
Direct hoof trauma eg concussion (kicking wall), landing on uneven surface/object, nail penetration through sole, fast work on hard tracks ( standardbres/trotters), less commonly due to hyperextension of the coffin joint, osteitis, laminitis. Clinical signs - acute severe lameness - may increase in first 24 hours. Increased digital pulsatio. May have heat in foot, solar pain on hoof testers, pain on flexioon, may have coffin joint effusion but only i fracture is articular. Signs subside slowly - horses usually walk sound after 4-8, can remain lame at diagnosed.
94
Describe how to treat the different types of pedal fractures
Type 1 - non articular wing fracture- treat by hoof immobilisation, average healing time = 11 months. good too excellent prognosis.
Type II - conservative treatment, average healing time 12 months. 50% prognosis for return to soundness. worse prognosis for older horses - neurectomy. Surgical treatment possible.
type III - surgical treatment - requires good aseptic technique, requires expertise and experience, Conservative treatment as a salvage procedure or for failed surgical repairs.
Type I fracture - lag screw fixation if large, arthroscoopy/arthrotomy for removal if smaller. Main long term complication = OA of DIP joint.
Type V - comminuted fracture, usually poor prognosis, usually some bad underlying pathology
Type VI fracture - solar margin fracture. often secondary to laminitis. other common cause is penetrating foreign body. conservative treatment unless infected. Treat primary cause.
95
Describe how splint bone fractures occur and the treatment
Proximal, mid or distal split bone fractures.
Fractures of the distal third - occur spontaneously - avulsion fractures?, external trauma, such as kicking especially to the lateral splint bone, or interference especially to the medial splint bone in the forelimbs.
Proximal fractures - caused by kicks to the lateral aspect of the hindlimb, concurrent injury of adjacent structures. MT3, suspensory ligament.
For distal or non complicated proximal fracture - conservative management. approx 76 percent of distal splint bone fractures without concurrent desmitis return to previous exercise.
Proximal intra articular fracture - use internal fixation
Fracture of mid portion - segmental ostectomy - excellent outcome
Open fractures - treated initially as open wounds, systemic and regional AB, lavage. Chance for successful healing is 3.5 times worse than with closed Fractures.
Removal - oof the distal 2/3 of the splint bone is safe. < proximal 1/3 of the split bone remaining > internal fixation. Entire Mt4 can be removed however the surgical outcome with this procedure is only 60 percent return to previous exercise. comminuted fractures of MT4 - usually no difference in surgical versus conservative treatment outcome, survival and return to exercise, other than conservative treatment tends too be cheaper.
96
What are the clinical signs of an olecranon fracture and how do these usually occur?
Affected animals have characteristic dropped elbow stance due to disruption of stay apparatus. Ddx from humerus fracture and radial paralysis.Usually the result of a kick injury with or without a wound. the olecranon is most frequently affected region of ulna ( types of which types III-V most common) can have considerable concurrent soft tissue injury/contaminatio. splint with carpus fixed in extension to allow weight bearing. Can be treated conservatively with non displaced non articular fractures i.e type V having best prognosis. Successful surgical treatment improves prognosis and allows earlier return to exercise therefore is optimal in most cases. Surgical repair of types III - V. a plate is contoured to the caudal aspect of the ulna after fracture reduction. aim for at least three screws proximal to the fracture and 4 distal. Plate removal is not necessary unless complications occur or the animal is <18 months old. Assisted recovery is vital.
97
When should you start to suspect a fracture?
If you cannot obtain pus from the foot after 1-2 days of poulticing max. the horse is lame at the walk (perhaps has improved a bit), there is obvious limb deviation, there is pain or oedema over a bone with or without a wound, there is a history of a kick or other severe trauma, or it is a racehorse.
98
What is the function of a tendon?
Tendons passively transfer force from muscle to bone to effect locomotion whereas ligaments restrict distraction of two bony surfaces.
99
How do you determine which structures ar einvolved in a tendon and ligament disease in horses?
Look at palmar aspect of metacarpus, it should be perfectly vertical with no evidence of bowiing, look at the level of the metacarpophalangeal joint, it will be dropped if there is significant injury to the SDFT. palpate all the palmar tendons and ligaments with the limb loaded and unloaded checking for heat, pain and adhesions. if the horse has sustained a wire wound the extent of thee tendon involvement can be determined by assisting the position of the foot and fetlock. if the SFT alone is fully transected then the metacarpophangeal joint will be dropped when the limb is loaded. if the DDFT and SDFT are transected then the horse will knuckle the toe upwards, when the SDFT, DDFT and SL are transected the horse has a plantarograde stance and metacarpophanageal joint bears weight.
100
Describe the pathogenesis of superficial digital flexor tendinopathy?
High speeds, hard grounds, fatigue, wight of horse and shoe. clinical superficial digital tendinopathy varies from individual collagen fibril slippage to single fibril or fibre rupture through to complete rupture of the whole tendon as the number of affected fibres increases. there are three main theories to describe the aetiopathogenesis of tendon injury:
1 - repetitive sub-threshold mechanical overstimulation resulting in microdamage and activation of degradative enzymes and extracellular matrix destruction. (most commonly accepted)
2. Under-stimulation - loss of local homeostatic strain results in activation of degradation enzymes (if never exposed too sress, more prone to dramage)
3. aberrant differentiation of resident progenitor cells causing lipid, cartilage or bone formation within the tendon and weakening mechanical properties.
101
How is diagnosis of superficial digital flexor tendinopathy made?
Horses typically present acutely severely lame with a soft painful bowed tendon in the mid canon region. when the limb is loaded the MCPJ can appear dropped if the SDFT injury is severe. Diagnosis is based on ultrasonography carried out 10-14 days after initial injury to confirm the extent of the fibre damage. tendons should be evaluated in both transverse and longitudnal. a central corse lesion is usually apparent (an anechoic black area within hyperechoic white tendon).
102
What is the treatment for superficial digital flexor tendinopathy?
There are 3 phases of tendon repair and treatment should be targeted accordingly. the acute inflammatory phase, the subacute fibroplastic phase, the chronic remodelling phase. Acute management in the inflammatory phase involves strict box rest, cold hosing for 15-20 minutes twice daily, supportive bandaging, non steroidal anti inflammatory medication (phenylbutazone) with controlled walking exercise introduced as soon as the horse is sound at the walk. The aim of treatment in the remodelling phase is to promote parallel longitudinal fibre alignment. Conservative management (12-18 months box rest and controlled exercise alone). typically b ox rest 0-8 wees the 9-32 weeks walking in hand, 32-50 weeks - begin to introduce canter work, from 52 weeks until full training, racing can commence. Intralesional treatments include hyaluronan, beta aminoproprionnitrate, bone marrow derived mesenchymal cells, adipose derived stem cells, platelet rich plasma thought to increase the metabolic activity and advance the maturation phase of repair, bone marrow aspirate, insulin like growth factor 1, polysulphated glycosaminolycans.
Surgery - desmotomy of the accessory ligament of the SDFT.
Thermocautery (pin or bar firing)
103
How does deep digital flexor tendinopathy occur?
Less common than injury to the SDFT injury but can occur at several locations;
Within the hoof capsule
Within the digital flexor tendon sheath
Within the tarsal sheath
Within the carpal sheath (associated with osteochondromas)
Associated with desmitis of the accessory ligament of the deep digital flexor tendon.
104
How is diagnosis of Deep digital flexor tendinopathy made and how is it treated?
Injury to the DDFT within the hoof capsule is most common in horses that jump and pleasure horses. clinically cases present with sudden onset severe unilateral lameness that resolves and recurs when exercise is introdued. lameness can sually be abolished by palmar digital analgesia. Ultrasonography is usually only useful if the DDFT lesions extends proximally to the level of the pastern. definitive diagnosis is made using magnetic resonance imaging with the horse standing and sedated. Three times of lesions are described within the hoof capsule (dorsal fibrillation, core lesions and sagittal splits). treatment is focussed on box rest, controlled exercise and corrective farriery. (raising the heels reduces the tendon on the DDFT but increase the tension on the SDFT and SL). Prolapse of tendon fibres into the navicular bursa can be treated surgically. Injury to the DDFT within the DFTS is most common in horses that jump. Marginal tears present with effusion of the DFTS ad sudden onset lameness. lameness is usually improved following intrathecal analgesia of the DFTS.
105
What is suspensory ligament desmopathy?
Can fail at several locations;
1. complete breakdwn when both proximal sesamoid bones fracture in the racehorse. horses pull up non weight bearing lame with a dropped fetlock, radiography can demonstrate bilateral PSBB fracture.
2. PRoximal suspensory desmitis in the forelimb - usually present as bilateral lameness with the lamer leg on the outside circle. Hind limb PSD more common in dressage hrses with an upright hock conformation.
3 - mid body suspensory desmitits
4. suspensory branch desmitis
5. Desmititis of the distal sesamoidean ligaments.
106
What is desmopathy of accessory ligament of the deep digital flexor tendon?
Present clinically as acute onset moderate to sever lameness with swelling of the ALDDFT. possibly a higher incidence in ponies and horses that jump. the typical ultrasnographic diagnosis demonstrates enlargement of the ALDDFT rather than core lesion formation as seen in the SDFT. Treatment is based on cotrolled walking exercise and box rest.
107
What is DIPJ collateral ligament desmopathy?
Recurrent forelimb lameness usually with no localising clinical signs. severe cases demonstrate palpable enlargement of the collateral ligament of the distal interphalangeal joint. lameness improves following PDNB but often requires ASNB to fully abolish lameness. some cases are apparent on ultrasonographic or scintigraphic evaluation but definitive diagnosis requires MRI. treatment is aimed at correcting hoof imbalance and maintaining box rest and controlled exercise for 6-12 moths. prognosis for return to athletic function is poor.
108
What is osteoarthritis?
It represents a progressive condition caused by gradual loss of articular cartilage usually with concomitant changes in the subchondral bone and synovium. OOA is also known as degenerative joint disease and osteoarthrosis.
109
Describe the anatomy of a synovial joint
A synovial joint consists of apposing hyaline articular cartilage covered surfaces resting on compliant subchondral bone plates that are in turn supported by cancellous bone. the synovial cavity is lined with synovium and held in place by the fibrous joint capsule and supporting ligaments. Hyaline cartilage is composed of water, type II collagen, proteoglycans and chondrocytes. The proteoglycans in cartilage draw water into the extracellular matrix and provide compressive stiffness and the arrangement of collagen fibrils provides tensile stiffness. Degradation is facilitated by matrix metalloproteinase enzymes and their proteolytic action is controlled by tissue inhibitors of metalloproteinases. These enzymes exist in a state of dynamic equilibrium, long term disruption of this balance between MMPs and TIMPs will have pathological consequences and lead to osteoarthritis.
110
Describe the pathogenesis of osteoarthritis?
Osteoarthritic disease Process can originate from various causes with trauma and synovitis being the most common as a result of overuse or poor conformation, leading to abnormal forces on normal cartilage. the alternative situation is normal forces on abnormal cartilage (young horses with osteochondrosis ) resulting in OA. macroscopic changes of the articular surface indicative of osteoarthritis include fibrillation, wear lines and erosion of the shiny white cartilage eventually down to Subchondral bone in severe cases. The subchondral bone cam become remodelled with the presence of osteochondral lesions and osteochondral splitting. these macrosopic and microscopic changes result from disruption to the normal equilibirum of the proteolytic MMPs and TIMPs.
111
How can osteoarthritis be managed medically?
Once hyaline articular cartilage is damages it is not capable of regeeration, deep cartilage lesions heal spontaneously by a progression from granulation to fibrous tissue that is remodelled to fibrocartilage. at 12 months post injury the type II collagen approaches normal but the proteoglycan levels are only about half that of normal. Treatmet;
1. Palliative drugs that reduce the pain and inflammation
2. Disease modifying osteoarthritis rugs that have a chondroprotective function so acting to slow the progression of the disease.
112
Which drugs are commonly used in osteoarthritis to manage medically?
NSAIDs - anti inflammatory agents that inhibit COX and reduce prostaglandin production. PBZ commonly used orally. Also flunixin meglumine, carprofen, meloxicam, ketoprofen.
Intra articular corticosteroids - potent anti inflammatory agents and they inhibit inflammation at all levels. Pan relief is attributed to inhibition of prostaglandin synthesis specifically by inhibiting the enzyme phosphor lipase A2. The 2 widely available corticosteroids for intra articular injection are triamcinolone (TA) and methyl prednisolone acetate (MPA).
Hyaluronan - HA is a large nonsulphated glycosaminoglycan component of synovial fluid responsible for viscoelasticity, boundary lubrication and steric hinderance. it is also an important component of proteoglycan in the cartilage matrix providing compressive stiffness. Thought to reduce neutrophil chemotaxis and phagocytosis, reduce PGE, IL1 and bradykinin production and scavenge free radials. HA ca be administered IV or Intra articularly.
PSGAGS -- polysulphatedglycosaminnoglycans - Adequan contains PSGAGS manufactured from a animal source (chondroitin sulphates extracted from bovine trachea). Shown to promote chondrocyte metabolic activity and inhibit the effects of cytokines and prostaglandins on cartilage and are therefore classed as DMOADS. PSGAGS have bee shown to potentiate the subinfective dose of staph aureus and therefore intra articular administration should be combined with concurrent intra articular antibiotic administration.
Pentosan polysulphate - this is A PSGAG extracted from plants licensed for IM use in horses. shown to achieve therapeutic levels in synovial fluid following IM injection.
Oral neutraceuticals: chondroitin sulphate and glucosamine - component of cartilage and the precursor molecules.
Tiludronate - a bisphosphoate that regulates bone remodelling through inhibition of bone resorption and therefore postulated it should ameliorate the remodelling process active in OA.
Autologous conditioned serum - Autologous conditioned serum generated from the horses blood that is incubated in a syringe containing chromium coated glass spheres. the chromium spheres stimulate white blood cells to produce anti inflammatory cytokines.
113
How can osteoarthritis be managed surgically?
Arthroscopic debridement of meniscal or ligamentous injuries - Minimally invasive surgery is increasingly available in equine practice and purports significant advantages over arthrotomy including reduced morbidity and convalescent time. Coonsequently debridement of intra articular ligamentous or meniscal injuries is widely practiced. Exposure of collagen fibrils within the synovial environment is thought to potentiate inflammation and predispose to OA hence debridement and reduction of fibrillated ligament or meniscus is thought to be beneficial.
Surgical arthrodesis - essentially facilitated ankylosis or fusing of the joint to obliterate any joint movement and therefore reduce pain. the low motion joints such as the proximal interphalangeal joint and tarsometatarsal joint are amenable to surgical arthrodesis in the horse and return to mild athletic activity. The high motion joints such as metacarpophangeal joint and carpus can be surgically arthrodesed if the goal of surgery is pasture soudness.
114
Describe how injury to the hip may cause Lameness in the horse?
Osteoarthritis of the coxofermoral joint is a rare cause of lameness in the horse and is usually secondary to trauma. Confirmation of the diagnosis would require a positive intraarticular block and radiographic evidence of periarticular bone remodelling or acetabular rim fragments. Hip luxation is also rare. trauma is the cause. the hip is usually displaced craniodorsally. Limb is shortened and held in an outwardly rotated poosition. Greater trochanter is very prominent and crepitus may be palpable. Can be distinguished from fractured pelvis by rectal examination. Closed reduction can occasionally work in the acute cases. Open reduction and excision arthroplasty has been reported as a salvage procedure in ponies or small horses. Prognosis is poor.
115
Describe the usual history and clinical signs seen
Fractures of the pelvis are regularly encountered in racehorse practice and result from trauma. the most common sites are the ilial wing or s haft. Ilial wing fractures may be caused by a one off incidet, or result from stress remodelling in horses working at high speeds. Tuber coxae fractures are usually due to hitting a fence post or stable dooor. tuber ischium fractures result from kick injuries or falling backwars, while other fractures are usually the result of a bad fall. Usually a single traumatic incident but stress fractures of the ilial wing may have a history of recurrent and transient hindlimb lameness from fast work. Clinical signs depend on site of fracture and degree of fragment displacement and vary from moderate uni or bi lateral hindlimb lameness to severe lameness or inability to rise, with obvious crepitus. Assymmetry of the tubera sacrale or coxae may be present and will be permanent. some cases may appear ataxic but have no neurological abnormalities when assessed. chronic cases invariably have marked muscle wastage, most prominent in the gluteal region. a rare complication is damage to the iliac arteries caused by displaced bone fragments.
116
How is diagnosis of a pelvic fracture made?
Rectal palpation for pain, haematoma, displacement.
Scintigraphy and ultrasonography are now the imaging modalities of choice for pelvic fractures. Radiography rarely performed as general anaesthesia is required for good quality images, and recovery from anaesthesia may further displace a fracture.
117
What is the treatment for pelvic fractures?
Fragments of tuber ischii or tuber coxae may be surgically removed. For most other pelvic fractures, prolonged rest is the only treatment . euthanasia is indicated where lameness persists or the horse remains recumbet. Prognosis - fracture of tuber coxae & ischii and non displaced ilial wing fractures = good, fractures of ilial shaft, pubis or involving acetabulum = poor.
118
How is diagnosis of equine back problems made?
Diagnosis made following a detailed and exhaustive clinical examinatio, the main purpose of which is to detect other conditions that may be the cause of the reported clinical signs. A full orthopaedic examination should be performed. if the signs are evident only during riding, the horse should be observed with the regular rider. In addition to direct plapation of the soft tissue structures, the hypaxial muscles should be palpated per rectum. levels of enzymes CK and AST can be measured following a period of struous exercise to detect exertional rhabdomyolsis. Other sources of pain can produce similar signs, so check saddle fit, teeth, bridle/bit. Palpation of the back too assess the degree of flexio an extension is an important test of whether back pain is present. Normal horses will show reflex back movements in response to stimulation. Diagnostic medication - a useful diagnostic test is to place the horse on a course of phenylbutazone and monitor the response, if any, when riden. no improvement during medication suggests that the problems are not due to paiin, although a painful incident may have triggered the now established behaviour. Diagnostic imaging - if it has been established that the horse does have 'back pain' - then diagnostic imaging is used to localise the pain. radiography and scintigraphy are established techniques.
119
What are the congenital abnormalities of the vertebral column possible in the horse?
Excessive curvature of the thoracolumbar spine can be ventral or dorsal or lateral. most of these deviations are mild and clinically insignificant. severe congenital or developmental deviations of the spine are rare but when present can interfere with the athletic use of the animal. as there is no firm evidence that horses with mild conformational abnormalities of the back are more likely to develop back pain, these animals should be managed as normal.
120
How may soft tissue lesions of the thoracolumbar vertebral spine cause pain in horses?
The soft tissues of the thoracolumbar and sacral regions include the muscles (epaxial and hypaxial), the ligaments interconnecting the vertebrae and those attaching the vertebral column to the hindlimbs at the sacroiliac joint. Acute soft tissue injuries occur either as a consequence of repeated low grade trauma or in a single acute incident such as a fall. Clinical signs in the horse are notoriously varied and can often be attributed to pain elsewhere or equitation problems. horse with back pain due to soft tissue lesions may have concomitant uni or bilateral hindlimb lameness, shortened stride length affecting the hindlimbs, poor performance and deterioration in temperament or other behavioural signs such as bucking. There may be palpable focal enlargement of the supraspinous ligament. the other ligaments can only be examined by ultrasound. Clinical signs in horses confirmed as having pain in the sacroiliac joint region in a recent report included asymmetric muscling, reduced or increased movement of thoracolumbar spine and gait abnormalities.
121
What is impingement of the dorsal spinous processes?
Overriding dorsal spinous processes.. Known to cause thoracolumbar pain in horses. the spaces between the dorsal spinous processes in the mid thoracic or the lumbar vertebral column narrow dorsally and the opposing bone surfaces remodel. Affected horses usually resent flexion or extension of the back when manipulated. radiography will confirm the impingement. positive response to local anaesthesia is required for confirmation of the diagnosis. Surgical treatment or local injections of steroid or surgical removal of impinging processes. a novel surgical treatment - involves cutting the interspinous ligament through small incisios. this will result in resolution of pain with a faster return to normal exercise than with removal of the spinous processes.
122
What is spondylosis?
Often encountered as an incidental finding when radiographing the soft tissues of the thorax in adult horses. considerable amounts of bone form on the ventral surface of the thoracolumbar vertebral bodies - unclear whether this is a source of pain.
