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surgery 3 > Horse > Flashcards

Horse Flashcards

1
Q

Thrush

A
  • infection with subsequent necrosis of the frog and sulci
  • characterised by foul- smelling odour and soft and slimy horse
  • if it reaches sensitive lamine = podo dermatitis
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2
Q

Factors influencing thrush

A

Urine and faeces present in the box that dissolve the horn due to presence of fungi and bacteria, so horses kept in bad environments are prone to thrush

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3
Q

Management of thrush

A

Good stall hygiene, hoof care and local treatment

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4
Q

Treatment for thrush

A
  • remove damaged horn and disinfect hoof (iodine, copper sulphate and formalin in small cotton balls applied into the sulci)
  • if podo dermatitis, bandage with povidone-iodine is applied. With adequate stall hygiene and hoof care the prognosis is good
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5
Q

White line disease

A
  • white line with a poor-quality horn allows the colonisation of bacteria and fungi with the resultant loss of bond between the hoof and sole
  • characterised by a keratinoly tic process that originates on solar surface of the hoof
  • with separation, there’s an increase in tensional forces that results in inflammatory processes into sensitive laminate and subsequent lameness
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6
Q

Factors influencing white line disease

A

Warm and humid climate

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7
Q

Treatment for white line disease

A

Improving stall hygiene, removal of altered Horn and bactericidas and fungicidal agents

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8
Q

Hoof wall cracks

A
  • longitudinal disruption of the hoof wall, parallel with horn tubules
  • it can have several lengths:
    > whole hoof wall length, only próximal/only distal hoof wall
    > can penetrate only superficial or extend into sensitive laminate
  • horizontal hoof cracks (parallel to the coronet) - hoof crevices
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9
Q

Causes of hoof wall cracks

A

Poor horn quality, abnormal hoof angles (tension gradients within the hoof wall), poor hoof hygiene, excessive workload, local trauma (proximal), uneven heals

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10
Q

Diagnosis of hoof wall cracks

A

By visual inspection

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11
Q

Treatment of hoof wall cracks

A
  • depends on the location and depth of the crack
  • improve hoof care and shoeing
  • all altered horn adjacent to the crack is removed, the defect is cleaned, a hoof bandage application and application of a bar shoe with clips on each side of the crack
  • trimming ht hoof wall just below the crack (reduces the movement of coronary band -> production of better horn)
  • fixation devices can be used (umbilical tape, clam,p, metal plates) over the crack (reduces movements against each other and unites two separate parts)
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12
Q

Prognosis of hoof wall cracks

A

Guarded to good, since crack often recurs

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13
Q

Keratoma

A
  • thickening of the hoof horn that extends towards the inside of the hoof
  • mostly columnar shaped (parallel to horn tubules) and less frequently a spherical form
  • typically formed in dorsal to dorsomedial and lateral parts of the hoof wall
  • it’s a space-occupying mass causing pressure necrosis of P3 and soft tissue
  • it causes drainage from the white line or coronary band and lameness
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14
Q

Diagnosis of keratoma

A

Radiography (smoooth, circumscribed lysis of the P3), CT and MRI better for surgery

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15
Q

Treatment for keratoma

A
  • complete keratoma removal with hoof wall support
  • removal of abnormal hoof wall and sensitive laminate, hoof wall defect filled with artificial Horn and shoe with large clips on either side of the defect
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16
Q

Prognosis of keratoma

A

Very good after srurgical treatment

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17
Q

Acute hoof abscesses

A

One of the most common cause of lameness that are caused by penetration of bacteria across the hoof wall - infection of sensitive lamellar - purulent material inside the hoof capsule

Pressure inside the hoof capsule causes severe pain

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18
Q

Aetiology of acute hoof abscess

A
  • horseshoe nail too close or directly into sensitive lamine
  • rocks/street nail penetrating the sole, complication of a sole bruise
  • nail prick-penetration of the sensitive hoof structure by a horseshoe nail
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19
Q

Signs of acute hoof abscess

A

Severe lameness, fever, warm foot, swelling of the distal limb, marked positive response to hoof tester

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20
Q

Treatmentt for acute hoof abscesss

A
  • shoe removal, location hoof tester, povidoine bandage to soften the horn -> location and subsequent drainage of the abscess
  • removal of necrotic and undermined Horn, cleaning with iodine of max 3% H2O2, iodine-soaked gauged and bandage
  • NSAIDs and ATB if deep structures are involve
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21
Q

Chronic hoof abscess

A
  • breaking at the coronary band, invading the coffin joint, undermining the sole, penetrating distal phalanx
  • opening of the abscess and removal of the undermined horn
  • if P3 is involved, curettage of the affected bone
  • systemic and local ATB therapy is often needed
  • treatment takes several weeks to months
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22
Q

Aseptic podo dermatitis

A

Very common cause of lameness and represents bruising of horn tissue of the hoof

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23
Q

Cause of aseptic pododermatitis

A

Poor shoeing technique, hard, dry, uneeven ground

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24
Q

Diagnosis of aseptic pododermatitis

A

Clinical exam -> foot is slightly warmer, increased pulsation of palmar arteries, positive reaction on hoof tester palpation

Palmar digital or a axial nerve block release lameness

Radiohtphy

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25
Q

Treatment for aseptic pododermatitis

A

Remove the cause, moist bandage for 3-5 days, followed by a dry bandage

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26
Q

puncture wound

A
  • nails in middle of the frog are most dangerous
  • penetration object is always contaminated
  • puncture wounds must be treated as an emergency
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27
Q

signs of puncture wounds

A
  • severe supporting limb lameness, warm hoof, increased pulsation of digital arteries, severe pain on hoof tester
  • radiography before removal (clean, examine hoof and remove object)
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28
Q

treatment of puncture wounds

A
  • surgical debridement of puncture wound, flushing involved synovial structures under GA
  • deep digital flexor tendon (DDFT) resection if penetrated, curettage if bone involvement
  • broad spectrum ATB
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29
Q

coronary laceration

A

laceration at transition between skin and hoof capsule

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30
Q

cause of coronary laceration

A

overreaching or trauma

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31
Q

signs of coronary laceration

A
  • severe lameness, infection within hoof capsule, risk of permanent damage to horn producing structures  abnormalities of hoof growth
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32
Q

treatment of coronary laceration

A
  • removal of the damaged horn, cleaning, primary closure, and hoof cast application
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33
Q

canker

A
  • abnormal horn proliferation, frog region (sole, wall, skin) not a true neoplasm, chronic inflammation-parakeratosis
  • hypertrophy of sensitive laminae and degeneration of superficial horn and corium
  • hind limbs are more often involved one or more hooves
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34
Q

predisposition of canker

A

moist, long-standing thrush, spirhochaetae, anaerobic bacteria/bovine papilloma virus

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35
Q

signs of canker

A
  • lesions involve primarily the frog sulci but can spread to other structures
  • rubber-like horn, friable horn, soft, greasy, cauliflower like growths
  • odour is present and horse reacts painfully to pressure and horn bleeds easily
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36
Q

diagnosis of canker

A

histology of resected material to confirm the diagnosis

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37
Q

treatment of canker

A
  • difficult due to reoccurrence
  • surgical debridement of abnormal horn under local anaesthesia, bandage until new horn grows, disinfection solution, and metronidazole local
  • systemic ATB in more severe cases, pred
  • biotin and zinc feed supplements
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38
Q

third phalanx fracture

A
  • common in both foals and adults horses
  • more common in forelimbs
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39
Q

cause pf P3 fracture

A

trauma (excessive work, kick)

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40
Q

different types of P3 fracture

A
  • abaxial without joint involvement
  • abaxial with joint involvement
  • axial/sagittal and peri sagittal fractures
  • fractures of the extensor process
  • comminuted (multi-fragment) fracture with joint involvement
  • solar margin fractures
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41
Q

signs of P3 fracture

A
  • acute, moderate-severe lameness, warm hoof, increased digital pulse and pain on the hoof tester
  • blood in synovial fluid in distal interdigital joint (DIJ) if joint involvement
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42
Q

radiology of P3 fracture

A
  • false negative possible, several views needed
  • negative radiology: stall rest and repeat after 7-10days
  • scintigraphy, MRI and CT
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43
Q

treatment of P3 fracture

A
  • type I: fibreglass casts, bar shoe with large side clips, 2-4months stall rest with reasonable prognosis for athletic function
  • type II, III: conservatively or surgical, surgery with intraoperative imaging-CT, lag screw technique. Complications-infection, abscess formation; conservative stall rest 4 month
  • type IV-hyperextension, avulsion injury, separate centre of ossification, OCD, lameness, nerve blocking necessary, removal of small fragments by arthroscopy. Stabilisation of large fragments with lag screws
  • type V: fibreglass cast, surgery, poor prognosis
  • type VI: high prevalence in young thoroughbred foals, trauma, after chronic laminitis, conservative, fragment removal if infected
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44
Q

navicular syndrome

A
  • palmar foot pain
  • lesions are present at distal sesamoid bone and surrounding structure
  • podotrochlear apparatus: navicular bone (NB), collateral sesamoideum ligaments (CSLs), distal sesamoideum ligament-impair (DSIL), navicular bursa, distal digital annular lig
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45
Q

predisposition of navicular syndrome

A
  • warmbloods, thoroughbreds, quarter horse, rare in finnhorse, arab, Friesian, ponies
  • mature horses are more common
  • conformation: long toe/underrun heel, small foot and large body mass subtle pain-no extension of the forelimb, short, choppy gait
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46
Q

signs of navicular syndrome

A

mild to moderate uni or bilateral forelimb lameness, exacerbation on the circle

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47
Q

diagnosis of navicular syndrome

A
  • toe first landing
  • no diagnostic test for pathognomonic for palmar foot pain
  • radiography (x-ray, CT, MRI) grading system 0-4/degrees of lameness poor correlation with radiology
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48
Q

treatment of navicular syndrome

A
  • trimming/shoeing: correct, preserve mediolateral, dorsopalmar balance, easy breakover, protection palmar aspect from concussion, straight hoof-pastern axis, adding concussion protection to the foot, allow hoof expansion
  • NSAIDs, intraarticular medication
  • bisphosphonate therapy-reduction of bone resorption and modelling
  • extracorporeal shock wave treatment
  • surgical treatment: tenoscopy, bursoscopy-visualisation of tendon injuries, desmotomy, etc
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49
Q

laminitis

A
  • inflammation of pedal laminae – decreased support between hoof wall and P3. Breakdown of CT suspensory apparatus of P3 and inside hoof wall  laminar attachment unable to support P3  P3 displaces
  • clinical syndrome associated with systemic disease (endocrine, sepsis, SIRS) Endocrinopatic is a predominant form
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50
Q

cause of laminitis

A
  • important to find the underlying cause
  • EMS, oral sugar test, PPID, etc
  • bacteria: strep bovis: rapidly proliferated in carb overload and after died releasing cellular components that could potentially pass mucosal barrier
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51
Q

pathophysiology of laminitis

A
  • pathological deformation of the lamellar attachment begins during the developmental phase. Enzymes are normal constituents of lamellar cells and respond to stress and strains to keep repair and remodelling in equilibrium
52
Q

trigger factors of laminitis

A
  • insulin: hyperinsulinemia  vasodilation in peripheral circulation
53
Q

phases of laminitis

A
  • developmental
  • acute: severe lameness, shifting weight from affected feet, reluctant to turn, walk, etc
  • chronic: misshaped hooves, deformed hooves, development of divergent hoof rings
  • post-chronic
54
Q

signs of laminitis

A
  • pain and inflammation from ischemia of secondary lamellae  cause of lameness
  • divergent hoof rings  most sensitive clinical signs of subclinical chronic laminitis
  • hoof on the heel growing faster, widening the white line, lack of concavity of the sole, and concavity of the dorsal hoof wall
55
Q

diagnosis of laminitis

A
  • increased digital pulse, increase in hoof wall temperature  positive hoof tester test
  • radiology: high quality, LM, DP, quick changes, venograms
56
Q

treatment of laminitis

A
  • acute laminitis:
    o treat underlying cause
    o minimise further damage
    o provide analgesia
    o monitor progression – radiology every few days, weeks, monthly
  • cryotherapy: vasoconstriction during developmental phase reduces exposure to circulating trigger factors and slows the kinetics of lamellar enzyme activity. Proximal metacarpal region and distal in a slurry of crushed ice for 24 hours
  • digital blood flow therapy: drugs such as ACP, and isoxsuprine shouldn’t be administered during developmental phase
  • mineral oil: 4 litres every 4 hours should be administered in case of carbohydrate overload and activated charcoal
  • swing: plaster of paris
  • pain management: NSAID
  • dietary management: metformin, thyro-L, pergolide
  • surgery: DDFT tenotomy as a salvage procedure (refractory laminitis with P3 rotation)
57
Q

direct fracture healing

A

(contact, gap healing) – rigid fixation and anatomical reduction resulting in no space between fragments; minimal intra-fragment motion/no periosteal callus formation between fracture ends.

58
Q

indirect bone healing

A
  • through both endochondral and intramembranous bone formation/formation of periosteal callus between fracture ends
  • acute inflammatory response  haematoma, proinflammatory molecules  granulation tissue is between bone ends  template for callus (Cartilaginous tissue forms soft callus)
  • repair phase-soft callus resorption and replacement with hard callus and subsequent woven bone
  • remodelling phase-remodelling of hard callus (resorbed by osteoclast) into bone (osteoblast) central medullar cavity
  • long bone healing time: adults 4 months, foals 3 months
59
Q

evaluation of healing: radiography

A
  • standard modality, at 2-3 weeks widening of fracture gaps, fracture line smooth as healing progresses, callus become evident (4 weeks)
  • 8 weeks bridging bony callus
  • 12 weeks transition from woven to lamellar bone
  • nuclear scintigraphy, CT, MRI, US
60
Q

complications of healing

A
  • infection
  • sequestra – localised bone trauma and disruption of blood supply
  • delay or failure of bony union
  • laminitis – if continuous lameness after fracture fixation, important stabilisation of fracture to return weight bearing
  • fixation failure
  • contralateral angular limb deformity (foals)
61
Q

non-surgical fracture management

A
  • stall rest, external coaptation splits (changed every 3-4days), fissure penetrating the joint  surgical treatment
  • slings
  • cast-changes important due to soft tissue problems, fibreglass, daily palpation for hot areas, foul odour, skin damage and necrosis under cast (first changes 3-4days)
62
Q

surgical mangement of fractures

A
  • external fixation – rare, but more used transfixation pin cast
    o communited fracture (fx) phalanges, distal MCIII, MtIII and breakdown fx of the fetlock joint
    o multifragmentation fractures have better results than one
    o complications: pin tract infection, sequestrum, pin breakage, osteoporosis
  • internal fixation
    o returning the full function of limb
    o early function  movement of joints, prevention of cartilage degeneration. Prevention of disuse osteoporosis
    o important preservation of blood supply of fractured bone and surrounding soft tissue
63
Q

tendon injury

A
  • extrinsic = percutaneous laceration
  • intrinsic = overstrain
  • sudden overloading
  • preceded by a phase of degeneration/cumulative fatigue and microdamage- high stresses>structural integrity of the tendon  clinical injury
64
Q

risk factor of tendon injury

A

speed, hard footing, fatigue

65
Q

phases of tendon injury

A
  • acute phase (inflammatory) – intratendinous haemorrhage oedema, infiltration of leucocytes, the release of proteolytic enzyme/1-2weeks
  • subacute phase (fibroblastic) – few days after injury (overlap with inflammatory), angiogenic response, fibroblast synthesised scar tissue-higher content collagen III
  • chronic phase (remodelling) – gradual, incomplete to higher content of collagen I/different structure persist  biomechanically interior to the primary tendon, increased stiffness and more prone to injury
66
Q

signs of tendon injury

A
  • inflammation, injury preceding exercise, lameness, alteration in posture, swelling, increased temp of the area, palpation in weight bearing and pain on deep palpation
67
Q

diagnosis of tendon injury

A
  • US: major severity at 7 days after injury
  • acute lesion: hypoechogenecity, reduced striated pattern longitudinally
  • chronic: variable echogenicity, irregular striated pattern-fibrosis
  • MRI-DDFT lesions (foot), SL (proximal region)
68
Q

treatment of tendon injury

A
  • non-surgical (physical): cold therapy, compression, shoeing, controlled exercise (up to 12-18months), ECSWT, laser
  • non-surgical (pharmacological): NSAIDs, intralesional medication – polysulfate glycosaminoglycans, HA
  • surgical: tendon splitting acute lesion, accessory ligament desmotomy, tenoscoly, prox SL-neurectomy
69
Q

fibrotic myopathy

A
  • unilateral hindlimb abnormality/abrupt cessation of the cranial phase of the stride, foot jerked caudal before hitting the ground, at walk most obvious
70
Q

predisposition of fibrotic myopathy

A

quarter horses and mares

71
Q

cause of fibrotic myopathy

A
  • traumatic injuries  adhesions and fibrosis of the semitendinosus (most common)
  • semimembranosus, biceps femoris, facilis
  • trauma-extreme tension on caudal limb, slipping, etc
72
Q

diagnosis of fibrotic myopathy

A
  • inspection of characteristic gait, not painful
  • mechanical restriction of affected tight muscle
  • ultrasound – fibrosis
  • radiology – osseous abnormalities
73
Q

treatment of fibrotic myopathy

A
  • transection of fibrotic tissue (standing sedation), semitendinosus tenotomy near insertion on medial tibia (GA)
74
Q

signs of string halt/equine reflex hypertonia

A
  • gait abnormality is characterised by involuntary, exaggerated flexion of one or both hindlimbs
  • cranial phase of stride limb jerked toward abdomen
    1. Classic stringhalt (idiopathic)
  • isolated cases, unilateral most, trauma dorsoproximal metatarsus, don’t resolve spontaneously
    2. Australian/plant-associated (dandelion)
  • outbreaks at pasture, late summer, fall, typically bilateral
  • signs from mild tho reluctant to move to hold hyper flexed leg for several minutes
  • diffuse peripheral neuropathy affects long myelinated nerve fibres
  • many recover without treatment
75
Q

treatment of stringhalt/ equine reflex hypertonia

A
  • prevention of plant ingestion
  • medical: phenytoin (anticonvulsant)
  • idiopathy – spontaneous recovery is rare, so surgery
    o lateral digital extensor tenectomy and partial myectomy to the attachment to the long digital extensor
76
Q

prognosis of stringhalt/ equine reflex hypertonia

A
  • fair for Australian type, some recover some severe
  • guarded-favourable-unpredictable for classical
77
Q

peroneus (fibularis) Tertius pathologies

A
  • entire tendinous muscle between long digital extensor tendon and tibialis cranialis muscle
  • from extensor fossa with a long digital extensor muscle
  • peroneus tertius (PT) divides into 4 tendons at distal attachment (central, 3rd, 4th, tarsal, MtIII and calcaneus)
78
Q

treatment of peroneus tertius pathologies

A
  • avulsion fx-arthroscopy
  • 6 weeks stall rest
  • controlled exercise for 3 months
  • lacerations – wound management
79
Q

pathogenesis of equine osteoarthritis

A
  • cyclic loading of collagen network/chondrocytes exposed to physical forces -> injury, metabolic changes/subchondral bone: increased cytokines, decreased support/sclerosis decreased shock absorption/ A group of disorders with a common end stage:
    o progressive deterioration of articular cartilage; changes in bone and soft tissue
80
Q

diagnosis of equine osteoarthritis

A
  • clinical examination: history, lameness, examination: diagnostic analgesia, diagnostic imaging
81
Q

therapy of equine osteoarthritis

A
  • ¬NSAIDs, corticosteroids, hyaluronan-disaharide, surgery of joint disease release
82
Q

osteoarthritis of the distal tarsal joint (bone spavin)

A
  • most common acquired pathology of tarsus/one of the most common pathologies causing hindlimb lameness
  • compression and rotation of the distal tarsal joints contribute to disease
83
Q

predisposition of osteoarthritis of the distal tarsal joint

A
  • dressage, western performance, standardbreds, islandic horses
84
Q

pathogenesis of osteoarthritis of the distal tarsal joint

A
  • crushing of central and third tarsal bone in dysmature neonates  juvenile OA of the tarsus
85
Q

signs of osteoarthritis of distal tarsal joint

A
  • lameness  common toe dragging
  • reduced foot flight, short cranial phase of the stride
  • axial deviation during the cranial phase followed by a rapid abaxial deviation at ground contact
86
Q

diagnosis of osteoarthritis of distal tarsal joint

A
  • routine lameness examination, uneven wear of shoes
  • flexion test often positive
  • palpation  enlargement over the dorsomedial tarsus
  • intraarticular anaesthesia of tarsometatarsal and distal intertarsal joint
  • Radiographic views
87
Q

treatment of osteoarthritis of distal tarsal joint

A
  • corrective shoeing – medial hoof wall is shortened + horseshoe with a wider thicker outside branch
  • lateral wedges  decreases pressure on the medial side of the tarsal joint
  • extracorporeal shock wave therapy
  • medically-NSAIDs, intraarticular steroids
  • chemical fusion by intraarticular injection of sodium monoiodoacetate, ethyl alcohol  chondrocyte death, cartilage necrosis, joint collapse, and fusion of distal tarsal joints
  • cunean tenectomy
88
Q

predisposition of osteochondrosis

A

young horses, beginning training

89
Q

pathogenesis of osteochondrosis

A
  • thick epiphyseal cartilage irrigated by vessels through cartilage canals
  • gradual obliteration – chondrification
  • premature disruption of the vascular supply of growth cartilage  necrotic areas in cartilage layers – OC
  • biomechanical damage-anastomotic branches that run through ossification
90
Q

diagnosis of osteochondrosis

A
  • radiology, US, arthroscopy
91
Q

nutrition of osteochondrosis

A
  • imbalance in minerals and trace elements
  • excess in energy intake  hyperinsulinemia  effect on endochondral loss
  • OC horses, increase postprandial glucose and insulin response
  • low copper  low ceruloplasmin
  • lysl oxidase
92
Q

treatment of osteochondrosis

A
  • conservative: rest, change in nutrition, controlled exercise, up to 1 year
  • surgical: lose fragments removed and surrounding tissue debrided
  • polydioxanone pins fixation of larger fragments
93
Q

prognosis of osteochondrosis

A

dependent on joints (fair to good)

94
Q

septic arthritis

A
  • abnormal exposure to pathogens/ abnormal weakness of host defence
  • fulminant inflammation  severe clinical signs
  • synovial membrane hyperaemia
  • increased vascular permeability  extravasation of fibrin, efflux of macrophages
  • stap. aureus produces toxins and enzymes  neg. effect on joint tissue
  • SF form infected joint increased collagenease, caseinase: decreased synthesis GAG, PGs, HA
  • microorganism enter the joint
    o 1. hematogenous – pathogens via synovial membrane
    o 2. per continuitatem
    o 3. perforating trauma
    o 4. iatrogenic following i.a injections (<0.1%), arthroscopy (0.7%)
95
Q

signs of septic arthritis

A
  • joint distension/periarticular swelling
  • pain at palpation
  • reduced POM
  • high-grade lameness
  • wounds – signs can obscure clinical signs of septic arthritis
96
Q

diagnosis of septic arhritis

A
  • bacterial culture
  • identify causative pathogens
  • determine susceptibility for antimicrobials
  • aerobic/anaerobic
  • blood culture medium
  • culture of synovial membrane biopsies
  • imaging: radiology; CT, MRI, scintigraphy
97
Q

treatment of septic arthritis

A
  • emergency arthroscopic lavage, synovial membrane debridement
  • antimicrobial therapy
  • local-regional limb perfusion, i.a, ATB-impregnated beads, collagen sponges
  • joint lavage, drainage
  • anti-inflammatory
  • rehabilitation: restriction of motion in acute stages. Physical therapy prevention of stiffening of periarticular area
98
Q

prognosis of septic arthriits

A
  • adults: 80% for dismissal, 70% full return to function
  • foals less favourable
  • fair to good for survival
99
Q

diagnosis of lameness

A
  • similar gait deficits exist for a variety of pathologies
  • application of diagnostic analgesia to localise source of pain causing lameness
  • clinical relevance
  • degree of lameness, gait characteristic, palpation findings  differential diagnosis
  • pathognomonic signs are rare  diagnostic analgesia mandatory
100
Q

characteristic gait of lameness

A
  • immediate and straightforward recognition and localisation of the problem
  • sweeny, fibrotic myopathy, upward fixation of the patella, stringhalt, shivers and radial nerve paresis
101
Q

lameness distribution

A

forelimb more common

102
Q

assessment of symmetry

A

comparison normal-abnormal sides
atrophy –> disuse/neurogenic

103
Q

swelling (lameness)

A

joint effusion, oedema, cellulitis, bleeding, fibrosis and bony swelling

104
Q

angular deformity (lameness)

A

developmental orthopaedic disease

severe forelimb lameness <2 years -> contralateral varus

luxation, subluxation of jointa

105
Q

foot size (lameness)

A
  • chronic lameness  disparity of foot
  • smaller foot ipsilateral to lameness (contracted, upright)
  • uneven feet
106
Q

posture (lameness)

A
  • information about the source of lameness
  • pointing
  • constant shifting of weight
  • dropped elbow
  • gastrocnemius rupture
    o extensive hock flexion while stifle in extension, point of hock drops, disruption of caudal component of reciprocal apparatus
107
Q

palpation (lameness)

A
  • systematic
  • bearing weight, again with elevated limb
  • be aware of false positive results
  • pressure
  • signs of inflammation: heat, pain, redness, swelling, loss of function
  • manipulation, flexion, extension
  • ROM, crepitus, skin lesions
  • foot temperature (palm side of hand)
  • strength of digital pulse/increased, elevated
  • complete absence-aortoiliac thromboembolism
108
Q

foot evaluation (lameness)

A
  • toe and heel length
  • hoof capsule conformation, condition and integrity
  • type of shoe and shoe position relative to the hoof capsule
  • hoof and pastern angle
  • medial-to-lateral hoof balance
  • coronary band conformation
  • palpation of coronary band, foot cartilage
109
Q

hoof tester examination

A
  • essential
  • amount of force varies
  • false negative and false positive possible
  • sole sensitivity, nails, frog, heels
  • 19/42 horses with navicular pain respond to hoof tester
110
Q

movement gait

A
  • GAIT-manner or style of walking
  • natural gaits: walk, trot, gallop (canter-collected gallop)
  • artificial gaits: pace, amble
  • BEAT-number of foot strikes in single-stride cycle
111
Q

walk

A
  • symmetrical
  • 4 beats gait
  • lameness evaluation
  • RH,RF,LH,LF
  • 1.37-1.82m/s
112
Q

trot

A
  • symmetrical
  • 2-5m/s
  • diagonal
  • 2 beat gait, moment of suspension between impact of each diagonal pair
  • essential for lameness evaluation
  • RH-LF, SUSP, LH-RF, SUSP
113
Q

centre-gallop

A
  • asymmetric
  • canter 3 beats (synchronised diagonal phase)
  • gallop 4 beats
  • leading lib- the last limb that strikes the ground before suspension
  • right: LH, RH, LF, RF, SUSP
  • 9-20m/s
114
Q

lameness evaluation

A
  • leading the horse
  • surface characteristics
  • horse temperament
  • riding evaluation
  • asymmetries
  • primary or base lameness
  • possibility of involvement or more limbs
  • classification:
    o supporting = pain during weight bearing, most lameness, worse on hard ground and circle (inner lame limb-worse)
    o swinging = primary affects the way the horse carries limb, shortening of cranial phase of stride, mechanical lameness, more evident when outside the circle
    o mixing
  • grading
  • alteration of phases of the stride
  • presence of abnormal limb fight
115
Q

AAEAP scale (grading)

A
  • 0 = lameness not perceptible under any circumstances
  • 1= lameness is difficult to observe and is not consistently apparent, regardless of circumstances
  • 2= lameness is difficult to observe at a walk, or when trotting in a straight line, but consistently apparent under certain circumstances
  • 3= lameness is consistently observable at a trot under all circumstances
  • 4= lameness is obvious at walk
  • 5= lameness produces minimal weight bearing in motion and/or at rest or a complete inability to move
116
Q

forelimb lameness

A
  • head nod increased during lame limb stance phase
  • head elevated when lame limb on the ground
  • head down when non lame limb on the ground
  • reduce in GRF
  • shortened stance duration-walk
  • increase stance duration-trot
117
Q

hindlimb lameness

A
  • ¬asymmetry of the lame side of the body increases
  • left hindlimb lameness: vertical motion of left tuber coxae diminished during left hindlimb stance, increased during right hindlimb stance
  • large motion amplitude of tuber coxae on the lame side
  • sacrum: less lowering and lifting during stance of lame limb
  • moderate/severe lameness-head drops on diagonal limb
118
Q

compensatory lameness/false

A
  • dropping of head as compensatory mechanism for hind limb lameness
  • mimic ipsilateral forelimb lameness
  • apparent lameness on opposite end of body due to kinematic changes caused by pain in one leg
  • forelimb lameness-compensatory contralateral hindlimb lameness
  • hindlimb lameness- compensatory ipsilateral forelimb
119
Q

law of sides

A
  • false ipsilateral lameness  primary hindlimb lameness
  • false contralateral hindlimb lameness  primary forelimb lameness
120
Q

flexion test

A
  • manipulation, exacerbation of lameness, lower limb flexion test, fetlock flexion test, carpal flexion test, upper limb manipulation, hindlimb flexion test
121
Q

diagnostic analgesia

A
  • localising the source of pain
  • perineural, intrasynovial, infiltration techniques
  • local anaesthetics
  • start distally in the limb and work proximally
  • improvement of 70-80% a positive response
  • smallest volume (1-5ml)
  • anatomy, basic technical skills, clinical experience
  • false positive, false negative
122
Q

objective lameness diagnostic

A
  • limitation of human eye
  • kinetic methods
  • kinematic methods: video assisted, inertial sensors
  • valuable for clinical use
123
Q

radiology

A

o information about bones and joints
o soft tissues  tendon, ligaments and joint capsule insertions
o sufficient number of views

124
Q

ultrasound

A

o diagnosis of soft tissue injuries (muscular, vascular, tendon, sheath, ligament etc)
o assessment of fluid accumulation
o evaluation of bony surface
o monitoring of the healing progress
o isoechoic = structure is normal, hypo = less, anechoic = lesion mostly black

125
Q

scintigraphy

A

o functional evaluation of bone at time of imaging- early detection of bone injury
o highly sensitive – can detect 10-13g radiopharmaceutical In bone
o radioisotopes emits radiation-captured by scintillation camera
o bone scan phases (vascular, soft tissue, bone)

126
Q

CT

A

o images map tissue density in the subject
o contrast-media – areas of increased blood supply, intraarticular is often used to identify soft tissue lesions
o interventional computed tomography

127
Q

MRI

A

o osseous and soft tissue with detailed anatomical resolution and some physiological information

surgery 3 (6 decks)

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