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surgery 3 > orthopaedics > Flashcards

orthopaedics Flashcards

1
Q

patient stabilisation

A
  1. Check and stabilise vitals
  2. Perform thorough physical, orthopaedic, and neurological examinations
  3. Pursue initial diagnostics, including blood analysis, thoracic and abdominal radiographs and a FAST ultrasound
  4. Resolve any life-threatening issues, which means surgery may need to be delayed for several days due to conditions
  5. Administer proper analgesia as soon as possible
    - Approx. 12-24 hrs following presentation, animal must be thoroughly re-evaluated
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2
Q

orthopaedic exam starts with

A
  • History (can give info about cause of limping, about previous problems or pathological conditions)
  • information on animal (age, sex, breed and reproductive status)
  • clinical examination
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3
Q

Bernese mountain dog and lab predisposition

A

elbow and hip dyslplasia

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4
Q

newfoundland predisposition

A

cruciate ligament rupture

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5
Q

greyhound and basset predisposition

A

very rare for cruciate ligament rupture

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6
Q

spaniels predisposition

A

incomplete ossification of the humerus condyles (IOHC)

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7
Q

mini poodle predisposition

A

hereditary medial shoulder instability

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8
Q
  1. test for cranial cruciate ligament rupture
A

sitting test
tibia compression test
drawer test

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9
Q

test for collateral ligametns

A

varus/valgus test

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10
Q

test for meniscus

A

by crepitation which occurs during passive knee movements

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11
Q

sitting test

A
  • Unspecific and indicate a problem with hips and spine
  • Dog is reluctant to sit down if cruciate ligaments rupture so changes position
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12
Q

tibia compression test

A
  • Knee in mild flexion and metatarsus of same leg in dorsiflexion
  • Index finger of other hand is put on tuberositas tibiae
  • At dorsal metatarsus flexion, tibia is shifting cranially which index fingers register
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13
Q

drawer test

A
  • Index finger of one hand is put on patella and thumb of same hand behind lateral sesamoid bone, fabella
  • Index finger of other hand put on tuberositas tibiae and thumb on fibula head
  • Moving lower leg relative to upper leg, causes shift
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14
Q

varus/valgus test

A
  • Thumb put on fibula head, index finger along the medial side of articular capsule
  • Using one hand to stabilise femur and other holds the end of tibia applying an inward force to joint (adduction)
  • If lateral ligament is torn an “opening” of joint is apparent
  • Vice versa
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15
Q

test for hip instability

A

ortolani test
Barlow
barden

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16
Q

ortolani test

A
  • Dysplastic changes and subluxation of the hip
  • Lateral recumbency or on back
  • Knee and hip are at 90 degrees
  • Femur grabbed by knee, adduct and push towards pelvis whilst other hand fixes pelvis
  • The pressure on trochanter, reduces femur head into acetabulum and make a thump
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17
Q

barden test

A

o Lifting femur from body in lateral position
o Instable hip will shift from joint socket dorsally when femur is lifted

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18
Q

barlow test

A

o Dog on back
o Both femurs in perpendicular position relative to body and by pressing knees downwards, are being pushed ventrally towards hip

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19
Q

panosteitis

A
  • Young German shepherds
  • Self limiting disease of long bones of large and giant breed dogs
  • Commonly affects ulna, followed by radius, humerus, femur and tibia
  • Cause = unknown
    o Maybe excessively high dietary protein or calcium administration that causes protein accumulation
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20
Q

signalment of panosteitis

A
  • 5-12 months, can up to 5 years of age
  • Males more commonly affected than females
  • Airedale terrier, Irish setter, great Dane, saint Bernard, newfoundland, golden/lab retrieves, GSD
  • Dogs weighing more than 23kg at increased risk
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21
Q

diagnosis of panosteitis

A
  • Based on signalment, history, physical examination, radiographic findings
  • Physical examination
    o Shifting leg lameness and pain on palpation on long bones
  • Radiography
    o Acute phase – they can be normal
    o As it progresses: medullary pattern changes to coarser than normal trabecular pattern
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22
Q

differentials of panosteitis

A
  • Hypertrophic osteodystrophy, Osteochondritis dissecans, hip dysplasia, fragmented medial coronoid process and united anconeal process
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23
Q

treatment of panostieits

A
  • Doesn’t appear to affect outcome
  • Exercise restriction and analgesics
  • NSAIDs but if hospitalised, IV and injectable opioids
  • Steroids and ATB isn’t necessary and should be avoided
  • Prevent excessive protein
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24
Q

hypertrophic osteodystrophy

A
  • Skeletal scurvy, metaphyseal dysplasia, etc
  • Young large and giant breed dogs
  • Radius, ulna and tibia mostly affected and usually bilateral
  • Cause: unknown, could be infectious
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25
Q

signalment of hypertrophic osteodystrophy

A
  • 2-6 months
  • Male dogs predisposed compared with females
  • Great Dane, Irish setter, boxer, GSD, golden and lab retrievers, Weimaraner (heritable)
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26
Q

diagnosis of hypertrophic osteodystrophy

A
  • Characterised by painful swelling of metaphyseal region of long bones In appendicular skeleton
  • Patients often systemically ill with fever, lethargy, inappetence or diarrhoea
  • X-ray critical in confirming the diagnosis
    o Characterised by lucent line in metaphyseal region parallel to physis (double physis)
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27
Q

differential of hypertrophic osteodystrophy

A
  • Septic arthritis, septic physitis, secondary nutritional hyperparathyroidism, retained cartilage cores, hypertrophic osteopathy and Panosteitis
  • Secondary disorder most often associated with pulmonary neoplasia
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28
Q

treatment of hypertrophic osteodystrophy

A
  • Self-limiting in days to months, signs may last for months
  • Mild cases: supportive care, NSAIDs
  • Severe cases: hospitalisation (aggressive supportive care and opioids)
  • Complete and balanced diet, Vit C and Vit d (questionable)
  • Blood cultures for immunosuppressed patients – then ATB accordingly
  • Weimaraner puppies = corticosteroids
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29
Q

avascular necrosis of femoral head other name

A

legs-calve-perthes diseasee

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30
Q

what is legg-calve-perthes diseae

A
  • Non-inflammatory local ischemia of femoral head and neck = deformation and lameness
  • In any dog, but those less than 12kg of BW it’s called Perthes disease
  • Cause: hereditary, conformation, infarction of femoral head, hormonal influence, increased intracapsular pressure – none is accepted as definite underlying cause
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31
Q

signalment of legg-calves-perthes-disease

A
  • 4-11 months
  • No sex
  • Small breed mostly affected, toy and terrier breeds increased risk
  • Mini poodles and Westies, trait is autosomal recessive
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32
Q

diagnosis of legs-calves-perthes

A
  • Physical examination: mild-severe, non-weight bearing lameness of the pelvic limbs
  • Radiographs are usually diagnostic, CT advised
    o Shows progressive radiopacity of the lateral epiphyseal area of femoral head, followed by lysis of the femoral head in a “moth-eaten” or “apple-core” appearance. After lysis, femoral head flattens, creating the potential for femoral neck fractures
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33
Q

differentials of LCP

A
  • Capital physeal trauma, epiphystitis, septic physitis, osteomyelitis and neoplasia
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34
Q

signs of LCP

A
  • Crepitation during passive movements, ROM, loss of muscle, lameness
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35
Q

treatment of LCP

A
  • Rest for 4-8 weeks
  • Lameness resolved with rest and NSAID therapy
  • Surgical options: femoral head and neck ostectomy or total hip replacement
  • Due to lytic appearance, sample should be sent for histopathology to rule of neoplasia
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36
Q

prognosis of LCP

A
  • Post-op is good, lameness resolving in 84-100% of cases
  • Physical rehab after surgery may help ensure a positive outcome
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37
Q

multiple cartilaginous exostosis

A
  • Benign bone disease of multiple, cartilage-capped bony protuberances that arise from the surface of any bone formed by endochondral ossification
  • Mostly affected: vertebrae, ribs, and long bones
  • Cause = unknown
  • Condition affects both cats and dogs
  • Exostosis may undergo malignant transformation to chondrosarcoma or osteosarcoma
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38
Q

signalment of multiple cartilaginous exostosis

A
  • No known sex or breed predilection, maybe Great Dane, saint Bernard’s
  • Inherited as autosomal dominant trait and seen in young growing patients
  • Exostosis appears and enlarges before skeletal maturity
  • Cats, associated with FeLV
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39
Q

diagnosis of multiple cartilaginous exostosis

A
  • Based on physical examination and radiographic findings, with excisional biopsy and histologic examination important for definitive diagnosis
  • Physical examination – pain maybe if exostosis is associated with a tendon, ligament, vessels or spinal cord compression
  • X-ray – single or multiple bony masses with a thin cortex and medullary cavity that is confluent with the host bone and has a distinct trabecular pattern
    o Full body – recommended as a monitoring tool
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40
Q

treatment of multiple cartilaginous exostosis

A
  • Depends on size and location
  • Rest and NSAIDs
  • Surgery indicated for single or large exostosis
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41
Q

osteomyelitis

A
  • Inflammation and infection of the medullary cavity, cortex and periosteum of bone
    Chronic osteomyelitis there’s two specific entities
  • Sequestrum
    o Piece of dead bone that has become separate during the process of necrosis from normal or sound bone
  • Involucrum
    o Is a complication of osteomyelitis and represents a thick sheath of periosteal new bone surrounding a sequestrum
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42
Q

predisposing factors of osteomyelitis

A
  • Inadequate fracture stabilisation
  • Unsterile surgery
  • Prolonged operating time
  • Poor technique  soft tissue damage
  • Primarily immunocompromised patient
  • Contaminated wound, inappropriate ATB
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43
Q

pathophysiology of osteomyeltiis

A
  • Inflammation  oedema and vascular congestion  depriving osteocyte of adequate oxygen  osteocytic death
  • Compromised blood supply to bound and tissue allows establishment of bacteria
  • Inadequate blood  poor invasion of site by host defences and poor ATB perfusion
  • Unresorbed bone  sequestrum and may wall off  involucrum
  • Chronic infections  granulation tissue production  fistulae
  • Bacterial toxins  further tissue damage  further isolating of the body’s defence mechanismpa
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44
Q

pathogenesis of osteomyelitis

A
  • Neonatal primary osteomyelitis occurs near growth plates because of tortuous course of BV allows bacterial to settle and multiply  infection
  • Results from poor surgical techniques, prolonged operating time, excessive soft tissue damage
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45
Q

cause of osteomyelitis

A
  • Bacteria infection introduced during orthopaedic surgery or contamination from wounds
  • Associated with Staph, strep, e.coli, proteus, Pasteurella, pseudomonas and B.canis
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46
Q

signs of osteomyeltiis

A
  • Acute/chronic
  • Lameness, pain, abscessation at the wound site, fever, anorexia and depression
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47
Q

diagnosis of osteomyelitis

A
  • Radiography can reveal bone lysis, sequestration, irregular periosteal reaction, loosening of implants and fistulous tracts
  • Deep FNA, cytology and blood cultures
  • Discharging sinuses, swelling at surgery site, limb dysfunction
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48
Q

treatment of osteomyeltiis

A
  • Early ATB (culture and sensitivity is essential)
  • Stabilisation of fractures and excision of necrotic material/bone sequestrate
  • Surgery: if chronic osteomyelitis
  • Wound debridement, lavage and removal of loose implants are recommended
  • Open or closed wound drainage and delayed autogenous, cancellous bone grafting
  • Chronic, refractory cases – limb amputation may be warranted
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49
Q

prognosis of osteomyelitis

A
  • Variable and based on severity and chronicity of the infection
  • Appropriate antimicrobial therapy based on bacterial culture and ATB sensitivity testing is mandatory for successful results
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50
Q

panostetitis

A
  • GSD, golden retrievers, bassets, Dobermans
  • In dog – specific painful bone condition involving the long leg bones of large dog breeds
  • 5-18 months
  • Males over females
  • There’s 2 types of marrow (fatty marrow and blood cells)
    o Fatty marrow is replaced with fibrous tissue
    o Fibrous tissue then replaced by a woven bone (which is represented by fluffy opacites seen on x-ray)
    o Marrow cavity can be nearly obliterated by encroaching woven bone
    o Eventually, bone remodelling occurs
    o Building new bone and dissolving bone where it shouldn’t be
    o Bone tissue is re-structured back to normal
51
Q

cause of panosteitis

A
  • Unknown
  • Could be a normal dog that receives a bone inoculation of marrow from an affected dog
52
Q

signs of panosteitis

A
  • Painful during its flare-ups
    o Pain can last 2-5 weeks
  • Lameness can shift from one leg to another
  • Fever
53
Q

diagnosis of panosteitis

A
  • Cloudiness in bone marrow cavities is visible on radiographs
54
Q

treatment of panosteitis

A
  • Pain relief, until dog outgrows
  • NSAIDs
55
Q

classification of fractures

A
  • By anatomic location (articular, physeal, epiphyseal, metaphyseal or diaphyseal)
  • Subclassified on anatomic locations (condylar, supracondylar, trochanteric or subtrochanteric)
  • Based on radiographs
    o Incomplete: fracture through only one cortex
    o Complete: fracture through both cortices
    o Comminuted: multiple fragments
    o Segmental: two or more separate fractures
  • Displacement should also be recognised when classifying fractures
    o Full orthogonal radiographs are needed
    o Degree of displacement of the distal segment in relation to proximal segment
  • Incorporate level of contamination – whether it’s open or closed fracture
    o Open fractures:
     Type I: < 1 cm puncture; fragment briefly penetrated the skin
     Type II: > 1 cm puncture; external trauma
     Type III: extensive wound; soft tissues damaged or absent. Further classified as
  • Type IIIa: Adequate skin to close the wound
  • Type IIIb: (**bad ** soft tissue)insufficient skin to close (degloving injury)
  • Type IIIc: (circulation issues) compromised vascular supply to the skin
    o Salter harris fractures: are growth plate (physeal) fractures in immature animals. Type I less likely and VI more likely to have long-term effects on mature bone length
     SH I fracture: involves a fracture through the physis itself
     SH II fracture: involves the physis and extends into the metaphysis
     SH III fracture: involves the physis and extends into the epiphysis; considered an intra-articular fracture
     SH IV fracture: involves physis and extends into both the metaphysis and epiphysis; considered an intra-articular fracture
     SH V fracture: compression fracture through the physis
56
Q

primary - direct bone healing

A

o 1. Contact healing
 When defect between the bone ends is less than 0.01mm
 with contact healing, cutting cones – an osteoclastic tunnelling process- develop, resulting in direct formation of lamellar bone oriented in the normal axial direction of the bone
o 2. Gap healing
 When bone ends are less than 0.8mm-1mm apart
 Initial fracture site undergoes intramembranous bone formation, with lamellar bone oriented perpendicular to the axial direction of bone
 Fracture site remains relatively weak
 Haversian remodelling begins 3-8 weeks after fracture fixation, allowing bone to develop in a more longitudinal fashion

57
Q

indirect- secondary bne healing

A
  • Occurs in unstable fractures or fractures treated with external coaptation as a primary means of fixation
  • Formation of intermediate callus prior to bone formation
  • As bone heals, the tissue pass through different stages of increasing stiffness and strength
  • The greater the instability, the greater amount of callus
58
Q

forces (6)

A

bending, rotation or torsion, shear, compression and tension

59
Q

primary methods of fracture repair

A
  • Bone plates – effective for nearly all forces
  • Interlocking nails – effective against rotation, bending, compression and shear
  • External skeletal fixation – effective for nearly all forces
    o Linear fixators
    o Ring fixators
  • Intramedullar pins – effective for bending, marginal for shear, ineffective for rotation
  • External coaptation – weak against all forces
60
Q

secondary methods of fracture repair

A
  • Cerclage wire – useful for maintaining fracture apposition and counteracting rotational, shearing and bending instability
  • Interfragmentary screws – useful for fragment apposition and counteracting rotational, shearing and bending instability
  • K-wires
61
Q

canine elbow dysplasia predisposition

A
  • Large bred dogs and can occur in any breed
  • Start to occur 4-8 months of age
62
Q

causes of elbow dysplasia

A
  • Multifactorial
  • Abnormal development of the bones in the joint, leading to variety of problems such as arthritis, lameness and pain
63
Q

signs of elbow dysplasi

A
  • Limping, reluctant activity, swelling of the elbow and difficulty moving the affecting limb as well as pain
64
Q

treatment of elbow dysplasi

A
  • Medications to reduce inflammation
  • Pain, weight management, physical therapy and surgery in severe cases
65
Q

non surgical treatment for elbow dysplasia

A
  • Supportive devices: braces/slings and changes to exercise routine (to reduce strain on joint)
  • Physical therapy
  • Proper nutrition: decreases weight so less strain and rich in nutrients supports joint health (glucosamine, chondroitin and omega-3 FA)
  • Environmental: comfortable space, safe, lots of water, exercises and managing pain
  • NSAIDs and glucocorticoids, joint supplements
  • Platelet-rich plasma (PRP) : using dog’s own platelets to stimulate healing in the joint
66
Q

conditions that cause elbow dysplasi

A

united anconeal process
fragment medial coronoid process
osteochondrosis dissecans
elbow incongruity

67
Q

UAP

A
  • Occurs when anconeal process, doesn’t fuse properly with the ulna
    o So joint doesn’t function properly, wear and tear and development of arthritis
  • By 20 weeks, if it’s not integrated into ulna and ossified – can assumed UAP (usually 10-13weeks)
  • Bilateral in 30% of cases
68
Q

predisposition of UAP

A
  • Males, large breed dogs (GSD, mastiff, newfoundland and greyhound)
69
Q

cause of UAP

A
  • over-long radius  causes focal overload and failure to fuse
70
Q

signs of UAP

A
  • lameness, external rotation of forearm and joint capsule effusion
  • pain during elbow hyperextension
71
Q

diagnosis of UAP

A

physical exam, x-ray

72
Q

treatment of UAP

A
  • both medical and surgical
  • medical: NSAIDs, corticosteroids
  • weight management – so less strain on elbow
  • physical therapy
  • surgery: ostectomy, osteosynthesis, proximal ulnar osteotomy, partial/total elbow replacement and arthrodesis
73
Q

FMCP

A
  • affects elbow joint in dogs
  • piece of medial coronoid process breaks off
74
Q

FMCP predisposition

A
  • large breed dogs, although can be any breed
  • 5-8 months
75
Q

signs of FMCP

A
  • External rotation of elbow joint, stiffness and lameness
  • Reduced ROM, crepitus
  • Weight bearing is painful
76
Q

diagnosis of FMCP

A
  • Physical therapy, x-ray, CT and arthroscopy
  • Pain/discomfort when palpating and moving the elbow
77
Q

treatment of FMCP

A
  • Same as UAP
  • Surgery: arthroscopy, arthrotomy, coronoidectomy, ostectomy
  • Deloading of coronoid process achieved by: PAUL (proximal abducting ulnar osteostomy) – specialised plate
78
Q

OCD

A
  • Disturbance of cell differentiation in the metaphyseal growth plates and articular cartilage
  • If it results in a fracture of an articular cartilage flap = OCD
79
Q

predisposition of OCD

A
  • Young (5-7months), rapidly growing dogs, medium/large/giant breeds
80
Q

pathogenesis of OCD

A
  • Occurs as endochondral ossification disorder (failure of bottom layer of articular cartilage to mineralise and integrate to the underlying subchondral bone
  •  focal areas of cartilage thickening
  •  focal areas thickened, unintegrated cartilage are prone to failure  cannot heal  arthritis and formation of loose pieces of cartilage in the joint (joint mice)
81
Q

signs of OCD

A
  • Lameness, swelling and difficulty moving affected limb
  • Pebble shoe = when cartilage flap breaks off completely
82
Q

diagnosis of OCD

A
  • Physical therapy, X-rays and other diagnostic tests
83
Q

treatment of OCD

A
  • Restrictive activity, medical (NSAIDs) and surgical intervention (arthroscopy  remove loose pieces of cartilage and smooth out rough areas of the joint)
  • Debridement and drilling into subchondral bone mesenchymal cell pools under the lesion
84
Q

EI

A
  • Bones of a joint don’t fit together properly and form a step  joints don’t function smoothly
  • EI plays important role in development of elbow dysplasia
85
Q

predisposition of EI

A
  • ¬large breeds (lab, golden retriever, GSD)
86
Q

cause of EI

A

genetics injury or abnormal growht

87
Q

diagnosis of EI

A
  • Manifests as radio-ulnar step (short radius  MCD/OCD and a short ulna  UAP)¬
88
Q

treatment of EI and consequences

A

Treatment
- Surgery might be needed to correct alignment of the bones and restore proper joint congruity
Consequences
- Development of osteoarthritis in affected joint
- Muscle imbalances and weakness in affected limb

89
Q

elbow luxation

A
  • Traumatic or congenital dislocation of elbow joint
  • Partial or complete displacement of joints articulating surfaces
  • Not common
90
Q

predisposition of elbow luxation

A
  • Congenital luxation = birth up until 3-4 months of age
91
Q

signs of elbow luxation

A
  • Lameness, pain and visible deformity (swelling) of the joint with a prominent lateral displacement of the radial head, elbow flexed and non-weight bearing, with resistance to flex/extend
92
Q

diagnosis of elbow luxation

A
  • Physical exam and radiograph
  • arthroscopy
93
Q

treatment of elbow luxation

A
  • Closed reduction of joint (realignment of articulating surfaces through manipulation, followed by immobilisation using a cast or splint)
    o Spica splint for 1st 2 weeks, CT needs 6-8 weeks to heal
    o External coaptation and cage rest
  • Surgery: repair ligaments, remove damaged cartilage, joint reduction
  • Surgery recommended for severe luxation or one that doesn’t respond to closed reduction or immobilisation
94
Q

cranial cruciate ligament (CCLD) prediposition

A
  • Rare in cats
  • Large and giant breeds most affected
  • Most affected: Rottweiler, newfoundland, staffies, mastiff)
  • Least affected: greyhound, dachshund, basset and old English sheepdog
  • Genetic mode of inheritance has been found in newfoundlands and labs
  • No sex predisposition
  • Neutered dogs have higher prevalence and smaller dogs affected later in life than larger
95
Q

cause of CCLD

A
  • Progressive degeneration of cranial cruciate ligament (CrCL)
  • Multifactorial aetiology (obesity, poor physical condition, genetics, breed, etc)
96
Q

signs of CCLD

A
  • Lameness and pain (with manipulation), crepitus
  • Medial buttress periarticular hypertrophy is often identified
  • Difficulty rising from sitting, difficulty sitting (positive sit test), trouble jumping, decreased activity
97
Q

diagnosis of CCLD

A
  • Sit test
  • Palpation: cranial drawer test and tibial compression test
  • Complete rupture is seen by gait observations, physical exam and radiographs
  • Sinus effusion palpable and most consistent radiographic finding
  • Arthrocentesis and radiographs (for more difficult tears)
  • Cranial socket laxity and cranial tibial traction: mainstay of diagnosis
98
Q

treatment of CCLD

A
  • Removal of damaged meniscus, then stabilising the knee
  • Extracapsular stabilisation, TPLO, lateral fabellotibilar suture (lateral suture), tightrope, fibular head transposition, intra-articular reconstruction, osteotomy…
  • Tibial plateau levelling osteotomy (TPLO)
    o Semi-circular cut around top of tibia and rotating its contact surface until it attains a near-level orientation (90o) relative to attachment of the quadriceps muscle
    o Stabilised by locking bone plate and screws
  • Tibial tuberosity advancement (TTA)
    o Linear cut along front of tibia (tibial tuberosity)
  • Choosing whether TPLO and TTA is just based on surgeons preference and experience
  • Post op: decrease excessive activities, physical therapy
99
Q

osteochondrosis

A
  • Developmental disorder of articular cartilage caused by failure of normal endochondral ossification
  • Cartilage in affected zone is thicker, receives less nutrition from synovial fluid and is less tolerant of biomechanical loading
  • Deeper zone of cartilage can become necrotic  fissure formation and development of detached flap  OCD
  • Lesion usually on medial aspect of lateral femoral condyle
100
Q

patella-luxation

A
  • Non-traumatic, generally associated with conformational abnormalities and may have multifactorial aetiology
  • Malposition of extensor mechanism leads to dislocation of patella
  • Various changes are identified in small breed dogs: angular deformities of femur and tibia (“genu varum”) hypoplasia of trochlear groove
  • Small and toy breeds – luxations are medial and commonly bilateral
  • Grade I: not obvious lameness, bilateral grade IV leads to significant debilitation
101
Q

diagnosis of patella luxation

A
  • Physical exam and palpation of patella during stifle manipulation
  • Direction of luxation and height of patella within trochlea ridge should be assessed
  • Cranial drawer and stifle stability needs to be evaluated
  • Radiographs
102
Q

treatment of patella luxation

A
  • Individualised to each patient
  • Trochleoplasty – sulcoplasty, chondroplasty or wedge/block recession is used to make a trochlea of the femur deeper
  • Tibial tuberosity transposition (TTT): done to realign the quadriceps
103
Q

hip dysplasia

A
  • Looseness that manifests in early age (4-12 months) and consequence is irregular and excessive load on joint surface, ligaments and joint capsule at the top
  • Genetically determined developmental irregularity in the structure of the hips
  • Most common hereditary orthopaedic disease in dogs
  • Occurs less often in cats – highest frequency in maine coone
  • Causes joint inflammation and secondary osteoarthrosis which leads to different degrees of clinical manifestation of the disease
  • Irregular development of hip joint mostly bilateral
104
Q

pathogenesis of hip dysplasi

A
  • Favourable environmental influences lead to expression of the responsible genes and phenotypic manifestation of the disease
  • Animals with rapid growth –> greater strain on the hips and causes joint instability
  • Develops in dogs during the growth phase as a result of several factors:
    o Collagen disease, dysfunction of adductor and abductor muscles, obese, etc
  • Stretching of joint capsule –> inflammation  pain  mechanical damage of acetabulum  painful microfractures
  •  leads to permanent and irreversible changes in hips and forms bone reactions, swelling and pathological changes
105
Q

pathogenically of hip dysplasia

A
  • 2 phases
    o 1st phase: marked instability of hips
    o 2nd phase: (late) noticeable and progressive osteoarthritic changes in hip joints
  • Changes to the joints in dysplasia
    o Increased volume of the round ligament
    o Oedematous articular cartilage
    o Increased synovial fluid
  • Young fast-growing breeds, excessive body mass of puppies, nutrition
    o Diets with high doses of Vit C, Vit D and Ca2+ cause a delay in enchondral ossification and skeletal remodellingd
106
Q

diagnosis of hip dysplasi

A
  • Clinical picture, orthopaedic exam, radiographs
  • 1st phase in younger patients with signs of instability are present
  • Second phase = signs of osteoarthritis
  • Orthopaedic exam
    o Performed to localise the symptoms and exclude or find other reasons for the appearance of symptoms that resemble hip dysplasia (panositis, osteochondrosis, etc)
    o Wide/ or later narrow stance of the hind limbs can be seen
    o Atrophy and/or insufficiently developed thigh muscles
    o Walk drifting to the side or swaying of the back part of spine
    o Animal reduces extent of hip extension and transfer the propulsion phase to spine
    o Musculature on the front is stronger than on the back

barden, Barlow and ortolani

  • Radiograph
    o In young dogs = penn hip method
     Measures hip distraction index measured by comparing 2 recordings, 1 in compression and 1 in joint distraction
     Physiological value is 0.3, values higher indicate increased looseness of the hips/hip laxity
107
Q

barden test

A
  • Lateral position, upper leg transverse to pelvic exam
  • Immediate epush, with 1 hand covering knee in lateral direction provokes lifting of the femur
  • Other hand supporting hip – can feel movement of greater trochanter laterally
  • Greater than 0.6mm = positive for barden and confirms hip laxity
108
Q

Barlow test

A
  • Supine position, pelvis parallel to table, femur in vertical position
  • Other femur, extended, parallel to table
  • Pressure of femur in dorsal direction axial compression, in unstable hips it provokes sliding of head of femur outside acetabulum felt by palpation
  • Proportional to degree of hip looseness
109
Q

ortolani test

A
  • sedated animal
  • tests stability of femoral heads within cups
  • supine/lateral position
  • (1 hand holds distal knee, other hip, knee is pushed towards other hand)
  • If positive – sudden movement will be felt, with a clunk
     Angles measured with orthopaedic goniometer
110
Q

signs of hip dysplasia

A
  • Mild discomfort to acute or chronic pain
  • Young: 4-12 months, juvenile, more severe form
    o Difficulty to stand up, mostly sitting, disinterest to play, avoidance of running and walking, “bunny hopping”
  • 2nd phase:
    o Chronic form
    o Same as above but might not be that noticeable
111
Q

treatment of hip dysplasi

A
  • Conservative
    o Limitation of activity, weight loss, NSAIDs and physical therapy
  • Surgery
    o Operating methods are divided into:
     Preventive methods at an early age and early stage of disease
  • Juvenile pubic symphysiodesis (JPS) , double pelvic osteotomy (DPO), DARthryoplasty
     Methods of treatmetn of the joint affected by osteoarthrosis
  • Removal of femoral head and neck (Femoral head and neck osteotomy FHO)
  • Installation of a hip prosthesis (total hip replacement THR)
     Palliative methods for removing pain
112
Q

juvenile pubic symphysiodesis (JPS)

A
  • Prevent development of dysplasia in puppies between 12-24 weeks of age
  • Stops growing in the pubic part of pelvic symphysis
  • Burning or cauterising cranial half of the pelvic symphysis, which necrotises the germinal cartilage layer
  • Goal = to stop further growth of ventral segment of acetabular part of pelvic
  • Recommended for puppies of risky breeds with positive Ortolani test (3-4 months)
113
Q

double pelvic osteotomy (DPO)

A
  • Enables intraoperative rotation of acetabular part of pelvis, resulting in better coverage of femoral head by acetabulum arch, stabilising unstable hip
  • Rotated acetabular part is permanently fixed with a plate
  • For dogs 5-9 months
  • Precondition for performing: absence/presence of slightly expressed hip arthritic changes and preserved acetabular roof
114
Q

femoral head and neck osteotomy

A
  • Done in degenerative dysplastic changes on hips, it’s conservative treatment and when implanting a prosthesis isn’t acceptable or possible
  • Excisional arthroplasty – removes pain and creates preconditions for the formation of a false fibrous joint
  • Small and medium-sized breed of dogs and cats
  • Aim = remove contact of articular surfaces of the hip, removing the pain - creates a “false joint”
115
Q

hip luxation

A
  • Most common joint luxation in dogs
  • Dislocation of femoral head from acetabulum
  • Need to be treated ASAP
  • Most treatments = conservatively and chronic cases = operative treatment
116
Q

hip luxation divided into

A
  • Craniodorsal luxation
    o Head of femur is located dorsally and cranially with acetabulum (most common)
  • Caudoventral luxation
    o Entrapment of femoral head inside of obturator opening (head located ventral to acetabulum)
  • Medial luxation associated with acetabulum fracture
    o Medial hip luxation occurs in case of acetabulum fracture
  • Caudodorsally luxation
    o Head of femur in relation to acetabulum is located caudal and dorsal
117
Q

signs of hip luxation

A
  • Animal shows high degree of lameness with hind leg, history of trauma
  • Clinical exam = crepitus and pain during flexion and extension
  • During palpation, narrowing of space between greater trochanter and ischial tuberosity is felt (caudodorsal luxation)
  • (craniodorsal) dorsal displacement can be palpated
    o Thumb between greater trochanter and ischial tuberosity during external rotation
  • (caudoventral) affected limb appears longer than the contralateral side
  • Radiological exam
118
Q

surgical treatment of hip luxation

A
  • Indicated if reduction is unsuccessful
  • Most common = craniolateral approach
  • Goal = remove soft tissue from inside of acetabulum that interferes with the reposition
  • Suturing the joint capsule
    o Non-resorbable or slow-resorbable suture materials, single or mattress suture
    o Postop hip is immobilised with Ehmer’s bandage (7-10days)
  • Synthetic capsule technique
    o After reduction, 2 screws placed on dorsal edge of acetabulum
    o Don’t penetrate articular cartilage itself
  • Toggle pin technique
    o If capsule is too damage or hip luxation is chronic = cannot stabilise the joint just by suturing so do tension anchor is placed through acetabular tunnel on medial side and then turned 90degrees, locked against medial wall of the acetabulum
    o After that, sutures passed through previously drilled tunnel in neck+ head of femur
    o ….
    o Greater trochanter repositioned with 2 kirschner wires and cerclage
119
Q

shoulder instability

A
  • Increased laxity or ROM between humeral head and glenoid fossa discomfort/dysfunction due to incompetence or disruption of joint stability mechanism
  • Predisposition: Small and mini breeds (poodles)
  • Cause: insufficient medial joint support (injury to the ligament)
  • Diagnosis: shoulder overabduction over 50o, X-rays
  • Treatment: stabilise shoulder by increasing strength (physical therapy), if fails, surgery (subscapular imbrication and medial collateral ligament prosthesis placement)
120
Q

shoulder luxation

A
  • Common if they’re predisposed due to their anatomy
  • Cause: trauma or congenital abnormalities
  • Signs: acute onset forelimb lameness with history of trauma
  • Diagnosis: shoulder asymmetry (visible or palpable), manipulation reveals ROM, pain and crepitus, X-rays
121
Q

treatment of shoulder luxation

A
  • Treatment:
    o conservative (closed reduction) under GA or sedation with myorelaxants with Velpeau sling (2-6 weeks)
    o medications to reduce pain and inflammation and physical therapy
    o when closed reduction isn’t successful = surgery, also necessary when fractured
    o salvage procedures are last minute and include excisional arthroplasty, bone fusion (arthrodesis)
    o rest and confinement
122
Q

bicep tendinopathy (tenosynovitis)

A
  • occurs when biceps tendon, originates at supraglenoid tubercule of scapula and passes over intertubercular groove on humerus, becomes inflamed or damaged  pain and weakness
  • cause: overuse or RSI
  • predisposition: medium to large dogs that participate in high-impact activities
  • sign: lameness or difficulty using affected limb, swelling or pain in shoulder, stiffness or reluctance to flex shoulder
  • diagnosis: physical exam, radiographs, US and arthroscopy
  • treatment: rest, NSAIDs, physical therapy, PRP, surgery if conservative fails
123
Q

fibrotic contracture of infraspintatus msucle

A
  • Occurs when normal muscle-tendon unit architecture is replaced with fibrous tissue, resulting in functional shortening of the muscle or tendon. Which may cause abnormal motion in adjacent joints
  • Predisposition: young, adult dogs of sporting breeds
  • Signs: lameness, discomfort
  • Diagnosis: characteristic gait with external rotation of shoulder and internal rotation of elbow and abduction of paw
  • Treatment: infraspinatus tenotomy, NSAIDs and physical therapy

surgery 3 (6 decks)

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