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
signalment of hypertrophic osteodystrophy
- 2-6 months - Male dogs predisposed compared with females - Great Dane, Irish setter, boxer, GSD, golden and lab retrievers, Weimaraner (heritable)
26
diagnosis of hypertrophic osteodystrophy
- 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)
27
differential of hypertrophic osteodystrophy
- Septic arthritis, septic physitis, secondary nutritional hyperparathyroidism, retained cartilage cores, hypertrophic osteopathy and Panosteitis - Secondary disorder most often associated with pulmonary neoplasia
28
treatment of hypertrophic osteodystrophy
- 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
29
avascular necrosis of femoral head other name
legs-calve-perthes diseasee
30
what is legg-calve-perthes diseae
- 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
31
signalment of legg-calves-perthes-disease
- 4-11 months - No sex - Small breed mostly affected, toy and terrier breeds increased risk - Mini poodles and Westies, trait is autosomal recessive
32
diagnosis of legs-calves-perthes
- 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
33
differentials of LCP
- Capital physeal trauma, epiphystitis, septic physitis, osteomyelitis and neoplasia
34
signs of LCP
- Crepitation during passive movements, ROM, loss of muscle, lameness
35
treatment of LCP
- 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
36
prognosis of LCP
- Post-op is good, lameness resolving in 84-100% of cases - Physical rehab after surgery may help ensure a positive outcome
37
multiple cartilaginous exostosis
- 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
38
signalment of multiple cartilaginous exostosis
- 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
39
diagnosis of multiple cartilaginous exostosis
- 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
40
treatment of multiple cartilaginous exostosis
- Depends on size and location - Rest and NSAIDs - Surgery indicated for single or large exostosis
41
osteomyelitis
- 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
42
predisposing factors of osteomyelitis
- Inadequate fracture stabilisation - Unsterile surgery - Prolonged operating time - Poor technique  soft tissue damage - Primarily immunocompromised patient - Contaminated wound, inappropriate ATB
43
pathophysiology of osteomyeltiis
- 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
44
pathogenesis of osteomyelitis
- 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
45
cause of osteomyelitis
- Bacteria infection introduced during orthopaedic surgery or contamination from wounds - Associated with Staph, strep, e.coli, proteus, Pasteurella, pseudomonas and B.canis
46
signs of osteomyeltiis
- Acute/chronic - Lameness, pain, abscessation at the wound site, fever, anorexia and depression
47
diagnosis of osteomyelitis
- 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
48
treatment of osteomyeltiis
- 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
49
prognosis of osteomyelitis
- 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
50
panostetitis
- 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
cause of panosteitis
- Unknown - Could be a normal dog that receives a bone inoculation of marrow from an affected dog
52
signs of panosteitis
- Painful during its flare-ups o Pain can last 2-5 weeks - Lameness can shift from one leg to another - Fever
53
diagnosis of panosteitis
- Cloudiness in bone marrow cavities is visible on radiographs
54
treatment of panosteitis
- Pain relief, until dog outgrows - NSAIDs
55
classification of fractures
- 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: **A**dequate 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
primary - direct bone healing
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
indirect- secondary bne healing
- 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
forces (6)
bending, rotation or torsion, shear, compression and tension
59
primary methods of fracture repair
- 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
secondary methods of fracture repair
- 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
canine elbow dysplasia predisposition
- Large bred dogs and can occur in any breed - Start to occur 4-8 months of age
62
causes of elbow dysplasia
- Multifactorial - Abnormal development of the bones in the joint, leading to variety of problems such as arthritis, lameness and pain
63
signs of elbow dysplasi
- Limping, reluctant activity, swelling of the elbow and difficulty moving the affecting limb as well as pain
64
treatment of elbow dysplasi
- Medications to reduce inflammation - Pain, weight management, physical therapy and surgery in severe cases
65
non surgical treatment for elbow dysplasia
- 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
conditions that cause elbow dysplasi
united anconeal process fragment medial coronoid process osteochondrosis dissecans elbow incongruity
67
UAP
- 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
predisposition of UAP
- Males, large breed dogs (GSD, mastiff, newfoundland and greyhound)
69
cause of UAP
- over-long radius  causes focal overload and failure to fuse
70
signs of UAP
- lameness, external rotation of forearm and joint capsule effusion - pain during elbow hyperextension
71
diagnosis of UAP
physical exam, x-ray
72
treatment of UAP
- 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
FMCP
- affects elbow joint in dogs - piece of medial coronoid process breaks off
74
FMCP predisposition
- large breed dogs, although can be any breed - 5-8 months
75
signs of FMCP
- External rotation of elbow joint, stiffness and lameness - Reduced ROM, crepitus - Weight bearing is painful
76
diagnosis of FMCP
- Physical therapy, x-ray, CT and arthroscopy - Pain/discomfort when palpating and moving the elbow
77
treatment of FMCP
- Same as UAP - Surgery: arthroscopy, arthrotomy, coronoidectomy, ostectomy - Deloading of coronoid process achieved by: PAUL (proximal abducting ulnar osteostomy) – specialised plate
78
OCD
- 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
predisposition of OCD
- Young (5-7months), rapidly growing dogs, medium/large/giant breeds
80
pathogenesis of OCD
- 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
signs of OCD
- Lameness, swelling and difficulty moving affected limb - Pebble shoe = when cartilage flap breaks off completely
82
diagnosis of OCD
- Physical therapy, X-rays and other diagnostic tests
83
treatment of OCD
- 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
EI
- 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
predisposition of EI
- ¬large breeds (lab, golden retriever, GSD)
86
cause of EI
genetics injury or abnormal growht
87
diagnosis of EI
- Manifests as radio-ulnar step (short radius  MCD/OCD and a short ulna  UAP)¬
88
treatment of EI and consequences
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
elbow luxation
- Traumatic or congenital dislocation of elbow joint - Partial or complete displacement of joints articulating surfaces - Not common
90
predisposition of elbow luxation
- Congenital luxation = birth up until 3-4 months of age
91
signs of elbow luxation
- 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
diagnosis of elbow luxation
- Physical exam and radiograph - arthroscopy
93
treatment of elbow luxation
- 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
cranial cruciate ligament (CCLD) prediposition
- 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
cause of CCLD
- Progressive degeneration of cranial cruciate ligament (CrCL) - Multifactorial aetiology (obesity, poor physical condition, genetics, breed, etc)
96
signs of CCLD
- 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
diagnosis of CCLD
- 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
treatment of CCLD
- 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
osteochondrosis
- 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
patella-luxation
- 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
diagnosis of patella luxation
- 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
treatment of patella luxation
- 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
hip dysplasia
- 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
pathogenesis of hip dysplasi
- 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
pathogenically of hip dysplasia
- 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
diagnosis of hip dysplasi
- 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
barden test
* 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
Barlow test
* 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
ortolani test
* 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
signs of hip dysplasia
- 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
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treatment of hip dysplasi
- 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
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juvenile pubic symphysiodesis (JPS)
- 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)
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double pelvic osteotomy (DPO)
- 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
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femoral head and neck osteotomy
- 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”
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hip luxation
- 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
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hip luxation divided into
- 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
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signs of hip luxation
- 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
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surgical treatment of hip luxation
- 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
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shoulder instability
- 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)
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shoulder luxation
- 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
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treatment of shoulder luxation
- 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
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bicep tendinopathy (tenosynovitis)
- 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
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fibrotic contracture of infraspintatus msucle
- 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