orthopaedics Flashcards
1
Q
patient stabilisation
A
- Check and stabilise vitals
- Perform thorough physical, orthopaedic, and neurological examinations
- Pursue initial diagnostics, including blood analysis, thoracic and abdominal radiographs and a FAST ultrasound
- Resolve any life-threatening issues, which means surgery may need to be delayed for several days due to conditions
- Administer proper analgesia as soon as possible
- Approx. 12-24 hrs following presentation, animal must be thoroughly re-evaluated
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
3
Q
Bernese mountain dog and lab predisposition
A
elbow and hip dyslplasia
4
Q
newfoundland predisposition
A
cruciate ligament rupture
5
Q
greyhound and basset predisposition
A
very rare for cruciate ligament rupture
6
Q
spaniels predisposition
A
incomplete ossification of the humerus condyles (IOHC)
7
Q
mini poodle predisposition
A
hereditary medial shoulder instability
8
Q
- test for cranial cruciate ligament rupture
A
sitting test
tibia compression test
drawer test
9
Q
test for collateral ligametns
A
varus/valgus test
10
Q
test for meniscus
A
by crepitation which occurs during passive knee movements
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
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
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
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
15
Q
test for hip instability
A
ortolani test
Barlow
barden
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
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
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
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
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
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
22
Q
differentials of panosteitis
A
- Hypertrophic osteodystrophy, Osteochondritis dissecans, hip dysplasia, fragmented medial coronoid process and united anconeal process
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
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
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)
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)
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
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
29
Q
avascular necrosis of femoral head other name
A
legs-calve-perthes diseasee
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
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
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
33
Q
differentials of LCP
A
- Capital physeal trauma, epiphystitis, septic physitis, osteomyelitis and neoplasia
34
Q
signs of LCP
A
- Crepitation during passive movements, ROM, loss of muscle, lameness
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
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
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
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
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
40
Q
treatment of multiple cartilaginous exostosis
A
- Depends on size and location
- Rest and NSAIDs
- Surgery indicated for single or large exostosis
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
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
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
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
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
46
Q
signs of osteomyeltiis
A
- Acute/chronic
- Lameness, pain, abscessation at the wound site, fever, anorexia and depression
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
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
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
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
