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SMALL ANIMAL > 20.9.1: Juvenile lame animal > Flashcards

20.9.1: Juvenile lame animal Flashcards

1
Q

Signalment and history associated with Perthe’s disease

A
  • Toy and small dogs under 6 months old
  • Inherited in Manchester terriers
  • Similar condition reported in the cat
  • Bilateral in 12-16% cases
  • Lameness with associated muscle atrophy (they don’t bear weight)
  • Reluctant to jump or go up and down stairs
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2
Q

Clinical signs of Perthe’s disease

A
  • Often marked muscle atrophy (particulary of the gluteal muscles)
  • Considerable pain on extension of the hips
  • Crepitus on manipulation of the hips
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3
Q

Radiographic findings associated with Perthe’s disease

A
  • Mottled appearance to femoral neck and head due to areas of lucency
  • A misshapen and often triangular shape to the femoral head
  • Secondary osteoarthritic changes
  • Loss of muscle mass
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4
Q

Pathogenesis of Perthe’s disease

A

Avascular necrosis of the femoral head

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5
Q
A

Perthe’s disease

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6
Q

Treatment and management of Perthe’s disease

A

Conservative management
* NSAIDs, neutraceuticals
* Physiotherapy
* Rarely successful as the dogs walk well on 3 legs and avoid using the painful one

Surgical management
* Femoral head and neck excision (FHNE)
* OR Total hip replacement (THR)

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7
Q

Management and progonsis after FHNE

A
  • Must encourage the animal to use the leg: small dogs can manage well on 3 legs and therefore rehab (physio, hydro, analgesia) is essential to encourage early use of the limb
  • Large dogs often do less well
  • The limb is always shorter and the hip has reduced extension; loss of length is compensated for by tilting the pelvis
  • If client can afford it, prognosis is better with total hip replacement compared to FHNE
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8
Q

Signalment of metaphyseal osteopathy

A
  • Only seen in dogs; unknown aetiology - suspected autoimmune
  • < 6 months old
  • Severe and excrutiating painful swelling to the metaphyseal region of all limbs
  • Pyrexic and systemically unwell
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9
Q

Clinical signs of metaphyseal osteopathy

A
  • Often unable to walk
  • Pyrexic and inappetant
  • Painful swelling associated with the distal limb (v painful)
  • Associated pitting oedema over the metaphyseal regions
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10
Q

Radiographic signs of metaphyseal osteopathy

A
  • Soft tissue swelling
  • Ill-defined lucency parallel to the physis (sometimes described as “extra growth plate”)
  • Periosteal lifting with mineralisation
  • Bridging of the physis by the inflammatory change can result in angular limb deformities (because bone bridges on one side of the growth plate but the other side continues to grow)
  • Need to tell the client about possible future problems
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11
Q
A

Metaphyseal osteopathy

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12
Q

Treatment and prognosis: metaphyseal osteopathy

A

Treatment
* Hospitalisation and IVFT
* Multi-modal analgesia including opioids, CRI
* Steroids may work better than NSAIDs
* Supportive feeding (tube if inappetant >3 days)

Prognosis: guarded; increased incidence of other autoimmune conditions when animal gets older.

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13
Q

Early cruciate disease may be seen in the juvenile animal in which breeds of dog?

A

Larger breeds: Mastiffs and Rotties

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14
Q

Patella subluxation is a cause of lameness in which breeds?

A

Both small and large breed dogs

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15
Q

How would you expect septic arthritis to present in the juvenile compared to the adult animal?

A

Juvenile - may have multiple joints affected
Adult - typically present for a single joint

Elbow = commonest site for joint sepsis

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16
Q

Polyarthritis may be seen after…

A

Infection (cats) or vaccination (dog)
* There is multiple sterile arthropathy

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17
Q

Humeral intracondylar fissures are most common in which breed?

A

Spaniels

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18
Q

How could you detect sesamoid disease on clinical exam?

A

There will be pin-point pain over the flexor sesamoids

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19
Q

Signalment and presentation of craniomandibular osteopathy

A

(This is an uncommon cause of juvenile lameness)
Signalment
* Small terries esp WHWT
* Has been reported in larger dogs e.g. Doberman
* <6 months old

Presentation
* Very painful condition of the mandibule, skill, and occasionally long bones
* Animals are systemically unwell and pyrexic
* With chronicity -> progressively difficult to open mouth (could become hard to intubate in future!)

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20
Q

Radiographic features of craniomandibular osteopathy

A
  • Characteristic palisading (battlement-like) new bone to the mandible, occipital crest, tympanic bullae
  • The temporomandibular joint may be involved
  • Similar changes seen in the long bones
  • Associated soft tissue swelling
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21
Q
A

Craniomandibular osteopathy

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22
Q

Treatment of craniomandibular osteopathy

A
  • Analgesia
  • Corticosteroids often required to manage this condition
  • Associated soft tissue swelling
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23
Q

Prognosis of craniomandibular osteopathy

A
  • Can be guarded as cases hard to manage and distressing for dog and owner
  • Long-term sequelae: reduced opening of the mouth -> eating, ET intubation difficult
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24
Q

Signalment and history of panosteitis

A

Signalment
* Common but often overlooked condition
* Seen in young dogs <1 y.o.
* GSDs and male over-represented

History
* Characteristic waxing and waning signs
* Often presents with shifting lameness that spreads from one limb to another

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25
Q

Clinical signs of panosteitis

A
  • Often dog is depressed and pyrexic
  • Lameness can be severe and dog may not weight bear
  • Pain on palpation of the diaphysis
  • May have had previous episode lasting ~1 week in another limb (shifting lameness)
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26
Q

Radiographic signs of panosteitis

A
  • Loss of normal trabecular pattern particularly around the nutrient foramen
  • Endosteal and periosteal new bone formation
  • Important to appreciate that sometimes clinical and radiographic signs may not overlap; sometimes good to radiograph 2 weeks after signs have been seen - changes may be subtle and client may not want to wait
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27
Q
A

Panosteitis

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28
Q

Treatment and prognosis for panosteitis

A

Treatment
* Rest and analgesia (NSAIDs)
* Advise the owner that this is an episodic condition; usually lasts a week and is self-limiting

Prognosis
* Excellent
* Episodes of acute lameness will become less severe and less frequent
* Most cases resolve by the time the dog is 1 y.o.; occasional reports of 5 y.o. dog but v rare
* Reassure the owner and make sure you aren’t missing anything e.g. elbow dysplasia

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29
Q

Signalment and clinical presentation of Rickets

A
  • Rare cause of lameness in the young animal
  • Associated with absolute lack of vitamin D often compounded by reduced exposure to sunlight and/or Ca:P imbalance

Clinical signs
* Pain and swelling around the physeal regions of the long bones and reluctance to move
* Growth plates widened due to poor / delayed mineralisation of the cartilage

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30
Q

Ddx and treatment of rickets

A

Ddx: nutritional secondary hyperparathyroidism

Treatment
* Provide a balanced diet containing adequate amounts of Vitamin D
* Ensure adequate exposure to sunlight

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31
Q

Pathogenesis and diagnosis of nutritional secondary hyperparathyroidism

A

Pathogenesis
* Poor skeletal mineralisation due to low Ca / high P diet (usually all meat diet)

Diagnosis
* Bones have thin, poorly mineralised cortices
* Prone to pathological fractures and vertebral body collapse
* Can be hard to appreciate contrast on radiography

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32
Q

Treatment of nutritional secondary hyperparathyroidism

A
  • Dietary correction
  • Analgesia
  • Exercise restriction
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33
Q
A
34
Q
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35
Q

Signalment of pituitary dwarfism

A

Pituitary dwarfism: congenital hereditary abormality caused by poituitary panhypopituitarism
* Pars distalis affected and results in somatotropic, adenotrophic, and TSH deficiencies.

Signalment
* Primarily GSDs; also Spitz, Manchester terrier

36
Q

Clinical signs of pituitary dwarfism

A
  • Proportionate dwarfism and alopecia with hypopigmentation
  • Physis remain open
  • No guard cells in the coat
  • Small testes / absent ostrus cycles
37
Q

Treatment and prognosis of pituitary dwarfism

A
  • Cortisol, thyroxine, progestogens

Side effects
* Common
* e.g. pyometra, insulin resistance, mammary hyperplasia

Prognosis: life expectancy reduced

38
Q

Cause and presentation of angular limb deformities

A
  • Many types of these deformities: antebrachial = most common
  • Occur in the young growing animal when one of two/ part of a growth plate closes prematurely
  • This arises from trauma or bridging with the periosteal bone
39
Q

Clinical signs and treatment of angular limb deformities

A

Clinical signs
* Lameness arising from joint pain due to abnormal stresses and associated subluxations

Treatment
* Depends on whether there is any growth left in the affected limb; many surgical options

40
Q

Valgus vs varus angular limb deformities

A

Valgus: lateral deviation of the distal limb.
Varus: medial deviation of the distal limb.

41
Q

Luxation

A

no contact between articular surfaces

42
Q

Subluxation

A

some contact between articular surfaces

43
Q

What is the most common form of angular limb deformity of the antebrachium?

A

Short ulna syndrome

44
Q

Pathogenesis and signalment of osteochondrosis

A
  • Very common developmental condition of the articular cartilage
  • Seen in juvenile animal but consequences extend into adult life

Pathogenesis
* Failure of ossification of the articular cartilage
* This might arise from abnormal stresses on the cartilage due to joint incongruity
* Results in thickened cartilage which fragments and allows contact of the synovial fluid with the subchondral bone (+ resulting inflammation, shown as sclerosis on radiographs)
* This cartilage can form a flap (osteochondrosis dissecans)
* The subchondral bone can fracture (fragmented coronoid process) or there may be failure of the physis to close (ununited anconeal process)

45
Q

Sites for osteochondrosis and their relative prognoses

A
  • Elbow - common, guarded prognosis
  • Shoulder - rare, good prognosis
  • Stifle - rare, poor prognosis
  • Hock - rare, poorest prognosis of all
  • Other sites - occasionally seen in lumbosacral joint
46
Q

What is elbow dysplasia?

A

Elbow dysplasia: broad term that encompasses all manifestations of osteochondrosis seen in the elbow
* Very common and has several manifestations
* All involve the medial aspect of the joint hence it is also known as medial compartment disease

47
Q

Signalment for elbow dysplasia

A
  • Polygenic inherited disease which may result in joint incongruity but also is affected by growth rate, diet, exercise regimes
  • Seen in many breeds but esp Labs, Rotties, GSDs, Basset hounds
  • Not reported in cats
  • Increased incidence in the male
  • 50-90% cases are bilateral
48
Q

History and clinical signs of elbow dysplasia

A
  • Insidious onset at 5-7 months old
  • Chronic lameness that is initially worse on rising after rest
  • Moderately responsive to NSAIDs at least initially
  • In chronic cases, muscle atrophy
49
Q

Clinical exam findings of the dog with elbow dysplasia

A
  • Holds the limb abducted and externally rotated (trying to take the pressure off the painful medial compartment)
  • Pain on manipulation, particularly internal rotation that loads the medial compartment of the joint
  • Pain on flexion with ununited anconeal process
  • In chronic cases -> muscle atrophy
  • Always check the contralateral limb!
50
Q

Components of elbow dysplasia and which breeds are most affected

A

Fragmented medial coronoid
* Common
* Affects Labs, Rotties, Bernese Mountain dogs

Osteochondrosis dissecans
* Lesion of medial humeral condyle
* May occur concurrently with FCP
* Seen in Labs

Ununited anconeal process
* Seen in GSDs and Basset hounds

Can also get incomplete ossification of the medial humeral epicondyle, but this is rarer. It’s unclear how this fits into elbow dysplasia.

51
Q

Describe how to undertake radiography in a case of suspected elbow dysplasia

A
52
Q

Which radiographic views do you need to take in the patient with suspected elbow dysplasia?

A

The lateral view is technically mediolateral.
The flexed mediolateral view is the most useful as it allows us to look for early degeneration (such as osteophytes forming around the anconeal process)

53
Q

What do we look for with regards to elbow dysplasia radiographs? What other imaging modality can help us?

A

Look for secondary changes
CT can be very useful

54
Q

What are some radiographic features consistent with osteochondrosis (elbow dysplasia)?
Describe how this would change according to each lesion location.

A
55
Q
A
56
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A
57
Q
A
58
Q
A
59
Q

Which type of elbow dysplasia is advanced imaging (CT) particularly useful for?

A

Fragmented coronoid process (this is hard to see on radiographs)

59
Q
A
60
Q
A
61
Q

Advantages of arthroscopy for diagnosis of elbow dysplasia

A

✅ Can detect lesions not seen with CT
✅ Facilitates treatment at the same time as diagnosis

62
Q
A

(Arthroscopy)

63
Q

Treatment options for fragmented coronoid process

A

Conservative management
* Weight control
* NSAIDs
* Platelet-rich plasma
* Stem cell therapy
* Nutraceuticals
* Cartrophen

Surgical options
* Removal of the fragment (arthroscopy) and ulna osteotomy to correct joint incongruency - helps short term but not long term
* Techniques to reduce weight bearing on medial aspect of joint e.g. PAUL, sliding medial humeral osteotomy
* Partial elbow replacement; total elbow replacements in infancy
* Elbow arthrodesis - salvage procedure, only if animal several lame

64
Q

Prognosis for fragmented coronoid process

A
  • Guarded
  • Irrespective of treatment technique employed, development of degenerative joint disease is inevitable
  • Anticipate long-term medical management due to the original lesion - warn the owner from the outset
65
Q

Treatment and prognosis of osteochondrosis dissecans

A
  • Surgical: remove the fragment and curette the deficit to promote the formation of fibrous cartilage
  • Prognosis is fair
66
Q

Treatment of ununited anconeal process

A

Options
* Remove the fragment -> this results in joint incongruity and OA
* Rettach fragment with screw
* Reattach fragment + ulna osteotomy to lengthen ulna

Results of all techniques = variable.
In the mature animal, this condition is treated medically.

67
Q

What initiatives are there to control elbow dysplasia?

A

BVA / Kennel Club scheme
* 2 views (flexed and neutral) required
* Each elbow has max score 3
* Highest score of either elbow = score the dog will be given
* Breeding discouraged from any animal with score >0
* Estimated breeding values available for different breeds; this only takes into account genetic merit and not environmental factors that may impact joint disease

68
Q

Signalment and history associated with shoulder osteochondrosis

A

Signalment
* Lab, Border Collies
* 6-8 months old
* This condition is now rarer than it used to be

History
* Lame on rising
* Worse after exercise
* Pain on shoulder extension
* Scapular muscle atrophy

69
Q

Diagnosis of shoulder osteochondrosis

A
  • Radiography
  • CT
  • Arthroscopy
  • Arthrogram not commonly done now
70
Q

Treatment and prognosis of shoulder osteochondrosis

A

Treatment
* Some advocate conservative management with vigourous exercise + analgesia to dislodge the flap
* Surgical management: remove fragment and debride deficit edges OR limited caudal arthrotomy with flexed shoulder and perform same procedure

Prognosis
* This has the best prognosis of any joint affected by osteochondrosis

71
Q

Signalment and clinical signs of stifle osteochondrosis

A

Signalment
* 6-12 months
* Lab, Staffies, reported in cats

Clinical signs
* Chronic lameness especially on rising
* Joint pain
* Joint effusion
* Ddx: early cruciate disease

72
Q

True/false: all young animal have a cranial draw but this comes to an abrupt halt when they get older and cruciate stabilises things.

A

True

73
Q

Diagnosis of stifle osteochondrosis

A
74
Q

Treatment and prognosis of stifle osteochondrosis

A

Treatment
* Surgery: arthroscopy/ arthrotomy -> remove fragment and curette deficit

Prognosis
* Fair to guarded

75
Q

Signalment and clinical signs of hock osteochondrosis

A

Signalment
* Labs and Rotties
* 6-12 months old

Clinical signs
* Lameness particularly after exercise
* Joint effusion to both medial and lateral aspects of the talocrural joint

76
Q

Diagnosis of hock osteochondrosis

A
  • Radiograph / CT
  • Arthroscopy (difficult in the hock)
77
Q

Radiographic findings consistent with hock osteochondrosis

A
78
Q

Treatment and prognosis of hock osteochondrosis

A
79
Q

Lumbosacral osteochondrosis: signalment and presentation

A
  • Rare condition
  • Does not commonly cause clinical signs
  • Can result in instability and disc extrusion / protrusion and back pain
80
Q

Which muscles atrophy with pathology in each of these area?
Hip -
Stifle -
Shoulder -

A

Hip - gluteal muscles
Stifle - quadriceps
Shoulder - scapula muscles

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