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Clinical Pod Med Exam 1 > 13 - Osteochondrosis > Flashcards

13 - Osteochondrosis Flashcards

1
Q

General features of osteochondrosis

A
  • Common during the middle years of growth
  • Affect boys>females
  • Lower limbs more frequently involved.
  • Approximately 15% are bilateral
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2
Q

Types of osteochondroses

A
  • Freiberg’s disease
  • Kohler’s disease
  • Buschke’s disease
  • Thiemann’s disease
  • Sever’s disease
  • Islen’s disease
  • Legg-calve-perthes disease
  • Osgood -schlatter’s disease

These are a group of conditions in which the primary or secondary center of ossification undergo aseptic necrosis

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3
Q

Phases of osteochondrosis

A
  • Early phase of necrosis (phase of avascularity)
  • Phase of revascularization w/ bone deposition and resorption
  • Phase of bone healing
  • Phase of residual deformity
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4
Q

Early phase of necrosis (phase of avascularity)

A
  • Osteocytes and bone marrow cells die
  • Ossific nucleus of the epiphysis ceases to grow
  • Articular cartilage remains alive and grows
  • Disuse atrophy (osteoporosis)
  • Asymptomatic
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5
Q

Phase of revascularization w/ bone deposition and resorption

A
  • Stage represents a vascular reaction of the surrounding tissue to dead bone
  • Ossification of the thickened pre-osseous cartilage resumes & new bone is laid down on dead trabeculae
  • Combination of irregular areas of bone deposition and resorption provides radiographic appearance of fragmentation.
  • The most vulnerable stage of osteochondrosis.
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6
Q

Phase of bone healing

A
  • Bone resorption ceases, but bone deposition continues

- Newly formed bone still exhibits biological plasticity

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7
Q

Phase of residual deformity

A
  • Once bony healing of the epiphysis is complete its contour relatively remains unchanged
  • If any residual deformity is present, it will remain, as well as the associated complications.
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8
Q

Legg-Calve-Perthes Disease (LCPD)

A
  • Ischemic necrosis of the femoral capital ossification center.
  • Males (4-8 years/old)
  • Avascularity (unknown-etiology)
  • Self limited disease
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9
Q

Etiology of LCPD

A

Occlusion of the blood supply to the femoral head

This can be caused by two things

  • Excessive fluid pressure of a synovial effusion (joint fluid)
  • Inflammatory or traumatic
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10
Q

Signs and symptoms of LCPD

A
  • Pain in the region of the hip (synovial effusion)
  • Antalgic gait (protect the hip)
  • Limited range of motion (abduction and internal rotation)
  • Disuse atrophy
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11
Q

Basic progression of LCPD

A
  • Femoral head becomes more dense with possible fracture of supporting bone
  • Fragmentation and reabsorption of bone
  • Reossification when new bone has regrown
  • Healing, when new bone reshapes
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12
Q

Four disease stages of LCPD

A
  • Incipient or synovitis phase
  • Aseptic necrotic / avascular stage
  • Regenerative / fragmentation stage
  • Residual stage
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13
Q

Incipient or synovitis phase of LCPD

A
  • Soft tissue change around the hip occurs

- This will last for 1-3 weeks

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14
Q

Aseptic necrotic or avascular stage of LCPD

A
  • The entire head or anterior half of the ossific nucleus is dead
  • This stage lasts for several months to years
  • The necrotic mass consists of dead bone marrow and dead bone in the marrow spaces
  • There is NO evidence of bone regeneration during this stage ***
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15
Q

Regenerative/fragmentation stage of LCPD

A
  • Radiographically, the femoral head appears compressed and fragmented
  • There is also ingrowing fibrous vascular tissue and immature bone present
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16
Q

Residual stage of LCPD

A
  • Rarefied area gradually disappers and normal trabecular patterns form
  • There will be a residual coxa magna (asymmetrical, circumferential enlargement and deformation of the femoral head and neck)
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17
Q

Treatment of LCPD

A
  • Aimed at preventing deformity of the femoral head and degenerative changes in the hip.
  • Preserve congruity of the joint
  • Abduction cast or some type of abduction brace.
  • Femoral osteotomy and innominate osteotomy (prevent or overcome subluxation)
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18
Q

Osgood’s Schlatter’s disease

A
  • Osteochondrosis of the tibial tuberosity
  • Males (10-15 years/old)
  • Radiographs are of no, or little use, variation of the apophysis tibial tuberosity
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19
Q

Clinical symptoms of Osgood’s Schlatter’s disease

A
  • Diagnosis chiefly determined by pain and soft tissue edema
  • Enlargement of the tibial tuberosity, with a maximum area of tenderness at the insertion of the patellar tendon.
  • Presumed etiology secondary to trauma
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20
Q

Differential diagnosis of Osgood’s Schlatter’s disease

A
  • Tendonitis
  • Osteogenic sarcoma
  • Infection
  • Tibial tubercle fracture
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21
Q

Radiographic findings during acute phase of Osgood’s Schlatter’s disease

A

Acute phase

- Soft tissue swelling anterior to the tibial tuberosity will be present

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22
Q

Radiographic findings during chronic phase of Osgood’s Schlatter’s disease (3 types of the chronic phase)

A

Chronic phase
1 - Type 1: tibial tuberosity is prominent and irregular
2 - Type 2: same as type 1, with small free particle of bone located at the anterior tuberosity
3 - Type 3: normal tuberosity with bone particle

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23
Q

Treatment of Osgood’s Schlatter’s disease

A
  • Withdrawal from active sports that cause pain
  • Ice, NSAIDs, pad to protect tuberosity, rest
  • Infrapatellar strap during activity
  • Steroid injection NOT recommended (risks; very questionable efficacy)
  • Cast immobilization for 6 weeks if severe symptoms (last resort) with crutches (non-weightbearing)
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24
Q

Complications of Osgood’s Schlatter’s disease

A

Complications: proximal segment fails to unite to the remainder of the tubercle (remains as a local source of pain)

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25
Q

Case study 1

A
  • Patient is a 12 year old black male who initially presented with a history of left knee pain for 4 months
  • On physical examination the patient had a prominent tibial tubercle which was swollen and tender
  • There was also no tenderness over the patellar tendon
  • There was full range of motion in the knee, but the patient had hamstring tightness
  • He also had pain with resisted knee extension
  • There was no instability to varus or valgus stress
  • McMurray test was negative
  • Lachman test was negative
  • Patellar tracking was normal, and there was no pain with loading of the patellofemoral joint
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26
Q

Radiographic findings in case study 1

A

Radiographs: ossicle (bone fragment) anterior to the tibial tuberosity

Tibial tuberosity is abnormally shaped, contributing to pain

Diagnosis is Osgood Schlatter’s disease

27
Q

Initial treatment for case study 1

A

Treatment:

- ibuprofen 600mg. Bid
- decrease activity

Wait and see how this patient does

28
Q

Kohler’s disease

A
  • Osteochondrosis of the navicular
  • 4x more frequent in males
  • Between the ages of (3-7)
  • Ossification (18-24 months for females) and (24-30 months in males) ***
  • Occasionally bilateral
  • May occur simultaneously with legg-perthes
29
Q

Etiology of Kohler’s disease

A
  • Mechanical theory
  • Compression theory
  • Weismann theory
  • Waught theory
30
Q

Mechanical theory of Kohler’s disease

A

Longitudinal strain during locomotion

31
Q

Compressive theory of Kohler’s disease

A

Compressive forces during locomotion–compromise the vascular source

32
Q

Weismann theory of Kohler’s disease

A

Weismann: talus projects further distally than normal (approx. 16-35%).

33
Q

Waugh theory of Kohler’s disease

A

Waugh theorized: during the vulnerable stage of single vessel supply of the ossific nucleus of the tarsal navicular, disruption of this vessel could produce ischemia, fragmentation of the ossific nucleus with collapse, reactive hyperemia and pain, i.e. Kohler’s disease.

34
Q

Symptom’s of Kohler’s disease

A
  • Antalgic gait (weight bearing on lateral side) – turn foot inward when walking
  • Local pain and tenderness over the navicular
  • Posterior tibial tendon inflamed at it’s insertion site
35
Q

Radiographic findings in Kohler’s disease - TWO PATTERS

A
  • Flattening of the navicular
  • Irregular rarefactions & sclerosis

Two radiographic patterns ***
1 - Flattened navicular w/ patchy areas of increased bone density and loss of normal trabecular (discoid navicular)
2 - Normal shape navicular w/ increased density

36
Q

Treatment of Kohler’s disease

A
  • Below knee walking cast (foot in 10-15 degrees of varus and 20 degrees of equinus) 6-8 weeks
  • First two weeks non-weightbearing

Once there is some improvement…

  • Decrease strenuous activity
  • Rigid orthoses or thomas heel
  • Follow through w/ soft longitudinal arch support
  • Prognosis very good
37
Q

Case study 2

A
  • A 6 year old male presents with a 3 week hx of right foot pain.
  • Radiographs are on slide 38
  • Navicular bone is much more sclerotic than the others
  • You can diagnose based on radiographs
  • Diagnosis is Kohler’s disease
  • Below the knee walking cast is the treatment
38
Q

Case study 3

A

3 year old girl presented with a complaint of left foot pain exacerbated by bearing weight.

Four weeks prior to this visit, the patient’s 4 year old sister had jumped onto her left foot during play resulting in pain and an antalgic gait. She had no pain in the left foot prior to this episode.

She was given a diagnosis of Kohler’s disease and instructed to restrict her activities. The patient continued to have a limp and frequently complained of pain in her left foot, especially after activity.

Follow up evaluation revealed fractures to the lesser metatarsals

Further treatment consisted of casting the left leg

39
Q

Freiberg’s infarction

A
  • Avascular necrosis of metatarsal head
  • Between ages 13-18 (females)
  • Generally unilateral
  • Structurally weak feet
  • Second met.–68%
  • Third met.–27%
40
Q

Differential diagnosis for Freiberg’s infarction

A
  • Fracture/Stress fracture
  • Synovitis/capsulitis
  • Extensor/flexor tendonitis
  • Metatarsalgia
  • Morton’s neuroma
  • JRA
41
Q

Etiology of Freiberg’s infarction - TWO ETIOLOGIES

A

Smillie theory: Occurs secondary to a traumatic process (stress)

Braddock theory: Secondary to fracture modified by its proximity to the epiphyseal plate

42
Q

Clinical presentation of Freiberg’s infarction

A
  • Local pain, tenderness, swelling

- Limitation of MPJ motion

43
Q

Classification of Freiberg’s infarction

A

Stage I: epiphyseal fissure fracture

Stage II: central portion of bone reabsorption

Stage III: metatarsal head begins to flatten

Stage IV: articular loose body

Stage V: complete flattening of the metatarsal

The progression will occur ONLY if there has been no treatment implemented

44
Q

Radiographic findings of Freiberg’s infarction

A
  • Widening of joint space with effusion***
  • Initial lesion (subchondral bone fracture)
  • Central and dorsal head detaches
  • Loose fragment becomes encompassed in a cavity
  • Collapse of lateral margin
45
Q

Treatment of Freiberg’s infarction

A
  • Acute stage: below the knee walking cast (3-4 weeks) or until symptoms subside
  • Use of metatarsal pad after cast removal
  • Orthoses
  • Adult: surgical intervention (arthroplasty, metatarsal head resection or implant) - almost like a hammertoe correction procedure
46
Q

Case study 4

A

HISTORY:

  • 15 year old female with left foot pain near the fourth toe for one year.
  • She had no antecedent trauma
  • She described her pain as a constant, dull ache which had been getting progressively worse.

PHYSICAL EXAM:

  • She complained of exquisite tenderness with flexion and extension of her left fourth toe.
  • She had tenderness to palpation over the dorsum of the fourth metatarsal phalangeal joint.
  • She was unable to toe walk without inverting her foot to relieve pressure from the fourth metatarsal head.

RADIOGRAPH

  • Metatarsal head is flattened
  • Osteopenic changes to the metatarsal head
  • This is a phase of new bone deposition
47
Q

Sever’s disease

A
  • Osteochondrosis of the calcaneus
  • Normal ossification appearance varies between 8-13 years old
  • Radiographs are non-contributory
  • Apophysis (a bony tubercle) usually has a greater density than the calcaneus
48
Q

Contributing factors to Sever’s disease

A
  • Gastroc-soleus equinus
  • Any foot deformity resulting in excessive pronation and decreased shock absorption
  • Cavus foot (high arch)
  • Obesity
  • Inflammatory conditions
  • Activity level
49
Q

Differential diagnosis for Sever’s disease

A
  • Fracture/ stress fracture
  • Lytic lesion
  • Infection
  • Tendonitis
50
Q

Radiographic findings in Sever’s disease

A
  • Diagnosis cannot be made
  • Contra-lateral films should be taken
  • Multiple centers of ossification, apophyseal (bony outgrowth/projection) sclerosis
51
Q

Clinical presentation of Sever’s disease

A
  • Pain, tenderness to palpation
  • Antalgic gait
  • Exacerbated by activity
  • Little pain in morning or after rest
  • Speculation that may be associated with trauma
52
Q

Treatment of Sever’s disease

A
  • Decrease in activity
  • Short leg cast 2-4 weeks
  • NSAIDs
  • Control pronatory force
  • Treat gastroc-soleus equinus
53
Q

Less frequently occurring osteochondroses

A
  • Thiemann’s disorder
  • Islen’s disease
  • Buschke’s disease
  • Diaz disease
  • Treve disease
  • Osteochondritis Dessicans
54
Q

Thiemann’s disorder

A
  • Osteochondrosis of the phalanges (proximal epiphyses)

- May be associated with activities (repetitive trauma)

55
Q

Islen’s disease

A

Osteochondrosis of the styloid process (on the lateral aspect of the foot - 5th metatarsal)

56
Q

Etiology of Islen’s disease

A
  • Traction apophysitis from the peroneus brevis

- Metatarsus adductus

57
Q

Buschke’s disease

A
  • Osteochondrosis of the cuneiform bones
  • Radiographs will show irregularity of contour and fragmentation
  • Occurs in children between ages 5-13
58
Q

Diaz disease

A

Osteochondrosis of the talus

59
Q

Treve disease

A

Osteochondrosis of the sesamoids

60
Q

Osteochondritis Dessicans

A
  • Juvenile and adult type
  • disturbance due to epiphyseal development
  • Trauma
  • Knee joint most commonly affected

Areas affected:

  • Medial femoral condyle
  • Femoral head
  • Talus
61
Q

Etiology of osteochrondritis Dessicans

A

Etiology

  • Primarily unknown
  • May be familial
  • May be associated with other osteochondrosis
  • May be associated with abnormality of the epiphysis
  • Local trauma may be the aggravating factor to initiate the lesion
62
Q

Symptoms of osteochondritis Dessicans

A
  • Intermittent pain in the joint
  • Stiffness
  • Swelling
  • Clicking and locking
  • Giving way
63
Q

Radiographic findings in osteochondritis Dessicans

A

A fragment of subchondral bone

64
Q

Treatment of osteochondritis Dessicans

A
  • Conservative
  • Long leg plaster cast
  • For a lesion of the talus a short leg cast
  • Arthrotomy and insertion of graft

Clinical Pod Med Exam 1 (17 decks)

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