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Diagnostic Imaging II > Part 16 Final > Flashcards

Part 16 Final Flashcards

(52 cards)

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1
Q

AVN definition

A

death of osseous cellular marrow compnents of bone

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2
Q

AVN has a predisposition for?

A

epiphyseal

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3
Q

when does epiphyseal necrosis become clinically evident?

A

when articular surfaces collapse

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4
Q

what is the latent period for AVN?

A

weeks to a year

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5
Q

what is the MC etiology for AVN?

A

spontaneous/idiopathic

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6
Q

types of AVN

A 
PLASTIC RAGS
pancratitis, pregnancy
lupus
alcoholism, atherosclerosis
steroids
trauma
idiopathic (leg-calve-perthes), infection
caisson disease, collagen disease

RA, radiation treatment
amyloid
gaucher disease
sickle cell/spontaneous

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7
Q

pathogenesis of AVN

A

obstruction of extra- and intraosseous vessels by aterial embolism, venous thrombosis, traumatic disruption, external compression
increased marrow space pressure

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8
Q

time frame from inital infarction to healed deformity?

A

variable, usually 2-8 years

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9
Q

etiology of AVN

A

external vessel compression (trauma, steroids, infection, gaucher’s, hyperlipidemia
vessel wall disorders (RA, LE, radiation, polyarteritis nodosa)
thrombo-emolic disorders (alcoholism, steroid, trauma, sickle-cell, caisson’s)

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10
Q

four stages of AVN

A

avasular
revascularization
repair
deformity

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11
Q

avascular phase

A

obliteration of epiphyseal blood supply precipitates death of the osteocyte and bone marrow cells
growth is altered, epiphyseal growth slows or stops and articular cartilate continues

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12
Q

what happens in revascularization phase?

A

infiltration of new vessels into necrotic bone results in deposition and resorption

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13
Q

deposition (AVN)

A

new bone is deposited directly on dead bone, theickening the trabeculation and increasing bone density (creeping substitution)

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14
Q

resorption of bone in AVN is due to?

A

secondary to phagocytosis, fibrosis and infiltration and produces bony fragmentation

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15
Q

where can fracture occur in an AVN?

A

articular cortex in the revascularization phase

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16
Q

repair and remodeling phase (AVN)

A

bony resorption is replaced by bony deposition

as in nectortic phase the new bone is easily modeled and deformity may be produced

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17
Q

deformity phase (AVN)

A

following healing, restitiution of the epiphysis to tis normal configuration occurs in varying degrees
residual deformity is due to how much compressive force is exerted on the necrotic bone during revascularization and repair phases

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18
Q

general radiological features of epiphyseal infarction

A 
collapse of articular cortex
fragmentation
mottled trabecular pattern
sclerosis
subchondral cysts
subchondral fracture
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19
Q

describe collapse of articular cortex

A

generally at region of max stress represents impaction fracture of necrotic bone, loss of normal smooth contour

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20
Q

describe fragmentation (AVN)

A

manifestation of resorption and weakening, radiolucent clefts appear

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21
Q

describe mottled trabecular pattern (AVN)

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A

reveals a thickened irregular pattern traversing the necrotic areas, most likely seen in the revascularization and repair phases

22
Q

sclerosis (AVN)

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A

occurs with revascularization new bone deposited around dead trabeculae typically occurs centrally, peripherally cortical margin or maybe a homogenous/patchy increased density

23
Q

subchondral cysts (AVN)

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A

patchy, well circumscribed areas of rarefaction identical to DJD cysts

24
Q

subchondral fractures (AVN)

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A

result from weakened subchondral bone, separates articular cortex from cancellous bone (rim sign or crescent sign)

25
metaphyseal/diaphyseal infarcts typically occur where?
distal femur proximal tibia proximal humerus usually medullary
26
other name for adult femoral head AVN
chandler's | just call it AVN of the femoral head
27
demographics for femoral head AVN
male, 30-70
28
symptoms of femoral head AVN
vague symptoms, pain in buttock, groin, thigh, knee or hip | gradual increase in pain and decreased motion over years, limping gait
29
radiographic signs of femoral head AVN
bite sign frequently articlar cortex separated from necrotic bone articular cortex collapse, impaction fracture of underlying necrotic area fragmentation occurs varying degrees of sclerosis and cystic radiolucencies subchondral fracture (rim sign/crescent sign) altered trabecular pattern core decompresssion involves removing a core of bone from the femoral neck and head
30
signs of AVN
snow cap sign crescent rim sign mushroom deformity hanging rope sign
31
what does a healed AVN look like?
``` articular deformity (early DJD) acetabular dysplasia hanging rope sign trochanteric overgrowth mushroom deformity ```
32
AVN on MRI
MRI scans demonstrate loss of marrow signal, particularly on T1 often bilateral may demonstrate joint effusion
33
legg-calve-perthes disease description
AVN of capital epiphysis before closure self limiting, resolving in 2-8 years affects boys, 4-8 years, bilateral in 10-20%
34
symptoms of legg-calve-perthes disease
groin pain, limping, pain, limitation of motion, particularly abduction and internal rotation
35
etiology of legg-calve-perthes disease
unknown hereditary, trauam, endocrine disorders, inflammation, nutrition, altered circulatory hemodynamics, distrubed venous drainage, intraosseous HTN
36
phases of legg-calve-perthes disease
avascular (0-12months) revascularization (6mo-4years) repair and remodeling (1-2 years) just like adult AVN
37
radiographic findings of legg-calve-perthes disease
soft tissue swelling small epiphysis lateral displacement of ossification center flattening, fissuring and fracture of ossification center metaphyseal widening and foreshortened widened irregular physis intraepiphyseal gas
38
soft tissue signs of hip joint disease
capsular swelling small obtruator increased tear drop distance
39
prognosis of legg-calve-perthes disease
dependant on early diagnosis and treatment age (better in younger patients) sex (poorer in females) poorer in advanced disease
40
epiphyseal disorders
``` osteochondritis osteochondrosis legg-calve-perthes disease AVN aseptic necrosis primary and secondary necrosis growth variations trauma ```
41
describe osteochondritis dessicans
represents a focal subchondral infarction of sub-articular bone the nectoric bone may heal spontaneously or become a free floating fragment separated fromt he parent bone
42
clinical features of osteochondritis dessicans
``` age: 11-20 males asymptomatic/vague complaints clicking, locking, limiting of motion swelling pain aggravated by motion history of trauma may be found ```
43
treatment goal for osteochondritis dessicans
goal is to preserve a smooth congruity between opposing articulating surfaces
44
location of osteochondritis dessicans
knee** (lateral aspect of medial femoral condyle) humeral head capitellum of elbow medial surface of elbow
45
radiology of osteochondritis dessicans
lesion at lateral aspect of medial femoral condyle defect usually concave and <2cm may detach into joint mouse purely cartilaginous fragment unrecognized on plain film fracture line parallels joint surface soft tissue swelling, joint effusion
46
spontaneous osteonecrosis
a diagnostic term applied to the aged knee
47
SONK
spontaneous osteonecrosis of the knee
48
osgood schlatter's disease
fragmentation of the apophsis of the tibial tuberosity | probably traumatic rather than a true necrosis
49
diagnosis of osgood schlatter's disease
must have the clinical findings!!
50
osgood schlatter's symptoms on the patella
sindig larsen johanssen disease
51
freiberg's disease
avascular necrosis of the metatarsal head (usually MTP 2)
52
who is freiberg's more common in? why?
females 13-18 | high heeled shoes

Diagnostic Imaging II (19 decks)

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