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Diagnostic Imaging II > Part 16 Final > Flashcards

Part 16 Final Flashcards

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)

A

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

22
Q

sclerosis (AVN)

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)

A

patchy, well circumscribed areas of rarefaction identical to DJD cysts

24
Q

subchondral fractures (AVN)

A

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

25
Q

metaphyseal/diaphyseal infarcts typically occur where?

A

distal femur
proximal tibia
proximal humerus
usually medullary

26
Q

other name for adult femoral head AVN

A

chandler’s

just call it AVN of the femoral head

27
Q

demographics for femoral head AVN

A

male, 30-70

28
Q

symptoms of femoral head AVN

A

vague symptoms, pain in buttock, groin, thigh, knee or hip

gradual increase in pain and decreased motion over years, limping gait

29
Q

radiographic signs of femoral head AVN

A

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
Q

signs of AVN

A

snow cap sign
crescent rim sign
mushroom deformity
hanging rope sign

31
Q

what does a healed AVN look like?

A 
articular deformity (early DJD)
acetabular dysplasia
hanging rope sign
trochanteric overgrowth
mushroom deformity
32
Q

AVN on MRI

A

MRI scans demonstrate loss of marrow signal, particularly on T1
often bilateral
may demonstrate joint effusion

33
Q

legg-calve-perthes disease description

A

AVN of capital epiphysis before closure
self limiting, resolving in 2-8 years
affects boys, 4-8 years, bilateral in 10-20%

34
Q

symptoms of legg-calve-perthes disease

A

groin pain, limping, pain, limitation of motion, particularly abduction and internal rotation

35
Q

etiology of legg-calve-perthes disease

A

unknown
hereditary, trauam, endocrine disorders, inflammation, nutrition, altered circulatory hemodynamics, distrubed venous drainage, intraosseous HTN

36
Q

phases of legg-calve-perthes disease

A

avascular (0-12months)
revascularization (6mo-4years)
repair and remodeling (1-2 years)
just like adult AVN

37
Q

radiographic findings of legg-calve-perthes disease

A

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
Q

soft tissue signs of hip joint disease

A

capsular swelling
small obtruator
increased tear drop distance

39
Q

prognosis of legg-calve-perthes disease

A

dependant on early diagnosis and treatment
age (better in younger patients)
sex (poorer in females)
poorer in advanced disease

40
Q

epiphyseal disorders

A 
osteochondritis
osteochondrosis
legg-calve-perthes disease
AVN
aseptic necrosis
primary and secondary necrosis
growth variations
trauma
41
Q

describe osteochondritis dessicans

A

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
Q

clinical features of osteochondritis dessicans

A 
age: 11-20
males
asymptomatic/vague complaints
clicking, locking, limiting of motion
swelling pain aggravated by motion
history of trauma may be found
43
Q

treatment goal for osteochondritis dessicans

A

goal is to preserve a smooth congruity between opposing articulating surfaces

44
Q

location of osteochondritis dessicans

A

knee** (lateral aspect of medial femoral condyle)
humeral head
capitellum of elbow
medial surface of elbow

45
Q

radiology of osteochondritis dessicans

A

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
Q

spontaneous osteonecrosis

A

a diagnostic term applied to the aged knee

47
Q

SONK

A

spontaneous osteonecrosis of the knee

48
Q

osgood schlatter’s disease

A

fragmentation of the apophsis of the tibial tuberosity

probably traumatic rather than a true necrosis

49
Q

diagnosis of osgood schlatter’s disease

A

must have the clinical findings!!

50
Q

osgood schlatter’s symptoms on the patella

A

sindig larsen johanssen disease

51
Q

freiberg’s disease

A

avascular necrosis of the metatarsal head (usually MTP 2)

52
Q

who is freiberg’s more common in? why?

A

females 13-18

high heeled shoes

Diagnostic Imaging II (19 decks)

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