Part 16 Final Flashcards
AVN definition
death of osseous cellular marrow compnents of bone
AVN has a predisposition for?
epiphyseal
when does epiphyseal necrosis become clinically evident?
when articular surfaces collapse
what is the latent period for AVN?
weeks to a year
what is the MC etiology for AVN?
spontaneous/idiopathic
types of AVN
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
pathogenesis of AVN
obstruction of extra- and intraosseous vessels by aterial embolism, venous thrombosis, traumatic disruption, external compression
increased marrow space pressure
time frame from inital infarction to healed deformity?
variable, usually 2-8 years
etiology of AVN
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)
four stages of AVN
avasular
revascularization
repair
deformity
avascular phase
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
what happens in revascularization phase?
infiltration of new vessels into necrotic bone results in deposition and resorption
deposition (AVN)
new bone is deposited directly on dead bone, theickening the trabeculation and increasing bone density (creeping substitution)
resorption of bone in AVN is due to?
secondary to phagocytosis, fibrosis and infiltration and produces bony fragmentation
where can fracture occur in an AVN?
articular cortex in the revascularization phase
repair and remodeling phase (AVN)
bony resorption is replaced by bony deposition
as in nectortic phase the new bone is easily modeled and deformity may be produced
deformity phase (AVN)
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
general radiological features of epiphyseal infarction
collapse of articular cortex fragmentation mottled trabecular pattern sclerosis subchondral cysts subchondral fracture
describe collapse of articular cortex
generally at region of max stress represents impaction fracture of necrotic bone, loss of normal smooth contour
describe fragmentation (AVN)
manifestation of resorption and weakening, radiolucent clefts appear
describe mottled trabecular pattern (AVN)
reveals a thickened irregular pattern traversing the necrotic areas, most likely seen in the revascularization and repair phases
sclerosis (AVN)
occurs with revascularization new bone deposited around dead trabeculae typically occurs centrally, peripherally cortical margin or maybe a homogenous/patchy increased density
subchondral cysts (AVN)
patchy, well circumscribed areas of rarefaction identical to DJD cysts
subchondral fractures (AVN)
result from weakened subchondral bone, separates articular cortex from cancellous bone (rim sign or crescent sign)
metaphyseal/diaphyseal infarcts typically occur where?
distal femur
proximal tibia
proximal humerus
usually medullary
other name for adult femoral head AVN
chandler’s
just call it AVN of the femoral head
demographics for femoral head AVN
male, 30-70
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
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
signs of AVN
snow cap sign
crescent rim sign
mushroom deformity
hanging rope sign
what does a healed AVN look like?
articular deformity (early DJD) acetabular dysplasia hanging rope sign trochanteric overgrowth mushroom deformity
AVN on MRI
MRI scans demonstrate loss of marrow signal, particularly on T1
often bilateral
may demonstrate joint effusion
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%
symptoms of legg-calve-perthes disease
groin pain, limping, pain, limitation of motion, particularly abduction and internal rotation
etiology of legg-calve-perthes disease
unknown
hereditary, trauam, endocrine disorders, inflammation, nutrition, altered circulatory hemodynamics, distrubed venous drainage, intraosseous HTN
phases of legg-calve-perthes disease
avascular (0-12months)
revascularization (6mo-4years)
repair and remodeling (1-2 years)
just like adult AVN
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
soft tissue signs of hip joint disease
capsular swelling
small obtruator
increased tear drop distance
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
epiphyseal disorders
osteochondritis osteochondrosis legg-calve-perthes disease AVN aseptic necrosis primary and secondary necrosis growth variations trauma
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
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
treatment goal for osteochondritis dessicans
goal is to preserve a smooth congruity between opposing articulating surfaces
location of osteochondritis dessicans
knee** (lateral aspect of medial femoral condyle)
humeral head
capitellum of elbow
medial surface of elbow
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
spontaneous osteonecrosis
a diagnostic term applied to the aged knee
SONK
spontaneous osteonecrosis of the knee
osgood schlatter’s disease
fragmentation of the apophsis of the tibial tuberosity
probably traumatic rather than a true necrosis
diagnosis of osgood schlatter’s disease
must have the clinical findings!!
osgood schlatter’s symptoms on the patella
sindig larsen johanssen disease
freiberg’s disease
avascular necrosis of the metatarsal head (usually MTP 2)
who is freiberg’s more common in? why?
females 13-18
high heeled shoes
