Avascular necross

“Avascular necrosis of
the bone is the death of
bone tissue due to an
impaired blood supply.”

Other names
Avascular necrosis
Osteonecrosis
Bone infarction
Aseptic necrosis
Bone death

 Ahlback disease: medial femoral
condyle, i.e. SONK
 Brailsford disease: head of radius
 Buchman disease: iliac crest
 Burns disease: distal ulna
 Caffey disease: entire carpus or
intercondylar spines of tibia
 Dias disease: trochlea of the talus
 Dietrich disease: head of metacarpals
 Freiberg infraction: head of the
second metatarsal
 Friedrich disease: medial clavicle
 Hass disease: humeral head
 Iselin disease: base of 5th metatarsal
 Kienbock disease: lunate
 Kohler disease: patella or navicular
(children)
 Kummel disease: vertebral body
 Legg-Calvé-Perthes disease: femoral
head
 Liffert-Arkin disease: distal tibia
 Mandl disease: greater trochanter
 Mauclaire disease: metacarpal heads
 Milch disease: ischial apophysis
 Mueller-Weiss disease: navicular
(adult)
 Panner disease: capitellum of
humerus
 Pierson disease: symphysis pubis
 Preiser disease: scaphoid
 Sever disease: calcaneal epiphysis
 Thiemann disease: base of phalanges
 Van Neck-Odelberg
disease: ischiopubic synchondrosis

 Osteonecrosis has been estimated to affect
20,000 new patients per year in the US
 75% of patients are between the ages of 30-
60 years old
 25% of patients with the condition are < 25
years of age
 The disease is more common in males
 7:3 males-females
 An important exception to this male-to-female
ratio is SLE

pathogenesis
 Avascular necrosis result from direct or indirect injury ,or
damage to the vascular flow.
 Ciculatory deficiency result in bone and bone marrow
cell death.(osteocyte , haematopoetic cell , adipocyte).
 The necrotic tissue triggers repair ,a reactive surface
develops at the boundary with the healthy bone.
 Revitalization of the necrosis due to ingrowth of blood
vessel and connective tissue from healthy surroundings
→abnormal and biomechanically weak bone
 Small lesions can heal , if not or incomplete →
subchondral bone will break from repeated microtrauma
and various significant defects will result.

 Cellular ischemia → death of hematopoietic cell in
6-12 hrs, osteocyte in 12-48 hrs and lipocyte in 2-5
days

Clinical Presentation
 Osteonecrosis can be asymptomatic and found incidentally on
imaging
 A high index of suspicion is necessary for patients with risk
factors
 Pertinent patient history includes history of steroid use, alcohol
abuse and clotting abnormalities
 Pain in the affected joint (although non-specific) is usually the
presenting symptom
 The initial physical exam findings may not be useful and are
often non-specific
 After osteonecrosis progresses, joint function deteriorates and
the patient may
 Have tenderness around the affected bone
 Have joint deformity and muscle wasting
 May even have a neurologic deficit if a nerve is compressed due to
necrosis and deformity of the affected bones

Late Presentation
 Unfortunately, most patients present late in the course of disease
 In the late stages, you may see highly deteriorated joint function
and a significant limp
 Without treatment, the patient would be more likely to present
with severe pain at rest and at night and would have more
restriction and pain with joint movements
 Joint deformity, muscle wasting and non union of fracture are
also more common with advanced osteonecrosis
 Medullary infarcts usually remain stable over time, while
subchondral infarcts often collapse and may predispose to
severe secondary osteoarthritis

Etiology :
1-Trauma (fracture or dislocation)
2-Dislocation
3-Collagen vascular disease
4-Sickle cell disease
5-Gaucher's disease
6-Caisson disease
7-Radiation
8-Pancreatitis, alcoholism
9-Hormonal (steroids, Cushing's disease)
10-Idiopathic (Legg-Calve-Perthes disease)
11-Pregnancy

the high prevalence and multifocal nature of AVN in
SLE patients during high dose steroid treatment
of disease exacerbation results from the co-
occurrence of two processes
1. Vascular Injury with widespread activation of
endothelium and inflammatory vasculopathy or
thrombosis disrupting the microcirculation
2. Lipid Deposition with interosseous fat
accumulation, secondary to glucocorticoid induced
abnormal lipid metabolism, increasing intramedullary
pressure (i.e. bony compartment syndrome) and
decreasing perfusion

Classification of the progress of the disease as
described in the association research circulation
osseous (ARCO)
 Initial stage (ARCO 0)
 An ischaemic attach.
 Still reversible and asymptomatic.
 Histologicaly minimal changes can be
found.
 Pathological perfusion can be shown by
dynamic contrast MRI.

Reversible early stage (ARCO
1)
 Edema of the bone marrow with extend
of medullary cavity necrosis.
 Start of repair process, with gradual
replacement of necrotic tisssue by
growth of fibrous vascullar tissue.
 Still no reactive surface.
 MRI

Non_reversible early stage
(ARCO 2)
 Histological bone process, in the sense of
bone resorption and formation of bone
marrow and the trabecula.
 vascular Granulation tissue attempts to
repair the necrotic area inside the
secleretic zone, which is directly opposed
to the area of the vital tissue.
 MRI (MR double line
sign)→pathognomonic in t2 ,it corresponds
to reactive interface.
 X-ray → blotchy change +seclerotic
changes are visible.

Transitional stage (ARCO 3)
 Mechanical failure of the affected bone
area lead to the subchonral microfracture.
 It usually begins at the margin of the
defect and is consequence of in sufficient
repair.
 X-ray → small suchonral crescent sign.
 MRI → MRI cresent sign , if subchondral
fracture filled with synovial fluid.

Late stage (ARCO 4)
 Secondary arthritic lesion (calcification
+resorptive cyst).
 Deformity
 Detect by any imaging method.

AP radiographic view of the pelvis shows flattening of the outer portion of
the right femoral head from avascular necrosis, with adjacent joint space
narrowing, juxta-articular sclerosis, and osteophytes representing
degenerative joint disease (stage IV)

Most common sites
 Head of humerus
 Head of femur
 Scaphoid
 Femur condyles
Affects bones with a single terminal blood
supply

Vascular supply around femoral
neck

diagnosis
 History
 Physical examination
 investigation
Plain radiography
There is significant delay between infarct onset and development of
radiographic signs. Classic description is of medullary lesion of sheet-
like central lucency surrounded by shell-like sclerosis with serpiginous
border. Discrete calcification and periostitis may also be seen.
CT
 Generally does not reveal much more than the plain film.
 The best modality for estimating the extent of bone death
 It is not as sensitive as MRI

MRI
 An important feature in differentiating bone infarct from other
medullary lesions is that the central signal usually remains that of
normal marrow. The marrow is not replaced.
 T1
 serpiginous peripheral low signal due to granulation tissue and to
lesser extent sclerosis
 peripheral rim may enhance post gadolinium
 central signal usually that of marrow
 T2
 acute infarct may show ill-defined non-specific area of high
signal
 double-line sign: hyperintense inner ring of granulation tissue
and a hypointense outer ring of sclerosis
 absence of double-line sign does not exclude bone infarct
 central signal usually that of marrow

GE (gradient echo)
 will also show double-line
 oedema obscured by susceptibility
Nuclear medicine
 bone scan
Bone scintigraphy is also quite sensitive (~85%) and is the second option
after MRI. It is a choice when multiple sites of involvement must be assessed
in patients with risk factors, such as sickle cell disease. The findings are
different accordingly to the time of the scan:
• early disease: often represented by a cold area likely representing the
vascular interruption
• late disease: may show a "doughnut sign": a cold spot with
surrounding high uptake ring (surrounding hyperaemia and adjacent
synovitis)
 no uptake (cold spot) where blood supply absent
 mildly increased uptake at periphery during acute phase

Biopsy
A biopsy is a surgical procedure in which a tissue
sample from the affected bone is removed and studied.
Although a biopsy is a conclusive way to diagnose
osteonecrosis, it is rarely used because it requires
surgery.
Functional Evaluation of Bone
Tests to measure the pressure inside a bone may be used
when the doctor strongly suspects that a patient has
osteonecrosis, despite normal results of x rays, bone
scans, and MRIs. These tests are very sensitive for
detecting increased pressure within the bone, but they
require surgery.

Imaging Method Findings Time to Diagnosis Comments
CT
reactive sclerosis
subchondral
collapse
months
sensitivity poor
specificity OK
radionuclide
imaging
decreased uptake
early, increased
uptake late
weeks
sensitivity good
specificity poor
MRI
decreased signal in a
segmental pattern
days to weeks
sensitivity excellent
specificity good
MRI or PET flow
study
decreased flow
through affected
bone
minutes
theoretically
possible, but not yet
proven

X-ray of head of femur (AVN)
 Crescent Sign
 Snowcapping
 Areas of lucency
 Flattening of joint surface

Luscent areas
Flattening of joint
surface

Snowcapping
Luscent areas
Flattening

Differential
Diagnostic Considerations
Other problems to consider in the differential diagnosis
of avascular necrosis include the following:
 Inflammatory synovitis
 Complex regional pain syndrome
 Labral tears
 Osteomyelitis
 Neoplastic bone conditions
Differential Diagnoses
 Osteoarthritis
 Osteoporosis

Various methods for treatment and delaying disease
progression
Non surgical –
Appropriate treatment for osteonecrosis is necessary to keep
joints from breaking down. Without treatment, most people with
the disease will experience severe pain and limitation in
movement. To determine the most appropriate treatment, the
doctor considers the following:
 the age of the patient
 the stage of the disease (early or late)
 the location and whether bone is affected over a small
or large area
 the underlying cause of osteonecrosis; with an ongoing
cause such as corticosteroid or alcohol use, treatment may not
work unless use of the substance is stopped.
The goal in treating osteonecrosis is to improve the patient’s
use of the affected joint, stop further damage to the bone, and
ensure bone and joint survival. To reach these goals, the doctor
may use one or more of the following surgical or nonsurgical
treatments.

Nonsurgical Treatments
Usually, doctors will begin with nonsurgical treatments,
alone or in combination. Unfortunately, although these
treatments may relieve pain or help in the short term, for
most people they don’t bring lasting improvement.
 Medications.
 Nonsteroidal anti-inflammatory drugs (NSAIDs) are often
prescribed to reduce pain.
 People with clotting disorders may be given blood
thinners to reduce clots that block the blood supply to
the bone.
 Cholesterol-lowering medications may be used to
reduce fatty substances (lipids) that increase with
corticosteroid treatment (a major risk factor for
osteonecrosis).
 Bisphosphonate
 Anticoagulants
 Vasodilators
 Biophysical modalities

 Reduced weight bearing. If osteonecrosis is diagnosed
early, the doctor may begin treatment by having the
patient remove weight from the affected joint. The doctor
may recommend limiting activities or using crutches. In
some cases, reduced weight bearing can slow the
damage caused by osteonecrosis and permit natural
healing. When combined with pain medication, reduced
weight bearing can be an effective way to avoid or delay
surgery for some patients.
 Range-of-motion exercises. An exercise program
involving the affected joints may help keep them mobile
and increase their range of motion.
 Electrical stimulation. This treatment has been used in
several centers to induce bone growth, and in some
studies has been helpful when used before femoral head
collapse.

Surgical –
A number of different surgical procedures are used to treat osteonecrosis. Most people
with osteonecrosis will eventually need surgery.
 Core decompression. This surgical procedure removes the inner cylinder of bone,
which reduces pressure within the bone, increases blood flow to the bone, and
allows more blood vessels to form. Core decompression works best in people who
are in the earliest stages of osteonecrosis, often before the collapse of the joint. This
procedure sometimes reduces pain and slows the progression of bone and joint
destruction.
 Osteotomy. This treatment involves reshaping the bone to reduce stress on the
affected area. Recovery can be a lengthy process, requiring several months of very
limited activities. This procedure is most effective for patients with early-stage
osteonecrosis and those with a small area of affected bone.
 Vascularised bone graft/muscle pedicle graft.This is the transplantation of
healthy bone from another part of the body. It is often used to support a joint after
core decompression. In many cases, the surgeon will use what is called a vascular
graft, which includes an artery and vein, to increase the blood supply to the affected
area. Recovery from a bone graft can take several months.
 Arthroplasty/total joint replacement. Total joint replacement is the treatment of
choice in late-stage osteonecrosis and when the joint is destroyed. In this surgery,
the diseased joint is replaced with artificial parts. Total joint replacement, or
sometimes femoral head resurfacing, is often recommended for people for whom
other efforts to preserve the joint have failed. Various types of replacements are
available, and people should discuss specific needs with their doctor.

Avascular necross

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