avascular necrosis
TRANSCRIPT
CASE HISTORY
41-year-old male presented with
PAIN Site: right sided low back, hip and knee pain Onset: from past six months. Fell from two meter high roof
land on his feet Intensity: worsening pain with time Pattern: antalgic limp and walked with the help of a cane. Radiation: into his right groin and anteromedial thigh region. Aggravating factors: walking and stair climbing. Relieving factors: sitting and resting.
NO ASSOCIATED SYMPTOMS
PAST HISTORY Flu vaccine 14 months prior to injury. He subsequently developed an allergic reaction and
was diagnosed with leukocytoclastic vasculitis skin eruptions.
Treated with four months of oral corticosteroid therapy with doses up to 50 mg per day. The skin lesions resolved with treatment.
However he developed corticosteroid-induced glucose intolerance subsequent to treatment.
Past history also revealed a nasal fracture six years ago which required two surgical interventions.
No other significant point.
PHYSICAL EXAMINATION
Severe pain and restricted movement across hip joint. Right hip region extreme tenderness Muscle atrophy noted in the right region Posterior joint provocation tests were painful for L4, L5. SI testing was painful for the right sacroiliac joint.
ON X-RAY
Irregularity to the right femoral head
Sclerosis
Subchondral lucency Mild collapse
DIAGNOSIS AVASCULAR NECROSIS (AVN)
DEFINITION
Cellular death of bone components due to interruption of the blood supply;
the bone structures then collapse, resulting in bone destruction pain loss of joint function.
ETIOLOGY TOXIC (alter lipid metabolism)
STEROID NOT LESS THAN TWO YEAR INTAKE ALCOHOL DRUD IMMUNOSUPPRESSIVE ANTI-INFLAMMMATORY
TRAUMATIC (vascular occlusion) IDIOPATHIC FRACTURES RADIOTHERAPY
INFLAMMMATORY SLE INFECTION RHEUMATOID ARTHRITIS
HEMOPOIETIC DISORDERS (intravascular coagulation) SICKLE CELL ANEMIA HAEMOPHILIA
MISCELLANEOUS
PATHOPHSIOLOGY
PATHOPHYSIOLOGY
Interruption of the blood supply to the bone Effected bone have single terminal blood supply such as
femoral head and condyles, epiphysis of long bone carpals, talus, humerus,
These bone have limited collateral blood supply Interruption of the vascular supply result in necrosis of bone marrow (2-5 days) Hemopoietic tissues (6-12 hours) Osteoblast, osteoclast, osteocystes (12-48 hours)
EPIDEMIOLOGY
RACE:- Associated with sickle cell anemia, hemoglobin S and SC SEX:- More common in men. Male to female ratio 8:1 AGE:- Middle age fourth or fifth decade of life
FICAT classification (5 stages) most commonly used
MITCHELL classification (4 types) Steinburg classification (7 stages)
RadiologicallyAVN Staging System:
No changes are visible. Plain film:
normal MRI:
normal Clinical symptoms:
nil
STAGE I
STAGE II plain film:
Normal or minor osteopenia Avascular areas are of
increased density (ostesclerosis)
MRI: Edema
bone scan: Increased uptake
clinical symptoms: Pain typically in the groin
STAGE III
Plain film: Mixed osteopenia Sclerosis Subchondral cysts
without any subchondral lucency
MRI: Geographic defect
Bone scan: Increased uptake
Clinical symptoms: Pain and stiffness
STAGE IV
Plain film: Crescent sign and cortical collapse
MRI: Same as plain film
Clinical symptoms: Pain and stiffness+/- radiation to knee and limp
Sub classification depends on the extent of crescent, as follows:
Stage a: Crescent is less than 15% of the articular surface. Stage b: Crescent is 15-30% of the articular surface. Stage c: Crescent is more than 30% of the articular surface.
STAGE V
plain film: End stage with evidence of secondary
degenerative change (joint space narrowing)
Collapsed MRI:
Same as plain film clinical symptoms:
Pain and limp Sub classification on the extent of collapsed
surfaces: Stage a: Less than 15% of surface is collapsed. Stage b: Approximately 15-30% of surface is
collapsed. Stage c: More than 30% of surface is collapsed.
MRI staging of AVN
CLASS TI WEIGHT IMAGE
T2 WEIGHT IMAGE
Grading lesion acuity
A BRIGHT INTERMEDIATE FAT SIGNAL
B BRIGHT BRIGHT BLOOD SIGNAL
C INTERMEDIATE BRIGHT FLUID/ EDEMA SIGNAL
D DARK DARK FIBROSIS SIGNAL
MODALITY OF CHOICE
X-RAY CT MRI RADIONUCLIDE BONE SCAN
X-RAY
Mild-to-moderate AVN Sclerosis (arrows) Changes in bone density (asterisk).
X- RAY
Advanced disease Bone deformities Flattening Subchondral radiolucent
lines (crescent sign) Collapse of the femoral
head
Computed Tomography
To assess the extent of the disease Calcification
Less sensitive then MRI
Computed Tomography
Sclerosis in the central part of femoral head asterisk sign (arrow head)
Low-density region (arrow)
Radionuclide Bone Scan
In early AVN Less sensitive than MRI Findings are nonspecific
Unilateral disease, Healthy side can be used for comparison
Bilateral disease: difficult to interpret
Early AVN Sensitivity of radionuclide bone scan is better than plain films . Central area of decreased uptake is surrounded by an area of
increased uptake. Doughnut sign (arrow):
The reactive zone surrounding the necrotic area.
Magnetic Resonance Imaging Most sensitive (~95%) modality Demonstrates changes well before plain film changes are visible. The progression is:
Diffuse oedema Focal serpentine low signal line with fatty center (most common
appearance) Double line sign on T2WI is diagnostic Osteochondral fragmentation: rim sign Secondary degenerative change
Magnetic Resonance Imaging
Decreased signal intensity in the subchondral region on both T1- and T2-weighted images, suggesting edema (water signal) in early disease.
Magnetic Resonance Imaging The next stage is characterized by a reparative process (reactive
zone) and shows Low signal intensity on T1-weighted scans ( band like area) High signal intensity on T2-weighted scans. (double line sign)
Advanced AVN
Deformity of the articular surface Calcification
TREATMENT
Medical management: Conservative measures
Limit weight bearing Pain medications.
Immobilization Bisphosphonates
Delay collapse of the femoral head Delay the need for surgical intervention.
Statin therapy Prevents corticosteroid-induced
Surgical Management: In early stages:
Core decompression with or without bone graft In late stages:
Total hip arthroplasty is the most appropriate treatment
COMPLICATIONS:
Total destruction of the joint may occur. Nonunion of fracture Secondary muscle wasting.
PROGNOSIS Depends on the disease stage at the time of diagnosis More than 50% of patients with AVN require surgical treatment
within 3 years of diagnosis. Half of patients with subchondral collapse of the femoral head develop
AVN in the contralateral hip.
Poor prognostic factors: Age older than 50 years Advanced disease (stage 3 or worse) at the time of diagnosis Non-modifiable risk factors such as cumulative dose of corticosteroids
(corticosteroid-induced AVN)
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