avascular necrosis

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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