Ischemic Osteonecrosis
- Ischemic Osteonecrosis (More accurate term) aka avascular necrosis AVN: this term describes subarticular (subchondral) bone death
- Intramedullary bone infarct: describes osteonecrosis within the medullary cavity of the bone (above x-ray image)
- Causes: m/c: trauma, systemic corticosteroids, diabetes, vasculitis in SLE. The list is long. Other important causes: Sickle cell disease, Gaucher disease, alcohol, caisson disease, SCFE, LCP, etc.
- Pathology: ischemia and bone infarct with resultant devitalized center surrounded by ischemia and edema with normal bone on the outer periphery (MRI double line sign)
- Sub-articular necrotic bone eventually collapses and fragments leading to progressive bone and cartilage destruction and rapidly progressing DJD
- Early Dx often missed but crucial to prevent svere DJD
M/C Sites
- Hips, shoulders, talus, scaphoid bone. Many peripheral idiopathic AVN sites are known by their eponyms (e.g. Kienbock aka AVN of the lunate bone, Preisier aka scaphoid AVN)
- Radiography is insensitive to early AVN and may only present as subtle osteopenia
- Some of the early appreciable rad features are increased patchy bone sclerosis followed by sub-articular bone collapse or “crescent sign” signifying stage-3 on Ficat
calssification (above) - Earliest detection and early intervention can be
acheived by MRI (most sensitive modality) - If MRI contraindicated or unavailable, 2nd most sensitive modality is radionuclide bone scan (
scinthigraphy ) - X-ray and CT scanning are of equal value
Coronal MRI Slice
- Fluid sensitive sensitive coronal MRI slice revealing bill ischemic osteonecrosis of the femoral head
- MRI findings: l
Tc99-MMDP Radionuclide Bone
- Bone scan reveals central area of photopenia (cold spot) d/t necrotic fragment surrounded by increased osteoblastic activity as increased uptake of Tc-99 MDP in the right hip
- The patient is a 30-year-old female with breast cancer and chemotherapy treatment who suddenly presented with right hip pain
Radiographic Progression of AVN
- Later stages present with articular collapse, subarticular cysts, increased patchy sclerosis and complete flattening of the femoral head with resultant severe DJD. Rx: THA
Management
- Early imaging Dx with MRI or bone scintigraphy is essential
- Referral to the Orthopedic surgeon
- Core decompression (above) can be used to revascularize the affected bone during earlier stages but produces mixed results
- Delayed changes of AVN: THA as IN severe DJD cases
B/L THA
- B/L THA in the patient with ischemic osteonecrosis of the right and later left hip
- When B/L hip AVN is present, typically consider systemic causes (corticosteroids, diabetes)
Inflammatory Arthritis Affecting the Hip
- Consider common systemic inflammatory condition such as RA and AS/EnA
- Hip RA may develop in 30% of patients with RA
- Key features to DDx inflammatory arthritis vs. DJD is symmertical/uniform aka concentric joint loss often leading to axial migration and Protrusion Acetabule in advanced cases
- Key feature between RA vs. AS: presence of RA bone erosion w/o productive bone changes or enthesitis in AS d/t inflammatory subperiosteal bone proliferation, whiskering/fluffy periostitis (collar-type enthesitis circumferentially affecting head-neck junction)
- Dx: Hx, PE, labs: CRP, RH, anti-CCP Ab (RA)
- CRP, HLA-B27, RF- (AS)
Septic Arthritis
- Gonococcal infections, iatrogenic causes, I.V. drug use
and some others - Routes:
haematogenous ,adjecent spread, direct inoculation (e.g. iatrogenic) - Clinically: pain and reduced ROM presented as
mononarthritis , generalized signs/symptoms. CBC, ESR, CRP changes. ARthrocentesis and culture are crucial - M/C pathogen Staph. Aureus & Neisseria Gonorrhea
- 1st step: radiography, often unrewarding in the early stage. Later (4-10 days) indistinctness of
white cortical line at the femoral articular epiphysis, loss of joint space, effusion aswidening of medial joint space (Waldenstrom sign) - MRI – best at early DX: T1, T2, STIR, T1+C may help with early. Early I.V. antibiotics crucial to prevent rapid joint destruction
Slipped Capital Femoral Epiphysis (SCFE)
- Important to diagnose but easily missed potentially leading to Ischemic Osteonecrosis of the femoral head aka AVN
- Presents typically in overweight children (more often boys), age over 8 years. Greater incidence in African-American boys
- 1st step: radiography, especially look for a widened physeal growth plate (so-called pre-slip). Later, slip and disturbed Klein’s line (above image). MRI – best modality for early Dx and early intervention
- The frog lateral view often demonstrates the medial slip better than the AP view
Clinically Limping Child or Adolescent
- M>F (10-18 years). African-Americans are at greater risk. 20% cases of SCFE are B/L. Complications: AVN >>DJD
- Radiography: AP pelvis, spot and frog leg may reveal slippage as Klein line failed to cross through the lateral aspect of the femoral head
- Additional features: physis may appear widened
- MRI w/o gad, is required for the earliest Dx and prevention of complications (AVN)
Normal and Abnormal Klein Line
- Consistent with SCFE. The physis is also widened. Dx: SCFE
- Urgent referral to the pediatric Orthopedic surgeon
Subtle Changes in Left Hip
- Note suspected subtle changes in the left hip that may require MR examination to confirm the Dx
- Delay in care may result in major complications
Perthes’ Disease
- aka Legg-Calves-Perthes Disease (LCP)
- Refers to Osteochondritis of the femoral head with osteonecrosis likely d/t disturbed vascularization of the femoral head
- Presents typically in children (more often boys) aged under 8 years as atraumatic “limping child.” 15% may have B/L Perthe’s
- Imaging steps: 1st step x-radiography, followed by MRI especially in stage 1 (early) w/o x-ray abnormalities
- Unspecific signs: joint effusion with Waldenstrome sign+ (>2-mm increase in medial joint space compared to the opposite side). Past approach: Fluoroscopic Arthrography (replaced by MRI)
- Pathologic-Radiologic Correlation: in well-established cases, the femoral head characteristically becomes sclerotic, flattened and fragmented due to avascular necrosis (AVN). Later on, an occasional Coxa Magna changes may develop (>10% femoral head enlargement)
- Management: symptoms control, bracing. Boys at younger ate show better prognosis d/t more immaturity and better chances of bone/cartilage reparir mechansisms. In advanced cases, operative care: osteotomy, hip arthrpoplasty in adulthood if advanced DJD develops
Common Neoplasms & Other Conditions Affecting Hip/Pelvis
- M/C hip & pelvis neoplasms in adults: bone metatasis ( above far left), 2nd m/c Multiple Myeloma (M/C primary bone malignancy in adults). Tips: remember Red Marrow distribution. Less frequent: Chondrosarcoma
- Paget’s disease of bone (above-bottom left image) is m/c detected in the pelvis and Femurs
- Children and young adults ‘limping child’ benign neoplasms: Fibrous Dysplasia (above middle image), Solitary Bone Cyst (21%), Osteoid Osteoma, Chondroblastoma. Malignant pediatric neoplasms: m/c Ewing Sarcoma (above middle right and bottom images) vs. Osteosarcoma. >2y.o-consider Neuroblastoma
- Imaging: 1st step: radiography followed by MRI are most appropriate.
- If Mets are suspected: Tc99 bone scintigraphy is most sensitive
Multiple Myeloma
- Multiple Myeloma in a 75-y.o male (AP pelvis view)
- Chondrosarcoma in a 60-y.o male (axial and coronal reconstructed CT+C slices in bone window)
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