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 as widening 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)

Hip Pelvis Arthritis & Neoplasms