AVN MANAGEMENT

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Based on the textbook content retrieved, here is a comprehensive summary of Avascular Necrosis (AVN) / Osteonecrosis Management:

Avascular Necrosis (AVN) — Management

Definition

AVN (also called osteonecrosis, aseptic necrosis, or ischemic necrosis) is skeletal infarction resulting from disruption of blood supply to bone. It can be asymptomatic, cause self-limited discomfort, or lead to painful subarticular bone collapse and joint destruction. — Goldman-Cecil Medicine

Causes / Risk Factors

CategoryExamples
TraumaticHip dislocation, femoral neck fracture
CorticosteroidsLong-term glucocorticoid therapy, Cushing disease
VascularSickle cell disease, fat emboli, caisson disease (dysbaric)
MetabolicEthanol abuse, diabetes mellitus, hyperuricemia, hyperlipidemia
OtherHIV/AIDS, renal dialysis, organ transplantation, irradiation, Gaucher disease, pancreatitis, pregnancy
The femoral head is the most commonly affected site at all ages. Non-traumatic AVN also affects the humeral head, femoral condyles, distal tibia, and talus.

Diagnosis

ModalityRole
MRIMost sensitive; detects bone marrow edema in early disease — modality of choice
Bone scintigraphyCan detect AVN before plain radiographs; SPECT more accurate for femoral head vascularity
Plain radiographsLate finding: patchy osteopenia + osteosclerosis reflecting skeletal repair
Crescent signLinear subchondral radiolucency = subarticular bone collapse (late, ominous sign)
MRI demonstrating bone marrow edema is especially sensitive for detecting early osteonecrosis. — Goldman-Cecil Medicine

Staging (Ficat & Arlet / ARCO System)

StageFeatures
INormal X-ray; MRI positive (marrow edema)
IISclerosis/cystic change; no collapse; X-ray changes present
IIICrescent sign — subchondral collapse; articular surface intact
IVCollapse of articular surface; secondary osteoarthritis

Management

Non-Operative (Conservative)

  • Protected weight-bearing — reduces mechanical stress on the affected joint
  • Analgesics / NSAIDs for pain control
  • SONK (spontaneous osteonecrosis of the knee): typically self-limiting — managed with limited weight bearing until resolution
  • Treat underlying cause (e.g., reduce corticosteroid dose if possible, manage sickle cell disease, alcohol cessation)
  • Adjuncts: bisphosphonates, statins, anticoagulants (limited evidence)

Operative — Joint-Preserving (Pre-Collapse, Stages I–III)

ProcedureIndication / Notes
Core decompressionGold standard for early stages (I–II); reduces intraosseous pressure, promotes revascularization; can be combined with bone grafting
Core decompression + bone graftingStructural support + biological stimulus; cancellous, cortical, or vascularized graft
Vascularized fibular graftProvides structural support and blood supply; best for larger lesions in young patients
Osteotomy (rotational/flexion)Rotates necrotic segment away from weight-bearing zone; used in selected cases in young patients

Operative — Joint Replacement (Post-Collapse, Stage III–IV)

ProcedureIndication
Total Hip Arthroplasty (THA)Most common definitive treatment for advanced femoral head AVN with collapse
HemiarthroplastyMay be used in elderly patients with femoral neck fractures leading to AVN
Total Knee Arthroplasty (TKA)For advanced osteonecrosis of the knee with articular destruction
Anatomic TSA / Reverse TSAFor advanced humeral head osteonecrosis depending on rotator cuff integrity
In undisplaced intracapsular femoral neck fractures, operative management is favored due to higher prevalence of nonunion, avascular necrosis, and fracture displacement in nonoperatively treated cases. — Rockwood & Green's Fractures in Adults

Humeral Head AVN (Special Consideration)

  • Traumatic causes: 3-part fractures → 15–35% incidence; 4-part fractures → ~90% incidence of osteonecrosis
  • Non-traumatic causes: steroids, alcohol, metabolic disorders, hemoglobinopathies, HIV
  • Staging similar to femoral head AVN
  • Treatment: conservative for early stages; anatomic TSA if rotator cuff intact; reverse TSA if rotator cuff deficient — Miller's Review of Orthopaedics

Key Principles Summary

  1. Early diagnosis (MRI) is critical — joint-preserving surgery is only possible before collapse
  2. Stage I–II → core decompression ± grafting (joint preservation)
  3. Stage III → consider vascularized graft vs. osteotomy vs. arthroplasty based on patient age and lesion size
  4. Stage IV → arthroplasty (THA/TKA/TSA as appropriate)
  5. Address the cause — stop steroids/alcohol when possible, treat underlying hematologic conditions
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