Avascular Necrosis (AVN).pptx................

Avascular Necrosis (AVN)

1. Avascular Necrosis (AVN) Dr. Madhu (PT)

2. Overview Avascular necrosis (AVN), also known as osteonecrosis , is the death of bone tissue due to a lack of blood supply. Without blood flow, the bone tissue dies, which can lead to the collapse of the affected bone and joint destruction. AVN most commonly affects the femoral head (hip joint) but can also occur in other bones like the humerus, knees, shoulders, and ankles.

3. Etiology and Risk Factors 1. Traumatic Causes: Fractures: Especially femoral neck fractures, which can disrupt blood supply to the femoral head. Dislocations: Hip dislocations can damage blood vessels, leading to AVN.

4. Etiology and Risk Factors 2. Non-Traumatic Causes: Steroid Use: Long-term corticosteroid use (e.g., for conditions like asthma or lupus) is a common cause of AVN. Alcohol Abuse: Excessive alcohol intake can interfere with the blood supply to the bone. Thrombosis and Embolism: Conditions like sickle cell anemia or hypercoagulable states can cause blockages in blood flow. Decompression Sickness: Also known as “the bends,” affects divers due to rapid changes in pressure. Vascular Disorders: Atherosclerosis or vasculitis can impair blood supply to the bones. Radiation: Radiation therapy can damage blood vessels, leading to AVN.

5. Etiology and Risk Factors 3. Other Associated Conditions: Autoimmune Diseases: Lupus erythematosus , rheumatoid arthritis. Infections: Osteomyelitis , septic arthritis. Gaucher’s Disease: A genetic disorder that affects bone metabolism. Chronic Pancreatitis: Linked to fat embolism, which may obstruct bone vasculature.

6. Pathophysiology 1. Ischemia: Due to interruption of blood supply, either from trauma or non-traumatic factors. 2. Bone Cell Death: Bone cells ( osteocytes ) die without oxygen and nutrients. 3. Resorption and Repair: The dead bone is resorbed and replaced by weaker bone, which is more prone to collapse. 4. Structural Collapse: The bone architecture becomes compromised, leading to joint collapse, especially in weight-bearing areas like the femoral head. 5. Secondary Osteoarthritis: If left untreated, AVN can lead to degenerative joint disease (osteoarthritis).

7. Clinical Features 1. Pain: - Initial Stages: Mild or asymptomatic, with pain developing gradually. Advanced Stages: Sharp pain, typically localized to the affected joint (hip, shoulder, knee). Pain worsens with weight-bearing activities. 2. Range of Motion: Decreased range of motion as the disease progresses. For hip AVN: Limited internal rotation and abduction. 3. Gait Changes: - Limping, antalgic gait in hip AVN. Difficulty with walking and standing. 4. Joint Deformity: Advanced stages show joint deformity and collapse, with symptoms of secondary osteoarthritis ( crepitus , stiffness).

8. Imaging Studies 1. X-ray: Early Stages: Often normal or show subtle changes. Later Stages: - Subchondral lucency (Crescent sign) – indicates bone collapse. - Flattening or collapse of the femoral head. 2. MRI (Magnetic Resonance Imaging): Gold Standard for early diagnosis. Can detect early ischemic changes before they are visible on X-ray. - Shows bone marrow edema, areas of bone death, and changes in bone structure.

9. Imaging Studies 3. CT Scan: - Useful in showing bony changes, collapse, and deformity. 4. Bone Scan: - Demonstrates areas of decreased blood flow in early disease and increased uptake in areas of repair.

10. Stages of Avascular Necrosis ( Ficat and Arlet Classification ) Stage I: Normal X-rays, MRI positive for bone marrow edema. - Symptoms: Mild pain. Stage II: X-ray shows sclerosis and cysts, but no collapse. - Symptoms: Increasing pain, difficulty in mobility. Stage III: - Crescent sign visible, subchondral collapse without flattening. - Symptoms: Significant pain, decreased range of motion. Stage IV: Complete collapse of the bone and joint space narrowing. - Symptoms: Severe pain, osteoarthritis features.

11. Management Non-Surgical Treatment: Medications: Bisphosphonates : To reduce bone resorption and prevent collapse. NSAIDs: For pain control. Anticoagulants: In cases of clotting disorders (e.g., sickle cell disease). 2. Physical Therapy: Range of motion exercises. Non-weight-bearing exercises to maintain joint mobility. 3. Core Decompression: Surgical drilling into the necrotic area to relieve pressure and stimulate blood flow. - Most effective in early-stage AVN (Stage I and II).

12. Surgical Treatment 1. Bone Grafting: Vascularized Graft: A bone graft is taken with its blood supply (e.g., fibula) to revascularize the affected bone. Non- Vascularized Graft: Bone grafts without a blood supply used in conjunction with core decompression. 2. Osteotomy : - Realignment of the bone to redistribute weight away from the necrotic area, delaying progression. - Mostly used in hip AVN. 3. Total Joint Replacement ( Arthroplasty ): Indicated in late-stage AVN (Stage III and IV) where there is significant joint destruction. Total Hip Arthroplasty (THA): Common for hip AVN with excellent functional outcomes. Partial Joint Replacement: May be considered in younger patients 4. Stem Cell Therapy - Experimental, involves using mesenchymal stem cells to promote healing and regeneration of bone.

13. Bone grafting

14. Osteotomy

15. Prognosis Early Diagnosis and Intervention: In early stages (I and II), treatments like core decompression or grafting can be successful in preventing bone collapse. Late Diagnosis (Stage III/IV): Surgical joint replacement is often required, with a good prognosis for pain relief and mobility restoration.

16. Complications Secondary Osteoarthritis: Due to joint collapse and cartilage damage. 2. Permanent Disability: If untreated, AVN can cause chronic pain, limited mobility, and severe functional impairment. 3. Increased Risk of Revision Surgery: Patients undergoing total joint replacement may require revision surgery if they are younger, as prostheses have a limited lifespan.

17. Follow-Up and Monitoring Regular Imaging: MRI or X-rays to monitor progression, especially in early stages or after core decompression. Physical Therapy: Post-surgical rehabilitation to restore function and strength. Long-Term Management: Monitoring for signs of secondary osteoarthritis and considering future surgical intervention.