Femoral Head Necrosis: Symptoms and Treatment

Femoral head necrosis

Avascular necrosis of the femoral head (osteonecrosis, aseptic necrosis) is a condition in which insufficient blood supply causes the death of bone tissue in the femoral head. Without treatment, the necrotic bone loses its structural integrity, the femoral head collapses, and disabling secondary osteoarthritis develops. Femoral head necrosis primarily affects adults between 30 and 50 years old, with a male prevalence (ratio 4:1), and accounts for 5-12% of hip replacements implanted each year.

Anatomy and Vascularization of the Femoral Head

The femoral head has a peculiar vascularization that makes it particularly vulnerable to ischemia:

• Femoral circumflex arteries (medial and lateral): branches of the deep femoral artery, they supply most of the blood flow to the femoral head through the retinacular vessels
• Artery of the ligamentum teres: variable and often insufficient contribution in adults
• Endosteal vascularization: minor contribution through the femoral neck

The vascularization is of a terminal type (without significant anastomoses), which means that the occlusion of a vessel cannot be compensated by collateral circulation. This makes the femoral head one of the most frequent sites of osteonecrosis in the human body.

Causes and Risk Factors

Traumatic causes

• Femoral neck fracture: the most frequent cause of post-traumatic necrosis (20-30% of displaced fractures)
• Hip dislocation: damage to the retinacular vessels
• Acetabular fractures

Non-traumatic causes

Corticosteroids (most common non-traumatic cause):

• Prolonged use of high-dose corticosteroids is the most significant risk factor
• Mechanism: fatty embolism of endosteal vessels, increased intra-osseous pressure
• Risk correlated with cumulative dose and duration of treatment
• Conditions requiring cortisone: autoimmune diseases, organ transplants, pulmonary pathologies

Alcohol abuse:

• Second most frequent non-traumatic risk factor
• Mechanism: fatty embolism, altered lipid metabolism, direct toxicity to osteocytes
• Significant risk with consumption exceeding 400 ml of pure alcohol per week

Other causes:

Idiopathic osteonecrosis:
In 10-20% of cases, a precise cause cannot be identified. This is referred to as idiopathic osteonecrosis.

Classification (Ficat and Arlet, modified ARCO)

The crescent sign on radiography is pathognomonic: a radiolucent subchondral line indicating the fracture of the necrotic bone beneath the articular surface.

Symptoms

Early stage (stages 0-I)

• Often asymptomatic or with vague and intermittent pain
• Mild groin pain after physical activity
• Diagnosis at this stage is often incidental (MRI for other reasons)

Intermediate stage (stage II)

• Progressive groin pain, radiating to the anterior thigh or knee
• Pain aggravated by weight-bearing and walking
• Initial joint stiffness, especially in internal rotation
• Intermittent limping

Advanced stage (stages III-IV)

• Constant pain, even at rest and at night
• Marked limping
• Severe limitation of joint ROM
• Shortening of the limb due to femoral head collapse
• Inability to perform normal daily activities

Warning signs

• Groin or hip pain in a young adult (30-50 years old) without obvious trauma
• Progressive pain in a patient on chronic corticosteroid therapy
• Bilateral pain (necrosis is bilateral in 40-80% of non-traumatic cases)

Diagnosis

Clinical examination

• Pain on internal rotation and flexion of the hip
• Reduced ROM: internal rotation is the first to decrease
• Antalgic gait
• Impingement test often positive

Instrumental examinations

Magnetic Resonance Imaging (MRI):

• Gold standard for diagnosis, sensitivity and specificity >95%
• Detects necrosis as early as stage I, before any radiographic changes
• Typical pattern: double line sign in T2
• Allows quantification of necrosis extension (fundamental for prognosis)

Radiography:

• Normal in early stages
• Progressively shows: sclerosis, cystic areas, crescent sign, collapse, osteoarthritis
• Useful for follow-up and staging

Bone scintigraphy:

• Area of hypofixation (early phase) or hyperfixation (reparative phase)
• Less specific than MRI

CT scan:

• Useful for highlighting the crescent sign not visible on radiography
• Surgical planning

Treatment

General principles

Treatment of avascular necrosis depends on the stage, extent of necrosis, patient’s age, and functional demands. The main goal is to prevent femoral head collapse whenever possible.

Conservative treatment (early stages I-II, small necrosis)

Joint unloading:

• Walking with crutches to reduce load on the femoral head
• Variable duration (6-12 weeks) depending on clinical response
• Efficacy of isolated unloading is controversial

Medications:

• Bisphosphonates (alendronate, zoledronate): can slow bone resorption and delay collapse. Promising but not definitive results
• Vasodilators (iloprost): improve bone perfusion, reduce intra-osseous edema
• Anticoagulants: in cases associated with thrombophilia
• NSAIDs for pain control

Pulsed electromagnetic fields (PEMF):

• Stimulation of vascularization and bone repair
• Encouraging results in early stages

Conservative surgical treatment (stages I-II, head preservation)

Core decompression:

• Perforation of the necrotic bone with a drill to reduce intra-osseous pressure and stimulate revascularization
• Indicated in stages I-II before collapse
• Success rate: 60-80% in stage I, 40-60% in stage II
• Can be combined with cancellous bone graft or mesenchymal stem cells

Vascularized bone grafts:

• Transfer of a bone segment with its vascular pedicle (e.g., vascularized fibula)
• Complex technique but with promising results for extensive pre-collapse necrosis

Osteotomies:

• Rotation of the femoral head to move the necrotic area out of the weight-bearing zone
• Used in specialized centers (e.g., Sugioka osteotomy)

Hip replacement (stages III-IV)

When the femoral head has collapsed or osteoarthritis is advanced, total hip replacement is the definitive treatment:

• Excellent functional results and pain control
• Average lifespan of the prosthesis: 20-25 years with modern implants
• In very young patients (< 50 years): resurfacing prostheses or femoral neck-preserving prostheses are considered

Rehabilitation

After core decompression

• Weeks 0-6: partial weight-bearing with crutches (10-20 kg), early hip mobilization
• Weeks 6-12: progressive weight-bearing up to full weight-bearing
• Months 3-6: muscle strengthening, complete functional recovery

After hip replacement

• Days 1-3: verticalization, walking with aids
• Weeks 1-6: progressive weight-bearing, mobility exercises and light strengthening
• Weeks 6-12: progressive strengthening, balance, walking without aids
• Months 3-6: return to daily activities and light sports

Rehabilitation program

Mobility exercises:

• Hip flexion-extension within the allowed range
• Abduction with heel slide
• Assisted rotations (respecting post-surgical limitations)
• Stationary bike without resistance

Muscle strengthening:

• Isometric gluteal contractions
• Glute bridge (bilateral, then unilateral)
• Hip abduction in side lying
• Hip extension in prone position
• Controlled mini-squat (after surgical authorization)

Balance and proprioception:

• Single-leg standing with support
• Proprioceptive board
• Walking on unstable surfaces

Recovery Times

Prevention

• Judicious use of corticosteroids: the lowest possible dose for the shortest necessary time
• MRI monitoring in patients on chronic corticosteroid therapy (hip MRI if groin pain appears)
• Limit alcohol consumption
• Stop smoking
• Management of thrombotic risk factors
• Early diagnosis: in case of unexplained persistent groin pain, especially in the presence of risk factors, an MRI of the hip should be requested

Frequently Asked Questions (FAQ)

Frequently Asked Questions

How is femoral head necrosis typically detected in its early stages?

Early detection often relies on recognizing persistent hip or groin pain, which may worsen with weight-bearing. Diagnostic imaging, such as MRI, is crucial for confirming the diagnosis before significant bone collapse occurs.

What non-surgical treatments are available for femoral head necrosis?

Non-surgical approaches for early-stage femoral head necrosis may include activity modification, pain management, and medication to improve blood flow or reduce bone breakdown. These treatments aim to alleviate symptoms and potentially slow disease progression.

What role does physical therapy play in the recovery from femoral head necrosis?

Physical therapy is essential for restoring hip function and strength following both conservative and surgical treatments. A physical therapist guides patients through exercises to improve range of motion, reduce pain, and facilitate a safe return to daily activities.

Can lifestyle changes help prevent femoral head necrosis?

While some risk factors are unavoidable, managing modifiable factors like excessive alcohol consumption and avoiding prolonged high-dose corticosteroid use when possible can reduce risk. Maintaining a healthy lifestyle generally supports overall bone health.

Sources and Scientific References

1. Konarski W et al. (2022). Avascular Necrosis of Femoral Head-Overview and Current State of the Art. Int J Environ Res Public Health. 19. DOI | PubMed
2. Goncharov EN et al. (2024). Conservative Treatment in Avascular Necrosis of the Femoral Head: A Systematic Review. Med Sci (Basel). 12. DOI | PubMed
3. Xiao M et al. (2022). Effect of Otago exercise programme on limb function recovery in elderly patients with hip arthroplasty for femoral neck fracture. Zhong Nan Da Xue Xue Bao Yi Xue Ban. 47:1244-1252. DOI | PubMed
4. Cohen-Rosenblum A et al. (2019). Osteonecrosis of the Femoral Head. Orthop Clin North Am. 50:139-149. DOI | PubMed
5. Goyal C et al. (2021). Legg-Calve-Perthes disease. Pan Afr Med J. 39:187. DOI | PubMed