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Avascular Necrosis of the Hip
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Contents
Other Names
- Osteonecrosis of the Hip
- Hip osteonecrosis
- AVN of the hip
- AVN of the femoral head (AVNFH)
- Atraumatic necrosis
- Ischemic necrosis
- Avascular necrosis (AVN)
Background
- This page refers to osteonecrosis or avascular necrosis of the femoral head, often referred to as avascular necrosis of the hip
History
Epidemiology
- Debilitating disease that can affect all ages, but most common in middle age men (ages 35-50)
- Around 20,000 new cases per year and accounts for roughly 5% - 12% of total hip arthroplasties (THAs) performed[1]
- Bilateral hips involved roughly 80% of the time (need citation)
Pathophysiology
- See: Avascular Necrosis (Main)
- Can be separated into traumatic versus nontraumatic
- Denomination “avascular” is very not entirely appropriate
- Femoral head blood supplying vessels do not disappear
- They suffer a pathological process which results in blood flow interruption
- Apoptosis of bone cells (bone marrow, osteoclasts, osteoblasts) results in bone collapse with involvement of overlaying cartilage
- Leads to flattening of the femoral head surface and development of secondary osteoarthritis
- Most use the term idiopathic for atraumatic causes, but a metabolic disorder background is the keystone behind the pathophysiology in almost all patients
- Hepatic metabolism altered by alcohol intake or administration of steroid medication
- Alcohol disturbs the phospholipid and cytokine metabolism and interrupts blood flow
- Both alcohol intake and streroid administration are dose dependent and account for more than 80 percent of atraumatic cases [2]
- Alcohol disturbs the phospholipid and cytokine metabolism and interrupts blood flow
- Other conditions increase tendency of intravascular coagulation
- Can be intraosseous (e.g. sickle cell disease) or extraosseous (e.g. Raynaud disease, decompression sickness)
- Hepatic metabolism altered by alcohol intake or administration of steroid medication
- Cultural, geographical and genetic circumstances have also been linked to idiopathic cases (Legg Calvé Perthes’ Disease (LCPD))
- Pathophysiology in adults and children the same process with an ischemic phase and regeneration phase
- Chilren's course depends on potential capability of the epiphyseal cartilage to synthesize new cartilage matrix
- Children under 4 have very good prognosis and children older than 9 have poorer prognosis
- Chilren's course depends on potential capability of the epiphyseal cartilage to synthesize new cartilage matrix
- Cases related to trauma have resulting osteonecrosis due to vascularity around the head being severely disturbed
- Mainly the medial femoral circumflex artery
Risk Factors
- Indirect[3]
- Alcohol use
- Prolonged corticosteroid use (greater than 20-40 mg per day for > 3 months)
- Usually related to chronic conditions (transplant, rheumatoid arthritis, etc.)
- Systemic Lupus Erythematosus (SLE)
- Sickle cell disease (SCD)
- Coagulation factor abnormalities (hypofibrinolysis or thrombophilia)
- Virus infection (hepatitis, HIV, CMV)
- Protease inhibitors (HIV medication)
- Direct
- Trauma (fracture)
- Hip dislocation
- Gaucher disease
- Radiation
- Decompression sickness (Caisson disease)
Differential Diagnosis
- Fractures And Dislocations
- Arthropathies
- Muscle and Tendon Injuries
- Bursopathies
- Ligament Injuries
- Neuropathies
- Other
- Pediatric Pathology
- Transient Synovitis of the Hip
- Developmental Dysplasia of the Hip (DDH)
- Legg-Calve-Perthes Disease
- Slipped Capital Femoral Epiphysis (SCFE)
- Avulsion Fractures of the Ilium (Iliac Crest, ASIS, AIIS)
- Ischial Tuberostiy Avulsion Fracture
- Avulsion Fractures of the Trochanters (Greater, Lesser)
- Apophysitis of the Ilium (Iliac Crest, ASIS, AIIS)
Clinical Features
- History
- Recognition of risk factors very important
- Most common presenting symptom is pain
- Can mimic joint pain with anterior hip pain radiating into groin
- May also have pain in buttocks and pain exacerbated with weight bearing
- Around 2/3 have pain at rest and 1/3 have night pain [4]
- Physical Exam: Physical Exam Hip
- Can be fairly nonspecific, but some have limitations in motion and pain in hip with passive and active range of motion
- Special Tests
- FADIR Test: May suggest hip etiology, not specific to AVN
Evaluation
Radiographs
- Standard Radiographs Hip
- Includes AP views and frog leg lateral views
- Close attention to superior portion of femoral head for subchondral abnormalities
- Crescent sign
- Refers to a linear area of subchondral lucency seen most frequently in the anterolateral aspect of the proximal femoral head
- Sign of imminent collapse
MRI
- MRI is the gold standard with sensitivity up to 100 percent
- Findings:
- T1 images appear dark with a low intensity band and T2 images have focal brightness or marrow edema
- Presence of marrow edema has been shown to predict worsening pain and future progression of disease [5]
- "Double line” sign that can be seen on T2 Spin echo or turbo spin echo sequences [6]
- Consists of a low signal intensity outer and a high signal intensity inner rim
- Sign or scheme was not ever used widely, as it did not correlate with radiographic staging, clinical presentation and prognosis
- Can be used to predict prognosis or risk of femoral head collapse (Kerboul combined necrotic angle) [7]
- Calculated by adding the arc of the femoral head necrosis on a midsagittal and mid-coronal MR image
- Less than 190 degrees can be characterized as low risk
- Between 190 and 240 degrees moderate risk
- Greater than 240 are high risk
- Calculated by adding the arc of the femoral head necrosis on a midsagittal and mid-coronal MR image
Bone Scintography
- Radionuclide testing (Technetium-99m)
- Can be used in patients with normal x-rays but suspected AVN
- Increased burn turnover increased uptake with cold surrounding area sometimes called the "doughnut" sign [8]
- Not used frequently and is less sensitive than MRI
Classification
Association Research Circulation Osseous (ARCO) System
- Stage 0
- All diagnostic techniques normal
- Stage 1
- Plain X-ray and CT-scan are normal but scintigraphy or MRI or positive
- Subdivided into 3 categories according to location of lesion (medial, central, lateral)
- Quantitation or area of femoral head involvement can be added: Minimal (<15%), Moderate (15-30%), Extensive (>30%)
- Stage 2
- No subchondral fracture or crescent sign
- Radiography shows a mottled aspect, sclerosis, osteolysis and focal porosis
- Femoral head remains spherical on AP and lateral views and CT scan.
- Can add quantitation or sub-classification as in stage 1.
- Stage 3
- Crescent sign on x-ray and femoral head fails mechanically
- Axial x-ray shows subchondral fracture line and spherical configuration starts to deteriorate and flatten
- Sub-classification and quantitation added (done by calculating the amount of flattening of femoral dome)
- This is performed by selecting most prominent crescent sign view and measuring depression
- Minimal = < 15% involvement or a depression of <2 mm.
- Moderate = 15-30% involvement or a depression of 2-4 mm.
- Extensive = > 30% involvement or a depression of more than 4 mm.
- Stage 4
- Progression to osteoarthritis
- The femoral articular surface is flattened and joint space narrows
- Associated with sclerosis, cysts, marginal osteophytes
- Complete destruction of joint eventually seen and sub-classification not needed
- ARCO: the most common staging system (need citation)
- Older staging systems are still used by some and include the Ficat-Arlet staging system, the Hungerford-Lennox system, the Steinberg classification system and the Ohzono system
Steinberg Classification (modification of Ficat classification)
- Stage: 0
- Radiographs: normal
- MRI: normal MRI and bone scan
- Stage: I
- Radiographs: normal
- MRI: abnormal MRI and/or bone scan
- Stage: II
- Radiographs: cystic or sclerosis changes
- MRI: abnormal MRI and/or bone scan
- Stage: III
- Radiographs: crescent sign (subchondral collapse)
- MRI: abnormal MRI and/or bone scan
- Stage: IV
- Radiographs: flattening of femoral head
- MRI: abnormal MRI and/or bone scan
- Stage: V
- Radiographs: narrowing of joint
- MRI: abnormal MRI and/or bone scan
- Stage: VI
- Radiographs: advanced degenerative changes
- MRI: abnormal MRI and/or bone scan
Management
Prognosis
- Increasing attention to nonoperative interventions aimed at preserving native joint or delaying THA
- Overall, THA outcome data less satisfactory compared to other indications
- Primarily related to limited lifetime, durability of THA in such young patients[9]
- Core decompression (CD)[10]
- Clinical success rate is only about 63.5%
- Rate for subsequent THA is about 33%
Nonoperative
- Indications
- Unclear
- Somewhat controversial with mixed results
- Treat & address risk factors
- Alcohol cessation
- Discontinue steroids if possible
- Correct coagulopathies
- Optimize management of SLE, SSD, etc
Pharmacologic Therapies
- Bisphosphonates
- One uncontrolled study showed improvement in pain, clinical function when taking alendronate 10 mg daily at three years, but not eight years[11]
- Another study with 40 patients showed less collapse [7 vs. 76 percent] while taking alendronate 70 mg weekly[12]
- However, 2016 meta-analysis concluded bisphosphonate therapy did not significantly reduce the progression to collapse[13]
- Statins
- Sometimes used to treat steroid-induced AVN
- Ongoing trials
Regenerative Therapy
Nonpharmacologic Therapy
- Electrical stimulation
- Hyperbaric Oxygen Therapy
- The evidence with hyperbaric oxygen is very limited
- One study in 68 patients showed improvement on MRI in 88% of patients with Steinberg stages I-II AVN, along with improvement in clinical scores[14]
- Extracorporeal Shock Wave Therapy (ESWT)
Operative
- Indications
- Most cases
- Technique
- Core Decompression +/- bone grafting
- Total Hip Arthroplasty
- Rotational Osteotomy
- Curettage and Bone Grafting
- Vascularized Free-fibula Transfer
- Total Hip Resurfacing
- Hip Arthrodesis
Rehab and Return to Play
Rehabilitation
- Needs to be updated
Return to Play
- Needs to be updated
Complications
- Chronic Pain
- Inability to return to sport
- Inability to participate in athletic activities
See Also
- Internal
- External
- Sports Medicine Review Hip Pain: https://www.sportsmedreview.com/by-joint/hip/
References
- ↑ Malizos KN, Karantanas AH, Varitimidis SE, Dailiana ZH, Bargiotas K, Maris T (2007) Osteonecrosis of the femoral head: etiology, imaging and treatment. Eur J Radiol 63:16–28.
- ↑ Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 1995;77:459–74
- ↑ Shah KN, Racine J, Jones LC, Aaron RK. Pathophysiology and risk factors for osteonecrosis. Curr Rev Musculoskelet Med. 2015;8(3):201–209. doi:10.1007/s12178-015-9277-8
- ↑ Mont MA, Hungerford DS. Non-traumatic avascular necrosis of the femoral head. J Bone Joint Surg Am 1995;77:459–74
- ↑ Ito H, Matsuno T, Minami A. Relationship between bone marrow edema and development of symptoms in patients with osteonecrosis of the femoral head. AJR 2006;186:1761–70.162:717.
- ↑ Mitchell DG, Rao VM, Dalinka MK, et al. Femoral head avascular necrosis: correlation of MR imaging, radiographic staging, radionuclide imaging, and clinical findings. Radiology 1987;162:709–15
- ↑ Ha YC, Jung WH, Kim JR, Seong NH, Kim SY, Koo KH. Prediction of collapse in femoral head osteonecrosis: a modified Kerboul method with use of magnetic resonance images. J Bone Joint Surg Am. 2006;88 Suppl 3:35–40
- ↑ Dumont M, Danais S, Taillefer R. "Doughnut" sign in avascular necrosis of the bone. Clin Nucl Med 1984; 9:44
- ↑ Lau RL, Perruccio AV, Evans HM, Mahomed SR, Mahomed NN, Gandhi R (2014) Stem cell therapy for the treatment of early stage avascular necrosis of the femoral head: a systematic review. BMC Musculoskelet Disord 15:156.
- ↑ Mont MA, Carbone JJ, Fairbank AC (1996) Core decompression versus nonoperative management for osteonecrosis of the hip. Clin Orthop Relat Res 324:169–178
- ↑ Agarwala S, Shah S, Joshi VR. The use of alendronate in the treatment of avascular necrosis of the femoral head: follow-up to eight years. J Bone Joint Surg Br 2009; 91:1013.
- ↑ Lai KA, Shen WJ, Yang CY, et al. The use of alendronate to prevent early collapse of the femoral head in patients with nontraumatic osteonecrosis. A randomized clinical study. J Bone Joint Surg Am 2005; 87:2155.
- ↑ Yuan HF, Guo CA, Yan ZQ. The use of bisphosphonate in the treatment of osteonecrosis of the femoral head: a meta-analysis of randomized control trials. Osteoporos Int 2016; 27:295.
- ↑ Malizos KN, Karantanas AH, Varitimidis SE, et al. Osteonecrosis of the femoral head: etiology, imaging and treatment. Eur J Radiol. 2007;63:16-22.
Created by:
John Kiel on 20 March 2020 19:04:15
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Last edited:
5 October 2022 13:05:28
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