Also called osteonecrosis of the hip, avascular necrosis of the hip refers to the death (necrosis) of the hipbone or femoral head, when blood supply to the bone is severely compromised. This causes initial degeneration and ultimate collapse of the femoral head.
The bone is a live tissue highly vascularised and constantly renewing itself.
Avascular necrosis of the hip consists in the partial or total blockage of blood supply to the hipbone or femoral head due to the damage to the vessels arising from the femoral neck.
When this occurs the hipbone is deprived of oxygen and minerals and gradually undergoes a degenerative process causing the death of bone cells. The femoral head becomes flat, fragile and no longer fits into the acetabulum. The condition ultimately ends in the wearing of the femoral head under the pressure of the body weight causing irreversible osteoarthritic changes of the hip joint.
The severity of avascular necrosis of the hip is defined using the Steinberg classification, which has been extended, from the Ficat classification. This includes six stages of avascular necrosis from normal to advanced degenerative changes based on the MRI scans of the hip joint.
Stage Radiographic findings
I Normal – minor osteopenia (bone loss)
II Cystic/sclerotic changes
III Crescent sign (imminent subchondral collapse)
IV Flattening of femoral head
V Narrowing of the hip joint
VI Advanced degenerative changes (A-mild, B-moderate, C-severe)
The origin of this pathology is not always clear and is defined as idiopathic, when arises spontaneously and the causes are unknown. It may also due to venous thrombosis, hypertension, chronic use of medications (e.g. corticosteroids), treatments (radiation) and preexisting autoimmune or blood conditions.
Other causes leading to avascular necrosis of the hip may depend on different forms of injuries while others arise from intrinsic vascular changes compromising blood flow to the femoral head.
Trauma includes fractures of femoral head 75-100%, basicervical or femoral head base 50%, cervico-trochanteric head-trochanter 25%
Hip dislocation (2-40%); higher risk with severe displacement and incorrect reduction.
The development of avascular necrosis of the hip has been attributed to a number of risk factors:
Iatrogenic (high dose corticosteroids, radiation, organ transplant)
Idiopathic (most common type: hypercoaguable disorder)
Blood diseases (leukaemia, sickle cell disease)
Autoimmune diseases (systemic lupus erythematosus)
Alterations in lipid metabolism
Viral and bacterial infections
The symptoms of the hip avascular necrosis may manifest at a late stage of the disease with an insidious onset displaying the following characteristics:
Pain to the groin area, buttock and anterior side of the thigh increasing with movement
Pain with weight bearing on the pathological hip side
Pain at rest
Pain during sleep
Stiffness of the hip joint
Difficulty in walking, limp
Clinical examination begins with medical history to acquire information on injuries, preexisting conditions, life style or drugs possibly leading to avascular necrosis of the hip.
Firstly the examiner will assess any changes in the range of movement of the hip, stiffness and abnormalities in the gait such as alimp.
X-ray imaging may reveal changes in the femoral head only when the pathology has advanced. This is improved with a bone scan following the injection of a contrast agent.
In the long term the hip will become typically arthritic, possibly masking the actual diagnosis of avascular necrosis of the hip. An MRI may be recommended in case the X-ray does not show bone alterations despite the clinical symptoms. The MRI is highly specific for the diagnosis of avascular necrosis of the hip showing a brighter femoral head indicative of bone loss, oedema and reduction in size.
Conservative treatment is the initial frontline of therapy following the diagnosis of avascular necrosis of the hip. Before the pathology has advanced to the collapse of the femoral head, conservative management aims at replenishing the bone with calcium via administration of bisphosphonates to prevent the later stages of bone degeneration. However, the reduction in blood flow to the bone itself cannot be restored with medications.
Additional treatment includes:
Pain management with analgesics
Non-steroidal antiinflammatory drugs (NSAIDs)
Reduction of weight bearing on the hip with crutches
Prior to the final collapse of the femoral head, the goal of surgery is to restore blood supply to the bone using various techniques.
Hip arthroscopy is used for decompression of the femoral head by drilling one or multiple holes in the head to stimulate angiogenesis (new vessel growth) and reduce the pressure within the femoral head to alleviate pain.
Fibular bone (strut) graft consists in the transplantation of bone fragment taken from the fibula (lower leg) into the femoral head to provide stability. The vessels originating from the fibula are joined with the vessels of the hip to restore blood flow to the femoral head.
Total hip replacement (arthroplasty) with an artificial prosthesis is performed when the hip has fully degenerated and becomes arthritic and cannot be repaired with other surgeries. It is mostly indicated in older patients (see hip fracture for further details on this technique).
Hip resurfacing surgery is a similar technique to prosthetic hip replacement but only a smaller portion of the bone is removed. This procedure is advised in young patients due to the short life span of hip prostheses.
Physical therapy is slightly different following conservative or postoperative treatment. In both instances it is recommended to reduce weight bearing on the hip temporarily with the use of crutches. This period can last up to 6-12 weeks in conservative patients. Simultaneously, the function of the hip is maintained with gentle exercise focusing on improving joint flexibility and strengthening of the pelvis, glutei and thigh muscles.
The use of crutches or a walker is longer in surgical patients lasting up to 6 months to prevent a fracture of the femur following either a prosthetic implant or a graft procedure.
Physiotherapy also management includes:
Exercise in the pool to reduce stress on hips
Activity modifying regime
Return to activity plan
Guided return to activity and sport
A variety of detrimental events can occur following both types of treatment for an avascular necrosis of the hip.
With conservative treatment:
Further femoral head degeneration and collapse
Arthritic changes of the hip joint
Requirement of hip replacement surgery
Bone fracture (during surgery)
Joint dislocation (after surgery)
Hip joint stiffness
Vessel or nerve damage
Deep venous thrombosis
Avascular necrosis of the hip cannot be easily prevented if arising from idiopathic causes. However, in patients with chronic medical diseases or prolonged use of steroids and immunosuppressants, a regular assessment of bone quality may be helpful.
A general check-up of patients’ wellbeing for the prevention of cardiovascular events can be achieved by regular monitoring for coagulopathies, high blood pressure (hypertension). Changes in life style involving the consume of alcohol, smoking and lack of exercise may also improve bone health and prevent the onset of avascular necrosis of the hip.
Additional treatments are recommended at the early stages of the disease:
Antiinflammatory drugs (NSAIDs)
Osteoporosis drugs to delay the progression of avascular necrosis
Medications to lower blood cholesterol to prevent fat embolism
Anticoagulant therapy or blood thinners such as warfarin to prevent deep venous thrombosis or clot formation