Avascular Necrosis of the Hip (Osteonecrosis of the Femoral Head)
What is Avascular Necrosis of the Hip?
Avascular necrosis (AVN), also known as osteonecrosis, of the femoral head occurs when the blood supply to the femoral head is interrupted. Without adequate blood supply, the bone cells die, leading to weakening of the bone and, eventually, collapse of the femoral head and secondary osteoarthritis of the hip joint.
Common risk factors include:
• Long term or high dose corticosteroid use
• Excessive alcohol consumption
• Previous hip trauma (fracture or dislocation)
• Sickle cell disease and other haemoglobinopathies
• Deep sea diving (decompression sickness)
• Autoimmune conditions such as systemic lupus erythematosus
• Chemotherapy and radiation therapy
• Idiopathic – no identifiable cause
Symptoms of Avascular Necrosis of the Hip
In the early stages, AVN is often asymptomatic. As the disease progresses, patients may develop:
Treatment options
Treatment depends on the stage of the disease, the size and location of the lesion and the patient’s age and activity level.
Non-surgical treatment: protected weight bearing, activity modification, pain relief and management of underlying risk factors. Non-operative management alone rarely halts disease progression.
Joint preserving surgery: in early stages, before collapse of the femoral head, core decompression (with or without bone grafting or biological augmentation) may be considered to reduce intra-osseous pressure and promote healing.
Joint replacement: once the femoral head has collapsed or secondary arthritis has developed, total hip replacement offers reliable pain relief and restoration of function.
Frequently Asked Questions (FAQ)
Hip arthritis usually develops over time rather than from a single cause. The most common reason is gradual wear of the joint cartilage with age. However, many people develop it earlier due to subtle issues with the shape of the hip, when the ball and socket don’t fit perfectly, it creates uneven pressure that slowly damages the joint. Previous injuries, such as fractures or dislocations, can also speed up this process. In some cases, genetics, inflammation, or increased load on the joint (including higher body weight or repetitive stress) contribute.
