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Avascular femoral head necrosis

Hyperbaric Oxygen Therapy for Avascular Necrosis of the Femoral Head

Avascular necrosis (AVN) or osteonecrosis of the femur head (ONFH) is the results of the prolonged interruption of blood supply to the femur head, which is enclosed by cartilage, restricting its access to local blood vessels.

"Hyperbaric oxygenation can break the vicious cycle of ischemia and hypoxia induced pain and bone destruction and is used as a non-surgical procedure to hip restoration and preservation." 

Hyperbaric oxygen increases oxygen availability in blood plasma to relieve ischemia caused by poor vascularization of the femur head. The reparative processes result in enhanced fibroblastic, angioblastic, osteoblastic, and osteoclastic activity, which are all extremely important in healing necrotic bone structures.

In a recent large and long term study, Koren (2015) showed 88% of the treatment group had improvement on MRI when AVN was treated in stage I and II for 68 patients (78 joints).  At 11.1±5.1 years follow-up a total of 54 patients (58 joints) were located and answered the questionnaires showing 93% survival rate of the joints. Earlier clinical studies (Reis 2003) showed similarly 81% of patients who received hyperbaric oxygen therapy returned to normal MRI in contrast to only 17% in the untreated group (Reis 2003).

Avascular necrosis (AVN) or osteonecrosis of the femur head (ONFH) is a result of an interruption of blood supply to the bone. The femoral head lays at the most remote part of the bone’s vasculature and is enclosed by cartilage. Its access to local blood vessels is restricted, making the femur head vulnerable to necrosis caused be ischemia (lack of blood supply). 

The possible causes may be idiopathic, alcohol- or drug-induced, blockage in a blood vessel supplying the femoral head, or fat embolism. Other causes are anemia, Gaucher disease, increase bone marrow pressure, impaired arterial supply, obstruction of venous drainage, vasculitis, intermedullary hemorrhage and hypofibrogenemia.

Hyperbaric oxygen therapy can positively address some of the causes of AVN such as: steroid or alcohol induced, anemia, Gaucher disease, increase bone marrow pressure, impaired arterial supply, obstruction of venous drainage or vasculitis, however presently, more clinical studies are needed.

Joint pain is usually the initial symptom which can either be dull, aching, sharp, or intermittent. Pain may be confined over the hip or radiating to the buttocks, gonads, or knee and is usually aggravated by standing or walking and relieved by rest. The pain can be debilitating, limiting the joint range of motion.

The main mechanism of AVN is hypoxia (lack of oxygen) to the bone which results in ischemia and death of the marrow and the osteocytes. This can be addressed by exposing the affected area to hyperbaric oxygen. Inhalation of hyperbaric oxygen increases the availability of plasma oxygen and restores oxygenation to the tissues. With the main therapeutic goal of preventing collapse of the femoral head and preserving the joint rather than replacing it, hyperbaric oxygen can accomplish this alongside with other orthopedic interventions. Predominantly, hyperbaric oxygen reduces joint edema, stimulates revascularization and boosts bone resorption and regeneration. 

Benefits of Hyperbaric Oxygen Therapy for Avascular Necrosis of the Femoral Head:

  • Hyperbaric oxygen is used as an addition to surgery or its replacement therapy with the main therapeutic goal of joint preservation and preventing collapse of the femoral head.
  • Hyperbaric oxygen reduces joint swelling and stimulates revascularization and bone resorption and regeneration. This will decrease pain and improve range of motion.
  • Hyperbaric oxygen therapy decreases edema and inflammation, thereby lowering intra-osseous pressure and restoring venous drainage.
  • Hyperbaric oxygen induces angiogenesis, improving the microcirculation which facilitates resorption of the necrotic dead bone and replacement with living bone.
  • Hyperbaric oxygen stimulates the body’s metabolism. Increased metabolism raises the rates of resorption, halting the further progression of the necrosis, conserving the femoral head, keeping its structural integrity and reducing the incidence of surgeries.
  • Hyperbaric oxygen promotes new bone formation or osteogenesis. HBO rebuilds and remodels the damaged bone by increasing the differentiation of stem cells to osteocytes, the bone-forming cells.
  • Hyperbaric oxygen therapy increases stem cell formation resulting in faster wound healing and recovery after hip arthroplasty or core decompression.
  • Hyperbaric oxygen reduces edema and decreases pain. Improvement of range of motion is noted when pain is reduced.
Further reading:
  1. Sen,RK; Management of Avascular Necrosis of the Femoral Heat at Pre-collapse Stage; Indian Journal of Orthopedics; 2009; 43-1:6-16
  2. Camporesi E, Vezzani G, Bosco G, Mangar D, Bernasek T; Hyperbaric Oxygen Therapy in Femoral Head Necrosis; Jouranl of Arthroplasty; 2010, 25-6:
  3. Reis ND, Schwartz O, Militanianu D, Ramon Y, Levin D, Norman D, Melamed Y, Shupak A, Goldsher D, Zinman C; Hyperbaric oxygen therapy as a treatment for stage-1 avascular necrosis of the femoral head; J Bone Joint Surg B; 2003; Apr;85(3);371-5.
  4. Koran N, Ginesin E, Melamed Y, Norman D, Levin D, Peled E; Hyperbaric Oxygen for stage I and II femoral head necrosis; Orthopedics; march 2015; 38(3);e200-5
  5. Yang JZ, Pan ZY, Gu H, Li N, Qian XJ, Zhai RY, Wu LH, Gao CJ; Quantitative study of therapeautic efficacy on early intervention to model steroid-induced avascular osteonecrosis of femoral head by multi-slice perfusion imaging; Zhonghua Yi Xue Za Zhi; 2008 Dec 9; 88(45);3210-6
  6. Gomez-Garcia F; Review of non-surgical treatment of avascular necrosis of the femoral head; Orto Acta Mex;2013 July-Aug; 27(4): 265-72
  7. Mei-Dan O, Hestroni I, Mann G, Melamed Y,Hiska M; Prevention of avascular necrosis in displaced talar neck fractures by hyperbaric oxygenation therapy: a dual case report; J Postgrad Med; 2008 Apr-Jun; 54(2):140-3

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