disease | Femoral Head Necrosis |
Femoral head necrosis, also known as avascular necrosis of the femoral head, is a disabling hip joint disease caused by ischemia of the femoral head, also referred to as ischemic necrosis. This condition is prone to misdiagnosis in primary hospitals, delaying crucial treatment time. Patients may suffer from disability in mild cases or lifelong paralysis in severe cases, earning it the nickname "undying cancer" in the medical field. Currently, there are approximately 30 million patients worldwide, with 4 million in China alone. The incidence rate is significantly higher among patients with a history of steroid use, hip trauma, alcoholism, or related diseases.
bubble_chart Etiology
(1) Trauma. Such as femoral neck fracture, hip dislocation, and hip joint contusion caused by external force impact.
(2) Heavy alcohol consumption. Long-term excessive drinking leads to the accumulation of alcohol in the body, causing elevated blood lipids, increased blood viscosity, slowed blood flow, altered blood coagulation, blocked blood vessels, and local ischemia, resulting in interrupted blood supply to the femoral head and subsequent necrosis.
(3) Excessive or prolonged use of adrenal glucocorticoids.
(4) Chronic cumulative strain.
(5) Bone metabolic disorders.
(6) Postoperative complications of hip surgery leading to necrosis.
(7) Osteoporosis.
(8) Changes in bone structure causing vascular compression and blood flow obstruction.
Stage 1: Clinical manifestations include progressive pain in the hip and knee joints, with Grade I limitation in hip joint movement. X-ray findings show normal appearance of the femoral head, with slightly blurred cartilage and trabecular structure, or patchy osteoporosis. CT reveals Grade I thickening of trabeculae in the central part of the femoral head, presenting a star-shaped structure with radial or pseudopod-like branches extending to the cartilage of the femoral head. Small cystic changes are visible in the subchondral area, along with small sclerotic joints. The abnormal grayscale area accounts for 10%–30% of the entire head.
Stage 2: Hip joint pain is the main symptom, with Grade I limitation in abduction and internal rotation. X-ray findings show subchondral cystic changes, with a mix of bone destruction and osteoporosis. CT reveals partial trabecular sclerosis in the medullary cavity. Subchondral medullary cavity shows cystic changes larger than 0.5 cm.Stage 3: Hip and knee pain worsens, weight-bearing tolerance decreases, and limping occurs. X-ray findings show subchondral microfractures, partial discontinuity of trabeculae, and collapse or flattening of the superolateral weight-bearing area of the femoral head, with possible bone fragments under the cartilage. CT findings include disordered trabeculae in the femoral head, enlarged cystic changes, bone fragmentation, femoral head deformation, localized hyperplasia and sclerosis, and acetabular osteophytes. The femoral head morphology changes, with necrotic area accounting for 30%–50%.
Stage 4: Hip joint movement is restricted, and severe cases may experience difficulty walking or loss of labor capacity. X-ray findings show narrowed joint space, flattened and collapsed femoral head deformity, and acetabular rim hyperplasia and deformation, presenting as osteoarthritis changes. CT reveals deformed femoral head contour, narrowed joint space, mixed sclerosis and cystic changes in the femoral head, and fragmented bone structure. The femoral head morphology is significantly altered, with abnormal grayscale area accounting for 50%–80% of the entire head.
bubble_chart Treatment Measures
1. Disease Cause Treatment
Eliminating the disease cause that leads to femoral head necrosis is a crucial and important step in the early treatment of femoral head necrosis. It creates certain conditions for the continued development of the femoral head and the treatment of femoral head necrosis, but it has its own limitations. The removal of the disease cause does not completely and thoroughly improve the ischemic necrotic lesion, and the effects of medication and treatment require considerable time, thus yielding slow results.
2. Traction and ImmobilizationThis method can relieve the weight-bearing pressure on the femoral head and the compression on the necrotic area, facilitating bone repair and recovery. At the same time, for the early aseptic inflammatory stage, it helps eliminate synovial membrane and joint swelling, congestion, and edema. However, this method is only suitable for the early stages of femoral head necrosis.
3. External Fixation Method
Traditionally, a hip spica cast is often used to create a brace, maintaining the hip joint at 45 degrees of abduction and 10 degrees of internal rotation. This changes the weight-bearing surface of the femoral head. The duration is one year to one and a half years, which is relatively long.
4. Joint Cavity Injection
A certain amount of medication is injected into the hip joint cavity. Before injecting the medication, a certain amount of joint fluid is extracted to decompress the joint, and then the medication is injected to promote blood circulation and resolve stasis.
5. Interventional Therapy
Developed on the basis of conservative treatment and surgical therapy, this method is minimally invasive and painless for patients. It has the effects of thrombolysis, improving femoral head microcirculation, and promoting blood circulation to resolve stasis.
6. Tuina Massage
Based on the principle of relaxing tendons and promoting blood circulation, techniques such as rolling, pressing, kneading, pulling, and rubbing are applied. The patient lies prone, and gentle rolling manipulation is performed on the affected hip, focusing on the hip joint, while coordinating with adduction, abduction, and rotation movements of the hip joint. This can alleviate symptoms but does not fundamentally improve the ischemia of the femoral head.
7. Functional ExerciseFunctional exercise plays a certain role in consolidating treatment effects. Active functional exercise without weight-bearing is adopted to enhance the therapeutic effect of femoral head necrosis and promote functional recovery. Specific therapeutic effects include improving sluggish blood circulation, preventing soft tissue atrophy and adhesion, and molding the joint to create conditions for early recovery. Functional exercise must be persistent and is a gradual process.
8. Hyperbaric Oxygen Therapy:
Increases blood oxygen content and the diffusion rate of oxygen, improving the hypoxic state of local tissues, reducing air bubbles, and improving blood circulation. It also has antibacterial effects. During hyperbaric oxygen therapy, care must be taken to prevent central nervous system toxicity.
The treatment outcome of femoral head necrosis is closely related to the severity of the condition, the timing of discovery, and the duration of the disease. The earlier the lesion is detected and the milder the condition, the better the treatment effect. Therefore, early diagnosis and early treatment of femoral head necrosis should be emphasized. The principles for early diagnosis of femoral head necrosis are as follows:
(1) For adults aged 20-50 who experience groin or hip pain radiating to the thigh (or knee pain on one side with subsequent hip pain after activity), with slow and progressive worsening, significant nighttime pain, and no response to general medication, and who have a history of trauma, alcoholism, or other predisposing factors or diseases that may cause femoral head necrosis, this condition should be considered first.
(2) For all patients with low back and leg pain, hip joint function should be routinely examined during physical examination. If restricted abduction and internal rotation of the affected hip joint are observed, the presence of this condition should be suspected.
(3) For patients with femoral neck fractures, follow-up should be conducted for 3-5 years post-injury. If a decrease in femoral neck height, nail track signs, or cystic changes are observed, along with clinical symptoms, this condition should be considered.
(4) For suspected cases, anteroposterior and frog-leg lateral X-rays of the hip joint must be taken first. If no abnormalities are found, close observation or further examinations such as CT, MRI, ECT, intraosseous pressure measurement, and arteriovenous angiography should be performed.