Aseptic necrosis of the femoral head, also known as ischemic necrosis of the femoral head, is caused by various causes of impaired blood supply to the femoral head, and is most common in children, with the highest incidence between the ages of 5 and 9. In recent years, aseptic necrosis of the femoral head has become increasingly common in adults, with a significantly higher incidence.
General information
1. Etiology: unclear. Most of them have a history of hormone overdose, and recently it has been reported that more than 60% have a history of hormonal drug treatment; 11.1% have a history of alcoholism, 15.2% have had trauma, and the others are of unknown origin.
2. Pathology: According to the development process of lesions, the disease can be divided into necrotic phase, repair phase and reconstruction phase.
In the early stage, the blood supply to the femoral head is impaired and various cells of the bone tissue are necrotic, followed by the repair phase, due to the congestion of the nearby normal bone, proliferation of granulation tissue, microvascular and fibrous connective tissue reaching into the necrotic area and bringing in osteoclasts and osteoblasts to gradually resorb the necrotic bone and produce new bone, and the new bone like tissue undergoes calcification and ossification to repair the bone again. This period is the key to treatment, and proper treatment can prevent deformity of the hip joint.
During this process, if the weight bearing of the affected hip exceeds the capacity of the necrotic or recovering femoral head, collapse of the femoral head bone cortex may occur, or if the necrosis and repair are repeated due to the persistence of the injurious force, deformity healing may occur and the affected hip will eventually form a flat hip and irreversibly lose its function.
Clinical manifestations and diagnosis
About 80% of patients are male, with a peak incidence of 40 to 50 years old. Early diagnosis can provide an opportunity to prevent collapse of the necrotic femoral head. In addition to detailed history taking and complete physical examination, good quality positive and lateral hip radiographs play an important role in making an accurate diagnosis of stage 2 to 4 lesions.
Hip pain is usually the first and main symptom, often starting as an insidious dull pain, often located in the groin area and radiating downward to the thighs, buttocks and knees, which can be easily confused with “low back pain” in Chinese medicine and misdiagnosed.
In patients with stage 0 to 1, the clinical characteristics are sudden pain in the groin, which may be progressive and radiating to the femur, and more painful in the evening, which is typical of ischemia. Nocturnal pain and intermittent claudication occur in the late stages. About 1/3 of patients have intermittent pain episodes. It often starts unilaterally, and the contralateral hip is often involved in about 60% of patients within 2 years. In most patients, the pain appears 2-6 months earlier than the abnormal radiographic presentation.
Hip motion is often limited, either in all directions or in one direction, especially in internal rotation or abduction. In the late stage, the limitation of joint movement is mainly limited in abduction – contracture of the adductor muscle group, which gradually worsens and may result in limb shortening, muscle atrophy and flexion-adduction deformity. The limitation of motion is of great importance and should be taken seriously.
Imaging manifestations
1.X-ray examination: It is still a reliable means to diagnose, determine the stage of the disease, guide the treatment and evaluate the efficacy.
Stage I: It is the early stage of the lesion, the clinical symptoms are mild, and there is often no performance on plain film, or osteoporosis and blurred trabeculae are seen, mainly located in the weight-bearing area above the femoral head.
Stage II: The femoral head has osteoporosis and cystic changes, and there are patches or strips of increased density in the upper weight-bearing area, mainly in the main pressure trabecular area.
Stage III: Fracture of the continuity of the femoral head bone cortex, “crescentic sign” with translucent area and fracture of the continuity of the femoral head bone cortex, surface unevenness, and translucent area of dead bone, fracture, sclerosis or cystic degeneration of the subcortical bone.
Stage IV: The femoral head is obviously flattened or deformed in a myxoid shape, containing diffuse or limited sclerosis or cystic areas, showing osteoarthritic changes. The femoral neck is thickened and hip subluxation may occur.
2, CT performance: higher sensitivity than the former, can detect the lesion earlier and help to choose the treatment plan early.
Stage I: femoral head stellate deformation, thickening of bone trabeculae, disorder, fusion of branches into clusters, mainly three kinds of alignment: along the normal femoral head stellate structure, from the center of the femoral head to the surrounding extension. It is crossed with the normal femoral head awning structure; it is accompanied by subcortical thickening at the edge of the femoral head or shows subcortical thickening.
Stage II: Small necrosis of the femoral head with limited cystic changes and lax areas, followed by necrosis of the femoral head with obvious weight-bearing areas, central wedge-shaped or surrounding crescentic bone density increase necrosis, hardening of the cystic edges, but the femoral head is intact without fracture.
Stage III: The femoral head has subchondral fracture deformation in the form of crescentic and bilateral signs, with cystic translucent areas, and femoral head deformation, fragmentation, collapse signs, irregular joint surface, the femoral head may have mild to moderate deformation, and there may be fragments of bone falling into the joint cavity.
Stage IV: further necrosis of the femoral head, obvious deformation, fragmentation, joint space narrowing, and typical osteoarthritic changes of the joint.
MR is the most sensitive means to diagnose ischemic necrosis of the femoral head, and the abnormal signal band of ischemic necrosis of the femoral head is often larger than that of X-ray plain film, and the shape can be linear, banded, wedge-shaped or crescent-shaped, mostly located in the anterior and superior part of the femoral head, with different sizes.
Treatment
Ischemic necrosis of the femoral head was once called “chronic bone cancer”, and its intractability is evident. For a long time, there has been no definitive treatment for this disease. At present, the traditional treatment is based on orthopedic decompression surgery and total hip arthroplasty, which has been developed in recent years. The former is used in the early stage of the disease, but the efficacy of independent use is not certain, and most patients inevitably develop into advanced stage, and eventually the total hip joint is replaced. The service life of the artificial joint is affected by the material of the equipment used, and currently its life span is only 10-15 years. Interventional therapy is a new treatment method developed in recent years, the main purpose of treatment is to restore the blood supply to the occluded femoral head, which can greatly delay the development of the disease to stage IV, and some patients can even achieve complete functional recovery to the level of normal people.
1.Non-surgical treatment: based on making the affected hip joint non-weight-bearing.
2.Orthopedic treatment: selection is mainly based on pathological stages
Stage I: treatment should be made to prevent partial collapse of the femoral head. Prefer medullary core decompression or cuneotomy
Stage II: medullary core decompression can still be chosen, but the failure rate is increased.
Stage III: In addition to osteotomy, hip arthroplasty is an alternative procedure.
Stage IV: total hip arthroplasty and joint fusion are the only valuable options.
3.Interventional treatment
Principle.
Aseptic necrosis of the femoral head is a disorder of blood supply to the femoral head, and from the vascular point of view, it is also a vascular embolism disease. Therefore, the treatment should follow the treatment principles of vasodilation, thrombolysis and platelet depolymerization. The specific drugs are: poppy bases, urokinase, low molecular dextrose or salvia injection.
Methods.
Local anesthesia was applied to the surface of the femoral artery at the root of the contralateral thigh, a small incision of 2-3 mm was made on the skin surface, and the femoral artery was directly punctured with a fine puncture needle, and a catheter for intervention was introduced to access the external iliac artery on the affected side for angiography to clarify the blood supply to the femoral head on the affected side, and the medial and lateral spinofemoral arteries were entered respectively, and slowly perfused with the above drugs after appropriate dilution. By comparing the blood supply angiogram of the femoral head before and after treatment, it was observed that the spasm of the blood supply vessels of the femoral head before treatment and the phenomenon of venous stagnation were relieved, and the sparse microvessels of the blood supply of the femoral head before treatment were significantly increased and enriched after treatment.