Idiopathic femoral head necrosis

Introduction to idiopathic femoral head necrosis Idiopathic femoral head necrosis, also known as ischemic femoral head necrosis, is a common disease. The etiology of femoral head necrosis is diverse, but its common pathological mechanism is bone tissue ischemia, so regarding the pathogenesis and blood supply. The blocked theory is the most acceptable. This theory believes that due to various intra- and extra-bone pathogenic factors, the bone tissue is reduced in nutrient blood flow, the intravascular vascular network is compressed or the venous occlusion is blocked, causing local blood supply disorders, and severe cases can cause ischemic necrosis of bone tissue. At the beginning of the disease, only a single major blood vessel can be damaged. As the disease progresses, if the residual circulating blood volume is insufficient to maintain the normal blood supply of the damaged bone cells, the bone marrow tissue will be damaged first, followed by osteonecrosis. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of infection: non-infectious Complications: hemiplegia

Idiopathic femoral head necrosis

(1) Causes of the disease

There are many causes of femoral head necrosis. It is generally believed that there are anatomical factors: due to anatomical structure characteristics, local blood supply is less, collateral circulation is less, such as trauma, strain or other reasons, it is easy to cause damage, loss of blood supply source and necrosis. Hemodynamic causes of biomechanics: Many reasons can increase the intraosseous pressure, thus reducing the amount of intraosseous circulation, causing tissue hypoxia, hypoxia can also cause bone marrow tissue to swell, swelling causes intramedullary pressure to rise Such a vicious circle, eventually causing bone ischemic necrosis, in addition, stress concentration in some parts can compress the bone, increase the intraosseous pressure, the same changes cause bone necrosis, biophysical factors: radiation, over Cold, overheating, etc. can cause local osteonecrosis. Also, after taking a large amount of adrenal corticosteroids, the body's fat embolus blocks the terminal blood vessels, causing blood supply to the epiphysis, and some people think that it is related to the abuse of indomethacin. Drug-related, as well as traumatic and non-traumatic classification.

Traumatic factor

The causes of femoral head necrosis can be divided into two categories: traumatic and non-traumatic. The commonality of both is due to the limited circulation of the collaterals between the various parts of the femoral head, which makes the femoral head vulnerable to ischemia and metabolic abnormalities. Injury, the proximal femur mainly receives blood supply from 3 groups of arteries: 1 femoral neck base joint capsule outer artery ring. 2 The cervical ascending branch from the outer ring of the joint capsule. 3 femoral head ligament arteries, the outer capsule of the joint capsule is composed of a branch of the medial circumflex femoral artery and a branch of the lateral circumflex femoral artery. The lower gluteal artery also has small branches, and the cervical ascending branch is between the intertrochanteric line and the femur. After the neck is issued by the arterial ring, it rises in the joint capsule, reaches and penetrates the edge of the epiphyseal cartilage. During the running process, it also branches to penetrate the femoral neck to the metaphysis, at the edge of the articular cartilage, the neck ascending branch Forming a subserosal joint capsule internal artery ring, the latter can be continuous or discontinuous due to anatomical variation, the branch of the epiphyseal artery is emitted from the intracapsular artery ring, penetrates into the femoral head to supply the epiphysis blood, and the epiphyseal artery is the terminal artery. There is almost no collateral circulation between them. The round ligament artery is a branch of the obturator artery or the medial femoral artery. It emits the medial epiphyseal artery, from the fossa ovalis, through the femoral head. Most patients, the lateral epiphyseal artery supplies the femoral head. For most of the blood supply, only 1/3 of the patients, the blood supply of the femoral head, is mainly supplied by the medial epiphyseal artery from the round ligament artery.

For traumatic osteonecrosis, there is a clear causal relationship between injury and outcome, that is, femoral neck fracture or hip dislocation causes mechanical damage to the blood flow of the femoral head, resulting in necrosis of the entire femoral head or part of it, of which, due to the lateral lateral branch The tearing of the blood vessel or the subtotal fracture of the proximal end causes the intraosseous portion of the lateral epiphyseal vessel to be destroyed. Therefore, the blood supply outside the femoral head is destroyed, and most of the femoral neck fracture remains after displacement. Or the blood supply of the femoral head, the lateral collateral blood vessels are mostly destroyed, at this time the femoral head relies on long-term survival of blood supply, mainly from the larger fossa ovalis, a small part from the residual medial The collateral vessels, because the blood vessels supplying the femoral head are located in the joint capsule, extra-bone. Therefore, when the hematoma is filled and the intracapsular pressure is increased after the injury, the blood supply of the femoral head will be damaged, which leads to the femoral head. Avascular necrosis.

2. Non-invasive factors

The causal relationship of non-traumatic osteonecrosis is difficult to determine. These patients usually have risk factors for osteonecrosis. The most common manifestations are osteonecrosis and subchondral fractures. However, for some individual risk factors, only a small part Symptomatic osteonecrosis occurs in patients. For some recognized risk factors, the corresponding non-invasive osteonecrosis animal model cannot be made, which makes it difficult to fully understand the basic biological processes of femoral head necrosis. According to different risk factors, the damage The mechanism may be intravascular coagulation, thromboembolism, vascular wall injury or vascular compression. For a patient, the size and location of the lesion is likely to indicate that the blood supply to the femoral head is unique and blood supply. The most vulnerable part of the junction, the upper part of the femoral head is the most commonly affected part, and there is no known risk factor or a history of non-traumatic femoral head necrosis commonly referred to as idiopathic femoral head necrosis.

The minimum amount of alcohol required for femoral head necrosis is estimated to be more than 400 ml of pure alcohol per week, for a total of 150 liters. Similarly, the risk of hormone use depends on the dose and time of use, but high doses do not increase its risk. Sex, the threshold of osteonecrosis may be 2000mg of continuous application of hormones, 20mg of hormones per day, the risk of osteonecrosis will increase by 5%, but the absolute safe dose of hormones is difficult to determine, but also caused by small doses of hormones Reports of femoral head necrosis suggest that there may be other individual-specific risk factors for the onset of femoral head necrosis.

(two) pathogenesis

For traumatic osteonecrosis, it is generally believed that due to the particularity of the local vascular supply system at a certain site, the interruption of blood supply after trauma, the incomplete vascularization and the local stress, typical osteonecrosis occurs. Non-traumatic osteonecrosis, due to the lack of animal models completely similar to human morbidity, the disease is still lack of understanding, the pathogenesis is unclear, but it is still closely related to the local blood supply status, due to many causes of osteonecrosis, but Osteonecrosis always occurs in certain anatomical parts, and is similar to the pathogenesis of osteophyte necrosis in children, such as femoral head, wrist scaphoid, scaphoid bone, lunate bone, talus, etc., local blood supply is very poor, so local The condition of blood supply is undoubtedly an important factor.

For non-traumatic osteonecrosis, there are mainly the following theories.

Fat embolism theory

The original cause of osteonecrosis is that the fat embolus is infarcted into the blood vessels of the bone. The fat embolus decomposes free fatty acids by lipase. The oleic acid causes the toxic reaction of the bone marrow, and the capillaries are peeled off, causing congestion and edema. Thus, the adiponectin is destabilized, and the bone marrow and fat pool collapse.

2. Intraosseous pressure increase theory

It is believed that osteonecrosis is similar to a fascial compartment syndrome, which is mainly caused by increased extravascular pressure inside the bone. For example, the extra-arterial pressure is unchanged, and the extra-vascular extravascular pressure can cause blood flow to decrease, leading to ischemia. Ischemia can cause bone marrow edema, which in turn causes increased intramedullary pressure, which in turn causes more severe ischemia, forming a vicious circle, which makes the condition worse, just as the early fascial incision of the compartmental septal syndrome can avoid soft tissue necrosis. In many cases, through early core decompression, reducing intramedullary pressure, breaking the vicious circle of ischemia, for extensive osteonecrosis, can reduce pain, stop bone changes, the increase of intraosseous pressure is mainly due to bone Various causes of necrosis are caused by extra-arterial factors, venous factors, intra-arterial factors, venous factors, extravascular factors, and cytotoxic factors.

3. Cumulative cell damage theory

It is believed that osteonecrosis is the result of many factors. Various pathogenic factors make bone tissue cells in a progressive disease state through multiple links, and the use of corticosteroids, through direct cytotoxicity, storage of intraosseous fat Increased intraosseous pressure and fat embolism, etc., cause the final fatal damage to bone tissue cells, and osteonecrosis always occurs in areas with poor blood supply such as femoral head, humeral head, talus, etc. Anatomical features are also a prerequisite for its onset.

Idiopathic femoral head necrosis prevention

Population prevention

In production activities and daily life, pay attention to avoid serious trauma and cumulative stress damage, such as large-volume training, excessive long-distance running, etc., involved in aviation or deep-water operations, etc., should strictly control the operating procedures to prevent decompression sickness caused by bone Necrosis, in the defense, industry, medical field, frequent contact or application of radioactive materials, should strengthen the management of radioactive materials and protective facilities for buildings and individuals, clinically necessary to apply adrenal corticosteroids or indomethacin treatment Patients should strictly control the indications and medication principles, do not abuse and regularly take pelvic tablets.

2. Individual prevention

(1) First-level prevention: create a good biomechanical environment, avoid stress over-concentration, excessive intensity of activities, work with large amount of activity, and work load should properly control the workload and work rhythm, pay attention to work and rest, Eliminate or reduce the local pressure on the epiphysis, strengthen the protection of radioactive substances and radiation, and pay attention to the principles of administration of adrenal corticosteroids and indomethacin.

(2) secondary prevention: femoral condyle necrosis can be based on mild pain in the hip, X-ray film shows that the ossification center is small, the epiphyseal density is uneven, the hardening cystic change, etc., the hip joint space widening for early diagnosis, The affected limb should be abducted with internal augmentation or abducted stent, 40° abduction, mild internal rotation, or cast with gypsum to incorporate femoral condyle into the acetabulum. Early patients, avoid weight-bearing and treatment with hyperbaric oxygen, early symptoms of obvious surgery, can be used for limb traction, to protect the stent with pain disappeared.

(3) Tertiary prevention: Commonly used osteophyte drilling in the aseptic necrosis of the femoral head, decompression to promote the reconstruction of necrotic callus; Phase II, III common resection of the major synovial or total resection plus femoral head drilling or simultaneous implantation Into the blood vessel and other methods, in recent years, the use of fetal cartilage implantation to repair the aseptic necrosis of the femoral head has achieved good results. The femoral condyle is all involved in the subluxation. It is feasible to use Salter pelvic osteotomy, sometimes with pelvic osteotomy. Rotate the osteotomy under the trochanter, and fix it with the "human" gypsum of the hip for 2 to 3 months, so that the femoral head is well covered.

Idiopathic femoral head necrosis complications Complications

Once the bone shape of the femoral head is deformed, it can cause permanent joint surface collapse.

Idiopathic femoral head necrosis symptoms Common symptoms Severe pain, greater rotator pain, buttocks can be touched up... Infectious fever

Pain is the most common early symptom, 50% of acute attacks, characterized by hip discomfort, uncertain position, can occur before or after X-ray film positive findings, may be related to increased intraosseous pressure, tissue ischemia or microfracture, Eventually, the joint surface collapses, causing the pain to be further aggravated. The lower limb activities, especially the internal rotation, are limited. Some patients have interspersed claudication. The symptoms are similar to those of chronic peripheral vascular disease. The symptoms are relieved at rest, and the activity and weight-bearing are aggravated. Patients should be especially vigilant:

1 Local pain of unknown cause, especially hip pain, occasional limp.

2 The contralateral hip joint has been diagnosed as osteonecrosis. Due to non-traumatic osteonecrosis, the bilateral bilateral lesions are as high as 30% to 80%.

3 obvious incentives, such as long-term or short-term use of large amounts of steroids, long-term heavy drinking, collagen disease (systemic lupus erythematosus, rheumatoid disease, etc.), sickle cell anemia, high snow tumor, decompression sickness, and the aforementioned causes Various medical history of osteonecrosis induced.

Examination of idiopathic femoral head necrosis

Hemodynamic examination of intramedullary cannula: The needle is inserted directly into the medullary cavity of the intertrochanteric region of the femur under local anesthesia or general anesthesia to determine intramedullary pressure in the lesion. This method is more conventional than X-ray and radionuclide. Bone scan examination can detect abnormal changes of bone tissue earlier, which has certain value for early diagnosis of femoral head necrosis. Normal intramedullary pressure is less than 4kPa (30mmHg). Patients with femoral head necrosis often exceed this value, such as injecting appropriate amount into the medullary cavity. The physiological saline, observed changes in pressure (impact test), help to further discover potential pathological changes.

1. Intramedullary vein X-ray photography The trocar of the intramedullary pressure is injected into the medullary cavity to inject contrast medium, and the X-ray film is continuously taken to observe the stroke and emptying of the angiography in the medullary cavity, thereby checking the blood vessels. The structure can provide a basis for the early diagnosis of femoral head necrosis. As with intramedullary pressure measurement, poor specificity and traumaticity are its disadvantages.

2. Histopathological examination can be used as the basis for the diagnosis of femoral head necrosis. Early stage of plasma stasis, interstitial edema, occasional foamy cells and yellow bone marrow small area eosinophilic necrosis, followed by eosinophilic necrotic area All the marrow cavity is filled with necrotic tissue, and trabecular bone necrosis occurs. Finally, the bone marrow is partially fibrotic, and the number of necrotic trabeculae is further increased, surrounded by new bone cells.

3. Imaging examination

(1) X-ray inspection:

It is the simplest and most practical method for diagnosing femoral head necrosis. The early stage of femoral head necrosis can be characterized as normal or mild loose bone. In some patients, the bone density of the lesion is relatively uniform due to the atrophy of the surrounding normal bone tissue. Phenomenon, it can be seen that the weight-bearing area has a wedge-shaped hardening zone or a cystic lesion of bone tissue, and a "new moon-shaped translucent band" which is equal to the articular surface is further appeared. The joint space is widened, and the cancellous bone supporting the articular subchondral bone plate is suggested. Bone fracture collapses. Finally, the subchondral bone plate and joint surface collapse, the bone contour changes, the step shape is discontinuous, the bone compression is aggravated, the acetabular joint surface is also damaged, the joint space is narrow, the callus is formed, and the entire joint is degenerative. Arthritis changes.

Note: Sterile necrosis of the femoral head is characterized by osteoporosis of the surrounding bone of necrotic bone tissue, and then a lateral triangle or crescent-shaped translucent area with a pointed tip pointing to the diaphysis, indicating that the necrotic bone tissue is from The granulation tissue in the marrow is removed or replaced, and the necrotic tissue around the lesion is covered by the new bone tissue, forming a hardening zone at the edge of the necrotic area. Repeated necrosis and new bone repair process form multiple capsules hardened around the necrosis of the femoral head. Orbital or irregular translucent area, late femoral head with heavy surface collapse, femoral head flattened, fragmented, joint space widened or subluxated, commonly used in clinical clinical Steinberg classification.

(2) Radionuclide scanning:

The clinical application of 99mTc phosphate bone scanning method in diagnosing various bone diseases has been more than 20 years. The sensitivity of AVN diagnosis is as high as 80%. It reflects the lesions earlier than conventional X-ray examination. The common bone display image shows lesions on the tracer. The absorption of the agent increases to form a hot zone, suggesting that local blood vessels and bone tissue are regenerated, and there is repair activity around the lesion area. The degree of absorption of the tracer is not positively correlated with the severity of the disease.

(3) Computed tomography (CT):

The normal femoral head cancellous bone appears as a star-shaped high-density shadow on the CT slice. In patients with early femoral head necrosis, there is little bone density change in the femoral head necrosis on the CT slice, so it cannot be used as an early diagnosis of femoral head necrosis. This aspect needs further observation.

(4) Magnetic resonance (MRI):

In other cases of negative and highly suspected ischemic necrosis, MRI should be performed. In MRI, normal osteochondral and bone marrow are low, medium and high, respectively, and cancellous bone with a large amount of bone marrow is whiter. Signal, bone ischemic necrosis is a local abnormally low signal in the sub-articular area, which can be divided into 4 types: uniform, uneven, ring-shaped, band-shaped. Currently, MRI is generally considered to be the best method for early diagnosis of femoral head necrosis. One.

Diagnosis and diagnosis of idiopathic femoral head necrosis

X-ray plain film can only identify advanced lesions as a basis for diagnosing femoral head necrosis. At present, MRI has become an important means of diagnosing femoral head necrosis earlier than X-ray films, even by clinical manifestations. By comparing bilateral symptomatic and asymptomatic For the joints, preclinical lesions can be found on MRI, and MRI abnormalities can be found in asymptomatic joints weeks before clinical manifestations are found.

The disease should be differentiated from early femoral head metastases, osteosarcoma, bone spot disease, femoral condyle spondylolisthesis or femoral condyle necrosis with severe joint degenerative changes.

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