Alcoholic necrosis of the femoral head

Introduction to alcoholic femoral head necrosis Alcoholic femoral head necrosis is a femoral head necrosis caused by a large amount of alcoholism. Simply speaking, it is the result of abnormal lipid metabolism. Clinical studies have shown that long-term heavy drinkers have a marked increase in blood lipids, resulting in lower clearance of liver lipids and fatty liver. Early clinical symptoms of alcoholic femoral head necrosis are not typical, and hip pain is the most common symptom. basic knowledge The proportion of illness: 0.001% Susceptible people: a large number of long-term drinkers Mode of infection: non-infectious Complications: osteoarthritis

Alcoholic femoral head necrosis

Lipid metabolism disorder (35%)

Alcohol metabolism is mainly carried out in the liver and produces acetaldehyde, which leads to lipid peroxidation. Lipid peroxide causes severe damage to the cell membrane, ischemia, and direct cytotoxicity of alcohol and its metabolites, making it under ischemia. Further damage to the bone cells leads to irreversible degeneration and necrosis.

Vasculitis (20%)

A large amount of alcohol stimulates the elevation of prostaglandins, causing local vasculitis. In the case of lesions in the femoral head microvessels, thrombosis is formed locally, and the blood vessels are blocked by ischemia. The ischemia causes bone cells to be damaged and leads to necrosis.

Osteoporosis (10%)

Drinking alcohol can cause metabolic disorders of vitamin D, hypothyroidism, decreased bone cell metabolism, reduced osteogenic capacity, osteoporosis, resulting in local stress area and high stress osteogenesis, bone cell destruction, subchondral A small fracture occurs, causing local intraosseous pressure rise and bleeding, leading to osteonecrosis.

Fatty liver (10%)

As a result of alcohol metabolism, fat accumulates in the liver, forming fatty liver. The liver activity of the damaged liver is reduced, the fat embolus continues to enter the blood, and the fat embolus is retained in the subchondral vascular bed, causing cartilage ischemia and necrosis.

At present, although there are many pathological mechanisms about femoral head necrosis, femoral head ischemia is the basic pathology of femoral head necrosis: after the femoral head is in an ischemic state, the normal metabolism and function of bone cells and bone tissue are affected and necrosis.

Alcoholic femoral head necrosis prevention

Do not eat chili, but drink alcohol, do not eat hormone drugs, pay attention to increase the intake of calcium, eat fresh vegetables and fruits, more sun, prevent weight, regular activities and other prevention of femoral head necrosis.

Alcoholic femoral head necrosis complications Complications osteoarthritis

The femoral head collapses, the joint space narrows, and finally leads to osteoarthritis, which causes the patient's hip joint dysfunction and causes disability.

Alcoholic femoral head necrosis symptoms Common symptoms Hip flexion and external rotation deformity

Early clinical symptoms of alcoholic femoral head necrosis are not typical, and pain in the internal rotation hip joint is the most common symptom. After the femoral head collapses, there may be a limited range of hip motion. Signs: local deep tenderness, tenderness of adductor muscles, and partial axonal pain may be positive. Early due to hip pain, Thomas sign, 4 word test positive; late due to femoral head collapse, hip dislocation, Allis sign and single leg independent test sign can be positive. Other signs include abduction, limited external rotation or limited internal rotation activity. The affected limb can be shortened, muscle atrophy, and even subluxation signs. Nelaton can also be moved linearly with hip dislocation, the bottom edge of the Bryant triangle is less than 5cm, and the Shenton line is discontinuous.

Examination of alcoholic femoral head necrosis

X-ray findings of alcoholic femoral head necrosis:

1. The shape of the early femoral head is complete, the bone surface is smooth, and the bone density is not changed. Only the trabecular bone is loosened, but there is no typical clinical symptoms and body disease in the clinic, and in the early stage of alcoholic femoral head necrosis. X-ray films can not show the necrosis of the femoral head. Therefore, it is difficult to diagnose the femoral head necrosis by X-ray film in the early stage. Patients need to do ECT, MRI and other tests to assist the diagnosis.

2. In the middle and late stage, a crescent-shaped transparent belt of 2-4 mm width appears below the osseous joint surface, which is the "new moon sign". The density of the top of the femoral head or the entire femoral head is increased, but there is a decrease in density and a sac-like translucent area. The dead bone is wedge-shaped and half-moon shaped, and there is a new bone band with a higher density. The femoral head collapsed and deformed into a mushroom shape. The articular surface of the bone is broken, the convex and concave are uneven, the joint space is narrowed, and the hip is subluxated. Often accompanied by osteoarthritis.

Diagnosis and diagnosis of alcoholic femoral head necrosis

diagnosis:

1. Clinical symptoms, signs and medical history: The joints of the groin, buttocks and thighs are the main joint pain, the hip internal rotation activity is limited, the history of hip trauma, the history of corticosteroid application, and the history of alcohol abuse.

2, X-ray film changes: femoral head collapse, without joint space narrowing; the femoral head has a hardened zone of the boundary; the subchondral bone has a X-ray band (new moon sign, subchondral fracture). Or X-ray film showed collapse of the femoral head with narrowing of the joint space, cystic or speckle-like hardening in the femoral head, and flattening of the upper part of the femoral head.

3. Nuclide scanning shows a cold zone in the hot zone of the femoral head.

4. The T1 weighted phase of the femoral head MRI is banded low signal (band type) or T2 weighted phase with double line sign.

5, bone biopsy showed more than 50% of the trabecular bone lacunae of the trabecular bone, and involving multiple trabecular bones nearby, with bone marrow necrosis. Or MRI shows a ribbon type of equal or heterogeneous low signal intensity without a T1 phase.

Differential diagnosis

1. Middle and late stage osteoarthritis: When the joint space is narrowed, it may be confused when subchondral cystic changes occur, but the CT manifestation is hardening and cystic change. MRI changes are mainly low signal, which can be identified accordingly.

2, acetabular dysplasia secondary to osteoarthritis: femoral head incomplete, acetabular line in the upper part of the femoral head, joint space narrowed, disappeared, osteosclerosis, cystic changes, similar changes in the corresponding area of the acetabulum, easy with ONFH Identification.

3, ankylosing spondylitis involving the hip joint: common in adolescent males, mostly bilateral ankle joint involvement, characterized by HLA-B27 positive, femoral head remains round, but the joint space narrows, disappears or even fuses, so not Difficult to identify. Long-term use of corticosteroids in some patients can be combined with ONFH, and the femoral head can collapse but is often not severe.

4, rheumatoid arthritis: more common in women, the femoral head remains round, but the joint space is narrowed and disappeared. Common femoral head articular surface and acetabular erosion, identification is not difficult.

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