Avascular necrosis of the femoral head(대퇴골두 무혈성 괴사) 2009년 논문

[문형철]

대퇴골두 무혈성 괴사 초기에 체중분산을 유도하고, 혈액공급을 원할케 하는 움직임 자극을 주고, 뼈 재생자극을 주면 

진행을 막을 수 있을까? 

왜 안된다고만 할까? cam and pincer impingement 조건을 없애주고..

진행을 늦추고, 유지하는게 가능하지 않을까? 거의 불가능!!

2015년 1월 1일 ...

대퇴골두 무혈성 괴사는 가능한 빨리 수술하여 2차적 관절 압박과 부정렬 악화를 방지하는 것이 중요함.

수술 후 재활치료도 쉬운 편

panic bird...

FACTORS RELATED TO DEVELOPMENT OF TRAUMATIC osteonecrosis o.pdf

Avascular necrosis of the femoral head. 2009.pdf

Avascular necrosis (AVN) is a disease that may affect several different bones as a result of temporary or permanent loss of the blood supply to these bones. The femoral head is most commonly affected by this disease. Usually, the patients are in their third, fourth or fifth decade of life at the time of diagnose. Initially, patients are asymptomatic, but, in time, AVN leads to joint destruction, requiring surgical treatment and, in latter stages, total hip replacement. It is essential that AVN of the femoral head is diagnosed early because delaying this disease by joint preserving measures has a much better prognosis and because the results of joint replacement are poorer in young individuals.

There are various conditions than can be incriminated as triggers for this disease. However, almost half of the patients diagnosed present none of these conditions. This type of avascular necrosis is termed primary, or idiopathic. All the other forms of this disease are secondary. Treatment has been facilitated by using widely accepted international classification systems and by effective earlier diagnosis using MRI and other imaging techniques. Although treatment has turned more and more towards surgery, no universally satisfactory therapy has been developed, even for early disease.

􀁺 Primary (idiopathic)

􀁺 Secondary to:

– Trauma – Fracture of the femoral neck

􀂃 Slipped capital femoral epiphysis

􀂃 Proximal femoral epiphysiolysis

􀂃 Dislocation of the femoral head

􀂃 Epiphyseal compression

􀂃 Vascular trauma

􀂃 Burns

􀂃 Radiation exposure

– Hemoglobinopathies

􀂃 Sickle cell disease

􀂃 Hemoglobin S or hemoglobin C

hemoglobinopathy

􀂃 Polycythemia

– Caisson disease – Dysbaric osteonecrosis

– Local infiltrative disease

􀂃 Gaucher disease

􀂃 Infection

􀂃 Neoplasms

– Hypercortisolism

􀂃 Corticosteroid medications

􀂃 Cushing disease

– Alcohol consumption

– Pancreatitis

– Chronic renal failure

– Cigarette smoking

– Collagen vascular diseases

– Congenital and developmental

􀂃 Congenital dislocation of the hip

􀂃 Ehlers-Danlos syndrome

􀂃 Heredity dysostosis

􀂃 Legg-Calve-Perthes disease

– Fabry disease

– Giant cell arteritis

– Gout and hyperuricemia

– Hemodialysis

– Hypercholesterolemia

– Hypercoagulable states

– Hyperlipidemia

– Hyperparathyroidism

– Intravascular coagulation

– Organ transplantation

– Pregnancy

– Systemic lupus erythematosus

– Thrombophlebitis

– Hemophilia

PHYSIOPATHOLOGY

1. Extraosseous arterial factors are the most important. The femoral head is at increased risk because the blood supply is an end-organ system with poor collateral development. Blood supply can be interrupted by trauma, vasculitis

(Raynaud disease), or vasospasm (decompression

sickness) (2,3).

2. Intraosseous arterial factors may block the microcirculation of the femoral head through circulating microemboli. These can occur in sickle cell disease (SCD), fat embolization or air embolization from dysbaric phenomena (2,9).

3. Intraosseous venous factors affect the femoral head by reducing venous blood flow and causing stasis. These factors may accompany conditions such as Caisson disease, SCD or enlargement of intramedullary fat cells (2,8).

4. Intraosseous extravascular factors affect the hip by the increasing the pressure, resulting in a femoral head compartment syndrome (2). 

For example:

1) Fat cells hypertrophy after steroid administration or abnormal cells, such as Gaucher and inflammatory cells, can encroach on intraosseous capillaries, reducing intramedullary circulation and contributing to compartment syndrome. 

2) Repeated microfractures in the weightbearing segment of the femur may cause multiple vascular lesions resulting in ischemia within fragile and poorly repaired bone.

3) Cytotoxic factors, such as alcoholism and steroid use, have a direct toxic metabolic effect on osteogenic cells (2).

4) Decreased concentrations of 1,25 dihydroxyvitamin D3 can cause a quantitative or qualitative deficiency in the bone

architecture, causing the bone to deform under pressure.

5. Extraosseus extravascular (capsular) factors involve the tamponade of the lateral epiphyseal vessels located within the synovial membrane, through increased intracapsular pressure. This occurs after as trauma, infection, and arthritis, causing effusion that may affect the blood supply to the epiphysis (2,3).