Osteonecrosis of the femoral head
*Aetiology :Femoral head is the commonest site of symptomatic osteonecrosis, mainly because of its peculiar blood supply which renders it vulnerable to ischemia from :
1- arterial cut – off.
2- venous stasis.
3- intravascular thrombosis.
4-intraosseous sinusoidal compression
5- or a combination of several of these.
Osteonecrosis can be :
A- post –traumatic : usually follows a displaced fracture of the femoral neck or dislocation of the hip.
B- non – traumatic : due to :
1- Infection : osteomyelitis , septic arthritis.
2- Haemoglobinopathy : Sickle cell disease.
3-Storage disorders : Gaucher s disease.
4- Caisson disease : dysbaric osteonecrosis.
5-Coagulation disorders : familial thrombophilia , hypofibrionlysis, throbocytopenic purpura.
6- other CAUSES :
-perthes disease
- cortisone usage.
- alcohol abuse.
-SLE ( systemic lupus erythematosus )
- anaphylactic shock , ionizing radiation and pregnancy ( fatty liver ,hypofibrinolysis ) .
Clinical features
**post- traumatic osteonecrosis : develops soon after injury to the hip , but symptoms and signs may take months to appear.**Non – traumatic osteonecrosis : is more insidious.
The presenting complaint is usually pain in the hip or ( in over 50 % of cases , both hips ) , which progresses over a period of 2-3 years to become quite severe.
However , in over 10 % of cases the condition is asymptomatic and discovered incidentally after x- ray or MRI.
**On examination :
There is limping and positive Trendelenburg sign.
The thigh is wasted and the limb may be 1 or 2 cm short.
Movements are restricted especially abduction and internal rotation.
-a characteristics sign : is a tendency for the hip to twist into external rotation during passive flexion.
This corresponds to the Sectoral sign in which , with the hip extended , internal rotation is almost full , but with the hip flexed it is grossly restricted.
There may be symptoms or signs of an associated causative disorder e e.g. Cortisone side effects.
Remember that even a short course of high dosage corticosteroids can result in osteonecrosis and the hip is the commonest target.
Imaging
X – ray :
During the early stages of osteonecrosis plain x- rays are normal.
The first signs appear only 6 – 9 months after the occurrence of bone death and are due mainly to reactive changes in the surrounding ( live ) bone.
Thus , the classic feature of increased density ( interpreted as sclerosis ) is a sign of repair rather than necrosis.
With time , destructive changes do appear in the necrotic segment.
Then increased distortion with eventual collapse of the articular surface of the femoral head will occur.
**MRI
*MRI shows characteristic changes in the marrow long before the
appearance of x- ray signs .
*The diagnostic feature is a band of altered signal intensity running through the femoral head ( diminished intensity in the T 1 weighted image and increased intensity in the STIR image ) .
*This band represents the reactive zone between living and dead bone . Thus demarcates the ischemic segment.
-Osteonecrosis of the femoral head = should be differentiated from =
1- x- ray features of destructive or sclerotic forms of osteoarthritis are sometimes mistaken for those of advanced osteonecrosis.
There may be elements of bone necrosis in some types of OA , but there is an important point of distinction between these two conditions.
In OA , the articular space diminished before the bone breaks up , whereas in osteonecrosis , the articular space is preserved to the last ( because it is not primarily a disease of articular cartilage ) .
2- transient osteoporosis of the hip .(marrow edema syndrome ).
*note : it is important to recognize that pathogenic factors are cumulative , so a patient with systemic lupus or a moderately severe alcohol habit may develop osteonecrosis following comparatively low doses of cortisone and occasionally even after prolonged or excessive use of topical corticosteroids.
**Staging :
In the past , Ficat and Alret s radiographic staging of the femoral head necrosis was widely used.
But , it dose not provide a guide to prognosis and therefore treatment in the early stages of the disease.
- Shimizu et al ( 1994 ) proposed a classification based on MRI images which defines the extent , location and intensity of the abnormal segment in the femoral head.
-the risk of femoral head collapse ( at least over a period of 2-3 years ) was related mainly to :
1- the extent = the area of the coronal femoral head image involvement.
2- location = the portion of the weight bearing surface in the initial MRI.
Note = the extent of the ischemic segment is determined at the outset and does not increase over time.
**according to Shimizu et al classification :
Grade 1= the lesion occupying less than one – quarter of the femoral head coronal diameter and involving only the medial third of the weight bearing surface .
- the lesion here rarely goes on to collapse.
-Grade 2 = lesions occupying up to one half of the femoral head diameter and involving between one –third and two- thirds of the weight bearing surface.
The lesion here is likely to collapse in about 30 % of cases.
Grade 3 = lesion occupying more than one – quarter of the femoral head diameter and involving more than two – thirds of the weight bearing surface .
- The lesion here will collapse within 3 years in over 70 % of cases.
-Treatment =
Treatment of post-traumatic osteonecrosis =
- Femoral head necrosis following fracture or dislocation of the hip usually ends in collapse of the femoral head.
Very young patients ( under 40 years ) . = in whom one is reluctant to perform hip replacement , can be treated by realignment osteotomy , with or without bone grafting of the necrotic segment.
They will probably require hip replacement at a later stage.
Older patients = will almost invariably require partial or total hip replacement.
Treatment of non – traumatic osteonecrosis =
-Early Shimizu grade 1 lesions =
The lesion progress very slowly or not at all , so all that is needed is symptomatic treatment and reassurance , but observation over several years is required .
Grade 2 lesions =
If the lesion is seen before there is any distortion of the femoral head , then conservative surgery is advised , which means core decompression and bone grafting of the femoral head .
The alternative is realignment osteotomy in younger patients and partial or total hip replacement in patients over 45 years old with increasing symptoms.
-Grade 3 lesion =
Decompression is unlikely to have a lasting effect.
For young patients , realignment osteotomy is the treatment of choice to displace the necrotic segment away from the maximal load bearing area.
A flexion osteotomy will be needed for most of cases.
Older patients are better treated by partial or total joint replacement.
Transient osteoporosis of the hip
( marrow edema syndrome )
**this is a well recognized , though uncommon , syndrome , characterized by pain and rapidly emerging osteoporosis of the femoral head and adjacent pelvis.
**Radionuclide scanning shows increased activity on both sides of the hip joint but not in the soft tissues.
**The condition was originally described in women in the last trimester of pregnancy , but it is now seen in patients of both sexes and all ages from early adulthood onwards.
**Typically the changes last for 6-12 months , after which the symptoms subside and x- ray gradually returns to normal.
**the cause is unknown , but MRI features are characteristic of marrow edema.
Treatment :
**The condition almost always resolves spontaneously and most patients require no more than symptomatic treatment .
**However , pain can be rapidly abolished by operative decompression of the femoral head.
**If there is any doubt about whether the MRI changes are due to osteonecrosis or marrow edema , operative decompression is recommended.