| Avascular necrosis |

Category: Practitioners

Avascular necrosis (AVN) (also known as osteonecrosis or aseptic necrosis) is the end result of a number of disease processes resulting in decreased blood flow to subchondral bone and cellular death of the components of bone.

Epidemiology

The exact incidence of AVN is unknown. The majority of cases occur in individuals under the age of 50 years and males are more commonly affected than females.

Aetiology and pathogenesis

AVN has been associated with trauma and a variety of non traumatic conditions. The latter include fractures of the femoral neck or hip dislocations, corticosteroid use, alcohol abuse, smoking, sickle cell anaemia and coagulopathies, systemic lupus erythematosis, hypercholesterolaemia, Gaucher’s disease and Caisson (decompression) disease. More recently an association between HIV and AVN has been reported. It is unclear as to whether the increased risk is due to the HIV infection itself, antiretroviral treatment, in particular protease inhibitors, or some other factor.

A mechanical interruption to the circulation of the subchondral bone, the region just beneath the surface of articular surface of the bone, occurs in most of the conditions. The slow flow and circuitous route of the vascular supply of this area predisposes the region to vascular compromise either by microemboli, vasospasms, or small increases in intra-osseous pressures.

In traumatic lesions gross disruption of the vessels can occur with a displaced fracture or a dislocation. However, the mechanism for the ischaemia and or necrosis in non traumatic AVN is less well understood. Several theories have been postulated. Fat embolism has been implicated and may result from a destabilization or coalescence of plasma lipoproteins, hyperlipaemia, or disruption of marrow fat. The fat globules may trigger endothelial damage, focal intravascular coagulation and platelet aggregation, eventually leading to thrombosis, ischaemia and AVN. Alcohol and corticosteroids are thought to cause alterations in fat metabolism leading to a fatty liver. Corticosteroids have also been shown experimentally to increase the size of the lipocytes in bone marrow thus increasing the intra-osseous pressure which may lead to collapse of small capillaries and resultant ischaemia.

In decompression disease and sickle cell disease, nitrogen bubbles and the rigid sickle cells may result in an engorgement of sinusoidal circulation.

Repeated microfractures in the weight-bearing area may induce microvascular lesions and ischaemia in fragile bone. However, AVN is not a recognized complication of postmenopausal osteoporosis.

Vascular problems in the arterial, venous or capillary part of the vascular network may predispose to AVN. This is supported by the fact that conditions associated with vascular disease at other sites e.g. corticosteroid use, diabetes, arteritis, alcohol abuse, hyperlipidemia and increased blood hyperviscosity are also associated with AVN. The increase risk of AVN with smoking is thought to be due to vascular spasm.

Clinical presentation

AVN commonly occurs at one site (unifocal) with the most common site involved being the femoral head. The distal femur, humeral head and small bones of the wrist and foot may also be affected. Less commonly multiple sites may affected.

In the early stages of the disease the patient is often asymptomatic and when symptoms do occur these are usually non specific. The onset of disease is usually gradual but may be sudden. In hip involvement the commonest symptom is persistent pain in the groin, buttock, thigh or knee which is exacerbated by weight-bearing. Later in the course of the disease the patient may develop a limp and decreased movement of the hip joint. Similarly, the physical examination may be normal until the advanced stage when the range of motion of the joint becomes limited, with pain at its extremes.

Differential Diagnosis

The diagnosis of ON is readily made in the presence known risk factors and characteristic radiographic changes i.e. the ‘crescent sign’ indicating collapse of the subchondral bone and/or the presence of flattening of the femoral head. However, in early and advanced disease this is more difficult.

In a patient presenting with persistent hip pain in the absence of characteristic radiographic findings, other diseases of the hip affecting bone, cartilage or synovial tissue must be considered in the differential diagnosis and excluded. An important differential is transient osteoporosis of the hip in which the same osteopaenia of the femoral head can be observed on X-ray, with the same uptake of radionuclide and possibly the same low-signal area on T1-weighted MRI. The only difference is on the T2-weighted image which displays a high signal as opposed to the low signal seen in AVN.

Management

Specific therapy for AVN can only be instituted early in the disease. Untreated, the majority of patients will progress to develop collapse of the femoral head and secondary osteoarthritis. Hence, early diagnosis is imperative.

Prevention

There are no specific measures to prevent AVN; however simple measures should be instituted in patients with a condition known to be associated with AVN.

These include:

Avoidance of decompression accidents with slow resurfacing with staged decompression

Control of hyperlipidemia and diabetes mellitus

Moderation of alcohol intake and cessation of smoking.

Appropriate use of corticosteroids with lowest effective dose and shortest duration necessary. In patients with AVN corticosteroids should be avoided and alternative agents should be used if immunosuppression is required.

Medical treatment is non specific and has a role in early disease when surgical intervention is not indicated. Patients should be advised to discontinue weight-bearing on the affected hip for at least 4–8 weeks in the acute stages and thereafter practice protected weight bearing with the use of assisted devices if necessary. In addition pain relief can be achieved with analgesics.

Surgical treatment

Several options are available depending on the stage of the disease.

In core decompression a core from the necrotic segment of bone is surgically removed using a trephine. This lowers intraosseous pressure, relieves pain, potentially stimulates vascular neogenesis and relieves ischaemia. Core decompression is indicated in early disease i.e. in the symptomatic patient with normal radiographs. Bone grafting may also provide decompression of the femoral head.

In an osteotomy the diseased section of the femoral head is removed from the region of major weight-bearing and replaced a normal portion of the femoral head. This procedure may be considered in young individuals with early radiographic changes of AVN and a little flattening.

Total hip replacement is indicated in late stages when collapse of the femoral head is present.

Published on 2005-06-08