Annals of African Medicine Annals of African Medicine Society ISSN: 1596-3519 Vol. 10, Num. 1, 2011, pp. 64-65

Annals of African Medicine, Vol. 10, No. 1, January-March, 2011, pp. 64-65

Letter to Editor

Bilateral osteonecrosis of the femoral heads in a patient with systemic lupus erythematosus

YZ Lawal¹, MO Ogirima¹, IL Dahiru¹, MI Maitama¹, FS Ejagwulu¹, K Abubakar²

¹ Department of Trauma and Orthopaedics, Ahmadu Bello University Zaria, Nigeria
² National Orthopedic Hospital Dala Kano, Nigeria

Correspondence Address: Y Z Lawal, Department of Trauma and Orthopaedics, Ahmadu Bello University Zaria, Nigeria, lawalyau@yahoo.co.uk

Code Number: am11015

PMID: 21311160

DOI: 10.4103/1596-3519.76594

Dear Sir,

Trauma is the leading cause of aseptic necrosis of the femoral head as a result of falls in the ever-increasing population of the aged. It results from intra-articular fractures of the neck of femur. ^[1] It may be seen in 2-30% of patients with systemic lupus erythematosus (SLE). It is also common in a wide array of conditions such as sickle cell disease, Gaucher′s disease, steroid usage, and deep-sea divers and in SLE and long-term survivors of leukemia and lymphomas. It is not commonly seen in steroid users or abusers who do not exceed 30 mg/day. ^[2]

We recently managed a 24-year-old male patient with a diagnosis of SLE on initial daily treatment with 15 mg of prednisolone and 150 mg of Diclofenac potassium in three divided doses for seven years. He was also on physiotherapy and walks with the assistance of a hand-held walking stick. He had a day′s history of acute aggravation of bilateral hip pains, which are worsened by walking and relieved by rest. There was no history of trauma. He smokes three to five sticks of cigarette in a day and takes alcohol occasionally. He has not been on any disease-modifying anti-rheumatic drugs (DMARDs). There was no family history of similar illness in the family. He has no history of thrombotic episodes. Examination revealed a chronically ill looking man walking with a waddling gait. His body mass index was 22 kg/m ² . There was no limb length discrepancy. He was able to raise the leg to 30º. He had cutaneous striae over the abdomen but his hernial orifices were normal. His body temperature was 37ºC. There was no stomatitis and no peri-articular swellings or vasculitis. The white blood cell count was 5.0 Χ 10 ⁹ /l and the erythrocyte sedimentation rate was 65 mm/h Westergren. He was HIV 1 and 2 antibodies negative. His activated partial thromboplastin time was 42 s, which is raised. His random blood sugar was 9.0 mmol/dl. His urea and electrolytes were normal and there were no raised hepatic transaminases.

He was resuscitated with intravenous saline, oral tramadol hydrochloride 150 mg in three divided doses and dynamic skin traction with 4 kg weight. He was counseled for bilateral total hip replacement. He did well and was discharged home after three weeks on admission. Patient however died of complications of chest infection and possible adrenal insufficiency. The X ray of the patient is seen in [Figure - 1].

Aseptic osteonecrosis of the femoral head is a common occurrence in people with a variety of illnesses including SLE and those on steroids. It is a slow process and occurs in stages. What is however striking in this patient is the fact that it occurred as a sudden event and reaching Ficat stage 4 within a week of onset of pain. This patient has had pain that is aggravated by walking and relieved by rest before the current presentation. However, the pain was attributed to the general symptoms of SLE. Radiographic findings appear as if the femoral neck was transected at the intertrochanteric line, thus making trauma a possible cause. However, there was no history of trauma and the apical aspects of the femoral heads show identical fragmentation. Dubois and Cozen made the first report of avascular necrosis of the femoral head (ANFH) related to SLE in 1960. It is believed that vasculitis, and increased tendency to thrombosis as components of lupus syndrome contribute to osteonecrosis in SLE. ^[3] Those patients with raised activated partial thromboplastin time or positive anticardiolipin antibody are more likely to have aseptic necrosis and the lupus syndrome. The main contributing factor to osteonecrosis in this individual is the steroid ingestion. There is correlation to the amount of steroid ingested and the occurrence of osteonecrosis. It tends to be present in situations where higher doses greater than 30 mg/day are used. ^[1] However the dose was low in this individual. Another factor might have been obesity. It also conforms to the finding that in 90% of SLE patients it is bilateral. Analgesia and enforced rest by skin traction is the main stay of treatment in the acute state. He was offered total hip replacement as a definitive treatment but patient died as a result of complicated pneumonia.

Bone necrosis does not only imply death of bone trabeculae but also of the intertrabecular marrow. The pathophysiology of ANFH differs from one cause to the other. However, necrosis tends to occur at sites of fatty marrow probably due to its poorer blood supply compared to that of hematopoietic marrow. Following necrosis, an attempt at repair begins as a result of revascularization. This is in two stages. The first stage is invasion of necrotic marrow by capillaries. Fat cells and cellular debris are mopped up by macrophages. This is followed by new lamellar bone deposition. Ficat ^[4] thus classified ANFH into five stages:

1. Silent hip, symptomless and no radiographic changes - no other side affected
2. Sudden pain in groin with some limitation of internal rotation and abduction; radiograph normal or subtle trabecular blurring.
3. Worsening symptoms, patchy or linear sclerosis - intact head.
4. Subchondral fracture, crescent line segmental flattening
5. Loss of articular cartilage, marginal osteophyte-osteoarthritis superimposed on deformed head.

In the early pre-collapse stages of osteonecrosis ^[1],[2],[3] restricted weight bearing may be all that is needed and spontaneous resolution have been reported. It has been observed that small-sized lesions less than 5 cm ³ progress slowly and long-term follow-up is recommended. In some, core decompression is done with a view to improving the blood supply and hence capillary invasion of the adjacent marrow. External biophysical methods such as extracorporeal shockwave lithotripsy, ^[1],[5] pulsed electromagnetic wave stimulation etc. have been reported to be of value in the earlier stages of the disease. Bone morphogenic protein injections, bone marrow mesenchymal cell grafting have also been used with variable successes. Hemiarthroplasty, total hip replacements are the methods of treatment for advanced diseases.

High index of suspicion is advocated to identify patients at early stage of disease to get better results.

References

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