Suspected Avascular Necrosis in a Runner

December 31, 2006

A 34-year-old man has had bilateralknee pain for the past 16 months andbilateral hip pain for the past 8 months.The pain is exacerbated by running, byweight bearing, and recently even by sittingfor extended periods. Moving froma sitting to a standing position is especiallydifficult. A week earlier, he visitedan urgent care center and was given naproxen and a 7-day course of prednisone,but neither medication alleviatedthe pain; in fact, he now feels worse.

A 34-year-old man has had bilateralknee pain for the past 16 months andbilateral hip pain for the past 8 months.The pain is exacerbated by running, byweight bearing, and recently even by sittingfor extended periods. Moving froma sitting to a standing position is especiallydifficult. A week earlier, he visitedan urgent care center and was given naproxen and a 7-day course of prednisone,but neither medication alleviatedthe pain; in fact, he now feels worse.Bell palsy was diagnosed 18months earlier, and the patient wasgiven a 14-day course of prednisone.He has never had surgery, has noknown allergies, and has no historyof drug, alcohol, or tobacco use.In his teens and twenties, the patientplayed soccer daily. When hestopped playing soccer, he started runningan hour every day. He ran upuntil 8 months ago, at which time hisinability to bear weight without painalso forced him to stop working.The patient walks with a stiff,slow gait, grimaces with each step, andholds onto the examination table forsupport. The knee examination revealsno limitation of flexion or extension andno effusion or joint line tenderness.Ligament evaluation shows no instability.Examination of the hips disclosestenderness in the groin and over thegreater trochanter bilaterally. Range ofmotion is limited bilaterally by pain:hip flexion is only 90 degrees (normal,120 degrees), and adduction and abductionare less than 10 degrees (normal,35 to 40 degrees). Internal rotationis 5 degrees at best (normal, 15 degrees) and elicits marked tenderness.Pain limits external rotation to 15 degrees(normal, 30 degrees). (When only1 hip is involved, the degree of differencethat is seen when the affected hipis compared with the good hip can beinformative. However, when both hipsare involved, as in this patient, such acomparison is not possible.)Femoral, popliteal, and dorsalispedis pulses are palpable and equal bilaterally.Although the patient's painlimits the extent of the neurologic examination,strength and sensation appearto be equal bilaterally. Other results ofthe physical examination are normal.Radiographs of the hips reveal lucenciesin both femoral heads and irregularityin the cortex with some flattening(Figure). The joint spaces are wellpreserved. No dislocations, subluxations,or fractures are seen. The sacroiliacjoints are symmetric, and the symphysispubis is well preserved. The rest of thevisualized soft tissues and bony structuresare unremarkable. The lucencies,cortical irregularity, and slight flatteningin the femoral heads suggest avascularnecrosisPOSSIBLE CAUSES OFAVASCULAR NECROSIS
Avascular necrosis (osteonecrosis)of the femoral head is seen in avariety of settings. It is the most commoncomplication of surgical repairof hip fractures; it has also been associatedwith alcohol abuse1 and theuse of corticosteroids.2 However, inmany patients, avascular necrosis hasno clear cause.The duration of corticosteroidtherapy associated with increasedrisk has been debated. Most studieshave been small case reports (eg, oneinvolved 71 patients and another, 77).One study concluded that 7 days ofcorticosteroid therapy is sufficient topredispose to avascular necrosis2The length of time from the beginningof corticosteroid therapy tothe onset of symptoms is also not clear. A case review by Koo3 showedthat the period of increased risk associatedwith long-term corticosteroidtherapy ranged from 1 to 16 months;he recommended monitoring patientsfor 1 year. (The prudent clinicianwould probably monitor patients bothduring corticosteroid therapy and forat least a year afterward.)This patient's avascular necrosishas no clearly defined cause. The2-week course of corticosteroids hereceived 18 months earlier for Bellpalsy may have provoked the condition(his symptoms began 10 monthslater). He denies alcohol use, so thatis probably not the cause. An untreatedstress fracture might have led tothe development of avascular necrosis;however, this is less likely becausestress fractures are usually unilateral.TREATMENT
Avascular necrosis carries apoor prognosis unless treated early.Nonsurgical treatment can be successfulif the femoral head has notcollapsed. In one study, 31% ofpatients with pre-collapse avascularnecrosis had a satisfactory clinicalresult without an operative procedure4 Various surgical proceduresare used, depending on the degreeto which the disease has advanced.Patients with more advanced osteonecrosismay require partial or fullprosthetic hip replacement. Becauseboth surgical and nonsurgical treatmentcan yield less than ideal results,consultation with an orthopedistexperienced in the care of hips isrecommended.In this patient, therapy was initiatedbased on a presumptive diagnosisof avascular necrosis. It includedoral naproxen, 500 mg bid; avoidanceof weight bearing (crutches were provided);range of motion exercises;and close follow-up at an orthopedicclinic. He was instructed to return tothe hospital if his pain remained uncontrolled.Before any invasive treatment treatmentcould be considered, avascularnecrosis would need to be confirmedwith MRI.OUTCOME OF THIS CASE
Unfortunately, the patient didnot return for follow-up. Thus, it isnot known whether the non-weightbearingtherapy was successful.

References:

REFERENCES:


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McKee MD, Waddell JP, Kudo PA, et al. Osteonecrosisof the femoral head in men following shortcoursecorticosteroid therapy: a report of 15 cases.

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Koo KH. Risk period for developing osteonecrosis of the femoral head in patients on steroid treatment.

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Ma M, Hungerford DS. Nontraumatic avascularnecrosis of the femoral head.

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1995;77:459-474.