Hematogenous osteomyelitis in childhood can relapse many years later into adulthood: A retrospective multicentric cohort study in France

Abstract

To describe the epidemiological, clinical, laboratory, and radiological features and the management of adult patients who experienced a relapse between 2003 and 2015 of an acute hematogenous osteomyelitis acquired in childhood.A retrospective multicentric cohort study was conducted in 5 centers in France.Thirty-seven patients were included. The median age was 40 years (28-56), and 26 (70%) were male. The first site of infection was the distal femur (n = 23, 62%). The median time between the osteomyelitis in childhood and the relapse in adulthood was 26 years (13-45). Thirty-four (92%) patients reported inflammatory local clinical manifestations, 17 (46%) draining fistula, 10 (27%) fever. Most patients had intramedullary gadolinium deposition (with or without abscess) on magnetic resonance imaging. Most relapses were monomicrobial infections (82%). Staphylococcus aureus was the most commonly found microorganism (82%), expressing a small colony variant phenotype in 3 cases. Most patients (97%) had a surgical treatment, and the median duration of antibiotics for the relapse was 12 weeks. All patients had a favorable outcome, no patient died and no further relapse occurred. We count 2 femoral fractures on osteotomy site.Osteomyelitis in childhood can relapse later in adulthood, especially in patients with lack of care during the initial episode. Osteotomy and prolonged antimicrobial therapy are required for clinical remission.

Figure 1

Localizations; time between the osteomyelitis in childhood and the relapse in adulthood; clinical manifestations and level of CRP. CRP = C-reactive protein.

Figure 2

Osteomyelitis with intraosseous abcess. (A) Tomodensitometry of the right thigh, note a medullary defect (arrow), thickening of the cortex and periosteal reaction (dashed arrow). (B) Magnetic resonance imaging of the right thigh (from left to right), note a low-signal medullary image in T1-weighted sequence (arrow); hyperintensity medullary image (arrow) and bone marrow oedema (arrowhead) in T2-weighted sequence with fat suppression; and in T1-weighted post contrast image the heterogen enhancement associated with the intraosseous abscess (dashed arrow). (C) Magnetic resonance imaging of the right thigh (from left to right), T2-weighted fat suppressed image shows intraosseous abscess cavity (arrow) with rim of surrounding oedema (arrowhead); T1-weighted post contrast image with fat suppression shows peripherical enhancement associated with the intraosseous abscess (dashed arrow).

Figure 3

Right femoral osteomyelitis and left chronic femoral osteomyelitis. (A) Anteroposterior and lateral X-rays of the right femur, note periosteal reaction (arrow) and sclerotic areas. (B) (from left to right) Coronal magnetic resonance imaging in T1-weighted post contrast with fat suppression of the right femur, shows osteomyelitis complicated by a soft tissue abscess (arrow) and an arthritis (dashed arrow); Coronal magnetic resonance imaging, in T1-weighted post contrast of the left femur, shows chronic osteomyelitis and a marrow oedema (large arrow). (C) Axial magnetic resonance imaging of the right and the left femur, in T1-weighted post contrast with fat suppression, shows soft tissue fluid collection (arrow) and inflammation around the lesion (dashed arrow) to the right femur and intraosseous abscess to the left femur (large arrow).

Figure 4

Comparison CRP level of osteomyelitis caused by MSSA PVL+ versus control. CRP = C-reactive protein, MSSA = methicillin-sensible Staphylococcus aureus, PVL + = Panton–Valentine leukocidin-positive.

Figure 5

Left distal tibia osteomyelitis. (A) Radiographic features (from left to right): initial X-ray, after surgical debridement and after 3 mo. (B) Axial and coronal magnetic resonance imaging, T1-weighted post contrast with fat suppression, note an intraosseous abscess (arrow) and marrow oedema (dashed arrow).