Osteomyelitisisaninfectionofthebone.Thethreedifferentmodesofacquiring the infection are hematogenous, direct inoculation, and local invasion. In children,osteomyelitisismostlyhematogenousinoriginandisusuallycaused by a bacterial infection. Risk factors for the hematogenous osteomyelitis in children are sepsis, hemoglobinopathies, and immunodeficiency disorders. The anatomic characteristic feature of the growing bone in children plays an important role in the pathogenesis and clinical feature of the disease. In children, the most common site of hematogenous osteomyelitis are in the long bones.
In children, osteomyelitis presents with nonspecific, systemic symptoms of low-grade fever and malaise, which is gradual in onset over several days to weeks. As the infection progresses, the patient presents with local symptomsofwarmth,swelling,pain,anddecreasedmobility.Themostcommon organisms causing hematogenous osteomyelitis in the normal host is Staphylococcus aureus. Other organisms causing hematogenous osteomyelitis are group A and B Streptococcus. Among children with sickle cell disease (SCD), Salmonella and other gram-negative organisms, such as Escherichia coli, can also cause osteomyelitis in addition to the typical organisms described above.
Osteomyelitis in SCD: Infections are a major cause of morbidity and mortality for patients with SCD. SCD patients are more susceptible to bacterial infections due to factors such as defective opsonins, and early loss of splenic function. These patients are more susceptible to osteoarticular infections, and osteomyelitis is one of the common infectious complications presenting in children with SCD.
Although S. aureus is the most common infectious agent causing osteomyelitis in the normal host, there still exists a controversy as to whether S. aureus or Salmonella is the most common infectious agent causing osteomyelitis in SCD patients. In their reviews, Burnett et al. and Chamber et al. have concluded that Salmonella is more common pathogen, followed by S. aureus in causing osteomyelitis infection in SCD. This has important implications for both the diagnosis and treatment of the disease.
Clinical Features and Diagnosis: The clinical diagnosis of osteomyelitis is often difficult because the presenting symptoms are similar to other common complications in these children (e.g., vaso-occlusive crisis). Both of these complication present with warmth, swelling, and local tenderness. Osteomyelitis should be considered in any patient who has fever, long-lasting pain, and decreased mobility associated with the above symptoms.
Blood tests, such as white blood cell count, erythrocyte sedimentation rate, and C-reactive protein, should be performed in suspected cases of osteomyelitis,eventhoughtheyarenotspecific.Bloodculturesshouldalsobe performed for suspected osteomyelitis, even though they are only positive in 50%ofthecases.Bonebiopsy,aspirations,andculturesareusuallydiagnostic and are the procedures of choice for suspected osteomyelitis.
Plain radiography is usually negative for the first 7 to 10 days except for soft tissue swelling, but can show destruction and new bone formation after 10 days. Magnetic resonance imaging is highly sensitive and specific for detecting bone involvement in suspected osteomyelitis. A bone scan with gallium or magnetic resonance imaging can help distinguish an infection from infarction.
The empirical antibiotic therapy for suspected osteomyelitis is based on the knowledge of the common pathogens causing the infection in SCD patients. Recommended regimens include treatment with a broad-spectrum cephalosporin, such as ceftriaxone or cefotaxime, in addition to an anti- Staphylococcus drug. If a specific pathogen is identified in culture, then antibiotic therapy needs to be specifically tailored. If the patient is responding to antibiotics, then the initial therapy is continued. The duration of intravenous antibiotic therapy is case-dependent based on the organisms identified and the clinical course of the disease. The key to diagnosis and treatment of osteomyelitis is to consider clinical symptoms, a positive culture, an abnormal imaging study, and the response to empirical antibiotic therapy.
Burnett MW, Bass JW, Cook BA. Etiology of osteomyelitis complicating sickle cell disease.
Pediatrics. 1998;101(2):296–297.
ChambersJB,ForsytheDA,BertrandSL,etal.Retrospectivereviewofosteoarticularinfections
in a pediatric sickle cell age group. J Pediatr Orthop. 2000;20(5):682–685.
Gill FM, Sleeper LA, Weiner SJ, et al. Clinical events in the first decade in a cohort of infants
with sickle cell disease. Cooperative Study of Sickle Cell Disease. Blood. 1995;86(2):776–
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Goergens ED, McEvoy A, Watson M, et al. Acute osteomyelitis and septic arthritis in children.
J Paediatr Child Health. 2005;41(1–2):59–62.
Karwowska A, Davies HD, Jadavji T. Epidemiology and outcome of osteomyelitis in the era of
sequential intravenous-oral therapy. Pediatr Infect Dis J. 1998;17(11):1021–1026.
Lampe RM. Osteomyelitis and suppurative arthritis. In: Behrman RE, Kliegman R, Jenson
HB. Nelson Textbook of Pediatrics. 17th ed. Philadelphia: Saunders; 2004, pages 2297–2302.
Lew DP, Waldvogel FA. Osteomyelitis. Lancet. 2004;364(9431):369–379.
Review other book chapters online related to Osteomyelitis:
Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Avoiding Common Pediatric Errors Authors: Anthony D Slonim MD, DrPH; Lisa Marcucci MD Publisher: Lippincott Williams & Wilkins Copyright: 2008 ISBN: 0-7817-7489-6 
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