What is the pathophysiology and treatment of osteomyelitis in children?

Pathophysiology of Osteomyelitis in Children

Pediatric osteomyelitis primarily results from hematogenous bacterial seeding, with infection localizing to the metaphysis of long bones due to unique vascular anatomy that creates a low-flow environment conducive to bacterial deposition. 1

Vascular Anatomy and Initial Infection

• The metaphysis is the primary site of infection because looping nutrient vessels slow blood flow in this region without traversing the growth plate (physis), creating an ideal environment for bacterial adherence and proliferation. 1

• In children ≤18 months of age, transphyseal vessels are present, allowing infection to spread from the metaphysis directly into the epiphysis and adjacent joint space, explaining the high rate of concurrent septic arthritis in this age group. 1

• In older children, transphyseal infection may be underestimated, though the physis typically acts as a barrier preventing epiphyseal spread. 1

Progression and Complications

• Infection spreads from the metaphysis to the subperiosteal space, either directly or through hematogenous seeding, leading to subperiosteal abscess formation. 1

• Subperiosteal abscesses cause bone ischemia and necrosis by stripping the periosteum from the cortex and compromising the periosteal blood supply, which is critical for bone viability. 1

• Concomitant osteomyelitis and septic arthritis occur in >50% of pediatric cases, particularly in neonates and infants where metaphyseal infection can directly seed the joint space. 1, 2

Microbiology

• Staphylococcus aureus is the predominant pathogen across all pediatric age groups, responsible for the majority of acute hematogenous osteomyelitis cases. 1, 3

• Age-specific pathogens must be considered: Group B streptococcus in neonates, Kingella kingae in children <4 years of age, and Salmonella species in patients with sickle cell disease. 1, 2

• Methicillin-resistant S. aureus (MRSA) has increased in prevalence, complicating empiric antibiotic selection and requiring broader initial coverage. 3, 4

Pathological Bone Remodeling

• Bacterial invasion triggers pathological bone remodeling through direct bacterial effects and inflammatory immune responses, leading to bone destruction and sequestration of infectious foci. 5

• Sequestration isolates bacteria from immune effectors and systemically delivered antibiotics, explaining why chronic osteomyelitis often requires surgical debridement in addition to prolonged antibiotic therapy. 4, 5

Age-Related Distribution

• Children <2 years are more likely to develop septic arthritis than osteomyelitis due to transphyseal vessels allowing direct joint seeding. 1, 2

• Children 2-10 years have slightly more osteomyelitis than septic arthritis, as the physis becomes a more effective barrier. 1, 2

• Half of all pediatric osteomyelitis cases occur in children <5 years of age, making this the highest-risk population. 1, 6

Treatment Principles

• Uncomplicated acute osteomyelitis is treated with short-course IV antibiotics followed by ≥3 weeks of oral antibiotics, with clinical examination, fever resolution, and C-reactive protein guiding the transition. 3

• Surgical debridement is indicated for subperiosteal abscesses, bone necrosis, or failed antibiotic therapy, as antibiotics alone cannot penetrate sequestered infectious foci. 1, 3, 4

• Osteomyelitis treatment duration must be ≥14 days and often longer (4-6 weeks for severe cases), as inadequate duration leads to chronic infection and recurrence. 7, 4

• Septic arthritis requires immediate surgical drainage (arthrotomy, irrigation, debridement) plus antibiotics, as bacterial proliferation and metabolites rapidly destroy articular cartilage. 1, 8

Critical Pitfalls

• Delayed diagnosis results in premature physeal arrest or permanent joint damage, making prompt recognition essential despite the fact that the classic triad of fever, pain, and diminished mobility occurs in only ~50% of cases. 1

• Radiographs are often normal in acute osteomyelitis, as bone changes require 10-14 days to become visible; MRI is the diagnostic modality of choice with 82-100% sensitivity. 1, 6, 3

• In children with sickle cell disease, distinguishing osteomyelitis from bone infarction is challenging, as both present similarly on imaging; subperiosteal fluid favors osteomyelitis. 1