Pathophysiology and Management of Osteomyelitis in Children

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, 2, 3
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, 2, 3
In older children, transphyseal infection may be underestimated, though the physis typically acts as a barrier preventing epiphyseal spread 1, 2

Infection spreads from the metaphysis to the subperiosteal space, either directly or through hematogenous seeding, leading to subperiosteal abscess formation 1, 2, 3
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, 2
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, 3, 4

Staphylococcus aureus is the predominant pathogen across all pediatric age groups, responsible for the majority of acute hematogenous osteomyelitis cases 1, 2, 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, 3, 4

Children <2 years are more likely to develop septic arthritis than osteomyelitis due to transphyseal vessels allowing direct joint seeding 1, 4
Half of all pediatric osteomyelitis cases occur in children <5 years of age, making this the highest-risk population 5, 6

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, 2, 3
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 5, 6
In children with sickle cell disease, distinguishing osteomyelitis from bone infarction is challenging, as both present similarly on imaging; subperiosteal fluid favors osteomyelitis 5, 6