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Acute transphyseal hematogenous osteomyelitis caused by Haemophilus influenzae with 5-year follow-up
1Department of Orthopaedics, Children's Hospital and Medical Center, Seattle, Washington.
Insights
Acute hematogenous osteomyelitis in children is typically Staphylococcus aureus. This case shows Haemophilus influenzae causing transphyseal osteomyelitis with complete resolution and no growth arrest, a rare outcome.
Area of Science:
- Pediatric infectious diseases
- Orthopedic surgery
- Microbiology
Background:
- Acute hematogenous osteomyelitis is common in children, usually caused by Staphylococcus aureus.
- Transphyseal involvement often leads to growth plate damage and subsequent growth arrest.
- Organism identification is crucial for appropriate treatment and prognosis.
Observation:
- A 4-month-old infant presented with acute hematogenous osteomyelitis.
- The infection was identified as transphyseal, involving the growth plate.
- The causative pathogen was identified as Haemophilus influenzae.
Findings:
- Complete resolution of the transphyseal osteomyelitis was achieved.
- The patient experienced no clinical or radiographic evidence of growth arrest at 5-year follow-up.
- This outcome is unusual given the typical sequelae of transphyseal osteomyelitis.
Implications:
- Haemophilus influenzae can cause severe bone infections in infants.
- Complete recovery without growth disturbance is possible even with transphyseal involvement.
- This case highlights the importance of pathogen-specific treatment in pediatric osteomyelitis.
Abstract:
Acute hematogenous osteomyelitis is a well-recognized entity in infants and children. Over 90% of cases are caused by coagulase-positive Staphylococcus aureus, with other organisms only rarely implicated. Transepiphyseal osteomyelitis, because of the presence of infection on either side of the physis, usually results in growth arrest. The authors report the case of a 4-month-old child who had a transphyseal acute hematogenous osteomyelitis caused by Haemophilus influenzae and document complete resolution of the infection at 5-year follow-up with no clinical or radiographic evidence of growth arrest.