OBJECTIVE: Epistaxis is very common in children but its cause remains unknown. We postulate that nasal colonization with Staphylococcus aureus leads to inflammation, crusting, and ultimately new vessel formation. STUDY DESIGN: A prospective case-control study. SUBJECTS AND METHODS: Sixty-seven children were recruited, 42 with epistaxis (22 had crusting in the nasal vestibule; 20 did not) and 25 control subjects. A microbiology swab was taken from the anterior nasal cavity of each child. RESULTS: All groups were equally likely to have a positive culture. S aureus was more common in the epistaxis group (P = 0.008) compared with the control group. There was no difference in the prevalence of S aureus between crust and noncrust groups. Epistaxis patients were much less likely to have isolates of respiratory pathogens or a skin commensal. CONCLUSION: Children with epistaxis are more likely to have nasal colonization with S aureus than controls. Our data would support the hypothesis that S aureus replaces existing nasal flora and causes inflammation and new vessel formation.
OBJECTIVE: Epistaxis is very common in children but its cause remains unknown. We postulate that nasal colonization with Staphylococcus aureus leads to inflammation, crusting, and ultimately new vessel formation. STUDY DESIGN: A prospective case-control study. SUBJECTS AND METHODS: Sixty-seven children were recruited, 42 with epistaxis (22 had crusting in the nasal vestibule; 20 did not) and 25 control subjects. A microbiology swab was taken from the anterior nasal cavity of each child. RESULTS: All groups were equally likely to have a positive culture. S aureus was more common in the epistaxis group (P = 0.008) compared with the control group. There was no difference in the prevalence of S aureus between crust and noncrust groups. Epistaxis patients were much less likely to have isolates of respiratory pathogens or a skin commensal. CONCLUSION:Children with epistaxis are more likely to have nasal colonization with S aureus than controls. Our data would support the hypothesis that S aureus replaces existing nasal flora and causes inflammation and new vessel formation.