Background
Pediatric pulmonary embolism (PE) incidence has shown a steady rise in recent years, underscoring a distinct and evolving etiological landscape. Infection-related PE, notably Mycoplasma pneumoniae (MPP), now accounts for an increasing proportion of pediatric PE cases, raising questions about a distinct in-situ thrombosis (ISPAT) pathophysiology. We aimed to systematically characterize the etiological spectrum of childhood PE and identify independent predictors of severe disease.
Methods
We conducted a 6-year retrospective cohort study of 113 pediatric PE pediatric patients diagnosed with PE at Department No.2 of Respiratory Medicine, Beijing Children's Hospital, from June 2018 to June 2024. Data included clinical and imaging findings, underlying conditions, and outcomes. Predictors of severe PE were assessed using multivariable logistic regression.
Results
The median age was 8.37 years. Infection was the leading etiology (89.4%), most commonly MPP (88.1%). Computed tomography pulmonary angiography (CTPA) revealed emboli were predominantly subsegmental/peripheral (80.5%), supporting the ISPAT phenotype. Post-infectious pulmonary vasculitis was identified in 8 patients, with NOD2, MPEG1, or CYBB variants detected in 3 cases. On multivariable analysis, infection−associated PE was independently linked to lower odds of severe PE (adjusted OR 0.12, 95% CI 0.03–0.54; p = 0.0055).
Conclusion
Pediatric PE is predominantly an ISPAT phenomenon driven by MPP-associated immunothrombosis. The distinct thrombotic pattern and better prognosis in the infection group support etiology based risk stratification. Furthermore, the observed links with post-infectious vasculitis and variants in NOD2, MPEG1, or CYBB suggest that occult immune dysregulation may modulate thrombotic risk in susceptible children.
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