Background and Objectives: We examined how health-related quality of life (HRQoL) in children with congenital heart disease (CHD) and caregiver stress/burnout relate in terms of lesion severity. Methods: We enrolled 72 child–caregiver dyads at a tertiary centre (May 2023–April 2025). Children completed PedsQL and CDI (anxiety assessment via SCARED-C was descriptive and not modelled in APIM); caregivers completed SF-36, PSS-10, and the Parental Burnout Assessment (PBA). Lesion severity (mild n = 22, moderate n = 34, severe n = 16) and LVEF were abstracted. Pearson correlations and actor–partner interdependence models (APIM) estimated within- and cross-partner effects. Results: Child PedsQL decreased with severity (mild 81.2 ± 7.4; moderate 70.9 ± 8.1; severe 63.3 ± 5.1; p < 0.001); caregiver SF-36 Mental Component Summary (MCS) showed a parallel gradient (66.8 ± 9.2; 59.7 ± 8.5; 54.1 ± 7.9; p < 0.001). Child HRQoL correlated with caregiver MCS (r = 0.46) and inversely with caregiver stress (PSS r = −0.42) and burnout (PBA r = −0.39). In APIM, caregiver stress predicted a caregiver’s own MCS (actor β = −0.38, p < 0.001) and the child’s PedsQL (partner β = −0.26, p = 0.002); higher child depressive symptoms predicted lower caregiver MCS (partner β = −0.22, p = 0.006). Each step up in lesion severity independently reduced child PedsQL by 7.9 points and caregiver MCS by 5.3 points (both p < 0.001). Dyads with unscheduled hospitalizations (n = 43) had poorer scores in both members. Conclusions: Psychological wellbeing in CHD dyads is strongly interdependent; caregiver stress relates to lower child HRQoL and child mood to caregiver mental health. Brief dyadic screening (PedsQL/SF-36 with PSS/CDI) and integrated, family-focused interventions may better target high-risk families, particularly with severe lesions or recent hospitalizations.
Background and Objectives: Surfactant protein-D (SP-D) enters the circulation when the alveolo-capillary barrier is injured. We synthesised evidence on the diagnostic and prognostic performance of circulating SP-D in children with acute infectious lung disease. Methods: We searched MEDLINE, Embase and Scopus (inception–1 June 2025) for human studies reporting serum/plasma SP-D in patients <18 years with community-acquired pneumonia (CAP), viral pneumonitis or paediatric ARDS (PARDS). Two reviewers independently screened, extracted data and assessed risk of bias (ROBINS-I). Primary outcomes were discrimination of severe versus non-severe disease and prediction of hard outcomes (mechanical ventilation, PARDS and mortality). Heterogeneity in assays and outcome definitions precluded meta-analysis; a narrative synthesis was undertaken. Results: Five studies (n = 723) from emergency and PICU settings met inclusion criteria. Admission SP-D was consistently higher in severe versus mild CAP; reported AUCs ranged 0.699–0.802. Thresholds of 110–180 ng/mL yielded sensitivities of 67–85% and specificities of 45–70%. In influenza-associated respiratory failure, SP-D correlated with ventilator days (r ≈ 0.45) and ICU length of stay (r ≈ 0.44). In multicentre PARDS cohorts, each 10 ng/mL increase in SP-D was associated with higher odds of severe PARDS and death (adjusted OR 1.02 per 10 ng/mL). Overall risk of bias across studies was low-to-moderate, with one study rated serious due to sampling and adjustment limitations. Conclusions: Across pathogens and care settings, elevated circulating SP-D correlates with radiographic consolidation, evolving PARDS and worse short-term outcomes. Although assay standardisation and external validation are needed, current evidence supports incorporating SP-D into multiparametric, age-aware risk-stratification algorithms for childhood pneumonia and viral lung injury.