Key result
Early stroke volume index drops link to higher troponin I in pediatric septic shock.
Why the study?
Pediatric septic shock is frequently associated with myocardial dysfunction and high mortality, but the correlation between USCOM-derived hemodynamic parameters and serum troponin I levels is not well understood.
Observational (n=32)
No
In pediatric septic shock, the severity of inotropic support independently predicts myocardial injury (elevated cTnI), and dynamic hemodynamic changes measured via USCOM correlate with troponin release, suggesting potential utility of multimodal bedside monitoring.
Answers are grounded in this paper and cite their sources.
USCOM parameters may reflect myocardial injury in pediatric septic shock; hypothesis-generating and requires prospective validation before clinical use.
Purpose: Pediatric septic shock is frequently associated with myocardial dysfunction and high mortality. Cardiac troponin I (cTnI) is a biomarker of myocardial injury, while the Ultrasonic Cardiac Output Monitor (USCOM) enables non-invasive hemodynamic assessment. This study aimed to explore the correlation between USCOM-derived hemodynamic parameters and serum cTnI levels in pediatric septic shock, and to examine the association of inotropic therapy with troponin levels. Patients and Methods: A prospective observational study was conducted in 32 pediatric patients with septic shock admitted to Hasan Sadikin Hospital, Bandung, between May and September 2025. Serial USCOM measurements were performed at 1, 3, 6, 12, and 24 hours to assess cardiac index (CI), stroke volume index (SVI), Smith-Madigan Inotropy Index (SMII), and systemic vascular resistance index (SVRI). Serum cTnI levels were measured at 6 and 24 hours using a high-sensitivity assay. Correlations were analyzed using Spearman's test, and multivariable regression was applied to explore independent associations. Results: Median cTnI levels increased significantly from 71 pg/mL at 6 hours to 201 pg/mL at 24 hours (p < 0.01). Early changes in SVI (1-6 hours) were negatively correlated with cTnI at 6 hours (r = -0.409; p = 0.020). SMII at 1 hour was positively correlated with cTnI at 24 hours (r = 0.409; p = 0.025), while SVI at 24 hours showed a positive correlation with cTnI at 24 hours (r = 0.387; p = 0.035). The number of inotropic agents was independently associated with higher cTnI levels at both 6 and 24 hours. Conclusion: Serum cTnI levels increased during the first 24 hours of pediatric septic shock and were associated with dynamic hemodynamic changes. These findings suggest a potential role for integrating serial troponin measurement with non-invasive hemodynamic monitoring. Further studies with larger cohorts are needed to validate these observations.
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Sandinirwan et al. (2026) conducted an observational in Pediatric septic shock (n=32). USCOM-derived hemodynamic parameters was evaluated on Correlation between early changes in stroke volume index (1-6 hours) and serum cardiac troponin I (cTnI) at 6 hours (r = -0.409, p=0.020). USCOM-derived hemodynamic parameters, including early changes in stroke volume index (r = -0.409), were significantly correlated with serum troponin I levels during the first 24 hours of pediatric septic shock.
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