SpO2 Infant and Pediatric Study

Assessment of TruSignal SpO2 Form, Fit and Clinical Performance With Infant and Child Patients

This study evaluates the pulse oximetry (SpO₂) sensor for clinical performance, form, and fit in hospitalized infants and children (28 days to 12 years). It compares SpO₂ measurements from the device to arterial oxygen saturation (SaO₂) values from arterial CO-oximetry, and assesses the reliability of usable data, performance across skin tones, and user feedback.

This prospective clinical study evaluates a pulse oximetry sensor in hospitalized infants (28 days to 23 months) and children (2-12 years) under routine clinical conditions. The primary objective is to assess the accuracy and agreement of SpO₂ measurements compared with reference SaO₂ values obtained from CO-oximetry analysis of simultaneously drawn arterial blood, using methods aligned with ISO 80601-2-61: 2026 3rd edition published in April 2026.

Secondary objectives include measuring the proportion of time the device produces invalid or unusable data to assess reliability for clinical use. The safety objective is to collect safety information, including type and number of AEs, SAEs, and device issues. Results may support product development, regulatory submissions, and marketing activities.

Inclusion Criteria:

• subjects are 1-23 months (infant cohort) or 2-12 years old (child cohort)
• requiring arterial blood samples per the site's standard of care.

Exclusion Criteria:

• Fractional Methemoglobinemia (FMetHb >2%) or Fractional carboxyhemoglobinemia (FCOHb >3%), within 24 hours of arterial blood draw.
• Severe anemia (tHb <7g/dL) within 4 hours prior to arterial blood gas draw.
• Hematocrit (Hct) <25 within 4 hours prior to arterial blood gas draw.
• Patients with injuries, deformities, or abnormalities which may prevent proper application of the sensor.
• Patients on Extracorporeal Membrane Oxygenation (ECMO).
• Patients receiving point of care (POC) testing for blood gases.
• Patients with diseases/conditions that may cause differential (or reverse differential) cyanosis including, but not limited to:
• Patent ductus arteriosus with pulmonary arterial hypertension.
• Pulmonary hypertension and left-heart abnormalities aortic arch hypoplasia, interrupted aortic arch, critical coarctation, and critical aortic stenosis.
• Children with transposition of the great arteries (TGA) and coarctation of the aorta or interrupted aortic arch, and TGA with suprasystemic pulmonary vascular resistance.
• At the discretion of the principal investigator or designee due to the subject health condition.