ABSTRACT
Objectives: To test the hypothesis that central venous to arterial carbon dioxide difference [Pcv-a CO[2]] may help as a global marker of tissue perfusion in resuscitated pediatric septic shock patients when the central venous oxygen saturation [ScvO[2]] goal has been reached
Study design: A prospective randomized observational study was conducted in a 9 -bedded pediatric intensive care unit. 49 patients aged from 1 month to 4 years with a new episode of septic shock were included. Patients were categorized into four predefined groups according to the Pcv-a CO[2] gap to a threshold of 6 mmHg evaluated on admission [T0] and six hours after early goal-directed therapy [EGDT] resuscitation protocol [T6]: [I] persistently high Pcv-aCO[2] [high at T0 and T6]; [II] increasing Pcv-aCO[2] [normal at T0, high at T6]; [III] decreasing Pv-aCO[2] [high at T0, normal at T6]; and [IV] persistently normal Pv-aCO[2] [normal at T0 and T6]. Patients were resuscitated according to the international guidelines for management of severe sepsis and septic shock using a 6 hour EGDT and 1 ry, 2ry outcomes were evaluated
Results: There was a significant difference among groups as regard Pcv-a CO[2] at T0, T6 [both p <0.001], ScvO[2] at T6 [p 0.003], T24 vasopressor inotrope score [VIS] among category I and II regarding failure to fulfill shock reversal [p <0.001] with T24 VIS AUC on ROC curve 0.960, [p <0.001] to predict failure of shock reversal among category I, II with 88.89% sensitivity and 100% specificity to predict failure of shock reversal. No significant difference among categories concerning demographic data, clinical, ICU mortality, and 28 day mortality rates
Conclusion: Despite of near normalization of oxygen parameters, that does not guarantee adequate tissue perfusion, and still high mortality rates among pediatric septic shock patients. We would advise to measure continuously all parameters [i.e. clinical, oxygen markers, Pcv-aCO[2], lactate] until proper resuscitation by early goal-directed therapy [EGDT] and reversal of shock. Further investigations are recommended to look for other markers of impaired microcirculatory or mitochondrial dysfunction as well as therapeutic approaches targeting these deficiencies