End-tidal carbon dioxide levels during resuscitation and carbon dioxide levels in the immediate neonatal period and intraventricular haemorrhage

Abstract

Abnormal levels of end-tidal carbon dioxide (EtCO 2 ) during resuscitation in the delivery suite are associated with intraventricular haemorrhage (IVH) development. Our aim was to determine whether carbon dioxide (CO 2 ) levels in the first 3 days after birth reflected abnormal EtCO 2 levels in the delivery suite, and hence, a prolonged rather than an early insult resulted in IVH. In addition, we determined if greater EtCO 2 level fluctuations during resuscitation occurred in infants who developed IVH. EtCO 2 levels during delivery suite resuscitation and CO 2 levels on the neonatal unit were evaluated in 58 infants (median gestational age 27.3 weeks). Delta EtCO 2 was the difference between the highest and lowest level of EtCO 2 . Thirteen infants developed a grade 3-4 IVH (severe group). There were no significant differences in CO 2 levels between those who did and did not develop an IVH (or severe IVH) on the NICU. The delta EtCO 2 during resuscitation differed between infants with any IVH (6.2 (5.4-7.5) kPa) or no .3) kPA) (p < 0.001) after adjusting for differences in gestational age. Delta EtCO 2 levels gave an area under the ROC curve of 0.940 for prediction of IVH.Conclusion: The results emphasize the importance of monitoring EtCO 2 levels in the delivery suite.

End-tidal capnography monitoring in infants ventilated on the neonatal intensive care unit

“…We have reported that abnormal levels of carbon dioxide, including large magnitude of difference in CO 2 levels during resuscitation contribute to IVH development [ 20 ]. A previous retrospective study reported the maximum PCO 2 during the first 72 hours after birth was a dose-dependent predictor of severe IVH development [ 21 ].…”

Feasibility of portable capnometer for mechanically ventilated preterm infants in the delivery room

“…During the first few days after birth, the respiratory and circulatory conditions of neonates undergo considerable changes. Some studies have shown that inappropriate EtCO 2 within a few days after birth in preterm infants is associated with PVL [ 2 , 3 ], IVH [ 1 , 11 , 12 ], and BPD [ 4 ]. Therefore, it is important to monitor CO 2 and control the PaCO 2 appropriately in preterm infants immediately after birth to reduce the risks of these diseases.…”

Neuroprotection of the Perinatal Brain by Early Information of Cerebral Oxygenation and Perfusion Patterns

“…Monitoring the pattern of cerebral oxygenation using NIRSdetermined rScO 2 as early after birth as possible, preferably already on the resuscitation table, at least up to postnatal day 4 in these vulnerable group of neonates can alert the clinician at an early point in time for hypercapnia-induced hyperoxygenation/hyperperfusion [25,35] and hypoxia-or hypocapnia-induced underoxygenation/hypoperfusion [32] of the immature brain. A very recent study from Tamura et al [37] showed that hypercapnia in the delivery room was associated with the occurrence of all grades of PIVH in a large cohort of preterm infants. Alderliesten et al [35] showed supranormal rScO 2 values [17] during 24 h preceding PIVH in a case-control study of 650 preterm infants below 32 gestational weeks.…”

“…It may be clear that prevention or early recognition and down tuning of cerebral hyper(hypo-)perfusion/-oxygenation and/or a fluctuating pattern of the cerebral blood flow potentially reduce or even prevent the occurrence and extension of PIVHs. In this respect it is especially important to aim for a stable arterial carbon dioxide level within normal limits (i.e., [35][36][37][38][39][40][41][42][43][44][45][46][47][48][49][50]. Monitoring the pattern of cerebral oxygenation using NIRSdetermined rScO 2 as early after birth as possible, preferably already on the resuscitation table, at least up to postnatal day 4 in these vulnerable group of neonates can alert the clinician at an early point in time for hypercapnia-induced hyperoxygenation/hyperperfusion [25,35] and hypoxia-or hypocapnia-induced underoxygenation/hypoperfusion [32] of the immature brain.…”