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  • Systematic Review
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16 November 2025

37 Pages

Acid–Base Status and Cerebral Oxygenation in Neonates: A Systematic Qualitative Review of the Literature

,
,
and
1
Division of Neonatology, Department of Paediatrics, Medical University of Graz, Auenbruggerplatz 34/2, 8036 Graz, Austria
2
Research Unit for Neonatal Micro- and Macrocirculation, Department of Paediatrics, Medical University of Graz, Auenbruggerplatz 34/2, 8036 Graz, Austria
*
Author to whom correspondence should be addressed.
Children2025, 12(11), 1549;https://doi.org/10.3390/children12111549
This article belongs to the Special Issue Advances in Neonatal Resuscitation and Intensive Care
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Highlights

What are the main findings?
  • Studies with the lowest risk of bias mostly showed no significant correlations between cerebral oxygenation and acid base status.
What is the implication of the main finding?
  • Further well-designed studies with minimal risk of bias are necessary to clarify this issue.

Abstract

Introduction: Blood gas analysis is utilized to assess parameters of oxygenation and ventilation, including acid–base status [pH value, base excess (BE) or base deficit (BD), and bicarbonate (HCO3)], to evaluate systemic metabolism status. Acid–base imbalances can have complex effects on the organism, potentially impacting oxygen delivery to tissue. Cerebral oximetry is a non-invasive monitoring technique using near-infrared spectroscopy (NIRS) for the continuous measurement of cerebral tissue oxygenation. The relationship between the acid–base status and cerebral tissue oxygenation in neonates remains unclear. This systematic qualitative review aims to analyze current knowledge of the potential correlations between different acid–base status parameters and cerebral tissue oxygenation measured via NIRS in neonates. Methods: A systematic search of PubMed and Ovid Embase was performed, focusing on cerebral oxygenation, neonates, and acid–base status. Risk of bias was assessed using the ‘‘Risk of Bias for Non-randomized Studies of Exposures’’ (ROBINS-E) instrument. Results: Fifty studies that measured parameters of the acid–base status and cerebral tissue oxygenation in the neonatal period were identified. Seven studies demonstrated a correlation between pH and cerebral tissue oxygenation, while eleven studies found no such correlation. Five studies demonstrated a correlation between the BE/BD and cerebral tissue oxygenation, while six studies found no such correlation. Three studies demonstrated a correlation between HCO3 and cerebral tissue oxygenation, while five studies found no such correlation. Discussion: Associations between acid–base status parameters and cerebral tissue oxygenation remain controversial. However, studies with the lowest risk of bias mainly demonstrated no significant correlation between any of the acid–base status parameters and cerebral tissue oxygenation.

1. Introduction

Cerebral injuries, such as intraventricular haemorrhage (IVH) or periventricular leukomalacia (PVL), remain persistent challenges in neonatology [1,2,3,4]. The neonatal cerebral autoregulation mechanism plays a crucial role in maintaining stable cerebral perfusion and oxygenation. Impairment of these mechanisms can result in hyperoxic or hypoxic conditions, potentially resulting in irreversible complications, such as IVH or PVL [2,3,5,6,7,8]. IVH and PVL are particularly common in extremely preterm infants, and they are associated with poor neurodevelopmental outcome or death [1,9,10,11]. Understanding the physiology and pathophysiology of neonatal cerebral autoregulation and its influencing factors is essential for the prevention of these irreversible severe complications. A major challenge remains—the timely recognition of impaired neonatal cerebral autoregulation and the subsequent imbalance in cerebral oxygen supply and consumption before cerebral complications occur. Unfortunately, current routine monitoring during the neonatal period, including pulse oximetry, electrocardiogram, and blood pressure measurement, does not assess cerebral oxygen delivery or cerebral oxygen consumption, thereby neglecting potentially critical cerebral oxygenation information [12,13,14,15].
Cerebral oximetry is a continuous, non-invasive, real-time method using near-infrared spectroscopy (NIRS) to detect cerebral tissue oxygenation [cerebral regional oxygen saturation (crSO2), tissue oxygenation index (TOI), and fractional tissue oxygen extraction (FTOE)]. Cerebral tissue oxygenation depends on cerebral oxygen delivery, cerebral oxygen consumption, and the arterial–venous volume ratio [16,17]. Therefore, using NIRS might be a promising tool for detecting impairments in cerebral perfusion and oxygenation even when routine monitoring parameters still remain within normal ranges [15,18,19]. Research has identified various variables, including cardiovascular and respiratory parameters, that may influence cerebral tissue oxygenation in neonates [17,20,21,22].
Blood gas analysis is a quick and non-invasive point-of-care method for assessing the acid–base status, identifying insufficient systemic oxygenation, and guiding counter-regulation in hypoxic conditions. Acid–base status parameters can serve as outcome predictors and indicators for interventions in neonates [23,24,25]. The pH level may affect neonatal vascular tone, subsequently influencing cerebral oxygen delivery and thus cerebral tissue oxygenation [26]. Furthermore, acidosis is associated with an increased risk for cerebral complications, such as hypoxic ischemic encephalopathy (HIE), IVH, or seizures [27,28,29]. Parameters such as base excess (BE) or its reversal, the base deficit (BD), and bicarbonate (HCO3) indicate the counter-regulation of an impaired acid–base status, and deviations are important predictors of neonatal morbidity, such as HIE, seizures, or respiratory complications [27,28,30,31]. Additionally, the administration of HCO3 in neonates with metabolic acidosis is a potential treatment option, although its benefits and harms remain controversially debated [29,32]. There is increasing research interest concerning the impact of acid–base status parameters on cerebral tissue oxygenation in neonates [33,34,35]. However, the effects of acid–base status parameters on the autoregulation mechanism and subsequently on cerebral oxygenation in the neonatal brain are unclear. The aim of this review is to provide an overview of the current literature regarding a potential association between parameters of the acid–base status and cerebral oxygenation in neonates during the neonatal period.

2. Materials and Methods

2.1. Search Strategy and Selection Criteria

Studies were identified using the stepwise approach outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA 2020) statement [36]. To ensure transparency and reproducibility, we pre-registered our study protocol in the International Prospective Register of Systematic Reviews database (PROSPERO, Registration ID: CRD420250655009).

2.2. Eligibility Criteria

Studies were included if they reported cerebral tissue oxygenation measurements with NIRS (crSO2 or FTOE), along with acid–base status parameters (pH, BE, BD, and HCO3), in neonates during the neonatal period.

2.3. Search Strategy

A systematic search was conducted on PubMed NCBI and Ovid Embase to identify studies published in the English language between July 1977—the first description of NIRS application in neonates—and May 2025. The search keywords included the following: near-infrared spectroscopy, fractional tissue oxygen extraction, regional cerebral tissue oxygen saturation, oxygenation, term neonates, preterm neonates, newborns, baby, caesarean delivery, vaginal delivery, transition, after birth, neonatal transition, metabolism, pH value, bicarbonate, base-excess, base-deficit, acidosis, alkalosis, acid-base balance, and acid-base imbalance.

2.4. Inclusion and Exclusion Criteria—Population

To be eligible, studies had to investigate human neonates with a postnatal age of less than 28 days. Studies that included both neonates with a postnatal age of less than 28 days and older infants or children were also included. Animal studies and studies without an available abstract were excluded.

2.5. Inclusion and Exclusion Criteria—Measurements (Exposure)

Studies using any NIRS device for cerebral oximetry were included if any additional measurements of neonatal capillary, venous, or arterial blood pH, BE/BD, or HCO3 values were reported.

2.6. Inclusion and Exclusion Criteria—Types of Publication

We included all studies published in the English language, excluding non-original articles, such as comments, book chapters, editorials, reviews, and methodological papers. Duplicates and publications in non-English languages were also excluded.

2.7. Study Selection

The articles identified in the literature review were independently evaluated by two authors (C.M. and G.P.) based on the titles and the abstracts. Full texts were then retrieved according to the eligibility criteria. In cases of uncertainty regarding inclusion based on the abstract, the full text was also assessed. Any disagreements were resolved through discussion and consensus between the two authors. Data were qualitatively analysed, including the study design, study population (preterm/term neonates), number of neonates, NIRS device used, NIRS measurement time point and duration, acid–base status parameter measurement time point, values of NIRS parameters and acid–base status parameters, the presence or absence of association, and the direction of correlation if an association was detected.

2.8. Risk of Bias in Individual Studies

During the planning process of this review, we primarily expected non-randomized observational studies. The bias assessment of non-randomized observational studies through standard bias assessment tools, such as the Newcastle–Ottawa Scale, resulted in a lack of feasibility. Hence, the Risk of Bias in Non-randomized Studies of Exposures (ROBINS-E) tool was used for studies presenting data on associations between parameters of the acid–base status and cerebral oxygenation [37]. The assessment process was conducted using the standardized ROBINS-E Excel implementation. ROBINS-E is a tool for assessing the risk of bias in non-randomized studies and includes seven items: (I) risk of bias due to confounding; (II) risk of bias arising from measurement of the exposure; (III) risk of bias in the selection of participants for the study; (IV) risk of bias due to post-exposure interventions; (V) risk of bias due to missing data; (V.) risk of bias arising from measurements of the outcome; and (VII) risk of bias in the selection of the reported result [36]. Each bias item was rated as low, some concerns, high risk, or very high risk of bias. Confounding factors were defined as follows: i. impaired cerebral autoregulation mechanism; ii. disorders of the cardiovascular system; iii. disorders of the respiratory system; iv. disorders resulting in increased oxygen consumption; and v. congenital malformation. Finally, a complete risk-of-bias rating was assigned to each study for the given answer on the observed presence or absence of association. Studies were categorized as low/some concerns (=low) risk of bias and high/very high (=high) risk of bias to address potential confounding.

3. Results

From the preliminary search, 4132 abstracts were identified and assessed for eligibility. Following the full-text review, 50 studies met the inclusion criteria for this systematic review [26,34,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85] (Figure 1).
Figure 1. PRISMA flow chart; NIRS = near-infrared spectroscopy.
In total, 21 studies [38,39,40,41,44,45,48,49,50,52,53,57,60,62,66,67,78,79,80,82,83] analyzed two parameters, and 9 studies [34,46,54,63,68,69,71,72,85] reported on all three parameters of the acid–base status in combination with NIRS measurements during the neonatal period. Table 1, Table 2 and Table 3 provide an overview of the basic data of all included studies.
Table 1. pH and cerebral oxygenation in the neonatal period.
Table 2. Base excess/base deficit and cerebral oxygenation in the neonatal period.
Table 3. Bicarbonate and cerebral oxygenation in the neonatal period.

3.1. pH Value and Cerebral Tissue Oxygenation

A total of 50 studies reported pH and cerebral NIRS measurements [26,34,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85] (Table 1).
Seven studies reported an association between the pH and cerebral tissue oxygenation (crSO2 and FTOE). Of these, four studies [34,38,72,83] found a positive correlation, while three studies [26,69,79] found a negative correlation. Eleven studies demonstrated no association [43,44,46,57,63,64,68,74,75,80,85], while thirty-one studies did not find an association [39,40,41,42,45,47,48,49,50,51,52,53,54,55,56,58,59,60,61,62,65,66,67,70,71,73,76,77,78,81,82].

3.2. Base Excess (BE) or Base Deficit (BD) and Cerebral Tissue Oxygenation

A total of 26 studies were identified that reported on BE or BD in combination with cerebral NIRS measurements [34,38,40,41,44,45,46,48,49,50,52,53,54,57,60,62,63,66,68,69,71,72,78,79,83,85] (Table 2).
Five studies found an association between BE and cerebral tissue oxygenation, with four studies [38,69,72,79] reporting a negative correlation and one study [34] reporting a positive correlation. Six studies found no associations [44,46,63,68,83,85], while fifteen studies did not find an association [40,41,45,48,49,50,52,53,54,57,60,62,66,71,78].

3.3. Bicarbonate (HCO3) and Cerebral Tissue Oxygenation

A total of 13 studies were identified that reported on HCO3 measurements in combination with cerebral NIRS measurements [34,39,46,54,63,67,68,69,71,72,80,82,85] (Table 3).
Three studies found an association between HCO3 and cerebral tissue oxygenation. Of these, one study [69] reported a negative correlation, while one study [72] reported a positive correlation. Additionally, one study reported a positive correlation between HCO3 and fractional tissue oxygen extraction (FTOE) only in term neonates but not in preterm neonates [34]. Five studies demonstrated no associations [46,63,68,80,85], while five studies did not find an association [39,54,67,71,82].

3.4. Quality Assessment and Risk of Bias Assessment

Eighteen of these studies provided data on the potential association between acid–base status parameters and cerebral tissue oxygenation [26,34,38,43,44,46,57,63,64,68,69,72,74,75,79,80,83,85]. Quality assessment and risk of bias were assessed for all included studies. Overall, study quality varied (Table 4).
Table 4. Quality of included studies as assessed using the Risk of Bias in Non-Randomized Studies of Exposure (ROBINS-E) tool.
No studies were categorized as low risk. Five studies (27.7%) were categorized as having some concerns, seven studies (38.8%) as high risk, and five studies (33.3%) as very high risk according to the ROBINS-E tool. Table 4 provides an overview of the risk-of-bias assessment. Most included studies were prospective observational studies (66%), followed by retrospective analyses (16%), randomized controlled trials (10%), cross-sectional studies (2%), and case–control studies (4%). An overview of the ROBINS-E assessment and the correlation between the acid–base status parameters and cerebral tissue oxygenation is presented in Table 5.
Table 5. Overview of ROBINS-E (risk-of-bias assessment) and correlations between parameters of the acid–base status and cerebral oxygenation in neonates during the neonatal period.

4. Discussion

This systematic qualitative review demonstrates that associations between acid–base status parameters and cerebral tissue oxygenation in neonates are controversial. These conflicting results may arise from different factors, including the diverse populations studied, variations in measurement timing, and differing clinical contexts.

4.1. pH Value and Cerebral Tissue Oxygenation

Low pH values may indicate inadequate oxygen supply and/or impaired gas exchange, potentially resulting in irreversible cerebral injury or death [27,28,29]. Studies have reported both negative and positive correlations between pH and cerebral tissue oxygenation. A negative correlation has been observed in neonates, infants, and young children undergoing pediatric heart surgery [26], in those with infantile hypertrophic pyloric stenosis in the perioperative setting [69], and in healthy full-term neonates during the first 10 min of extrauterine life [79]. Conversely, positive correlations have been reported in fetuses shortly before delivery [38]; in preterm and term neonates during the first 15 min after birth [34]; in extremely preterm neonates on the first day after birth [72]; in term-born asphyxiated neonates immediately before the initiation of therapeutic hypothermia [83]; and in preterm neonates with and term neonates without respiratory support during the first 15 min after birth [85]. These discrepancies may be attributed to variations in sample size, timing, and interval between measurements of acid–base status parameters and cerebral tissue oxygenation, and the clinical setting (e.g., HCO3 administration, surgical procedures).

4.2. Base Excess (BE) or Base Deficit (BD) and Cerebral Tissue Oxygenation

The BE or BD, in combination with the pH, is used alongside clinical and neurological parameters to evaluate neonatal well-being and assess the likelihood and severity of perinatal asphyxia. Furthermore, BE or BD may also assist in guiding therapeutic decisions, such as the initiation of hypothermia therapy for neonates experiencing hypoxic ischemic events [83,86].
Some studies have shown a negative correlation between BD and cerebral tissue oxygenation in fetuses shortly before delivery [38] and in extremely preterm neonates on the first day after birth [72]. Against these, some studies have shown a negative correlation between BE and cerebral tissue oxygenation in neonates and infants suffering from infantile hypertrophic pyloric stenosis in the perioperative setting [69] and in healthy full-term neonates during the first 10 min of extra-uterine life [79]. Finally, one study reported a positive correlation between BE and cerebral tissue oxygenation in preterm and term neonates during the first 15 min after birth [34]. These differences may be due to variations in the number of included neonates, the timing and interval between measurements of acid–base status parameters and cerebral tissue oxygenation, and the clinical setting (e.g., HCO3 administration, surgical procedures).

4.3. Bicarbonate (HCO3) and Cerebral Tissue Oxygenation

HCO3 is a critical predictor of neonatal morbidity, and it is used to correct metabolic acidosis, thereby improving hemodynamic parameters. The benefits and harms of HCO3 administration in neonates are debated in the literature [34,46,63,68,69,72,80]. Three studies analyzed the effect of HCO3 administration on HCO3 levels and cerebral tissue oxygenation [34,69,72], whereby two studies [34,72] found a positive association, while one study [69] reported a negative correlation. These differences may be due to variations in the number of included neonates, the gestational age of the neonates, the timing and interval between measurements of acid–base status parameters and cerebral tissue oxygenation, and the clinical setting (e.g., HCO3 administration, surgical procedures).

4.4. Studies Involving Neonates with Cardiovascular System Impairments

Four studies focused on neonates with congenital heart disease [26,57,64,80]. Except for the study by Amigoni et al. [26], no association was found between acid–base status parameters and cerebral tissue oxygenation in these neonates [57,64,80]. As discussed in the Introduction, the cardiovascular system significantly influences cerebral tissue oxygenation in neonates. Impairments in the cardiovascular system, as observed in neonates with congenital heart diseases, may act as confounders, resulting in potential bias and the absence of observed associations between acid–base status parameters and cerebral tissue oxygenation. This confounding effect might also depend on the severity of congenital malformation, which varied significantly among the included studies. Additionally, two studies [26,57] measured acid–base status parameters and cerebral tissue oxygenation during surgery involving a cardiopulmonary bypass procedure.

4.5. Studies During the Transition from Intra- to Extrauterine Life

The immediate postnatal period is characterized by unique physiological conditions. Studies examining neonates during and immediately after the transition from intra- to extrauterine life have reported both positive and negative correlations between acid–base status parameters and cerebral tissue oxygenation [34,38,79]. Notably, in the study by Aldricht et al. [38], cerebral tissue oxygenation was measured during childbirth prior to the clamping of the umbilical cord. Both Aldricht et al. [38] and Mattersberger et al. [34] found positive correlations between acid–base status parameters and cerebral tissue oxygenation in neonates during delivery and immediately after birth, respectively. In contrast, Leroy et al. [79] found a negative correlation in healthy full-term singleton neonates during uncomplicated transition. Mattersberger et al. [34] observed differences in correlations between preterm and term neonates. These differences suggest that gestational age-related differences may, at least in part, explain the variability in correlations observed across studies investigating the immediate transition after birth.

4.6. Studies on Term and Preterm Neonates

The physiological differences between preterm and term neonates may impact the relationship between acid–base status parameters and cerebral tissue oxygenation. As already mentioned, Mattersberger et al. [34] found associations between capillary measured pH/BE levels and brain oxygenation in preterm neonates, whereas associations between HCO3 and cerebral tissue oxygenation were observed in term neonates. Against them, Dusleag et al. [85] found no associations between the pH/BE/HCO3—measured with respect to the umbilical cord blood—and cerebral tissue oxygenation in preterm neonates with and term neonates without respiratory support during the first 15 min after birth [85]. Unfortunately, no other study compared preterm and full-term neonates. However, some studies included preterm neonates [43,46,63,68,72,74], while others included full-term neonates [75,79,83], yielding controversial results (Table 1, Table 2 and Table 3) that suggest that gestational age has an impact on the influence of acid–base status on cerebral tissue oxygenation.

4.7. Proposed Explanatory Model

4.7.1. pH and Cerebral Oxygenation

Acidosis can reduce the contractility of cardiomyocytes and diminish cardiac responsiveness to catecholamines, which may both lower cardiac output and cerebral oxygen delivery [87]. However, in hemodynamically stable preterm infants, myocardial function remains largely unaffected during the early transitional period, even with markedly low pH levels, and there appears to be no clear relationship between pH and cardiac output in the first three days after birth [88]. The vascular response to acidosis is developmentally regulated. From day 4 to 14 after the transition, systemic vascular resistance decreases and left ventricular output increases, while no association between pH and vascular tone is seen during the first three days [88]. These observations may demonstrate that the effect of pH on vascular tone—and consequently on regional blood flow—is dependent on postnatal age and therefore differs according to postnatal age. In addition, acidosis causes cerebral vasodilation, resulting in increased cerebral blood flow and oxygenation [26]. These effects could explain an increase in cerebral blood supply and, consequently, cerebral oxygenation.

4.7.2. Base Excess (BE) or Base Deficit (BD) and Cerebral Tissue Oxygenation

A possible explanation for the association between BE or BD and cerebral oxygenation is that BE or BD is calculated from the pH value. Furthermore, BE is an indicator of shock, resuscitation efficacy, and volume deficit, and a decreased BE likely indicates centralization, with resulting hemodynamic effects on cerebral oxygen delivery [89,90].

4.7.3. Bicarbonate (HCO3) and Cerebral Tissue Oxygenation

A possible explanation for the correlation between HCO3 and cerebral oxygenation may be the strong link between pH and HCO3 levels. However, a study in healthy males demonstrated that bicarbonate concentration affects cerebral blood flow (CBF) independently of pH and CO2 levels [91].

4.8. Risk-of-Bias Assessment of Studies Describing Correlations Between Parameters of Acid–Base Status and Cerebral Oxygenation

Only one study [79], categorized as “low risk of bias” or “some concerns”, demonstrated a correlation of pH level and BE with cerebral tissue oxygenation in neonates. Six studies [26,34,38,69,72,83], categorized as “high risk” or “very high risk of bias”, also described such an association (Table 5). Using the ROBINS-E tool for risk of bias assessment, the main factors for increased risk of bias were a lack of consideration of confounders, selection bias, post-exposure intervention bias, and missing data (Table 4). In some studies, acid–base status parameters were secondary outcome parameters [57,64,68,75,83,85]. These methodological weaknesses may contribute to the incongruent results regarding potential associations.

5. Conclusions

This review reveals controversial associations between acid–base status parameters and cerebral tissue oxygenation in neonates. The variability in findings can be attributed to heterogeneity in study populations, especially concerning gestational age, timing of measurements, and clinical contexts. However, the studies with the lowest risk of bias mostly demonstrated the absence of association between the acid–base status parameters and cerebral tissue oxygenation, suggesting the need for more consistent methodologies and further research in this area.

Author Contributions

All authors contributed substantially to the conception and design of this study, data acquisition, analysis, and interpretation. Conceptualization, methodology, original draft preparation, writing—review and editing, and validation: C.M., B.S., N.B.-S., and G.P. Data collection and formal analysis: C.M., B.S., N.B.-S., and G.P. Writing review, visualization and editing, and supervision: C.M., B.S., N.B.-S., and G.P. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

Not applicable.

Data Availability Statement

No new data were created.

Conflicts of Interest

The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results.

Abbreviations

The following abbreviations are used in this manuscript:
ad.Administration
BDBase deficit
BEBase excess
CDHCongenital diaphragmatic hernia
CO2Carbon dioxide
CPBCardiopulmonary bypass
crSO2Cerebral regional oxygen saturation
EAEsophageal atresia
FTOEFractional tissue oxygen extraction
HCO3Bicarbonate
HIEHypoxic ischemic encephalopathy
IVHIntraventricular hemorrhage
LVOLeft ventricular output
minMinutes
NIRSNear-infrared spectroscopy
n.rNot reported
PAPerinatal asphyxia;
PH-IVHPulmonary and intraventricular hemorrhage
PVLPeriventricular leukomalacia
RBCRed blood cell
RVORight ventricular output
U.A.Umbilical artery
U.V.Umbilical venous

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