The use of intravenous analgesics during emergency cesarean section may lead to adverse neonatal outcomes. In our study, we observed no significant differences in neonatal outcomes between the esketamine and non-esketamine groups, including umbilical arterial-blood gas analysis, Apgar score, and total days spent by the neonate in the hospital. Additionally, our study showed a similar hemodynamic performance in parturients between the two groups during operation.

A woman who receives an emergency cesarean section may have a more negative birth experience, greater anxiety, and an increased risk of post-traumatic stress disorder (PTSD) than a woman who has an elective cesarean Sects.  [8,9,10] Therefore, we must pay attention to the quality of perioperative analgesia during emergency cesarean sections. At the same time, neonatal safety must be ensured before parturients receive any intervention. The analgesic of choice should have minimal transfer across the placental barrier and minimal or no side effects on the fetus.

Ketamine has been used to provide anesthesia and analgesia for decades. It can be transferred to the neonate via the placenta, [11] and its adverse effects are dose-dependent. The recommended dose of ketamine is 1–1.5 mg/kg. A subanesthetic dose of ketamine is defined as < 1 mg/kg i.v. Even a subanesthetic dose of ketamine might be able to block central sensitization [12, 13]. Because it has fewer side effects, such a dose can be administered in clinical practice. Ketamine is a racemic mixture of 50% R (−)-ketamine and 50% S (+)-ketamine. As the S + isomer of ketamine, esketamine possesses similar pharmacological characteristics but causes fewer adverse effects. Given the 2:1 potency ratio of ketamine/esketamine, the dose of esketamine should be 0.5–0.75 mg/kg. In this study, we selected a single i.v. dose of 25 mg esketamine for parturients weighing 67 kg on average, and the dose used in our study was in the safe range.

In terms of maternal hemodynamics, SBP and DBP at 5 and 10 min were significantly higher in the esketamine group in comparison with the non-esketamine group. There may be a slight increase in BP caused by esketamine. However, the overall group effect revealed that there were no significant differences in maternal SBP, DBP, HR and SPO2 between the two groups. To evaluate the safety of esketamine, We assessed some adverse effects including hypotension, arrhythmia, nausea and vomiting, dizziness, shivering, and psychic symptoms. Psychic symptoms and dizziness were observed in the esketamine group and not in the non-esketamine group, but the symptoms were short-lived and not statistically significant. As mentioned above, esketamine causes fewer adverse effects than ketamine and its adverse effects are dose-dependent. Accordingly, the dose of esketamine used in our study was safe for mothers.

Acute fetal acidosis is the most commom manifestation of fetal distress, and it usually occurs during delivery. Basically, it is caused by a disturbance of the maternal-fetal gas exchange. In such circumstances, there are many factors that may lead to fetal acidosis in utero. These factors include problems with the placenta and umbilical cord, excessive uterine contractions, hemodynamic instability in the mother, or anesthetic interventions. Thus, we ruled out some parturients with placental and umbilical cord problems. In the meantime, we did not observe any significant diferences in hemodynamic characteristics between the two groups during operation. As a decrease in blood pressure may compromise uterine blood flow and foetal circulation, leading to hypoxia and acidosis in the fetus [14].

Brambrink AM found that it was sensitive to the apoptotic effects of ketamine in the developing rhesus macaque brain at both fetal and neonatal periods; an exposure duration of 5 h was sufficient to cause significant neuronal apoptosis [15]. However, briefer periods of fetal exposure were not studied. In this regard, S (+)-ketamine has been shown to have neuroprotective efficacy after axonal transection and glutamate exposure in polarized rat hippocampal neurons 7 days post-insult [16]. It is not clear how to account for these contrasting results. Differences in dose, timing of administration, and the type of ketamine might contribute to the different results. Hence, more research is needed on the use of ketamine and its isomer in neonates. Based on our clinical study, we found no difference in neonatal outcomes between our two groups.

Since 1952, Apgar score has been widely used to evaluate the parturient environment of the fetus [17]. Apgar score includes heart rate, respiration, color, muscle tone, and reflexes. It can help the doctor quickly judge the neonate’s clinical status and decide on the next steps. Apgar score assessment can be biased by the evaluator’s experience and subjectivity even though there is a single standard. Furthermore, a number of factors can affect the score, including low gestational age, congenital malformations, intrauterine infection, and overuse of anesthesia. It is therefore inappropriate to diagnose asphyxia neonatorum using the Apgar score alone.

Recently, UABGA was acknowledged as the most reliable index for assessing fetal oxygenation and acid–base status. According to the American College of Obstetricians and Gynecologists (ACOG), pH < 7.00 or BE < − 12 mM in UABGA indicate significant perinatal morbidity and poor prognosis [18]. UABGA can detect even subtle effects of anesthesia on neonates, but its results can be affected by factors such as the timing of sample and test, the way of delivery. In our study, BE in the esketamine group was − 5.54 ± 2.38 mM, versus − 6.63 ± 3.21 mM in the non-esketamine group. Despite the slightly lower BE in the esketamine group, the difference was not statistically significant. BE levels among our participants were higher than those found in a previous study: −0.5 ± 1.6 mM in the supine group, and − 0.6 ± 1.5 mM in the tilt group [19]. This discrepancy might have been due to the difference in participants; that study enrolled parturients scheduled for elective cesarean section, whereas our subjects had been given labor analgesia, failed to deliver their neonates, and turned into cases of emergency cesarean section.

UABGA combined with Apgar score can reflect the metabolic state of the fetus during delivery and predict the risk of adverse events. Neonates with an Apgar score of ≤ 7 at 1 min and an umbilical-artery pH of < 7.20 can be diagnosed with mild asphyxia. In our study, two cases of mild asphyxia were recorded in the esketamine group, while one case was in the non-esketamine group. This difference between the two groups did not reach statistical significance. Furthermore, compared with the non-use of esketamine, the use of esketamine did not prolong the total days that neonates stayed in the hospital.

There were several limitations to our study. First, we did not collect concentrations of esketamine in maternal or fetal serum to provide more potent evidence. Second, we only paid attention to perioperative outcomes; the risks of long-term adverse effects, such as delayed neurological symptoms, remain unknown. Third, there was the potential to mistake umbilical venous blood for an arterial sample. The pH of umbilical arterial blood was lower than that of venous blood by at least 0.02 [20]; therefore, we might have had some errors in data analysis.