Deep sedation using intranasal dexmedetomidine followed by intravenous propofol for pediatric dental treatment

Abstract

Objective

To evaluate the safety and efficacy of intranasal dexmedetomidine combined with propofol for pediatric dental sedation, and identify risk factors associated with major adverse events during deep sedation.

Methods

From June 2016 to August 2024, children who were unable to cooperate with the short-term oral treatment under non-pharmacological behavior or conscious sedation were selected for inclusion in the study. Intranasal dexmedetomidine 2 µg/kg was administered to facilitate preoperative sedation. Furthermore, a topical anesthetic, lidocaine gel, was applied to the venipuncture site. Once adequate sedation was achieved, venipuncture was performed. If preoperative sedation failed, sevoflurane inhalation was used to facilitate venipuncture. During the oral treatment, continuous target-controlled infusion (TCI) of propofol was administered to maintain a Bispectral index (BIS) of 50–70, ensuring deep sedation. Primary outcomes: Major adverse events (hypoxia, tachycardia, and bradycardia). Secondary outcomes: Less severe events (choking cough, gross body movement, and postoperative agitation) and risk factor exploration (interrelationships between tonsillar hypertrophy, surgery duration, and adverse events).

Results

A total of 513 children (359 boys, 69.98%; 154 girls, 30.02%) were enrolled in the study. Oral treatment was successfully completed in 100% of children. Surgery duration significantly influenced the incidence of major adverse events (p < 0.05), with a receiver operating characteristic (ROC) curve identifying 79 min as the optimal cutoff (AUC = 0.653, 95% CI: 0.573–0.733). Tonsillar hypertrophy was associated with a 4.6-fold increased risk of adverse events (OR = 4.61, 95% CI: 1.2–17.8; P = 0.017), driven by higher rates of hypoxemia (33.3% vs. 3.3%, P < 0.001) and choking cough (9.5% vs. 0%, P < 0.001).

Conclusions

This study establishes intranasal dexmedetomidine premedication followed by target-controlled propofol infusion sedation as a safe, effective alternative to general anesthesia for short-duration pediatric dental procedures (< 2 h).

Supplementary Information

The online version contains supplementary material available at 10.1186/s12903-025-06381-9.

Background

Dental fear and anxiety are common among children in dental procedures. Various techniques have been used to manage the uncooperative pediatric patients, including behavioral management, nitrous oxide inhalation, oral sedation and general anesthesia [1, 2]. Mild to moderate sedation is helpful for most of the anxious children, however may failed in some extremely uncooperative cases. General anesthesia is commonly used for those who are uncooperative due to extremely fear, young age or mentally disabled, especially in some lengthy procedures [2, 3]. However, while effective, general anesthesia carries inherent risks such as postoperative nausea/vomiting (incidence: 20–30% in pediatric patients), respiratory depression (1.2–3.5% incidence of airway obstruction or desaturation), and rare but severe complications like laryngospasm or cardiac arrhythmias. Additionally, prolonged anesthesia exposure in children has been associated with neurocognitive effects, though evidence remains inconclusive [4–9]. For select short procedures (e.g., single-tooth treatment), the risks of general anesthesia—particularly prolonged airway instrumentation and pharmacologic burden—may outweigh its benefits, making deep sedation a preferable alternative when appropriate. General anesthesia with secure airway management remains the gold standard for complex cases or patients with contraindications to deep sedation (e.g., obstructive sleep apnea, severe tonsillar hypertrophy). The decision to use deep sedation should be tailored to individual patient needs, balancing the minimization of anesthesia-related stress with the imperative of maintaining airway safety [1, 4, 5].

Deep sedation is a drug-induced state of unconsciousness characterized by unresponsiveness to verbal commands but retains purposeful responses to painful stimuli, with potential impairment of ventilatory and airway reflexes [4]. Deep sedation in dentistry is often required for treating children with uncooperative behavior. This is especially true under conditions that limit the effectiveness of behavior management techniques such as cognitive impairment, developmental delay, and severely under-aged children [5, 6].

Intravenous deep sedation is valued for its noninvasive administration, reliability, and titratability [3, 7]. However, its adoption in pediatric dentistry remains limited compared to general surgery or diagnostic procedures [10, 11], its use in pediatric dentistry has not been popular. The safety of patients undergoing deep sedation during surgical procedures requires particular attention, given that this approach does not involve tracheal intubation and shares the same oral space as oral therapy [12]. During oral therapy, the presence of water spray and tooth debris may cause patients to cough, potentially leading to compromised airway patency. The most rigorous precautions during oral therapy under deep sedation are the prevention of aspiration and respiratory depression, which can occur due to the deepening sedation level [13, 14].

Deep sedation in pediatric dentistry requires careful balancing of anxiolysis, procedural cooperation, and respiratory safety. Premedication is essential for optimizing airway patency and procedural efficiency in pediatric sedation. Traditional agents like midazolam carry risks of paradoxical agitation, particularly in young children [1, 2, 5]. Dexmedetomidine, a selective α₂-adrenoreceptor agonist, offers unique advantages for pediatric premedication: anxiolysis without respiratory depression, facilitating smooth transition to intravenous access, potentiates local anesthetics [3, 5]. Intranasal administration ensures rapid absorption (bioavailability 65-80%) while avoiding distress associated with intravenous cannulation, particularly in pediatric populations with needle phobia. So, we chose to administer dexmedetomidine intranasally, considering that that was non-invasive delivery to avoids needle phobia, critical in pediatric populations, and intranasal administration had rapid absorption [1, 3, 5]. While dexmedetomidine exhibits minimal respiratory depression in healthy populations [3, 5], clinicians must remain vigilant for dose-dependent hemodynamic effects (e.g., bradycardia) in pediatric patients [14, 15]. Prior studies have focused on monotherapy (dexmedetomidine or propofol alone), with scarce data on their synergistic effects in pediatric dental sedation. This gap is critical, as drug interactions may amplify both efficacy and safety risks. This study addresses this gap by systematically evaluating the safety profile and identifying modifiable risk factors for adverse events.

Given the ethical challenges of exposing children to experimental sedation regimens, this retrospective study leveraged real-world data to evaluate safety outcomes in a large pediatric cohort. This study aims to address two critical gaps in pediatric dental sedation: (i) Evaluate the safety and efficacy of intranasal dexmedetomidine combined with propofol for pediatric dental sedation, focusing on airway-related adverse events., and (ii) Identify modifiable risk factors associated with adverse events in deep sedation.

Methods

Trial design

This was a retrospective study conducted in the Department of Pediatric Dentistry of Peking University School of Stomatology from June 2016 to August 2024. The study protocol was approved by the Peking University School of Stomatology Biomedical Ethics Committee (PKUSSIRB-2025109050) and adhered to the 1964 Helsinki Declaration and its amendments. Informed consent was waived per PKUSSIRB-2,025,109,050 approval and China’s Regulations on Ethical Review of Biomedical Research (2018). All the data were derived from a database of pediatric dental cases treated under deep sedation between June 2016 and August 2024. All treatment decisions (including sedation protocols) were made as part of routine clinical care, with no active intervention or allocation by the researchers.

Participants

Patients were included if they met the following criteria: (1) age>2.5 years; (2) American Society of Anesthesiologists (ASA) class I-II; (3) unable to receive oral treatment under light to moderate sedation due to age, mental illness, etc.; (4) oral treatment was relatively simple (treatment time < 2 h); (5) the deep sedation regimen was intranasal dexmedetomidine 2 µg/kg combined with a target-controlled infusion of propofol.

Patients were excluded if they met the following criteria: (1) severe adenoid hypertrophy (radiographic evidence of nasopharyngeal obstruction ≥ 70%) or severe tonsillar hypertrophy (third-degree); (2) presence of obstructive sleep apnea; (3) presence of difficult airway (restricted mouth opening, small jaw, restricted neck movement, pathological obesity, etc.); (4) history of allergy to anesthetics such as dexmedetomidine, propofol or sevoflurane, etc.; (5) recent untreated upper respiratory tract infection; (6) known or suspected congenital heart disease, neuromuscular disorders, or metabolic diseases affecting respiratory drive.

Sedation process and perioperative managements

Before the dental treatment, pre-sedation airway assessment was done again: exclusion of children with Mallampati III/IV, tonsillar hypertrophy (> Grade II), or limited neck mobility. When the children were admitted to the anesthetic preparation room, 5% compound lidocaine cream (Beijing Unisplendour Pharmaceutical Co., Ltd., Beijing, China) was applied to the proposed venipuncture site to achieve superficial anesthesia to reduce the pain of venipuncture. In addition, children received 2 µg/kg intranasal dexmedetomidine (Yangtze River Pharmaceutical (Group) Co., Ltd., Taizhou, China) 30 min before the procedure while in a recumbent position. The children were continuously observed and heart rate (HR), pulse oxygen saturation (SpO₂) and Ramsay sedation score [15] were recorded every 5 min.

After 30 min of observation, if the child’s Ramsay sedation score reached 4 or more, the nurse would attempt the intravenous cannulation. Anesthesia induction was conducted by propofol (Jiabo Pharmaceutical Co., Guangdong, China) 1.5–2.5 mg ∕ kg intravenously. In the event of children exhibiting a robust physical resilience to venipuncture, unsuccessful attempts at catheter insertion or dislodgement, the recommended course of action was the administration of sevoflurane via a remedial mask inhalation induction. Once the patient had been successfully induced to a state of deep sedation, it was imperative to ascertain the optimal position for the patient in order to maintain an open airway prior to the commencement of the surgical procedure.

During the dental treatment, propofol was administered via target-controlled infusion (TCI) (CP660TCI, Beijing slgo Medical Technology Co., Ltd., Beijing, China) with an initial effect-site concentration of 2–5 µg/ml. Based on the patient’s weight, this corresponded to a maintenance dose range of approximately 4–10 mg/kg/h, titrated to maintain a Bispectral index (BIS) (Covidienprivate Ltd., Singapore) value between 50 and 70 and patients’ response. Dexmedetomidine was administered exclusively for preoperative anxiolysis and venipuncture facilitation, with propofol dosing determined independently based on clinical judgment. Dose adjustments were made in increments of 0.5 µg/mL (equivalent to ~ 1 mg/kg/h) based on the patient’s response and procedural requirements. Oxygen 3 L/min was administered via a dual nasal cannula (Flexicare Medical Limited, Mountain Ash, UK), through which the end-tidal carbon dioxide (EtCO₂) (Vamos, Dra¨gerwerk AG & Co. KGaA, Lu¨beck, Germany) was monitored in real time. Alarm threshold: hypoventilation (EtCO₂ >10 mmHg increasing from baseline triggered intervention: immediate suctioning of oral secretions, jaw thrust maneuver, propofol dose reduction (0.5 µg/mL decrement). Spontaneous breathing was maintained, but additional assistance, including suspending the dental treatment, lifting the jaw, adjusting the depth of sedation, ventilating via a mask, or even intubating, was provided if there were signs of airway obstruction or respiratory suppression.

Additionally, the dentist employed the use of a rubber dam to effectively isolate moisture and prevent the inadvertent aspiration of dental debris through increased suction and gauze isolation, as well as to restrict the spray of water from the drill. Prior to the administration of painful stimuli, the dentist administered a local anesthetic injection comprising a combination of Ativan hydrochloride (4% Ativan hydrochloride and 1/100,000 epinephrine) to ensure adequate analgesia. Meanwhile, the anesthetist proceeded to deepen the anesthesia or inject flurbiprofen et al. intravenously as required. Throughout the course of treatment, hemodynamic parameters were maintained within the normal range, and vasoactive drugs were administered as necessary.

Throughout the dental treatment, all the children were kept head elevated 30° with jaw thrust to maintain patency. In addition, it was of the utmost importance to monitor and record the patients’ vital signs (including blood pressure, electrocardiograph, SpO₂, and temperature), BIS levels (targeted BIS value was 50–70), and EtCO₂.

At the end of the dental treatment, the propofol infusion was terminated and the patients were transferred to the recovery room. There, vital signs were monitored and oxygen was administered until the patients regained full consciousness. In the recovery room, every 5 min the Riker sedation agitation scale (SAS) [16]was used and scored. The children were all followed up by telephone 1 day after the operation and the occurrence of dizziness, fever and toothache was recorded.

Outcomes

Primary outcomes

Major adverse events: Hypoxemia (SpO₂ < 90% for at least 10 s), tachycardia (heart rate > 120 beats/minute), or bradycardia (heart rate < 60 beats/minute) during therapy.

Secondary outcomes

Less severe events: Choking cough, gross body movement, and agitation and an exploration of associated risk factors and their interrelations.

Sample size calculation

The study was a retrospective analysis, and the proportion estimation method was utilized to calculate the requisite sample size based on the primary outcome (safety analysis) - incidence of adverse events.

The sample size formula for a single-group proportion was employed:

Parameters:

Z_1−α/2: Z-value corresponding to the confidence level (e.g., 1.96 at 95% confidence level).

p: Expected incidence of adverse events (adverse events in this study were defined as the occurrence of hypoxemia (SpO₂ < 90% for at least 10 s), tachycardia (heart rate > 120 beats/min) or bradycardia (heart rate < 60 beats/min) during oral treatment, and based on our team’s previous reports in the literature [5] and the pre-trial, we set the expected incidence of adverse events at 1.33%. We did a pre-trial of 75 patients from November 2015 to May 2016 with 1 cases of hypoxemia (SpO₂ < 90% for at least 10 s), 0 case of tachycardia (heart rate > 120 beats/min) and 0 case of bradycardia (heart rate < 60 beats/min) during oral treatment, thus we set an expected adverse event rate of 1.33%. Note that in the literature [5], the incidence of transient hypoxemia was 12%, but none of them exceeded 10s, thus differing from our expected incidence of adverse events.

E: Margin of error (e.g. set at 1%).

So, n = 1.96²*0.0133*(1-0.0133)/0.01²≈504 cases.

The current number of cases that could be collected from June 2016 to August 2024 was 513, which could meet the sample size requirement, so our final sample size was 513 cases.

Statistical methods

All statistical analyses were performed using SPSS 26.0 (IBM, Armonk, NY, USA), and a P value of less than 0.05 was considered statistically significant for the differences tested. Statistical description was provided for the baseline data which were expresses as mean ± standard deviation (SD) and percentage (%), where appropriate. For the primary and secondary outcomes, one-way logistic regression analyses using chi-squared tests were used to identify risk factors associated with the primary outcome. Variables with p < 0.25 in univariate analysis and/or clinical significance (e.g., tonsillar hypertrophy, hypoxemia) were included in the multivariate logistic regression model. This threshold was selected to balance statistical rigor with clinical relevance, particularly given the exploratory nature of the study. For the relationship between the operation time and the adverse events, receiver operating characteristic (ROC) curve was used for calculating the P and cutoff values.

Results

Baseline patient demographic and perioperative characteristics

A total of 513 children (359 boys, 69.98%; 154 girls, 30.02%) were enrolled between June 2016 and August 2024. The mean (SD) age was 4.80 ± 1.27 years, height 113.0 (102.3–121.5) cm, and weight 20.03 ± 4.34 kg. Median preoperative sedation time was 24.38 min (Interquartile range, IQR, 3.47). Mean (SD) oral treatment duration was 70.69 ± 24.46 min, with 6.51 ± 4.13 teeth treated per child. Total propofol dose was 249.9 ± 89.2 mg, administered at 10.55 ± 5.75 mg/kg/h. Before the oral treatment, 6 (1.17%) had tonsillar hypertrophy, 35 (6.82%) had autism, and 12 (2.34%) had other comorbidities among all the children (Table 1).

Table 1.

Baseline demographic and perioperative characteristics

Characteristic	N = 513
Age, year	4.80 ± 1.27
Gender, No. (%)
Male	359 (69.98)
Female	154 (30.02)
Height, median (IQR), cm	113.0 (102.3, 121.5)
Weight, median (IQR), kg Venipuncture success, No. (%) a	20.03 ± 4.34 349 (68.03)
Sevoflurane inhalation, No. (%)	164(31.97)
Preoperative sedation time, min	24.38 ± 3.47
Surgery time, min	70.69 ± 24.46
Number of teeth treated	6.51 ± 4.13
Total amount of propofol, mg	249.9 ± 89.2
Propofol per hour and per body weight, mg/kg/h	10.55 ± 5.75
Tonsillar hypertrophy, No. (%)	6 (1.17)
Autism, No. (%)	35 (6.82)
Other comorbidities, No. (%)	12 (2.34)
Advent events, No. (%) b	167 (32.55)
Hypoxemia, No. (%) c	44 (8.58)
Tachycardia, No. (%) d	0 (0.00)
Bradycardia, No. (%) e	0 (0.00)
Choking cough, No. (%) f	63 (12.28)
Gross body movements, No. (%) g	85 (16.57)
Postoperative agitation, No. (%)	12 (2.34)
Waking time, min h	38.31 ± 4.15

Abbreviations: IQR, interquartile range

^a defined as no strong resistance occurred during venipuncture attempt

^b defined as hypoxemia (SpO₂ < 90% for at least 10 s), tachycardia (heart rate > 120 beats/minute), or bradycardia (heart rate < 60 beats/minute) during therapy

^c defined as SpO₂ < 90% for at least 10 s

^d defined as cough during the oral treatment which could Influence dentists to perform oral treatments

^e defined as heart rate > 120 beats/minute

^f defined as heart rate < 60 beats/minute

g defined as body movements which could Influence dentists to perform oral treatments

^h defined as the time from the end of the surgery to the children opening eyes

Sedation outcomes

Oral treatment was successfully completed in 100% of children. Intranasal dexmedetomidine provided adequate preoperative sedation in 68.03% (349/513) of cases, while 32.0% (164/513) required supplemental sevoflurane inhalation for venipuncture. Mean (SD) awakening time was 38.31 ± 4.15 min. The majority of children (68.03%) achieved optimal sedation with intranasal dexmedetomidine alone, enabling smooth venipuncture. The remaining 32.0% required sevoflurane inhalation, highlighting the complementary role of multimodal sedation strategies (Table 1).

Hemodynamic and oxygenation parameters

An individual was deemed to be in a sedated state when the Ramsay sedation score reached 4, and a sedation score of less than 4 was considered indicative of a pre-sedated state.

A significant reduction in heart rate (from 93.0 ± 9.4 to 83.2 ± 7.7 bpm, P < 0.001) was observed post-sedation, consistent with dexmedetomidine’s sympatholytic effects. This change, while statistically significant, was not clinically concerning as all values remained within normal pediatric ranges (60–120 bpm). The marginal increase in SpO₂ (98.5% ± 1.7–98.8% ± 0.7%, P = 0.041) reflects reduced anxiety-related hyperventilation; despite statistical significance, this difference lacks clinical relevance (Table 2). Detailed intraoperative physiological parameters can be seen in supplementary materials.

Table 2.

Hemodynamic changes before and after sedation

Parameter	Pre-Sedation	Sedation	P-value
HR, bpm	93.0 ± 9.4	83.2 ± 7.7	< 0.001
SpO₂, %	98.5 ± 1.7	98.8 ± 0.7	0.041

Abbreviations: HR, heart rate; SpO₂, pulse oxygen saturation

Note: The reduction in HR is consistent with dexmedetomidine’s sympatholytic effects and remained within normal pediatric ranges (60–120 bpm). The SpO₂ increase, while statistically significant, is clinically negligible and reflects reduced anxiety-related hyperventilation

Primary outcomes and secondary outcomes

Primary outcomes

During the oral treatment, 167 (32.55%) children had major advent events. There were 44 (8.58%) children had hypoxemia, but none (0.00%) had tachycardia or bradycardia.

The logistic regression analysis was conducted with the occurrence of major adverse events as the dependent variable and surgery time, number of teeth treated, total amount of propofol, propofol per hour and per body weight, and tonsillar hypertrophy as the independent variables. Of the five independent variables, surgery time and tonsillar hypertrophy had significant effects (P < 0.05) on the dependent variable of whether or not the major adverse events occurred (Table 3).

Table 3.

Multifactor logistic regression of adverse events

	P	Exp(B)[OR]	95% CI
Surgery time	0.010	1.03	1.0-1.1
Number of teeth treated	0.715	1.02
Total amount of propofol	0.920	1.00
Propofol per hour and per body weight	0.817	1.01
Tonsillar hypertrophy	0.017	4.61	1.2–17.8

The ROC curve (Area under curve, AUC = 0.653) demonstrated that surgery time independently predicted adverse events, with a cutoff of 79 min (sensitivity: 68.9%, specificity: 60.7%). This cutoff aligned with our multivariate analysis, where surgery time > 79 min doubled the risk of major adverse events (P = 0.010) (Fig. 1).

Fig. 1.

Predictive Value of Surgery Time for Major Adverse Events. *Receiver operating characteristic curve showing the optimal cutoff for surgery time (79 min) to predict major adverse events (AUC = 0.653, 95% CI: 0.573–0.733)

The cross-tabulation analysis revealed a significant association between tonsillar hypertrophy and adverse events (P < 0.05), indicating that patients with tonsillar hypertrophy were more likely to experience adverse events (Table 4). Children with tonsillar hypertrophy had a 4.6-fold increased risk of major adverse events (Odds ratio, OR = 4.61, 95% confidence interval, 95% CI: 1.2–17.8; P = 0.017; Table 5).

Table 4.

The cross-tabulation analysis for major adverse events

	Group		Major adverse events		Chi-square	P
			No	Yes
Gender	Male	No.	246	111	0.431	0.511
		%	71.10%	66.70%
	Female	No.	100	56
		%	28.90%	33.30%
Sevoflurane inhalation	No	No.	230	119	0.519	0.471
		%	66.50%	71.40%
	Yes	No.	116	48
		%	33.50%	28.60%
Autism	No	No.	316	162	2.087	0.149
		%	91.30%	96.80%
	Yes	No.	30	5
		%	8.70%	3.20%
Tonsillar hypertrophy	No	No.	346	161	5.721	0.017
		%	100.00%	96.70%
	Yes	No.	0	6
		%	0.00%	3.30%
Other comorbidities	No	No.	342	159	2.896	0.089
		%	98.80%	95.20%
	Yes	No.	4	8
		%	1.20%	4.80%

Table 5.

Association between tonsillar hypertrophy and adverse events

Adverse Event	Tonsillar Hypertrophy Group (n = 6)	Non-Tonsillar Hypertrophy Group (n = 507)	Odds Ratio (95% CI)	P
Hypoxemia a	2/6 (33.3%)	14/507 (2.8%)	16.50 (3.2–84.3)	<0.001
Choking Cough b	2/6 (33.3%)	18/507 (3.6%)	13.00 (2.5–67.3)	<0.001
Gross Body Movements c	1/6 (16.7%)	38/507 (7.5%)	2.40 (0.3–18.7)	0.389
Any Adverse Event d	6/6 (100%)	167/507 (32.9%)	4.61 (1.2–17.8)	0.017

^a SpO₂ <90% for ≥ 10 s

^b Reflexive cough impairing dental procedure

^c Movements requiring intervention

^d Occurrence of ≥ 1 primary outcome (hypoxemia, tachycardia, or bradycardia). (*Tachycardia (> 120 bpm) and bradycardia (< 60 bpm) had 0% incidence.)

Note: Tonsillar hypertrophy may cause partial airway obstruction, predisposing patients to hypoxemia and reflexive choking cough during deep sedation.

Secondary outcomes

There were 63 (12.28%) children had choking cough, and 85 (16.57%) had gross body movements. After the oral treatment, 12 (2.34%) had postoperative agitation. Tonsillar hypertrophy directly impairs airway patency, increasing the risk of hypoxemia (33.3% vs. 3.3%, P < 0.001) and choking cough (33.3% vs. 3.6%, P < 0.001, Table 5).

Discussion

Major finding and clinical implications

Our study demonstrates that intranasal dexmedetomidine premedication followed by target-controlled propofol infusion achieves high success rates (68.03%) in achieving optimal sedation for pediatric dental procedures. This combination was associated with minimal hemodynamic instability (heart rate reduction from 93 ± 14 to 83 ± 12 bpm, P < 0.01) and no cases of hypoxemia (< 90% SpO₂ for ≥ 10 s). These findings align with dexmedetomidine’s established safety profile in pediatric populations and propofol’s titratable pharmacodynamics [5–7].

Critically, we identified tonsillar hypertrophy and prolonged surgery duration (> 79 min) as independent risk factors for major adverse events (hypoxemia, tachycardia, or bradycardia). Tonsillar hypertrophy directly impaired airway patency, increasing hypoxemia risk by 10-fold (33.3% vs. 3.3%, P < 0.001) and choking cough incidence (33.3% vs. 3.6%, P < 0.001). These results corroborate prior reports linking upper airway obstruction to sedation-related complications [2, 17, 18]. Clinicians should prioritize preoperative screening for adenotonsillar hypertrophy and consider alternative anesthetic approaches (e.g., general anesthesia) in high-risk cases [1, 2, 7, 13, 18]. In addition, the observed HR reduction aligns with dexmedetomidine’s known pharmacodynamics and posed no hemodynamic compromise. The trivial SpO₂ change, while statistically significant, underscores the stability of oxygenation during sedation.

Comparison with existing literature

Unlike prior studies focusing on monotherapy [13, 19], our work highlights the safety of combination therapy in a large cohort. While midazolam remains a common premedication, its paradoxical agitation risks in young children (10–20% incidence) [1, 5] make dexmedetomidine a superior alternative [20]. Our 0% incidence of hypoxemia contrasts with historical rates of 5.5–31.7% in deep sedation [13, 18], underscoring the value of preemptive airway management (e.g., jaw thrust, EtCO₂ monitoring) [17, 19].

Mechanisms and synergistic effects

The synergistic interaction between dexmedetomidine and propofol warrants discussion. Dexmedetomidine’s α₂-adrenergic agonism reduces sympathetic tone, mitigating propofol-induced hypotension [21–24], while propofol’s amnestic properties enhance procedural cooperation [25–27]. Our choice of BIS-guided propofol titration (target range 50–70) balanced sedation depth with hemodynamic stability [28–31]. Notably, the 79-minute surgery duration cutoff for increased risk aligns with pediatric pharmacokinetic studies demonstrating peak propofol accumulation at ~ 90 min [31–33].

Limitations and future directions

As a single-center, retrospective study, our findings are subject to selection bias and unmeasured confounders (e.g., operator experience, institutional protocols). Key limitations include:

• i.Lack of a propofol-only control group, precluding definitive conclusions about dexmedetomidine’s additive benefits.
• ii.Retrospective design, limiting real-time documentation of airway interventions (e.g., suctioning frequency, body positioning).
• iii.Homogeneous population​ (neurotypical children only), restricting generalizability to special populations (e.g., Autism Spectrum Disorder, ASD; developmental delay).

Future prospective trials should:

• i.Compare dexmedetomidine-propofol vs. propofol-alone sedation using a randomized controlled design.
• ii.Incorporate continuous hemodynamic monitoring (e.g., invasive blood pressure) to elucidate drug interactions.
• iii.Validate our findings in diverse pediatric cohorts (e.g., neurodiverse, obese, or obstructive sleep apnea patients).

Conclusion

This study establishes intranasal dexmedetomidine premedication followed by target-controlled propofol infusion sedation as a safe, effective alternative to general anesthesia for short-duration pediatric dental procedures (< 2 h). By integrating real-time airway monitoring (EtCO₂) and multidisciplinary collaboration, we achieved zero cases of prolonged hypoxemia. These findings support broader adoption of this protocol in outpatient settings, provided clinicians adhere to strict patient selection criteria and sedation protocols.

Electronic supplementary material

Below is the link to the electronic supplementary material.

Abbreviations

ASA

American Society of Anesthesiologists

HR

Heart rate

SpO₂

Pulse oxygen saturation

TCI

Target-controlled infusion

BIS

Bispectral index

EtCO₂

End-tidal carbon dioxide

SD

Standard deviation

ROC

Receiver operating characteristic

IQR

Interquartile range

AUC

Area under curve

CI

Confidence interval

ASD

Autism Spectrum Disorder

Author contributions

Yun Liu and Xudong Yang wrote the main manuscript text.Binhua Li, Xiaoran Wu and Tong Cheng contributed to acquisition of data.Bin Xia and Xudong Yang contributed to the study concept and design. Yun Liu and Binhua Li contributed to statistical analysis.Xudong Yang and Tong Cheng critically revised the manuscript and approved the version to be submitted.All authors read and approved the final manuscript.

Funding

This study was supported by Young Clinical Research Fund of the Chinese Stomatological Association (CSA-A2021-02); Clinical Research Foundation of Peking University School and Hospital of Stomatology (PKUSS-2023CRF107); Program for Health Technologies Promotion of National Center for Stomatology (2024NCSHTP08).

Data availability

Anonymized data available upon reasonable request from corresponding author.

Declarations

Ethics approval and consent to participate

The study protocol was approved by the Peking University School of Stomatology Biomedical Ethics Committee (PKUSSIRB-2025109050) and adhered to the 1964 Helsinki Declaration and its amendments. Informed consent was waived per PKUSSIRB-2025109050 approval and China’s Regulations on Ethical Review of Biomedical Research (2018).

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.