Emergence from general anaesthesia is a complex transition from unconsciousness to purposeful interaction. During this interval, patients may develop transient non-purposeful movement, restlessness, disorientation, shouting, or combative behaviour, collectively described as emergence agitation. Although the phenomenon has been extensively studied in paediatric anaesthesia, clinically important EA is also encountered in adults. Its incidence varies with age, anxiety, surgical procedure, pain, anaesthetic technique, and the instrument used for assessment.¹ Sevoflurane is widely used because of its low blood-gas solubility and predictable, relatively rapid recovery. The same rapid change in anaesthetic concentration that facilitates prompt awakening may, however, be accompanied by behavioural dysregulation during early recovery. Adult studies have demonstrated clinically relevant EA after sevoflurane and have shown that modifying the emergence strategy can influence postoperative behaviour.²˒³ Dexmedetomidine is a highly selective α2-adrenergic agonist that produces sedation resembling physiological sleep, sympatholysis and relative preservation of respiratory drive. By reducing central noradrenergic activity, it may attenuate the autonomic and behavioural response accompanying abrupt emergence. A meta-analysis of randomized adult trials reported a reduction in EA with perioperative intravenous dexmedetomidine compared with placebo, while also emphasizing the importance of dose selection because bradycardia, hypotension and delayed recovery can occur.⁴˒⁵ Propofol is a short-acting intravenous hypnotic with rapid onset and offset. It potentiates GABA-mediated inhibition and is commonly used for induction, maintenance and selected emergence strategies. Transitioning from sevoflurane to propofol near the end of surgery has been shown to reduce EA, although some studies have reported modest effects on recovery timing.⁶ Thus, propofol represents a clinically relevant comparator when assessing dexmedetomidine-based emergence strategies. The present prospective comparative study was designed to compare dexmedetomidine and propofol for prevention of sevoflurane-induced EA in adults. In addition to the primary behavioural endpoint, the study assessed the severity of agitation, serial cardiovascular and respiratory parameters

Study design and setting: A prospective comparative study was conducted in the Department of Anesthesiology and Critical Care, Raipur Institute of Medical Sciences, Raipur, Chhattisgarh, India. Institutional scientific and ethics approvals were obtained and written informed consent was taken. Participants: Adults aged 18–65 years, ASA physical status I–II, scheduled for elective surgery under general anaesthesia with endotracheal intubation were eligible. Exclusion criteria included ASA ≥III, significant cardiovascular or respiratory disease, psychiatric illness or cognitive impairment, relevant drug allergy, BMI outside 18–30 kg/m², uncontrolled hypertension and recent participation in another clinical trial. Allocation and intervention: The thesis describes computer-generated allocation with concealed envelopes. The final analysed dataset comprised 50 patients, 25 in each group. The dexmedetomidine group received 0.5 μg/kg diluted in 100 mL normal saline over 30 minutes; the propofol group received 0.5 mg/kg diluted in 100 mL normal saline over 30 minutes. Both infusions were started after induction and discontinued at the end of surgery. Anaesthetic technique: Standard monitoring included ECG, SpO₂ and non-invasive blood pressure. Induction consisted of midazolam 0.05 mg/kg, propofol 2–2.5 mg/kg, nalbuphine 0.2 mg/kg and atracurium 0.5 mg/kg. Sevoflurane was titrated to a BIS of 40–60 for maintenance. Neuromuscular blockade was reversed with neostigmine 0.05 mg/kg and glycopyrrolate 0.008 mg/kg. Extubation was performed when tidal volume exceeded 5 mL/kg and the Aldrete score was ≥9. Outcome assessment: EA within 15 minutes after extubation was the primary endpoint and was defined as RSAS ≥5. RSAS, HR, MAP and SpO₂ were recorded immediately after extubation (T0), at 5 minutes (T1), 15 minutes (T2) and 30 minutes (T3). PONV was assessed on a four-point scale, and QoR-15 was assessed at 24 hours. Statistical analysis: Continuous variables were summarized as mean±SD and categorical variables as counts and percentages. Between-group comparisons used independent-sample tests for continuous variables and chi-square or Fisher exact testing for categorical variables, with p<0.05 considered statistically significant. The thesis also states that intention-to-treat and per-protocol analyses were conducted. Data integrity note: The thesis contains an internal discrepancy in the methodology section, where one passage describes 30 patients per intervention group although the sample-size calculation and final analysed cohort are 25 per group. The present manuscript uses the final analysed cohort of 50 patients (25 per group), as reflected consistently in the reported outcome tables. This discrepancy should be reconciled against the original master chart before journal submission.

Participant characteristics and baseline comparability The final analysis included 50 adults, equally divided between dexmedetomidine (DEX; n=25) and propofol (PRO; n=25). The groups were comparable across age, sex, ASA physical status and anthropometric measures. Age-category distribution was also balanced: 18–30 years, 6 versus 7; 31–45 years, 12 versus 12; and 46–65 years, 7 versus 6 in DEX and PRO, respectively (χ²=0.154, df=2, p=0.926). Mean age was 41.04±13.04 years in DEX and 39.24±13.72 years in PRO (p=0.636). Table 1. Baseline demographic, clinical and anthropometric characteristics. Variable Dexmedetomidine (n=25) Propofol (n=25) p value Age, years 41.04±13.04 39.24±13.72 0.636 Female, n (%) 17 (68) 17 (68) 1.000 Male, n (%) 8 (32) 8 (32) 1.000 ASA I, n 11 13 0.571 ASA II, n 14 12 0.571 Height, cm 163.44±9.618 162.88±9.628 0.838 Weight, kg 70.24±13.189 69.56±12.343 0.851 BMI, kg/m² 26.64±6.27 26.36±5.03 0.862 The identical sex distribution and similar ASA composition reduce concern that the primary outcome difference was driven by major baseline imbalance. Similarly, the small numerical differences in height, weight and BMI were not statistically significant. Primary outcome: emergence agitation EA within 15 minutes of extubation occurred in 7 of 25 patients (28%) in the DEX group compared with 16 of 25 (64%) in the PRO group. The between-group difference was statistically significant (χ²=6.522, p=0.022). The absolute risk reduction was 36 percentage points. Based on the reported event counts, the relative risk was 0.438 (95% CI 0.219–0.876) and the corresponding approximate number needed to treat was 2.8. These latter measures are derived calculations from the thesis data and should be interpreted cautiously because of the small single-centre sample. Table 2. Primary outcome and derived effect measures. Outcome Dexmedetomidine Propofol Between-group result EA, n (%) 7 (28) 16 (64) χ²=6.522; p=0.022 No EA, n (%) 18 (72) 9 (36) — Absolute risk difference — — −36 percentage points Relative risk (derived) — — 0.438 (95% CI 0.219–0.876) Approx. NNT (derived) — — 2.8 Severity of emergence agitation At 15 minutes after extubation, mean RSAS was 3.40±1.607 in DEX and 4.96±1.904 in PRO. The mean difference was −1.56 points and was statistically significant (t=−3.131, df=48, p=0.003). The standardized difference calculated from the reported means and SDs was approximately 0.89, indicating a substantial separation between the two group means in this sample. Table 3. RSAS score at 15 minutes (T2). Group n Mean RSAS at T2 SD SE p value Dexmedetomidine 25 3.40 1.607 0.321 0.003 Propofol 25 4.96 1.904 0.381 — Serial cardiovascular parameters Heart rate remained comparable at all four measured recovery points. At extubation, HR was 78.96±3.034 beats/min in DEX and 80.16±3.223 beats/min in PRO (p=0.182). The mean values then remained closely aligned at 5 minutes, 15 minutes and 30 minutes. No time point showed a statistically significant difference. Table 4. Serial heart rate during emergence and early recovery. Time point DEX mean±SD (beats/min) PRO mean±SD (beats/min) p value T0 (extubation) 78.96±3.034 80.16±3.223 0.182 T1 (5 min) 77.64±2.970 77.96±2.950 0.704 T2 (15 min) 75.72±2.923 75.52±3.057 0.814 T3 (30 min) 73.68±3.497 74.76±2.891 0.240 Mean arterial pressure showed a similarly stable pattern. MAP at T0 was 88.72±6.523 mmHg in DEX and 88.40±7.200 mmHg in PRO (p=0.870). At T1, T2 and T3, values remained comparable, with all p values >0.80. Thus, within the limits of this sample and observation window, the reduction in EA was not accompanied by a detectable between-group difference in recovery blood pressure. Table 5. Serial mean arterial pressure during emergence and early recovery. Time point DEX mean±SD (mmHg) PRO mean±SD (mmHg) p value T0 (extubation) 88.72±6.523 88.40±7.200 0.870 T1 (5 min) 86.64±7.376 86.20±7.439 0.835 T2 (15 min) 83.76±6.924 84.08±7.466 0.876 T3 (30 min) 88.00±6.545 87.52±7.078 0.804 Oxygen saturation SpO₂ remained high and stable throughout the reported recovery measurements. The thesis reports the same group means at T0–T3: 96.92±1.038% for DEX and 97.48±1.085% for PRO, with p=0.068. No significant between-group difference was identified at any reported time point. The repeated identical values in the thesis table should nevertheless be checked against the original master chart before final submission, because repeated values across four postoperative time points may reflect data transcription or summarization. Table 6. Reported SpO₂ values during recovery. Time point DEX mean±SD (%) PRO mean±SD (%) p value T0 96.92±1.038 97.48±1.085 0.068 T1 96.92±1.038 97.48±1.085 0.068 T2 96.92±1.038 97.48±1.085 0.068 T3 96.92±1.038 97.48±1.085 0.068 Quality of recovery Patient-centred recovery at 24 hours was significantly different between groups. Mean QoR-15 was 137.20±7.455 in the DEX group compared with 123.88±6.654 in the PRO group, with t=6.665, df=48 and p=0.001. The between-group mean difference was 13.32 points. The standardized mean difference calculated from the reported summary statistics was approximately 1.89, indicating a large separation in QoR-15 scores in this sample. Table 7. Quality of Recovery-15 score at 24 hours. Group n QoR-15 mean SD SE t df p value Dexmedetomidine 25 137.20 7.455 1.491 6.665 48 0.001 Propofol 25 123.88 6.654 1.331 — — — Postoperative nausea and vomiting PONV scores were distributed similarly between groups. In the DEX group, 15 patients had score 0, 8 had score 1 and 2 had score 2. In the PRO group, the corresponding counts were 12, 11 and 2. No patient was reported with score 3 in either group. The chi-square statistic was 0.807 with df=2 (p=0.668). Table 8. Distribution of PONV scores between groups. PONV score Dexmedetomidine, n (%) Propofol, n (%) 0 15 (60) 12 (48) 1 8 (32) 11 (44) 2 2 (8) 2 (8) 3 0 (0) 0 (0) Overall test χ²=0.807, df=2 p=0.668 Overall interpretation of the results Taken together, the results show a consistent separation in the primary behavioural outcome and the patient-centred recovery outcome. The incidence of EA was lower and the 15-minute RSAS score was lower with dexmedetomidine. In contrast, the physiological recovery variables—HR, MAP and SpO₂—were comparable between groups, and PONV did not differ significantly. This pattern suggests that the observed difference in emergence behaviour occurred without a measurable between-group penalty in the routinely monitored cardiovascular and respiratory parameters during the first 30 minutes after extubation.

Principal findings The principal finding of this prospective comparative study was that dexmedetomidine was associated with a lower incidence of sevoflurane-induced EA than propofol in the analysed adult cohort. EA was observed in 7/25 (28%) patients in the DEX group versus 16/25 (64%) in the PRO group. The difference of 36 percentage points was statistically significant. Importantly, the reduction was accompanied by lower agitation severity at 15 minutes, with RSAS values of 3.40 versus 4.96. The direction of these findings is consistent with adult evidence suggesting that perioperative dexmedetomidine can reduce EA.⁴ The present study therefore adds a direct comparison with propofol rather than comparing dexmedetomidine only with placebo or usual care. This distinction is clinically relevant because propofol itself has established effects on emergence quality and is used routinely in perioperative practice. Randomized work has shown that propofol administered around the end of sevoflurane anaesthesia can reduce EA, making the current 64% incidence in the propofol arm a clinically meaningful comparator rather than an untreated control.⁶ Magnitude and clinical interpretation of the reduction in agitation The absolute reduction in EA was 36 percentage points, corresponding to an approximate NNT of 2.8 based on the observed rates. The derived relative risk of 0.438 indicates that the observed risk of EA in the dexmedetomidine group was less than half that in the propofol group. The 95% confidence interval for the derived relative risk (0.219–0.876) remains below 1.0, but the interval is relatively wide because only 50 patients were analysed. Therefore, the effect estimate should be viewed as supportive rather than definitive evidence of the exact magnitude of benefit. The reduction is also supported by the severity analysis. Mean RSAS at 15 minutes was lower by 1.56 points. The RSAS findings are important because an intervention that merely shifts the number of patients classified as agitated without reducing the intensity of agitation would have more limited practical relevance. Here, both the frequency and measured severity moved in the same direction. Possible pharmacological explanation Dexmedetomidine has a pharmacological profile that provides a plausible explanation for smoother emergence. α2-adrenergic agonism reduces central sympathetic outflow and produces a sedative state resembling physiological sleep, with relative preservation of spontaneous ventilation. During emergence, this may attenuate the abrupt autonomic and behavioural activation associated with rapid loss of volatile anaesthetic concentration. The mechanism is distinct from propofol, which primarily enhances GABA-A receptor-mediated inhibition and has rapid onset and offset.⁴˒⁵ The present findings should not, however, be interpreted as evidence that sevoflurane itself is the sole cause of agitation. EA is multifactorial and can be influenced by pain, anxiety, surgical stimulation, environmental factors, opioid exposure and the speed of awakening. The standardized anaesthetic approach in this study reduces some variability, but the available dataset does not provide enough detail to quantify the contribution of each of these factors. Comparison with previous evidence The direction of the current result agrees with the adult meta-analysis by Zhang and colleagues, which found a reduction in EA with perioperative intravenous dexmedetomidine across randomized trials.⁴ Adult procedure-specific studies have likewise reported lower agitation with dexmedetomidine in sevoflurane-based anaesthesia.² The current study is therefore broadly concordant with the existing pharmacological evidence, while providing a direct dexmedetomidine-versus-propofol comparison in an adult cohort. The paediatric literature has also repeatedly demonstrated anti-agitation effects of dexmedetomidine and propofol, although extrapolation from children to adults should be cautious because age, anxiety, neurodevelopmental factors and the phenotype of EA differ between populations. The current adult findings are consequently useful as population-specific evidence rather than as confirmation that paediatric effect sizes apply directly to adults. Propofol remains a rational comparator because randomized studies have demonstrated that a transition to propofol after sevoflurane can reduce EA.⁶ Its rapid redistribution and short duration can be advantageous when rapid awakening is prioritized. Thus, the present finding does not negate the utility of propofol; rather, within this specific dosing and study framework, the observed agitation outcomes favoured dexmedetomidine. Haemodynamic safety A potential concern with dexmedetomidine is dose-related bradycardia or hypotension. The current study did not demonstrate a statistically significant difference in HR or MAP at any measured time point. HR declined progressively in both groups over the 30-minute observation window, but the group means remained close: at T0, 78.96 versus 80.16 beats/min; at T3, 73.68 versus 74.76 beats/min. Similarly, MAP ranged from 83.76 to 88.72 mmHg in DEX and 84.08 to 88.40 mmHg in PRO across the measured points, with all p values >0.80. These findings suggest that the studied dose was tolerated in the selected ASA I–II population. Nevertheless, absence of a statistically significant difference should not be equated with proof of haemodynamic equivalence, especially in a small sample. Rare adverse events may not be detected, and the exclusion of patients with major cardiovascular disease limits generalizability to higher-risk populations. Dose, infusion rate, intravascular volume and concomitant anaesthetic drugs all influence the haemodynamic response to dexmedetomidine. Respiratory profile Oxygenation remained stable in both groups. The thesis reports SpO₂ values of 96.92±1.038% for dexmedetomidine and 97.48±1.085% for propofol, with p=0.068 and the same reported means at each recovery time point. This supports the absence of a detectable oxygenation disadvantage during the observed recovery period. The result is biologically consistent with the relative preservation of respiratory drive described with dexmedetomidine. The repeated identical SpO₂ values across T0–T3 should be verified from the original master chart before publication. This is particularly important because serial physiological measurements are generally expected to vary over time, and accurate reporting of repeated-measures data strengthens the credibility of the manuscript. Quality of recovery and patient-centred outcomes The QoR-15 result extends the findings beyond immediate emergence behaviour. Mean QoR-15 at 24 hours was 137.20 in DEX versus 123.88 in PRO, a between-group difference of 13.32 points (p=0.001). The derived standardized mean difference of approximately 1.89 indicates a large separation in this sample. QoR-15 is particularly valuable because it integrates multiple dimensions of postoperative recovery rather than focusing only on a single physiological or behavioural endpoint. Several mechanisms could contribute to the higher QoR-15 observed with dexmedetomidine. Its sedative and analgesic-sparing properties may facilitate a calmer emergence and better early postoperative experience. Reduced agitation may itself decrease distress and the need for additional rescue medications. However, the present study did not report sufficiently detailed postoperative analgesic consumption, pain trajectories or rescue medication requirements to establish mediation of the QoR-15 difference. The association should therefore be interpreted as an observed outcome rather than proof of a specific mechanism. PONV PONV did not differ significantly between groups (p=0.668). Sixty percent of DEX patients and 48% of PRO patients had a PONV score of 0, while the remaining observations were predominantly score 1. No score-3 events were reported. This finding is compatible with a clinically neutral PONV profile in this small adult cohort. Because the study was not powered specifically for PONV, the absence of statistical significance does not establish equivalence between the agents. Propofol has recognized antiemetic properties, which can be an important consideration when selecting an emergence strategy.⁵ In the present dataset, however, the anti-agitation difference occurred without a detectable PONV difference. Future studies should prospectively record rescue antiemetic use, timing and clinically meaningful vomiting events to provide a more complete assessment. Strengths and limitations Strengths include a prospective comparative design, equal group size, a clinically relevant primary endpoint, standardized early recovery time points and inclusion of both behavioural and patient-centred outcomes. Baseline age, sex, ASA status and anthropometric characteristics were well balanced. The combination of EA incidence, RSAS severity, serial HR/MAP/SpO₂ and QoR-15 provides a multidimensional assessment of emergence quality. Several limitations need emphasis. First, the study was single-centre and included only 50 patients, limiting precision and generalizability. Second, only ASA I–II adults aged 18–65 years were included; the results cannot automatically be extrapolated to elderly patients, children, patients with significant cardiovascular disease or ASA III–IV populations. Third, follow-up was limited to 24-hour QoR-15, with no detailed assessment of later cognitive outcomes or persistent postoperative behavioural symptoms. Fourth, the available manuscript does not provide sufficient stratification by surgical type, duration, pain severity or opioid exposure, all of which may influence EA. Fifth, details of blinding and inter-rater reliability for RSAS assessment are limited. Sixth, the thesis contains an internal discrepancy between a planned group size of 30 per arm in one methodology passage and the final analysed sample of 25 per arm. Finally, the identical SpO₂ values reported at each time point warrant verification against the master chart before publication. These limitations do not negate the observed associations, but they define the level of certainty with which the findings should be presented. A larger multicentre randomized trial with prespecified stratification, standardized analgesia, blinded outcome assessment and complete reporting of adverse events would provide stronger evidence.

In this prospective comparative adult cohort undergoing general anaesthesia with sevoflurane, dexmedetomidine was associated with a lower incidence of emergence agitation and lower RSAS severity at 15 minutes than propofol. Dexmedetomidine was also associated with a higher QoR-15 score at 24 hours. Serial HR, MAP and reported SpO₂ values were comparable between groups, and PONV distribution did not differ significantly. The observed 36-percentage-point absolute reduction in EA is clinically notable, but the small single-centre sample and methodological reporting limitations warrant confirmation in larger, rigorously controlled studies.

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