Abstract
Introduction
Spinal anesthesia is widely used for lower-extremity surgery, but the duration of sensory and motor blockade is finite and may not cover longer procedures or early postoperative analgesic needs. Intravenous dexmedetomidine, a highly selective α2-adrenoceptor agonist, provides sedative, sympatholytic, and analgesic-sparing effects with relatively limited respiratory depression, making it a clinically relevant adjunct during regional anesthesia [1,2].
Evidence from randomized trials and meta-analysis indicates that intravenous dexmedetomidine can prolong sensory and motor blockade after spinal anesthesia. In a meta-analysis of seven randomized trials including 364 patients, intravenous dexmedetomidine prolonged sensory and motor block and delayed the first analgesic request, while increasing transient reversible bradycardia without a clear increase in hypotension [3]. Subsequent randomized studies have generally confirmed prolonged block duration, although effects on block onset and hemodynamics have varied according to dose and protocol [4-7].
The present study evaluated whether intravenous dexmedetomidine, administered as a loading dose followed by a low-dose maintenance infusion, was associated with changes in the onset and duration of spinal sensory and motor block and perioperative heart rate and blood pressure in adults undergoing lower-extremity orthopedic surgery.
Methods
Study design and setting
This was a single-center, randomized, controlled, parallel-group study conducted at Hospital General Nacional “Dr. Ángel Larralde” between June and August 2025. Participants were prospectively assigned to an active intravenous intervention or saline control.
Participants
Eligible participants were adults aged 18-65 years with American Society of Anesthesiologists (ASA) physical status I or II, body mass index ≤30 kg/m², scheduled for lower-extremity orthopedic procedures under spinal anesthesia, and willing to provide written informed consent. The study enrolled 25 participants using a nonprobability volunteer sample.
Exclusion criteria were refusal to participate; ASA physical status III or higher; pregnancy; first- or second-degree atrioventricular block; unexplained hypotension; conversion to or combination with another anesthetic technique; refusal of spinal anesthesia; allergy to α2-agonists; hemodynamic instability; planned surgery shorter than 1 hour or longer than 3 hours; renal disease; or abnormal coagulation testing.
Randomization and study groups
After enrollment, each participant selected a sealed envelope indicating group assignment. Twelve participants were assigned to the dexmedetomidine group (Group D) and 13 to the saline control group (Group C). The study documentation did not describe generation of the allocation sequence, allocation concealment beyond the sealed-envelope procedure, or blinding of participants, clinicians, or outcome assessors.
Anesthetic protocol
Thirty minutes before spinal anesthesia, participants received the study center's standard preanesthetic regimen: intravenous ketoprofen 100 mg, omeprazole 40 mg, dexamethasone 8 mg, metoclopramide 10 mg, and cefazolin 2 g. Baseline systolic blood pressure, diastolic blood pressure, and heart rate were recorded in the operating room.
Group D received intravenous dexmedetomidine 1 µg/kg over 10 minutes before spinal anesthesia, followed by a continuous infusion of 0.2 µg/kg/h in 0.9% saline beginning with the anesthetic technique. Group C received an equivalent-volume 0.9% saline infusion. Spinal anesthesia was performed using a midline approach with a 25-gauge Quincke needle; after confirmation of cerebrospinal fluid, 10 mg of isobaric bupivacaine was administered intrathecally. Hypotension or bradycardia could be treated with intravenous ephedrine 5-10 mg and/or atropine 0.02 mg/kg according to clinical judgment.
Outcomes and measurements
Sensory block was assessed by pinprick and motor block by the Bromage scale. Sensory and motor onset times were recorded. Sensory block duration was measured from block establishment until the first return of nociceptive sensation, and motor block duration until regression to Bromage grade I. Heart rate and systolic and diastolic blood pressure were recorded at baseline, during the spinal anesthetic technique, immediately after the subarachnoid block, 15 and 40 minutes after initiation of the study infusion, at the end of the infusion, and 40 minutes after infusion discontinuation in the post-anesthesia care unit.
Ethics
The protocol was reported as approved by the Bioethics Committee of Hospital General Nacional “Dr. Ángel Larralde.” The study was conducted in accordance with the Declaration of Helsinki and the Venezuelan Code of Ethics for Life. All participants provided written informed consent, and confidentiality was maintained through alphanumeric coding and anonymization. An ethics approval number was not provided in the source documentation.
Statistical analysis
Data were entered in Microsoft Excel and analyzed using SPSS version 22.0. Quantitative and ordinal variables were summarized as medians and minimum-maximum ranges. Between-group comparisons were performed using the Mann-Whitney U test. A two-sided p value <0.05 was considered statistically significant. No a priori sample-size calculation or multiplicity adjustment was reported.
Results
Participant characteristics
Twenty-five participants were analyzed: 12 in Group D and 13 in Group C. Each group included three women. Age was reported by sex rather than as an overall group summary (Table 1).
Table 1. Participant characteristics Characteristic Group D (n=12) Group C (n=13) Female sex, n (%) 3 (25.0) 3 (23.1) Male sex, n (%) 9 (75.0) 10 (76.9) Age among women, y, median (min-max) 37 (34-60) 30 (18-47) Age among men, y, median (min-max) 32 (19-55) 33 (20-43)
Sensory and motor block
Dexmedetomidine was associated with modestly faster sensory and motor block onset and substantially longer sensory and motor block duration (Table 2).
Table 2. Sensory and motor block characteristics Outcome Group D median (min-max) Group C median (min-max) p value Sensory block onset, min 1.0 (0.5-1.5) 1.2 (0.70-1.8) 0.040 Motor block onset, min 2.0 (1.0-3.5) 2.5 (2.0-4.0) 0.025 Sensory block duration, min 125 (75-155) 85 (55-117) <0.001 Motor block duration, min 102.5 (60-145) 65 (40-109) 0.002
Blood pressure
Blood pressure was generally lower in Group D at several post-baseline time points, but none of the between-group comparisons met the prespecified p<0.05 significance threshold. Systolic blood pressure at 40 minutes yielded p=0.050 and was treated as borderline rather than statistically significant (Table 3).
Table 3. Perioperative systolic and diastolic blood pressure Time point / parameter Group D median (min-max) Group C median (min-max) p value Baseline SBP, mmHg 130 (100-142) 121 (102-140) 0.052 Baseline DBP, mmHg 82 (65-95) 71 (62-100) 0.300 During technique SBP, mmHg 120 (105-135) 118 (100-140) 0.935 During technique DBP, mmHg 71 (62-89) 75 (60-85) 0.940 Post-spinal SBP, mmHg 108 (74-125) 115 (100-125) 0.325 Post-spinal DBP, mmHg 68.5 (44-77) 65 (50-82) 0.703 15 min SBP, mmHg 104 (69-164) 111 (98-124) 0.107 15 min DBP, mmHg 64.5 (30-107) 70 (50-80) 0.368 40 min SBP, mmHg 101.1 (92-158) 115 (100-135) 0.050 40 min DBP, mmHg 67 (52-109) 80 (61-95) 0.703 End infusion SBP, mmHg 100 (99-145) 117 (97-130) 0.075 End infusion DBP, mmHg 66.5 (55-79) 74 (47-84) 0.252 40 min post-infusion SBP, mmHg 112.5 (100-151) 120 (103-130) 0.072 40 min post-infusion DBP, mmHg 62.5 (50-80) 74 (55-90) 0.056
Heart rate
Baseline heart rate was similar between groups. Heart rate was lower in Group D at every subsequent time point; the difference during the anesthetic technique was p=0.050 and did not meet the prespecified p<0.05 threshold, while differences after the technique, at 15 and 40 minutes, at the end of infusion, and 40 minutes post-infusion were statistically significant (Table 4).
Table 4. Perioperative heart rate Time point Group D median, bpm Group C median, bpm p value Baseline 70 75 0.913 During anesthetic technique 65 75 0.050 Immediately post-spinal 62 72 0.049 15 min 62 70 0.025 40 min 60 71 0.001 End of infusion 58.5 75 0.005 40 min post-infusion 60 80 0.003
No severe hemodynamic events such as severe hypotension or cardiac arrest were reported. However, adverse events and rescue-medication use were not tabulated systematically.
Discussion
In this small randomized controlled study, intravenous dexmedetomidine added to spinal anesthesia was associated with substantially longer sensory and motor block duration and modestly faster block onset. The principal hemodynamic finding was a sustained reduction in heart rate after spinal anesthesia, whereas blood pressure differences did not meet the study’s prespecified p<0.05 threshold.
The approximately 40-minute difference in median sensory block duration and 37.5-minute difference in median motor block duration are directionally consistent with prior evidence. Abdallah et al. reported in a meta-analysis of seven randomized trials that intravenous dexmedetomidine prolonged sensory block by approximately 38% and motor block by approximately 21%, while also delaying the first request for analgesia [3]. Randomized studies by Kılıç and Aydın, Sekar et al., Thakkar et al., and Chahal et al. likewise support prolongation of spinal block or postoperative analgesic duration with intravenous dexmedetomidine [4-7].
The faster onset observed in this study should be interpreted cautiously. Sekar et al. found no significant difference in sensory or motor onset, and a 2025 randomized trial by Chahal et al. also reported similar onset times between groups [5,7]. Because the current sample included only 25 participants and tested numerous outcomes and time points without a reported multiplicity adjustment, the onset findings may be more susceptible to random variation.
The lower heart rate in the dexmedetomidine group is pharmacologically plausible. Dexmedetomidine reduces central sympathetic activity through α2-adrenoceptor agonism, and bradycardia and hypotension are recognized dose-related effects [1,2]. The 2013 meta-analysis found a 3.7-fold increase in transient reversible bradycardia with intravenous dexmedetomidine, without a significant increase in hypotension [3]. This pattern resembles the present findings, in which heart-rate differences were more consistent than blood-pressure differences.
The maintenance infusion of 0.2 µg/kg/h was relatively low compared with several later randomized protocols using 0.5 µg/kg/h [5-7]. A 2018 randomized study also used a 0.2 µg/kg/h infusion during spinal anesthesia and documented lower hemodynamic measures and improved block-related outcomes, although its protocol was not identical to the present study [4].
These findings do not establish a definitive safety advantage or justify routine adoption of dexmedetomidine for all patients undergoing spinal anesthesia. The study was small, adverse events were not systematically tabulated, and clinically important outcomes such as sedation scores, oxygen saturation, postoperative pain, opioid consumption, and time to first rescue analgesia were not reported. Larger studies with prespecified primary outcomes are needed to determine the optimal dose and the balance between prolonged block and cardiovascular effects.
Limitations
This study has several limitations. It was single-center and included only 25 volunteers without a reported a priori sample-size calculation, limiting precision and external validity. Although allocation used sealed envelopes, sequence generation, concealment procedures, and blinding were not described. Repeated between-group testing at multiple perioperative time points was performed without a reported multiplicity adjustment. The study did not provide a CONSORT-style participant flow, systematic adverse-event counts, rescue-medication use, oxygen saturation, sedation, postoperative pain, opioid consumption, or longer-term outcomes. No prospective trial-registration information was provided. In addition, some source-table values were internally inconsistent; values that could not be reconciled reliably were not reproduced in this report.
Conclusion
Among 25 ASA I-II adults undergoing lower-extremity orthopedic surgery under spinal anesthesia, intravenous dexmedetomidine 1 µg/kg followed by 0.2 µg/kg/h was associated with longer sensory and motor block duration and modestly faster block onset compared with saline. Heart rate was lower at several perioperative time points, while between-group blood pressure differences were not statistically significant under the prespecified p<0.05 threshold. Larger, prospectively registered and adequately powered trials are required before firm conclusions regarding efficacy and safety can be drawn.
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