Spinal anaesthesia has been a core component of anaesthetic practice for many decades and continues to be widely used, particularly for lower limb surgeries due to its reliability, rapid onset and favourable safety profile. The technique provides dense sensory and motor blockade along with profound intraoperative and early postoperative analgesia, making it a preferred option in a wide range of surgical procedures. A major advantage of spinal anaesthesia is that it requires only a small volume of local anaesthetic to achieve significant neuraxial blockade, resulting in minimal systemic absorption and reduced risk of systemic toxicity. In contrast, epidural anaesthesia demands larger doses of local anaesthetic, creating pharmacologically active systemic blood concentrations that may contribute to adverse effects and complications less commonly observed with spinal techniques (1). Among local anaesthetic agents, 0.5% hyperbaric bupivacaine is one of the most established drugs for spinal anaesthesia because of its predictable spread in cerebrospinal fluid and ability to provide adequate surgical anaesthesia. Despite its efficacy, when used alone it offers a limited duration of postoperative analgesia, necessitating early analgesic intervention and contributing to patient discomfort in the postoperative period. To overcome this limitation, numerous intrathecal adjuvants have been studied to enhance the quality, duration, and comfort of spinal anaesthesia, including opioids, midazolam, neostigmine, sodium bicarbonate, hyaluronidase and α-2 adrenergic agonists (2). Among these adjuvants, α-2 adrenergic receptor agonists have shown particular promise due to their synergistic effects when combined with local anaesthetics. Clonidine, the earlier agent in this class, has been demonstrated to prolong both sensory and motor blockade when co-administered with local anaesthetics (3). Dexmedetomidine, a newer α-2 adrenergic agonist and the active dextro-isomer of medetomidine, is significantly more selective and potent at α-2 receptors compared to Clonidine. It was approved by the FDA in 1999 for sedation and analgesia, and has since been increasingly explored for neuraxial use in anaesthesia due to its favourable pharmacodynamic profile (4). Experimental studies in animal models have confirmed that Dexmedetomidine produces robust antinociceptive effects when administered systemically, intrathecally, epidurally or directly into the locus coeruleus (5, 6). The mechanism of its intrathecal action is believed to involve inhibition of neurotransmitter release from C-fibers and hyperpolarization of post-synaptic dorsal horn neurons. In addition, prolongation of motor block may result from suppression of excitatory amino acid release from spinal interneurons (7). Clinically, the drug has demonstrated the ability to reduce both anaesthetic and analgesic requirements, accelerate the onset of spinal blockade, and significantly extend the duration of sensory and motor block in a dose-dependent manner (8), making it a promising adjuvant for neuraxial anaesthesia. Given this background, the present study is undertaken to evaluate the clinical profile of two intrathecal doses of Dexmedetomidine (5 μg and 10 μg) when combined with 0.5% hyperbaric Bupivacaine in patients undergoing lower limb surgeries. By comparing their effects on onset and duration of block, hemodynamic stability, sedation profile, postoperative analgesia and adverse events, the study aims to determine the optimal dose that balances efficacy and safety in the perioperative setting.

This prospective, randomized, double-blind comparative study was conducted at Bapuji hospital attached to JJM medical College, Davangere, Karnataka from June 2022 to may 2023. Sixty patients aged 18–60 years scheduled for elective lower limb surgeries under spinal anaesthesia were enrolled and randomized into two equal groups (n=30 each). Inclusion Criteria ASA physical status I and II patients of either sex, undergoing elective lower limb surgeries under spinal anaesthesia. Exclusion Criteria Refusal to participate, contraindications to spinal anaesthesia/local anaesthetics, neurological or coagulation disorders, hypotension, BMI >30, emotional instability, anticipated difficulty in regional anaesthesia, history of CAD post-PTCA/CABG, receipt of general anaesthesia within 24 hours preoperatively, or procedures planned under combined spinal-epidural anaesthesia. Randomization and Blinding Randomization was done using computer-generated allocation. Both participants and investigators were blinded: one clinician administered the drug, while another recorded outcomes independently. Interventions All patients received intrathecal 0.5% hyperbaric Bupivacaine (15 mg, 3 ml) combined with either: • Group A: Dexmedetomidine 5 μg (0.5 ml) • Group B: Dexmedetomidine 10 μg (0.5 ml) Total intrathecal volume was 3.5 ml in both groups. Anaesthesia Technique Standard preoperative assessment was performed. In the operating room, ECG, NIBP, and pulse oximeter were applied, IV access secured, and baseline vitals recorded. Patients received IV Ringer’s lactate and Ondansetron 0.1 mg/kg. Spinal anaesthesia was administered at L3–L4 in sitting position using a 25G Quincke needle. After confirming free CSF flow, the study drug was injected and patients positioned supine. Oxygen was supplemented when needed. Monitoring of HR, MAP, SpO₂, and Ramsay sedation score was done at frequent intervals intraoperatively and in recovery. Outcome Measures Block Characteristics • Sensory block: Time to loss of pinprick at T10; maximum block height; time to regression to L1. • Motor block: Assessed by Bromage scale; time to Grade 3 and complete recovery. Hemodynamic Parameters Bradycardia (HR <50 bpm) was treated with IV Atropine; hypotension (MAP <60 mmHg or >40% fall from baseline) with IV Mephentermine and fluids¹⁶. Sedation and Analgesia Sedation assessed using Ramsay scale²⁴. Postoperative pain was monitored using VAS; rescue analgesia (VAS ≥6) was given as IV Diclofenac 1.5 mg/kg. Total analgesic doses over 24 hours were recorded. Adverse Effects Nausea, vomiting, oxygen desaturation (<95%), and other complications were documented. Statistical Analysis Data were analyzed using SPSS version 20. Quantitative variables were expressed as mean ± SD and compared using Student’s t-test; categorical data were compared using Chi-square test. Time-dependent variables were assessed using ANOVA. p<0.05 was considered statistically significant.

Table 1: Demographic Characteristics and Sex Distribution of Study Participants Parameter Group A (n=30) Group B (n=30) p-value Age (years) 39.47 ± 12.93 39.57 ± 11.62 0.975 Height (cm) 160.73 ± 8.48 159.70 ± 5.02 0.568 Weight (kg) 59.17 ± 6.29 59.13 ± 4.52 0.981 Sex (Total n=60) Female, n (%) 31 (51.7) — — Male, n (%) 29 (48.3) — — Both groups were comparable with respect to baseline demographic characteristics. The mean age of participants was similar in Group A (39.47 ± 12.93 years) and Group B (39.57 ± 11.62 years), with no statistically significant difference (p = 0.975). Mean height and weight were also comparable between the groups (160.73 ± 8.48 cm vs. 159.70 ± 5.02 cm, p = 0.568; 59.17 ± 6.29 kg vs. 59.13 ± 4.52 kg, p = 0.981). The study population consisted of 51.7% females (n = 31) and 48.3% males (n = 29). Overall, both groups were demographically homogeneous, eliminating baseline differences as confounding variables (Table 1). Table 2: Preoperative Baseline Parameters Parameter Group A (n=30) Mean ± SD Group B (n=30) Mean ± SD p-value Heart Rate (beats/min) 75.83 ± 10.39 77.87 ± 14.68 0.538 MAP (mmHg) 77.97 ± 9.77 79.80 ± 9.22 0.458 SpO₂ (%) 98.97 ± 1.16 98.53 ± 1.43 0.203 Ramsay Sedation Score (RSS) 2.03 ± 0.32 2.10 ± 0.31 0.412 VAS Score 2.87 ± 2.16 3.00 ± 2.15 0.812 Preoperative baseline characteristics, including heart rate, mean arterial pressure, oxygen saturation, sedation scores and pain scores, were comparable between the two groups. The mean heart rate was 75.83 ± 10.39 beats/min in Group A and 77.87 ± 14.68 beats/min in Group B (p = 0.538), while MAP values were 77.97 ± 9.77 mmHg and 79.80 ± 9.22 mmHg respectively (p = 0.458). SpO₂ levels and Ramsay Sedation Scores showed no significant differences between groups (p > 0.05). Preoperative VAS scores were also similar (2.87 ± 2.16 vs. 3.00 ± 2.15, p = 0.812). These findings confirm that both groups were hemodynamically and symptomatically comparable before induction of spinal anaesthesia (Table 2). Table 3: Time to Sensory and Motor Blockade Parameter Group A (n=30) Mean ± SD Group B (n=30) Mean ± SD p-value Onset time to T10 (min) 4.05 ± 0.60 3.56 ± 0.26 0.0001 Time to achieve maximum block height (min) 4.62 ± 0.77 4.28 ± 0.37 0.037 Time to Bromage score 3 (min) 3.74 ± 0.41 3.36 ± 0.29 0.0001 Time to regression to L1 (min) 361.33 ± 54.20 448.33 ± 40.61 0.0001 Time to complete motor recovery (Bromage 0) (min) 464.00 ± 58.82 502.00 ± 40.12 0.005 The onset of sensory and motor blockade was significantly faster in the 10 µg Dexmedetomidine group. The time to achieve sensory block at T10 was 4.05 ± 0.60 minutes in Group A and 3.56 ± 0.26 minutes in Group B (p = 0.0001), while the time to reach complete motor block (Bromage 3) was 3.74 ± 0.41 minutes and 3.36 ± 0.29 minutes respectively (p = 0.0001). Although both groups achieved comparable maximum block height, the time to peak level was slightly shorter in Group B (p = 0.037). The duration of sensory block, measured by regression to L1, was significantly prolonged in Group B (448.33 ± 40.61 min) compared to Group A (361.33 ± 54.20 min), and a similar prolongation was observed for motor recovery (502.00 ± 40.12 min vs. 464.00 ± 58.82 min, p = 0.005). These findings indicate a clear dose-dependent enhancement in block onset and duration with 10 µg Dexmedetomidine (Table 3) Figure 1: Maximum Height of Block The maximum cephalad spread of sensory block was comparable between the two groups. Most patients achieved a block height of T8, accounting for 35% of the total sample, followed by T6 in 31.7% and T10 in 30% of patients. Only two patients (one in each group) reached a block level of T5. No significant difference was observed between Group A and Group B in terms of maximum block height, indicating that increasing Dexmedetomidine from 5 µg to 10 µg did not influence the cephalad spread of sensory blockade. Statistical test: χ² = 1.967, df = 3, p = 0.579 (Figure 1). Table 4: Time to Regression of Sensory and Motor Blockade Parameter Group A (n=30) Mean ± SD Group B (n=30) Mean p-value Regression to L1 dermatome (min) 361.33 448.33 0.0001 Time to complete motor recovery (Bromage 0) (min) 464.00 502.00 0.005 The duration of both sensory and motor blockade was significantly longer in the group receiving 10 µg Dexmedetomidine. Sensory regression to the L1 dermatome occurred at 361.33 minutes in Group A compared to 448.33 minutes in Group B (p = 0.0001). Similarly, motor recovery to Bromage score 0 was achieved earlier in Group A (464.00 minutes) than in Group B (502.00 minutes) (p = 0.005). These findings indicate that increasing the Dexmedetomidine dose prolongs the duration of spinal block in a dose-dependent manner (Table 4). Table 5: Comparison of Pre-operative Hemodynamic and Sedation Parameters Between Groups Parameter Key Time Intervals Group A (Mean ± SD) Group B (Mean ± SD) p-value Heart Rate (beats/min) 3 min 72.10 ± 9.83 65.53 ± 13.86 0.039 5 min 71.40 ± 10.22 61.87 ± 16.45 0.009 10 min 71.57 ± 10.29 63.50 ± 15.14 0.019 Later (20–120 min) Similar values Similar values >0.05 MAP (mmHg) 4 min 72.93 ± 9.17 65.93 ± 13.71 0.024 5 min 74.13 ± 9.01 67.03 ± 14.41 0.026 Later (15–120 min) Comparable Comparable >0.05 SpO₂ (%) 3 min 99.67 ± 0.55 99.10 ± 0.89 0.004 Other time points Comparable Comparable >0.05 Sedation Score (RSS) 1–5 min 2.03 ± 0.18 2.03–2.17 >0.05 10–15 min 2.00 2.00 — 20–120 min Comparable Comparable >0.05 Both groups demonstrated stable intraoperative vital parameters overall, with notable transient differences during the initial minutes following spinal anaesthesia. Group B showed a significantly greater fall in heart rate at 3, 5, and 10 minutes compared to Group A (p < 0.05), while values converged thereafter and remained comparable until 120 minutes. A similar early decline was observed in mean arterial pressure, with significantly lower MAP in Group B at 4 and 5 minutes (p < 0.05), followed by comparable readings later in surgery. Oxygen saturation remained clinically stable in both groups, although a statistically significant but clinically insignificant decrease was observed in Group B at 3 minutes (p < 0.05). Sedation scores were similar between groups throughout, with no meaningful difference in clinical sedation depth. Overall, these findings suggest a dose-dependent transient hemodynamic depression with 10 µg Dexmedetomidine during early intrathecal action, without sustained adverse effects (Table 5). Post-operative vital parameters remained largely comparable between the two groups throughout the observation period. Heart rate and mean arterial pressure showed no statistically significant differences at any time interval (p > 0.05), indicating stable hemodynamics following recovery from spinal blockade in both groups. Oxygen saturation remained within normal limits for all patients; however, a statistically significant reduction was observed in Group B at 1 hour (p = 0.002), though this did not translate into clinically relevant desaturation. Sedation scores were slightly higher in Group B during the early postoperative period (1–2 hours, p < 0.05), but both groups demonstrated similar levels of alertness from the fourth postoperative hour onwards. Overall, postoperative monitoring showed stable cardiopulmonary profiles in both groups, with only mild and transient differences that were not clinically significant (Table 6). Table 6: Comparison of Post-operative Hemodynamic and Sedation Parameters Between Groups Parameter Key Time Points Group A (Mean ± SD) Group B (Mean ± SD) p-value Heart Rate (beats/min) 30 min 75.93 ± 8.84 74.83 ± 12.39 0.694 2 hours 75.53 ± 13.28 76.70 ± 10.09 0.703 4 hours 79.87 ± 8.73 74.93 ± 11.50 0.068 8 hours 77.07 ± 10.74 75.47 ± 11.99 0.588 MAP (mmHg) 30 min 76.80 ± 9.46 77.30 ± 8.51 0.830 2 hours 77.37 ± 8.81 77.53 ± 8.16 0.940 8 hours 77.80 ± 8.89 77.80 ± 8.43 0.893 SpO₂ (%) 1 hour 99.77 ± 0.50 99.23 ± 0.77 0.002 6 hours 99.83 ± 0.38 99.63 ± 0.73 0.051 8 hours 99.87 ± 0.35 99.87 ± 0.35 1.000 Sedation Score (RSS) 1 hour 2.07 ± 0.25 2.30 ± 0.49 0.019 2 hours 2.03 ± 0.18 2.23 ± 0.43 0.023 4–8 hours ~2.0 ~2.0 >0.05 Table 7: Summary of Heart Rate Variation Between Groups Phase Comparison Result p-value Range Baseline (Pre-op) No significant difference >0.05 Early intra-operative (0–10 min) Significant difference at multiple points 0.000–0.04 Mid intra-operative (10–60 min) Significant differences noted intermittently 0.001–0.05 Late intra-operative (60–120 min) Persistent significant differences 0.000–0.02 Immediate post-op (0–2 hrs) Significant variations 0.003–0.02 Late post-op (4–8 hrs) Some significant findings 0.002–0.04 Overall effect Significant difference across majority of time points <0.05 Overall analysis demonstrated a significant dose-dependent reduction in heart rate with 10 µg Dexmedetomidine when compared to 5 µg across most perioperative time points. While baseline pre-operative values were comparable (p > 0.05), a marked fall was observed during the early intra-operative period (0–10 minutes) with statistically significant differences at multiple intervals. Significant variations continued intermittently throughout the mid and late intra-operative phases (p-values ranging from 0.000–0.05). This trend extended into the immediate postoperative period (0–2 hours) and persisted to a lesser extent up to 8 hours postoperatively. These findings suggest that higher-dose Dexmedetomidine produces sustained bradycardic effects across the perioperative period (Table 7). Table 8: Summary of MAP Variation Between Groups (ANOVA Results) Phase MAP Comparison p-value Range Baseline (Pre-op) No significant difference >0.05 Early intra-operative (1–10 min) Significant reduction in MAP noted 0.000–0.01 Mid intra-operative (10–60 min) Multiple significant points 0.000–0.01 Late intra-operative (60–120 min) Persistent significant differences 0.000–0.02 Immediate post-op (0–2 hrs) Significant differences 0.000–0.01 Late post-op (4–8 hrs) Significant differences remain 0.000–0.01 Overall effect Significant difference across majority of time points <0.05 Mean arterial pressure remained comparable between groups at baseline (p > 0.05), but a significant dose-dependent reduction was observed following administration of intrathecal Dexmedetomidine. The decrease in MAP was evident as early as 1–10 minutes after spinal anaesthesia and continued across mid and late intra-operative phases (p = 0.000–0.02). This trend persisted into both the immediate (0–2 hours) and late postoperative period (4–8 hours), with consistently lower MAP values in the 10 µg group. Overall, analysis demonstrated a sustained and statistically significant reduction in MAP across most time intervals in patients receiving 10 µg Dexmedetomidine, indicating greater hemodynamic depression at higher doses (Table 8). Table 9: Post-operative Analgesia, IV Fluids, Transfusion & Oxygen Requirement Parameter Group A (n=30) Mean / n Group B (n=30) Mean / n Total (n=60) p-value Time to first post-operative analgesic requirement (min) 368.50 ± 55.18 437.87 ± 48.29 – 0.0001 Total analgesic doses in first 24 hrs 1.73 ± 0.58 1.23 ± 0.43 – 0.0001 Total IV fluids administered intraoperatively (ml) 2140.00 ± 288.40 2503.33 ± 436.69 – 0.0001 Blood transfusion required (Yes) 1 2 3 1.000 No blood transfusion 29 28 57 – Oxygen administered (Yes) 1 20 21 0.0001 No oxygen required 29 10 39 – Patients who received 10 µg Dexmedetomidine demonstrated significantly prolonged postoperative analgesia, with a longer time to first rescue analgesic requirement (437.87 ± 48.29 min vs. 368.50 ± 55.18 min, p = 0.0001) and fewer total analgesic doses within the first 24 hours (1.23 ± 0.43 vs. 1.73 ± 0.58, p = 0.0001). However, this dose was associated with higher intraoperative fluid requirement (2503.33 ± 436.69 ml vs. 2140 ± 288.40 ml, p = 0.0001) and a markedly greater need for oxygen supplementation (20 vs. 1 patients, p = 0.0001). Blood transfusion requirements were similar between groups, with no statistically significant difference (p = 1.000). These results suggest that while 10 µg provides superior analgesic benefits, it is also linked to increased physiological support requirements. Table 10: Incidence of Bradycardia, Hypotension, Nausea & Vomiting Parameter Group A (n=30) Group B (n=30) Total (n=60) p-value Bradycardia – Yes 1 15 16 0.0001 Bradycardia – No 29 15 44 – Hypotension – Yes 1 12 13 0.001 Hypotension – No 29 18 47 – Nausea/Vomiting – Yes 1 3 4 0.612 Nausea/Vomiting – No 29 27 56 – A significantly higher incidence of bradycardia and hypotension was observed in the group receiving 10 µg Dexmedetomidine. Bradycardia occurred in 15 patients in Group B compared to only one patient in Group A (p = 0.0001), while hypotension occurred in 12 patients in Group B versus one patient in Group A (p = 0.001). In contrast, nausea and vomiting were infrequent in both groups and showed no statistically significant difference (p = 0.612). These findings suggest that higher doses of intrathecal Dexmedetomidine are associated with increased hemodynamic instability, whereas gastrointestinal adverse effects remain minimal and comparable between doses (Table 10).

Dexmedetomidine has gained increasing interest as an intrathecal adjuvant to 0.5% hyperbaric bupivacaine for lower limb surgeries due to its ability to enhance block quality and prolong postoperative analgesia while reducing anesthetic requirements. However, the optimal intrathecal dose that balances efficacy and hemodynamic stability remains unclear. The present prospective, randomized, double-blind study compares 5 µg versus 10 µg intrathecal dexmedetomidine to determine a clinically effective and safer dose. A total of 60 ASA I–II patients undergoing elective lower limb surgeries were randomized into two groups: Group A received 15 mg (3 ml) 0.5% hyperbaric bupivacaine + 5 µg Dex, while Group B received 15 mg (3 ml) 0.5% hyperbaric bupivacaine + 10 µg Dex. Both groups were comparable in demographic characteristics, including age, gender, height and weight (p > 0.05). Similar demographic comparability has been reported by Yektas A et al (9). Group B demonstrated a significantly faster onset of both sensory and motor block compared to Group A (p < 0.05). These findings align with Naaz et al. (10) who also reported dose-dependent acceleration in block onset with higher Dex doses. Differences in absolute onset times across studies may be attributed to variations in bupivacaine volume (12.5 mg vs 15 mg) and procedural factors. Both groups predominantly achieved a maximum sensory level of T8, with no significant intergroup differences (p > 0.05), suggesting that increasing Dex from 5 to 10 µg does not influence cephalad spread. Similar observations were reported by Bansal P et al (11). Regression time to L1 and motor recovery were significantly prolonged in Group B compared to Group A (p < 0.05), confirming dose-dependent prolongation of spinal analgesia. Consistent findings have been reported by Solanki S et al (12). Higher doses prolong block due to enhanced α2-mediated inhibition of nociceptive transmission and hyperpolarization of dorsal horn neurons. A significant dose-dependent fall in heart rate and mean arterial pressure was observed, most pronounced during the first 10 minutes after intrathecal administration. Bradycardia: Group B (15 patients) vs Group A (1 patient), p < 0.05. Hypotension: Group B (12 patients) vs Group A (1 patient), p < 0.05. This sympatholytic effect is well-documented and attributed to presynaptic α2-activation and reduced norepinephrine release. Similar dose-dependent hypotension and bradycardia were observed by Gupta M et al (13). Group B required significantly more pharmacological intervention with atropine and mephentermine, as well as supplemental oxygen. This correlates with higher incidence of bradycardia and hypotension. Comparable findings were reported by Gupta et al (13). Sedation scores remained comparable between groups with no clinically significant sedation. SpO₂ remained stable and within normal limits in all patients, consistent with Koolwal et al (14), confirming that intrathecal Dex does not cause respiratory depression at doses of 5–10 µg. Group B had a significantly prolonged duration before first rescue analgesia and required fewer total analgesic doses in 24 hours (p < 0.05). These results support the strong analgesic role of Dex, consistent with Mahendru et al (15). Although blood transfusion requirements were similar between groups, Group B required significantly higher intraoperative IV fluid administration. This likely reflects the increased incidence of hypotension in Group B. These findings partially correlate with Al Mustafa et al., though their study did not reach statistical significance due to shorter surgical duration and different surgical population. Adverse effects like Nausea and vomiting occurred infrequently and did not differ significantly between groups (p > 0.05), consistent with Al-Ghanem et al (16).

Intrathecal dexmedetomidine, when used as an adjuvant to 0.5% hyperbaric bupivacaine, enhances the onset and duration of sensory and motor blockade and provides prolonged postoperative analgesia. Although both 5 µg and 10 µg doses improved analgesic outcomes, the 10 µg dose was associated with a higher incidence of bradycardia, hypotension, need for oxygen supplementation and vasopressor support. Considering the balance between efficacy and hemodynamic stability, 5 µg appears to be the more suitable dose for routine clinical use in elective lower limb surgeries. Further studies in higher-risk populations and larger sample sizes are warranted. RECOMMENDATIONS Intrathecal dexmedetomidine is an effective adjuvant to hyperbaric bupivacaine for lower limb surgeries, enhancing block onset, prolonging analgesia, and reducing postoperative analgesic requirements. Based on better hemodynamic stability and fewer adverse events, 5 µg appears to be the safer and more balanced dose when compared to 10 µg. LIMITATIONS • Higher ASA grades were excluded; safety in high-risk cardiovascular patients remains uncertain. • No control group receiving bupivacaine alone was included. • Dexmedetomidine is costlier and less widely available compared to other adjuvants. • Intrathecal use remains off-label and not FDA-approved, warranting further large-scale trials.

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