Scalp block has emerged as a highly effective technique for providing perioperative anesthesia and analgesia in neurosurgical and certain extracranial procedures. It has gained widespread acceptance among anesthesiologists due to its efficacy in maintaining hemodynamic stability and minimizing the need for systemic analgesics1. Initially used primarily for patients at high risk for general anesthesia, the indications for scalp block have now expanded significantly. Presently, it is employed both as a supplement to general anesthesia and as a sole anesthetic technique in procedures performed under sedation, such as burr hole surgeries, craniotomies, and awake craniotomies.2 It also finds application in chronic headache management and minor scalp procedures. By providing excellent pain control, scalp block reduces sympathetic stimulation, thereby preventing fluctuations in blood pressure and heart rate—crucial factors in neurosurgical patients, where hemodynamic instability may adversely influence intracranial pressure and cerebral perfusion3.Pain, often referred to as the “fifth vital sign,” remains a major concern following neurosurgical interventions. Conventionally, postoperative pain is managed using systemic agents like opioids and NSAIDs, along with local techniques such as infiltration or regional blocks4. However, opioids, despite their potent analgesic effect, are associated with multiple side effects including nausea, vomiting, respiratory depression, sedation, and delayed recovery. Their use in neurosurgical patients is further limited due to their potential to cause hyperalgesia and possible association with tumor angiogenesis and recurrence in brain tumor cases. NSAIDs, though effective, are also avoided in such settings because of their tendency to increase the risk of postoperative bleeding, which may have serious neurological consequences5.Local anesthetics such as bupivacaine offer an attractive alternative, providing safe and long-lasting analgesia by blocking sodium channels and thereby preventing the propagation of nerve impulses. Bupivacaine’s high potency and prolonged duration of action make it an ideal agent for scalp block6. Regional anesthesia with bupivacaine ensures targeted pain control, minimizes systemic adverse effects, and facilitates early recovery. Moreover, scalp block during cranial surgeries effectively blunts the sympathetic surge induced by scalp incision, preventing sudden increases in intracranial pressure. To prolong the duration and improve the quality of local anesthesia, several adjuvants have been studied, including opioids, alpha-2 agonists, vasoconstrictors, steroids, and other agents. Among these, dexmedetomidine—a highly selective alpha-2 adrenergic agonist—has shown great promise due to its analgesic, sedative, and anesthetic-sparing effects.7,8 When added to bupivacaine, dexmedetomidine enhances the depth and duration of analgesia, reduces pain transmission, and provides sedation without respiratory depression. Recent studies suggest that scalp block using bupivacaine with dexmedetomidine offers superior intraoperative anesthesia, prolonged postoperative pain relief, and marked opioid-sparing effects. AIM To assess the effect of scalp block using Dexmedetomidine as an adjuvant with Bupivacaine (0.5%) under sedation with Dexmedetomidine for Burr hole surgery patients.

This study is a prospective randomized controlled trial conducted in the Department of Anesthesiology, Sardar Patel Medical College and Associated Group of Hospitals, Bikaner. The study was initiated after obtaining approval from the Institutional Ethical Committee and written informed consent from all participating patients. It was designed as a hospital-based prospective study and carried out over a period of one and a half years, from August 2023 to March 2025. The study population comprised patients aged between 18 and 70 years who were scheduled to undergo elective or emergency burr hole surgery. Participants had a body mass index (BMI) between 18 and 30 kg/m² and belonged to the American Society of Anesthesiologists (ASA) physical status grade I or II, ensuring inclusion of patients who were either healthy or had only mild systemic disease. Patients were excluded from the study if they refused to participate or had a known allergy to any of the drugs used in the study protocol. Patients with hepatic, renal, or cardiorespiratory failure were not included due to potential risks associated with drug metabolism and anesthesia. Individuals undergoing emergency procedures, those unable to understand or communicate using the Modified Behavioural Pain Score (MBPS), or those scheduled for postoperative sedation were also excluded from participation. Furthermore, patients with a history of previous craniotomy incision were excluded to avoid confounding factors related to altered scalp innervation or scar tissue sensitivity.

Table 1: Comparison of mean age between the two groups. (N = 20) Age of the patient in years Mean (SD) p-value Group D (N = 20) Group B (N = 20) 58.35 (19.52) 61.25 (15.77) 0.608 The table compares the mean age of patients in two groups, Group D and Group B, with each group having 20 patients (N = 20). The mean age for Group D is 58.35 years with a standard deviation (SD) of 19.52, while the mean age for Group B is 61.25 years with a standard deviation of 15.77. The p-value of 0.608 suggests that there is no statistically significant difference in the mean age between the two groups. Table 2: Comparison of mean anthropometric measurements and ASA grade of the patient in two groups. (N = 20) Anthropometric measurements Mean (SD) p-value Group D (N = 20) Group B (N = 20) Height in cm 169.25 (7.69) 170.7 (6.52) 0.524 Weight in Kg 70.8 (6) 72 (7.62) 0.584 BMI in Kg/sqm 24.77 (2.21) 24.7 (2.23) 0.925 ASA grade Grade I 17 (85%) 14 (70%) 0.256 Grade II 3 (15%) 6 (30%) The table compares anthropometric parameters and ASA grade distribution between Group D and Group B (N = 20 each). Both groups show similar mean height, weight, and BMI values, with no statistically significant differences (p > 0.05). ASA grading also shows comparable distribution, with most patients in Grade I and few in Grade II. Overall, the groups are demographically and clinically comparable, indicating baseline homogeneity. Table 3: Comparison of mean heart rate between the two groups. (N = 20) Heart rate (bpm) Mean (SD) p-value Group D (N = 20) Group B (N = 20) T0 81.0 (6.32) 82.25 (7.08) 0.559 T1 64.35 (4.44) 67.25 (4.84) 0.056 T2 62.05 (2.21) 64.9 (1.55) <0.001 T3 62.55 (2.09) 66 (2.58) <0.001 T4 62 (2.45) 66.9 (3.84) <0.001 T5 62.55 (2.56) 66.25 (3.31) <0.001 T6 63 (2.34) 68.8 (2.19) <0.001 T7 62.55 (3.58) 68.30 (2.90) <0.001 T8 62.7 (3.47) 66.8 (4.56) 0.003 T9 62.05 (3.73) 68.9 (5.47) <0.001 The table compares mean heart rates between Group D and Group B (N = 20 each) across time points T0–T9. Baseline heart rates were comparable (p = 0.559), while at T1 the difference approached significance (p = 0.056). From T2 onward, Group D consistently demonstrated significantly lower heart rates (p < 0.05, many < 0.001), indicating better heart rate control compared to Group B. The tables compare systolic and diastolic blood pressure (SBP and DBP) between Group D and Group B (N = 20 each) across time points T0–T9. At baseline (T0), both groups showed similar SBP (p = 0.596) and DBP (p = 0.631). From T1 to T6, Group D consistently exhibited significantly lower SBP than Group B, with highly significant differences at T1, T2, T4, T5 (p < 0.001), and T6 (p = 0.001), while T3 showed a near-significant difference due to a transient rise during surgical incision. From T7 to T9, SBP differences diminished and became non-significant (p > 0.05), suggesting stabilization of blood pressure in both groups. Throughout the study, DBP values remained comparable between the two groups, indicating that Group D mainly influenced systolic rather than diastolic blood pressure. Table 4: Comparison of median MBPS between the two groups. (N = 20) MBPS Mean (SD) p-value Group D (N = 20) Group B (N = 20) T3 3.25 (0.44) 4.20(0.77) <0.001 T4 3.05 (0.22) 3.40 (0.50) 0.007 T5 3.15 (0.37) 3.40(0.50) 0.080 T6 3.05 (0.22) 3.25 (0.44) 0.077 T7 3.10 (0.31) 3.30 (0.47) 0.120 T8 3.05 (0.22) 3.35 (0.49) 0.017 T9 3.05 (0.22) 3.40 (0.50) 0.007 The table compares MBPS scores between Group D and Group B (N = 20 each) from T3 to T9, showing consistently lower scores in Group D, indicating better pain control. Statistically significant differences favoring Group D were observed at T3, T4, T8, and T9, reflecting both earlier onset and prolonged analgesic action. Overall, Group D demonstrated superior and sustained pain relief compared to Group B throughout the observation period. Table 5: Distribution of cases according to sedation score of the patient in two groups. (N = 20) Sedation score Median (IQR) p-value Group D (N = 20) Group B (N = 20) T0 5.15 (0.81) 4.90(0.72) 0.305 T1 1.55 (0.69) 1.95 (0.51) 0.042 T2 0.1 (0.3) 1.6 (0.5) <0.001 T3 0.15 (0.37) 1.2 (0.41) <0.001 T4 0.3 (0.47) 1.1 (0.45) <0.001 T5 0.35 (0.49) 1.1 (0.45) <0.001 T6 0.40 (0.50) 1.1 (0.55) <0.001 T7 0.50 (0.51) 1.1 (0.44) <0.001 T8 0.85 (0.58) 1.2 (0.41) <0.001 T9 1.05 (0.76) 1.4 (0.50) 0.093 The table presents a comparison of sedation scores between Group D and Group B (N = 20 each) at different time intervals (T0–T9). At baseline (T0), there was no significant difference between the groups (p = 0.305). However, from T1 to T8, Group D consistently demonstrated significantly lower sedation scores (p < 0.05 to < 0.001), indicating deeper and more sustained sedation compared to Group B. By T9, the difference was no longer significant (p = 0.093), suggesting that sedation levels in both groups eventually equalized over time. Table 6: Comparison of mean duration of effective analgesia and mean number of rescue analgesics given in the first 24 hours between the two groups. (N = 20) Duration of effective analgesia in hours Mean (SD) p-value Group D (N = 20) Group B (N = 20) 16.2 (0.41) 9.2 (1.06) <0.001 Number of rescue analgesics given in first 24 hours 1.10 (0.31) 1.4 (0.5) 0.0283 The table compares the mean duration of effective analgesia and the number of rescue analgesics between Group D and Group B (N = 20 each). Group D showed a significantly longer duration of analgesia (16.2 ± 0.41 hours) compared to Group B (9.2 ± 1.06 hours, p < 0.001). Additionally, Group D required fewer rescue analgesics within 24 hours (1.10 ± 0.31) than Group B (1.4 ± 0.5), with this difference also being statistically significant (p = 0.0283). Table 7: Distribution of cases according to side effects and complications in two groups. (N = 20) Side effects and complications Group D (N = 20) Group B (N = 20) p-value Bradycardia 3 (15%) 0 (0%) 0.133 Hypotension 1 (5%) 3 (15%) None 16 (80%) 17 (85%) The table shows that bradycardia occurred in 15% of patients in Group D and none in Group B, while hypotension was seen in 5% and 15% respectively. Most patients in both groups had no complications, and the difference in bradycardia incidence between groups was not statistically significant (p = 0.133).

The two groups in this study were comparable in baseline characteristics. The mean age for Group D was 58.35 years, while Group B had a mean of 61.25 years (p = 0.608), indicating no statistically significant age difference. Furthermore, the ASA physical status classification was predominantly Grade I in both groups, ensuring comparability in physical fitness preoperatively. Both groups remained hemodynamically stable. Group D exhibited lower heart rates than Group B from T2 through T9 (p < 0.001). This bradycardic effect is consistent with dexmedetomidine's known pharmacological profile, which includes sympatholytic properties leading to reduced HR. Systolic blood pressure (SBP) and mean arterial pressure (MAP) also followed a similar trend. Group D had significantly lower SBP compared to Group B (p < 0.001 at several time points). A randomized trial by Bekker et al [2008]9 demonstrated that dexmedetomidine minimized the hemodynamic surges during craniotomy pin insertion. Pain management outcomes were distinctly superior in Group D. The duration of effective analgesia was significantly longer—16.2 hours versus 9.2 hours in Group B (p < 0.001). Modified Behavioral Pain Scale (MBPS) scores were significantly lower in Group D at most measured intervals, particularly from T3 to T9, with the most notable difference at T3 (3.25 vs. 4.2, p < 0.001). While both groups received bupivacaine, the earlier onset, extended analgesia and lower pain scores in Group D are attributable to the addition of dexmedetomidine, these findings suggest that Group D experienced earlier onset and prolonged duration of effective analgesia, as evidenced by lower pain scores across multiple time points. Therefore, Group D demonstrated superior pain control indicating favorable recovery profile compared to Group B. Furthermore, a study by Marhofer et al [2013]10 highlighted that dexmedetomidine has both central and peripheral actions that potentiate the analgesic effect of local anesthetics. Patients in Group D required significantly fewer rescue analgesics in the first 24 hours following surgery compared to those in Group B(p value < 0.001). This suggests that Group D experienced better postoperative pain control, likely due to the enhanced analgesic effect provided by the addition of dexmedetomidine in the scalp block. The reduction in the need for supplemental pain medications reinforces the superior analgesic efficacy of the regimen used in Group D. A study by Zhang et al[2023]11 also reported reduced analgesic consumption when dexmedetomidine was used as an adjuvant in axillary brachial plexus blocks . A remarkable finding in this study was the deeper sedation levels observed in Group D, evident from significantly lower sedation scores from T1 to T8 (all p < 0.05). At T2, for instance, Group D recorded a mean score of 0.1 compared to 1.6 in Group B (p < 0.001). This pattern continued consistently until T8. The scores began to converge by T9 (p = 0.093), likely reflecting the waning pharmacodynamic effect of dexmedetomidine. Dexmedetomidine’s sedative action results from its α2-adrenergic receptor agonism, particularly affecting the locus coeruleus, a key brainstem area regulating arousal. Unlike other sedatives, it provides "cooperative sedation," where patients remain arousable and communicative—a significant advantage in neurosurgical settings. This characteristic has been widely discussed in trials including those by Raimann FJ et al [2002]12, where patients undergoing awake craniotomies were reported to tolerate procedures better when dexmedetomidine was included. Adverse events were relatively low in both groups, with Group D reporting three cases of bradycardia (15%) and one case of hypotension (5%). In contrast, Group B had three instances of hypotension (15%) but no bradycardia. While these events were not statistically significant, they are consistent with the known profile of dexmedetomidine, which can cause bradycardia due to Vago mimetic effects. The hemodynamic changes seen in this study did not lead to significant morbidity and were effectively handled, supporting the safety of dexmedetomidine in scalp block protocols. Moreover, the fact that the majority of patients in both groups experienced no side effects (80% in Group D and 85% in Group B) supports the overall safety and tolerability of scalp block techniques in this setting.

This study evaluated the effectiveness of using scalp block with dexmedetomidine as the sole anesthetic technique in patients undergoing burr hole surgery. We concluded that addition of dexmedetomidine to bupivacaine scalp blocks significantly enhances the quality of anesthesia and analgesia, demonstrated superior outcomes in terms of early onset and prolonged duration of analgesia, sedation depth, pain scores, heart rate and blood pressure stability, satisfaction levels with minimal and manageable side effects. Furthermore, larger sample size and multicentric studies are required to establish these facts.

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