“For all the happiness mankind can gain is not in pleasure, but in prevention of pain.” – John Dryden

Craniotomy procedures are among the most stimulating and invasive neurosurgical interventions, frequently associated with intense nociceptive responses and marked hemodynamic fluctuations. One of the most noxious components during such surgeries is the application of skull pins, required to immobilize the patient's head using a Mayfield head clamp. This stimulation can lead to abrupt increases in heart rate (HR) and blood pressure (BP), potentially escalating intracranial pressure (ICP) and jeopardizing cerebral perfusion, thereby increasing the risk of intraoperative complications such as hemorrhage and brain edema (1,2).

Effective control of these responses is paramount to maintaining perioperative stability and optimal neurosurgical conditions. Regional anesthesia techniques, particularly scalp nerve blocks, are widely employed to blunt nociceptive input during skull pin insertion. These blocks involve the administration of local anesthetics to various sensory nerves of the scalp, thereby attenuating afferent pain signals and stabilizing hemodynamic parameters during craniotomy (3,4).

Ropivacaine, a long-acting amide-type local anesthetic, is favored for such blocks due to its efficacy and reduced potential for cardiotoxicity and motor blockade when compared with bupivacaine (5,6). However, its limited duration of action may be insufficient for prolonged neurosurgical procedures. To enhance and prolong its analgesic efficacy, various adjuvants have been investigated. One such agent is dexmedetomidine, a highly selective α2-adrenoceptor agonist with sedative, analgesic, and sympatholytic properties (7,8).

Dexmedetomidine has shown promise in regional anesthesia due to its ability to potentiate local anesthetics, prolong analgesia, and reduce opioid requirements. It also contributes to intraoperative hemodynamic stability by decreasing sympathetic tone and catecholamine release (9,10). Studies have shown that combining dexmedetomidine with ropivacaine in scalp blocks may further attenuate the pressor response associated with skull pin insertion and skin incision during craniotomy (11,12). For example, Sahni et al. demonstrated that the addition of dexmedetomidine to ropivacaine significantly prolonged analgesia and blunted hemodynamic responses to noxious stimuli during craniotomies (11). Similarly, Verma et al. observed a significant reduction in HR and BP responses in patients receiving dexmedetomidine-enhanced scalp blocks (12).

Study Design and Setting:

This prospective, hospital-based, observational, cross-sectional study was conducted in the Department of Anesthesiology, Pain Management, and Critical Care at Mahatma Gandhi Medical College and Hospital, Jaipur. The study spanned a duration of 1.5 years, from January 2023 to June 2024, after obtaining institutional ethical clearance and written informed consent from all participants.

Sample Size and Group Allocation:

A total of 60 adult patients scheduled for elective neurosurgical procedures requiring skull pin head holder application were enrolled. Patients were randomly allocated into two groups, each comprising 30 individuals:

• Group 1: Received a scalp block with 0.25% ropivacaine combined with dexmedetomidine.
• Group 2: Received a scalp block with 0.25% ropivacaine alone.

Inclusion Criteria:

• Patients aged 18–65 years.
• Both male and female patients.
• ASA (American Society of Anesthesiologists) physical status grade I or II.
• Undergoing elective craniotomies with skull pin fixation.

Exclusion Criteria:

• Age <18 or >65 years.
• ASA grade III, IV, or V.
• Patients with uncontrolled hypertension, preoperative bradycardia, ischemic heart disease, cardiac arrhythmias, hepatic or renal impairment.
• Known allergy to study medications.
• History of previous craniotomy.
• Pregnant or lactating women.

Blinding and Preparation:

The study drugs were prepared by an independent anesthesiologist not involved in patient care or data analysis. The attending anesthesiologist and outcome assessors were blinded to group assignments.

Anesthetic Protocol and Scalp Block Technique:
Preoperatively, patients underwent routine assessment and pre-anesthetic check-up. No sedative premedication was administered outside the operation theatre. Standard monitoring including ECG, NIBP, SpO₂, respiratory rate, and EtCO₂ was initiated. Following pre-oxygenation, general anesthesia was induced using fentanyl (1–2 mcg/kg), propofol (1.5–2 mg/kg), and vecuronium (0.08–0.1 mg/kg). Anesthesia was maintained with propofol infusion (4–12 mg/kg/h) and 0.5 MAC isoflurane with a 50:50 oxygen-air mixture. Mechanical ventilation was adjusted to maintain EtCO₂ between 30–35 mmHg. Radial artery cannulation was performed for invasive blood pressure monitoring.

Scalp block was administered bilaterally with 15 ml of the prepared solution per side, targeting the following nerves:

• Supraorbital and Supratrochlear Nerves: 1.5 ml at the supraorbital foramen and 1 cm medial to it.
• Zygomaticotemporal Nerve: 3 ml above the zygoma at the posterior arch.
• Auriculotemporal Nerve: 3 ml anterior to the tragus at the zygomatic level, avoiding the superficial temporal artery.
• Greater Occipital Nerve: 3 ml midway between the occipital protuberance and mastoid process.
• Lesser Occipital Nerve: 3 ml along the superior nuchal line, ~5 cm lateral to the occipital protuberance.

Intraoperative Monitoring and Management:
Hemodynamic parameters including HR, SBP, DBP, and MAP were recorded at multiple time points: baseline (pre-induction), post-induction, post-skin incision, 10 minutes after incision, at dura opening, and every 30 minutes thereafter. Any increase in HR or MAP >20% from baseline was managed by increasing propofol infusion and administering fentanyl (2 mcg/kg). If unresponsive, labetalol was used and such patients were excluded from analysis. Hypotension (MAP <70 mmHg) was managed with inhalational agent adjustments, mephentermine (6–12 mg), or noradrenaline infusion as needed. Bradycardia (HR <40/min) was treated with IV atropine (0.6 mg).

Postoperative Monitoring and Analgesia:

Pain was evaluated using a 10 cm Visual Analogue Scale (VAS) at 0, 1, 3, 6, 12, 18, and 24 hours postoperatively by a blinded investigator. Rescue analgesia (IV paracetamol 1 mg/kg) was given for VAS >4. Time to first rescue analgesia and total 24-hour analgesic requirement were recorded. Nausea or vomiting was treated with IV ondansetron (4 mg).

Study Tools and Data Collection:

A structured data collection form captured the following:

• Patient demographics and ASA status.
• Surgical details.
• Intraoperative vitals (HR, SBP, DBP, MAP).
• Pain scores and analgesic use.

Hemodynamic Monitoring Modalities:

• ECG: Continuous monitoring for heart rate and rhythm disturbances.
• NIBP/IBP: MAP >70 mmHg was targeted to ensure adequate perfusion.
• EtCO₂: Monitored via capnography for adequacy of ventilation and perfusion.
• SpO₂: Assessed using pulse oximetry to monitor oxygenation.

Statistical Analysis:

Data were analyzed using SPSS software.

The study involved 60 patients randomly divided into two equal groups of 30 each. Group 1 received 0.25% ropivacaine with dexmedetomidine, and Group 2 received 0.25% ropivacaine alone. The demographic and baseline vitals were comparable across groups. Hemodynamic parameters—systolic blood pressure, mean arterial pressure, and heart rate—were closely monitored post-induction to evaluate the effects of the intervention. (Table 1)

Table1: Comparison of Systolic Blood Pressure Between Both Groups After Induction (N=60)

Systolic blood pressure in Group 1 was significantly lower than Group 2 from 45 minutes to 1.5 hours (p < 0.05 to p < 0.01). However, a notable increase in SBP was observed in Group 1 after 3 hours, surpassing that of Group 2. This biphasic response is suggestive of dexmedetomidine’s sympatholytic and later vasoconstrictive effects.

Table 2: Comparison of Mean Arterial Pressure Between Both Groups After Induction (N=60)

Interpretation (Table 2):

Group 1 exhibited significantly lower MAP values than Group 2 during the initial 1.5 hours post-induction (p < 0.01), indicating dexmedetomidine’s hypotensive effect. This trend later reversed after 3 hours, with Group 1 exhibiting higher MAP at 3 and 3.5 hours (p < 0.01).

Table 3: Comparison of Heart Rate Between Both Groups After Induction (N=60)

Interpretation (Table 3):

Group 1 consistently exhibited significantly lower heart rates from 15 minutes to 2 hours, with the difference most pronounced at 30 minutes and 4 hours (p < 0.01). This confirms the bradycardic effect of dexmedetomidine, necessitating close intraoperative monitoring, especially during prolonged procedures.

The addition of dexmedetomidine to ropivacaine significantly influenced hemodynamic parameters. As shown in Table 5, systolic BP was significantly lower in Group 1 during early phases, then reversed later. Table 7 highlights a similar biphasic pattern in MAP. Table 8 demonstrates sustained bradycardia in the dexmedetomidine group. These findings underscore the need for individualized anesthetic planning and vigilant monitoring when using this combination.

This prospective observational study evaluated the hemodynamic effects of adding dexmedetomidine to 0.25% ropivacaine for scalp blocks in patients undergoing elective neurosurgical procedures. The findings revealed that the combination produced distinct and time-dependent alterations in blood pressure and heart rate, suggesting enhanced autonomic modulation. The outcomes have potential implications for anesthetic practice, especially in scenarios requiring stable intraoperative hemodynamics.

The demographic characteristics between the two study groups were comparable in terms of age and sex, with most patients falling within the 21–40-year age bracket and a slight male predominance. A significant proportion of patients belonged to ASA grade I, minimizing the influence of comorbidities on the hemodynamic variables studied. Such demographic parity is crucial for reducing confounding and ensuring the internal validity of the results (1,2).

The primary observation was a biphasic hemodynamic pattern in the dexmedetomidine group. Initially, a significant reduction in systolic, diastolic, and mean arterial pressures was noted, lasting up to approximately 90 minutes post-induction. This phase is attributable to the central sympatholytic action of dexmedetomidine, mediated through presynaptic α2-adrenergic receptor activation, which inhibits norepinephrine release and reduces sympathetic outflow (3,4). Similar trends have been documented in both intravenous and perineural dexmedetomidine use, confirming its role in producing dose-dependent hypotension (5,6).

Interestingly, this initial hypotension was followed by a delayed hypertensive trend, particularly evident in systolic blood pressure after 3 hours. This phenomenon is consistent with previous studies demonstrating that peripheral α2B-receptor stimulation can lead to vasoconstriction and rebound hypertension once central sympatholysis diminishes (7,8). This biphasic response has been reported by Ebert et al. in intravenous dexmedetomidine infusions and appears to persist when the agent is used as an adjuvant in regional blocks (9).

The mean arterial pressure (MAP), an integrated reflection of systemic perfusion, followed a similar trend: reduced during the early intraoperative period and rising during the later stages. These MAP fluctuations may be clinically beneficial in neurosurgical settings. Controlled hypotension early in the procedure can reduce cerebral blood flow and intracranial pressure, optimizing the surgical field (10). Conversely, restoration of MAP during closure may safeguard cerebral perfusion as anesthetic depth decreases (11).

The heart rate in the dexmedetomidine group showed a marked and sustained decline, beginning from 15 minutes post-induction and persisting throughout the observation period. This bradycardia is consistent with dexmedetomidine’s known ability to enhance vagal tone and reduce sympathetic activity (12). The prolonged nature of this effect aligns with findings from previous investigations, indicating that perineural dexmedetomidine provides a depot-like effect resulting in extended systemic absorption (13,14).

From a pharmacodynamic perspective, these results suggest that the combination of dexmedetomidine with ropivacaine offers a balanced anesthetic profile. The early hypotensive phase reflects its central effects, while the delayed hypertensive response likely results from peripheral receptor activation. Notably, the consistent bradycardia throughout supports the dominance of central autonomic modulation over peripheral cardiovascular tone (15).

Previous meta-analyses and randomized controlled trials have shown that dexmedetomidine, when used as an adjuvant to local anesthetics, enhances the quality of regional blocks, prolongs sensory and motor block duration, and reduces postoperative opioid requirements (16,17). While this study did not assess analgesia duration or pain scores, the hemodynamic stability achieved, especially during later surgical stages, supports its potential in neurosurgical applications.

Furthermore, the consistent bradycardia seen here, though typically benign, underscores the importance of patient selection. Caution is advised in patients with pre-existing conduction system disorders or those on beta-blockers (8). Extended monitoring is also warranted due to the prolonged hemodynamic effects associated with dexmedetomidine.

The hemodynamic pattern observed in this study may also support cerebral perfusion management. Controlled reductions in blood pressure can be advantageous during dura opening, while later increases can be beneficial during closure and emergence phases. This aligns with recommendations for individualized blood pressure targets during neurosurgical procedures to balance cerebral autoregulation and perfusion pressure (9).

Despite the promising outcomes, limitations exist. The relatively small sample size and inclusion of mostly ASA I–II patients limit generalizability. Moreover, the absence of direct postoperative outcomes such as pain scores or analgesic consumption is a limitation. Future studies should evaluate these clinical endpoints alongside cerebral perfusion indices and dexmedetomidine plasma levels to better understand its systemic kinetics when administered via scalp blocks.

In conclusion, this study reinforces the role of dexmedetomidine as a valuable adjuvant in regional anesthesia for neurosurgical procedures. The biphasic hemodynamic response and sustained bradycardia highlight both the efficacy and considerations necessary when using this agent. With careful patient selection and vigilant monitoring, dexmedetomidine combined with ropivacaine may offer enhanced hemodynamic control and potential opioid-sparing benefits in neurosurgery.

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