Hypertension following Intravenous Dexmedetomidine Infusion for Total Intravenous Anaesthesia in a Case of Posterior Fossa Surgery

Dear Sir, Dexmedetomidine, an alpha-2 adrenoceptor agonist, is widely employed for sedation in intensive care settings and operating rooms. While effective, it carries common side effects including hypotension and bradycardia.[1] Notably, transient hypertension may occur during the initial infusion phase due to stimulation of α2-adrenoceptors, although this typically requires no direct intervention and can often be managed by reducing the infusion rate.[2,3] This report details a case of sustained intraoperative hypertension linked to dexmedetomidine during total intravenous anaesthesia (TIVA) for posterior fossa surgery. We present the case of a 49-year-old male patient with a body mass index of 22.5 kg/m² scheduled for a translabyrinthine craniotomy to excise a space-occupying lesion, likely a schwannoma, in the right cerebellopontine angle. Following the application of Standard American society of Anesthesiologists (ASA) monitors, anaesthesia was induced using a combination of lignocaine (60 mg), propofol (90 mg), fentanyl (100 μg) and vecuronium (6 mg). An invasive arterial catheter and subclavian vein catheter were placed, with BIS monitoring employed to assess the depth of anaesthesia. The maintenance regimen included a propofol infusion administered at a target concentration of 3–3.5 μg/mL through a target-controlled infusion pump, along with dexmedetomidine at 0.5 μg/kg/h and fentanyl at 1 μg/kg/h, to facilitate intraoperative neurophysiological monitoring of the facial nerve. One hour following the initiation of TIVA, blood pressure gradually rose, reaching 180/96 mmHg over a 30-min interval while maintaining a BIS index between 30 and 40. Noteworthy, hypertension was observed in both invasive arterial blood pressure and non-invasive blood pressure measurements [Figure 1]. Despite administering boluses of labetalol (up to 40 mg), no resolution of hypertension occurred. Attempts to deepen anaesthesia with a 5-mg morphine intravenous bolus were similarly ineffective. Consequently, we decided to discontinue the dexmedetomidine infusion while continuing with propofol, fentanyl and sevoflurane at 0.2–0.3 minimum alveolar concentration. Gradually, the patient’s blood pressure returned to 126/70 mmHg baseline over the next 45 min. Resuming the dexmedetomidine infusion at a lower dose (0.2 μg/kg/h) demonstrated a similar hypertensive response, reinforcing our conclusion that the hypertension was indeed driven by dexmedetomidine. The infusion was halted again, and the surgery was completed over 6 h, with the patient remaining haemodynamically stable thereafter.Figure 1: Trend of blood pressure. SBP: Systolic blood pressure, DBP: Diastolic blood pressureThis case emphasises an important clinical consideration: while dexmedetomidine is valued for its sedative effects, it poses a risk for significant haemodynamic changes. Prior literature has noted instances of hypertension related to dexmedetomidine due to its pharmacological mechanisms, specifically through the activation of alpha-2 adrenergic receptors, which can induce vasoconstriction and subsequently elevate blood pressure. Studies have documented similar occurrences in both paediatric and adult populations, shedding light on the potential for dose-dependent responses, including hypertension at higher infusion rates and hypotension at lower concentrations.[4,5] Thus, this experience advocates for vigilant monitoring of haemodynamic parameters when administering dexmedetomidine, particularly in patients undergoing anaesthesia for extensive surgical procedures. The need for individualised patient care becomes particularly apparent, as what may be an appropriate dosage for one individual can lead to instability in another. The article contributes to understanding the complexities of anaesthetic management involving dexmedetomidine and emphasises the importance of individualised patient care. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

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Journal
Journal of Medical Evidence
Published
2025-04-01
DOI
https://doi.org/10.4103/jme.jme_35_25
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Anesthesia and Sedative Agents
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article
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article

Hypertension following Intravenous Dexmedetomidine Infusion for Total Intravenous Anaesthesia in a Case of Posterior Fossa Surgery

Mayank Gupta, Ravi Chaudhary, Amar Jeet Yadav, Anil Pargi
Journal of Medical Evidence
Anesthesia and Sedative Agents
article

Hypertension following Intravenous Dexmedetomidine Infusion for Total Intravenous Anaesthesia in a Case of Posterior Fossa Surgery

Mayank Gupta, Ravi Chaudhary, Amar Jeet Yadav, Anil Pargi
article en

Abstract

Dear Sir, Dexmedetomidine, an alpha-2 adrenoceptor agonist, is widely employed for sedation in intensive care settings and operating rooms. While effective, it carries common side effects including hypotension and bradycardia.[1] Notably, transient hypertension may occur during the initial infusion phase due to stimulation of α2-adrenoceptors, although this typically requires no direct intervention and can often be managed by reducing the infusion rate.[2,3] This report details a case of sustained intraoperative hypertension linked to dexmedetomidine during total intravenous anaesthesia (TIVA) for posterior fossa surgery. We present the case of a 49-year-old male patient with a body mass index of 22.5 kg/m² scheduled for a translabyrinthine craniotomy to excise a space-occupying lesion, likely a schwannoma, in the right cerebellopontine angle. Following the application of Standard American society of Anesthesiologists (ASA) monitors, anaesthesia was induced using a combination of lignocaine (60 mg), propofol (90 mg), fentanyl (100 μg) and vecuronium (6 mg). An invasive arterial catheter and subclavian vein catheter were placed, with BIS monitoring employed to assess the depth of anaesthesia. The maintenance regimen included a propofol infusion administered at a target concentration of 3–3.5 μg/mL through a target-controlled infusion pump, along with dexmedetomidine at 0.5 μg/kg/h and fentanyl at 1 μg/kg/h, to facilitate intraoperative neurophysiological monitoring of the facial nerve. One hour following the initiation of TIVA, blood pressure gradually rose, reaching 180/96 mmHg over a 30-min interval while maintaining a BIS index between 30 and 40. Noteworthy, hypertension was observed in both invasive arterial blood pressure and non-invasive blood pressure measurements [Figure 1]. Despite administering boluses of labetalol (up to 40 mg), no resolution of hypertension occurred. Attempts to deepen anaesthesia with a 5-mg morphine intravenous bolus were similarly ineffective. Consequently, we decided to discontinue the dexmedetomidine infusion while continuing with propofol, fentanyl and sevoflurane at 0.2–0.3 minimum alveolar concentration. Gradually, the patient’s blood pressure returned to 126/70 mmHg baseline over the next 45 min. Resuming the dexmedetomidine infusion at a lower dose (0.2 μg/kg/h) demonstrated a similar hypertensive response, reinforcing our conclusion that the hypertension was indeed driven by dexmedetomidine. The infusion was halted again, and the surgery was completed over 6 h, with the patient remaining haemodynamically stable thereafter.Figure 1: Trend of blood pressure. SBP: Systolic blood pressure, DBP: Diastolic blood pressureThis case emphasises an important clinical consideration: while dexmedetomidine is valued for its sedative effects, it poses a risk for significant haemodynamic changes. Prior literature has noted instances of hypertension related to dexmedetomidine due to its pharmacological mechanisms, specifically through the activation of alpha-2 adrenergic receptors, which can induce vasoconstriction and subsequently elevate blood pressure. Studies have documented similar occurrences in both paediatric and adult populations, shedding light on the potential for dose-dependent responses, including hypertension at higher infusion rates and hypotension at lower concentrations.[4,5] Thus, this experience advocates for vigilant monitoring of haemodynamic parameters when administering dexmedetomidine, particularly in patients undergoing anaesthesia for extensive surgical procedures. The need for individualised patient care becomes particularly apparent, as what may be an appropriate dosage for one individual can lead to instability in another. The article contributes to understanding the complexities of anaesthetic management involving dexmedetomidine and emphasises the importance of individualised patient care. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Journal of Medical EvidenceVol. 6(2)
All India Institute of Medical Sciences Rishikesh (IN)
Zero hunger
Openalex Percentile: Top 77%
Anesthesia and Sedative Agents
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