Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 7  |  Issue : 3  |  Page : 423-427

Conscious sedation during diagnostic cerebral angiography: A comparative study between dexmedetomidine and midazolam


1 Department of Anesthesiology, Intensive Care, and Pain Management, Faculty of Medicine, Benha University, Benha, Egypt
2 Ain Shams University, Cairo, Egypt

Date of Submission06-Jan-2014
Date of Acceptance10-Feb-2014
Date of Web Publication27-Aug-2014

Correspondence Address:
Ahmed Mostafa Abd El-Hamid
Department of Anesthesiology, Intensive Care, and Pain Management, Faculty of Medicine, Benha University, 12111 Benha
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.139586

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  Abstract 

Objective
To compare the efficacy and safety of dexmedetomidine versus midazolam in conscious sedation during diagnostic cerebral angiography.
Patients and methods
This prospective randomized, double-blind, comparative study was conducted on 66 patients scheduled for diagnostic cerebral angiography, who were randomly allocated into two equal groups: group I (dexmedetomidine group), in which patients received infusion of dexmedetomidine 1 mcg/kg administered over 10 min followed by continuous infusion of 0.2-0.7 mcg/kg/h; and group II (midazolam group), in which patients received midazolam 0.05-0.15 mg/kg administered over 10 min followed by infusion of 0.02-0.1 mg/kg/h. Intraoperative sedation levels were titrated to achieve a bispectral index score between 70-80 and Ramsay sedation score between 3-4. Hemodynamic variables (heart rate, mean arterial pressure) and ventilation (respiratory rate, peripheral oxygen saturation) were recorded at 15 min before drugs were administered, 5 min after the infusion of the bolus dose, and then every 10 min until 1 h after the end of the procedure. The onset of sedation and the recovery time were also recorded.
Results
Group I showed significant decrease in heart rate, but this decrease did not require treatment. No other significant differences between groups were found with regard to main blood pressure, ventilation parameters, and the onset of sedation. Group I showed significant decrease in recovery time in comparison with group II.
Conclusion
Dexmedetomidine is a good alternative to midazolam for intravenous sedation during diagnostic cerebral angiography, because it seems to be reliable and safe, providing a satisfactory sedation level without any serious side effects.

Keywords: conscious sedation, dexmedetomidine, diagnostic cerebral angiography, midazolam


How to cite this article:
Abd El-Hamid AM, Elrabiey MI, Youssef OR. Conscious sedation during diagnostic cerebral angiography: A comparative study between dexmedetomidine and midazolam. Ain-Shams J Anaesthesiol 2014;7:423-7

How to cite this URL:
Abd El-Hamid AM, Elrabiey MI, Youssef OR. Conscious sedation during diagnostic cerebral angiography: A comparative study between dexmedetomidine and midazolam. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2020 Mar 29];7:423-7. Available from: http://www.asja.eg.net/text.asp?2014/7/3/423/139586


  Introduction Top


Cerebral angiogram is a diagnostic procedure that provides images of the blood vessels in the brain. It can help to diagnose conditions such as the presence of a blood clot, fatty plaque that increases the patient's risk of stroke, cerebral aneurysm, or other vascular malformations [1].

A cerebral angiogram requires that a special dye be injected into the arteries of the head or brain [2]. Under the direction of an expert physician, this procedure is performed by inserting a flow-directed microcatheter into the blood vessels through the femoral artery under local anesthesia and manipulated through the carotid or vertebral vessels. When the catheter is in the correct position, the dye is then injected. At this point, the cerebral angiogram can generate the images of the blood vessels [3].

Conscious sedation is the most reliable technique for endovascular diagnostic procedures. It offers the advantage of conferring the ability to conduct intermittent neurological examination and allow the rapid return to consciousness at the conclusion of the procedure, which is important to facilitate neurological evaluation [4].

A variety of sedation regimens is available, and specific choices are based on the experience of the practitioner and the goals of anesthetic management. Frequently used agents include midazolam and fentanyl, low-dose propofol, remifentanil, or dexmedetomidine [5].

Dexmedetomidine is a selective α2 -agonist with sedative properties [6]. It has 1600-fold greater sensitivity toward α2 than α1 receptors. It produces its sedative effects by action on α2 receptors in the locus ceruleus [7]. Dexmedetomidine reduces cerebral blood flow without affecting oxygen metabolism, but it does not produce cerebral ischemia. The reduction in cerebral blood flow is secondary to cerebral vasoconstriction through postsynaptic α2 receptors [8].

Midazolam was selected as the comparator medication, because it is the only benzodiazepine approved for continuous infusion and is commonly used for long-term sedation in many countries [9].

This study aimed to compare the efficacy and safety of dexmedetomidine versus midazolam in conscious sedation during diagnostic cerebral angiography.


  Patients and methods Top


After local ethical committee approval and patients' informed written consent, this prospective randomized, double-blind, comparative study was conducted on 66 patients with ASA I : III scheduled for diagnostic cerebral angiography, and were randomly allocated by closed envelope into two equal groups, with 30 patients each.

Group I (dexmedetomidine group)

Patients received infusion of dexmedetomidine 1 mcg/kg administered over 10 min (bolus dose) followed by continuous infusion of 0.2-0.7 mcg/kg/h.

Group II (midazolam group)

Patients received midazolam 0.05-0.15 mg/kg administered over 10 min (bolus dose) followed by infusion of 0.02-0.1 mg/kg/h.

All medications were started 15 min before the procedure and stopped at the end of the procedure.

Intraoperative sedation levels were titrated to achieve a bispectral index score between 70-80 and Ramsay sedation score between 3-4.

Patients and all study personnel except the authors were blinded to the treatment assignment.

Patients with disturbed conscious level, Glasgow coma scale less than 13, patients with impaired liver or kidney functions, clinical history or ECG evidence of heart block, ischemic heart disease, bronchial asthma, sleep apnea syndrome, alcohol consumption, pregnancy, patient refusal, known psychiatric illness, chronic sedative or analgesic use, or patients who received any drugs that augment the effect of any of the investigating drugs were excluded from the study.

The following parameters were recorded.

Primary outcome

Recovery time

0This is the time from the stop of infusion until the bispectral index score reached 95 and Ramsay sedation scale reached between 1 and 2.

Secondary outcomes

(1) Sedation level: bispectral analysis and Ramsay sedation scale [Table 1].
Table 1 Ramsay sedation scale

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(2) Hemodynamic variables: heart rate and mean arterial blood pressure.

(3) Ventilation: respiratory rate and peripheral oxygen saturation.

These parameters were recorded at 15 min before the administration of the drugs, 5 min after the infusion of the bolus dose, and then every 10 min until 1 h after the end of the procedure.

(4) The onset of sedation: this is the time from the start of infusion until it reached the target sedation level.

Statistical analysis

Sample size was estimated as follows: assuming α error = 0.05 (two-tailed), β error = 0.1 and a power of 80% to detect an assumed clinically significant difference of 5% (effect size d = 0.6) or more between the paired measurements of the recovery time difference between the two groups (primary outcome). T-test for matched pairs was used to estimate the sample size, which stated that a sample of 60 patients will detect the difference with the above-mentioned accuracy.

Statistical analysis was performed using SPSS version 16 (IBM, New York, USA). All data were presented as mean and SD and were analyzed by using student t-test, except for age and ASA physical status that were presented as numbers and were analyzed by using χ2 -test. A P-value less than 0.05 was considered statistically significant, whereas less than 0.01 was considered highly significant.


  Results Top


Demographic characteristics showed no statistical significance between the two groups with regard to age, sex, weight, ASA physical status, and time of the procedure [Table 2].
Table 2 Demographic characteristics

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Hemodynamic variables

Heart rate

Group I showed statistically significant decrease in mean heart rate in comparison with group II, but this decrease did not require any treatment [Table 3].
Table 3 Heart rate

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Mean arterial blood pressure

There was no statistical difference between the two groups with regard to mean arterial pressure [Table 4].
Table 4 Mean arterial blood pressure

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Ventilation

Respiratory rate

0There was no statistical difference between the two groups with regard to mean respiratory rate [Table 5].
Table 5 Respiratory rate

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Oxygen saturation

There was no statistically significant difference between both groups [Table 6].
Table 6 Oxygen saturation

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The onset of sedation

There was no statistically significant difference between the two groups [Table 7].
Table 7 Difference between groups with regard to the onset of sedation and the recovery time

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Recovery time

Group I showed statistically highly significant decrease in the recovery time in comparison with group II [Table 7].


  Discussion Top


The aims of conscious sedation are to keep patients comfortable, relieve them of their pain, reduce anxiety, and protect the agitated patient from self-harm or from interfering with critical medical treatments and status assessments [11].

The ideal sedative should provide predictable effects, a rapid onset, and a rapid recovery. It should be easy to administer and titrate, cause few adverse effects with little or no interaction with other drugs, and minimal or no accumulation of metabolites, leaving no withdrawal effects [12].

The side effects of traditional sedatives led to the search for other drugs with different mechanisms of action, pharmacological properties, and alternative efficacy and tolerability profiles [13].

Midazolam is a widely used sedative drug, with rapid onset time in adults, and its effects after a single dose disappear rapidly [14]. However, intravenous infusion for more than 1 h increases its deposition in the tissues. Therefore, the effects of midazolam continue after the infusion has been stopped, owing to release from the tissues to blood [15].

Dexmedetomidine produces effective sedation. It has opioid-sparing properties and can alleviate withdrawal symptoms. It is also unique that it can reduce sympathetic activity by a central sympatholytic effect [16].

This study compares the sedative effects of dexmedetomidine with that of midazolam during diagnostic cerebral angiography, and documents that dexmedetomidine is a good alternative to midazolam for intravenous sedation because it seems to be reliable and safe, providing a satisfactory sedation level without any serious side effects. This is in agreement with by Panzer et al. [17], who document that dexmedetomidine has become one of the frequently used drugs in anesthetic armamentarium, along with routine anesthetic drugs, because of its hemodynamic, sedative, anxiolytic, analgesic, neuroprotective, and anesthetic-sparing effects. It also has minimal respiratory depression with cardiac protection, CNS protection, and renal protection, thus making it useful at various situations, including outpatient procedures. In the present study, there is a significant decrease in heart rate in the dexmedetomidine group in comparison with the midazolam group; however, this decrease did not require any treatment. This was in agreement with the meta-analysis performed by Tan and Ho [18], where it was observed that the incidence of bradycardia requiring intervention increased in studies that used both a loading dose and maintenance doses of dexmedetomidine in excess of 0.7 μg/kg/h, which is much greater than the dose administrated in the present study. This was also in agreement with Grounds [19] who compared dexmedetomidine with propofol in 20 adults expected to require mechanical ventilation, and found that patients sedated with dexmedetomidine required three times less analgesia than did those receiving propofol. They also found that heart rate was significantly lower in the dexmedetomidine group. Because of its central sympatholytic effect, dexmedetomidine is useful in decreasing hemodynamic responses in the perioperative period, which was agreed by this study. Saπύroπlu et al. [20] successfully used intravenous doses of dexmedetomidine, varying from 0.25 to 1 μg/kg for attenuating intubation response, and found that the optimal dose for attenuating the response was 1 μg/kg and lesser doses were not effective, and also documented that infusion continued into the postoperative period had been associated with reduced hemodynamic fluctuations and decreased in plasma catecholamines. Ebert et al. [21] studied the effects of increasing plasma concentrations of dexmedetomidine in humans, and found that doses in the range of 0.5 μg/kg not only attenuated the extubation response, but also reduced the emergence reaction and analgesic requirement to extubation after rhinoplasty and neurosurgery. With regard to the recovery time, this study documents that dexmedetomidine had rapid recovery time in comparison with midazolam. This was agreed with by Turan et al. [22] and Aksu et al. [23] who documented that there was no delay in recovery or prolonged sedation when boluses were administered before induction or before extubation. Similar was the observation when the duration of infusion was within 2 h.


  Conclusion Top


This study documents that dexmedetomidine is a good alternative to midazolam for intravenous sedation during diagnostic cerebral angiography, because it seems to be reliable and safe, providing a satisfactory sedation level without any serious side effects).


  Acknowledgements Top


 
  References Top

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9. Riker RR, Shehabi Y, Bokesch PM, Ceraso D, Wisemandle W, Koura F, et al. Dexmedetomidine vs midazolam for sedation of critically ill patients: a randomized trial. JAMA 2009; 301:489-499.   Back to cited text no. 9
    
10.Ramsay, MAE, Savege, TM, Simpson, BRJ, Goodwin, R. Controlled sedation with alphaxalone-alphadolone. Br Med J 1974; 2:656-659.  Back to cited text no. 10
    
11.Mirski MA, Lewin JJ. Sedation and pain management in acute neurological disease. Semin Neurol 2008; 28:611-630.  Back to cited text no. 11
    
12.Ostermann ME, Keenan SP, Seiferling RA, Sibbald WJ. Sedation in the intensive care unit. A systematic review. JAMA 2000; 283:1451-1459.  Back to cited text no. 12
    
13.Gowing L, Farrell M, Ali R, White JM. Alpha2-adrenergic agonists for the management of opioid withdrawal. Cochrane Database Syst Rev 2009; 2:CD002024.  Back to cited text no. 13
    
14.Nitsun M, Szokol JW, Saleh HJ, Murphy GS, Vender JS, Luong L, et al. Pharmacokinetics of midazolam, propofol, and fentanyl transfer to human breast milk. Clin Pharmacol Ther 2006; 79:549-557.  Back to cited text no. 14
    
15.Peruzzi WT, Hurt K. Approach to sedation in the ICU. Perioperative medicine and pain. Semin Anaesth 2005; 24:27-33.  Back to cited text no. 15
    
16.Nelson LE, Lu J, Guo T, Saper CB, Franks NP, Maze M. The alpha2-adrenoceptor agonist dexmedetomidine converges on an endogenous sleep-promoting pathway to exert its sedative effects. Anesthesiology 2003; 98:428-436.  Back to cited text no. 16
    
17.Panzer O, Moitra V, Sladen RN. Pharmacology of sedative-analgesic agents: dexmedetomidine, remifentanil, ketamine, volatile anesthetics, and the role of peripheral mu antagonists. Crit Care Clin 2009; 25:451-469.  Back to cited text no. 17
    
18.Tan JA, Ho KM. Use of dexmedetomidine as a sedative and analgesic agent in critically ill adult patients: a meta-analysis. Eur J Anaesthesiol 2011; 28:3-6.  Back to cited text no. 18
    
19.Grounds RM. Comparison between dexmedetomidine and propofol for sedation in the intensive care unit: patient and clinician perception. Br J Anaesth 2001; 87:684-690.  Back to cited text no. 19
    
20.Saðýroðlu AE, Celik M, Orhon Z, Yüzer S, Sen B. Different doses of dexmedetomidine on controlling haemodynamic responses to tracheal intubation. Int J Anesthesiol 2010; 27:2.  Back to cited text no. 20
    
21.Ebert T, Hall JE, Barney JA, Uhrich TD, Colinco MD. The effects of increasing plasma concentrations of dexmedetomidine in humans. Anesthesiology 2000; 93:382-394.  Back to cited text no. 21
    
22.Turan G, Ozgultekin A, Turan C, Dincer E, Yuksel G. Advantageous effects of dexmedetomidine on haemodynamic and recovery responses during extubation for intracranial surgery. Eur J Anaesthesiol 2008; 25:816-820.  Back to cited text no. 22
    
23.Aksu R, Akýn A, Biçer C, Esmaoðlu A, Tosun Z, Boyaci A. Comparison of the effects of dexmedetomidine versus fentanyl on airway reflexes and hemodynamic responses to tracheal extubation during rhinoplasty: a double-blind, randomized, controlled study. Curr Ther Res 2009; 70:209-220.  Back to cited text no. 23
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7]



 

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   Abstract
  Introduction
  Patients and methods
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