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 Table of Contents  
Year : 2020  |  Volume : 34  |  Issue : 2  |  Page : 118-123

Effect of intravenous versus intrathecal dexmedetomidine on the characteristic of spinal anesthesia in patients undergoing infra umbilical surgeries

Department of Anaesthesia, Sawai Man Singh Medical College, Jaipur, Rajasthan, India

Date of Submission22-Oct-2019
Date of Decision10-Dec-2019
Date of Acceptance08-Jun-2020
Date of Web Publication06-Aug-2020

Correspondence Address:
Dr. Mamta Khandelwal
Flat No. 21, B 80, Jona Enclave, Rajendra, MARG, Bapunagar, Jaipur - 302 015, Rajasthan
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijpn.ijpn_88_19

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Background: Dexmedetomidine have been used as an adjuvant to local anaesthetic in subarachnoid block and as intravenous medication for postoperative pain relief and sedation. In higher doses, it may produce adverse effect on haemodynamic. Aim: This study compares the effects of low-dose intravenous (IV) dexmedetomidine or Intrathecal dexmedetomidine with hyperbaric bupivacaine on spinal characteristic, total duration of analgesia, and sedation. Objective: the primary objective of our study evaluate the total duration of analgesia and a secondary objective was to assess and compare the onset time and duration of sensory block, changes in hemodynamic parameter and side effect. Materials and Methods: In this prospective, randomised, double-blinded study, 240 American Society of Anaesthesiologist Status I and II patients were randomly allocated into two groups: Group IV: Patients received dexmedetomidine 0.5 μg/kg body weight diluted up to 10 ml with normal saline intravenously by infusion pump and 3 ml of 0.5% hyperbaric bupivacaine diluted in 0.5 ml of normal saline intrathecally.Group IT: Patients received 10 ml of normal saline intravenously by infusion pump and 3 ml of 0.5% hyperbaric bupivacaine with 0.5 ml (5 μgm) of dexmedetomidine intrathecally. Onset and duration of sensory and motor block, first request for analgesia, hemodynamic, VAS score, and sedation score were assessed. Results: Time to two segment regression was more in group IT (127.7 ± 16.69 min) as compared to group IV (116 ± 16.2 min). Total duration of analgesia was also prolonged in group IT (274.68 ± 58.21 min) than group IV (211.37 ± 32.87 min)(P < 0.001). Conclusion: IT dexmedetomidine as compared to IV dexmedetomidine as an adjuvant to intrathecal bupivacaine prolonged the time to first request for analgesia, without any significant adverse effect.

Keywords: Bupivacaine, dexmedetomidine, intrathecal, intravenous

How to cite this article:
Kumar P, Bafna U, Khandelwal M, Chatterji R. Effect of intravenous versus intrathecal dexmedetomidine on the characteristic of spinal anesthesia in patients undergoing infra umbilical surgeries. Indian J Pain 2020;34:118-23

How to cite this URL:
Kumar P, Bafna U, Khandelwal M, Chatterji R. Effect of intravenous versus intrathecal dexmedetomidine on the characteristic of spinal anesthesia in patients undergoing infra umbilical surgeries. Indian J Pain [serial online] 2020 [cited 2020 Nov 26];34:118-23. Available from: https://www.indianjpain.org/text.asp?2020/34/2/118/291556

  Introduction Top

Spinal anesthesia provides excellent anesthesia for lower abdominal surgery with good muscle relaxation and sensory blockade. It is easy to administer, has a faster onset of sensory and motor block, reduces the risk of pulmonary aspiration, spares spontaneous respiration, and reduces intraoperative blood loss.[1] The management of postoperative pain using short-acting local anesthetic in spinal anesthesia still proves to be a major obstacle. The efficacy of spinal anesthesia can be improved by the addition of adjuvants.

Dexmedetomidine is a highly selective alpha 2 (α2)-adrenergic agonist. Intrathecal dexmedetomidine is found to have an antinociceptive action for both somatic and visceral pain. Low-dose dexmedetomidine has anxiolytic and hypnotic properties and added advantage of hemodynamic stability without respiratory depression.[2],[3] Binding of dexmedetomidine to α2 receptors in the locus coeruleus causes sedation and anxiolysis while action at laminae VII and VIII of the ventral horn of the spinal cord produces analgesia.[4]

In previous studies intravenous dexmedetomidine has been used as a bolus dose followed by continuous infusion, in our study, we have given a single dose of intravenous dexmedetomidine over 10 min and compared it with intrathecal dexmedetomidine to find the clinical efficacy and safety of both the routes.

The primary objective of our study was to evaluate the total duration analgesia and the secondary objectives were to assess and compare the onset time and duration of sensory block, changes in hemodynamic parameters and side effects of intravenous and intrathecal administration of dexmedetomidine as an adjuvant to 0.5% hyperbaric bupivacaine in patients underwent infra-umbilical surgeries under spinal anesthesia.

  Methodology Top

This prospective, randomized, double-blinded study was conducted at a tertiary care hospital from December 2017 to November 2018, after approval from the institutional ethics committee. Two hundred and forty patients of the American Society of Anesthesiologists (ASA) Grade I and II, aged between 20 and 50 years underwent elective infra-umbilical surgeries under spinal anesthesia were included in this study. Patients who were not willing to participate in the study, patients having any contraindication to spinal anesthesia, history of chronic disease such as hypertension, diabetes mellitus, respiratory disease, epilepsy and cardiac disease, chronic history of headache and backache, any absolute or relative contraindication to study drug, uncooperative patients, and failure of spinal anesthesia in any patient were excluded from the study.

Written informed consent was obtained on the day of surgery. A total of 260 patients were assessed for eligibility, of which 240 patients were randomized into two groups by using computerized randomization method (Random Allocation Software), and the allocated group number of each patient was kept sealed in an opaque envelope. Twenty patients were excluded from the study because they were not meeting the inclusion criteria [Figure 1].
Figure 1:Consort diagram

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  • Group IV (n = 120): Intravenous dexmedetomidine group
  • Group IT (n = 120): Intrathecal dexmedetomidine group.

In OT, all patients were prehydrated with 10 ml/kg of Ringer's lactate solution through 18G, intravenous cannula. Standard monitors such as noninvasive blood pressure (BP), electrocardiogram, and SpO2 were attached, and baseline readings were noted.

Group IT patients received 10 ml of normal saline intravenous bolus over 10 min by infusion pump and Group IV patients received 0.5 μg/kg dexmedetomidine diluted up to 10 ml with normal saline as an intravenous bolus over 10 min by infusion pump.

After 5 min of completion of intravenous infusion, under all aseptic precautions, spinal anesthesia was given at L3–L4 interspace with 25 G Quincke needle in the left lateral position.

Group IV patients received 3 ml of 0.5% hyperbaric bupivacaine with 0.5 ml of normal saline in spinal anesthesia, and Group IT patients received 3 ml of 0.5% hyperbaric bupivacaine with 0.5 ml (5 μg) of dexmedetomidine.

Patients were placed supine with head low tilt. One milligram, of midazolam was given for sedation. Sensory block was assessed by the loss of pinprick sensations, bilaterally along the mid-clavicular line with a 25G hypodermic needle at 2 min interval, and the time required to reach the highest level of sensory block was recorded. The time from injection of the study drug to the time taken to achieve the T6 dermatomal level was taken as onset time of the sensory block. The time taken for the sensory block to regress by two dermatomal segments from the highest level achieved was defined as regression of sensory block. Modified Bromage scale[5] was used to assess the motor block at 2-min interval. Time elapsed from the maximum to the lowest Bromage score was taken as duration of motor block.

It was a double-blinded study as an anesthetist who recorded readings was different from anesthetist who gave spinal anesthesia, and both were blinded to the groups to which the patient was allotted.

BP, pulse rate, and SpO2 were monitored at every 5-min interval throughout the surgery. Any fall of MAP >20% from the baseline or systolic BP <90 mm of Hg has treated with intravenous fluid and incremental doses of mephentermine 5 mg intravenously. Bradycardia was defined as heart rate (HR) <55, was treated with injection atropine 0.6 mg IV.

The pain assessment was done by visual analog scale (VAS) between 0 and 10 (0 = no pain, 10 = most severe pain). VAS score was assessed at every 30 min in the postoperative period. Intravenous injection of diclofenac 75 mg was given as rescue analgesia to the patient on a VAS score of 3. The total duration of analgesia (time from the intrathecal administration of study drug to the administration of rescue analgesia) was documented. This was the endpoint of our study.

“Four-Point Sedation Scale” was used to assess the sedation level. Patients were monitored for 24 h, and any adverse events such as nausea, vomiting, hypotension, and bradycardia were logged and treated accordingly.

Statistical analysis

The sample size was calculated to be 129 subjects in each group at 95% confidence interval and power 80% assuming the minimal detectable difference in the meantime to first analgesic request with intravenous dexmedetomidine and intrathecal dexmedetomidine to be 14 ± 35 min[6] so, 224 patients were enrolled for the study.

Categorical variables were summarized as frequency and percentage and were analyzed using the Chi-square test/Fiscer's exact test as applicable. Continuous variables were expressed as mean and standard deviation and analyzed using the Student t-test. A P < 0.05 was considered statistically significant. All statistical analyses were performed using Epi info version (CDC, Atlanta, GA, USA).

  Results Top

Both groups were comparable with respect to age, ASA status, weight, height, type of surgery, and duration of surgery [Table 1] and [Table 2].
Table 1: Demographic data

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Table 2: Type of surgery

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The onset of sensory block was faster in Group IT (6.09 ± 1.13 min) than in Group IV (6.52 ± 0.092 min). The highest level of the sensory blockade was similar in both the groups, and it was not statistically significant (P > 0.05). The time for two-segment regression was substantially longer in Group IT (127.7 ± 16.69 min) as compared to Group IV (116 ± 16.2 min) it was statistically significant (P < 0.001) Time to first dose of rescue analgesia was 274.68 ± 58.21 min in Group IT and 211.37 ± 32.87 min in Group IV respectively which was statistically significant. The duration of motor block was also considerably longer in Group IT as compared to Group IV [Table 3].
Table 3: Characteristics of sensory and motor block

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There was no significant difference between the mean HR and MAP in Group IT and Group IV throughout the intraoperative period [Table 4] and [Table 5]. Incidence of bradycardia was equivalent in both the groups Although, the incidence of hypotension was greater in Group IV (33.3%) in comparison to Group IT (26.7%), it was not statistically significant (P > 0.05) [Table 6]. None of the patients had nausea, vomiting, hypotension, or bradycardia in the postoperative period.
Table 4: Trend of mean heart rate among study groups

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Table 5: Trend of mean blood pressure among study groups

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Table 6: Comparison of intra-operative bradycardia and hypotension

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The median VAS scores were significantly less in Group IT as compared to Group IV for up to 4.5 h (P < 0.001) [Table 7].
Table 7: Comparison of visual analog scale score among study groups (median and interquartile range)

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Sedation scores were inconsequential between both groups throughout the observation period [Table 8].
Table 8: Comparison of sedation score among study groups (median and interquartile range)

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  Discussion Top

The use of intrathecal adjuvants with local anesthetics in spinal anesthesia has become a popular practice for superior postoperative analgesia and enhanced quality of block. Opioids as adjuvants are associated with numerous side effects such as respiratory depression, pruritus, nausea, vomiting, and hemodynamic instability.[7]

In our study, the addition of intrathecal dexmedetomidine lead to faster onset of sensory block, extended duration of sensory and motor block, provided adequate intraoperative and postoperative sedation, at the same time curtailing the need for rescue analgesia. All of these properties prove beneficial for surgery under spinal anesthesia.

Dexmedetomidine acts by inhibition of nociceptive neurons by stimulation of α-adrenoreceptors at the substantia gelatinosa of the dorsal horn in the spinal cord, activation of both α2C and α2A receptors situated in the neurons of superficial dorsal horn especially lamina II, directly preventing pain transmission by reducing the release of pro-nociceptive transmitter, substance P and glutamate from primary afferent terminals and by hyperpolarization of spinal interneurons through G-protein mediated activation of potassium channels.[8]

Prolongation of the subarachnoid block after IV administration of dexmedetomidine is by supraspinal action. This action of dexmedetomidine occurs due to the stimulation of the adrenoceptors in the locus coeruleus.[4] Hyperpolarization of noradrenergic neurons which suppresses neuronal firing in the locus coeruleus leads to inhibition of the descending medulospinal noradrenergic pathway and inhibition of norepinephrine release results in hypnotic and supraspinal analgesic effects of dexmedetomidine.[9]

This produces a differential blockade by selective blocking of myelinated A α-fibers involved in sensory conduction over unmyelinated C fibers involved in motor conduction. Such selectivity may be useful when prolonged analgesia is desirable, but not necessarily motor block.[6]

Anxiolysis, sedation, and analgesia are mediated by a drop in the outflow of norepinephrine preventing its action on presynaptic α2 receptor in the central nervous system.[10]

Continuous infusion of dexmedetomidine may result in increased activation of alpha-2 receptors in the spinal cord resulting in inhibition of nociceptive impulse transmission. The effect seems to be mediated through both presynaptic and the postsynaptic alpha-2 receptors.[4] The results of the study done by Hadil magdy et al. showed that infusion of dexmedetomidine leads to faster onset of sensory block, though the onset of motor blockade was not affected.[11]

The study showed that IT dexmedetomidine (5 μg) quickened the onset and prolonged the duration of sensory block and first request of analgesia. Magdy et al.[11] conducted a study to compare the effects of hyperbaric bupivacaine, IT dexmedetomidine (5 μg) with hyperbaric bupivacaine and IV dexmedetomidine (0.5 μg/kg/h) with hyperbaric bupivacaine in cesarean section. They found that the onset of sensory blockade was fastest in the Group IT. In another study, Ahmed and Talaat.[6] compared dexmedetomidine 0.5 μg/kg IV immediately after spinal anesthesia and dexmedetomidine 3 μg intrathecally. Significant lengthening of the duration of sensory block was observed in group IT as compared to group IV dexmedetomidine. Our results are consistent with these studies.

The faster onset and delayed recovery from sensory block may be due to inhibition of nociceptive impulse transmission by α2 receptor activation. Prolongation of the duration of spinal anesthesia may be attributed to delayed absorption of local anesthesia, as α2 receptor agonism in the substantia gelatinosa causes vasoconstriction and analgesic action.[10]

When α2 agonists were administered in the form of a loading dose followed by an infusion, prolongation of sensory and motor block was observed in other studies also.[12],[13]

Studies conducted by Magdy et al.[11] and Ahmed and Talaat.[6] showed that the time for the first request of analgesia was more in group IT as compared to group IV dexmedetomidine. These results are analogous to our study. Kubre et al.[14] also found that intravenous dexmedetomidine surpassed the control group in terms of a total duration of analgesia, i.e., 234.67 ± 7.649 min versus 164.17 ± 6.170 min, respectively.

All the studies have estimated that the addition of α2 agonists with local anesthetics leads to prolongation of analgesia, which may be attributed to the supraspinal and direct analgesic actions of dexmedetomidine.

In intravenous dexmedetomidine group, the need for rescue analgesia for 75 percent patients did not arise until 180 min, whereas in intrathecal dexmedetomidine group 75, it was 210 min [Table 7].

In both intravenous and intrathecal dexmedetomidine groups, 75% of patients opened their eyes on command after 240 min [Table 8].

The groups were comparable with respect to intraoperative and postoperative pulse rate, mean arterial pressure, systolic, and diastolic BP (P > 0.05). The incidence of hypotension was not appreciably different in the groups. Direct stimulation of beta-adrenoceptor in vascular smooth muscle can be attenuated by a slow infusion of dexmedetomidine over 10 min, as demonstrated in our study, which prevents a transient increase in BP and subsequent reflex decrease in HR.

Reddy et al.[15] and Kaya et al.[2] examined the effect of single-dose dexmedetomidine 0.5 μg/kg IV versus placebo and observed an increase in the incidence of bradycardia and hypotension with dexmedetomidine, but it was statistically insignificant. None of the patients showed any neurological deficits in follow-up visits. Many animal studies using intrathecal dexmedetomidine in the dose range of 2.5–100 mcg have not reported any neurological deficits or neurotoxicity.[16]

All patients were easily arousable and co-operative at the end of the study in both groups.

Since the total analgesic requirement during 24 h was not documented, this could be the limitation of our study.

  Conclusion Top

Intrathecal dexmedetomidine prolonged postoperative analgesia, duration of sensory and motor blockade compared to IV dexmedetomidine without any significant adverse effects and hemodynamic perturbation. So, we concluded that the addition of 5 μg dexmedetomidine as an adjuvant to 0.5% hyperbaric bupivacaine intrathecally can be a better alternative to provide a satisfactory and longer duration of analgesia as compared to IV dexmedetomidine.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Brown DL. Anesthesia. In: Miller RD, editor. Spinal, Epidural and Caudal Anesthesia. Philadelphia: Churchill-Livingstone; 2000. p. 1492-8.  Back to cited text no. 1
Kaya FN, Yavascaoglu B, Turker G, Yildirim A, Gurbet A, Mogol EB, et al. Intravenous dexmedetomidine, but not midazolam, prolongs bupivacaine spinal anesthesia. Can J Anaesth 2010;57:39-45.  Back to cited text no. 2
Venn RM, Bradshaw CJ, Spencer R, Brealey D, Caudwell E, Naughton C, et al. Preliminary UK experience of dexmedetomidine, a novel agent for postoperative sedation in the intensive care unit. Anaesthesia 1999;54:1136-42.  Back to cited text no. 3
Jorm CM, Stamford JA. Actions of the hypnotic anaesthetic, dexmedetomidine, on noradrenaline release and cell firing in rat locus coeruleus slices. Br J Anaesth 1993;71:447-9.  Back to cited text no. 4
Sachan P, Kumar N, Sharma JP. Efficacy of premixed versus sequential administration of clonidine as an adjuvant to hyperbaric bupivacaine intrathecally in cesarean section. Anesth Essays Res 2014;8:20-5.  Back to cited text no. 5
  [Full text]  
Ahmed MS, Talaat SM. Effect of intravenous versus intrathecal low-dose dexmedetomidine on spinal block in lower limb orthopedic surgery. Ain Shams J Anaesthesiol 2014;7:205.  Back to cited text no. 6
Campora E, Merlini L, Pace M, Bruzzone M, Luzzani M, Gottlieb A, et al. The incidence of narcotic-induced emesis. J Pain Symptom Manage 1991;6:428-30.  Back to cited text no. 7
Ishii H, Kohno T, Yamakura T, Ikoma M, Baba H. Action of dexmedetomidine on the substantia gelatinosa neurons of the rat spinal cord. Eur J Neurosci 2008;27:3182-90.  Back to cited text no. 8
Guo TZ, Jiang JY, Buttermann AE, Maze M. Dexmedetomidine injection into the locus ceruleus produces antinociception. Anesthesiology 1996;84:873-81.  Back to cited text no. 9
Westfall TC, Westfall DP. Adrenergic agonists and antagonists. In, Brunton LL, Chabner BA, Knollman BC, eds. Goodman & Gilman's the pharmacological basis of therapeutics. 12th ed. New York: McGraw-Hill, 2011. pp. 277-333.  Back to cited text no. 10
Magdy H, Mohsen M, Saleh M. The effect of intrathecal compared with intravenous dexmedetomidine as an adjuvant to spinal bupivacaine anaesthesia for cesarean section. Ain Shams J Anaesthesiol 2015;8:93-9.  Back to cited text no. 11
Harsoor S, Rani DD, Yalamuru B, Sudheesh K, Nethra S. Effect of supplementation of low dose intravenous dexmedetomidine on characteristics of spinal anaesthesia with hyperbaric bupivacaine. Indian J Anaesth 2013;57:265-9.  Back to cited text no. 12
[PUBMED]  [Full text]  
Al-Mustafa MM, Abu-Halaweh SA, Aloweidi AS, Murshidi MM, Ammari BA, Awwad ZM, et al. Effect of dexmedetomidine added to spinal bupivacaine for urological procedures. Saudi Med J 2009;30:365-70.  Back to cited text no. 13
Kubre J, Sethi A, Mahobia M, Bindal D, Narang N, Saxena A. Single dose intravenous dexmedetomidine prolongs spinal anesthesia with hyperbaric bupivacaine. Anesth Essays Res 2016;10:273-7.  Back to cited text no. 14
[PUBMED]  [Full text]  
Reddy VS, Shaik NA, Donthu B, Sannala VK, Jangam V. Intravenous dexmedetomidine versus clonidine for prolongation of bupivacaine spinal anaesthesia and analgesia: A randomized double blind study. J Anaesth Clin Pharm 2013;29;342-6.  Back to cited text no. 15
Onttonen T, Pertovaara A. The mechanical antihyperalgesic effect of intrathecally administered MPV-2426, a novel alpha2 -adrenoceptor agonist, in a rat model of postoperative pain. Anesthesiology 2000;92:1740-5.  Back to cited text no. 16


  [Figure 1]

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8]


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