Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 8  |  Issue : 1  |  Page : 93-99

The effect of intrathecal compared with intravenous dexmedetomidine as an adjuvant to spinal bupivacaine anesthesia for cesarean section


Department of Anesthesia, Intensive Care, and Pain Management, Ain Shams University, Cairo, Egypt

Date of Submission03-Sep-2014
Date of Acceptance03-Oct-2014
Date of Web Publication25-Mar-2015

Correspondence Address:
Hadil Magdy
Department of Anesthesia, Intensive Care, and Pain Management, Ain Shams University, 12345 Cairo
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.153949

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  Abstract 

Introduction
The aim of this study was to evaluate the effect of intrathecal compared with intravenous dexmedetomidine as an adjuvant to spinal bupivacaine anesthesia for pregnant women undergoing cesarean section on intraoperative and postoperative analgesia with special emphasis on their sedative properties and on the neonatal outcome.
Patients and methods
A total of 105 women of ASA physical status I or II at term pregnancy were enrolled randomly into three groups. Patients in group I received spinal anesthesia with hyperbaric bupivacaine. In group II, 5 μg dexmedetomidine was added to bupivacaine. In group III, after administration of spinal anesthesia with bupivacaine and an intravenous infusion of 0.5 μg/kg/h dexmedetomidine throughout the surgery, the incidence of hypotension, bradycardia, the onset, and the duration of sensory and motor block and the postoperative pain score were assessed.
Results
No differences were observed in the rate of occurrence of hypotension and bradycardia between the three groups. The time to reach the peak sensory level was shorter in group II and group III with a longer duration compared with group I. The duration of motor block was shorter in group I compared with the two other groups with no significant difference between the three groups in the onset of motor block. The onset of postoperative pain was significantly earlier in group I, and more patients in group I needed supplementary analgesia. No significant difference was noted between the three groups regarding the Apgar score and the incidence of maternal side effects such as nausea, vomiting, and dryness of the mouth.
Conclusion
The use of intrathecal dexmedetomidine or intravenous dexmedetomidine as an adjuvant to spinal bupivacaine in women undergoing elective cesarean section improved the intraoperative condition and the quality of postoperative analgesia without neonatal or maternal side effects.

Keywords: bupivacaine, dexmedetomidine, intrathecal, intravenous, spinal anesthesia


How to cite this article:
Magdy H, Mohsen M, Saleh M. The effect of intrathecal compared with intravenous dexmedetomidine as an adjuvant to spinal bupivacaine anesthesia for cesarean section. Ain-Shams J Anaesthesiol 2015;8:93-9

How to cite this URL:
Magdy H, Mohsen M, Saleh M. The effect of intrathecal compared with intravenous dexmedetomidine as an adjuvant to spinal bupivacaine anesthesia for cesarean section. Ain-Shams J Anaesthesiol [serial online] 2015 [cited 2021 Oct 24];8:93-9. Available from: http://www.asja.eg.net/text.asp?2015/8/1/93/153949


  Introduction Top


Spinal anesthesia is a preferred and popular technique used in cesarean section as it allows the parturients to participate in the birth process of their babies, while avoiding the risk of general anesthesia [1] .

Different agents such as opioids and α2-adrenergic agonists have been used as adjuncts to local anesthesia to improve the quality of intraoperative and postoperative analgesia [2],[3],[4],[5] .

The addition of low-dose fentanyl to spinal anesthesia augments the analgesia produced by intrathecal local anesthetics, but a high incidence of undesirable side effects such as pruritus or postoperative nausea and vomiting are well known [6] .

Dexmedetomidine is a highly selective α2-adrenergic agonist with an affinity eight times greater than that of clonidine [7] . When used as an adjuvant in regional anesthesia, dexmedetomidine has both analgesic and sedative properties [8] .

Dexmedetomidine has also been used for premedication and as an adjuvant to general anesthesia. Intravenous dexmedetomidine can be titrated to the desired level of sedation with decreased inhalational anesthesia and opioid requirements during general anesthesia [8] .

We hypothesize that intravenous dexmedetomidine might prolong the duration of spinal analgesia similar to intrathecal dexmedetomidine.

Accordingly, the aim of this prospective randomized study was to evaluate the effect of intrathecal compared with intravenous dexmedetomidine as an adjuvant to spinal bupivacaine anesthesia in pregnant women undergoing cesarean section on intraoperative and postoperative analgesia with special emphasis on their sedative properties and on the neonatal outcome.


  Patients and methods Top


After approval of the local institutional ethical committee, the study was conducted in Ain Shams University Hospital between April 2013 and January 2014.

Inclusion criteria were healthy women (ASA I or II) carrying a singleton fetus at term, scheduled to undergo elective cesarean section under spinal anesthesia. Patients with body weight more than 110 kg or height less than 150 cm, patients refusing spinal anesthesia, or those who had any contraindication to regional anesthesia were excluded from the study.

After a detailed preanesthetic check-up, informed written consent was obtained from the parturients on presenting at the labor ward.

On arrival to the operating room, standard anesthesia monitors were attached to the patient including pulse oximetry, ECG, and noninvasive blood pressure, and the baseline readings were recorded. An intravenous cannula was placed, and the patients were preloaded with lactated Ringer's solution (15 ml/kg) infused over 20 min. Spinal anesthesia was performed in the sitting position at the L4-L5 level or at the L3-L4 level through a midline approach using a 25-G Quincke spinal needle (B. Braun Medical, Bethiehem, USA) under proper aseptic conditions.

Using a computer-generated random list, patients were assigned to one of the three groups. Group I received 2 ml of 0.5% hyperbaric bupivacaine (Astra Zeneca, Luton, UK) +0.5 ml normal saline. Group II received 2 ml of 0.5% hyperbaric bupivacaine+5 μg dexmedetomidine (Precedex 100 μg/ml; Hospira, Lake forest, USA) diluted to 0.5 ml in normal saline. Group III received 2 ml of 0.5% hyperbaric bupivacaine (Astra Zeneca)+0.5 ml normal saline as in group I. Immediately after spinal injection, all patients were turned into the supine position. Patients allocated to group III received an intravenous infusion of dexmedetomidine (0.5 μg/kg/h) through an intravenous infusion pump, which started after patients lay back and was continued till the end of the surgery. The other two groups received an intravenous infusion of normal saline in the same calculated volume.

The intravenous formulae were prepared by an anesthetist who was not involved in the study or care of the patients. Both the patient and the anesthetist performing the block were blinded to the study drug.

Oxygen (3 l/min) was applied to all patients through nasal prongs, and patients' ECG, with heart rate (HR), systolic blood pressure, diastolic blood pressure, mean arterial blood pressure, and peripheral oxygen saturation were monitored and recorded throughout the surgery at 1-min intervals for the first 10 min, and then every 3 min till the end of the procedure, and then every 15 min in the postanesthesia care unit (PACU) until the patient was discharged to the ward.

Any decrease in the mean arterial pressure (MAP) greater than 20% from the baseline value was treated with a 5 mg bolus of intravenous ephedrine injection and administration of 300 ml of lactated Ringer's solution over 10 min, with an increasing degree of left uterine displacement. In the event of bradycardia (HR < 50 beats/min or >20% from the baseline HR value), intravenous atropine (0.5 mg) was administered. Other side effects such as nausea, vomiting, dryness of the mouth, headache, or shivering were recorded.

Sensory and motor block were assessed every 2 min for the first 10 min and thereafter every 5 min during surgery and postoperatively till discharge from the PACU.

The sensory block was assessed using a cotton swab and cold (iced tube) in the midaxillary line bilaterally. Measurement included the onset (the time from the induction of spinal anesthesia to reach a T10 sensory level), the highest dermatome level achieved, and the duration of the sensory block (the time of sensory regression to S1).

The motor block was assessed using the Modified Bromage score (0 = no paralysis, 1 = unable to raise the extended leg, 2 = unable to flex the knee, 3 = unable to the flex ankle) [7] . Measurements included the onset (the time from the induction of spinal anesthesia till Bromage = 3) and the duration of the motor block (the time to return to Bromage = 0).

Patients were discharged from the PACU after sensory regression to S1 dermatome and Bromage scale = 0.

Sedation was recorded by a five-point scale (1 = completely awake; 2 = awake, but drowsy; 3 = asleep, but responsive to verbal commands; 4 = asleep, but responsive to tactile stimulus; 5 = asleep and not responsive to any stimulus) [9] . The recording was obtained just before the initiation of surgery and thereafter every 15 min till the end of the procedure.

Insufficient intraoperative analgesia (on patient's request) was treated with an intravenous bolus of fentanyl (50 μg) increments or general anesthesia, and patients were excluded from the study.

After delivery of the fetus, umbilical blood gas analysis for pH and PO 2 were measured. The Apgar score of the newborn was recorded at 1 min and at 5 min after birth.

In the postoperative period, pain and sedation scores were assessed immediately at the PACU, and then every hour for the first 6 h and then every 6 h in the first 24 h. Postoperative analgesia was assessed by a 10-point verbal rating scale, in which 0 represented no pain and 10 represented the worst possible pain. Patients with pain greater than 4 were given 1.5 mg/kg intramuscular diclofenac. The time of the first request for postoperative analgesia and the number of patients who required supplemental analgesia were recorded.


  The study outcome Top


The primary outcome of this study was the duration of postoperative analgesia (the time to the first analgesic request) and secondary outcomes were the onset and the duration of sensory and motor blockade, possible dexmedetomidine side effects (hypotension, excessive sedation, bradycardia), and side effects in the newborn (newborn Apgar scores and umbilical cord blood gas analysis).

Statistical analysis and sample size

On the basis of previous studies, we assumed that at least 29 participants per group were needed to demonstrate a difference in the duration of postoperative analgesia (50% increase) with an α-error of 0.05 and a power of 90%. To account for possible loss, we decided to include 35 patients in each group.

All statistical analyses were performed using SPSS version 16.0 for Windows (SPSS Inc., Chicago, Illinois, USA). Numerical variables were presented as mean and SD, whereas categorical data were presented using counts and percentages.

Analysis of variance was used for the analysis of continuous variable. The χ2 -test or Fisher's exact tests were used for categorical variables. A post-hoc test was applied using the Bonferroni method for adjusting for multiple comparisons. P-value less than 0.05 was considered to indicate statistical significance.


  Results Top


In our study, total 105 parturients were randomized (35 patients in each group). After randomization, five patients could not be analyzed: two patients withdrew consent after randomization (one patient in group II and one in group III), and in three patients, spinal anesthesia was converted to general anesthesia (one in each group).

The demographic data and the mean duration of surgery are shown in [Table 1], with no statistically significant difference between the three study groups.

The baseline MAP and HR were comparable in all groups. After performing the spinal anesthesia and throughout the first 24 h, the mean values of MAP and HR showed no significant difference between the three groups and the lowest HR and MAP recorded during the study period were ~15% lower than the baseline values, with no differences among groups ([Table 2]).
Table 1: Patients demographic and surgery data

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Table 2: Patients' clinical characteristics

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However, seven patients in group III and six patients in each of the other two groups developed intraoperative hypotension, which was treated with ephedrine (5 mg) and an increasing rate of intravenous crystalloid fluid infusion with left uterine displacement.

Regarding bradycardia, three patients in group II compared with four patients in group III and three patients in group I had bradycardia and returned to normal with boluses of 0.3-0.5 mg atropine.

There were no changes in oxyhemoglobin saturation (SpO 2 ) at any time throughout the study period in all enrolled patients, and no woman had an SpO 2 lower than 94% during the first 24 h after spinal anesthesia ([Table 2]).

The incidence of postoperative complications, such as nausea, vomiting, headache, dryness of the mouth, and shivering, were similar in all the groups ([Table 3]). Regarding the outcomes of the newborn, there were no significant differences regarding the newborn's birth weight. The Apgar score at 1 and 5 min and the umbilical cord blood gas analysis were comparable in all groups ([Table 4]).
Table 3: Incidence of adverse events

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Table 4: Neonatal outcome

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Insignificant differences were recorded between the three study groups regarding the maximal dermatomal sensory blockade level achievement. However, the onset of sensory blockade was slower (the time to reach T10), with a shorter duration (the time for sensory regression to S1) in group I compared with the other two groups (7.1 ± 0.1 vs. 3.5 ± 0.6 or 3.8 ± 0.4, respectively, and 180.9 ± 14.1 vs. 257.2 ± 14.1 or 266 ± 12.1, respectively) ([Table 5]).
Table 5: Sensory block characteristics

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The mean onset time of motor blockade (the time to reach Bromage scale = 3) was insignificantly different between the three groups. However, the time to motor regression (the time to reach Bromage = 0) was significantly shorter in group I compared with the two other groups (160 ± 5.1 vs. 188 ± 8.1 or 185 ± 5.1) ([Table 6]).
Table 6: Motor block characteristics

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The visual analogue scale pain score recorded postoperatively at T0 (at PACU) and till T3 (3 h after arrival to the PACU) was comparable in the three groups with no significant difference. However, the pain score assessed at 4, 5, and 6 h postoperatively were significantly higher in group I compared with groups II and III, with insignificant differences between groups II and III throughout the study period ([Table 7]). The time to the first request for postoperative analgesia was significantly shorter in group I (143 ± 27 vs. 221 ± 35 or 235 ± 25, respectively); in addition, more patients required analgesia (diclofenac) during the first 24 h after spinal anesthesia in group I than in the other two groups (16 patients, eight patients, and seven patients, respectively) ([Table 8]).
Table 7: The postoperative pain score (VAS)

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Table 8: Postoperative analgesic requirements

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Intraoperative and postoperative sedation (till 6 h postoperatively) was greater in group II and group III than in group I ([Table 9]). However, no significant difference between the three groups was recorded at T12 or T24 postoperatively ([Table 9]). Excessive sedation (Ramsay score>5) was not observed in any patients in the three groups ([Table 3]).
Table 9 Intraoperative and postoperative Ramsay sedation scores

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  Discussion Top


Dexmedetomidine is a highly selective α2-adrenergic agonist drug with an affinity 8-10 times greater than that of clonidine [10],[11] . α2-Adrenergic agonists have both analgesic and sedative effects by binding to α2-receptors in the locus coeruleus, which diminishes the release of norepinephrine and inhibits sympathetic activity [12],[13],[14] . The mechanism of action by which dexmedetomidine prolongs the effect of local anesthetics is not well known. The α2-adrenoceptor agonist acts by binding to presynaptic C fibers and postsynaptic dorsal horn neurons, thus depressing the release of C fiber transmittors and hyperpolarizing dorsal horn postsynaptic neurons. Therefore, this may cause an additive synergistic effect to the mechanism of action of local anesthetics [12] .

Intravenous dexmedetomidine may also augment the effect of the intrathecal block. Although the mechanism remains unclear, the supraspinal direct analgesic and the vasoconstrictive effect of dexmedetomidine are likely to be involved [13],[14],[15] . Kaya and colleagues found that intravenous dexmedetomidine has supraspinal action, which could explain the prolongation of spinal anesthesia after intravenous administration of dexmedetomidine. Neurons in the locus coeruleus are connected to the noradrenergic nuclei in the brain stem. The activity of noradrenergic neurons is decreased by agonists acting at α2-adrenergic receptors in the locus coeruleus cell bodies, and therefore exerts a descending inhibitory effect on nociception in the spinal cord [14] .

To date, there have been a number of clinical studies that investigated the synergistic interaction between dexmedetomidine and local anesthetics [13],[14],[15],[16],[17],[18],[19],[20] . Dexmedetomidine was infused in many studies [13],[14],[15],[16] , whereas the intrathecal dexmedetomidine route was used in many other studies [17],[18],[19],[20],[21] to augment the effect of spinal anesthesia.

In four studies that used intravenous dexmedetomidine, two of them used a loading dose of dexmedetomidine of 1 μg/kg over 10 min, and then a maintenance dose of 0.5 or 0.4 μg/kg/h [13],[16] , and in the other two studies, a single dose of dexmedetomidine 0.5 μg/kg [14] or 1 μg/kg [15] was used. However, in the studies that used intrathecal dexmedetomidine, a low dose of 5 μg was compared with high-dose 10 μg dexmedetomidine [18] or low-dose clonidine [16] with low-dose fentanyl [21] .

In these studies [13],[14],[15],[16],[17],[18],[19],[20],[21] , dexmedetomidine prolonged the duration of sensory and motor block of spinal anesthesia when used intravenously or intrathecaly. In the current study, the addition of a low-dose intrathecal or intravenous infusion of dexmedetomidine as an adjuvant to spinal bupivacaine accelerated and prolonged the sensory block and to a lesser extent prolonged the motor block of bupivacaine. Dexmedetomidine may exert its effect on sensory and motor block through the supraspinal, spinal, and peripheral action of the α2-agonist effect [22] . There may be a direct inhibition of impulse conduction in large myelinated Aa-fibers, and the 50% effective concentration of α2-agent measured approximately four-fold that needed for C fibers [16] . This may explain the lesser effect on motor block compared with sensory block observed in our study.

The addition of low-dose dexmedetomidine intrathecally or intravenously to spinal anesthesia for cesarean sections in our study resulted in a significant reduction in the visual analogue scale pain score with consequent delay in the time to the first request of analgesia postoperatively. Dexmedetomidine is a selective α2-agonist with a dose-dependent analgesic effect and a sedative effect. It has been known that patient sedated with low-dose dexmedetomidine remain cooperative and easily arousable [23] . In our study, low-dose dexmedetomidine intravenously or intrathecally provided sedation intraoperatively and postoperatively till the first 6 h. Excessive sedation (Ramsay score = 5) was not observed in our patients. Sedating the patient provided better conditions for the surgeon and the patient, provided the hemodynamic stability was preserved. Previous studies have demonstrated the safety of dexmedetomidine in spinal anesthesia [13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27] . However, it has been shown that dexmedetomidine in relatively high doses can lead to hypotension when administered either neuroaxially or intravenously [15] . Low-dose dexmedetomidine with sufficient preoperative hydration was used in our study, and thus the patients remained hemodynamically stable, and the hypotension that occurred in some patients was easily treated with ephedrine and left uterine displacement. Our results showed that dexmedetomidine would not increase the risk of side effects such as nausea, vomiting, headache, and shivering. Previous studies [13],[15],[18],[19] reported the use of dexmedetomidine without any neurological consequence within 2 weeks after surgery with no or minimal respiratory depression effect.

Bradycardia during spinal anesthesia is believed to be secondary to decreased venous return and from the blockade of sympathetic stimulation to the heart that arise from the first four thoracic spinal segments [24],[25],[26],[27] . Therefore, bradycardia with low-dose spinal anesthesia is uncommon, and this result is in line with our study results, which recorded only three cases of bradycardia (in group I and group II) and four cases (in group III) that required atropine. However, the addition of dexmedetomidine to low-dose spinal anesthesia in previous studies [13],[16],[18],[19] was found to increase the risk of bradycardia requiring atropine. In all these studies, the bradycardia could be reversed by atropine with no serious side effects. The bradycardia-inducing effect of dexmedetomidine in these studies may be explained by the decreased sympathetic outflow and the circulating effect of catecholamines [12] .

Using sedatives and narcotics in a pregnant woman have always been a challenge as these drugs may cross the uteroplacental barrier and can lead to deleterious effects on the baby. Dexmedetomidine has a high placental retention (0.77 maternal/fetal index), and it is a highly lipophilic drug. As a result, it is retained in the placental tissue [28],[29] , and therefore, it does not cross the uteroplacental barrier or crosses in a negligible concentration.

Intravenous dexmedetomidine at a dose of 0.4-0.6 μg/kg/h attenuates maternal hemodynamics and the hormonal response to cesarean section without adverse effects [30],[31],[32],[33] , and a single low-dose dexmedetomidine (2.5 μg) intrathecally added to spinal anesthesia prolonged the duration of analgesia significantly without adverse effects such as respiratory depression to the mother or the newborn.

In the current study, all babies are delivered with a normal Apgar score.

In conclusion, we have shown that low-dose dexmedetomidine intravenously or intrathecally prolonged the sensory blockade and the analgesic effect of spinal anesthesia during cesarean section. It also provided sedative effect to the mother without significant adverse effects to the mother or the newborn.


  Conclusion Top


Adding intrathecal dexmedetomidine or intravenous dexmedetomidine as an adjuvant to spinal bupivacaine in women undergoing elective cesarean section improved the intraoperative condition and the quality of postoperative analgesia without neonatal or maternal side effects.


  Acknowledgements Top


Conflicts of interest

None declared.

 
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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6], [Table 7], [Table 8], [Table 9]


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  In this article
   Abstract
  Introduction
  Patients and methods
  The study outcome
  Results
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