Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 7  |  Issue : 3  |  Page : 388-392

Comparing the effect of adding dexmedetomidine versus dexamethasone on prolonging the duration of intrathecal bupivacaine in lower abdominal operations


Department of Anesthesia, Faculty of Medicine, Cairo University, Cairo, Egypt

Date of Web Publication27-Aug-2014

Correspondence Address:
Nashwa Sami Elzayyat
Department of Anesthesia, Faculty of Medicine, Cairo University, Cairo
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.139574

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  Abstract 

Objective
The aim of this study was to evaluate the efficacy of adding dexmedetomidine compared with dexamethasone to bupivacaine to prolong the duration of spinal anesthesia and analgesia in lower abdominal operations.
Patients and methods
This randomized double-blind study included 60 ASA I or II patients, aged between 25 and 55 years old, scheduled for lower abdominal operations. They were administered 0.5% intrathecal bupivacaine injection and randomly divided into one of three groups: control group (GC), in which patients were administered additional 1 ml of saline; GDX group, in which patients were administered 4 mg dexamethasone; and GDM group, in which patients were administered 10 μg dexmedetomidine. The patients were monitored for heart rate, mean arterial pressure, oxygen saturation, onset and duration of sensory and motor block, intraoperative and postoperative sedation and pain, and adverse events.
Results
Compared with GC, GDM had significantly faster onset of sensory block (P = 0.006), longer duration of sensory block (P < 0.001), longer duration of motor block (P = 0.013), longer duration of postoperative analgesia (P < 0.001), and significantly higher sedation score (P < 0.001). Compared with GDX, GDM had significantly longer duration of sensory block (P = 0.025) and longer duration of postoperative analgesia (P < 0.001). Compared with GC, GDX had significantly longer duration of sensory block (P < 0.001) and longer duration of postoperative analgesia (P < 0.001). The three groups were comparable in terms of the onset of motor block (P = 0.637) and frequency of adverse events.
Conclusion
Intrathecal dexmedetomidine and dexamethasone are safe and effective adjuncts to intrathecal bupivacaine anesthesia in lower abdominal surgery. Dexmedetomidine showed to provide more rapid onset and longer duration of sensory block, longer duration of motor block, and longer postoperative analgesia.

Keywords: dexamethasone, dexmedetomidine, spinal anesthesia


How to cite this article:
Elzayyat NS, Ahmed Nagy HI, Girgis K. Comparing the effect of adding dexmedetomidine versus dexamethasone on prolonging the duration of intrathecal bupivacaine in lower abdominal operations. Ain-Shams J Anaesthesiol 2014;7:388-92

How to cite this URL:
Elzayyat NS, Ahmed Nagy HI, Girgis K. Comparing the effect of adding dexmedetomidine versus dexamethasone on prolonging the duration of intrathecal bupivacaine in lower abdominal operations. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2017 Jun 27];7:388-92. Available from: http://www.asja.eg.net/text.asp?2014/7/3/388/139574


  Introduction Top


Spinal anesthesia is the safest during lower abdominal operations; many studies have been concerned about prolonging the duration of spinal anesthesia by adding different adjuvants. One of these additives is dexamethasone, which has been proved in many studies to prolong the duration of peripheral blocks both in animal and human studies [1].

It is known that dexamethasone has anti-inflammatory and analgesic action by inhibition of transmission in nociceptive C-fibers and neural discharge. When given as an additive in peripheral nerve blocks or in intrathecal anesthesia, it prolongs the duration of anesthesia [2].

Dexmedetomidine is a selective α2-adrenergic agonist that is used as an adjuvant to general anesthesia, and also by acting on the intrathecal α2-receptors, it can be added and used as an adjuvant in spinal anesthesia, prolonging both motor and sensory block [3,4]. Dexmedetomidine is eight times more specific and a highly selective α2- adrenoreceptor agonist compared with clonidine, thereby making it a useful and safe adjunct in diverse clinical applications [4].

The aim of this study was to compare the effect of adding dexmedetomidine versus dexamethasone to bupivacaine for prolonging the duration of spinal anesthesia and analgesia in lower abdominal operations, and to evaluate any possible side effects.


  Patients and methods Top


This is a randomized prospective double-blind study conducted in the Anesthesia Department of Kasr El-Aini Hospital between November 2012 and April 2013 after obtaining approval of the local ethical and scientific committees.

A total of 60 patients scheduled for lower abdominal operations (herniorrhaphy, varicocelectomy, and hemorrhoidectomy) participated in the study after providing informed consent. They fulfilled the inclusion criteria: age of 25-55 years, and ASA I or II. Patients were excluded from the study if they had major cardiac, respiratory, hepatic or renal diseases, hypersensitivity to used drugs, uncontrolled diabetes, coagulopathy, or infection at the site of injection.

Methods

On arrival to the operating room, an 18-G intravenous cannula was inserted into the cephalic vein under local infiltration anesthesia and all monitors were attached (noninvasive blood pressure, pulse oximetry, and five-lead ECG), and then lactated Ringer's infusion 10 ml/kg was started as preload. Baseline readings were recorded.

All patients were prepared for spinal anesthesia using 2.5 ml bupivacaine (0.5%). The patients were randomly divided into one of three groups: control group (GC), in which patients were administered an additional 1 ml of saline, dexamethasone group (GDX), in which patients were administered 4 mg dexamethasone in 1 ml saline, and dexmedetomidine group (GDM), in which patients were administered 10 μg dexmedetomidine in 1 ml saline.

Intrathecal anesthesia was administered using a 22-G spinal needle inserted into the L3-L4 space with the patient in the sitting position with complete sterilization. Then the patient was allowed to be in the supine position. The patients were monitored for heart rate, mean arterial pressure, and oxygen saturation every 5 min after injection for 30 min, and then every 15 min. Sensory block was assessed using pin prick every 2 min while the patient was supine till proper level was reached (T10 dermatome), and Bromage scale was measured to reach Bromage 3 before surgery. Any decrease in heart rate below 60/min was treated with intravenous atropine (0.01 mg/kg), and any decrease in mean arterial pressure below 20% of the basal reading was treated by fluid bolus and 5 mg intravenous increments of ephedrine.

Patient sedation was tested using Ramsay scale both intraoperative and postoperative till discharge (no sedation was given from the start). Pain in postanesthesia care unit was assessed with visual analogue scale (VAS) between 0 and 10 (0 = no pain, 10 = the most severe pain) every 1 h. If the postoperative VAS was higher than 3, it was treated by intramuscular meperidine. All times were recorded from the end of spinal injection as a zero point. Postoperative nausea and vomiting was managed if intolerable with metoclopramid 10 mg intravenously.

Bromage scale (0-3) [5]:

0: The patient is able to move the hip, knee and ankle.

1: The patient is unable to move the hip, but can move knee and ankle.

2: The patient is unable to move the hip and knee but can move the ankle.

3: The patient cannot move the hip, knee and ankle.

Ramsay scale (1-6) [6]:

1: Anxious, agitated or restless.

2: Cooperative, oriented.

3: Respond to commands.

4: Asleep but responsive to stimulation.

5: Asleep with sluggish response to stimuli.

6: Asleep no response.

Statistical methods

Assuming α- value of 0.05 (two-tailed), β- value of 0.1, and given that the time to two-segment regression (sensory) with bupivacaine was reported to be 95.38 ± 17.41 min, a total sample size of 38 patients, equally allocated into two equal groups (19 per group), will be required to detect an assumed clinically significant difference of 20% (effect size 'd' = 1.096) or more in the time to two-segment regression (sensory) between groups, with a power of 90%. Estimation of sample size was carried out using computer program G*Power 3 (Franz Faul, Universitδt Kiel, Germany); independent samples t-test was used. Data were analyzed using SPSS version 20. Data were presented as mean (SD) or patient's n (%). χ2 -test was used to examine the relation between qualitative variables. Comparison between the three groups was made using analysis of variance test, and then post-hoc 'Scheffe test' was used for pairwise comparison. A P-value less than 0.05 was considered significant.


  Results Top


[Table 1] shows demographic and clinical characteristics of the three studied groups. The three groups were comparable in age, sex, and type of surgery.
Table 1 Demographic and clinical characteristics of the three studied groups

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The onset of sensory block was significantly faster in GDM compared with the control group (P = 0.006) but comparable to GDX (P = 0.225). There was no significant difference in the onset of sensory block between the GDX and control groups (P = 0.116). The three groups were comparable in terms of the onset of motor block (P = 0.637). The time to two-segment regression was significantly longer in the GDM group compared with the control group (P < 0.001) and the GDX group (P = 0.025), and it was significantly longer in the GDX group compared with the control group (P < 0.001). On the contrary, the time to motor block regression to Bromage 0 was significantly longer in the GDM group compared with the control group (P = 0.013) but not compared with the GDX group (P = 0.301). There was no significant difference in motor block regression to Bromage 0 between the GDX and control groups (P = 0.095). Sedation scores of all patients was 2-3, indicating adequate and acceptable sedation and was comparable between the three groups; however, the patients receiving dexmedetomidine were more sedated with no statistically significant difference. Time to first call for analgesics was significantly longer in the GDM compared with the GDX and control groups and in the GDX group compared with the control group (P < 0.001) [Table 2].
Table 2 Block onset and regression times (min)

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The immediate postoperative VAS score and score after 12 h were significantly lower in the GDM and GDX groups compared with the control group [Figure 1].
Figure 1: Postoperative visual analogue scale (VAS) score during the fi rst 24 h in the three studied groups. T0 = immediate postoperative. *Significant compared with control group.

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The mean sedation score was significantly higher in GDM. Patients with sedation score greater than 3 were 70% in the GDM group compared with 25 and 15% in the GDX and control groups, respectively.

The proportions of adverse effects are summarized in [Table 3]. The frequency of bradycardia, hypotension, nausea, and vomiting were comparable between the three groups.
Table 3 Proportion of adverse events in the three studied groups

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  Discussion Top


The originality of this study arises from comparing intrathecal dexmedetomidine/bupivacaine versus dexamethasone/bupivacaine as very few studies, if any, compared both drugs.

This study found that dexmedetomidine added to intrathecal bupivacaine was associated with a faster onset and longer duration of the sensory blockade compared with addition of dexamethasone in lower abdominal surgeries under spinal anesthesia. In addition, it causes longer duration of motor block and more sedation. Meanwhile, addition of dexamethasone prolonged duration of sensory block. Postoperatively, dexmedetomidine produced longer duration of analgesia. Frequency of adverse events was limited in all groups.

Dexmedetomidine's ability to prolong sensory and motor blockade could be explained by being a highly selective α2-adrenergic receptor agonist. In addition, it has a sedative, analgesic, perioperative sympatholytic, anesthetic-sparing, and hemodynamic-stabilizing properties [7]. Moreover, it has the advantage of no respiratory depression [8]. In the spinal cord, it activates α2-adrenergic receptors in the neurons of the superficial dorsal horn [9]. It directly reduces pain transmission by reducing the release of pronociceptive transmitter, substance P, and glutamate from primary afferent terminals, and by hyperpolarizing spinal interneurons by G-protein-mediated activation of potassium channels [10].

The possible explanation of the effect of adding dexmedetomidine to intrathecal bupivacaine lies in its synergistic effect being selective α2-adrenergic receptor agonist, which binds to the presynaptic C-fibers and postsynaptic dorsal horn neurons. Thus, it produces analgesia by depressing the release of C-fiber transmitters, hyperpolarization of postsynaptic dorsal horn neurons, whereas bupivacaine as a local anesthetic acts by blocking sodium channels [11].

The study results went in line with the study conducted by Shukla et al. [12] who compared dexmedetomidine versus magnesium sulfate added to intrathecal bupivacaine and found that dexmedetomidine shortened the onset and prolonged the duration of spinal anesthesia. Another recent study proved superiority of intrathecal dexmedetomidine in comparison with clonidine and fentanyl. It provided prolonged motor and sensory block and reduced demand of additional analgesics [13].

The current study results were in agreement with the two studies comparing clonidine and dexmedetomidine in different doses (5 and 3 μg, respectively) as adjuncts to bupivacaine. Both found the duration of sensory and motor block to be prolonged with dexmedetomidine compared with clonidine. Postoperative analgesia was comparable in these two groups and superior compared with bupivacaine alone [14,15].

Dexmedetomidine was tried as an adjunct to spinal bupivacaine through the intravenous route. It was found to prolong sensory and motor block with a good sedative effect [16]. Compared with midazolam, intravenous dexmedetomidine had prolonged sensory block and longer time to first request for postoperative analgesia, whereas duration of motor block was similar [17]. Similarly, premedication with intravenous dexmedetomidine is better than clonidine to provide intraoperative sedation and postoperative analgesia during bupivacaine spinal anesthesia for orthopedic lower limb surgery [18]. In post-thoracotomy patients, intravenous dexmedetomidine demonstrated effective analgesia when used as an adjunct to thoracic epidural bupivacaine infusion [19].

Dexmedetomidine has also been studied as an epidural adjuvant and was found to prolong duration of sensory and motor block and postoperative analgesia. It was reported to be without serious adverse effects [20]. Furthermore, dexmedetomidine was reported to be successful in promoting analgesia in children undergoing lower abdominal surgeries under caudal bupivacaine anesthesia [21].

Almost all of the previously mentioned studies as well as the current study confirmed safety and hemodynamic stability of dexmedetomidine, whether administered intravenously or intrathecally as an adjuvant to spinal bupivacaine anesthesia.

On the contrary, in this study, dexamethasone was found to prolong the sensory blockade and prolong the time to first call for analgesia when added to intrathecal bupivacaine compared with bupivacaine alone. Intrathecal dexamethasone as an analgesic could be explained by influencing prostaglandin production. Corticosteroids are capable of reducing prostaglandin synthesis by inhibition of phospholipase A2 through the production of calcium-dependent phospholipid-binding proteins called annexins, and by the inhibition of cyclooxygenases during inflammation [22].

The results of the current study regarding dexamethasone went in line with a study conducted by Bani-Hashem et al. [2] who reported an increase in the duration of sensory block associated with the addition of intrathecal dexamethasone.

The study results showed that adding dexmedetomidine to intrathecal bupivacaine prolonged the sensory blockade duration by 38% compared with bupivacaine alone, although the sensory blockade duration was prolonged by 23% when adding dexamethasone to intrathecal bupivacaine. The cost effectiveness of dexmedetomidine versus dexamethasone is an issue of conflict, as tangible cost of dexmedetomidine is higher than dexamethasone; yet the intangible costs (hospital stay, wound infection, nausea and vomiting, ICU stay if needed, antibiotics …. etc.) need to be considered in drug selection.


  Conclusion Top


Addition of dexmedetomidine to intrathecal bupivacaine enhances onset and prolongs duration of sensory and motor block, and prolongs postoperative analgesia compared with dexamethasone when added to intrathecal bupivacaine.


  Acknowledgements Top


 
  References Top

1.Movafegh A, Razazian M, Hajimaohamadi F, Meysamie A. Dexamethasone added to lidocaine prolongs axillary brachial plexus blockade. Anesth Analg 2006; 102:263-267.  Back to cited text no. 1
    
2. Bani-Hashem N, Hassan-Nasab B, Pour EA, Maleh PA, Nabavi A, Jabbari A. Addition of intrathecal dexamethasone to bupivacaine for spinal anesthesia in orthopedic surgery. Saudi J Anaesth 2011; 5:382-386.  Back to cited text no. 2
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3. Gupta R, Bogra J, Verma R, Kohli M, Kushwaha JK, Kumar S. Dexmedetomidine as an intrathecal adjuvant for postoperative analgesia. Indian J Anaesth 2011; 55:347-351.  Back to cited text no. 3
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4. Gupta R, Verma R, Bogra J, Kohli M, Raman R, Kushwaha JK. A comparative study of intrathecal dexmedetomidine and fentanyl as adjuvants to bupivacaine. J Anaesthesiol Clin Pharmacol 2011; 27:339-343.  Back to cited text no. 4
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5. Bromage PR. A comparison of the hydrochloride and carbon dioxide salts od lidocaine and prilocaine in epidural analgesia. Acta Anaesthesiol Scand 1965; 16:55-69.  Back to cited text no. 5
    
6. Ramsay MA, Savage TM, Simpson BRJ, Goodwin R. Controlled sedation with alphaxalone-alphadalone. BMJ 1974; 2:656-659.  Back to cited text no. 6
    
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9. 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; 27:3182-3190.  Back to cited text no. 9
    
10.Stone LS, Broberger C, Vulchanova L, Wilcox GL, Hokfelt T, Riedl MS, et al. Differential distribution of alpha2A and alpha2C adrenergic receptor immunoreactivity in the rat spinal cord. J Neurosci 1998; 8:5928-5937.  Back to cited text no. 10
    
11.Kanazi GE, Aouad MT, Jabbour-Khoury SI, Al Jazzar MD, Alameddine MM, Al-Yaman R, et al. Effect of low-dose dexmedetomidine or clonidine on the characteristics of bupivacaine spinal block. Acta Anaesthesiol Scand 2006; 50:222-227.  Back to cited text no. 11
    
12.Shukla D, Verma A, Agarwal A, Pandey HD, Tyagi C. Comparative study of intrathecal dexmedetomidine with intrathecal magnesium sulfate used as adjuvants to bupivacaine. J Anaesthesiol Clin Pharmacol 2011; 27:495-499.  Back to cited text no. 12
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13.Solanki SL, Bharti N, Batra YK, Jain A, Kumar P, Nikhar SA. The analgesic effect of intrathecal dexmedetomidine or clonidine, with bupivacaine, in trauma patients undergoing lower limb surgery: a randomised, double-blind study. Anaesth Intensive Care 2013; 41:51-56.  Back to cited text no. 13
    
14.Al-Mustafa MM, Badran IZ, Abu-Ali HM, Al-Barazangi BA, Massad IM, Al-Ghanem SM. Intravenous dexmedetomidine prolongs bupivacaine spinal analgesia. Middle East J Anesthesiol 2009; 20:225-231.  Back to cited text no. 14
    
15.Kaya FN, Yavascaoglu B, Turker G, Yildirim A, Gurbet A, Mogol EB, Ozcan B. Intravenous dexmedetomidine, but not midazolam, prolongs bupivacaine spinal anesthesia. Can J Anaesth 2010; 57:39-45.  Back to cited text no. 15
    
16.Reddy VS, Shaik NA, Donthu B, Reddy Sannala VK, Jangam V. Intravenous dexmedetomidine versus clonidine for prolongation of bupivacaine spinal anesthesia and analgesia: A randomized double-blind study. J Anaesthesiol Clin Pharmacol 2013; 29:342-347.  Back to cited text no. 16
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18.Bajwa SJ, Bajwa SK, Kaur J, Singh G, Arora V, Gupta S, et al. Dexmedetomidine and clonidine in epidural anaesthesia: a comparative evaluation. Indian J Anaesth 2011; 55:116-121.  Back to cited text no. 18
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19.Salgado PF, Sabbag AT, Silva PC, Brienze SL, Dalto HP, Modolo NS, et al. Synergistic effect between dexmedetomidine and 0.75% ropivacaine in epidural anesthesia. Rev Assoc Med Bras 2008; 54:110-115.  Back to cited text no. 19
    
20.Saadawy I, Boker A, Elshahawy MA, Almazrooa A, Melibary S, Abdellatif AA, Afifi W. Effect of dexmedetomidine on the characteristics of bupivacaine in a caudal block in pediatrics. Acta Anaesthesiol Scand 2009; 53:251-256.  Back to cited text no. 20
    
21.El-Hennawy AM, Abd-Elwahab AM, Abd-Elmaksoud AM, El-Ozairy HS, Boulis SR. Addition of clonidine or dexmedetomidine to bupivacaine prolongs caudal analgesia in children. Br J Anaesth 2009; 103:268-274.  Back to cited text no. 21
    
22.Yao XL, Cowan MJ, Glawin MT, Lawrence MM, Angus CW, Shelhamer JH. Dexamethasone alters arachidonate release from human epithelial cells by induction of P11 protein synthesis and inhibition of phospholipas A 2 activity. J Biol Chem 1999; 274:17202-17208.  Back to cited text no. 22
    


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