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ORIGINAL ARTICLE
Year : 2020  |  Volume : 14  |  Issue : 3  |  Page : 521-524  

Is spinal dexmedetomidine aggravating hypotension after tourniquet deflation?


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

Date of Submission17-Jan-2021
Date of Decision24-Jan-2021
Date of Acceptance25-Jan-2021
Date of Web Publication22-Mar-2021

Correspondence Address:
Dr. Mohamed Maher El Baz
5st 1 Takseem Khattab, Mansoura
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aer.AER_7_21

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   Abstract 

Background and Aims: The addition of dexmedetomidine to spinal anesthesia decreases the incidence of tourniquet pain but may aggravate hypotension after tourniquet deflation. Methods: Fifty patients were included in this prospective, double-blinded, randomized study, randomly divided into two equal groups of 25 patients each. Spinal anesthesia was performed using 2.5 mL of 0.5% hyperbaric bupivacaine plus 0.5 mL of normal saline in control group (Group C) or 2.5 mL of 0.5% hyperbaric bupivacaine plus 0.5 mL (5 μg) of dexmedetomidine in (Group D). Tourniquet pain was treated by 50 mg of meperidine and repeated in a dose of 20 mg, and the total meperidine consumption was calculated. After tourniquet deflation, heart rate and mean blood pressure were measured for 15 min in the operating room and at these times: before induction of anesthesia (baseline), after inflating tourniquet (inflation), 1 min before deflating tourniquet (predeflation), after tourniquet deflation (10 min postdeflation), and maximum blood pressure and heart rate changes. Duration of time that started before the minimum blood pressure and maximum heart rate was changed until recovery was recorded. Results: Pain after torniquet inflation was significantly higher in the Group C compared to the Group D. The maximal change of blood pressure was lower in the dexmedetomidine than in the control group. The mean time between the maximal change in blood pressure reached and started to recover was 135 ± 14 s in the dexmedetomidine group and 80 ± 31 s in the control group (P < 0.01) and maximal heart rate change was lower in dexmedetomidine group than the control group. The time between the maximal heart rate changes until recovery was 113.2 ± 19 s in the dexmedetomidine group and 53.2 ± 11 s in the control group P < 0.01. Conclusion: Adding dexmedetomidine to spinal anesthesia decreases the incidence of tourniquet pain but aggravates the hemodynamic effect of tourniquet deflation.

Keywords: Dexmedetomidine, hypotension, spinal, tourniquet


How to cite this article:
El Baz MM, Farid AM. Is spinal dexmedetomidine aggravating hypotension after tourniquet deflation?. Anesth Essays Res 2020;14:521-4

How to cite this URL:
El Baz MM, Farid AM. Is spinal dexmedetomidine aggravating hypotension after tourniquet deflation?. Anesth Essays Res [serial online] 2020 [cited 2021 Apr 20];14:521-4. Available from: https://www.aeronline.org/text.asp?2020/14/3/521/311722


   Introduction Top


Applying a tourniquet to the extremities results in bloodless field which decreases blood loss during operation but sometimes accompanied by dull, aching tourniquet pain even when using adequate regional block.[1]

Adding dexmedetomidine to lidocaine decreases tourniquet pain and analgesics requirement in Bier block.[2]

Dexmedetomidine has a central sympatholytic effect, so improves the quality of neuraxial blocks by postsynaptic central alpha 2 adrenoceptors (α2-ARs) activation, causing hypotension and bradycardia, decreasing stress response of surgery.[3]

Dexmedetomidine when added to local anesthetic in subarachnoid block can prolong the duration of analgesia, this action can be additive or synergistic and lipophilicity of dexmedetomidine may play a role in its effects on local anesthetics.[4]

Deflation of tourniquet can cause acute hypotension and rarely, fatal hemodynamic instability.[5] So that, there is a question is raised, is intrathecal dexmedetomidine may aggravate the acute hypotension after tourniquet deflation or not?

Hypothesis of the study

We hypothesized that the addition of dexmedetomidine to spinal anesthesia may aggravate hypotension after tourniquet deflation.

Aim of the study

The primary goal of this study is to evaluate the effect of intrathecal dexmedetomidine on hemodynamics after tourniquet deflation in knee arthroscopy.

The second goal of this study is to evaluate the efficacy of addition dexmedetomidine in spinal anesthesia in decreasing the incidence of tourniquet pain and analgesic requierments.


   Methods Top


After agreement from the Institutional Review Board (IRB) of anesthesia and surgical intensive care department (IRB number R/16.01.75) of Mansoura University on January 26, 2016, this study was done according to the Declaration of Helsinki and good clinical practice (Brazil, 2013). This prospective double-blind randomized comparative clinical trial done by closed envelop methods was conducted by the Department of Anesthesia at Mansoura University Hospital starting from January 2016 and after obtaining written consents from all the study patients after patients information about the use of the patient data for research and educational purposes. Patient inclusion criteria included patients of either gender between 20 and 40 years of age, ASA I-II, and patients planned for elective knee arthroscopy under spinal anesthesia. Exclusion criteria were patient refusal to spinal anesthesia, patient with risk factors for spinal anesthesia, increased intracranial tension, bleeding tendency, infection around skin puncture site, neurological disorder, hepatic and renal insufficiency, heart block/dysrhythmia, and known hypersensitivity to bupivacaine or dexmedetomidine. We enrolled 50 patients undergoing lower-limb surgery and patients devolped severe hypotension requierd ephedrine. Patients were divided into two groups: control group (Group C) and dexmedetomidine group (Group D), 25 patients each using a closed envelop method. Before entering the operation room, a baseline reading was recorded (heart rate and blood pressure using invasive method and peripheral pulse oximetry). Patients were prehydrated with normal saline 10 mL.kg−1; dural puncture was performed between L3–4 and L4–5 interspace, under complete aseptic technique putting patients in the sitting position, using a 25-gauge Quincke needle. Spinal anesthesia was performed using 2.5 mL of 0.5% hyperbaric bupivacaine plus 0.5 mL of normal saline in control group (Group C) or 2.5 mL of 0.5% hyperbaric bupivacaine plus 0.5 mL (5 μg) of dexmedetomidine in (Group D). Dexmedetomidine was diluted to 10 μg.mL−1 using normal saline. During the study period arterial blood pressure was measured by invasive blood pressure moitoring using arterial cannula, heart rate, pulse oximetry and electrocardiogram were monitored intra and postopertively.

A tourniquet was placed on the limb planned for surgery and inflated 15–20 min after spinal anesthesia. After inflating the tourniquet, the operation was started. All patients were learned about tourniquet pain. Meperidine 100 mg was used in a concentration of 10 mg.mL−1. Initial 50 mg of meperidine (5 mL) was given on the patient complaint of tourniquet pain and repeated according to the patient's need in a dose of 20 mg, and total meperidine consumption was calculated. After finishing surgery, the limb was straightened on the operating table then deflating the tourniquet. After deflation, we continuously recorded heart rate and mean blood pressure for 15 min in the operating room and at these times: before induction of anesthesia (baseline), after inflating tourniquet (inflation), 1 min before deflating tourniquet (predeflation), after tourniquet deflation (10 min postdeflation), and maximum blood pressure and heart rate changes. Duration of time that started before the minimum blood pressure and maximum heart rate were changed until recovery was recorded. We considered critical hypotension when systolic blood pressure fell below 80 mmHg and bradycardia was critical when heart rate was <45 beats/min. Once happened, ephedrine or atropine was given until stable hemodynamics reached and the patient was excluded from the study.

Statistical analysis

We found approximately 20 patients were enough in each group to ensure a power of 0.8 to detect a significant difference of 15% or more in duration of hypotension after tourniquet deflation.[6] Data were collected and analyzed by SPSS version 16 (SPSS Inc. Released 2007. SPSS for Windows, Version 16. Chicago, SPSS Inc.). The numbers of patients increased to 25 in each group to compansate for drop out cases.. P < 0.05 was statistically significant. The Mann–Whitney U-test was used to compare between patient characteristics and to compare between hemodynamics between the groups. Maximal changes were compared to predeflation readings in both the groups. The Chi-square test was used for patient characteristics. All values were reported as mean ± standard deviation, P values were considered significant if <0.05.


   Results Top


Fifty-three patients started the study group, one in the control group and two patients in the dexmedetomidine group were excluded because of hypotension requiring ephedrine after deflating the tourniquet, so 50 patients completed the study. We found no statistically significant difference between the two groups regarding patient characteristics, but pain tourniquet after was significantly higher in the control group compared to the dexmedetomidine group [Table 1].
Table 1: Patients' characteristics data (mean±standard deviation) or number

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Mean blood pressure was lower after deflating tourniquet compared to predeflation and basal blood pressure [Table 2] in both the groups and at maximal change, blood pressure was lower in the dexmedetomidine than in the other group [Table 2]. The mean time between the maximal change in blood pressure reached and started to recover was 135 ± 14 s in the dexmedetomidine group and 80 ± 31 s in the control group P < 0.01 [Table 3].
Table 2: Heart rate in the study groups (data are in mean±standard deviation) beat/min

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Table 3: Duration of time that elapsed before the minimum value of blood pressure and maximum value of heart rate started to recover will be recorded

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Heart rate was significantly higher after deflating tourniquet compared to predeflation heart rate in both the groups, and maximal heart rate change was lower in dexmedetomidine group than in the other group [Table 4]. The mean time between the maximal heart rate changes until recovery was 113.2 ± 19 s in the dexmedetomidine group and 53.2 ± 11 s in the control group P < 0.01 [Table 3]. Meperidine dose was significantly lower in dexmedetomidine group compared to control Group (P = 0.04) [Table 5].
Table 4: Mean blood pressure in the study groups (data are in mean±standard deviation)

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Table 5: Meperidine dose in study groups (data are in mean±standard deviation)

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   Discussion Top


α2-adrenergic agonists when added to intrathecal local anesthetics increase the motor and sensory block of it, these additive or synergistic effects are secondary to the different mechanisms of action of the local anesthetic. The local anesthetics block nerve conduction by blocking sodium channels, whereas analgesic and sedative effects of intrathecal α2-AR agonists are caused by inhibiting the release of substance P at the level of the dorsal root neuron in the nociceptive pathway and by α2-AR activation in the locus coeruleus. The inhibition of the descending noradrenergic pathway decreases nociceptive neurotransmission and stops pain signal propagation.[7] These effects explain why dexmedetomidine prolongs the sensory block when added to spinal local anesthetics. In addition, intrathecal α2-adrenergic agonists can prolong the motor block of spinal anesthetics in a dose-dependent manner,[8] this effect results from the action of α2-adrenergic agonists on dorsal horn motor neurons.[9]

In the spinal cord, α2 C and α2-ARs are situated in superficial dorsal horn neurons, particularly lamina II, activation of both receptors reduces pain transmission by decreasing the release of glutamate and substance P from primary afferent neurons, activation of both receptors also activates potassium channels results in hyperpolarization of spinal interneuronsby an effect mediated by G-protein. Central α2-ARs' postsynaptic activation has sympatholytic effect results in hypotension and bradycardia, which attenuate the stress response of surgery.[3],[10],[11] It has more selective action on α2-ARs so that dexmedetomidine can be used in pain treatment. Dexmedetomidine has opiate like effect so used in management of acute and chronic postoperative pain, as myofascial pain, sympathetic pain as complex regional pain syndrome, neuropathic pain, and chronic headaches, also dexmedetomidine was used as adjuvant analgesic either intravenously or by intrathecal infusion, and in treatment protocols for cancer pain refractory to other analgesics.[12],[13],[14]

Previous studies used intrathecal small dose of dexmedetomidine as (3 μg) with bupivacaine for spinal anesthesia in human and found a more rapid onset of motor block with prolongation of motor and sensory block with stable hemodynamics and no sedation.[5]

After tourniquet deflation, acute hypotension is a common finding and a few reported fatal cases of circulatory collapse.[15] Tourniquet deflation results in peripheral vascular resistance fall and venous flow increase in the affected limb. These decrease venous return to the heart and decrease in cardiac output.[16] Return of metabolites to the systemic circulation from the ischemic limb occurs after tourniquet deflation.[17],[18] These metabolites, like adenosine and lactic acid, have a direct vasodilator action and can alter heart function. Normally, rapid changes in blood pressure alter the baroreflex change activity of the sympathetic nervous system. Response of baroreflex to stress hypertension mainly results in vagal hyperactivity, while the response to hypotension is a predominant sympathetic activity.[19]

Intrathecal dexemedetomidine-related side effects such as bradycardia were reported in seven trials before especially in high-dose dexemedetomidine group increase the risk of bradycardia than when a small dose is used. Hypotension also was reported in seven trials. High-dose dexemedetomidine group increases the risk of hypotension also. Meta-analysis by Yong Zhang searched for the effect of different doses of dexmedetomidine on spinal anesthesia.[20]


   Conclusion Top


Adding dexmedetomidine to spinal anesthesia decreases the incidence of tourniquet pain but aggravates the hemodynamic effect of tourniquet deflation.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Hagenouw RR, Bridenbaugh PO, van Egmond J, Stuebing R. Tourniquet pain: A volunteer study. Anesth Analg 1986;65:1175-80.  Back to cited text no. 1
    
2.
Memiş D, Turan A, Karamanlioğlu B, Pamukçu Z, Kurt I. Adding dexmedetomidine to lidocaine for intravenous regional anesthesia. Anesth Analg 2004;98:835-40.  Back to cited text no. 2
    
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Candiotti KA, Bergese SD, Bokesch PM, Feldman MA, Wisemandle W, Bekker AY, et al. Monitored anesthesia care with dexmedetomidine: A prospective, randomized, double-blind, multicenter trial. Anesth Analg 2010;110:47-56.  Back to cited text no. 3
    
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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. 4
    
5.
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;50:222-7.  Back to cited text no. 5
    
6.
Sarkar S, Acharya A, Pahari S. effect of oral clonidine premedication on haemodynamic response to tourniquet deflation following epidural anesthesia for lower extremity surgeries. Indian J Anasth 2006;50:266-70.  Back to cited text no. 6
    
7.
Grewal A. Dexmedetomidine: New avenues. J Anaesthesiol Clin Pharmacol 2011;27:297-302.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Yaksh TL. Pharmacology of spinal adrenergic systems which modulate spinal nociceptive processing. Pharmacol Biochem Behav 1985;22:845-58.  Back to cited text no. 8
    
9.
Smith C, Birnbaum G, Carter JL, Greenstein J, Lublin FD. Tizanidine treatment of spasticity caused by multiple sclerosis: Results of a double-blind, placebo-controlled trial. US Tizanidine Study Group. Neurology 1994;44:S34-42.  Back to cited text no. 9
    
10.
Stone LS, Broberger C, Vulchanova L, Wilcox GL, Hökfelt T, Riedl MS, et al. Differential distribution of alpha2A and alpha2C adrenergic receptor immunoreactivity in the rat spinal cord. J Neurosci 1998;18:5928-37.  Back to cited text no. 10
    
11.
Arain SR, Ebert TJ. The efficacy, side effects, and recovery characteristics of dexmedetomidine versus propofol when used for intraoperative sedation. Anesth Analg 2002;95:461-6.  Back to cited text no. 11
    
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Grosu I, Lavand'homme P. Use of dexmedetomidine for pain control. F1000 Med Rep 2010;2:90.  Back to cited text no. 12
    
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Roberts SB, Wozencraft CP, Coyne PJ, Smith TJ. Dexmedetomidine as an adjuvant analgesic for intractable cancer pain. J Palliat Med 2011;14:371-3.  Back to cited text no. 13
    
14.
Ugur F, Gulcu N, Boyaci A. Intrathecal infusion therapy with dexmedetomidine-supplemented morphine in cancer pain. Acta Anaesthesiol Scand 2007;51:388.  Back to cited text no. 14
    
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Valli H, Rosenberg PH, Kyttä J, Nurminen M. Arterial hypertension associated with the use of a tourniquet with either general or regional anaesthesia. Acta Anaesthesiol Scand 1987;31:279-83.  Back to cited text no. 15
    
16.
Kahn RL, Marino V, Urquhart B, Sharrock NE. Hemodynamic changes associated with tourniquet use under epidural anesthesia for total knee arthroplasty. Reg Anesth 1992;17:228-32.  Back to cited text no. 16
    
17.
Collis MG. The vasodilator role of adenosine. Pharmac Ther 1989;41:143-62.  Back to cited text no. 17
    
18.
Benzon HT, Toleikis JR, Meagher LL, Shapiro BA, Ts'ao CH, Avram MJ. Changes in venous blood lactate, venous blood gases, and somatosensory evoked potentials after tourniquet application. Anesthesiology 1988;69:677-82.  Back to cited text no. 18
    
19.
Dohi S, Tsuchida H, Mayumi T. Baroreflex control of heart rate during cardiac sympathectomy by epidural anesthesia in lightly anesthetized humans. Anesth Analg 1983;62:815-20.  Back to cited text no. 19
    
20.
Zhang Y, Shan Z, Kuang L, Xu Y, Xiu H, Wen J, et al. The effect of different doses of intrathecal dexmedetomidine on spinal anesthesia: A meta analysis Int J Clin Exp Med 2016;9:18860-7.  Back to cited text no. 20
    



 
 
    Tables

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



 

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