Abstract
Objective
To investigate the sensory block onset time, duration time, and side effects of adding dexmedetomidine to ropivacaine for cervical plexus block.
Methods
Forty American Society of Anesthesiologists (ASA) Class I or II adult patients who were scheduled to undergo thyroid surgery were randomly allocated to the following groups to receive cervical plexus block: 30 mL of 0.375% ropivacaine combined with 1 μg kg−1 of dexmedetomidine; 30 mL of 0.375% ropivacaine combined with saline (control). The sensory block onset time, duration of analgesia, mean arterial pressure (MAP), heart rate (HR), and the incidences of side effects, such as hypotension, bradycardia, and hypoxemia were recorded.
Results
The addition of dexmedetomidine to ropivacaine (Group D) shortened the sensory block onset time compared with the ropivacaine group (Group C) (95% confidence interval [CI] 4.18–5.26; p < 0.05). The duration of analgesia of cervical plexus block in Group D was significantly longer than that in Group C (95% CI 295.96–311.12; p < 0.05). The Ramsay sedation score at 5, 10, 20, 40, 60, 90, and 120 minutes after local anesthetic administration in Group D was significantly higher than that in Group C (p < 0.05). MAP level and HR level in Group D were significantly lower than that in Group C (p < 0.05).
Conclusion
The addition of 1 μg kg−1 dexmedetomidine to ropivacaine for cervical plexus block could shorten the sensory block onset time and extend the duration of analgesia, and increased the quality of analgesia, with the patients being sedated and arousable.
Keywords
anesthetics, local: ropivacaine; cervical plexusdexme; detomidine; nerve block;
1. Introduction
Dexmedetomidine is a highly selective α2 adrenergic receptor agonist. Its main site of action is in the brainstem locus coeruleus. It plays an important central antisympathetic role when it is used as a sedative for patients, and it may preserve physiological sleep better than any other sedative, while at the same time it can produce analgesic1 and anxiolytic2 effects. However, it causes slight respiratory depression. Because of its pharmacological characteristics, it is now widely used in situations such as intensive care unit sedation and anesthesia, especially in regional anesthesia.
Cervical plexus block is a regional anesthetic, in which patients are awake and arousable. It is mostly used in neck surgery, especially in some of types of thyroid surgery (e.g., thyroid adenoma, Hashimoto's goiter, and nodosity thyroiditis). Most of the patients are young or middle-aged, and most surgeons prefer cervical plexus block to general anesthesia to avoid injury to the recurrent laryngeal nerve and superior laryngeal nerve.
Because of the small defect of the cervical plexus block, some of the patients who receive this type of anesthesia will feel stress, anxiety, or pain when they are kept awake. Several adjuvant drugs, such as midazolam, fentanyl, remifentanil, and clonidine, were used to provide better surgical conditions to make patients more comfortable. However, side effects (e.g., oversedation, respiratory depression, hypoxemia, and hypotension) would follow after the use of these drugs. Other adjuvant drugs with different dosages were investigated by researchers in recent years in an attempt to identify ones that are safer for patients.
Dexmedetomidine is a new adjuvant for regional anesthesia; Esmaoglu et al3showed that the addition of 1 μg kg−1 dexmedetomidine to lidocaine for intravenous regional anesthesia (IVRA) improves the quality of anesthesia and postoperative analgesia without causing side effects. In the study by Kaygusuz et al,4 the use of dexmedetomidine has been reported to be safe when used as an addition to local anesthetic for brachial plexus block; it can prolong the duration of anesthesia and analgesia. In a case report by Plunkett et al,5 it was shown that dexmedetomidine (1 μg kg−1) intravenous infusion along with local anesthesia administered by the surgeon for an awake thyroidectomy was safe and without respiratory depression. However, its use in cervical plexus block as an addition to local anesthetic has not been reported.
In our study, we investigated the onset time of sensory block, duration time, and side effects of adding dexmedetomidine to ropivacaine for cervical plexus block.
2. Methods
2.1. General information
Our study had been approved by the Ethical Committee of Human Research of the first Affiliated Hospital of Guangxi Medical University. Forty ASA Class I or Class II patients who underwent thyroid surgeries (included thyroid adenoma, Hashimoto's goiter, nodosity thyroiditis) were enrolled in a prospective, double-blind controlled trial. The median age of the patients was 35 years. Those who were receiving adrenoreceptor agonist or antagonist therapy, or had a history of cardiac, respiratory, hepatic, or renal failure or diabetes mellitus were excluded. Patients in this study were randomly allocated to two groups: dexmedetomidine group (n = 20, Group D) and control group (n = 20, Group C).
2.2. Anesthesia
In all patients, premedication was omitted. After arrival at the operating room, all patients were monitored with electrocardiogram and pulse oximetry, and noninvasive blood pressure was assessed.
The cervical plexus block comprised deep and superficial plexus block. A single injection of 10 mL of the local anesthetic solution was delivered with a short-bevel needle at C4 onto the cervical transverse process, 2∼3 cm deep from the skin and 1 cm posterior to the posterior border of the sternocleidomastoid. The superficial block was completed on two sides by subcutaneous injection of the remaining 20 mL (10 mL for each side) of the solution along the posterior border of the middle point of the sternocleidomastoid. Before injection, the absence of blood in the needle hub was checked by aspiration. Patients were randomly allocated using a sealed envelope technique to receive either 30 mL of ropivacaine 0.375% with 1 mL of saline added into the solution (Group C, n = 20),or 30 mL of ropivacaine 0.375% with 1 mL (1 μg kg−1) of dexmedetomidine being added to the solution (group D, n = 20) in a double-blind procedure. The drug solutions were prepared by an anesthesiologist not involved in the study.
All the cervical plexus blocks were performed by the same anesthesiologist and were assessed by another anesthesiologist who was unaware of the group assignments.
Those who complained of pain (visual analog scale (VAS) > 7) during operating procedures were given additional local infiltration anesthesia with 1% lidocaine.
2.3. Observation items
Sensory blocks and the Ramsay sedation score were evaluated every 2 minutes until 20 minutes after injection, and then every 20 minutes after surgery until the operation was completed. Sensory block was evaluated by VAS (0–10).
The sensory block onset time and duration time should be recorded. Onset time was defined as the time interval between the end of injection of local anesthetic to VAS < 3. Duration time was defined as the time interval between VAS < 3 to VAS > 7. The Ramsay sedation score, heart rate (HR), and mean arterial pressure (MAP) should be recorded 0, 5, 10, 20, 40, 60, 90, and 120 minutes after local anesthetic administration. The sensory block onset time, duration time, Ramsay sedation score, HR, MAP, and the incidences of side effects in the two groups should be compared.
2.4. Statistics
Data were processed using SPSS version 13.0 (SPSS Inc., Chicago, IL, USA). The values were expressed as mean ± standard error of mean for all data. Differences between the two groups were analyzed by Student t-test. Results were considered significant at p < 0.05.
3. Results
The demographic data were similar in each group (Table 1).
Sensory block onset time in Group D is shorter than in Group C; the difference was statistically significant (Table 2, p < 0.05).
Sensory block duration time in Group D is longer than in Group C; the difference was statistically significant (Table 2, p < 0.05).
The Ramsay sedation score at 5, 10, 20, 40, 60, 90, and 120 minutes after local anesthetic administration in Group D was significantly higher than in Group C. (Fig. 1, p < 0.05).
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The MAP level in Group D at 5, 10, 20, and 40 minutes was significantly lower than in Group C (Fig. 2, p < 0.05). HR in Group D at 5, 10, 20, 40, 60, 90, and 120 minutes was significantly lower than in Group C. (Fig. 3, p < 0.05).
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In Group D, two patients experienced bradycardia (the lowest heart rate in these two patients was 49 bpm and 51 bpm) and were treated with atropine. There was no bradycardia in Group C.
4. Discussion
The main result of our study demonstrated that the addition of 1 μg kg−1dexmedetomidine to ropivacaine for cervical plexus block can shorten sensory block onset time and extend the duration of analgesia. These findings coincide with those of Brummett et al6, 7 and Gaumann et al.8 Meanwhile, study Group D had more hemodynamic stability than Group C. The Ramsay sedation score was higher in Group D, so we predict that the local area use of dexmedetomidine also can produce sedation.
Although dexmedetomidine is commonly used as an intravenous agent, interest in the addition of perineural dexmedetomidine to local anesthetic is increasing. There are several studies on perineural dexmedetomidine use.6, 7, 9 Brummett et al9 showed that dexmedetomidine enhanced duration of bupivacaine anesthesia and analgesia of sciatic nerve block in rats without any damage to the nerve. In another study in rats, Gaumann et al8 showed these same results. In addition to animal studies, human studies on the addition of dexmedetomidine to local anesthetic were performed. Esmaoglu et al3 and Ammar and Mahmoud10 showed that the use of dexmedetomidine was safe as an addition in local anesthetic for brachial plexus block. Another study11carried out on volunteers showed that dexmedetomidine could be used as an additive to local anesthetics for various regional anesthetic techniques, while simultaneously prolonging perineural nerve block.
Dexmedetomidine is well known as a highly selective α2 adrenoreceptor agonist shown to have both sedative and analgesic effects.12, 13, 14 Its intravenous role has been well recognized as sedative, analgesic, and anxiolytic, its resultant of respiratory depression is slightly and will not achieve mechanical ventilation conditions.15, 16 Although several studies on animals or humans exist, the mechanism of dexmedetomidine in peripheral nerve blocks is not fully understood.
It is well known that in peripheral myelinated and nonmyelinated fibers, membrane hyperpolarization develops that can produce sensory effects and pain during or after stimulation and mainly results from the activation of the sodium-potassium pump after the transient influx of sodium ions.17 Dalle et al18 found that clonidine (an α2 adrenoreceptor agonist) enhances the sensory blockade by blocking the inhibiting hyperpolarization activated cation current to enhance the level of hyperpolarization and thus inhibits subsequent action potentials. In the study of rats by Gaumann et al,8 it was shown that the analgesic effect of peripheral perineural dexmedetomidine might be caused by enhancement of the hyperpolarization-activated cation current, which prevented the nerve returning from a hyperpolarized state to resting membrane potential for subsequent firing. This conclusion is consistent with that of Dalle et al.18 Another effects may be the mechanism of α2 adrenoreceptor agonist in peripheral nerve by reducing release of norepinephrine and causing α2 receptor independent inhibitory effects on nerve fiber action potentials.
The use of clonidine in peripheral nerve blocks has been reported to be safe and beneficial (it prolongs the duration of anesthesia and analgesia) by Singelyn et al.19, 20 Dexmedetomidine is a selective α2 adrenoreceptor agonist similar to clonidine; its effect on the peripheral nerve may be the same as or more potent than that of clonidine. It is unknown whether the mechanism of dexmedetomidine in peripheral nerve blocks is associated with membrane hyperpolarization or activation of the sodium-potassium pump; additional research is required.
Although most of the studies were on animals, the addition of α2 adrenoreceptor agonist to local anesthetics has been reported to be safe and beneficial. In studies on humans, Esmaoglu et al,3 Kaygusuz et al,4 and Rancourt et al21 showed that dexmedetomidine was safe when used as an addition to local anesthetic for brachial plexus block and posterior tibial nerve sensory blockade. Esmaoglu et al3 and Kaygusuz et al4 also showed that when dexmedetomidine is used as an addition to local anesthetic, it can provide faster onset and longer duration for brachial plexus block, but resulted in some side effects, such as hypotension and bradycardia.
Because of the defect of cervical plexus block, patients who undergo it will be anxious and experience discomfort. On the basis of our discussions, we assumed that the addition of dexmedetomidine to the local anesthetic for cervical plexus block could provide the same effect as that of the study by Esmaoglu et al.3 In our study, the addition of dexmedetomidine (1 μg kg−1) to local anesthetics extended the duration of anesthesia and increased the quality of analgesia, and patients were sedated and arousable, thus avoiding the use of intravenous sedatives that may induce respiratory depression. The possible mechanism is that the dual role of dexmedetomidine of the central and peripheral, which include slight intravenous effect that cause by the tissue capillary absorption and its direct effect on the peripheral nerves.
Dexmedetomidine has a double effect, playing an anticentral sympathetic role and activating the vagus nerve to lower plasmas catecholamine levels which can lower blood pressure (BP) and HR, providing stable hemodynamics. However, it also has a dosage-related inhibition for BP and HR. Esmaoglu et al22 showed some side effects such as hypotension and bradycardia in their test group (100 μg of dexmedetomidine added to levobupivacaine for brachial plexus block), along with its effects such as sedation and anxiolysis. In our study, HR in Group D was lower than that of the control group, but the incidence of bradycardia was lower than that recorded in the study by Esmaoglu et al22 (2/20 vs. 7/30); the difference may be because the dose of dexmedetomidine (1 μg kg−1 vs. 100 μg) was lower in our study, and was tolerant and reversible without adverse effects to the patients. We assume that the occurrence of hypotension and bradycardia may be associated with individual sensitivity to dexmedetomidine.
In conclusion, the addition of 1 μg kg−1 dexmedetomidine to ropivacaine for cervical plexus block can decrease sensory block onset time and extend the duration of analgesia, and increased the quality of analgesia so that patients were sedated and arousable. However, perineural dexmedetomidine added to local anesthetic may also cause some side effects (e.g., hypotension and bradycardia), and it may be associated with dosage or individual sensitivity. Further studies are needed to determine the safe optimal dose of dexmedetomidine adding to local anesthetics for cervical plexus block, and further studies to determine the effect of neurotoxicity on the human nerve are required.