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Department of Anesthesiology, Clinique Générale, Annecy, France
To the Editor:
I read with interest the article by Sia et al. (1) about the effect of epinephrine-containing anesthetic solutions on the incidence of hypotensive/bradycardic events (HBE) during shoulder surgery in the sitting position under interscalene brachial plexus block (ISB). I agree with the authors that preventive measures need to be assessed because of the large frequency (13%–28%) of this acute and life threatening complication. The most likely cause of these events is the activation of the Bezold-Jarisch reflex (BJR). Beta-blocking drugs have been proven to prevent this phenomenon by decreasing the sympathetic tone (2,3). Sedation could also decrease endogenous catecholamine level and protect from HBE, but this remains to be demonstrated in a prospective manner (4).The hypothesis that exogenous epinephrine (via local anesthetic solutions or arthroscopic irrigating solutions) could increase the incidence of HBE has been proposed by Kinsella but never been proven (5). In their article, Sia et al. report a reduction of the incidence of HBE from 29% to 11% by withdrawing epinephrine from the lidocaine-bupivacaine mixture (1). I would like to make some comments about this work.
As it is mentioned in their Discussion section, the use of a vasodilating drug like urapidil to improve the visualization of the surgical field is a very important concern. The understanding of the paper could have been made clearer if the 30 patients who had received urapidil or metoprolol had been excluded from the analysis. Instead of focusing on the effects of epinephrine, the authors define a new entity called "urapidil or non-urapidil induced HBE" that makes the reading of their study rather difficult. Furthermore, it is obvious that the injection of a vasodilator increases venous pooling in lower limbs and may induce an experimental BJR.
However, even when they consider only the 85 patients who did not receive urapidil or metoprolol, the authors find that the incidence of HBE is more frequent in the epinephrine group (29% vs 4%). I think that the consequences of such a very small dose of epinephrine added to an anesthetic solution and administered in a plexus sheath are surprising. If we believe the authors’ statements, in this setting, epinephrine withdrawal from the local anesthetic solution could decrease blood pressure and heart rate enough to reduce the bleeding in the surgical field, the urapidil use, and above all the incidence of HBE (<5%). Does that mean that HBE occurring during shoulder surgery in the sitting position under ISB is no more a clinical concern? We regret that plasma concentrations of epinephrine have not been monitored. In a study about the hemodynamic responses to epinephrine-containing perianal lidocaine, Barber et al. (6) have compared lidocaine 0.5% with or without 1:200,000 epinephrine. They have shown that despite increasing plasma concentrations, there were no changes in blood pressure, heart rate, or plasma norepinephrine levels. I do not understand why the same doses of epinephrine injected in the interscalene space could produce more hemodynamic effects than in the perianal region.
References
Department of Anesthesiology, Centro Traumatologico Ortopedico, Firenze, Italy
In Response:
I read with interest the letter from Dr. Souron regarding the major critical aspect of our study, i.e., the need to administer an antihypertensive drug during the surgical procedure.
He suggested that the patients who received urapidil or metoprolol should be excluded from the analysis to cut out any possible influence of these drugs on the recorded incidence of HBE. On the basis of this argument, he considered 4% as the actual incidence of HBE in the "control group" instead of the recorded 11%. I do not agree on this point.
The most likely cause of HBE in patients undergoing shoulder surgery in the sitting position under interscalene block (ISB) is a form of vasovagal syncope mediated by the Bezold-Jarisch reflex, which occurs when venous pooling (caused by the sitting position) and increased sympathetic tone (due to increased blood levels of epinephrine), induce a low-volume, hypercontractile ventricle (1,2).
Significantly larger intraoperative levels of heart rate (HR) and blood pressure (BP) were recorded in patients who had an HBE when compared with those who did not (3). This may confirm that a state of increased sympathetic tone could predispose susceptible patients to subsequent vasovagal episodes. The 30 patients who were treated for tachycardia and/or hypertension had a state of increased sympathetic tone; we thought that it would not have been correct to exclude them from the analysis, because they are probably more susceptible to vasovagal episodes than the remaining 85 patients. Therefore, we decided to consider as the actual result of the study the incidence of HBE recorded in all the 55 patients included in each group, and to indicate as "urapidil-induced HBE" the vasovagal events occurred within 15 min of administration of the drug.
We recorded an 11% incidence of HBE, despite the use of plain local anesthetic solutions for ISB. These data are comparable with those recorded by Souron et al. (4), who found a 5.7% incidence of HBE in patients undergoing shoulder surgery under ISB and sedation with target-controlled infusion of propofol. I think that HBE is still a clinical concern and that future studies will define the interventions that might cause a reduction in the incidence of this complication. Avoidance of epinephrine-containing solution for ISB might be, in my opinion, the first step.
Dr. Souron was surprised at the hypertensive effect of exogenous epinephrine recorded in our study (10–14 mm Hg increase of systolic BP). I think that the hemodynamic effects of injected epinephrine in a patient placed in the sitting position should not be compared with those recorded in patients who are placed in a different position, because the interaction between the effects of the sitting position and those of injected epinephrine have not been studied. The present is the first study that compared the hemodynamic effects of injected local anesthetic solution, with and without epinephrine, in the sitting position. Analogous with our results, D’Alessio et al. (1) recorded significantly higher levels of BP in a subgroup of patients who received a dose of exogenous epinephrine significantly larger than that administered to the patients of the other subgroups. I think that the results recorded in the study by Barber et al. (5), in which a knee-chest position and an IV premedication with diazepam 10 mg and meperidine 100 mg were used cannot be compared with ours.
References
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