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Background: The purpose of this study was to evaluate the efficacy and safety of episcleral single-injection anesthesia in a large number of patients., Methods: Over a period of 5 yr, in four institutions, anesthesiologists involved in this prospective study completed a standardized form to evaluate single-injection medial canthus high-volume episcleral anesthesia. The success rate of the block was rated according to an akinesia score. The study parameters included demographic data, surgical procedure, and anesthetic management. All patients were followed up at least until postoperative day 1, and all complications, pain, and discomfort were noted. Statistical analysis was done to assess the risk factors for complications., Results: A total of 2,031 patients were included in the study. The most frequent surgical procedures performed were phacoemulsification and posterior chamber artificial lens implantation (91.0%). A total of 66 complications (3.3%) occurred in 60 patients. One patient had a retrobulbar hemorrhage, and 59 had one or two more minor incidents or pain/discomfort with the procedure. The complications consisted of subconjunctival hematoma (1.3%), ocular hypertonia (0.4%), and chemosis (0.30%). Statistical analysis revealed that inexperience in the technique represented a risk factor for complications., Conclusions: This is the first survey of a large experience in episcleral single-injection anesthesia, a form of anesthesia that does not preclude sharp-needle complications and does require training. Only one complication occurred among 2,031 patients; however, a larger number of patients is needed to definitively evaluate the safety of episcleral single-injection anesthesia.

Background: Some reports suggest that activation of the autonomic nervous system by bupivacaine could participate in its cardiotoxicity. This is based in part on the fact that hexamethonium suppresses cardiac disturbances in anesthetized rabbits given small intracerebroventricular doses of bupivacaine. The aims of the current study were to determine, in anesthetized dogs, (1) whether the activation of the autonomic nervous system is deleterious after a large intravenous dose of bupivacaine and (2) whether the parasympathetic or sympathetic system is implicated in the bupivacaine-induced deleterious activation of the autonomic nervous system., Methods: We used an electrophysiologic model in closed-chest dogs anesthetized with sodium pentobarbital. In group 1 (n = 6), dogs were given 4 mg/kg intravenous bupivacaine over 10 s. In group 2 (n = 6), dogs were given the same dose of bupivacaine 5 min after having received 0.2 mg/kg intravenous atropine sulfate. In group 3 (n = 9), dogs were pretreated with 10 mg/kg intravenous hexamethonium and then given bupivacaine 4 mg/kg. In addition, in group 3, the right atrium was paced at a basic cycle length of 400 ms to obtain a heart rate similar to that of group 1., Results: Bupivacaine in group 1 induced significant bradycardia; lengthening of PR, atria-His, His-ventricle, and QTc intervals; and QRS widening. The first derivative of left ventricular pressure was significantly decreased, whereas left ventricular end-diastolic pressure was increased. Atropine pretreatment did not modify cardiac disturbances induced by bupivacaine. Hexamethonium pretreatment induced significantly less QRS widening and QTc lengthening than was seen in group 1 but worsened the bupivacaine effects on bradycardia, atria-His and PR intervals, mean aortic pressure, and first derivative of left ventricular pressure. Moreover, atrial pacing in group 3 induced alterations of QRS similar to those in group 1., Conclusions: Considering that marked slowing of ventricular conduction velocity (i.e., QRS widening) is known to facilitate reentrant ventricular arrhythmias, we conclude that (1) the activation of the autonomic nervous system by bupivacaine is not as deleterious as previously suggested; (2) the parasympathetic system is not markedly implicated in the worsening of direct bupivacaine cardiotoxicity; and (3) the sympathetic nervous system acts only by inducing a less marked bradycardia, which slows ventricular conduction velocity in a use-dependent manner, facilitating reentrant arrhythmias.