Temporary bilateral blindness after acute lidocaine toxicity
Temporary bilateral blindness after acute lidocaine toxicity
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DOI：
10.1097/00000539-200207000-00040
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发表时间：
2002-07-01
影响因子：
5.7
通讯作者：
von Schroeder, H
中科院分区：
文献类型：
--
作者：
Sawyer, RJ;von Schroeder, H
讨论利多卡因是一种酰胺类局麻药，因其用途广泛、起效快、作用持续时间中等以及相对安全性而受到广泛欢迎。然而，意外血管内注射、过量剂量或快速吸收导致有毒血浆水平是其在局部麻醉中使用的公认并发症。利多卡因广泛用于 IVRA，起效快，手术麻醉效果良好。使用利多卡因进行 IVRA 后出现严重并发症的情况极为罕见 (1, 2)。大剂量的局麻药可导致急性心血管和中枢神经系统 (CNS) 毒性。利多卡因毒性通常会导致口周/舌部麻木、烦躁、幻视（物体出现振动）、言语不清、癫痫发作，最终导致呼吸衰竭、昏迷和死亡。心血管毒性可能导致严重的心动过缓、心律失常和心搏停止 (3)。此前曾报道过急性利多卡因中毒后出现异常症状和体征，包括急性可逆性失语 (4) 和脑干反射完全可逆性丧失 (5)。松开止血带后，该患者接受了大剂量的利多卡因快速静脉推注。不幸的是，没有获得血清利多卡因浓度。然而，静脉注射利多卡因的药代动力学已得到充分研究 (6, 7)，大多数研究表明，当静脉浓度达到 5 g/mL 或更高时，就会出现毒性症状和体征 (8)。初始推注后，计算出的血清浓度（Cpmax 药物剂量/VD）将为 6.59 g/mL。然而，由于前臂隔离，这并没有占药物与手臂组织结合的很大比例（20%–80%）（7）。袖带闭塞时间和利多卡因血浆浓度之间存在反比关系 (7)，并且不同止血带放气循环技术的效果会导致达到峰值动脉浓度 (Cpmax) 的时间 (Tmax) 变慢，但不会显着影响 Cpmax (9)。阐明该患者双侧失明的确切机制很困难。失明也可能是由于视网膜小动脉或视觉皮层的栓子引起的，或者可能是由于静脉血栓形成导致视网膜静脉充血造成的。对于该患者，我们排除了这一诊断，因为视觉症状迅速且逐渐消失，而
DiscussionLidocaine is an amide local anesthetic enjoying wide popularity because of its versatility, rapid onset, and intermediate duration of action, as well as its relative safety. Accidental intravascular injection, excessive dosage, or rapid absorption resulting in toxic plasma levels are, however, recognized complications of its use in regional anesthesia. Lidocaine is widely used for IVRA with rapid onset of good surgical anesthesia. Serious complications after IVRA with lidocaine are extremely rare (1, 2).Large doses of local anesthetics can lead to acute cardiovascular and central nervous system (CNS) toxicity. Lidocaine toxicity usually results in symptoms of perioral/tongue numbness, restlessness, visual hallucinations (objects appear to oscillate), slurring of speech, seizures, and ultimately respiratory failure, coma, and death. Cardiovascular toxicity may result in profound bradycardia, arrhythmias, and asystole (3). Unusual symptoms and signs have been previously reported after acute lidocaine toxicity and include acute reversible aphasia (4) and complete reversible loss of brainstem reflexes (5). After tourniquet release, this patient received a large, rapid IV bolus dose of lidocaine. It is unfortunate that a serum lidocaine concentration was not obtained. However, the pharmacokinetics of IV lidocaine have been well studied (6, 7), and most studies indicate that symptoms and signs of toxicity appear at venous levels of 5 g/mL or more (8). Calculated serum concentration (Cpmax drug dose/VD) would be 6.59 g/mL, after the initial bolus injection. However, this does not account for a significant percentage (20%–80%) of the drug bound to the arm tissues as a result of forearm isolation (7). An inverse relationship exists between cuff occlusion time and plasma concentrations of lidocaine (7) and the effect of varying tourniquet deflation cycling technics would have resulted in a slower time (Tmax) to peak arterial concentration (Cpmax), but would not have significantly influenced Cpmax (9). Elucidating the exact mechanism of this patient’s bilateral blindness is difficult. Blindness may also be caused by emboli to the retinal arterioles or visual cortex, or it may result from venous thrombosis resulting in venous congestion of the retina. In this patient, we excluded this diagnosis because of the swift and progressive resolution of the visual symptoms while