Cunningham A J, Barry P
Can Anaesth Soc J. 1986 Mar;33(2):195-208. doi: 10.1007/BF03010831.
The major factors controlling intraocular pressure during surgery are the dynamic balance between aqueous humour production in the ciliary body and its elimination via the canal of Schlemm; the auto-regulation and chemical control of choridal blood volume; the extraocular muscle tone and vitreous humour volume. Prior to surgical incision of the anterior chamber in open intraocular procedures, a low-normal intraocular pressure is mandatory to avoid the hazards of iris or lens prolapse and vitreous loss associated with sudden decompression. In general, the central nervous system depressant drugs, hypnotics, narcotics, major tranquillizers, volatile anaesthetic agents are associated with a reduction in intraocular pressure, with the exception of ketamine and possibly trichloroethylene. The mechanism of action of anaesthetic agents in reducing intraocular pressure may involve a direct effect on central diencephalic control centres, reduction of aqueous production, facilitation of aqueous drainage or relaxation of extraocular muscle tone. Succinylcholine administration is associated with a significant rise in intraocular pressure, with a peak increase between two to four minutes following administration and a return to base line values after six minutes. The intraocular hypertensive effect may be due to a tonic contraction of the extraocular muscles, choroidal vascular dilatation or relaxation of orbital smooth muscle. Despite many claims to the contrary, no reported method to date has been shown to consistently prevent the intraocular hypertensive response to intravenous succinylcholine administration. Because the non-depolarizing relaxants are associated with a reduced intraocular pressure, a barbiturate-non-depolarizing relaxant technique utilizing preoxygenation and cricoid pressure has evolved as the most commonly employed induction technique for the emergency repair of a penetrating eye injury. The alternative non-depolarizing relaxant pretreatment-barbiturate-succinylcholine technique may offer the advantages of more rapid onset of relaxation with only minor increases in intraocular pressure and in a carefully controlled rapid sequence induction technique may be the most acceptable method of handling emergency penetrating eye injuries.
手术期间控制眼压的主要因素包括睫状体房水生成与经施莱姆管排出之间的动态平衡;脉络膜血容量的自动调节和化学控制;眼外肌张力和玻璃体液容量。在开放性眼内手术切开前房之前,必须维持略低于正常的眼压,以避免虹膜或晶状体脱垂以及与突然减压相关的玻璃体丢失的风险。一般来说,中枢神经系统抑制药物、催眠药、麻醉性镇痛药、强效镇静剂、挥发性麻醉剂都与眼压降低有关,但氯胺酮和可能的三氯乙烯除外。麻醉剂降低眼压的作用机制可能涉及对中枢间脑控制中心的直接作用、房水生成减少、房水引流促进或眼外肌张力松弛。使用琥珀酰胆碱会使眼压显著升高,给药后2至4分钟达到峰值,6分钟后恢复至基线值。眼压升高的效应可能是由于眼外肌的强直性收缩、脉络膜血管扩张或眼眶平滑肌松弛。尽管有许多相反的说法,但迄今为止,尚无报告表明哪种方法能始终如一地预防静脉注射琥珀酰胆碱引起的眼压升高反应。由于非去极化肌松药与眼压降低有关,一种采用预充氧和环状软骨压迫的巴比妥类-非去极化肌松药技术已发展成为穿透性眼外伤急诊修复最常用的诱导技术。另一种非去极化肌松药预处理-巴比妥类-琥珀酰胆碱技术可能具有起效更快、眼压仅轻微升高的优点,在精心控制的快速顺序诱导技术中,可能是处理穿透性眼外伤急诊最可接受的方法。