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Editor,—Ten years on from Davis and Mandel’s1 description of the technique, and despite the popularity of the method, the exact role of, and rationale for, ocular compression in peribulbar anaesthesia remains somewhat obscure. Whatever the facts of the matter this would appear particularly undesirable since a body of evidence from clinical,2cadaveric,3 and animal4 work would suggest certain potential risks associated with its employment. In their recent paper, published in this journal in May 1996,5 Bowmanet al correctly admit that comparison of their results with those obtained by other workers is difficult since so many published studies attempt to draw conclusions from surgeons with widely differing practice. Final clarification of the controversy remains elusive.
While conducting a study of a separate but related aspect of peribulbar anaesthesia, we were interested to establish the details of current consultant practice and surveyed 60 consultant members of the Scottish Ophthalmic Club with 42 (70%) questionnaires returned. Of consultants surveyed 55% were using peribulbar, 23% retrobulbar, 17% sub-Tenon’s, and 5% topical anaesthesia. Of those using peribulbar techniques, 62% considered compression with the balloon essential. In this group the minimum acceptable time for compression was quoted at between 5 and 20 minutes (average 9 minutes).
Despite the theoretical risks from oculopression, especially in eyes with actual or potentially impaired optic nerve head blood flow, thankfully there is a relative paucity of reports of serious adverse effects in clinical practice.
Editor,—Bowman and coauthorsdemonstrated in their well performed study that there is a marked rise in intraocular pressure (IOP) after peribulbar anaesthesia. They injected a total of 10 ml of the anaesthetic, divided, into two different locations. The pressure could be lowered again with the help of oculopressure.
I have been using peribulbar anaesthesia for intraocular procedures for some years now, injecting 1.5 ml of a mixture of 2% lignocaine and 0.5% bupivacaine in the upper fornix, then 1.5 ml in the lower fornix. The anaesthetic effect is very good and sufficient even for long and complicated operations. By using these relatively small quantities of local anaesthetics, the IOP rises only slightly, thus preventing complications and making ocular compression unnecessary. I would recommend this technique for most intraocular procedures.
Editor,—We knew that the use of oculocompression after peribulbar anaesthesia is not universal and we were interested to learn from Ellis and Kearns’s survey of the Scottish Ophthalmic Club that only 62% of the users of peribulbar anaesthesia considered oculocompression essential. We wonder whether those users of peribulbar anaesthesia who do not employ oculocompression afterwards were aware of our findings of the immediate mean pressure rise of 11.44 mm Hg with an injectate volume of 10 ml. We disagree with Ellis and Kearns that the rationale of the technique remains obscure: we have shown that oculocompression for 20 minutes with the Honan’s balloon after peribulbar anaesthesia produces a mean fall in intraocular pressure of 11.05 mm Hg.
As Schipper points out, lower volumes of anaesthetic do not produce such a significant pressure rise. Oculocompression may not be necessary with smaller volumes of anaesthetic or topical anaesthesia. However, we continue to recommend the use of oculocompression to reduce the ocular pressure if the technique of peribulbar anaesthesia reported by Davis and Mandel is employed.