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Editor,—In this case a grand mal seizure occurred after a short peribulbar anaesthetic needle was used, permanent visual loss resulted, and magnetic resonance imaging (MRI) confirmed optic nerve damage.
A 49 year old myopic woman was diagnosed as having normal tension glaucoma. A year previously she underwent uncomplicated right trabeculectomy with 5-fluorouracil under local anaesthetic, and surgery to the left eye was planned. Her medication included levobunolol HCl 0.5% twice daily to the left eye, and atenolol for hypertension.
Before left trabeculectomy, with 5-fluorouracil, corrected vision was 6/9 right eye, and 6/5 left. Intraocular pressures were 12 mm Hg and 20 mm Hg respectively.
A painless peribulbar anaesthetic of prilocaine 4% was administered with a 25 mm 27 gauge needle. One injection of 3 ml was given inferotemporally and a second injection of 2.5 ml at the medial canthus.
The eye remained in the primary position throughout. Light ocular compression was applied and after 10 minutes she was prepared for surgery. She then felt cold and started to shiver, and after 5 minutes developed a grand mal fit. Her vital signs remained stable and oxygen and diazemuls were administered. The convulsion lasted 90 seconds and by 20 minutes she had recovered, was fully lucid, and surgery proceeded uneventfully.
The following day corrected vision in the left eye was reduced to hand movements. A bleb was formed, the anterior chamber was deep and the intraocular pressure measured 4 mm Hg. There was a dense afferent pupillary defect and fundal examination revealed cupping of the optic disc as preoperatively.
An unenhanced computed tomograph scan performed a week later showed no abnormality of the orbits or optic nerves. An MRI was performed at 4 weeks. T1 and T2 weighted, fat suppressed 4.0 mm images were performed axially at 0.4 mm intervals through the orbits. The images demonstrated swelling of the left optic nerve over a distance of 8 mm immediately behind the globe (Fig 1). The surrounding optic nerve sheath was effaced (Fig 2), and the nerve returned an abnormally low signal on T2 weighted images. No other abnormalities were detected.
Six weeks after the operation she underwent intravenous pulsed methylprednisolone 1 g a day for 3 days; however, there was no improvement in visual acuity. Her intraocular pressures remain less than 12 mm Hg.
A follow up MRI scan at 6 months demonstrated complete resolution of the optic nerve swelling and restoration of the nerve sheath with the development of optic atrophy particularly in the portion of the optic nerve behind the globe. A gradient echo sequence confirmed the absence of any optic nerve haemorrhage.
Peribulbar anaesthesia has been advocated as a safer technique than retrobulbar anaesthesia as the risk of optic nerve damage is significantly less.1 Injection of anaesthetic in the optic nerve sheath can cause brainstem anaesthesia and is well described with retrobulbar blockade.2-5 The risk of brainstem anaesthesia increases with the length of needle used, and if the eye is in the Atkinson position.1 2 5 Even with planned peribulbar block it has been estimated that an intraconal anaesthetic has been given in 1.3% of cases.1
Direct trauma to the optic nerve can occur after orbital block, characteristically without associated brainstem anaesthesia.6 7 The visual loss may be associated with signs of a retinal artery occlusion,8 subhyaloid haemorrhage,7 or a retinal vein occlusion.9In some of these cases the optic nerve sheath swelling was confirmed by ultrasonography or CT, and intraneural sheath haemorrhage was treated in one case by optic nerve sheath decompression with limited visual improvement.9
Prilocaine (Citanest) was used as the anaesthetic agent; it is similar to lignocaine, and has the advantage of being 50% less toxic, with reduced local irritation and slower systemic absorption.10Contraindications include anaemia and at high concentrations it can cause methaemoglobinaemia.
In this case we suggest that some prilocaine was injected into the nerve sheath causing a grand mal fit, with loss of the cerebrospinal fluid space and local optic nerve swelling. The latter may be due to direct injection into the optic nerve or an associated ischaemic swelling.
This complication occurred, despite using a 25 mm needle with the eye in the primary position, and when the anaesthetic was administered by an experienced anaesthetist (more than 8000 orbital blocks).
The MRI images were able to demonstrate the subtle changes in the optic nerve and sheath that were undetected by the CT scans. Our experience was that it provided superior detail, and the gradient echo sequence would demonstrate if haemorrhage was present.
Earlier corticosteroid treatment would be advised, although it is not known whether the initial optic nerve swelling was reversible. Unfortunately treatment was given 6 weeks after the event and was of no benefit.
To our knowledge there are no published reports of optic nerve changes of this type following brainstem anaesthesia.6