Indian Journal of Ophthalmology

: 1998  |  Volume : 46  |  Issue : 2  |  Page : 109--110

Lens expulsion into sub-conjunctival space following peribulbar anaesthesia

M Nagpal, PN Nagpal 
 Asopalov Eye Hospital, Ahmedabad, India

Correspondence Address:
M Nagpal
Asopalov Eye Hospital, Ahmedabad

How to cite this article:
Nagpal M, Nagpal P N. Lens expulsion into sub-conjunctival space following peribulbar anaesthesia.Indian J Ophthalmol 1998;46:109-110

How to cite this URL:
Nagpal M, Nagpal P N. Lens expulsion into sub-conjunctival space following peribulbar anaesthesia. Indian J Ophthalmol [serial online] 1998 [cited 2023 Jun 1 ];46:109-110
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Full Text

Various studies have shown that there is an incidence of ocular penetration during peribulbar and retrobulbar anaesthesia of <0.1% for eyes having axial length <26mm,[1],[2] and an incidence of <1% for eyes of axial length >26 mm.[3] Damage to the globe after penetration can result from either toxic effects of anaesthetic drugs[4] or from mechanical injury caused by the needle itself. Mechanical injury from the needle can be from a single penetration or a double perforation of the globe or from direct optic nerve penetration.

 Case Report

We would like to report the occurrence of an ocular explosion after peribulbar anaesthesia. A 65-year-old male was referred to us with a report suggesting a subconjunctival cyst in the supero-temporal quadrant of his right eye (Figure). This swelling had been noticed by the referring ophthalmologist immediately after giving the patient a peribulbar block 2 months earlier for a planned cataract surgery. About 5 cc of anaesthetic (combination of 2% xylocaine and 0.5% sensorcaine) had been injected in each of the superonasal and inferotemporal peribulbar sites. No digital massage was given since the swelling appeared immediately after the injection. Surgery was abandoned and the patient was referred to our centre.

On examination we found that the lens of the patient had been expelled into the subconjunctival space. The overlying and surrounding conjunctiva was mildly hyperemic. We thoroughly examined the sclera of the same eye as well as the other eye to look for any predisposing thin areas or signs of previous scleritis but could find none. Pupil was drawn superotemporally towards the site of the displaced lens. The eye was aphakic and there were no capsular remnants seen. Vitreous face was broken and a few strands were seen in the anterior chamber. A minimal resolving vitreous haemorrhage was noticed in the inferior part. Rest of the fundus looked normal and inspite of thorough peripheral examination with scleral indentation no needle entry wound was found. Ultrasonography confirmed the clinical findings of inferior vitreous haemorrhage, and axial length was found to be 24.5 mm. The best corrected visual acuity was counting fingers at 1.5 ft with +11 D which could not be explained as the media were clear and there were no obvious posterior pole changes. The intraocular pressure (IOP) in the right eye was 7.1 mm Hg and in the left eye 14.6 mm Hg with Schiotz tonometer.

We scheduled the patient for lens removal from the subconjunctival space and carefully dissected the lens from the overlying conjunctiva and underlying sclera. On removal of the lens the underlying sclera showed a brownish coloured sealed defect. The lens tissue measured 9 mm in diameter and the sealed defect was 7.5 mm. The uveal tissue had sealed the gap. We did not try to dissect it further lest the wound give way. The conjunctiva was resutured.

Three months after the surgery, the vision was still unchanged. The IOP was 12.2 mm Hg and pupil was updrawn and not reactive to light. The disc and the macula appeared normal but there was still a resolving vitreous haemorrhage in the inferior part.


We could not explain the poor visual acuity since the posterior pole was seemingly normal and despite a non-reactive pupil there was no obvious optic atrophy. Probably it might develop in due course. Transient visual loss has been described due to intraocular xylocaine toxicity[5] but none that would last so long. Hypotony in the immediate post lens expulsion period could be explained due to the sudden rupture of the globe leading to decompartmentalisation of the eye and possibly a ciliary shock which recovered in due course. The site of perforation was possibly in the region of the resolving vitreous haemorrhage and thus could not be seen.

A similar case has been reported recently, in which the lens prolapsed into the subconjunctival space after an accidental perforation of the globe while giving peribulbar anaesthesia.[6] The authors of this report conducted an experimental study where they ruptured 21 cadaver eyes with intraocular saline injections. Of the 21 eyes, 11 ruptured in the perilimbal region while 10 ruptured in the equatorial area. Of the 11 perilimbal ruptures, 3 had lens extrusion into the subconjunctival space. The extremely high IOP achieved just before globe rupture was preceded by corneal whitening and a marked resistance to further advancement of the injecting syringe plunger. These signs should be considered to strongly suggest an impending disaster. Also, a sudden localised swelling coming up in the subconjunctival space immediately after a peribulbar injection could quite possibly be a lens expelled due to the raised volume in the posterior chamber.


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2Schechter RJ. Management of inadvertent intraocular injection. Ann Ophthalmol 1985;17:771-75.
3Hay A, Flynn Jr HW, Hoffman JI, Rivera AH. Needle penetration of the globe during retrobulbar and peribulbar injections. Ophthalmology 1991;
4Kimble JA, Morris RE, Witherspoon CD, Feist RM. Globe perforation from peribulbar injection. Arch Ophthalmol 1987;105:749.
5Lincoff H, Kreissig I. Local anaesthesia with accidental perforation of the eye: an acute emergency. Klin Monatsbl Augenheilkd 1986;188:128-32.
6Magnante DO, Bullock JD, Green WR. Ocular explosion after peribulbar anaesthesia. Ophthalmology 1997;104:608-15.