|Year : 2014 | Volume
| Issue : 2 | Page : 83-85
Temporary complete vision loss after intracameral lignocaine in a post-vitrectomy eye: A single case report
Sanjiv Kumar Gupta1, Ajai Kumar2
1 Department of Ophthalmology, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of Ophthalmology, Jan Kalyan Eye Hospital, Lucknow, Uttar Pradesh, India
|Date of Web Publication||5-Jun-2015|
Dr. Sanjiv Kumar Gupta
Department of Ophthalmology, King George's Medical University, Lucknow - 226 016, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
We report a case of temporary complete vision loss in a phakic patient after intracameral lignocaine solution injection percolated to the posterior segment of the eye and anesthetized the retina. The main reason of this seepage of lignocaine solution from the anterior chamber to the posterior segment was presumably the hypotony and absence of the vitreous body as the patient had undergone pars plana vitrectomy for intravitreal cysticercus. Once the duration of anesthesia effect of lignocaine elapsed, the patient gained good vision with no obvious retinal damage as seen on fundus imaging and ocular coherence tomography. Thus, one should keep the possibility of intracameral medications to reach the posterior segment in therapeutic/toxic concentrations, especially in postvitrectomy eyes with hypotony.
Keywords: Intracameral lignocaine, intra-ocular cysticercus, postvitrectomy, retinal anesthesia, temporary blindness
|How to cite this article:|
Gupta SK, Kumar A. Temporary complete vision loss after intracameral lignocaine in a post-vitrectomy eye: A single case report. Egypt Retina J 2014;2:83-5
|How to cite this URL:|
Gupta SK, Kumar A. Temporary complete vision loss after intracameral lignocaine in a post-vitrectomy eye: A single case report. Egypt Retina J [serial online] 2014 [cited 2020 Apr 5];2:83-5. Available from: http://www.egyptretinaj.com/text.asp?2014/2/2/83/158226
| Introduction|| |
Retina is considered an extension of the brain tissue as also evident by the embryology. Retina develops from the neuroectoderm and it will be logical to conclude that the anesthetic agents which affect the nerves and neural tissue will have a similar effect on the retina. We report a case where such an effect caused unpleasant, but temporary surprise to both the patient and the surgeon.
| Case Report|| |
A 22-year-old male underwent sutureless 23 g pars plana vitrectomy under topical anesthesia for intravitreal live cysticercus in right eye. The patient was phakic, and the crystalline lens was clear, so it was not disturbed. On day 1 postoperative patient reported diminution of vision with mild pain in the eye. On examination, the best corrected visual acuity (BCVA) was 3/60 with moderate ciliary tenderness and marked hypotony. A provisional diagnosis of sclerostomy leak was made, and the patient was advised tight pad and bandage for providing tamponade to the sclerostomy sites and was advised to return after a day. Next day the hypotony persisted, and the patient was shifted to the operation theater for exploration and suturing of sclerostomy if needed.
One of the sclerostomy superotemporal site corresponding to the surgeons right hand, used for vitrectomy cutter was found to be leaking and thus was sutured under topical anesthesia supplemented with intracameral 0.05% lignocaine solution through a preexisting limbal paracentesis site. Subsequently, intracameral irrigation with balanced salt solution was used to build up the pressure, to achieve normal intra-ocular pressure.
Although, the leakage was from a sclerostomy but still we preferred to inject fluid in the anterior chamber instead of the sclerostomy due to the number of reasons. Firstly intracameral lignocaine augmented topical anesthesia, which was important for postoperative painful and the tender eye. Second, there was a preexisting paracentesis site available (this was made during the Pars Plana Vitrectomy for intracameral mydriasis and anesthesia augmentation using lignocaine 1% solution), hence injecting fluid through it was preferred to avoid choroidal detachment while entering through the preexisting sclerostomy in an eye with hypotony.
Significant deepening of the anterior chamber was observed at the time of intracameral injection, and hence fluid was injected in episodes so as to allow fluid to travel to the posterior segment through the lens zonules.
Patient was shifted out of the OT with no patch as the procedure was done under topical anesthesia. Few minutes later the patient self-reported that he cannot see with the operated eye. The vision was no perception of light, and there was the absence of consensual pupillary reaction in the other eye. Fundus appeared normal with no disc pallor or vascular abnormality. Intra-ocular pressure was 10 mm Hg with Goldman's applanation tonometer Provisional diagnosis of retinal anesthesia due to significant amounts of intracameral lignocaine solution reaching posterior segment was made and patient was assured and was asked to report after 24 h and to continue topical antibiotic steroid eye drops and cycloplegic eye drops.
On the subsequent visit after 24 h the patient was comfortable with gain in vision. On examination, the BCVA was 6/24 and intra-ocular pressure was 10 mm Hg on applanation. Fundus examination of the right eye showed clear media with attached retina and laser spots in the inferior periphery around the area of attachment of the cysticercus cyst [Figure 1] which was done during the vitrectomy for removal of the cysticercus. At the time of preparation of this report, 2 months had passed since the event and patient was stable with further visual gain to BCVA 6/18. At this time, an ocular coherence tomography (OCT) macular map was done which showed epiretinal membrane in the nasal quadrant of macula [Figure 2].
|Figure 1: Fundus photograph of the eye showing scar and laser spots at the site of attachment of cysticercus cyst|
Click here to view
| Discussion|| |
Anatomically and developmentally, the retina is known as an extension of the central nervous system (CNS); it consists of retinal ganglion cells, the axons of which form the optic nerve, whose fibers are, in effect, CNS axons.  Due to this retinal tissue is vulnerable to same anesthetic agents which are able to anesthetize the nerves and spinal cord as in nerve blocks and spinal anesthesia. In the case described a similar phenomenon occurred as the intracameral lignocaine solution reached the posterior segment through the permeable space formed by the lens zonules. Once the anesthetic solution came in contact with the retina and diffused into the tissue the patient's retina lost all the nerve conduction properties and hence was temporarily unable to generate and conduct the visual signals to the visual pathway.
The retinal anesthesia was so profound that the patient was unable to perceive light in the affected eye. And there was absolute afferent pupillary defect in the affected eye, as seen by the absence of consensual pupillary reaction in the other eye. However, this was a reversible phenomenon and after recovery from anesthesia, the patient gained full preoperative vision and complained of no other symptoms. The OCTs were normal for macular map and optic disc retinal nerve fiber layer thickness at 4 weeks from the event.
Similar case report is there in the literature involving inadvertent retinal anesthesia causing profound temporary visual loss.  In that case also, hypotony due to a perforated leaking anterior chamber allowed seepage of lignocaine solution from the anterior chamber into the posterior segment and anesthetized the retina. Similarly in our case, the combination of hypotony and anterior chamber infusion with anesthetic solution to build-up the intra-ocular pressure caused seepage of anesthetic solution to the posterior segment via the zonular "sieve."
Thus, one must keep the possibility of retinal anesthesia when using intracameral anesthesia especially in situations of ocular hypotony, even in phakic eyes. This may be an unpleasant surprise for both the surgeon and the patient as both expect immediate visual recovery after the procedure, whereas there is temporary absolute vision loss due to this phenomenon. In such a situation, one must realize that the vision loss is temporary, and there is usually complete recovery once anesthesia effect is gone with no residual damage. At the same time, this phenomenon also highlights the possibility of any medication delivered in the anterior chamber to reach the posterior segment in therapeutic/toxic concentration and this should be kept in mind, especially if there is hypotony and an attempt is made to build up the pressure.
| References|| |
London A, Benhar I, Schwartz M. The retina as a window to the brain-from eye research to CNS disorders. Nat Rev Neurol 2013;9:44-53.
Hoffman RS, Fine IH. Transient no light perception visual acuity after intracameral lidocaine injection. J Cataract Refract Surg 1997;23:957-8.
[Figure 1], [Figure 2]