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Editor,—Since the initial identification of macular holes as pathological entities in the middle of the 19th century,1 there has been an evolution in the understanding of their aetiology. Tangential macular traction by perifoveal vitreous cortex is now accepted as the causative factor in the development of idiopathic macular holes.2 3
With the widespread use of extracapsular cataract extraction procedures, posterior capsule opacification is a frequent complication. YAG laser capsulotomy, although a non-invasive procedure, has been associated with a number of complications, including retinal detachment, cystoid macular oedema, and raised intraocular pressure (IOP).4 5 A much rarer complication of YAG capsulotomy herein reported is the formation of a macular hole after YAG capsulotomy.4
A 71 year old woman underwent an uncomplicated extracapsular cataract extraction with posterior chamber lens implantation in her left eye. Her ocular history was significant for chronic open angle glaucoma. In the immediate postoperative period, there was an acute rise in IOP to 40 mm Hg that responded to Diamox (acetazolamide) orally. Three months postoperatively, best corrected visual acuity was 20/20 in both eyes with IOPs of 17 mm Hg in the right eye and 13 mm Hg in the left.
Two years later, the best corrected visual acuity was found to have decreased to 20/80 in the left eye attributable to significant posterior capsule opacification. Posterior capsulotomy was performed with a Nd:YAG laser (4.1 mJ/pulse, total energy 109.5 mJ). Postoperatively, there was no increase in IOP and no vitreous prolapse into the anterior chamber. Two weeks after the Nd:YAG laser capsulotomy, the patient noted a decrease in visual acuity, along with a black spot in her central vision. On examination, a stage 3 macular hole was seen with best corrected visual acuity 20/400 left eye. Retinal consultation confirmed the diagnosis and the patient underwent a pars plana vitrectomy, with C3F8 gas instillation and facedown positioning.
Evaluation of the patient 4 weeks after surgery revealed an improvement of visual acuity in the left eye to the level of 20/25. Visual acuity 6 months after surgery remained at the level of 20/25 with the macular hole closed.
The most common complication of extracapsular methods is a late opacification of the posterior capsule. Surgically opening the posterior capsule has been shown in several studies to increase the incidence of both cystoid macular oedema and retinal detachment.4 5 With the advent of the Nd:YAG laser, the ease of posterior capsulotomy has been greatly simplified. Retinal complications following YAG laser capsulotomy are well documented.4 5 Winslow and Taylor4 reported one retinal flap, two macular holes, six cases of cystoid macular oedema, and 10 retinal detachments following YAG laser capsulotomy. In this series, macular hole formation occurred 1 and 3 months after capsulotomy while in our case it occurred within 2 weeks.
Over the years, several mechanisms have been proposed to explain the increased incidence of retinal complications following posterior capsulotomy including increased vitreous liquefaction, changes in vitreous composition, acoustic transients, and direct retinal damage. Osterlin6 reported a greater decline in the hyaluronic acid content in vitreous samples from monkey eyes having undergone intracapsular cataract extraction as opposed to extracapsular cataract extraction. He postulated that in the eyes that had undergone intracapsular cataract extraction, hyaluronic acid in the vitreous had diffused anteriorly, resulting in the vitreous instability and subsequent retinal complications. Thus, the intact capsule acts as a diffusion barrier for hyaluronic acid. This concept of a diffusion barrier was again employed by Miyake7 to theorise a role for the posterior capsule in the development of cystoid macular oedema due to iris synthesised prostaglandins.
Significant liquefaction of the vitreous, postulated to be the result of acoustic transients accompanying the laser irradiation, has been documented in monkey and rabbit eyes following Nd:YAG laser irradiation of the posterior capsule.8 Other more direct injuries to the retina with the formation of macular holes have been reported in industrial accidents involving the Nd:YAG laser.9
In a case report by Blacharski and Newsome,10 bilateral macular holes were reported following Nd:YAG laser posterior capsulotomies. In the first eye, a macular hole formed 21 days after capsulotomy in the absence of vitreous prolapse or an elevated IOP post laser. In the second eye, careful biomicroscopy was performed before Nd:YAG capsulotomy and despite the absence of complication, a macular hole formed 10 days after treatment. These authors believed it unlikely that the shock wave generated by the pulse directly caused the macular hole as relatively low energies were used on both occasions (18 mJ and 29 mJ).
In our case, we propose that the macular hole was formed secondary to the perifoveal vitreous contraction initiated by the YAG capsulotomy. The possible mechanisms of Nd:YAG laser initiation of vitreous contraction could include the well documented acoustic transients generated by a YAG laser pulse, as well as vitreous instability secondary to the vitreous liquefaction demonstrated in both human and monkey eyes following YAG posterior capsulotomy.4
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