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Retinal Detachment With a Dislocated Posterior Chamber Intraocular Lens
Arch Ophthalmol. 2001;119:909-911.
INTRODUCTION
Subluxation and complete dislocation of posterior chamber intraocular lenses (PCIOLs) into the vitreous cavity are well described complications of cataract surgery. A variety of approaches to their management have been reported.1-3 We report a case in which a dislocated PCIOL was left in the vitreous cavity. Some time later, this PCIOL appears to have contributed to a rhegmatogenous retinal detachment.
Report of a Case
In 1993, an 82-year-old woman underwent an uncomplicated cataract extraction in her left eye. In 1995, the PCIOL became subluxated to the extent that the superior edge of the optic was just visible at the inferior pupillary margin. An anterior chamber intraocular lens (ACIOL) was implanted after an unsuccessful attempt to remove the subluxated PCIOL in March 1995. Immediately after surgery, the patient developed a hyphema and a vitreous hemorrhage and she was referred for management 25 days postoperatively.
When in the retina service, her visual acuity was hand motions OS. A 20% hyphema, a vitreous hemorrhage, and a well-positioned ACIOL were noted. The intraocular pressure (IOP) was 20 mm Hg. A B-scan ultrasonogram demonstrated that the retina was attached; we began a period of observation. During this observation period, her IOP rose to 40 mm Hg OS on postoperative day 46. Though medical therapy was initially successful in controlling her IOP, the pressure began to rise despite treatment. In May 1995, a pars plana vitrectomy (PPV) and an anterior chamber washout were performed. During the PPV, the PCIOL completely dislocated into the posterior chamber and it was not removed at that time.
Nine weeks postoperatively, her visual acuity had improved to 20/70 OS. The anterior chamber was quiet with a well-positioned ACIOL, and the IOP was 12 mm Hg. A preretinal membrane was present in the posterior pole, and the PCIOL was noted to be lying on the retina in the 6-o'clock position. The patient denied symptoms attributable to the PCIOL.
Two weeks later, the patient developed a macula-involving retinal detachment, with the causative break located in the periphery in the 10:30-o'clock position. This detachment was treated with a scleral buckling procedure, cryotherapy, and instillation of pure perfluoropropane periphery intraocular gas. Since the dislocated PCIOL was not in proximity to the break, it was not believed to have played a role in the retinal detachment. The PCIOL was left in the vitreous cavity at that time.
The patient's visual acuity subsequently improved to 20/40–2; however, in September 1997, the patient developed a macula-involving temporal retinal detachment. Although the original retinal break at the 10:30-o'clock position remained closed, 1 of the haptics of the dislocated PCIOL was noted to pass through the causative retinal break located just temporal to the meridian in the 6-o'clock position in the inferior periphery (Figure 1).
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Detail of the inferior retina in which haptic of the dislocated posterior chamber intraocular lens is passing into the subretinal space through the causative retinal break.
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At this point, another surgeon performed a PPV with meticulous dissection of the vitreous near the PCIOL. Perfluorocarbon liquid was used to flatten the retina up to the level of the retinal break. Owing to the high specific gravity of the perfluorocarbon liquid, the relatively buoyant lens was able to "float" on the meniscus of the perfluorocarbon liquid.4 The PCIOL was gently grasped with vitreoretinal surgical forceps and removed from the retina. Next, the PCIOL was repositioned into the anterior chamber between the iris and the ACIOL. Following this, the PCIOL was removed via a limbal incision, without removing the secondary ACIOL. After the retinal break was treated with endolaser photocoagulation, air-fluid and gas-air exchanges with isovolumetric perfluoropropane were performed.
As of September 1997, her retina has remained attached and her visual acuity has remained counting fingers OS. Since this operation, she has had visually significant corneal edema that has failed to clear. As of her most recent examination in November 1999, she continues to refuse a penetrating keratoplasty.
Comment
This case raises 3 main concerns in the management of dislocated intraocular lenses. The first issue is how to manage a subluxated or fully dislocated lens in the absence of any retinal complications. A number of different strategies have been reported elsewhere including observation alone, repositioning the PCIOL in the sulcus (with or without sutures), and removal of the lens with or without implantation of a secondary intraocular lens.1-3
In this case, an unsuccessful attempt was made to remove the PCIOL via a limbal approach. Since the PCIOL was out of the visual axis, the surgeon simply implanted an ACIOL at that time. This patient developed a hyphema, a vitreous hemorrhage, and elevated IOP all of which ultimately made a PPV necessary. Perhaps this patient would have only required a single operation if a PPV technique along with lens exchange or lens repositioning had been performed when the lens first became subluxated. Furthermore, it would have been reasonable to have removed the PCIOL (or to have repositioned the PCIOL and removed the ACIOL) during the May 1995 PPV.
The second dilemma is how to repair a retinal detachment in the presence of a posteriorly dislocated intraocular lens. Scleral buckling and PPV have both been successfully used to manage retinal detachments in this setting.1 When this patient had the retinal detachment in July 1995, she was treated with scleral buckling surgery with initial success. As in this case, a significant limitation of the scleral buckling technique is that the dislocated lens cannot be removed by this approach alone.
In contrast, PPV has the advantage that the vitrectomy instruments allow removal or repositioning of the dislocated intraocular lens at the same time as the retinal detachment repair. When this patient went on to develop another retinal detachment in 1997, a PPV with the aid of perfluorocarbon liquid was used to reattach the retina and to manipulate the dislocated PCIOL.4 The PCIOL was first positioned in the anterior chamber and subsequently removed at the surgical limbus. Removing the lens at the pars plana instead of the limbus possibly could have avoided the long-term corneal decompensation that occurred.
The final point of discussion is whether the dislocated PCIOL contributed to either of the retinal detachments in this case. In regard to the July 1995 retinal detachment, the location of the causative break at the 10:30-o'clock position was in line with a sclerotomy site and may have resulted from the initial PPV. Although it is possible that this retinal tear may have resulted from contact with the superior haptic, there is no convincing evidence that the PCIOL caused the break. In September 1997 when the patient had a second retinal detachment, the haptic of the lens was found within the causative retinal break.
One explanation for our clinical findings is that the lens haptic caused a retinal break and migrated through the break into the subretinal space. After the May 1995 PPV, the PCIOL was completely dislocated into the posterior pole. Since the vitreous gel had been removed, the dislocated lens was probably mobile, and perhaps this increased mobility may have contributed to the retinal break.
Alternatively, it is conceivable that the haptic passed into an existing (ie, spontaneous) retinal tear, but the authors believe that this is unlikely. On review of the intraoperative video and preoperative photographs, the size of the break was only slightly larger than the haptic. Also, there was a moderate amount of tissue resistance when the lens haptic was removed from the break suggesting a fairly snug fit. Moreover, the midperipheral location of this break would have been unlikely for a spontaneous tear. Finally, an iatrogenic tear from the May 1995 vitrectomy would have likely manifested itself sooner. In our opinion, both of these observations suggest that it would have been difficult for the haptic to have become engaged in a preexisting break of that size.
This case illustrates a complication likely resulting from a dislocated PCIOL in a previously vitrectomized eye. Leaving a dislocated PCIOL in the vitreous cavity may not be safe, especially in patients who have undergone prior vitrectomy.
AUTHOR INFORMATION
This study was supported by an unrestricted grant from Research to Prevent Blindness Inc, New York, NY. Dr Shah was supported by the HEED Ophthalmic Foundation, Cleveland, Ohio.
None of the authors have any proprietary interests in the contents of this article.
Corresponding author and reprints: Brian P. Connolly, MD, 900 Walnut St, Philadelphia, PA 19107-5598 (e-mail: drbpconn{at}yahoo.com).
Brian P. Connolly, MD;
J. Arch McNamara, MD, FRCSC;
Gaurav K. Shah, MD
Philadelphia, Pa
Caroline R. Baumal, MD, FRCSC
Boston, Mass
REFERENCES
1. Brod RD, Flynn HW Jr, Clarkson JG, Blankenship GW. Management options for retinal detachment in the presence of a posteriorly dislocated intraocular lens. Retina. 1990;10:50-56.
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2. Smiddy WE, Flynn HW Jr. Management of dislocated posterior chamber intraocular lenses. Ophthalmology. 1991;98:889-894.
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3. Tassman W, Annesley WH Jr. Retinal detachment in prosthetophakia. Arch Ophthalmol. 1966;75:179-88.
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4. Lewis H, Sanchez G. The use of perfluorocarbon liquids in the repositioning of posteriorly dislocated intraocular lenses. Ophthalmology. 1993;100:1055-1059.
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SECTION EDITOR: W. RICHARD GREEN, MD
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