Cataract Surgery | Aug 2005
A Forward Vaulting IOL
Christoph Kranemann, MD, FRCS, DABO; D. Matthew Bushley, MD; Terry Kim, MD; Michael L. Nordlund, MD, PhD; Iqbal Ike K. Ahmed, MD, FRCSC; and Juan J. Mura, MD
As CHRISTOPH KRANEMANN, MD, FRCS, DABO
First and most significantly, the IOL seems to be upside down. It appears to be an MA60 (Alcon Laboratories, Inc., Fort Worth, TX), which, when placed properly, has a 10º posterior angulation of the haptics that causes the optic to vault posteriorly. The lens' reversed position alone would account for a significant forward vaulting effect. The problem is aggravated by a significant amount of retained cortex temporally. Quite possibly, there is also vitreous prolapse via the posterior capsular tear.
Clearly, the status quo, including the use of cycloplegics, is unacceptable in this case. The patient has a long-term risk of secondary pigmentary dispersion as well, and the surgeon must address the retained cortex and probably prolapsed vitreous.
It would be insufficient simply to reverse the IOL's position. Flipping the lens in the anterior chamber would pose a significant risk to the endothelium. If the surgeon pursued such an approach, it would be less traumatic to explant the IOL by making a 3- to 4-mm cut in the optic and rotating it out of the eye, as previously described by Osher and Dodick.1
Still, any new IOL should have its optic captured posterior to the capsule. The least traumatic approach would therefore be to capture the optic of the existing IOL posterior to the capsule and only to perform a lens exchange if the patient's refractive demands and current IOL power required it. Quite likely, the IOL in place was calculated for a position in the capsular bag and would be of the appropriate power. The surgeon would simultaneously need to remove the bulk of the remaining cortex, enlarge the capsular opening, and remove any prolapsed vitreous.
My preference would be a bimanual vitrectomy approach with an anterior chamber maintainer at the limbus and the vitrector inserted through a pars plana incision. After debulking the anterior vitreous, I might have to employ a viscoelastic to open the remaining capsular bag. I could then use the vitrector to remove the remaining cortex as well as to enlarge the capsular opening. Thereafter, I could capture the optic posterior to the capsule.
Alternatively, one could perform the bimanual vitrectomy via two limbal incisions. Because this technique can cause the vitreous to move forward, I prefer the aforementioned scenario. If approaching the IOL solely from the limbal side, I would first place a dispersive viscoelastic to isolate the vitreous and open the capsular bag. I would proceed as described earlier. One of the technical challenges is that a dispersive viscoelastic can clog the vitrector in this situation. Either approach may be performed under topical anesthesia.
D. MATTHEW BUSHLEY, MD, AND TERRY KIM, MD
We assume that cycloplegia relieved the patient's symptoms, although this information is not provided. Our first step would be to perform a thorough ophthalmologic examination, with particular attention to the IOP, gonioscopy, the anterior chamber depth, the IOL's position, and the anterior and posterior capsules' integrity. We would also conduct a complete, dilated, fundoscopic examination with B-scan ultrasonography to look for conditions that may cause or predispose the patient to pupillary block in the postsurgical setting.
Figure 1 provides few clues. The IOL in the sulcus is upside down, which positions the optic in a more anterior position. The capsulorhexis is small. Depending on its location and size, a large, grayish, homogenous mass behind the IOL temporally could further displace the lens implant anteriorly.
Potential conditions at play here include choroidal effusion or detachment, retinal detachment, a choroidal mass, or retained lens material after a complicated cataract surgery. Swollen cortical material, especially if entrapped within the capsular bag, could displace the sulcus-supported lens implant anteriorly while the associated intraocular inflammation would explain the increase in floaters noted by the patient. An examination and ultrasonography should promote a rapid differential diagnosis.
We recommend creating a peripheral iridotomy, repositioning the IOL in the ciliary sulcus such that it is correctly oriented under the protection of copious amounts of a dispersive viscoelastic, and removing retained lens material via anterior vitrectomy, if indicated. We would also consider capturing the IOL's optic through the intact anterior capsulorhexis to minimize any chance for pupillary capture or block.
Another clinical scenario that could present in this manner but that may not respond to cycloplegia alone is aqueous misdirection syndrome. In such a case, we would expect the patient's anterior chamber to be shallow and her IOP to be high, despite pupillary dilation beyond the edge of the IOL's optic. Figure 1 does not provide sufficient detail for assessment, however, and the status of the anterior hyaloid membrane is unknown here.
Contributing to the anterior vaulting of the IOL in this scenario would be the small capsulorhexis, which the IOL's optic can block and thus prevent the misdirected aqueous from entering the anterior chamber. The persistence of symptoms despite a patent peripheral iridotomy would confirm this diagnosis. The aforementioned treatment of anterior vitrectomy, peripheral iridotomy, and a repositioned lens should be curative for this disorder.
MICHAEL L. NORDLUND, MD, PhD
Pupillary block after phacoemulsification and the placement of a PCIOL are uncommon.2,3 The usual etiologies are aqueous misdirection syndrome, iris synechiae to the anterior capsule or IOL, anatomical risk factors such as nanophthalmos, and a misplaced IOL. In this case, the surgeon experienced a capsular tear and apparently placed a multipiece IOL in the ciliary sulcus. Although such placement is appropriate in this case, Figure 1 demonstrates that the lens was placed upside down. Thus, the haptics, which normally extend 5º to 10º anteriorly from the optic, are angled posteriorly in the eye. The posterior extension of the haptics causes anterior vaulting of the optic and the subsequent pupillary block.
To correct the pupillary block, one could perform a laser peripheral iridotomy. If the iris is markedly displaced anteriorly, however, I would be concerned about chronic iritis and cystoid macular edema. Additionally, in Figure 1, it appears that there are significant cortical remnants temporally that could contribute to intraocular inflammation. Thus, if laser peripheral iridotomy and aggressive topical steroid treatment did not quickly resolve the pupillary block and inflammation, I would proceed with an IOL exchange.
The details of the surgical approach depend on specifics that are not provided in the case presentation, such as the extent of the posterior capsular tear and whether the anterior hyaloid membrane is intact. If the anterior hyaloid is undamaged, it may be possible to perform the IOL exchange and manually aspirate the cortical remnants without a vitrectomy. With a violated anterior hyaloid face, however, a vitrectomy will likely be required. If a vitrectomy is necessary, I would use a bimanual technique in which I performed irrigation through a paracentesis and passed the vitreous cutter through a pars plana stab incision, 3.5mm posterior to the limbus. The pars plana approach is particularly useful in this eye, because the anterior capsulorhexis is quite small.
I would remove the IOL through the established wound. I would create space between the capsule and the IOL with a dispersive viscoelastic and bisect the IOL with lens-cutting scissors. I prefer this method to refolding the lens in an eye with an open capsule, because I feel it allows me to remove the lens with less posterior pressure and to control better the movement of the haptics relative to the capsular bag. After removing the IOL, I would manually aspirate the residual cortical material with a J-cannula. During this maneuver, it is important to hold the vitreous back with the dispersive viscoelastic.
Having removed the IOL and cortex, I would replace the lens. If the capsular tear were large and the posterior capsule were unstable, I would reinsert a multipiece acrylic PCIOL in the ciliary sulcus. If the tear were small and central, however, I would attempt a posterior capsulorhexis to stabilize the capsular bag further, prior to inserting the lens in the bag. In the case of a small, eccentric posterior capsular tear, I would place the lens without performing a posterior capsulorhexis. I would attempt to reinflate the capsular bag and place a single-piece acrylic IOL, with its haptics aligned perpendicular to the location of the tear. I prefer a single-piece IOL in this situation, because it exerts less radial tension on the capsule and has excellent centration.
Typically in eyes with posterior rents, I try to capture the optic in the anterior capsulorhexis. In this case, it appears too small for optic capture, so I would not try to enlarge the capsulorhexis in this eye, because a small radial tear could significantly compromise the stability of the IOL's placement and the outcome of the surgery. After positioning the IOL, I would remove the viscoelastic with gentle I/A and place a suture in the wound to minimize the risk of a leaking wound and the anterior displacement of the vitreous.
IQBAL IKE K. AHMED, MD, FRCSC, AND JUAN J. MURA, MD
It appears that the IOL was implanted upside down within the ciliary sulcus in the presence of an open posterior capsule and retained cortical material. This situation may produce a minimal-to-large myopic refractive error, depending on the IOL optic's design. For example, a plano-convex design placed upside down can cause a large myopic shift.4
The IOL in this case appears to be a three-piece acrylic lens designed with posterior vaulting (ie, 10º) when placed correctly. In a reversed-optic position, the IOL vaults anteriorly and thus has a propensity for iris chafing, which could lead to pigmentary dispersion glaucoma (most likely the mechanism of IOP elevation in this case),5 optic capture, and pupillary block. Additional causes of anterior IOL vaulting include capsular block syndrome,6 vitreous block, malignant glaucoma, supraciliary effusion/choroidal detachment, and retained cortex.
The ophthalmologist should examine this patient for evidence of iris chafing and pigmentary dispersion, including iris transillumination defects, Krukenberg's spindle, and excessive pigmentation of the trabecular meshwork. Peripheral fundoscopy and/or ultrasound biomicroscopy would be of additional help to rule out the other aforementioned causes of posterior-pushing mechanisms.
The appropriate management of this patient would begin with a pars plana anterior vitrectomy (infusion with an anterior chamber maintainer through a limbal stab incision) to clear the anterior segment of vitreous adhesions and to remove retained cortex. This approach is preferable to limbal vitrectomy, because it will allow the surgeon adequate access to residual cortical material. It is critical to remove the significant amount of retained lens material in order to prevent persistent uveitis, glaucoma, and/or cystoid macular edema.
Next, the surgeon should retain the preexisting anterior capsule shelf while enlarging the capsulorhexis to between 5.0 and 5.5mm to permit the capture of the optic (the capsulorhexis currently appears to be approximately 3 to 4mm). A capsulorhexis forceps is preferable for this step, but the surgeon may also use a vitreous cutter.
The surgeon should then reposition the IOL in situ by tumbling it with the aid of abundant viscoelastic placed anterior and posterior to the IOL.7 Thereafter, he should attempt to capture the optic through the capsulorhexis. If impossible to do so, the surgeon would place the IOL in the ciliary sulcus and ensure its correct orientation.
Section Editors Robert J. Cionni, MD; Michael E. Snyder, MD; and Robert H. Osher, MD, are cataract specialists at the Cincinnati Eye Institute in Ohio. They may be reached at (513) 984-5133; rcionni@cincinnatieye.com.
Iqbal Ike K. Ahmed, MD, FRCSC, is Assistant Professor at the University of Toronto and Clinical Assistant Professor at the University of Utah in Salt Lake City. He states that he holds no financial interest in the products or companies mentioned herein. Dr. Ahmed may be reached at (905) 820-3937; ike.ahmed@utoronto.ca.
D. Matthew Bushley, MD, is Clinical Associate, Cornea and Refractive Surgery Services, Duke University Eye Center in Durham, North Carolina. He states that he holds no financial interest in the products or companies mentioned herein. Dr. Bushley may be reached at (919) 681-3568; mbushley@aol.com.
Terry Kim, MD, is Associate Professor of Ophthalmology, Cornea and Refractive Surgery Services, at Duke University Eye Center in Durham, North Carolina. He states that he holds no financial interest in the products or companies mentioned herein. Dr. Kim may be reached at (919) 681-3568; terry.kim@duke.edu.
Christoph Kranemann, MD, FRCS, DABO, is Lecturer at the University of Toronto. He states that he holds no financial interest in the products or companies mentioned herein. Dr. Kranemann may be reached at (416) 289-4000; kranemann@globalserve.net.
Juan J. Mura, MD, is an instructor for the Ophthalmology Department at the Universidad de Chile in Santiago, Chile. He states that he holds no financial interest in the products or companies mentioned herein. Dr. Mura may be reached at (905) 820-3937; juan.mura@rogers.com.
Michael L. Nordlund, MD, PhD, is Assistant Professor for the Department of Ophthalmology at the University of Cincinnati College of Medicine and Cincinnati Eye Institute. He states that he holds no financial interest in the products or companies mentioned herein. Dr. Nordlund may be reached at (513) 984-5133; mnordlund@cincinnatieye.com.
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