I was consulted on a 72-year-old white male who had previously undergone bilateral cataract surgery by another surgeon. The patient had received multifocal lens implants and was very unhappy with the quality of his vision, partly due to some underlying ocular pathology, including an epiretinal membrane in his right eye and mild amblyopia in his left.
One year after undergoing cataract surgery, the patient returned to his surgeon and requested that the lenses be exchanged for monofocal IOLs. He underwent a lens exchange in his right eye. Prior to both this surgery and the initial cataract procedure, the patient's corneal endothelial cell counts were measured and found to be healthy in both eyes at approximately 2,000 cells/mm2 OU. One week after the lens exchange procedure, the patient's glare had disappeared in his right eye, and his UCVA was 20/40, similar to the acuity both before and immediately after the cataract surgery. The eye was quiet, and the patient was pleased with the eradication of his photic phenomenon.
One month after the lens exchange surgery, however, the patient presented to the operating surgeon with complaints of pain and blurred vision in his right eye. His cornea showed moderate edema in addition to some iritis with a mild-to-moderate cellular reaction in the anterior chamber. The surgeon treated him appropriately with topical steroids, hyperosmotics, and atropine for the pain. One month later, although his eye had quieted, his corneal edema persisted, and his vision could be improved to no better than 20/100 OD.
At this point, the patient was referred to me for a corneal consultation. I noted the patient's moderate corneal edema and quiet anterior chamber in the right eye. I treated him aggressively with topical steroids every hour in addition to Muro 128 (Bausch & Lomb Surgical, San Dimas, CA) every 2 hours. Corneal endothelial cell counts revealed a normal count of 2,400 cells/mm2 in the left eye (Figure 1A). The cell counts were unrecordable in the right eye (Figure 1B). The patient returned 3 weeks later after adhering to the aggressive topical regimen with no change in his edema or his visual acuity.
What was unusual about this case was that the patient saw well immediately after his lens exchange procedure. I asked the original, experienced surgeon how he had removed the lens, and he informed me that the surgery had proceeded “atraumatically” and used the Mackool Lens Removal System (Impex, Inc., Staten Island, NY). My initial impression was that the corneal edema had probably resulted from trauma during the lens exchange. However, the patient's good visual acuity immediately after the exchange followed by corneal decompensation and anterior chamber inflammation 1 month later did not quite fit with this explanation.
A MINISCULE DISCOVERY
The patient ultimately required a corneal transplant in his right eye. I removed his cornea, sutured the graft into place, and irrigated the viscoelastic out of his eye. As I performed the anterior chamber irrigation, I noticed an object in the anterior chamber shimmering and dancing around. Under high magnification, I confirmed the presence of a small foreign body. I removed the foreign body, which appeared to be a sliver of the extracted silicone lens (Figure 2) that the original surgeon had removed. Next, I completed the transplant and sent the cornea for pathologic evaluation, which demonstrated a total absence of endothelial cells. I thought I now knew the cause for the patient's corneal decompensation.
I discussed my discovery with the surgeon, and he stated that he had needed to cut through the lens twice in order to completely transect it. I suspect that cutting twice through the lens somehow created a small sliver that, because of its size, fell into the inferior angle unnoticed. Although the patient's inflammation may possibly have contributed to damaging the endothelial cells, it was most likely this small fragment's bouncing around in the anterior chamber that eventually destroyed the endothelium. Contact between the fragment and corneal endothelium damages cells and creates what is termed an endothelial sink. During this process, remaining healthy cells will continue to slide over the areas of bare Descemet's membrane and then subsequently become damaged by the fragment until the density of endothelial cells drops below the threshold that will allow the corneal to remain clear.
CORNEAL DECOMPENSATION AND IOLs
The causes of corneal decompensation associated with IOLs are numerous. Some of the more common ones include (1) pre-existing corneal endothelial disease (this was not the case with this patient); (2) intraoperative trauma (which the operating surgeon denied in this case); (3) vitreous prolapse that comes into contact with the cornea; (4) toxic intraocular medications; and (5) an IOL touching the endothelium. A literature search for cases of lens fragments causing corneal decompensation revealed only two reports: one of a haptic from an anterior chamber IOL that had broken off, and another of a haptic from a posterior chamber IOL that broke off many years after the initial implantation. Reports in the literature of a retained, fragmented foldable lens that had been exchanged did not exist. Whether or not this scenario has happened before is difficult to determine.
To avoid a complication such as this one, I recommend the following. First, after performing a lens exchange, irrigate the angle of the eye with BSS (Alcon Laboratories, Inc., Fort Worth, TX) to dislodge any occult fragments. Second, regardless of the instrument used to transect the IOL, remove and place all IOL fragments on the surface of the eye and reassemble them like pieces of a jigsaw puzzle to ensure that you have a complete lens outside of the eye.
I performed a surgery recently in which I replaced a lens that had developed a crack in it during insertion. I used a wire-snare to cut it in half, but, because I had cut through the crack, I had actually created three pieces of lens instead of the expected two. I could easily have left a fragment in the eye (with the same consequences as described earlier) had I not noticed a small piece in the subincisional area. I removed the three fragments and reassembled them on the patient's ocular surface, thereby demonstrating that the entire IOL was indeed now outside of the eye (Figure 3). This step ensured that there were no occult fragments left in the eye.
If after performing a lens exchange you encounter a similar situation in which the patient's cornea begins to deteriorate many weeks after surgery, particularly in the inferior region, you should suspect a foreign body. Perform gonioscopy, and, if you find a foreign body, you can remove it before the cornea completely decompensates. If you are able to intervene one-half or one-third of the way into the corneal endothelial sink process, many times the cornea will recover, and the patient will not require a transplant. In this particular case, the endothelium had already been damaged beyond recovery.
Approximately 9 months after the patient's transplant surgery, all but two of his interrupted sutures had been removed, and his visual acuity had returned to 20/40 with a +0.50 + 1.50 X 60 correction (Figure 4). This outcome is similar to that which the patient had achieved 1 week after his lens exchange procedure, and he is currently satisfied. As one might expect, he elected not to undergo a lens exchange in his left eye.