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Patient reports deteriorating vision after cataract surgery
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A 63-year-old female presented to the clinic for evaluation of reduced vision. She had undergone uneventful cataract surgery during which a +25-D three-piece acrylic intraocular lens was placed in each eye at our facility approximately 3 months previous. The refractive target for both eyes was emmetropia. As the patient did not live locally, her postoperative care was provided by her referring optometrist.
Although the recovery was reported as uneventful, with the eye healing normally, both the doctor and the patient were concerned about a poorer visual outcome than expected with the left eye. The patient described a well-healed, comfortable right eye. She was happy with the visual improvement she achieved there. The left eye, however, she described as having poor vision, which had continued to deteriorate overtime.
Her presenting acuity with an updated spectacle prescription (which was written 1 month after surgery) was 20/20 OD and 20/50 OS. The glasses prescription was 0.50 D -1.00 D x 180 OD and -1.50 D -0.75 D x 175 OS. Uncorrected acuities were 20/25 OD and 20/200 OS. Pinhole testing yielded 20/20 OU visual acuity, and autorefraction showed 0.50 D -1.00 D x 168 to 20/20 OD and -2.50 D -1.00 D x 170 to 20/30 OS.
Entrance testing consisting of pupils, extraocular muscle function and confrontation fields was normal in both eyes. IOP by ICare tonometry was 12 mm Hg OU.
Dilated slit lamp examination of the right eye showed a normally healed postoperative eye with healthy anterior and posterior structures and a well-positioned and clear three-piece IOL The left eye was also grossly normal. The eye was white and quiet; cornea, nerve and retina all appeared normal; and the IOL was a clear three-piece lens, well-centered, without posterior capsular opacification.
There was a significant difference, however, between the two eyes in the depth of the anterior chamber. This was plainly visible on slit lamp exam and also measurable with biometrics. Pentacam (Oculus) showed an aqueous depth (depth from corneal endothelium to anterior lens) of 3,360 m OD and 2,290 m OS – preoperatively, aqueous depth was symmetric at 2,130 m and 2,230 m.
What’s your diagnosis?
While cystoid macular edema (CME) would be on the differential list for visual acuity reduction in this time frame after cataract, the fact that this patient still corrects well all but eliminates the potential for this, and CME should not impact the depth of the anterior chamber.
To make to our diagnosis we need to answer the following questions: Why does the patient have unintended and worsening myopia in the left eye (as evidenced by the continued myopic shift after her postoperative glasses prescription was dispensed)? Why does she have a narrow anterior chamber on the left eye relative to the right when preoperative measures suggested symmetry? Are these two findings tied together?
Focus on anterior chamber
Attention to the anterior chamber is really the key component and can guide our clinical exam further, as sources of shallow anterior chamber after cataract surgery are quite limited. The effect of cataract surgery on anterior chamber depth should be almost universal deepening, as the thicker cataractous natural lens is replaced with a thinner profile IOL. This change allows the iris plane to settle more posteriorly and opens the anterior chamber.
There are three exceptions to this rule. The most common exception is if early in the postoperative course there would be a significant wound leak. While chamber depth will remain established with mild wound leaks, severe ones will cause flattening. Wound leaks this prominent are rare after modern uneventful cataract surgery and are relatively easily identified, both with Seidel testing and with IOP, which in the case of a flat/shallow anterior chamber will be close to 0. Remember that, in our case, the chamber was formed, it was just shallow relative to the fellow eye.
Next, malignant glaucoma or aqueous misdirection may rarely occur during cataract surgery and manifest in the early postoperative course. These eyes will have extremely shallow central anterior chambers and highly elevated IOPs; following the same basic trend would be those eyes with a mediation-induced anterior rotation of the ciliary body, such as that which occasionally occurs with use of the anticonvulsant topiramate. Further, in both of these cases, because the IOL has been displaced forward by either posterior vitreous pressure or anterior movement of the ciliary body, a myopic shift will result: The further forward the lens or IOL sits, the more effectively myopia is induced. Examining the patient with malignant glaucoma or anterior rotation of the ciliary body will reveal no special anatomic disruption other than shallowing of both the peripheral and central anterior chamber and high IOP, which, depending on its extent, may generate corneal edema as well.
The last source for anterior chamber flattening in a postcataract patient is a phenomenon that is seldom discussed in optometry: capsular distension syndrome. Capsular distension syndrome occurs when fluid fills the space between the posterior IOL and posterior capsule (PC). In most cases, this space collapses over the first few days postoperatively and results in a PC that is in direct contact with the IOL. Occasionally, however, fluid remains trapped in the space and does not clear. In my experience, the most common type of capsular distension then results as this stagnant fluid becomes turbid and cloudy over time, which then roughly mirrors the effects of posterior capsular opacification. Occasionally, however, fluid is continuously introduced into this space, either via a trap-door mechanism through the ciliary process or through production of fluid from retained lens material in the capsule itself, which results in a continuous, insidious expansion of this trapped fluid and subsequent ballooning of the space between the IOL and PC. At some threshold level, the PC cannot easily further expand into the vitreous, and the IOL is driven anteriorly by the intracapsular pressure.
As with malignant glaucoma, this anterior displacement of the lens results in a myopic shift. The extent of myopia generated is determined by both the IOL power and the distance it is displaced from the intended lens position; an average +20 D lens will generate about 2 D of error for every millimeter it is displaced. Rarely, if the process progresses further, an asymmetric rise in IOP from narrowing of the chamber or pigment dispersion from IOL/iris chaffing may occur.
Easy diagnosis
In our case, the primary suspicion, given the entire constellation of findings, is that this is a case of capsular distention syndrome, a phenomenon that is easy to diagnose if you suspect it, but also incredibly easy to overlook if you are unaware of it. This is because in marked cases the posterior capsule will be driven so far into the vitreous that it will not be visible as you look at the IOL. This can lead the clinician into believing that the capsule is clear and in place as normal. However, if you push your slit beam further forward into the vitreous, you will encounter the ballooned surface of the posterior capsule and be able to identify it, in which case the diagnosis is made.
So, the key to this diagnosis of capsular distension is awareness of the condition and a suspicion that you may be dealing with it. This will drive your slit lamp exam to a part of the eye that is seldom directly assessed, the mid-vitreous.
This patient’s management
In our patient’s case, capsular distention was the diagnosis, as confirmed by the ballooning of her posterior capsule. The treatment of this condition is one of the quickest and most satisfying in all of eye care, a YAG capsulotomy. Simply performing a YAG on a distended posterior capsule will result in immediate egress of fluid from this space, a collapse of the capsular ballooning, posterior settling of the IOL and a subsequent regression of myopia. In some eyes this reduction will occur over several minutes. In others, it may take a week, but, in all cases, YAG is a definitive treatment and provides a relatively quick resolution. In cases like these, a small capsular opening is usually produced, as the end result size that abuts to the IOL is unpredictable due to redundant capsule. This smaller opening can always be expanded later if necessary.
At our patient’s 1-week follow up, her uncorrected acuity had returned to 20/30, her autorefraction was -0.75 DS and her symptoms of blurred vision had resolved. Scheimpflug imaging showed an aqueous depth of 3,160 m. Slit-lamp exam showed an appreciable deepening of the anterior chamber. The posterior capsule had contracted down to contact the IOL. Radial “stretch marks” were apparent on the capsule due to sudden collapse of the ballooned capsule after YAG, which were not bothersome to the patient, but could be removed with further YAG laser if they became so.
As with many conditions, the key to diagnosing capsular distension is a suspicion it may be present. If you keep it on your differential for postoperative myopia and postoperative asymmetric shallowing of the anterior chamber, you will not miss the diagnosis.
For more information:
Aaron Bronner, OD, is a staff optometrist at Pacific Cataract and Laser Institute in Kennewick, Wash. He can be reached at abronner@gmail.com.
Edited by Leo P. Semes, OD, FAAO, a Primary Care Optometry News Editorial Board member. He may be reached at leopsemes@gmail.com.
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