CASE REPORT

Long-lasting hyperopic shift and irregular astigmatism after selective laser trabeculoplasty

Farrokhi, Sanaz MD; Steinberg, Johannes MD, PhD, FEBO; Spitzer, Martin S. MD, PhD, FEBO; Linke, Stephan J. MD, PhD

Author Information
doi: 10.1097/j.jcro.0000000000000028
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Abstract

Selective laser trabeculoplasty (SLT) is a frequently performed laser procedure for the treatment of primary open-angle glaucoma and is generally considered a safe and effective method for reducing intraocular pressure (IOP). Most complications related to SLT are transient and readily managed, such as ocular discomfort, postprocedure IOP elevation, and anterior chamber inflammatory reaction. Serious complications are rare.1

A rare but perhaps underrecognized or underreported adverse side effect is a refractive shift after uneventful SLT treatment, which is only reported in a few case studies.2–5 In all 7 cases, the authors have shown an acute corneal edema with subsequent stromal thinning and hyperopic shift after routine SLT. We here present a case with a well-documented follow-up of more than 3 years, revealing a remarkable and long-lasting hyperopic shift after SLT.

CASE REPORT

A 59-year-old man was referred in September 2016 for blurred and reduced visual acuity in the right eye after undergoing uneventful SLT in both eyes 7 weeks before.

The initial diagnosis of normal-tension glaucoma was made in 2015 based on a maximum IOP of 16 mm Hg in both eyes, and Humphrey visual field testing revealed a paracentral field defect in the right eye, with the inferior, superior, and nasal nerve fiber layer losses observed on optical coherence tomography in the right eye, no Humphrey visual field defects in the left eye but superior and nasal nerve fiber layer losses, and a cup-to-disc ratio of 0.50 bilaterally. Central corneal ultrasound pachymetry measured 589 µm in the right and 580 µm in the left eye. Owing to allergic reaction to multiple topical antiglaucomatous drugs (ie, all prostaglandin analogs, carbonic anhydrase inhibitors, beta blockers, and adrenergic agonists), SLT was performed in another clinic. After the procedure, the patient was discharged on topical medication, diclofenac eyedrops and dexamethasone eyedrops each 4 times a day for 1 week to limit postoperative inflammation. The pre-SLT IOP-lowering topical medications (dorzolamide-timolol fixed combination and latanoprost) were discontinued.

Owing to persistently foggy and reduced vision in the right eye, 7 weeks after SLT the patient was referred to our clinic. The corrected distance visual acuity (CDVA) was 20/200 in the right eye and 20/25 in the left eye. Slitlamp examination showed age-adequate, normal findings and the cornea found to be free of any defects, such as corneal haze or edema.

Goldmann applanation tonometry was 18 mm Hg in the right eye and 21 mm Hg in the left eye without topical medication. Corneal endothelial cell count was of normal density (2452 cells/mm2 in the right eye and 2939 cells/mm2 in the left eye) and morphology. Also, macula optical coherence tomography was regular in both eyes.

In the right eye, corneal topography (Galilei G4, Ziemer Ophthalmic System AG) revealed a significant central flattening of the cornea with paracentral steepening and a decreased central total corneal power (TCP) to 36.38 diopters (D) (Figure 1). Central corneal thickness (CCT) was reduced to 504 µm, resulting in an irregular shape of the anterior and posterior cornea in the right eye. The midperipheral TCP was 42.47 D in the right eye. In the left eye, corneal topography revealed minimal central flattening with superior and inferior steeping, whereas CCT (574 μm) and central TCP (41.35 D) were stable (Figure 2). The midperipheral TCP was 42.33 D in the left eye.

Figure 1.
Figure 1.:
Seven weeks after selective laser trabeculoplasty: Corneal topography showing a significant central flattening of the cornea with paracentral steepening, a decreased central total corneal power to 36.38 D, and a reduced central corneal thickness to 504 µm in the right eye.
Figure 2.
Figure 2.:
Seven weeks after selective laser trabeculoplasty: In the left eye, corneal topography revealed minimal central flattening with superior and inferior steeping, whereas central corneal thickness (574 μm) and central total corneal power (41.35 D) were normal.

Although the pre-SLT refraction was −7.50 D −0.5 D × 6 in the right eye and −6.25 D −1.50 D × 158 in the left eye, the post-SLT refraction showed a marked hyperopic shift to +3.00 D −1.75 D × 93 in the right eye and −5.25 D −0.75 D × 152 in the left eye. Clinically, the corneal changes lead to a massive hyperopic shift in the right eye with a decrease in the spherical equivalent from −7.75 D to +2.25 D and a decrease in the CDVA to 20/200. In the left eye, the spherical equivalent decreased from −7.00 D to −5.75 D, whereas the CDVA was relatively stable with 20/25 (Table 1).

Table 1.
Table 1.:
Illustration of a marked hyperopic shift and irregular astigmatism of post-SLT refraction in the right eye and attenuation of the hyperopic shift and irregular astigmatism within 3 years using RGPCLs.

We suspected the massive corneal changes in the right eye were caused by secondary tissue heating and/or inflammation because of high energy input, as Lee et al. described in a study; hence, systemic methylprednisolone (80 mg) was initiated daily for 3 days and tapered over a 3-week period (every 3-day reduction: 60 mg, 40 mg, 30 mg, 25 mg, 20 mg, 17.5 mg, 15 mg, 12.5 mg, and 10 mg).6

Over the subsequent weeks, there was no change in the topography and refraction, as well as the visual acuity, which remained 20/200 in the right eye. We stopped the therapy with methylprednisolone and suggested rigid gas-permeable contact lens (RGPCL) fitting for the right eye. Immediately, the patient observed an improvement in CDVA (20/20), and contact lenses were well tolerated.

On the follow-up visit, 5 months after SLT as well as 10 months after SLT, in the right eye a concomitant decrease in the central corneal flattering and paracentral irregularity was observed on topography (central TCP: 36.68 D and 37.64 D; midperipheral TCP: 41.46 D and 41.83 D) and an attenuation of the hyperopic shift (Figures 3 and 4 and Table 1).

Figure 3.
Figure 3.:
Right eye, 5 months after selective laser trabeculoplasty: Corneal topography showing a decrease in the central corneal flattening and paracentral irregularity. Contact lens–induced artifacts can be seen.
Figure 4.
Figure 4.:
Right eye, 10 months after selective laser trabeculoplasty: Corneal topography showing a decrease in the central corneal flattering and paracentral irregularity artifacts can be seen on Figure 3.

At the last follow-up, 3 years after the SLT procedure, the right eye had a manifest refraction of −4.00 D −0.25 D × 160 and the left eye had a manifest refraction of −5.50 D −0.75 D × 150. The regression to myopia in the right eye was paralleled by an increase in CCT to 551 μm and central TCP to 38.90 D (Figure 5). The CCT and central TCP of the left eye were 579 μm and 41.71 D, respectively (Figure 6). The patient's IOP was well controlled, measuring 11 mm Hg and 13 mm Hg.

Figure 5.
Figure 5.:
Last follow-up, 3 years after selective laser trabeculoplasty: In the right eye, the regression to myopia was paralleled by increased central corneal thickness (551 μm) and increased central total corneal power (38.90 D).
Figure 6.
Figure 6.:
Last follow-up, 3 years after selective laser trabeculoplasty: In the left eye, the regression to myopia was paralleled by increased central corneal thickness (579 μm) and increased central total corneal power (41.71 D).

DISCUSSION

SLT has become a common treatment option for open-angle glaucoma. A recent review summarized reported complications, such as IOP spikes, iritis, hyphema, macular edema, foveal burn, and corneal haze.1 Furthermore, some unusual postprocedure reactions have been discussed in case reports, namely, peripheral anterior synechiae, corneal edema secondary to herpetic stromal keratitis, endothelial injuries, and persistent IOP elevation.7–9 A hyperopic shift after SLT, due to acute cornea edema and stromal haze, and ensuing corneal thinning in 8 patients has been reported in the literature.2–5 In our case, we report remaining hyperopic shift after SLT with the follow-up of 3 years.

Post-SLT corneal edema has been previously reported to have an incidence of approximately 0.8%.10 Although the etiology is unknown, there are few postulated theories about corneal edema resulting in stromal thinning and hyperopic shift.

Knickelbein et al. reported 4 cases of corneal hydrops, a condition characterized by acute corneal edema followed by stromal thinning.5 Because all patients were highly myopic, the authors suspected a break in Descemet membrane causing edema due to pressure of contact trabeculoplasty lens, patient eye rubbing, or a combination of both. Our patient was also highly myopic; however, no preexisting ectatic pathology has been seen on clinical examination before treatment.

Other corneal changes, such as endothelial spots, were noted on slitlamp examination, 1 to 2 hours after SLT. These were transient and without any impact on cell count or visual acuity.11 Also, whitish spots in the corneal endothelium after SLT have been described by Ong et al., which can result in endothelial dysfunction and corneal edema.12 In our case, however, no endothelial changes were seen in the postoperative course after SLT. Moreover, endothelial dysfunction would result in an increase of CCT rather than corneal thinning, which was shown in a recent study.13

Lee et al. reported a significant thinning of CCT after a single session of SLT, which the authors postulated to be caused by laser energy heat escaping into the corneal stroma, which led to temporary thermal contractions of the stromal collagen fibers.6 Although the CCT decrease was reported to be transient (1 week), our patient had a thinner CCT for over 3 years.

Few reports have described diffuse stromal edema followed by corneal thinning, which seemed to be caused by a reactivation of an occult herpes simplex infection due to the inflammatory cascade, which was induced by SLT.2,7,14 There was no preexisting history of iritis in our patient, and there was no vascularization and scarring typical for herpes keratitis.

It is well known that SLT stimulates cytokine production, such as interleukin-1 α, interleukin-1 β, tumor necrosis factor α, and activation of matrix metalloproteinases, which are involved in destructive inflammatory responses and can enhance collagen degeneration by corneal fibroblasts.14

The risk of an inflammatory response is higher in patients undergoing SLT compared with argon laser trabeculoplasty. Song et al. supposed that this could be caused by the spot size of the SLT, which affects a larger surface area of tissue, so the surrounding structures such as the ciliary body and the iris root can be affected and, hence, extend the inflammation to the cornea.5 In this study, the patient showed diffuse corneal edema and subsequently marked corneal thinning and stromal haze sparing the posterior corneal stroma, which lead to flattering of the anterior corneal curvature with a corresponding hyperopic shift similar to our case.

Our patient had a TCP of 36.68 after the procedure. The TCP increased to 37.64 10 months and to 38.90 3 years after using the RGPCL. RGPCLs have been the mainstay of contact lens correction of keratoconus for many decades. Although soft toric contact lenses, hybrid contact lenses, and scleral lenses have been introduced into the clinical practice for vision correction in keratoconic eyes, RGPCLs improve visual acuity more efficiently.15 In our case, an improvement of vision by wearing scleral lenses cannot be ruled out, but even if improvement were possible, the vision correction/quality would be inferior compared with RGPCLs, because of a massive irregularly shaped cornea.

We suspect the changes in the keratometry values were caused by tissue heating owing to a higher threshold, which affected the corneal tissue, by contraction and shrinking, thus leading to corneal curvature alteration.

Although hyperopic shift after SLT is a rare and maybe underreported complication and its underlying mechanism is obscure, ophthalmologists should be aware of this side effect and its effective symptomatic treatment with a hard contact lens. As a treatment, we recommend RGPCLs because in our case the patient regained his full visual acuity.

WHAT WAS KNOWN

  • Although most complications related to selective laser trabeculoplasty (SLT) are transient and readily managed, a refractive shift after uneventful SLT treatment might be an underrecognized adverse side effect.
  • Hyperopic shift after SLT might be due to acute cornea edema and stromal haze and ensuing corneal thinning. Also, reactivation of an occult herpes simplex infection could lead to diffuse stromal edema, followed by hyperopic shift after the procedure.

WHAT THIS PAPER ADDS

  • A significant refractive shift post-SLT lasted for over 3 years, with no abnormal morphological findings such as corneal haze or edema.
  • Due to tissue heating owing to a higher threshold, the corneal tissue could be affected by contraction and shrinking, leading to corneal curvature alteration and changes in k values.
  • Hard rigid gas-permeable contact lenses were for symptomatic treatment and lead to full visual acuity.

REFERENCES

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2. Regina M, Bunya VY, Orlin SE, Ansari H. Corneal edema and haze after selective laser trabeculoplasty. J Glaucoma 2011;20:327–329.
3. Marquis RE. Keratitis and hyperopic refractive shift induced by SLT. Glaucoma Today 2010:18–22.
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12. Ong K, Ong L, Ong LB. Corneal endothelial abnormalities after selective laser trabeculoplasty (SLT) J Glaucoma 2015;24:286–290.
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14. Bradley JMB, Anderssohn AM, Colvis CM, Parshley DE, Zhu X, Ruddat MS, Samples JR, Acott TS. Mediation of laser trabeculoplasty-induced matrix metalloproteinase expression by IL-1beta and TNFalpha. Invest Ophthalmol Vis Sci 2000;41:422–430.
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