Sudden refractive change 1 month after phakic intraocular lens implantation

Abstract

Editor, This letter describes a case of corticosteroid-induced hypertension detected because of a sudden refractive change as late as 1 month following phakic intraocular lens (IOL) implantation with 1-year follow-up data. Sudden astigmatic refractive changes can be caused by a preliminary suture break or cheese-wiring. Usually, a with-the-wound shift occurs 1–3 months after surgery depending on the incision size, location, wound construction and the suture material used. Corticosteroid-induced hypertension is a serious complication that occurs as early as 2 weeks after ocular surgery. It is usually reversible within 3–7 days (Deng et al. 1999) when treatment is limited to a period of less than 12 months (Sapir-Pichhadze & Blumenthal 2003). A 24-year-old woman presented to our refractive clinic with a best-corrected visual acuity (BCVA) of 20/20 with the refraction −8.0–3.5 × 172° (right eye) and −10.0–1.5 × 167° (left eye), intraocular pressure (IOP) 11 mmHg (both eyes) and a regular with-the-rule corneal astigmatism (both eyes) in the corneal topography. Preoperatively, an Nd-YAG-iridotomy was performed in the left eye. Phakic IOL implantation (Verisyse™; AMO, Ettlingen, Germany; −11.5 D) via a 6.1 mm limbal incision closed by a running 10.0-nylon suture was uneventful in the left eye. Dexamethasone 0.1% and ofloxacin four times daily (qid) were given postoperatively. One week after surgery, uncorrected visual acuity was 20/25 and BCVA 20/16 with a refraction of +0.25–1.5 × 148°, IOP 18 mmHg. Examination showed a well-centred phakic IOL with an unremarkable incision suture and no irritation. Local treatment was reduced to dexamethasone twice daily (bid). An uneventful Mitomycin-C-augmented LasEk was performed on the right side. Postoperative fluorometholone 1% was used in the right eye. One month after phakic IOL implantation, the patient presented with a sudden subjective loss of visual acuity on the left phakic IOL side, no other discomfort, an uncorrected visual acuity of 20/32 (decreased), BCVA of 20/16 (unchanged) with refraction of +0.75–1.75 × 100° (astigmatic change of roughly 3 D of cyl in comparison to the previous examination), no irritation, corneal oedema or flare on slit-lamp examination (Fig. 1). Wound architecture and the suture looked perfectly normal. Remarkably, the IOP was 45 mmHg. A quiet eye with a centred phakic iris-claw intraocular lens. Steroid treatment was discontinued; the new treatment was a non-steroidal anti-inflammatory agent three times daily (tid) on the right side, apraclonidine bid on the left side and oral acetazolamide 250 mg bid. Three days later, uncorrected visual acuity was 20/20 and IOP 10 mmHg so oral acetazolamide was discontinued. One week and 1 month after hypertension, IOP was 13 mmHg in the left eye. Apraclonidine treatment was discontinued after 1 month. At the 1-, 3- and 12-month follow-up visits, uncorrected visual acuity remained at 20/20 and BCVA 20/16 with a returned refraction of +0.25–0.75 × 120°. IOP was normal without anti-glaucoma treatment. Slit-lamp examination showed a perfect postoperative situation. At all follow-up visits the right eye showed a normal IOP. This is a rare case of a sudden astigmatic change of almost 3 D cyl as the only presenting manifestation of a corticosteroid-induced hypertension after 1 month of steroid treatment. The condition is definitely related to a large sutured corneal incision relaxed by high IOP. Nowadays a foldable phakic lens design with a sutureless sclerocorneal or clear corneal incision can solve this problem. An extremely large refractive shift (−8.0 D) has been described with malignant glaucoma (Sii & Shah 2006) but no cases similar to ours exist. This case demonstrates the difference between weak (fluorometholone right eye) and strong (dexamethasone left eye) steroids on IOP. In conclusion, the case presented illustrates that a sudden change in refraction as late as 1 month after the implantation of a phakic IOL could be the first manifestation of a late-onset, steroid-induced glaucoma.