CORRESPONDENCE

Progressive hyperopia secondary to RK or justnormal physiology?

Theodore P. Werblin, MD, PhD, Steve Phillips, MD,Daniel Krider, PhD

In the 1990s, when radial keratotomy (RK) was invogue, we as refractive surgeons were very active inthis technology. In recent years, RK has essentiallybeen replaced by laser in situ keratomileusis (LASIK)and related laser procedures. Clearly, the laser ap-proach to refractive corneal surgery has several advan-tages over RK with respect to accuracy, predictability,and stability.1,2 In addition, in recent years, a largenumber of RK patients have demonstrated a progres-sive flattening of the cornea, termed progressivehyperopia or hyperopic shift.3–5 We were fully expect-ing to see a similar form of instability in the cornea fol-lowing laser procedures, but to date this does notappear to be happening; however, other corneal insta-bilities have occurred.6,7 In light of these issues of cor-neal instability, one of us was particularly impressedby a recent patientwho hadRK in 1 eye almost 10 yearsago andhashadno surgery in the felloweye. Yet, a sim-ilar amount of hyperopic shift occurred in both eyes. Ifthis is truly a physiological event and not unique to thisparticular patient (and we do not see that it should be),might we not expect to see the same refractive instabil-ity over time after other corneal refractive modalitiesbut not related to corneal instability?

CASE REPORT

A 49-year-old white woman had uneventful 4-incisionRK in the left eye inApril 1997. The preoperative cyclo-plegic refraction was �2.75 C 0.75 � 162 in the righteye and �2.00 C 0.25 � 170 in the left eye, with kera-tometry readings of 45.37/46.50 @ 90 and 45.75/47.25@ 90, respectively. (Cycloplegiawas performed per theCasebeer system8 and consisted of 1 drop of phenyl-ephrine hydrochloride 2.5% and tropicamide 1%followed 5 minutes later by another drop of

Q 2007 ASCRS and ESCRS

Published by Elsevier Inc.

tropicamide 1%. Approximately 15 to 20 minutesafter the instillation of drops, cycloplegic refractionswere performed.) The best corrected visual acuitywas 20/20 in both eyes, and the uncorrected visualacuity (UCVA) was 20/400 in the right eye and20/200 in the left eye. The aim of surgery was tocreate monovision, with the left eye corrected fordistance and the right eye uncorrected for near.

In June 2000, the patient had an RK enhancementprocedure for residual astigmatism. At that time, thecycloplegic refraction was �2.50 C 1.00 � 159 in theright eye and �0.25 C 1.25 � 14 in the left eye. A 2-in-cision T-cut RK was performed to eliminate the astig-matism. At the conclusion of the procedure, the UCVAwas 20/20 in the left eye and J1 without correction inthe right eye, which was the intended result.

The patient returned in December 2006, complain-ing of progressively poor vision in the left eye. TheUCVA was 20/25 in the right eye and 20/200 in theleft eye. The cycloplegic refractions were �0.75 C0.75 � 172 and C1.75 sphere, respectively, and thekeratometry readings, 45.37/46.50 @ 92 and 43.12/45.25 @ 92, respectively. If one looks at the changein the spherical equivalent in the 2 eyes over time(Table 1), it is apparent that the right eye, which hadnot had surgery, had a progressive hyperopic shift of2.0 diopters (D) (estimated to be 1.3 D for the same6-year period of observation as the left eye) and theleft eye, which did have RK surgery, had a progressivehyperopic shift of about 1.4 D. Keratometry in the righteye remained stable throughout this entire period.

DISCUSSION

Because the right eye of the patient had not had RK,weconcluded that some change in thepower of the crystal-line lens had created the hyperopic shift we observed.Hyperopic shift as a function of age is a well-knownphenomenon.9 A mean shift of 0.035 D a year accountsfor only 0.32 D over 9 years in the patient’s right eyeand 0.21 D over 6 years in the left eye. Although

Table 1. Change in SE from 1997 to 2006.

Date Procedure Cycloplegic Refraction SE* K

04/24/1997 RK OS OD: �2.75 C0.75 OD: �2.375 OD: 45.37/46.50OS: �2.00 C0.25 OS: �1.875 OS: 45.75 /47.25

06/29/2000 Enhancement RK OS OD: �2.50 C1.00 OD: �2.00 d

OS: �0.25 C1.25 OS: C0.375 d

12/18/06 Follow-up visit OD: �0.75 C0.75 OD: �0.375 OD: 45.37/46.50OS: C1.75 OS: C1.75 OS: 43.12/45.25

K Z keratometry; RK Z radial keratotomy; SE Z spherical equivalentOD Z C2.00 (1997–2006); estimate C1.33 (2000–2006)OS Z C1.38 (2000–2006)*Change in SE

0886-3350/07/$dsee front matter 1343doi:10.1016/j.jcrs.2007.03.039

Intraocular pressure rise and recurrenceof capsular block syndrome afterneodymium:YAG laser anterior capsulotomy

Ahmet Colakoglu, MD, Necmettin Kucukakyuz, MD,Iffet E. Topcuoglu, MD, Solmaz Akar, MD, PhD

Capsular block syndrome (CBS) occurs when thecontinuous curvilinear capsulorhexis (CCC) marginis occluded by the intraocular lens (IOL) optic.1,2 Wereport a case of intraocular pressure (IOP) rise andrecurrence of capsular bag distension after neody-mium:YAG (Nd:YAG) laser anterior capsulotomyperformed for late postoperative CBS with opaquecontents.

CASE REPORT

An 85-year-old man, who had had cataract extractionwith phacoemulsification and IOL implantation in theright eye 6 years earlier, presented with a complaint ofblurred vision in the right eye, with a best corrected vi-sual acuity (BCVA) of 20/800. Slitlamp examinationshowed a circumferential adhesion between the mar-gin of the anterior capsule opening and the anteriorsurface of the peripheral IOL optic and mild posteriorcapsule opacification (PCO). There was a pool of ho-mogeneous milky-white fluid between the posteriorsurface of the IOL optic and the posterior capsule.White fragments of moderate size were also observedin the capsular bag, but the optical axis was free ofthese fragments. The posterior capsule was vaultedposteriorly. No cells or flare were observed in the an-terior chamber, and no abnormalities were observedin the cornea, vitreous body, or retina. The milky-white substance in the pocket was thought to be themain cause of the reduced vision, aside from themild PCO, and a posterior capsulotomy was sched-uled to eliminate the substance.

The aiming beam of the Nd:YAG laser could not befocused on the posterior capsule because of the intenseopacity of the contents in the hyperdistended capsularbag. Surgical drainage of the turbid fluid via the parsplana approach was proposed, but the patient de-clined. He accepted the anterior capsulotomy alterna-tive. Wide dilation of the pupil was achieved to exposethe anterior capsule at the 6 and 12 o’clock positions.Inferior and superior anterior capsulotomies were per-formed beyond the edge of the IOL using a Nd:YAG

1344 CORRESPONDENCE

somewhat extreme, the amount of hyperopic shift seenin our patient suggests that this represents an ‘‘outlier,’’as cited in previously performed studies.9 Given thesedata, one needs to wonder how much hyperopic shiftseen in post-RK eyes is actually caused by RK10 com-pared with that which occurs naturally with age.

This patient may be an extreme event in biology;however, we definitely have the impression that thereare hyperopic changes apparent in our patient popula-tions, as noted in previous studies,9 in the fifth andsixth decades of life. Since this is a general phenome-non, we should see these changes in the long-termfollow-up of non-RK corneal refractive procedures. Itis hypothesized that these changes are due to age-related progressive changes in ciliary muscle tone.11

Therefore, one unavoidable conclusion would be thatrefractive surgery that replaces the crystalline lenscould uniquely avoid this variable and unpredictablephenomenon. If loss of ciliary tonicity causes a netloss in the dioptic power of the crystalline lens due toa change in the lens shape, one would expect that sim-ply replacing the crystalline lens with a conventionalintraocular lens (IOL) would prevent this hyperopicshift. However, if the change in tonicity is associatedwith a positional change of the crystalline lens, thehyperopic shift would persist even with the lensexchange and an adjustable IOL would be requiredfor refractive stability.12

REFERENCES1. Kymionis GD, Tsiklis N, Pallikaris AI, et al. Long-term results of

superficial laser in situ keratomileusis after ultrathin flap crea-

tion. J Cataract Refract Surg 2006; 32:1276–1280

2. Rajan MS, O’Brart D, Jaycock P, Marshall J. Effects of ablation

diameter on long-term refractive stability and corneal transpar-

ency after photorefractive keratectomy. Ophthalmology 2006;

113:1798–1806

3. CharpentierDY, GarciaP,Grunewald F,etal.Refractive resultsof

radial keratotomy after 10years. JRefractSurg1998;14:646–648

4. Waring GO III, Lynn MJ, McDonnell PJ. Results of the Prospec-

tive Evaluation of Radial Keratotomy (PERK) Study 10 years af-

ter surgery; the PERK Study Group. Arch Ophthalmol 1994;

112:1298–1308

5. Deitz MR, Sanders DR, Raanan MG. Progressive hyperopia in

radial keratotomy; long-term follow-up of diamond-knife and

metal-blade series. Ophthalmology 1986; 93:1284–1289

6. Randleman JB, Caster AO, Banning CS, Stulting RD. Corneal

ectasia after photorefractive keratectomy. J Cataract Refract

Surg 2006; 32:1395–1398

7. Tabbara KF, Kotb AA. Risk factors for corneal ectasia after LA-

SIK. Ophthalmology 2006; 113:1618–1622

8. Werblin TP, Stafford GM. The Casebeer system for predictable

corneal refractive surgery; one year evaluation of 205 consecu-

tive eyes. Ophthalmology 1993; 100:1095–1102

9. Hirsch MJ. Changes in refractive state after the age of forty-five.

Am J Optom Arch Am Acad Optom 1958; 35:229–237

10. Werblin TP, Stafford GM. Hyperopic shift after refractive keratot-

omy using the Casebeer System. J Cataract Refract Surg 1996;

22:1030–1035

J CATARACT REFRACT SU

11. Walton WG Jr. Refractive changes in the eye over a period

of years. Am J Optom Arch Am Acad Optom 1950; 27:

267–286

12. Werblin TP. Why should refractive surgeons be looking beyond

the cornea? The Barraquer Lecture. J Refract Surg 1999;

15:357–376

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