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Case report

Axial myopic progression following phakic intraocular lens implantation

Apel, Warren MB BS*; Apel, Andrew FRANZCO; Stephensen, David FCCLSA; Versace, Patrick FRANZCO

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Journal of Cataract & Refractive Surgery: September 2013 - Volume 39 - Issue 9 - p 1435-1438
doi: 10.1016/j.jcrs.2013.06.012
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Abstract

The Implantable Collamer Lens phakic intraocular lens (pIOL) (Staar Surgical Co.) is a reversible surgical procedure used to treat ametropia.1 The artificial IOL is placed in the posterior chamber of the anterior segment with a haptic zone resting in the ciliary sulcus.2 More traditional refractive surgeries such as photorefractive keratectomy (PRK), laser in situ keratomileusis, and radial keratotomy are associated with optical aberrations, poor quality of vision, and poor predictability when used to correct high myopia.3 Studies show that the pIOL is an effective management for high myopia with advantages such as reversibility, immediate correction, stability, and relative simplicity.3 Several studies have shown that the pIOL is an effective and predictable treatment for moderate to high myopia.1,2 Complications of pIOLs include cataract formation, endothelial cell loss, pigmentary glaucoma, and pupillary block.1,2

While most refractive errors stabilize by approximately 15 years of age, myopic changes can occur later in a small proportion of adults.4 Adult myopic progression is an increase in myopia in existing myopes, and several studies describe myopic progression in patients in their fourth decade of life.4,5 Myopic progression is of increasing clinical interest and can affect long-term patient satisfaction following refractive procedures.5

Case report

A 45-year-old white woman presented to her ophthalmologist (A.A.) complaining of worsening vision after implantation of a pIOL approximately 10 years earlier. Prior to the pIOL surgery, the patient was highly myopic with a refractive error of −11.25 diopter sphere (DS) in the right eye and −10.00 DS in the left eye. The axial length (AL) measured by contact ultrasound biometry was 28.28 mm in the right eye and 27.90 mm in the left eye. At that time, the mean keratometry (K) was 43.40 D and 43.80 D, respectively. Meridional power values could not be obtained. Ocular history consisted of high myopia; there was no significant ocular family history. There was no other significant medical history.

The pIOL surgery in the right eye was performed in August 2000 using a Visian Implantable Contact Lens ICM125v4 −14.0 D. The surgery was performed in the left eye in October 2000 with the same pIOL and power. Surgery was uneventful and the postoperative course routine.

In late 2000, 3 months after the first surgery, the uncorrected distance visual acuity (UDVA) in the right eye was 6/18, corrected to 6/6 with −1.25 DS and 1.00 D cylinder (DC) of astigmatism. The vault between the posterior pIOL surface and the anterior surface of the crystalline lens was 400 μm. The UDVA in the left eye was 6/6 with only 0.5 DC of astigmatism. The vault was 800 μm.

In July 2001, the UDVA was 6/30 in the right eye and 6/7.5 in the left eye. The manifest refraction without cycloplegia was −2.50 DS and −0.50 DS, respectively.

In April 2010, the patient was seen by a refractive surgeon and the UDVA was recorded as 6/60 in the right eye and 6/24 in the left eye and the corrected distance visual acuity as 6/9 and 6/7.5, respectively. The AL was measured using partial coherence interferometry (PCI) (IOLMaster, Carl Zeiss Meditec AG) and was noted to have increased to 30.25 mm in the right eye and 29.22 mm in the left eye. Intraocular pressures (IOP) were within normal range at 13 mm Hg and 14 mm Hg, respectively. The pIOLs were observed to be in good positions, the crystalline lenses were clear, and the retinal examination was unremarkable except for myopic macular and optic disc changes. The K values were stable at 42.61 × 26/43.77 × 116 in the right eye and 42.37 × 166/44.06 × 76 in the left eye. The subjective refraction was −4.50 −1.25 × 120 and −2.50 DS, respectively.

Following a discussion with the patient regarding various refractive choices, the use of reading spectacles was agreed on and options such as monovision to compensate for emerging presbyopia were discussed. After careful consideration of options and the risks of further intraocular surgery, bilateral PRK was performed in May 2010. In July, the UDVA was 6/9 in the right eye and 6/6 in the left eye. Keratometry values following PRK were 39.20 × 10/39.50 × 100 and 40.47 × 147/41.26 × 57, respectively (Table 1).

Table 1
Table 1:
Axial length over a 10-year period.

Discussion

It is generally agreed that axial elongation is the main anatomical change in adult myopic progression.6 Studies by Jiang and Woessner,6 McBrien and Adams,7 and Grosvener and Scott8 report that myopia is axial in origin, demonstrating increased vitreous chamber depth and consequently increased AL. Grosvener and Scott8 suggest that corneal steepening occurs early or as a precursor to myopia but subsequent progression is due to axial elongation. Fledelius and Goldschmidt9 report that the mean AL increased significantly from 26.7 mm at age 26 years to 27.5 mm at age 54 in 29 highly myopic patients. Another study by Meng et al.10 reports that AL elongation exhibits a bimodal distribution in an adult myopic population with the first peak at 24.0 mm and the second peak at 30.0 mm, suggesting that different pathological mechanisms occur in varying severities of myopia. That study also reports that the AL reaches its fastest rate of change in the year prior to the onset of myopia and then progresses relatively slowly.

Saka et al.11 report that the AL can increase in patients older than 45. Posterior staphyloma growth with increasing age is considered a key factor in AL elongation in adults with high myopia, although it is unclear whether it is a cause or consequence of increasing AL. Saka et al. suggest that older individuals with posterior staphyloma are more susceptible to larger increases in the AL as they may be more susceptible to IOP changes, leading to stretching of the sclera and thus increased AL.

Although PCI (IOLMaster) has been calibrated against high-precision immersion US and thus correlates well with immersion techniques, previous studies have shown that it measures a greater AL than contact US.12–14 Explanations for the discrepancy include that PCI is noncontact and therefore does not cause indentation of the cornea, that it measures along the visual axis while US measures along the anatomical axis, and that it measures from the tear film to the retinal pigment epithelium while US measures from the cornea to the vitreoretinal interface.12,13 In a study by Bai et al.,12 the PCI AL measurements were on average 0.56 mm greater than contact US recordings in 121 subjects. However, this difference is insufficient to account for the increase in AL measurements of 1.97 mm and 1.31 mm in our patient’s right eye and left eye, respectively, which were initially measured by contact US and subsequently by PCI.

Several observations describing structural changes in myopic progression have been proposed, including equatorial stretching, global expansion of the vitreous chamber, and posterior pole elongation.15 A recent study by Atchison et al.15 using 2-dimensional (2-D) magnetic resonance imaging (MRI) shows that although myopic eyes expand in all directions, the growth occurs more in the axial plane than the vertical plane and more in the vertical plane than the horizontal plane. The authors propose that this phenomenon is due to either an anatomical constraint such as bony walls or regional variations in an eye’s susceptibility to grow in certain directions in response to a particular stimulating factor.15 The latter hypothesis suggests that defocus sensitivity or growth factor gradients vary vertically and horizontally.15 A study by Moriyama et al.16 using 3-D MRI divides myopic eyes into 4 abnormal shapes—barrel, cylinder, nasally distorted, and temporally distorted—and shows that these classifications are comparable between eyes in 78.3% of patients with bilateral high myopia.

Retinal defocus, in particular abnormal peripheral retinal input, may also cause myopic progression.17 It has been assumed that visual signals to the fovea controlled the emmetropization process, as the fovea possesses the highest visual acuity and greatest sensitivity to optical defocus.17 However, clinical work has shown that children with peripheral retinal abnormalities and relative peripheral hyperopia are more likely to develop myopic shift at the fovea.18 A study by Smith et al.19 uses lenses to produce form deprivation in the periphery of infant rhesus monkeys producing axial myopia. Another recent animal study by Smith et al.18 shows that the ablation of monkey foveas do not alter the course of emmetropization and conclude that visual signals to the peripheral retina in isolation determine axial growth. In a further study on rhesus monkeys, Huang et al.20 conclude that the alterations in patterns of peripheral refractions that accompanied central axial myopia are strongly correlated with changes in the shape of the posterior globe. In particular, relative peripheral hyperopia develops because the eye becomes more prolate as the central AL increases.20

In our patient, a stable foveal image was not sufficient to prevent or alter axial myopic progression. The right eye did not possess a stable foveal image following pIOL placement as it was left myopic at −1.25 DS postoperatively in comparison with the left eye, which was left plano postoperatively and thus possessed a stable foveal image. Despite the difference in foveal image stability, both eyes progressed myopically by approximately 2.0 DS over the following 10 years. This shows that the stable foveal image produced in 1 eye did not influence the natural progression of AL growth or myopia in that eye compared with the fellow eye.

In conclusion, surgeons should not reason that age and recent stability are sufficient criteria to assume that a patient with myopia is no longer progressing in their magnitude of axial myopia. Our patient’s refractive error was initially assessed as stable and then subsequently progressed myopically. As such, patients should be advised that there is a small but real risk that myopia will continue to advance following pIOL surgery.

It can be concluded from this case that implantation of a pIOL and induction of a stable, constant, and focused foveal image were not sufficient to prevent further axial myopia progression. When a myopic refraction is obtained on a patient following pIOL placement, it should not be assumed that there was an adverse outcome postoperatively. For the purpose of uncovering myopic progression after implantation, we recommend that surgeons record the AL in all pIOL cases prior to and after surgery.

The decision to proceed with further intraocular surgery in a high myope as opposed to extraocular surgery needs to be carefully considered. In our patient, the decision to perform bilateral PRK proved effective. This decision must be based on the patient’s visual needs, refractive history, and current refractive measurements.

References

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