American Journal of Ophthalmology
Volume 134, Issue 5 , Pages 645-660, November 2002

Pathologic myopia: where are we now?1

  • Yasuo Tano, MD

      Affiliations

    • Corresponding Author InformationInquiries to Yasuo Tano, MD, Department of Ophthalmology, Osaka University Medical School, Rm E-7, 2-2 Yamadaoka, Suita, Osaka 565-0871 Japan; fax: (+81)-6-6879-3459
    • Department of Ophthalmology, Osaka University, Medical School, Osaka, Japan

Accepted 29 August 2002.

Article Outline

Abstract 

PURPOSE: To describe current concepts and available treatments for pathologic myopia.

DESIGN: Review of experimental and clinical studies.

METHODS: The demography, natural history, medical and surgical treatments for choroidal neovascular membrane, vitreoretinal interface disorders and future strategies for pathologic myopia are reviewed.

RESULTS: Several medical and surgical modalities are currently available to treat various complications of pathologic myopia. Macular translocation appears to stabilize or improve visual function in many eyes with choroidal neovascularization.

CONCLUSION: Newer strategies are emerging to better ameliorate or prevent the complications of pathologic myopia.

 

Pathologic myopia is a major cause of legal blindness in many developed countries.1, 2, 3 The prevalence of pathologic myopia with a refractive error greater than −7.9 diopters was reportedly 0.2% to 0.4% in the general population of the United States.3 Pathologic myopia is especially common in Asia and the Middle East.4 In Japan, pathologic, degenerative, or high myopia reportedly affects 6% to 18% of the myopic population and 1% of the general population.5

Duke-Elder defines pathologic myopia as degenerative myopia, that is, the type of myopia which is accompanied by degenerative changes occurring particularly in the posterior segment of the globe.6 Another definition states that high myopia accompanied by visual dysfunction is pathologic myopia.5 Since myopic eyes with a refractive error greater than −8 diopters are frequently associated with visual dysfunction, high myopia is defined as an eye with a refractive error greater than −8 diopters and this definition has been employed as a diagnostic criteria for pathologic myopia in Japan.5

High myopia is often associated with excessive and progressive elongation of the globe, resulting in a variety of fundus changes, with or without posterior staphyloma.6, 7, 8, 9, 10 These fundus changes are associated with varying degrees of visual deterioration in highly myopic eyes.

A fundamental approach for preventing visual deterioration in myopic eyes is to develop agents to slow down the excessive axial elongation. Animal models of myopia were developed to study the mechanisms of progressive elongation in growing eyes11 and have greatly expanded our knowledge concerning the plasticity of eye growth and the development of refractive error. Studies using these animal models indicate that the absence of a clear retinal image triggers a cascade of pathological events which ultimately result in axial elongation.12 Several neurotransmitters in the retina are reportedly involved in this process.13, 14, 15 For example, atropine, an antagonist of muscarinic acetylcholine receptors, was demonstrated to affect eye and scleral growth.14

There have been few nonsurgical treatments proposed to prevent myopia. Atropine eye drops have been shown in one randomized control study to retard the progression of myopia.16 However, the potential long-term adverse effects of such anticholinergic agents needs to be evaluated in growing eyes. In addition, from a more practical point of view, the effect of continuous cycloplegia on patient quality of life needs to be considered.

In contrast, the surgical treatment of refractive complications of myopia has undergone rapid development over the last decade. Yet, refractive surgical procedures such as laser in situ keratomileusis (LASIK) and photorefractive keratectomy (PRK) have been reported to be associated with a variety of retinal complications including macular hemorrhage,17, 18, 19, 20 retinal detachment,21, 22 and macular hole23 following these procedures. The scleral compression and transient ocular hypertension induced by the suction ring in LASIK, and/or the shockwave delivered to the eye by the excimer laser itself, may trigger some of these disease processes. However, since many of these retinal lesions are also commonly seen in the natural course of patients with myopia, especially pathologic myopia, a cause-effect relationship needs to be investigated with well-controlled trials.

Refractive surgery in eyes with a higher degree of myopia also appears to be associated with an increased incidence of iatrogenic keratectasia24 and corneal haze,25 with deterioration of optical quality induced by higher-order wavefront aberrations.26 At the least, patients with severe myopia considering such treatment should be well-informed of the higher postoperative risks of keratectasia, haze, suboptimal visual function, and retinal disease.

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Natural history of pathologic myopia 

Fundus changes observed in high myopia include tigroid fundus (choroidal vessels being visible through the retina, often with lacquer cracks in Bruch’s membrane), geographic atrophy of the retinal pigment epithelium (RPE) and choroid (diffuse or patchy), posterior staphyloma, and choroidal neovascularization (CNV) that is also referred to as Fuchs’ spot at its later stage.27, 28, 29, 30 The prevalence of these fundus changes in a Japanese study of eyes with myopia greater than −8 diopters is shown in Figure 1. 31

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  • FIGURE 1. 

    The prevalence of fundus changes in 1,584 consecutive eyes with high myopia.31 Definition of terminology used: tigroid fundus, choroidal vessels visible through the retina in the posterior pole; diffuse atrophy, diffuse chorioretinal atrophy in which the color of the posterior pole changes to yellowish-white; patchy atrophy, chorioretinal atrophy in which well-defined grayish-white lesions are observed in the posterior pole; Fuchs’ spot, small mature choroidal neovascularization in the posterior pole.

Diffuse fundus atrophy is relatively common in highly myopic eyes, even with relatively preserved visual acuity (Figure 2), 30 however, some eyes with diffuse atrophy and/or posterior staphyloma may suffer visual loss due to macular hole formation or retinoschisis.

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  • FIGURE 2. 

    Visual acuity (Log MAR) with different fundus changes in 1,584 consecutive eyes with high myopia.31 Visual acuity was worst in eyes with Fuchs’ spot, followed by those with patchy atrophy, diffuse atrophy, and tigroid fundus.

Among all the myopic fundus pathologies, macular CNV is the most common vision-threatening complication32, 33, 34 reported to occur in 5%–10% of patients with high myopia.4, 35 To clarify the long-term visual outcome of this complication, Yoshida and associates studied 25 consecutive patients (27 eyes) with myopic CNV who were observed without treatment for more than 10 years (Ohno-Matsui K, written communication, April 27, 2002). The characteristics of these patients are summarized in Table 1. Visual acuity at 10 years after CNV onset was examined and the overall follow-up period ranged from 120 to 159 months (mean, 132 months). As Figure 3 shows, most of the patients lost visual acuity over the course of the study. At initial examination, 22.2% of eyes had a visual acuity of greater than 20/40, while 29.6% of eyes had a visual acuity of less than 20/200. However, at final examination, only one eye retained a visual acuity of greater than 20/40 and 96.3% of eyes had a visual acuity of less than 20/200 during the follow-up of more than 10 years. Hemorrhage associated with CNV was absorbed over an average of 7.6 months from time of onset (range, 1–15 months) and rebleeding was not common (observed in only 22% of CNV eyes). At 5 and 10 years after onset, all CNVs were observed to have regressed completely, becoming flat and sometimes unrecognizable (Ohno-Matsui K, written communication, April 27, 2002). This suggests low activity and a self-limiting course for myopic CNVs, as also reported by Avila and associates.32 However, chorioretinal atrophy gradually developed around the regressed CNV in 20 of 27 eyes (74.1%) by 3 years after initial examination. At 5 years after onset and at final examination, chorioretinal atrophy had developed in 26 of the same 27 eyes (96.3%). Furthermore, the size of the area of chorioretinal atrophy was noted to gradually enlarge (Figure 4). This enlargement of chorioretinal atrophy caused further decentration of fixation, resulting in a decrease in central vision over time.

TABLE 1. Baseline Characteristics of 27 Eyes of 25 Patients With Myopic CNV∗
Gender
number of men (number of eyes)5 (5)
number of women (number of eyes)20 (22)
Age46.9 years (12.7 years)
Refractive error−15.4 D (4.2 D)
Axial length29.3 mm (2.3 mm)
Initial Snellen visual acuity, number of eyes (percentage)
> 20/406 (22.2%)
20/40 to 20/20013 (48.1%)
< 20/2008 (29.6%)
LogMAR visual acuity0.75 (0.48)
CNV size0.92 DD (0.6 DD)
CNV location, number of eyes (percentage)
subfoveal22 (81.5%)
juxtafoveal5 (18.5%)

CNV = choroidal neovascularization; D = diopters; DD = disc diameters.

∗ Mean given with standard deviation in parentheses, except where indicated.

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  • FIGURE 3. 

    Long-term visual outcome of choroidal neovascularization (CNV) in 27 eyes with high myopia. The majority of eyes experienced a drop in visual acuity to less than 20/200 within 10 years after the onset of myopic CNV.

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  • FIGURE 4. 

    Progression of chorioretinal atrophy in the right eye of a 39-year-old man with high myopia.(Top left) Fundus photograph just after onset of macular hemorrhage associated with choroidal neovascularization. (Top right) Fundus photograph of the same patient 3 years after onset. (Bottom left) Fundus photograph 5 years after onset. (Bottom right) Fundus photograph 10 years after onset.

The long-term visual outcome of these myopic CNV eyes was extremely poor. Visual acuity dropped to less than 20/200 within 10 years after CNV onset in almost all eyes. A progressive and steady visual decline over the long-term (greater than 5 years) secondary to chorioretinal atrophy enlargement may be characteristic of myopic CNV. Based on this evidence, it is clear that treatments need to be developed to help eyes with myopic CNV avoid progressive visual impairment.

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Treatments for CNV in pathologic myopiá 

The natural course of visual function in eyes with pathologic myopia is poor. In particular, eyes with CNV have an increased risk of losing reading vision. Medical treatments including thermal laser and photodynamic therapy and surgical interventions including removal of the choroidal neovascular membrane and macular translocation have been used in the attempt to treat myopic CNVs with varying success.

Limitations and complications of thermal laser treatment 

Prior to the 1990s, thermal laser photocoagulation was the only approach available for the management of CNV associated with pathologic myopia.27, 32, 36, 37, 38, 39 Although the efficacy and safety of thermal laser treatment for myopic CNV had not been examined in randomized controlled trials, laser treatment for juxtafoveal CNVs in myopia was well-accepted. Laser ablation of juxtafoveal lesions may be useful in preventing enlargement of the CNV into the fovea and in improving the initial visual disturbance. However, thermal laser treatment of subfoveal CNV lesions does not seem justified based upon the available evidence including recent studies on photodynamic therapy for this condition. Even in cases of juxtafoveal CNVs, many studies have subsequently shown that good visual acuity cannot be maintained over the long-term. In one study of 16 eyes that received argon green laser treatment for myopic CNV, all CNVs were shown to be completely closed, with visual acuities being maintained or improved in six eyes at one-year of follow-up.32 However, with longer observation, the visual acuities were found to have deteriorated in all eyes by the time of last follow-up (range, 21–52 months). A separate study using krypton laser photocoagulation in patients younger than 55 years of age with myopic CNV showed that there was no statistically significant difference in visual acuity between treated and untreated eyes after 5 years of follow-up.36 Another long-term study comparing natural history with laser treatment for myopic CNV found that laser treatment was associated with preservation of visual acuity only over the first 2 years of follow-up.39 The difference between treated and untreated eyes in terms of mean decrease in visual acuity lost significance by the 5 year follow-up point.

A high rate of CNV recurrence is another major problem associated with thermal laser treatment. Lacquer cracks arising after laser treatment are often observed and may be a risk factor for CNV recurrence.40 In one recent study, recurrences were observed in 72% of treated eyes overall, with 36% of treated eyes having a subfoveal recurrence associated with a mean visual acuity of 20/154.39 Recurrence rates varying from 31% to 72% have been reported, with recurrent CNVs arising most commonly from the edge of laser scars.27, 36, 37, 38, 39

Focal macular photocoagulation for CNV is associated with several vision-threatening complications such as inadvertent foveal ablation, subretinal hemorrhage, and retinal pigment epithelial tears. Furthermore, laser scar expansion (also referred to as “atrophic creep”) is a well-recognized and severe complication after laser treatment in eyes with pathologic myopia. Previous studies have shown that expansion of laser scars occurs in 92% to 100% of myopic eyes treated with various wavelengths.27, 32, 36, 37, 38, 39, 41, 42, 43 Both the laser scar and the surrounding area of atrophy may enlarge progressively with long-term observation.39 The increase in size of the atrophic area may cause loss of central vision when the fovea is affected. In a previous study, we investigated visual function and light sensitivity of the retina in areas of laser scar expansion using scanning laser microperimetry.43 We found that the fixation point after laser treatment shifted to the edge of the atrophic area (Figure 5) and that light sensitivity in the region of retinal atrophy had decreased markedly, causing a relative scotoma to occur even before the atrophy “crept” in to the fovea (Figure 5).

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  • FIGURE 5. 

    Laser scar expansion after photocoagulation of a juxtafoveal choroidal neovascularization (CNV). (Top left) Fundus photograph shows a juxtafoveal CNV (arrow) surrounded by a small subretinal hemorrhage. (Top right) Fundus photograph at 3 months after laser treatment reveals expansion of the laser scar (arrows) into the fovea with retinal pigment epithelial atrophy. The original laser scar is indicated by a black arrowhead. (Bottom left) Microperimetry using a scanning laser ophthalmoscope shows that fixation had shifted to the temporal margin of the expanded laser scar. Blue and red points indicate the location of preferred fixation at each examination session. (Bottom right) Reduced light sensitivity is noted not only over the original laser spot, but also in the area of laser scar expansion as demonstrated by the relative scotoma. The red letters “F” indicate locations where a 5 dB light intensity stimuli was not seen by the patient. The blue letters indicate stimuli detected by the patient. Reprinted with permission from Lippincott, Williams & Wilkins from Oshima Y, Harino S, Tano Y. Scanning laser opthalmoscope microperimetric assessment in patients with successful laser treatment for juxtafoveal choroidal neovascularization. Retina 1998;18:109–117.

Although the mechanism of laser scar expansion remains unclear, mechanical stretching of the chorioretinal complex is thought to occur easily in eyes with pathologic myopia. The chorioretinal complex is thinner and more atrophic in eyes with pathologic myopia than in eyes of healthy subjects or eyes affected by other ocular diseases such as age-related macular degeneration (AMD). In fact, the incidence of laser scar expansion in myopic eyes is much higher (92%–100%) than that observed in eyes with other diseases (63%–70%).38, 41, 42, 43 The untreated (RPE) and choroid surrounding the area of initial laser therapy in myopic eyes may be sensitive to the effects of the thermal energy indirectly delivered by photocoagulation, playing a possible role in subsequent laser scar expansion and retinal dysfunction. This spontaneous enlargement of atrophy associated with laser scars, a vision-threatening complication in laser treatment, should be considered when the decision is made to photocoagulate either subfoveal or especially juxtafoveal CNVs in eyes affected with pathologic myopia.

New and potential laser applications 

Due to the limitations and complications associated with thermal laser photocoagulation of myopic CNVs, alternative treatment modalities have been investigated, including photodynamic therapy (PDT) and transpupillary thermotherapy (TTT). Photodynamic therapy with Visudyne involves the administration of a photosensitive dye intravenously which accumulates preferentially in the CNV, followed by long-exposure, large spot size irradiation of the CNV using a 689 nm diode laser in order to activate the accumulated dye. Trans pupillary thermotherapy involves long-exposure, large spot size irradiation of the CNV using an 810 nm diode laser, associated with a higher thermal output than that used for PDT, but without administration of a photosensitive dye. Both PDT and TTT were initially developed for the treatment of subfoveal CNV in AMD and both are also under investigation for the possible treatment of CNV associated with pathologic myopia.

Photodynamic therapy 

The ongoing Verteporfin in Photodynamic Therapy (VIP) clinical trial is evaluating the use of the photosensitive dye verteporfin (Visudyne, Novartis Ophthalmics, Duluth, Georgia USA) in PDT for non-AMD diseases including pathologic myopia. In this VIP study, 120 patients with subfoveal CNV associated with pathologic myopia were randomly assigned to verteporfin therapy (81 eyes) or placebo (39 eyes). For entry, the greatest linear dimension of the lesion had to be no more than 5,400 microns, with a best-corrected visual acuity of approximately 20/100 or better. The 1-year results showed a statistically significant benefit of PDT for the treatment of myopic CNVs.44 The visual acuity of the verteporfin-treated group had a greater chance of remaining stable compared with the placebo-treated group. Seventy-two percent of verteporfin-treated patients lost fewer than eight letters (P < .01) compared with 44% of placebo-treated patients. Fluorescein leakage was absent from classic CNVs in 35% of the verteporfin-treated group compared with 28% of the placebo-treated group. The mean greatest linear dimension of CNV leakage decreased to 1,865 microns in the verteporfin-treated group compared with an increase to 3,085 microns in the placebo-treated group (P < .01). Despite these acceptable short-term results, however, recently published 2-year data showed no statistical significance in benefit on visual acuity in verteporfin-treated patients.45 Interestingly, the 2-year results of the Treatment of Age-Related Macular Degeneration with Photodynamic Therapy (TAP) study showed that AMD patients with predominantly classic CNV were more likely to have improved visual acuity with PDT using verteporfin46 and predominantly classic CNV was found in about 80% of pathologic myopia eyes enrolled in the VIP study. One may speculate that the difference in 2-year results between AMD and pathologic myopia might be due to the intrinsic nature of the chorioretinal complex having a greater tendency to atrophy in pathologic myopia. The potential damage for RPE by PDT was suggested from animal studies based on the RPE damage demonstrated by fluorescein angiography, histopathologic examination,47 and some RPE atrophy was seen after multiple administrations and repeated laser treatments in the TAP study.48 As with the phenomenon of laser scar expansion observed following focal laser photocoagulation, PDT-induced chorioretinal damage may occur more easily and may be even more pronounced in the more susceptible myopic eyes. Experimental and clinical studies with longer follow-up are clearly needed to evaluate this possibility.

Transpupillary thermotherapy, which showed the therapeutic potential for the management of occult CNVs associated with AMD in a pilot study,49 may represent another alternative for the management of myopic CNVs. However, most CNVs associated with pathologic myopia are of the classic type and are smaller in size and with less exudation compared to classic CNVs observed in AMD. It is possible that TTT in these eyes with little or no subretinal fluid may cause damage to the neurosensory retina. Moreover, since the amount of diode laser energy absorbed depends greatly upon the amount of melanin, the most effective light absorber in the chorioretinal layers, TTT protocols need to be developed that take into account appropriate laser settings for patients of differing racial background and therefore differing fundus pigmentation as well as for myopic patients with highly attenuated RPE and choroid. Ultimately, a randomized prospective trial evaluating TTT for the treatment of myopic CNVs in patients of varying racial backgrounds may be necessary.

Surgical treatments for myopic CNV 

Surgical treatments have been increasingly considered as a viable alternative for the treatment of subfoveal CNV in pathologic myopia, in part because of the inability to restore vision with nonsurgical methods such as PDT and TTT. Surgical options include CNV removal and macular translocation and these procedures have been performed for CNV due not only to AMD,50, 51, 52, 53, 54 but also due to pathologic myopia.55, 56, 57, 58, 59, 60

Surgical removal of CNV 

Several studies have examined the role of surgical removal of subfoveal CNV in pathologic myopia.55, 60, 61 Uemura and associates reported that visual acuity improved in 39%, was unchanged in 26%, and worsened in 35% of eyes following surgical removal of CNV in 23 patients.55 However, Ruiz-Moreno and associates analyzed the results of 22 eyes and concluded that the surgical removal of myopic CNV does not achieve any significant improvement in best-corrected visual acuity.61 Recurrence of CNV occurred at relatively high rates, ranging from 18%–57% in these studies.55, 60, 61 In addition to recurrence or enlargement of the CNV, progressive expansion of RPE atrophy following CNV removal may result in deterioration of vision with longer follow-up.

Macular translocation 

Macular translocation is an innovative procedure first reported by Machemer and Steinhorst.51 The rationale of macular translocation is to displace sensory retina originally lying over a subfoveal CNV onto healthier RPE. Macular translocation surgery has been performed in eyes with CNV due to pathologic myopia as well as due to AMD. Although several surgical techniques have been developed for macular translocation, we have concentrated on performing either limited macular translocation or macular translocation involving a 360-degree retinotomy.51, 52, 53

Limited macular translocation 

When compared to macular translocation utilizing a 360-degree retinotomy, limited macular translocation (LMT) has both the advantage of less tissue manipulation and the disadvantage of less foveal displacement. When compared to surgical removal of CNV, a recent study by Hamelin and associates reported that LMT achieved better results.60

The surgical procedure consisted of four major steps: three-port standard vitrectomy with complete posterior vitreous detachment; artificial retinal detachment; scleral shortening and partial fluid-air exchange. The posterior hyaloid was thoroughly separated and removed, extending to the posterior edge of the vitreous base. After peripheral vitreous shaving at the ors serrata with indentation, we created retinal detachment in the superotemporal 180 degrees of the globe by injecting balanced saline solution into the subretinal space using a 39 gauge rigid cannula connected to a pressure-controlled fluid injection system (VFC, Accurus, Alcon, Fort Worth, Texas, USA). After confirmation that the retinal detachment extended from the optic nerve head to the ora serrata, scleral shortening was performed either with scleral infolding or outfolding. We employed mattress sutures for infolding and titanium clips for outfolding. Partial fluid-air exchange was performed with air occupying approximately 40% of the vitreous cavity. After surgery, the patient’s head was positioned as follows: nasal side up for 15 to 30 minutes, superonasal side up (laying on temporal side with head up approximately 45–60 degrees) for 4 to 8 hours, upright overnight, superotemporal side up (laying on nasal side with head up approximately 45–60 degrees) for half a day, and temporal side up for 2 days until the air bubble disappeared.

We performed LMT in 17 eyes of 16 patients (six men and ten women) with subfoveal CNV in association with high myopia. Patient age ranged from 38 to 82 years (mean, 56 years). The mean preoperative visual acuity was 20/140 (range, 20/1000 to 20/50). The LMT surgical procedure performed was similar to that described in previous reports.53, 54, 57, 62, 63, 64 Either scleral infolding or scleral outfolding was used to shorten the sclera. Follow-up ranged from 6 to 68 months (mean, 26 months).

The fovea was displaced inferiorly in all 17 eyes and was completely separated spatially from the CNV in 12 of 17 eyes (71%). The mean distance of foveal displacement was 1,245 microns, ranging from 484 to 2,190 microns. Visual acuity initially improved by two lines or more in 14 eyes (82%), was unchanged in two eyes (12%), and decreased in one eye (6%). The mean visual acuity at postoperative best was 20/48 (range, 20/200–20/20). Visual acuity initially improved four or more lines in ten of the 17 eyes (59%) and was 20/30 or better in nine eyes (53%). However, the final visual outcome was not as satisfactory, with a mean final visual acuity of 20/124. At final analysis, the visual acuity improved by two lines or more in five eyes (29%), was unchanged in seven eyes (41%), and worsened in five eyes (29%). Final visual acuity decreased from best postoperative visual acuity in 12 eyes (71%). The reasons for this decrease included CNV enlargement in nine eyes (75%) and atrophy of the retina/RPE/choroid in three eyes (25%). Enlarged CNV was removed in seven patients. CNV enlargement appears to be the most important factor in the visual outcome of LMT for myopic CNV.

Macular translocation with 360-degree retinotomy 

We performed macular translocation with 360-degree retinotomy in 28 eyes of 28 patients (nine men, 19 women) with subfoveal myopic CNV between October 1996 and June 2001. Our surgical technique has been described previously.56, 59

Briefly, the crystal lens was removed with phacoemulsification aspiration technique through a sclero-corneal incision (20 cases) or through the pars plana (two cases) in 22 phakic patients followed by intraocular lens implantation. Intensive vitrectomy was performed following separation of posterior vitreous. A retinal detachment was created by injecting balanced salt solution into the subretinal space with a 39- or 41-gauge needle. Balanced salt solution was injected into the subretinal space with 20-gauge silicone-tipped needle in some cases to facilitate retinal detachment following creation of local retinal detachment. A circumferential 360-degree retinotomy was created near the ora serrata using the vitreous cutter and/or the vertical scissors. Choroidal neovascular membrane was removed in 11 of 28 eyes and was left untouched in 17 eyes. The retina was rotated superiorly following the injection of a small amount of perfluorooctane, which was injected onto the retina to stabilize the retina.

Perfluorooctane was filled after the appropriate rotation of the retina followed by photocoagulation to the edge of the retinotomy and the intentional retinal holes. Finally, the perfluorooctane was directly exchanged with silicone oil. Silicone oil was removed 2 to 3 months after the translocation surgery. Extraocular muscle surgery was performed to counter-rotate the eye globe, simultaneously with the translocation surgery (19 patients) or 2 months after the translocation surgery (eight patients), while no extraocular muscle surgery was needed in one patient, because of no complaint of diplopia.

Patient age ranged from 44 to 84 years (mean, 62 years). All patients were followed for at least 6 months postoperatively, with a mean follow-up period of 20.0 months. The mean CNV size was 1,850 microns, ranging from 780 microns to 3,260 microns. Preoperative visual acuity ranged from 20/700 to 20/40, with a mean of 20/115. The new fovea was displaced superiorly and was completely separated spatially from the choroidal lesion in all eyes postoperatively. The distance of foveal displacement ranged from 550 microns to 6,090 microns (mean, 2,970 microns).

At postoperative best, the visual acuity improved two lines or more in 21 eyes (75%), was unchanged in three eyes (11%), and decreased in four eyes (14%). After a mean follow-up of 20 months, most patients maintained this vision. The final visual acuity improved two lines or more in 18 eyes (64%), was unchanged in four eyes (14%), and decreased in six eyes (21%) (Figure 6). A final visual acuity of 20/20 or better was achieved in four eyes (14%), 20/30 or better in nine eyes (32%), 20/70 or better in 16 eyes (57%), and 20/200 or better in 21 eyes (75%).

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  • FIGURE 6. 

    (Left) Preoperative visual acuity and final visual acuity in 17 eyes of 17 patients after limited macular translocation performed at Osaka University Hospital (nine eyes) and Kyoto Prefectural University Hospital (eight eyes). (Right) Preoperative visual acuity and final visual acuity in 28 eyes of 28 patients after macular translocation with 360-degree retinotomy performed at Osaka University Hospital.

Long-term preservation of improved postoperative vision is of the utmost importance. Twelve eyes were followed for longer than 2 years with a mean follow-up of 27.6 months. The mean preoperative visual acuity for these 12 eyes was 20/125 and this improved to 20/80 at 6 months, 20/77 at 12 months, and 20/61 at 24 months postoperatively (Figure 7). Maintenance of improved vision, or even further improvement over 2 years of follow-up, is a major advantage of macular translocation with 360-degree retinotomy over limited macular translocation.

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  • FIGURE 7. 

    Mean visual acuity of 12 eyes of 12 patients followed for longer than 2 years (mean follow-up: 27.6 months) after macular translocation with 360-degree retinotomy performed at Osaka University Hospital.

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Case report 

A 64-year-old woman complained of visual loss in her right eye. At presentation, the best-corrected visual acuity was 20/200 in the right eye. Fundus examination and fluorescein angiography revealed a subfoveal choroidal neovascular membrane of 1,220 microns in size in the right eye (Figure 8). Macular translocation with 360-degree retinotomy combined with extraocular muscle surgery was performed. A comparison of preoperative and postoperative fundus photographs showed clockwise rotation of the retina by 23 degrees and counterclockwise rotation of the globe by 23 degrees. The fovea was displaced 2,260 microns superiorly. Visual acuity gradually improved to 20/20 by 12 months after surgery and this has been maintained for at least 2 years postoperatively.

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  • FIGURE 8. 

    Macular translocation with 360-degree retinotomy (Top left) Fundus photograph of a 64-year-old woman with a preoperative best-corrected visual acuity of 20/200. The size of the subfoveal choroidal neovascularization (CNV) was 1220 microns. (Top right) Fluorescein angiography clearly demonstrates the subfoveal CNV. (Bottom left) After translocation with 360-degree retinotomy combined with extraocular muscle surgery, the fovea was displaced superiorly by 23 degrees and the globe was counter-rotated by 23 degrees. The new fovea was located outside of the area of the CNV lesion. (Bottom right) Fluorescein angiography confirmed spatial separation between the CNV and the new fovea.

Progression of chorioretinal atrophy after macular translocation with 360-degree retinotomy 

Improvement in visual acuity and large foveal shift were obtained by macular translocation with 360-degree retinotomy in eyes with myopic CNV.58 However, it is well-known that enlargement of chorioretinal atrophy around a Fuchs’ spot65 or around the excision site after surgical CNV removal may result in deterioration of vision in the long-term. Therefore, if chorioretinal atrophy progresses after macular translocation surgery, the visual acuity may deteriorate over time. In order to assess this potential complication, we retrospectively evaluated the progression of chorioretinal atrophy after macular translocation with 360-degree retinotomy for myopic CNV in 13 eyes of 13 patients (two men, 11 women). The CNV was removed during macular translocation surgery in six eyes and was not removed and left untouched in seven eyes.

Two fundus images were taken during the postoperative period at varying times in each patient. The first fundus image was taken at a mean of 5.2 months postoperatively for eyes that underwent CNV removal in addition to macular translocation and at a mean of 4.4 months in eyes that underwent macular translocation alone. The second fundus image was taken at mean of 19.0 months and 17.6 months after surgery for each group, respectively. The differences in postoperative times at which the images were taken for the two groups were not statistically significant. The intervals between the time at which the two fundus images were taken were also not statistically significant (mean, 13.1 months for eyes that underwent CNV removal and 13.5 months for eyes that did not). The chorioretinal atrophy and the optic disk were outlined on each fundus image and areas were calculated using NIH image (http://rsb.info.nih.gov/nih-image/). The area of chorioretinal atrophy (A) was expressed in units of disk area (DA). The time course of myopic progression in two representative eyes is shown in Figure 9.

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  • FIGURE 9. 

    Progression of chorioretinal atrophy after macular translocation with 360-degree retinotomy. (Top left) Fundus photograph from a 54-year-old woman 11 months after macular translocation surgery with CNV removal. Choroidal atrophy measuring 2.58 disk areas was observed. (Top right) Fundus photograph of the same patient 26 months after surgery. The area of choroidal atrophy had enlarged to 3.62 disk areas. (Bottom left) Fundus photograph from a 55-year-old woman 16 months after macular translocation surgery without CNV removal. Choroidal atrophy measuring 0.89 disk area was observed. (Bottom right) Fundus photograph of the same patient 30 months after surgery. Only mild progression of choroidal atrophy (now measuring 1.04 disc area) was observed.

The rate of increase of chorioretinal atrophy (RIA) was calculated using the following formula: RIA = A (late) − A (early)/months between the two examinations. This rate is expressed in units of DA/month. The RIA in eyes that underwent CNV removal (0.043 ± 0.054 DA/month) was significantly greater than that for eyes that did not undergo CNV removal (0.00035 ± 0.0047 DA/month, P = .045, Figure 10). Although the number of eyes studied was small and the follow-up period was less than 3 years, there appeared to be a clear difference between the two groups, with progression of chorioretinal atrophy being greater when removal of the myopic CNV was performed during macular translocation surgery. One may speculate that the RPE and choroidal tissues surrounding the CNV are either damaged by CNV removal or are particularly vulnerable to other factors at the time of CNV removal, causing progressive atrophy which ultimately affects the overlying retina as well.

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  • FIGURE 10. 

    Rate of progression of chorioretinal atrophy after macular translocation with 360-degree retinotomy. The rate of progression of chorioretinal atrophy was significantly greater in eyes with CNV removal compared with those without CNV removal (P = .045).

Even if the chorioretinal atrophy enlarges over decades after macular translocation surgery, a larger distance between the new fovea and the edge of the RPE atrophy may prevent involvement of the CNV lesion into the new fovea. Therefore, among the currently available surgical treatments for myopic CNV, macular translocation with 360-degree retinotomy may offer the best results for preserving foveal function in the long run until more fundamental treatments to prevent chorioretinal atrophy and/or axial elongation are developed.

Complications of surgical treatment 

Three surgical procedures for the treatment of CNV associated with pathologic myopia have been described here including CNV removal, limited macular translocation, and macular translocation with 360-degree retinotomy. Submacular surgery involving removal of the CNV is technically the easiest procedure to perform and involves the least amount of tissue manipulation, while macular translocation with 360-degree retinotomy is probably the most challenging from a technical point of view and is also accompanied by the highest risk of postoperative complications. Although direct comparisons are difficult, it appears that surgical CNV removal achieves better visual results in eyes with myopic CNV than in eyes with AMD.50, 55 Moreover, the results for myopic CNV appear to be improved further by limited macular translocation60 and more so by macular translocation with 360-degree retinotomy. Indeed, one of our patients who underwent limited translocation in the left eye and macular translocation with 360-degree retinotomy in the right eye was found to have better visual improvement in the eye that underwent the macular translocation with 360-degree retinotomy.59

One possible reason for the difference in final visual outcome between the two surgical procedures may be the distance between the new fovea and the edge of the choroidal lesion which includes any RPE atrophy and the CNV itself. Displacement of the fovea following limited macular translocation is much less than that following macular translocation with 360-degree retinotomy. Enlargement or recurrence of the CNV, or expansion of chorioretinal atrophy, could involve the new foveal location more frequently in eyes that have undergone limited translocation. Indeed, when “best” postoperative results were examined, limited macular translocation appeared to achieve the same improvement observed in macular translocation with 360-degree retinotomy. A lower rate of involvement of the new fovea by the choroidal lesion may be the key factor in the better final visual outcomes seen in macular translocation with 360-degree retinotomy.

Several complications developed following translocation surgery. A postoperative retinal detachment including proliferative vitreoretinopathy developed in four of 17 eyes (24%) following the limited translocation and in eight of 28 eyes (29%) following translocation with 360-degree retinotomy. In addition, translocation with 360-degree retinotomy was associated with the development of macular hole in two eyes (8%) and hypotony in two eyes, the latter after several retinal reattachment surgeries for retinal detachment. Corneal astigmatism of 3 diopters or more was observed in five eyes (29%) after limited translocation and in one eye (4%) after translocation with 360-degree retinotomy.

Serious concerns regarding the frequency of postoperative complications, including proliferative vitreoretinopathy,66 will hopefully be overcome by future advances in surgical techniques.

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Retinoschisis and macular hole in highly myopic eyes 

There is a significant correlation between rhegmatogenous retinal detachment (RRD) and axial myopia. Factors associated with myopia and RRD include greater vitreous liquefaction, increased frequency of posterior vitreous separation, lattice degeneration, and asymptomatic retinal breaks.67 It is believed that the prevalence of RRD is related to the degree of myopia.68

In addition to peripheral retinal abnormalities, alteration of the vitreoretinal interface at the posterior pole is believed to play a role in the pathogenesis of RRD in highly myopic eyes. One of the manifestations of such vitreoretinal interface alteration is macular hole formation and associated retinal detachment. Initially, macular hole retinal detachment was treated with scleral buckling over the macula and retinopexy involving cryotherapy, diathermy, or laser photocoagulation. However, this procedure fell out of favor as it was associated with extensive postoperative scarring of the macular region and poor vision. Subsequently, the important role of the posterior vitreous cortex in causing traction and consequent macular hole formation in nonmyopic eyes was recognized.69 Pars plana vitrectomy with separation of posterior vitreous cortex from the inner retinal surface was then successfully performed to release vitreous traction at the hole edge.70 Gas tamponade without vitrectomy was also shown to be effective in some eyes without vitreous traction.71

Yet, the reattachment rate for simple vitrectomy combined with gas tamponade remains approximately 70% with one surgical procedure in highly myopic eyes.72 Many attempts have been made to improve this success rate, particularly for highly myopic eyes which have an even lower initial success rate.73 In order to preserve as much potential vision as possible, a method for retinal reattachment without surrounding retinopexy has been sought.74 To this end, various techniques have been developed to relieve traction due to epiretinal membrane (ERM) and/or residual vitreous cortex,75, 76 believed to be the root cause of recurrent macular hole formation and subsequent retinal detachment. One approach is to eliminate residual cortical vitreous using an abrading instrument, such as the diamond-dusted membrane scraper (DDMS),77 while another involves peeling the internal limiting membrane (ILM) after indocyanine green (ICG) staining.78, 79 Although the number of reported cases is still small, the reattachment rate improved with both of these techniques.77, 78, 79 Macular buckling without retinopexy is an alternative approach to decreasing vitreous traction or changing the vector force of vitreous traction at the macular hole edge and a higher success rate compared to vitrectomy and gas tamponade was reported (approximately 90%).72

Another serious disorder at the vitreomacular interface in highly myopic eyes is retinoschisis and foveal retinal detachment. This condition was first reported by Takano and Kishi in 1999.80 The pathogenesis of this condition was unclear at the time. However, since pars plana vitrectomy with vitreous cortex separation from the retina and ILM peeling with81 or without82 combined gas tamponade is effective in this disease, it may be deduced that vitreous traction is the cause of retinoschisis and foveal retinal detachment in high myopia (Figure 11). 81, 82 Although the exact relationship between retinoschisis and macular hole formation is not known, it has been suggested that retinoschisis develops prior to macular hole. This suggestion is based in part on the observation of patients in whom retinoschisis and macular hole coexist.83 However, retinoschisis is not always present in myopic eyes with foveal retinal detachment. Further study is needed to determine the relationship between retinoschisis and macular hole formation.

  • View full-size image.
  • FIGURE 11. 

    Preoperative fundus photograph (Top left) and ocular coherence tomography (OCT) results (Bottom left) of a patient with retinoschisis and foveal retinal detachment. The white arrow indicates the fovea. The corrected visual acuity was 16/200. Phacoemulsification and intraocular lens implantation, followed by pars plana vitrectomy, internal limiting membrane peeling, and gas tamponade were performed. Fundus photograph (Top right) and OCT examination (Bottom right) 6 months after surgery revealed resolution of the retinoschisis. The visual acuity improved to 20/60.

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New strategies for the treatment of pathologic myopia 

Although many advances have been made in the management of pathologic myopia, these advances will certainly be improved further utilizing ever-evolving new ideas and technology. For example, since scleral thinning and changes in collagen fibril bundle organization are characteristic of myopic eyes,84 prevention of these changes in the posterior sclera early in the course of disease may be useful. Indeed, scleral reinforcement, a procedure developed decades ago by Snyder and Thompson involving overlaying grafts of collagenous tissues to give support to the thinned sclera of the posterior globe,85 had been reported to be effective in preventing progressive visual loss in highly myopic patients with evidence of posterior pole myopic degeneration.86, 87 A reappraisal of this scleral reinforcement technique should be considered with the introduction of newer implant materials. Among synthetic polymer materials, polytetrafluoroethylene seems to be the most promising due to its tensile strength and biocompatibility.88

Recent experiments using animal models of myopia have elucidated biochemical changes in the sclera that occur with visual deprivation.89, 90 Scleral remodeling during the development of myopia was caused by dramatic changes in proteoglycan synthesis.91, 92, 93 These findings suggest that manipulation of scleral proteoglycan synthesis might inhibit the development of ocular elongation.94 Further studies are needed to establish the utility of pharmacological treatment to promote normalization of scleral remodeling.

Recently, various investigators have aggressively sought a pharmacological anti-angiogenic treatment for CNV. Angiogenic factors such as vascular endothelial growth factor (VEGF)95 have been major targets. Both a monoclonal anti-VEGF receptor and a soluble VEGF-receptor chimeric protein have been shown to inhibit retinal ischemia-induced retina and iris neovascularization in animals.96, 97 Furthermore, a recent study has demonstrated that intravitreal injections of an antigen-binding fragment of recombinant humanized monoclonal anti-VEGF antibody (rhuFab VEGF) prevents CNV formation in a laser-induced cynomolgus monkey model.98 Clinical trials of rhuFab VEGF intravitreal injections are currently being considered for the therapy of age-related macular degeneration.99 Corticosteroid therapy is another anti-angiogenic approach, which has been suggested for the treatment of CNV due to both ocular histoplasmosis and AMD.100, 101 While the mechanism of angiogenesis inhibition by corticosteroids remains unclear, it has been speculated to involve suppression of leukocytes that release angiogenic factors.102 Blockade of growth factor signaling could also be effective in inhibition of CNV development. Troglitazone, an agent that inhibits the mitogen-activated protein kinase signaling pathway, was shown to inhibit laser-induced CNV development in rats and primates.103 Similarly, CGP 41251, an inhibitor of several protein kinase C isoforms, inhibited laser-induced CNV in a murine model.104 By extrapolation, these pharmacological approaches are presumed to be effective in myopic CNV as well, however, further experimental and clinical evaluation is needed prior to their clinical use in myopia.

Finally, there is extensive scientific evidence to support a major role for genetics in the development of myopia. Yet there is no consensus to date with respect to the mode of inheritance of myopia. It is likely that the development of myopia is multifactorial and quite complicated. New techniques in genetic analysis may be able to identify susceptibility genes that predispose individuals to myopia. However, certain forms of high myopia may have a simpler pattern of inheritance compared to that for low grade myopia.105 In fact, Young and associates reported the discovery of a chromosomal locus that appears to show a simple autosomal dominant inheritance pattern of high myopia.106 This remarkable result may lead to the identification of genes linked to the development of high myopia and stimulate new research into possible therapies to arrest the progression of myopia.

Pathologic myopia has long been one of the major challenges for ophthalmologists worldwide. Some myopic complications, previously considered to be untreatable, can now be helped by new modalities such as photodynamic therapy, macular translocation, and subretinal surgery. Accumulation of knowledge and further sophistication of surgical and laser techniques are expected to improve current treatment results in the near future. Finally, newer strategies including various pharmacological approaches and gene therapy are emerging to better ameliorate or prevent the complications of pathologic myopia.

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  • 1 Internet Advance publication at ajo.com Sept 17, 2002.

PII: S0002-9394(02)01883-4

American Journal of Ophthalmology
Volume 134, Issue 5 , Pages 645-660, November 2002

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