Degenerative Myopia

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Degenerative Myopia Updated November 2007 Overview Myopia is a condition whereby images come into focus in front of the eye, resulting in a blurred image on the retina. The more severe the nearsightedness, the farther the image is from the retina, which results in more blurry vision in the distance. Myopia causes light rays to focus on the front of the retina. As a result, close objects are seen clearly, while distant objects appear blurred. Near vision, however, can deteriorate to a level where reading even close to the face can become difficult. There are three ways for an eye to become myopic: The front surface of the eye (the cornea) is too curved and, therefore, too powerful. The eyeball itself is too long. A combination of both of the above. In many cases, myopia will stabilize when the growth process has been completed, and glasses can offer normal vision. Higher levels of myopia, however, tend to be hereditary, meaning that if there is a moderately or highly nearsighted parent, the odds are higher for one of the children to be myopic. Myopia that develops in childhood is often called juvenile onset myopia, which almost always increases in severity with the progression into adulthood. In the more severe chronic cases ("degenerative" or "pathological" myopia), there is the possibility of sight loss. The deformation of the eye creates stress on the retina, which can become damaged or detached, and this can then provoke additional changes. This is especially true in degenerative

Transcript of Degenerative Myopia

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Degenerative Myopia

Updated November 2007

Overview

Myopia is a condition whereby images come into focus in front of the eye, resulting in a blurred image on the retina. The more severe the nearsightedness, the farther the image is from the retina, which results in more blurry vision in the distance.

Myopia causes light rays to focus on the front of the retina. As a result, close objects are seen clearly, while distant objects appear blurred. Near vision, however, can deteriorate to a level where reading even close to the face can become difficult.

There are three ways for an eye to become myopic:

The front surface of the eye (the cornea) is too curved and, therefore, too powerful. The eyeball itself is too long.

A combination of both of the above.

In many cases, myopia will stabilize when the growth process has been completed, and glasses can offer normal vision. Higher levels of myopia, however, tend to be hereditary, meaning that if there is a moderately or highly nearsighted parent, the odds are higher for one of the children to be myopic.

Myopia that develops in childhood is often called juvenile onset myopia, which almost always increases in severity with the progression into adulthood.

In the more severe chronic cases ("degenerative" or "pathological" myopia), there is the possibility of sight loss. The deformation of the eye creates stress on the retina, which can become damaged or detached, and this can then provoke additional changes. This is especially true in degenerative myopia, which can lead to macula problems (not to be confused with age-related macular degeneration).

There are at least four other clinical types of myopia: simple, nocturnal, pseudo, and induced. For the purposes of this article, degenerative myopia is described here.

Degenerative Myopia

Degenerative myopia is the seventh leading cause of legal blindness, occurring in about 2% of the U.S. population. It is most often seen in people of Chinese, Japanese, Middle Eastern and Jewish descent. This condition can start at birth, but most often starts during the pre-teen years. It is believed to be hereditary.

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Degenerative myopia is more severe than other forms of myopia and is associated with retina changes, potentially causing severe vision loss. It progresses rapidly, and visual outcome depends largely on the extent of fundus and lenticular changes. The diagnosis of degenerative myopia is accompanied by characteristic chorioretinal degenerations. Pathologic myopes, particularly those with higher refractive errors, are at risk for retinal detachment and macular changes.

Patients with degenerative myopia typically complain of decreased vision, headaches, and sensitivity to light. If retinal degeneration or detachment is present, patients may also report light flashes and floaters, which are associated with retina changes. Those with degenerative myopia have an increased incidence of cataract formation (nuclear cataracts are most typical).

Some of the most typical features of degenerative myopia are:

Vitreous liquefaction and posterior vitreous detachment Peripapillary atrophy appearing as temporal choroidal or scleral crescents or rings around

the optic disc

Lattice degeneration in the peripheral retina

Tilting or malinsertion of the optic disc, usually associated with myopic conus

Thinning of the retinal pigment epithelium with resulting atrophic appearance of the fundus

Ectasia of the sclera posteriorly (posterior staphyloma)

Breaks in Bruch's membrane and choriocapillaris, resulting in lines across the fundus called "lacquer cracks"

Fuch's spot in the macular area.

Myopic degeneration is similar to age-related macular degeneration AMD) in that it causes loss of central vision due to degeneration of the photoreceptor cells. This is caused by separation of the retina as a result of abnormal elongation of the eyeball. This usually happens because the back of the eye is larger than normal when the eye is very nearsighted. Marked thinning and stretching may lead to break down of the macula, surrounding retina and it's underlying tissue. This will cause a varying amount of blurred vision.

Even after the eyeball has fully grown (by adulthood), weakness in the sclera (the white outer shell) can lead to development of a posterior staphyloma. This is a distention of the sclera at the back of the globe where the optic disc and macula are located. Breaks in Bruch's membrane and atrophy of the choroid layer of the retina (where the blood vessels are) can create lesions known as lacquer cracks. Blood vessels may protrude through the cracks and leak into the subretinal space beneath the photoreceptor cells. Known as "choroidal neovascularization," this hemorrhaging can lead to scarring, retinal separation, and profound sight loss in the central field. If this occurs, immediate treatment is needed, which may be in the form of photodynamic therapy, antiangiogenic drug treatment or both.

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Treatment for Prevention of Degenerative Myopia

Two treatments are showing promise. One is scleral buckling, which can be read about in the article, "Degenerative Myopia: a Review of its Nature and its Treatment", on this site. The other is early systemic treatment with 7-methylxanthine, which has been shown to normalize the abnormal growth pattern of myopic eyes in children aged 8-13.

In the abstract, "Effect of 7-methylxanthine on eye growth in myopic children" (Ophthalmic and Physiological Optics, Vol. 26, Suppl. 1, August 2006), researchers Klaus Trier and Soren Munk Ribel-Madsen reported that "axial growth in the 7-methylxanthine group was reduced by 22% in the low axial growth stratification layer and by 8% in the high axial growth layer compared with placebo. The myopia progression in the two layers was reduced by 21% and 12%." This study was based upon the success of earlier research, in which 7-methylxanthine increased the content of collagen and proteoglycans (connective tissue components of the sclera) as well as the diameter of collagen fibrils in rabbits. Excessive eye elongation is related to abnormal organization and reduced content of these components.

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Principal source: www.revoptom.com

Chapter 126 – Degenerative Myopia

Chapter 126 – Degenerative Myopia

 

BRAD J. BAKER

RONALD PRUETT

 

 

 

 

 

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DEFINITION

• A poorly understood form of excessive axial myopia that can be associated with potentially blinding complications.

 

KEY FEATURES

• Progressive global expansion with posterior staphyloma formation and secondary macular degeneration.

 

ASSOCIATED FEATURES

• Premature cataract formation.

• Vitreous syneresis, rhegmatogenous retinal detachment, and glaucoma.

 

 

 

INTRODUCTION

Myopia is a common optical aberration. Physiological myopia, by far the most prevalent, is less than -6D in magnitude and is considered a normal biological variation. Eyes that have errors greater than -6D are said to have high myopia. The greater the myopia, the more likely are complications that can threaten vision. A subgroup of high myopes have axial lengths that fail to stabilize during young adulthood. The pathophysiology of this progressive, degenerative form of myopia is unknown.

EPIDEMIOLOGY AND PATHOGENESIS

Not all eyes that have myopia greater than -6D progress; nor does every eye that has progressive myopia develop degenerative complications. The worldwide distribution of those who have truly degenerative myopia is unknown, but the prevalence of progressive “pathological” myopia was surveyed by Fuchs[1] more than 40 years ago. Among 15 countries in the study, progressive myopia was found in 0.3% (Egypt) to 9.6% (Spain) of their populations. Asians are known to have a high prevalence of myopia. That of progressive myopia in Japan was 8.4%. This wide variation implies that there is a genetic influence.

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In the multiethnic United States, the prevalence was estimated at 2.1% in a U.S. Public Health Service study.[2] Women are affected twice as commonly as men, and black Africans infrequently have progressive myopia. It is the seventh leading cause of blindness in the United States, and its effects generally occur at an earlier average age than those of diabetic retinopathy and age-related macular degeneration.

The pathogenesis of myopia in general, and progressive myopia in particular, is unclear, but both heredity and environment play a role.[3] The mode of inheritance may be autosomal recessive or dominant, but it also can appear sporadically. Progressive myopia occurs commonly in association with

 

 

Ocular Manifestations of Degenerative Myopia

 

 

ANATOMICAL MANIFESTATIONS

Corneal astigmatism

 

Deep anterior chamber

 

Angle iris processes

 

Zonular dehiscences

 

Vitreous syneresis

 

Lattice retinal degeneration

 

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Scleral expansion and thinning

 

Decreased ocular rigidity

 

Increased axial length

 

Posterior staphyloma

 

Tilted disc

 

Temporal crescent or halo atrophy

 

Macular lacquer cracks

 

Pigment epithelial thinning

 

Choroidal attenuation

 

FUNCTIONAL MANIFESTATIONS

Image minification

 

Anisometropic amblyopia

 

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Subnormal visual acuity

 

Visual field defects

 

Impaired dark adaptation

 

Abnormal color discrimination

 

Suboptimal binocularity

 

 

 

 

 

 

Marfan’s, Ehlers–Danlos, and Stickler’s syndromes, and twin studies confirm its genetic basis.

The most widely accepted environmental influences are excessive near work and increasing formal education. Sustained accommodation and intraocular pressure (IOP), both basal and phasic, are suspected to influence axial elongation in eyes that have decreased scleral resistance,[4] [5] but recent evidence questions both of these hypotheses. Topical atropine slows the progression of myopia in children,[6] but this may be via a mechanism independent of accommodation. Further, it appears that at least some degree of active scleral growth and remodeling appears to be involved in pathological myopia. This may be regulated by various local growth factors, independent of central nervous system control. Experimentally, ocular growth can be governed by the application of plus or minus spectacles,[7] and children who have threshold retinopathy of prematurity develop less myopia following peripheral retinal ablation.[8] Understanding of these and other influences upon development of myopia is still too fragmentary to permit therapeutic application.

OCULAR MANIFESTATIONS

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The more important anatomical and functional abnormalities found in extremely myopic individuals are listed in Box 126-1 .[9]

Patients who have excessive myopia often have strabismus, especially exophoria and exotropia, and are more likely to develop premature nuclear sclerosis or, in some cases, posterior subcapsular lens opacities. Glaucoma is more common among highly myopic eyes and is particularly insidious. Its prevalence is related to the degree of myopia. Curtin[10] found glaucoma in 3% of eyes that had axial lengths less than 26.5?mm, in 11% that had

 

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Figure 126-1 A 28-year-old Caucasian woman experienced a central light flash followed by blurred vision in her -23.50D right eye. A, A subretinal hemorrhage is present in the fovea. B, A small wishbone-shaped lacquer crack was observed 13 months later. C, At 27 months from the original bleed, another such crack was noted along a temporal extension of the growing lacquer crack pattern. This was asymptomatic and the corrected acuity was 20/60 (6/18).

axial lengths in the range 26.5–33.5?mm, and in 28% of eyes that had axial lengths over 33.5?mm. Determination of glaucomatous changes are especially difficult in highly tilted optic discs, with posterior staphyloma adjacent to the myopic disc complicating the evaluation of visual field defects. Also, pigmentary and normal-tension glaucoma occurs more frequently in myopes.

Among the other serious complications of progressive myopia are vitreous syneresis and rhegmatogenous retinal detachment that results from peripheral tears. Such detachments usually are spontaneous, but they may occur after blunt ocular trauma or subsequent to cataract surgery, especially when complicated by capsular rupture and vitreous loss.

The abnormality seen in the myope that justifies use of the term degenerative is posterior staphyloma (ectasia), with its devastating secondary effects in the posterior pole. The progressively myopic eye expands in all its posterior dimensions, and the formation of an equatorial staphyloma with scleral dehiscence is not uncommon, especially in the superotemporal quadrant. Visual loss is most often due to macular involvement of a posterior

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pole staphyloma. [11] The deformity occurs in various locations, described by Curtin[12] as posterior polar (disc and macula central), macula centered with the disc at the margin, peripapillary, inverse (in which the depression extends nasally from the optic nerve head), and an inferior type that involves the lower portion of the disc and the fundus below it. Complex patterns are termed compound staphylomata. Usually, the edge of the defect is sharper closer to the disc and more blended away from it. Staphylomata that are clear edged and deep in a young person may occasionally lose some definition as the scleral envelope enlarges with age.[11]

As the scleral shell expands, the neural retina, pigment epithelium, and choroid stretch and thin to accommodate the area they cover. Tissue attenuation causes the fundus to have a pale, tessellated appearance. The pigment epithelial cells are flattened, and a reduction occurs in the thickness of the choriocapillaris and in the larger vessel layers and pigment of the choroid. This is evident especially within the staphyloma itself, where the fundus pallor is exaggerated by the increased visibility of the underlying sclera.

With time and progression, traction and tension phenomena are observed. The first is a pale, temporal crescent at the disc as the pigment epithelium and choriocapillaris are retracted from the disc’s margin toward the deepest area of the staphyloma. Bruch’s membrane is noncellular and elastic but has a limited capacity to stretch. If its elastic limit is exceeded, the internal tension is relieved by formation of microdehiscences called lacquer cracks. Acute lacquer crack formation near the fovea occasionally is signaled by photopsias and metamorphopsia ( Fig. 126-1 ). Defects in the overlying pigment epithelium may appear punctate, but eventually a linear pattern develops that coincides with the breaks in Bruch’s membrane. Continued break formation results in a reticular pattern that usually is most obvious in the deepest recess of the staphyloma and portends a guarded prognosis for central vision.

The lacquer crack defects usually slowly increase in width and grow in number. Other isolated, round, or irregular pigment epithelial and choriocapillaris defects may develop along the margin or within the staphyloma. If a choroidal neovascular membrane invades a crack, an abrupt macular hemorrhage may be produced. Although usually self-limited, the hyperpigmented fibrovascular scar that evolves (Förster–Fuchs’ spot) causes a central or paracentral scotoma. An area of choroidal and pigment epithelial atrophy develops and surrounds the scar ( Fig. 126-2 ). This extends and coalesces with areas of atrophy that advance from other lacquer cracks, eventually to produce large geographical areas of destruction in which sclera can be seen through the transparent neural retina. The process is usually bilateral and insidious. As paracentral fixation areas diminish, even low-vision aids become useless and ambulatory sight is all that remains.

Macular hole formation in extreme myopes may occur, but the exact mechanism is unknown. Whether attenuation of the neural retina and its supportive pigment epithelium and choroid are responsible is speculative. Vitreous syneresis and posterior vitreous detachment are more common and occur at an earlier age among high myopes than among others[13] ; usually they are not accompanied by vitreomacular traction or an epiretinal membrane and only rarely produce a posterior rhegmatogenous retinal detachment.

DIAGNOSIS AND ANCILLARY TESTING

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Myopes are recognized easily by their poor distance visual acuity that is improved by negative-power lenses. Degenerative myopia is a diagnosis made when clinical findings and extreme axial length occur together, as cause and effect.

The need for ancillary diagnostic testing is dictated by the preliminary findings. If a posterior staphyloma is detected or questioned, A and B scan ultrasonography can confirm its presence. Fluorescein angiography and, in some cases, indocyanine green angiography may demonstrate more extensive lacquer crack formation than is detected by ophthalmoscopy and can be used to rule out choroidal neovascularization.

DIFFERENTIAL DIAGNOSIS

The clinician who has taken a careful history and performed a meticulous examination will have no difficulty in diagnosing

 

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Figure 126-2 Sudden loss of vision. This male Caucasian myope (right eye, -8.00D; left eye, -9.00D) suddenly lost vision to 20/400 (6/120) in the right eye at 35 years of age. A, A choroidal neovascular membrane invades the fovea. B, Fluorescein angiography demonstrates the central membrane that had not been treated. C, The patient underwent a scleral reinforcement procedure on both eyes. Fifteen years later the area of central choriocapillary atrophy has enlarged, but corrected visual acuity is a surprising 20/80 (6/24).

progressive myopia. Its signature deformity is posterior staphyloma. Although patients who have retinitis pigmentosa are frequently myopic, show secondary cataract and vitreous liquefaction, can develop macular degeneration, and have peripheral visual field defects, these are easily distinguished by other findings in most cases. Peripapillary atrophic changes, punched-out defects in the pigment epithelium, and macular neovascular lesions are seen in ocular histoplasmosis syndrome. Myopes are unprotected from acquiring this infection, but its characteristics are not easily confused with those of degenerative myopia.

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SYSTEMIC ASSOCIATIONS

Myopia of different degrees and incidence may be associated with a wide variety of disorders. Many of these are hereditary and all forms of inheritance are represented.[14] [15] A selected listing is presented in Box 126-2 . Environmental factors also determine expression, but because the complex development of the eye can be misdirected by a number of code sequence errors leads to an unavoidable conclusion—no single “myopia gene” exists.

Some systemic disorders are diagnosed easily, conditions such as albinism and trisomy 21; others are more subtle. Because the cardiovascular complications of Marfan’s syndrome and congenital rubella and the orthopedic disabilities associated with Ehlers–Danlos and Stickler’s syndromes may produce morbidity and even mortality, prompt referral to medical and surgical colleagues is indicated if the patient has not been referred already.

PATHOLOGY

Typically, the extremely myopic eye is enlarged in all its posterior dimensions, but particularly in its axial length. Anteriorly, the cornea may be slightly thinner and flatter than normal, with a deeper anterior chamber, and the angle recess shows iris processes attached to the trabeculum. The lens has a tendency to show early nuclear sclerosis. Defects in the zonular membrane are common and may present a challenge during cataract surgery. The ciliary body may be smaller than normal, although considerable variability exists.

Generalized scleral thinning is associated with increased scleral elasticity, or decreased ocular rigidity. Especially when combined with zonular dehiscence, this results in rapid vitreous fluid egress and global collapse when the eye is opened to atmospheric pressure. Sudden hypotony can result in a serous or hemorrhagic choroidal detachment during intraocular surgery. Anatomically, the sclera is not only thin but also has an abnormal constitution. The classic electron microscopic findings of Garzino[16] have been corroborated by others. The collagen fibers are of much smaller average diameter than in a normal eye.

 

 

Systemic Associations of Degenerative Myopia

Albinism

 

Congenital rubella

 

de Lange’s syndrome

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Down’s syndrome

 

Ehlers–Danlos syndrome

 

Fetal alcohol syndrome

 

Gyrate atrophy—hyperornithinemia

 

Laurence–Moon–Bardet–Biedl syndrome

 

Marfan’s syndrome

 

Pierre Robin’s syndrome

 

Stickler’s syndrome

 

 

 

 

Further, the fibrils show greater interfibrillar separation and the normally tightly opposed and interwoven architecture of the collagen bundles[17] gives way to a more uniformly lamellar and eventually amorphous appearance.[18] Choroidal neovascularization may be evident through Bruch’s membrane dehiscences. [19]

TREATMENT

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The ultimate goal is to prevent myopia progression and posterior staphyloma with its associated visual loss, but currently no proven method exists by which to accomplish this.

In children, topical atropine can effectively slow enlargement of the myopic eye and the effect is sustained even after the drug has been withdrawn. [6] However, the possibility of long-term light damage to eyes that have dilated pupils has been investigated insufficiently. If this method is chosen, a thorough informed consent is required, and sun shielding and filters are advised. The effectiveness of atropine in eyes genomically destined to become pathologically myopic is unknown. Other approaches presumed to act via modification of accommodation include the use of bifocals, undercorrection of myopia, and part-time spectacle wear. Clinical trials report contradictory results,[20] but the regulation of young primate eye growth has proved possible by using plus and minus lenses to blur the retinal image.[7]

Because highly myopic eyes have reduced scleral resistance plus a tendency to develop glaucoma, many investigators have postulated that scleral expansion is caused by raised IOP.[4] Pärssinen[21] found a significant correlation between raised IOP and myopic progression among boys, but not among girls, while Quinn et al.[5] noted that ocular tension is higher in children who have myopia than in nonmyopes. Controlled trials of IOP reduction have been reported. [22] [23] [24] Timolol maleate was employed,

 

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all the subjects were children, and the focus was not on progressive degenerative myopia. Goldschmidt’s pilot study of 10 children showed a tendency for the children who had a reduction in IOP to slow in their progression of myopia,[23] but Jensen’s 2-year study of 94 children did not prove timolol to be effective. [24] The possibility remains that optical and pharmacological methods, alone or in concert, may be devised to retard axial elongation.

If advancing myopia in children continues beyond pubertal years, follow-up at least yearly is indicated. A stereoscopic, indirect ophthalmoscopic, and biomicroscopic search for staphyloma formation is important and, if suspected, staphyloma formation is investigated further using A and B scan ultrasonography. Some of these eyes eventually stabilize as highly myopic but with no posterior complications. The ongoing evaluation of any peripheral lattice degeneration lesions that may be evident, especially in the event of blunt trauma or an acute posterior vitreous separation, is critical.

If staphyloma formation is detected, further caution is warranted. Biannual examinations may reveal lacquer crack development that is not heralded by a photopsia or blurred central vision. Once lacquer crack formation or areas of choriocapillary and pigment epithelial atrophy are present in a young adult, it becomes likely that the central vision will be threatened in time by advancing atrophy, choroidal neovascularization, or both. The traditional option in the United States at this stage has been to continue observation, while ophthalmologists in some eastern European countries advocate the use of various tissue extract injections, vasodilators, and scleral reinforcement. Although the value of reinforcement surgery is unproved,[25] [26] it may have

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application in selected and obviously endangered eyes in which the disease continues to advance.[27]

One step short of surgery, or in addition to it, is to lower IOP. No controlled trial has been used to confirm efficacy or assured safety. Until such information is available, and in the absence of other contraindications, the use of a tension-reducing agent in “normal” eyes seems not unreasonable and has been recommended.[27] Relative ocular hypotension in eyes prone to develop tears in Bruch’s membrane may help to prolong central vision.

Other conservative measures include avoidance of eye rubbing, trauma, Valsalva exertion, and regular use of anticoagulants such as aspirin (unless required for systemic disease). Because topical corticosteroids frequently provoke a rise in IOP in the highly myopic eye, these also should be used with caution and with frequent tension checks.

Myopia-related choroidal neovascularization is a major cause of visual loss, especially when located in a subfoveal location. Photodynamic therapy has shown a statistically significant reduction in visual loss when compared with a placebo group after 1 year for subfoveal choroidal neovascularization associated with pathological myopia.[28] The lesion could be classic or occult on fluorescein angiography if either was at least 50% of the total area. The median visual acuity following treatment was 20/64+2 in the treatment group and 20/80–2 in the control group, with 77% of treated patients losing fewer than 8 letters compared with 44% of the placebo group at 12 months. The average patient received 3.4 treatments during the study. Extrafoveal choroidal neovascularization may also be treated with argon laser photocoagulation. Confluent argon laser burns of diameter 100–200?µm delivered over 0.2–0.4 seconds are most effective. Whether laser treated or allowed to involute spontaneously, the cicatricial lesion eventually becomes surrounded by a zone of atrophy that slowly enlarges with time. This atrophy typically is relentless and may progress to compromise the central vision.

Macular hole formation and the less frequently encountered detachment of the posterior retina are problems that confront those who care for patients who have degenerative myopia. Even for those patients who are attended by surgeons trained and practiced in modern vitreoretinal surgical skills, these complications result in a poorer prognosis and increased risk. Modern vitreoretinal surgical techniques can restore vision in select cases.

COURSE AND OUTCOME

Because the degenerative form of progressive myopia is among the leading causes of legal blindness is testimony that today’s treatment methods do not offer a cure. Affected individuals cannot share in the optimism of the more numerous patients with low myopia that the development of keratorefractive techniques will help them, because the fundamental nature of their disease, axial elongation and posterior staphyloma, is not altered by such techniques. Hopefully, laboratory and clinical evidence will provide practical methods by which to reduce the risk of progressive myopia. Meanwhile, the management of degenerative myopia is that of its complications and the prognosis for patients is guarded.

 

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REFERENCES

 

1. Fuchs A. Frequency of myopia gravis. Am J Ophthalmol. 1960;49:1418–9.

 

2. Roberts J, Slaby D. Refraction status of youths 12–17 years. Pub No (HRA) 75–1630. Washington, DC: US Dept Health, Education and Welfare; 1974.

 

3. Mutti DO, Zadnik K, Adams AJ. Myopia, the nature versus nurture debate goes on. Invest Ophthalmol Vis Sci. 1996;37:952–7.

 

4. Pruett RC. Progressive myopia and intraocular pressure: what is the linkage? Acta Ophthalmol. 1988;185:117–27.

 

5. Quinn GE, Berlin JA, Young TL, et al. Association of intraocular pressure and myopia in children. Ophthalmology. 1995;102:180–5.

 

6. Kennedy RH. Progression of myopia. Trans Am Ophthalmol Soc. 1995;93:755–800.

 

7. Hung LF, Crawford MLJ, Smith EL. Spectacle lenses alter eye growth and the refractive status of young monkeys. Nat Med. 1995;1:761–5.

 

8. Algawi K, Goggin M, O’Keefe M. Refractive outcome following diode laser versus cryotherapy for eyes with retinopathy of prematurity. Br J Ophthalmol. 1994;78:612–4.

 

9. Curtin BJ. The myopias, basic science and clinical management. Philadelphia: Harper & Row; 1985:277–385.

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10. Curtin BJ. Myopia: a review of its etiology, pathogenesis and treatment. Surv Ophthalmol. 1970;15:1–17.

 

11. Steidl SM, Pruett RC. Macular complications associated with posterior staphyloma. Am J Ophthalmol. 1997;123:181–7.

 

12. Curtin BJ. The posterior staphyloma of pathologic myopia. Trans Am Ophthalmol Soc. 1977;75:67–86.

 

13. Morita H, Funata M, Tokoro T. A clinical study of the development of posterior vitreous detachment in high myopia. Retina. 1995;15:117–24.

 

14. Curtin BJ. The myopias, basic science and clinical management. Philadelphia: Harper & Row; 1985:72–97.

 

15. Fong DS, Pruett RC. Systemic associations with myopia. In: Albert DM, Jakobiec FA, eds. Principles and practices of ophthalmology. Philadelphia: WB Saunders; 1994:3142–51.

 

16. Garzino A. Modificazione del collagene scleralae nella miopia maligna. Ross Ital Ottal. 1956;25:241–74.

 

17. Komai Y, Ushiki T. The three-dimensional organization of collagen fibrils in the human cornea and sclera. Invest Ophthalmol Vis Sci. 1991;32:2244–58.

 

18. Curtin BJ, Teng CC. Scleral changes in pathological myopia. Trans Am Acad Ophthalmol Otolaryngol. 1957;62:777–90.

 

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19. Pruett RC, Weiter JJ, Goldstein RB. Myopic cracks, angioid streaks, and traumatic tears in Bruch’s membrane. Am J Ophthalmol. 1987;103:537–43.

 

20. Goss DA. Effect of spectacle correction on the progression of myopia in children, a literature review. J Am Optom Assoc. 1994;65:117–28.

 

21. Pärssinen O. Intraocular pressure in school myopia. Acta Ophthalmol. 1990;68:559–63.

 

22. Goldschmidt E, Jensen H, Marushak D, et al. Can timolol maleate reduce the progression of myopia? Acta Ophthalmol. 1985;63(Suppl):90.

 

23. Jensen H. Timolol maleate in the control of myopia. Acta Ophthalmol. 1988;185:128–9.

 

24. Jensen H. Myopia progression in young school children. A prospective study of myopia progression and the effect of a trial with bifocal lenses and ß blocker eye drops. Acta Ophthalmol. 1991;69:1–79.

 

25. Curtin BJ. The myopias, basic science and clinical management. Philadelphia: Harper & Row; 1985:415–21.

 

26. Thompson FB. Scleral reinforcement. In: Thompson FB, ed. Myopia surgery: anterior and posterior segments. New York: MacMillan; 1990:267–97.

 

27. Pruett RC. Posterior segment. In: Roy FH, ed. Master techniques in ophthalmic surgery. Philadelphia: Williams & Wilkins; 1995:994–1006.

 

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28. Photodynamic therapy of subfoveal choroidal neovascularization in pathologic myopia with verteporfin. 1-year results of a randomized clinical trial—VIP report No 1. Verteporfin in Photodynamic Therapy Study Group. Ophthalmology. 2001;108:841–52.

Degenerative Myopia: a Review of its Nature and Current Treatment

byBrian Ward, Ph.D., M.D.

December 2011

    Degenerative myopia deserves our recognition as one of the truly neglected areas of ophthalmology. It is reported to be the seventh ranking cause of legal blindness in the United Sates of America the fourth ranking cause in Hong Kong and the second in parts of China and Japan. Degenerative myopia is an important world-health issue with an unfortunate history of ineffectual treatments that have led most eye specialists to believe that it is something of a "lost cause." As a result, this condition, which is responsible for the loss of vision in so many people during the middle years of life and in old age, seems destined to run its natural course, save for attention to correction of the refractive error and the treatment of some of its other complications.

    To summarize the course of this condition: It presents for the majority of people, as an inherited genetic condition. This is why the incidence of this condition varies so much between the various ethnic groups. The genetic defects responsible may be transmitted between the generations in a variety of ways, and may produce very different degrees of myopia in different family members.

    An affected individual will show accelerated growth of the size of the eye during the normal growth-periods of childhood and adolescence, so that, by the late teens, or the early twenties, the eye is much longer than normal. The eye is said to have high axial myopia (nearsightedness). Distant objects are focused in front of its retina and are thus out of focus. If objects are brought close to the eye, a point is reached when they come into focus. This is known as the far point of the eye. The defocusing of the retinal image may be corrected by spectacle lenses, contact lenses or by refractive surgery. In all of these cases, the distant object appears to the eye to be situated at its far point and is therefore in focus on the retina.

    Unfortunately, this form of myopia frequently progresses in adult life, with small intermittent steps of elongation being observable at any age. The adult progression appears to be due to the stretching of the walls of the eye. Genetically weak elements of the scleral wall are prone to thinning and stretching. One of the major forces at work in this stretching process appears to be the normal intra-ocular pressure.

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    Much of the sight loss in high axial myopia is thought to be due to the damaging effects of the stretching and thinning of the inner parts of the eye. The sclera, the choroid, the retina and the interface between the retina and the vitreous gel are all affected by deformation. In the central retina, damage to the functioning of the macula results in fine central-vision loss. This process of macular scarring is termed myopic macular degeneration. Stresses in the retina and the adjacent parts of the vitreous gel are also partly responsible for a predisposition to peripheral retinal tears, which may go on to admit vitreous fluid into the sub-retinal space, producing retinal detachment.

    Highly myopic eyes are also liable to loss vision from cataract and glaucoma. They have an increased vulnerability to the damage effects of eye trauma, which must include the higher incidence of complications in some ophthalmic surgical procedures. Of all of these sight-threatening complications, myopic macular degeneration is the most common. It is because of these degenerative complications, that this disorder is called degenerative myopia

    Early attempts to protect the macula from the damaging effects of stretching, involved surgical procedures to reinforce the thinned weak sclera at the back of the eye. It had been observed that a bulge (a staphyloma) could often be observed behind the macula. This very severe localized scleral thinning results in especially severe stretching of the inner layers in the region of the macula and especially severe damage to its tissues. Various natural materials had been used for staphyloma support, but it was donor-sclera that was finally selected for by most surgeons. Today, the results of these various early operations are difficult to assess, in terms of their safety and their effectiveness.

    In the U.S.A. two prominent groups advocated scleral reinforcement for degenerative myopia. Dr Brian Curtin lead the effort in New York, while a California-based group of surgeons used rather different procedures. The "West Coast" approach evolved from pioneering work by Borley and Snyder at the Stanford medical campus in San Francisco. Curtin tried different approaches before finally concluding that these had been ineffective, and noting some significant complications in some of their cases. Meanwhile, on the West Coast, Snyder, Thompson and Miller continued to develop their surgical approaches to scleral reinforcement, with no reports of adverse safety issues. These surgeons had a firm conviction that they were stabilizing axial myopia progression through their efforts. It is unfortunate that their published reports are somewhat anecdotal and lack any controlled studies. Perhaps because of the widespread disappointment with Curtin's conclusions, and the lack of controlled studies on other techniques, the interest in surgical treatments was largely lost.

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    In retrospect, these initial attempts at myopia control by scleral grafting are seen to have been important pioneering innovations, which may have lead to some modest contributions to saving sight. They were, in retrospect, perhaps providing support which was rather "too little and too late."

    Personal experience with Thompson's technique had showed it to be safe, and a pilot study indicated an encouraging degree of axial myopia control when compared to its progression in the unsupported eyes. Thompson's basic approach of "scleral reinforcement" was found to become more effective when the concept was extended to one of the buckling of the posterior pole of the eye, by providing a firm structural connection between the thin weak sclera at the back of the eye and the thicker tissue at the front of the globe. A gently tensioned sling was positioned over the back of the eye, under general anesthesia, and its ends were firmly anchored to the thick sclera in the anterior part of the globe. With this approach, adult eyes showed more stability of their axial myopia and, unexpectedly, some patients reported small subjective improvements in their quality of vision. In retrospect, there are some theoretical reasons why some small vision improvement might have occurred in some patients.

    In collaboration with Prof. Elena P. Tarutta, of Moscow, a clinical study was designed to follow and to evaluate buckled and unbuckled eyes for a period of five years. Fellow eyes, with similar degrees of high myopia, were designated as the control eyes, and followed according to the same protocol. The majority of the 59 buckled adult eyes showed stabilization of their axial myopia. The five-year follow up data illustrated this fact and also confirmed that a limited visual acuity improvement had occurred after buckling in some eyes. The relative stability after surgery meant that it became appropriate to offer the treatment for the patient's second eye during the study period; especially where a clear increase in axial length was evident in the control eye. Parts of this study were presented at the International Myopia Conference in Singapore in August of 2006. It is the first study to show good safety of a procedure and a statistically significant efficacy in terms of axial myopia control.

    In the study, reported after its conclusion in 2009, it was found that one of the treated eyes had had a form of myopic macular schisis and local traction detachment. Post-operatively, this complication was found to have been corrected (incidentally). The basic buckling surgical procedure has now been modified for the optimal treatment of this new indication– myopic macular schisis. The effectiveness of buckling for treating existing macular schisis suggests that the buckles being applied for axial myopia control might well serve to prevent the development of macular schisis and detachments.

    Today the indication for buckling surgery, in cases of Degenerative Myopia, is the

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risk of further axial extension in an eye, which is at least 26mm in axial length, at almost any age. The measurement of 26mm is used, as it is the threshold axial length for the development of myopic macular degeneration. The refractive error present may be as little as -6.00 diopters, but it is generally much greater. The risk of Macular degeneration increased with both the passage of time (i.e. the age of the patient) and with the magnitude of the axial length of the eye. Buckling adult eyes can stabilize axial length and minimize future macular degeneration, but it cannot prevent the continuation of degenerative processes, which are already at work.

    The appropriateness of buckling surgery for high axial myopia should be considered on a case-by-case basis.

    Degenerative myopia may be preventable in the future. Today, however, the usual treatments are limited to optical correction, intra-ocular pressure control, and attention to complications that may occur. The use of scleral buckling can prevent axial extension and minimize the toll of myopic macular degeneration on future visual function. At-risk eyes deserve careful evaluation and follow-up, with early treatment where appropriate. New buckling materials are being evaluated for their use in the more severe cases in all age groups. These are eyes in which greater areas of support and stronger buckling forces may be helpful. As always, the safety of any treatment needs to be evaluated in terms of its risk-to-benefit ratio.

    It should also be remembered that the prevention of axial myopia increase is also of value in stabilizing the power of the required corrective lens. This is especially important where refractive surgical correction is being considered. This benefit of axial myopia stabilization applies equally to ensuring stability of the effectiveness of the intraocular lens implant, following cataract surgery.

Brian Ward, Ph.D., M.D. Retinal Diagnostic Center3395 S. Bascom Ave, Suite 140Campbell, California 95008

Journal of Ophthalmology

Volume 2010 (2010), Article ID 175613, 4 pages

doi:10.1155/2010/175613

Case Report

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Pathology of Macular Foveoschisis Associated with Degenerative Myopia

Johnny Tang,1,2 Michael B. Rivers,3 Andrew A. Moshfeghi,4 Harry W. Flynn Jr.,4 and Chi-Chao Chan5

1Research Service, Louis Stokes Cleveland VA Medical Center, Cleveland, OH 44106-5068, USA

2Department of Ophthalmology and Visual Sciences, University Hospitals Eye Institute, University Hospitals Case Medical Center, Case Western Reserve University, 11100 Euclid Avenue, LKSD 4107, Cleveland, OH 44106-5068, USA

3The Retina Group of Washington, Fairfax, VA 22031-4621, USA

4Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami, Miller School of Medicine, Miami, FL 33136, USA

5Section of Immunopathology, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892-3655, USA

Received 24 March 2010; Revised 9 June 2010; Accepted 13 July 2010

Academic Editor: Darius M. Moshfeghi

Copyright © 2010 Johnny Tang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

This is a clinicopathological paper on the histologic findings in myopia-associated macular foveoschisis. The findings on ophthalmic pathological study of a 73-year-old woman with high myopia are reviewed. Multiple retinoschisis cavities involving both the macula and retinal periphery were disclosed. Our paper offers tissue evidence and supports recent ocular coherence tomography reports of eyes with high myopia and associated macular foveoschisis.

1. Introduction

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Myopic foveoschisis (MFS) in highly myopic eyes is a more recently recognized clinical entity whose clinical description has been facilitated via optical coherence tomography (OCT) studies. [1, 2]. Previously, myopic foveoschisis has been poorly characterized and may have been mistaken for macular holes or shallow retinal detachments [1, 3]. The first description of this entity was by Phillips who noted that localized posterior retinal detachment over posterior staphyloma can occur even in the absence of a retinal hole [4]. Myopic foveoschisis affects 9% to 20% of myopic eyes with staphylomas [5, 6]. Utilizing OCT, it is now known that MFS can lead to the development of subtle shallow retinal detachments and/or macular holes in patients with high myopia and account for previously unknown causes of vision loss in these patients [1, 7]. To date, pathology of such eyes has not been well illustrated. Herein, we describe a clinicopathologic case of MFS associated with high myopia.

2. Case Report

A 73-year-old woman with high myopia was referred with complaints of bilateral worsening vision. She did not report symptoms of photopsias or scotomas. The best-corrected visual acuity was 20/70 OD and 20/80 OS with a refraction of

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.

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1

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 OD and

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 OS. Anterior segment was remarkable for only mild nuclear sclerotic cataracts OU. Fundus examination revealed bilateral staphylomas, optic nerve crescents, and degenerative myopic changes (Figures 1(a) and 1(b)). Fluorescein angiography (Figures 1(c) and 1(d)) revealed a normal choroidal pattern, window defects in the macular regions and staining of the optic nerve crescents in both eyes.

fig1

Figure 1: (a) Clinical photographs of the fundus of the right and (b) left eyes. Bilateral optic nerve crescents and staphylomas are seen in both eyes. There are also degenerative changes seen in the macular areas of both eyes. (c) Fluorescein angiogram of the right eye in the early (a) and late (b) phases demonstrating staining of the optic nerve crescents and small window defects along the macular region.

Two years later, she died of unrelated causes without interval ocular examination. We do not know if her vision continued to deteriorate during that time. This study was performed prior to the widespread availability of OCT. Both eyes were obtained within 24 hours for autopsy under a protocol approved by the Institutional Review Board of the National Eye Institute.

Grossly, the right globe measured

2

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 mm in the anterior-posterior, horizontal and vertical diameters, respectively. The anterior segment appeared normal, vitreous was clear and retina in place. A posterior staphyloma was noted temporally to the disc.

Histologically, the right eye demonstrated degenerative retinoschisis with interbridging strands in the outer plexiform layer of the macular region (Figures 2(a) and 2(b)). A staphyloma with loss of photoreceptors, attenuated inner nuclear layer, absence of retinal pigment epithelium, and choroid resting against sclera were present at the temporal peripapillary region. A thin fibroglial preretinal membrane was adherent to the internal limiting membrane (ILM) in the macula. Interestingly, there were multiple cystic degeneration in the outer plexiform layer, and there appeared to be folding of the inner layers of the retina. These histopathologic observations are not readily apparent during OCT analysis of MPS patients [7, 8]. Artifactual retinal detachments are noted in the figures secondary to tissue processing.

fig2

Figure 2: (a) Photomicrograph of the right eye demonstrating areas of macular foveoschisis. A region containing the staphyloma is also seen (black arrow). (b) Higher magnification of macular foveoschisis seen in multiple layers of the retina including the outer plexiform layer, inner plexiform layer, nerve fiber layer, and the outer plexiform layer in the perifoveal region. A thin fibrous preretinal membrane is seen (black arrow). (hematoxylin and eosin, original magnification, (a) x50; (b) x100). (c) Photomicrograph of the left eye demonstrating classical retinoschisis in the outer plexiform layer, ganglion cell layer, and nerve fiber layer. (d) Higher magnification demonstrating neuronal bridges between both nuclear layers (asterisk). A fibrous preretinal membrane is seen (black arrow). (hematoxylin and eosin, original magnification, (a) x50; (b) x100).

The fovea, perifovea, and optic nerve head in the left eye were missing. Peripherally, classical age-related retinoschisis in the outer plexiform layer, ganglion cell layer, and nerve fiber layer was noted. Additionally, a thin fibrous preretinal membrane was present (Figures 2(c) and 2(d)).

3. Discussion

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High myopia predisposes patients to degenerative conditions that range from development of lacquer cracks and neovascular membrane formation to development of retinal detachments. The etiology of myopic degeneration is still not clear, but it is believed to stem from a combination of genetic and environmental factors [9]. Published OCT imaging studies have demonstrated that high myopia along with the presence of staphyloma may lead to the development of MFS [7, 8]. Prior to OCT, it was difficult to differentiate these schisis cavities from shallow retinal detachments, macular holes or macular edema [7, 8]. Even with more recent OCT, it was difficult to determine the exact nature and components of the schisis cavity. This study illustrates that retinal schisis cavities can form in various layers of the neurosensory retina in high myopes.

Myopic foveoschisis leads to decreases in visual acuity because of disruption of the neurosensory elements and predisposes patients to foveal retinal detachments [1, 3, 7]. Johnson reviewed the interactions between the vitreous and retina that are thought to be causes of these vitreoretinal interface abnormalities [10]. He discusses that MFS is likely caused by a relative stiffness of the inner retina compared with the outer retina within the concavity of the staphyloma resulting from cortical vitreous remnants after incomplete posterior vitreous detachment (PVD) [10]. Also, possibly contributing is a nondistensible ILM and inner retinal blood vessels [10]. The fibroglial preretinal membrane that was adherent to the ILM in our specimen supports OCT and more recent ultrastructural studies that the preretinal membranes and incomplete PVD in highly myopic patients contribute to MFS formation [6, 10, 11]. Gaucher et al. reported the presence of vertical column-like structures seen on OCT which are consistent with findings seen in our sections (Figure 2(d)) [12].

A long-term evaluation of 29 eyes with MFS demonstrated that the natural evolution of this disease is rather diverse [12]. Fortunately, patients may remain stable for many years without affecting VA [12]. Risk factors for worsening VA increases when there are associated premacular structures such as epiretinal membranes or a partially detached vitreous cortex [12]. Several studies propose that vitrectomy is a reasonable consideration in these cases [13–18].

Financial Disclosures

The authors have no financial interests to disclose.

Acknowledgments

This work was supported in part by the Veterans Affairs Career Development Award 2, Veterans Affairs Foundation Award, and the NEI Intramural Research Program.

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References

1. M. Takano and S. Kishi, “Foveal retinoschisis and retinal detachment in severely myopic eyes with posterior staphyloma,” American Journal of Ophthalmology, vol. 128, no. 4, pp. 472–476, 1999. View at Publisher · View at Google Scholar · View at Scopus

2. J. Akiba, S. Konno, E. Sato, and A. Yoshida, “Retinal detachment and retinoschisis detected by optical coherence tomography in myopic eye with a macular hole,” Ophthalmic Surgery and Lasers, vol. 31, no. 3, pp. 240–242, 2000. View at Scopus

3. Y. Ikuno, F. Gomi, and Y. Tano, “Potent retinal arteriolar traction as a possible cause of myopic foveoschisis,” American Journal of Ophthalmology, vol. 139, no. 3, pp. 462–467, 2005. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus

4. C. I. Phillips, “Retinal detachment at the posterior pole,” British Journal of Ophthalmology, vol. 42, no. 12, pp. 749–753, 1958.

5. T. Baba, K. Ohno-Matsui, and K. Ohno-Matsui, “Prevalence and characteristics of foveal retinal detachment without macular hole in high myopia,” American Journal of Ophthalmology, vol. 135, no. 3, pp. 338–342, 2003. View at Publisher · View at Google Scholar · View at Scopus

6. G. Panozzo and A. Mercanti, “Optical coherence tomography findings in myopic traction maculopathy,” Archives of Ophthalmology, vol. 122, no. 10, pp. 1455–1460, 2004. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus

7. N. Benhamou, P. Massin, B. Haouchine, A. Erginay, and A. Gaudric, “Macular retinoschisis in highly myopic eyes,” American Journal of Ophthalmology, vol. 133, no. 6, pp. 794–800, 2002. View at Publisher · View at Google Scholar · View at Scopus

8. M. Ip, C. Garza-Karren, J. S. Duker, E. Reichel, J. C. Swartz, A. Amirikia, and C. A. Puliafito, “Differentiation of degenerative retinoschisis from retinal detachment using optical coherence tomography,” Ophthalmology, vol. 106, no. 3, pp. 600–605, 1999. View at Scopus

9. M. F. Rabb, I. Garoon, and F. P. LaFranco, “Myopic macular degeneration,” International Ophthalmology Clinics, vol. 21, no. 3, pp. 51–69, 1981. View at Scopus

Page 29: Degenerative Myopia

10. M. W. Johnson, “Posterior vitreous detachment: evolution and complications of its early stages,” American Journal of Ophthalmology, vol. 149, no. 3, pp. 371–382, 2010. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus

11. H. Bando, Y. Ikuno, J.-S. Choi, Y. Tano, I. Yamanaka, and T. Ishibashi, “Ultrastructure of internal limiting membrane in myopic foveoschisis,” American Journal of Ophthalmology, vol. 139, no. 1, pp. 197–199, 2005. View at Publisher · View at Google Scholar · View at PubMed

12. D. Gaucher, B. Haouchine, R. Tadayoni, P. Massin, A. Erginay, N. Benhamou, and A. Gaudric, “Long-term follow-up of high myopic foveoschisis: natural course and surgical outcome,” American Journal of Ophthalmology, vol. 143, no. 3, pp. 455–462, 2007. View at Publisher · View at Google Scholar · View at PubMed

13. H. Kobayashi and S. Kishi, “Vitreous surgery for highly myopic eyes with foveal detachment and retinoschisis,” Ophthalmology, vol. 110, no. 9, pp. 1702–1707, 2003. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus

14. S. Kanda, A. Uemura, Y. Sakamoto, and H. Kita, “Vitrectomy with internal limiting membrane peeling for macular retinoschisis and retinal detachment without macular hole in highly myopic eyes,” American Journal of Ophthalmology, vol. 136, no. 1, pp. 177–180, 2003. View at Publisher · View at Google Scholar · View at Scopus

15. Y. Ikuno, K. Sayanagi, and K. Sayanagi, “Vitrectomy and internal limiting membrane peeling for myopic foveoschisis,” American Journal of Ophthalmology, vol. 137, no. 4, pp. 719–724, 2004. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus

16. R. F. Spaide and Y. Fisher, “Removal of adherent cortical vitreous plaques without removing the internal limiting membrane in the repair of macular detachments in highly myopic eyes,” Retina, vol. 25, no. 3, pp. 290–295, 2005. View at Publisher · View at Google Scholar · View at Scopus

17. K. Hotta and J. Hotta, “Retinoschisis with macular retinal detachment associated with vitreomacular traction syndrome,” Retina, vol. 24, no. 2, pp. 307–309, 2004. View at Publisher · View at Google Scholar · View at Scopus

18. K. Sayanagi, Y. Ikuno, and Y. Tano, “Reoperation for persistent myopic foveoschisis after primary vitrectomy,” American Journal of Ophthalmology, vol. 141, no. 2, pp. 414–417, 2006. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus

FAQ - Myopia, Degenerative(Powered by Yahoo! Answers)

Does anyone know how common the "degenerative myopia" is?

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I am very shortsighted (-9.5D) and just heard about "degenerative myopia". I wonder how many high degree myopia people will have "degenerative myopia".

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2% of the population has this. You are nearsighted. Any person with a high degree of myopia has a higher risk of retinal detachment. It is not likely that you have this but an ophthalmologist (not an optometrist) should be consulted if you feel you may have it.  (+ info)

Do I have degenerative myopia?

I have been wearing glasses for myopia since 5th grade, and I've had to get new glasses about each year. I spend a lot of time in front of electronics. I see spots and have a lot of headaches recently. I want to know what cures there are and what to do to stop my eyesight from worsening.

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See an eye doctor to discuss options. Also check out this site: http://www.tlcvision.com/why_famouspeople_tiger.fxml  (+ info)

Degenerative myopia?

How can I tell if I have it or not? I'm 13 and my vision has been getting worse every year for just about the past 7 years. I believe there was one year when my vision actually got better, but I dunno. Last I checked, my vision was -9 and -7 in my right and left eye, and I know it's gotten worse this year. Do I have degenerative myopia?Sorry, I misunderstood. Thanks to everyone who answered. I was under the impression progressive myopia never gets better, lol. Thanks again. :)

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What you are describing is referred to as "progressive" myopia. Progressive myopia is a genetically inherited condition. The classical presentation of progressive myopia tends to follow this time line -- Most first notice a shift into myopia causing a blurring of distance around second to third grade (7 to 8 years of age). The individual then consistantly and continually increases in nearsightedness until about the age 17 to 19 at which time most then become somewhat stable in their degree of nearsightedness for many years until other vision issues such as cataract may cause changes. Since I am also a progressive myope, you and I have a common ancestor somewhere. I received my first set of eyeglasses from my uncle who was an eye doctor. I became stable at age 18. I have had laser vision correction and have remained stable for years following my laser vision correction. Hope this helped.  (+ info)

Could I Have Degenerative Myopia?

Could I? What are the symptoms? How can I tell?

I have -9.00 diopters in my right eye and -7.00 in my left. I'm not even an adult yet and my vision seems to keep getting worse even if I don't use it much.

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"degenerative myopia" is a form of myopia where the retinal health is affected:

http://www.revoptom.com/handbook/oct02_sec5_3.htm

it is different from garden-variety juvenile myopia progression, in which teens get increasingly nearsighted.

the only way to know if you have degenerative myopia is to have a dilated eye examination and have an eye doctor (optometrist or ophthalmologist) make that diagnosis for you. your retina either has a degenerated appearance or it does not. no way to tell by just the spectacle Rx (whether you are -9.00 or not) or whether you are becoming increasingly nearsighted or not  (+ info)

Degenerative Myopia??

I'm 25, and was born with congenital glaucoma and nystagmus so I've always worn glasses. About a year ago my vision changed again from a -3 in both eyes to a -5 in the left and -4.50 in the right, and it seems to be getting worse. I've been to 2 Opth. who can find no reason for it, and neither have made any remarks about problems with my retina etc. although I do see floaters and such. Do I have degenerative myopia? I mean, normally eyes stabilize before your 25 right? Thanks

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A big change in your need for glasses over a short time period (and at your age) could have more to do with your congenital glaucoma. If it's been a while since you're been to the ophthalmologist, you should have your eye pressures checked. While you're there you can ask about having your retina examined (usually requires dilating drops). If you don't feel comfortable with the ophthalmologists you've seen, maybe you should get another opinion from a different ophthalmologist.

Floaters are pretty normal, unfortunately. If your vision is suddenly grey, like you're looking through a curtain, call your ophthalmologist immediately.

Good luck to you!  (+ info)

How much are colored contacts for a person with myopia?

I have myopia and I want to get hazel prescription contacts, does any body have any idea how much that would cost?How much are regular contacts then?

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Do you wear hard lens, if so they don't make color contacts. If you wear soft lens then they are about 30 dollars a box.  (+ info)

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Is Degenerative Disc Disease and Disc Space Narrowing the same thing?

The chiropractor told me I had disc space narrowing. Is that the same as degenerative disc disease? It's extremely painful and I can't sit or stand for long periods of time. Thanks for the help.

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No, they are referring to two different things. DDD is the actual bone of the spine degenerating. DSN is the intervertrebral disc, ie the cushion is failing.  (+ info)

What is Degenerative Spine and why are there wings involved?

Okay, so, my doctor said I have degenerative spine. Two people have TRIED to explain what it is, but they use big words that mean nothing to me. Give me a break, I only took one semester of high school medical terminology. Could you explain in SIMPLE terms what's going on with my back, and why he said there were "two little wing looking things coming off the base" of my spine? Why are they there? Also, is there any way to make my tailbone STOP hurting? Please help. Thank you.

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Go here:

http://www.lajollaspine.com/sdds.shtml  (+ info)

Is there any way to reduce the power(myopia) in the eyes without surgery?

I really can't undergo surgery. But I want to know if there is any way of reducing this eye defect(myopia) without surgery.

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It's posible but unfortunatly most people are too lazy and don't believe in self healing. I have a read a book with studies where people ranging in different ages had their eye sight fixed by just exercizing their eyes. You know the table with the letters? Look at the line where it already gets blurry. Keep on looking at it, blinking, tryng to see the letters. When you see the letter are getting bette, stop. Do this for about 5 mins. 3 times a day? Don't stress urself. Keep on wroking on that one line until you see it crearly from the start of the 'workout'. Then, go onto the next line. It isn't silly. It WORKS because the eyes contain muscles that contract and lenses that keep on adjusting.

(Example: Running builds up muscles and breathing so after running many times you won't have breathing problems-)

You always have to persuate yourself that YOU CAN fix your eye sight. I know some people who were able to do it. Try it. Take some time. MOst people are lazy and won't do it. Others lack belief in self healing. This is the only way I know without an operation. =D good luck!  (+ info)

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What kind of profession is most suitable for people with high degrees of myopia?

What kind of profession is most suitable for people who suffer from high degrees of myopia (nearsightedness) or what kind of work they should perform in order not to hurt their eyes?

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Well this optometrist gets to -14.25 in the worst meridian of my worst eye.It's given me some insight (sorry) and empathy with at least my high myope patients.

It's a question better tackled from the other end.High myopes are marginally more prone to retinal detachment, so occupations exposed to vibration or shocks are to be avoided: pneumatic drills, driving heavy machinery...High diver, professional football player (USA)

Some occupations require good vision without glasses or contact lenses... principally branches of the military and the fire service, but heavy goods vehicle driving is also legally barred from high myopes on grounds of a minimum vision without glasses requirement in most countries.

Otherwise go for it! Ski instructor, if you are happy in contacts(glasses steam up!)  (+ info)

Klasifikasi myopia berdasarkan besarnya derajat refraksi anomaly, antara lain :1. Myopia ringan : Spheris - 0.25 Dioptri s/d Spheris - 3.00 Dioptri2. Myopia sedang : Speris - 3.25 Dioptri s/d Spheris - 6.00 Dioptri

3. Myopia tinggi : lebih dari Spheris - 6.25 Dioptri

Klasifikasi berdasarkan laju perubahan besarnya derajat anomaly secara klinik, antara lain :

Myopia simplek/stasioner/fisiologik

Myopia simplek biasanya timbul pada usia yang masih muda kemudian akan berhenti. Tetapi dapat juga naik sedikit kemudian berhenti. Dapat juga naik sedikit pada masa puber sampai sekitar umur 20 tahun. Besar dioptrinya kurang dari S -5.00 Dioptri atau S -6.00 Dioptri. Tetapi kalau dikoreksi dengan lensa yang sesuai dapat mencapai normal yaitu 6/6 atau 20/20.

Myopia progresif

Myopia ini ditemukan pada segala umur. Pada keadaan ini akan terjadi kelainan fundus yang khas untuk myopia tinggi ( myopia lebih dari Speris -6.00 Dioptri )

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Myopia maligna

Myopia ini disebut juga dengan myopia patologis/degeneratif karena disertai penuaan dari koroid dan bagian lain dalam bolamata ( lensa, koroid, badan siliar ).

Myopia berdasarkan faktor penyebab dapat dibedakan menjadi dua, yaitu :

Myopia axial

Myopia axial ini dapat terjadi sejak lahir oleh karena faktor hereditas, komplikasi penyakit lain seperti gondok, TBC, dan campak maupun karena konginetal. Selain itu juga dapat karena anak biasa membaca dalam jarak yang selalu dekat sehingga mata luar dan polus posterior yang paling lemah dari bolamata memanjang. Orang yang berwajah lebar akan menyebabkan konvergensi berlebihan saat melakukan pekerjaan dekat, karena peradangan atau melemahnya lapisan yang mengelilingi bolamata disertai tekanan yang tinggi. Myopia ini dapat bertambah terus sampai dewasa.

Myopia axial merupakan suatu keadaan dimana jarak fokus media refrakta lebih pendek dibandingkan sumbu orbitnya. Dalam hal ini jarak fokus media refrakta normal 22,6 mm sedangkan jarak sumbu orbitnya adalah > 22,6 mm.

Myopia refraktif

Myopia refraktif merupakan suatu keadaan dimana jarak fokus media refrakta lebih pendek ddibandingkan sumbu orbitnya. Namun dalam hal ini sumbu orbit normal 22,6 mm sedangkan jarak fokus media refrakta < 22,6 mm

Sumber: http://id.shvoong.com/medicine-and-health/ophthalmology/2174948-klasifikasi-myopia/#ixzz1towVNYVj

Chapter 243 – Complications of Glaucoma Surgery and Their Management

Chapter 243 – Complications of Glaucoma Surgery and Their Management

 

J. WILLIAM DOYLE

M. FRAN SMITH

 

INTRODUCTION

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In the ideal world, surgery proceeds smoothly and outcomes are uncomplicated. Unfortunately, in the real world, despite a surgeon’s best efforts, complications may occur. This is especially true in the field of glaucoma—glaucoma surgery, unlike many other ocular procedures, is not particularly “forgiving” in nature. Nonetheless, good final outcomes may often be achieved in spite of the occurrence of complications. The key to success is for the surgeon to be alert and be able to identify and address any problems promptly.

FILTRATION SURGERY

Before the discussion of complication management in filtration surgery, it is worth repeating an old surgical axiom. Without a doubt, the best surgical complication management is avoidance of the complication in the first place. Preoperatively, ensure that the patient stops the intake of all aspirin-like products, and discontinue topical epinephrine (adrenaline) compounds to decrease the quantity of superficial bleeding. Consider the use of preoperative topical antibiotics. Intraoperatively, meticulous attention to detail is important, especially if antimetabolites are being used. It is imperative to handle the conjunctiva gently. When the partial-thickness trabeculectomy flap is being closed, consider using extra, releasable-style sutures. If intraocular pressure (IOP) is too high postoperatively, a stitch may be pulled easily. But if too much drainage occurs postoperatively, an insidious cycle of overdrainage may be established—and this cannot always be corrected readily.

Nonetheless, complications intermittently occur. Filtration surgery complications are most easily categorized as intraoperative, early postoperative, and late postoperative.

Intraoperative Complications

CONJUNCTIVAL BUTTONHOLE.

In no other situation is the axiom given before more appropriate—the best complication management of the buttonhole is initial avoidance of the complication. Toothed forceps are the problem here—they should not be on the glaucoma tray. Bishop-Harmon or suture-tying forceps are preferable when conjunctiva is handled. Better yet, the use of a dry cellulose sponge, with its tip cut off, to stretch conjunctiva up and away from the area of interest is safe. If a buttonhole occurs anyway, management requires patient, complete hole closure if successful surgery is to ensue. If a buttonhole cannot be closed in a watertight fashion and detection of the hole has occurred early in the surgery, consideration must be given to rotation of the site of the trabeculectomy flap to a different area, away from the hole. Also, if antimetabolite use was planned but not initiated prior to discovery of the buttonhole, the surgeon must consider no exposure, or limited exposure, to antimetabolite, applied well away from the buttonhole.

Closure technique for a conjunctival buttonhole depends on its location, size, and shape. The most easily closed buttonhole

 

 

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Figure 243-1 Repair of buttonhole close to limbus.

 

 

Figure 243-2 Two-layer closure of intraoperative buttonhole in central bleb zone. Following Tenon’s layer closure, conjunctiva is closed.

is the short limbal tear, which may be closed with a horizontal mattress suture of double-armed 10-0 nylon. Cornea just anterior to the tear is deepithelialized. One arm of the suture is passed to one side of the hole, through conjunctiva and partial-thickness anterior Tenon’s layer, and into the cornea in front of the tear. The other needle of the double-armed suture is passed similarly on the other side of the hole. When the two ends are tied, conjunctiva is pulled safely down, with considerable overlap, onto clear cornea. The deepithelialized cornea quickly heals to the underside of the overlapped conjunctiva ( Fig. 243-1 ).

Linear tears of conjunctiva away from the limbus are probably best closed in two layers with a running suture. An 8-0 polyglactin suture on a vascular needle is used first to close Tenon’s layer, from the Tenon’s layer side. For conjunctival layer closure, the conjunctival flap is flapped over and 10-0 or 11-0 nylon sutures are used, preferably on a vascular needle ( Fig. 243-2 ). Similarly, small, round holes can be closed using a two-layer technique and purse-stringing the suture around the hole.

 

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Figure 243-3 Peripheral intraoperative buttonhole closure. Repair by inclusion in conjunctival incision closure.

Finally, linear tears in conjunctiva near a fornix incision are frequently best addressed by incorporation of the tear into the final incision closure (see Fig. 243-3 ).

After buttonhole repair, it is essential that watertightness be tested before proceeding further. Balanced salt solution may be squirted vigorously at one side of the closure and any seepage through to the other side carefully sought. Also, after final incision closure, it is best to recheck for leakage using fluorescein dye. Inflation of the bleb with balanced salt solution through the corneal paracentesis and application of fluorescein dye is a simple way to mark any leaks. The time to address such leaks is while the patient has good anesthesia and is still in the operating room. Postoperatively, when inflammation occurs and the conjunctiva has become thinned because of aqueous flow, definitive surgical repair may not be possible.

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TRABECULECTOMY SCLERAL FLAP TEAR/DISINSERTION.

Occasionally, despite the surgeon’s attempt to dissect up a sufficiently thick (about two thirds of the total scleral thickness) scleral flap, tissues are such that a “ratty” flap is produced. These flaps tend to tear or disinsert. If the tear is found early and is small enough, direct suture closure using 10-0 nylon may be attempted. Similarly, if the flap base is disinserted partially, an attempt may be made to reposit the flap using a double-armed horizontal mattress suture externalized through clear cornea ( Fig. 243-4 ). Some surgeons have reported successful reposition of a totally disinserted flap using two 10-0 nylon sutures through the flap base and out the peripheral cornea.[1] However, total disinsertion and large tears are usually a reflection of exceptionally poor quality (ratty) sclera; such flaps do not tolerate sutures well and tend to “cheesewire,” which results in larger defects. Rather, this complication may be best addressed by placement of an additional cover over the problem flap.

Tenon’s tissue is readily available in all eyes. The surgeon may choose to excise a 4 × 3?mm piece of redundant Tenon’s tissue from up in the superior fornix near the incision or alternatively from the inferior fornix if excess tissue is not present superiorly. This excised rectangular piece of tissue may be sutured at its four corners over the full-thickness sclerotomy. [2] If excess leakage is noted after anterior chamber reformation, additional sutures may be placed. Other choices of coverage material are donor sclera,[3] dura, pericardium, or even fascia lata.[4] Most operating rooms have at least one of these materials present in a convenient prepackaged form. The material is hydrated in balanced salt solution, a rectangle of material (approximately 2?mm larger and wider than the trabeculectomy flap) is cut out, and the cover is sutured into place, with at least one 10-0 nylon suture to each corner of the material. Postoperatively, these sutures may be lysed using an argon laser to increase drainage as desired, so secure closure on the operating table is warranted ( Fig. 243-5 ).

VITREOUS LOSS.

Especially in pseudophakes after complicated cataract extraction or in aphakes, the surgeon may encounter vitreous prolapse after the iridectomy. Careful clearance

 

 

Figure 243-4 Repair of disinserted flap.

 

 

Figure 243-5 Donor dura flap to replace disinserted flap.

from the sclerotomy of all vitreous is key because vitreous is a very effective sclerotomy plug. A limited vitrectomy with a combination of scissors dissection, cellulose sponge, and automated

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vitrector should be performed. The goal is no vitreous present at the sclerotomy when checked using a cellulose sponge. Extra care is required in these eyes to avoid a postoperative shallow anterior chamber because this may bring further vitreous forward to block the sclerotomy. Therefore, consider the placement of extra releasable sutures (or sutures that may be lasered) to prevent early overdrainage.

INTRAOPERATIVE BLEEDING.

Excess bleeding from the iris root and/or ciliary body after iridectomy must be addressed because blood may also cause sclerotomy blockage. Cold balanced salt solution, dripped slowly over several minutes, with or without low-concentration epinephrine added, usually results in stoppage of the bleeding. Alternatively, a monopolar wet-field 23gauge cautery may be applied carefully to the bleeding vessel if the site can be visualized. It is rare for these areas to rebleed postoperatively, but if they do, it is usually in situations with hypotony; again, a tight closure with extra releasable sutures is considered. Viscoelastic material can be left in the eye at the conclusion of surgery to act as a “tamponade” and also to help avoid postoperative hypotony.

Suprachoroidal hemorrhage (SCH) is the other type of intraoperative bleeding. In these cases the eye should be closed as quickly as possible. Avoidance is paramount because an expulsive

 

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SCH is disastrous. Preoperative intravenous mannitol (100?ml of 20% solution over 15 minutes), with Foley catheter placement, may be considered in eyes that undergo trabeculectomy with a preoperative IOP >40?mmHg (5.3?kPa). Theoretically, less chance exists of SCH if eye pressure at the time of internal sclerotomy does not suddenly drop from 45?mmHg (6.0?kPa) to zero. In addition, the paracentesis may be performed earlier to decompress the eye gradually prior to internal block removal.

CHOROIDAL EFFUSION.

Usually effusions develop postoperatively, not intraoperatively. However, patients who have Sturge-Weber syndrome or markedly elevated episcleral venous pressure may develop effusions intraoperatively. Their occurrence is signaled by sudden anterior chamber shallowing. Management consists of drainage via inferior linear sclerotomies, located 5–6?mm from the limbus. If the plan is to carry out surgery on the second eye of a patient who has developed intraoperative choroidal effusions in the first eye (the disease is bilateral), placement of a preliminary posterior sclerotomy prior to internal block removal may be considered.

Early Postoperative Complications

UNDERDRAINAGE.

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In the early postoperative period, initial underdrainage, not associated with sclerotomy blockage, is addressed effectively by sequential release of scleral flap sutures. If so-called permanent sutures have been placed, the 10-0 nylon may be lysed with the argon laser and a Hoskins (or Ritch) lens.[5] Krypton red (or blue-green argon), 50?µm spots, at 300?mW are usually effective. Rarely, a nylon suture cannot be visualized, secondary to overlying subconjunctival hemorrhage or thick Tenon’s tissue. To avoid this occurrence, place at least half of the scleral flap sutures using a “releasable”-suture technique. [6] This involves tying the suture with a slip knot that may be released easily with a pull on the cornealized free suture end ( Fig. 243-6 ). Because endophthalmitis has been reported to develop from a freely moving, cornealized releasable suture, the externalized suture end must be buried in clear cornea.[7] The superficial unburied segment of the suture is epithelialized quickly, which decreases risk of endophthalmitis and still allows the surgeon easy assess.[8] To maintain expansion of the subconjunctival space with fluid (aqueous) in the early postoperative period, and when it is too early to lyse a stitch, another option is local scleral compression. This involves gentle application of pressure over the conjunctiva using a moistened cotton-tip applicator, just at the edge of the scleral flap. Such pressure “burps” free an aliquot of aqueous, which lowers IOP. Gonioscopy is recommended to check that the internal sclerostomy is not blocked by vitreous, iris, and so forth.

A blocked sclerotomy is handled differently. If fibrin or blood blocks outflow, tissue plasminogen activator may be helpful.[9] [10]

 

 

Figure 243-6 Releasable sutures (arrow).

Doses of 6–25?µl have been injected into the anterior chamber safely, with resumption of flow through the sclerotomy. Because recurrent bleeding is a risk with tissue plasminogen activator use, lower doses, 6–12?µl, are now recommended. Also, fibrin frequently recurs unless high-dose corticosteroids, topical, subconjunctival, and/or oral, are used to reduce inflammation.

THE SHALLOW ANTERIOR CHAMBER.

If a shallow anterior chamber is present, the reason for shallowing—overdrainage or some other process—must be ascertained. Overdrainage is associated with low IOP, which usually results from inadequate scleral flap closure (with a high bleb present) or from a bleb leak (no or low bleb present).

Overdrainage with no bleb leak can be tedious to manage. If the bleb is high and no corneal-lens touch or “kissing” choroidal effusion occurs, observation with cycloplegic prescription is appropriate. However, if anterior chamber shallowing is progressive, early placement of an oversized, bandage soft contact lens may help to prevent later, more difficult problems.[11] [12] Such lenses seem to limit excessive bleb extension and/or excess bleb transconjunctival aqueous flow ( Fig. 243-7 ). Usually, their use may be discontinued after 1–2 weeks. Alternatively, a Simmon’s shell may be applied to the eye. The shell has a plate that can be positioned over the

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sclerotomy site for maximum tamponade. However, patients may tolerate it poorly, and daily ocular examination is required. Also, corneal epithelial defects occur frequently.

Another option some surgeons use in these cases is gentle pressure patching, in which pressure is applied directly over the trabeculectomy flap to limit outflow. One concern with this option is that, when the patient looks up (or exhibits Bell’s phenomenon, with sleep), the pressure patch may transfer pressure over the cornea, which results in lens-corneal touch. Sometimes, injection of viscoelastic material into the anterior chamber may provide sufficient time (24–48 hours) to allow the eye to “catch up” with itself.[13] We have found greater viscosity viscoelastic to be particularly useful in such cases. This is best attempted early, rather than late, in the course. Finally, if overdrainage continues with the development of choroidal effusions that touch, or of lens-corneal touch, the surgeon may need to return the patient to the operating room for further flap closure, anterior chamber reformation, and effusion drainage.

Initial overdrainage with bleb leak is frequently the result of a buttonhole missed at the time of surgery. Postoperatively, a buttonhole is far more difficult to manage. As already noted, suture repair at this time is often ineffective, especially if intraoperative antimetabolites were used and/or the conjunctiva is cystic or excessively thinned. Suturing at this time may result in a larger hole. Patching, bandage soft contact lenses, and Simmon’s shell may be used, with variable results. The surgeon must watch the bleb carefully because the preceding “solutions” often fail to

 

 

Figure 243-7 A 17?mm contact lens compresses an overdraining bleb. Edge of bandage contact lens indicated by arrows.

 

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seal the leak and only act to exacerbate episcleral/conjunctival healing and adhesion. Other alternatives include autologous fibrin tissue glue,[14] autologous blood injection (see Fig. 243-8 ),[15] [16] [17] and cyanoacrylate glue with contact lens application. [18] Most of these alternatives seem to work better on small, late-postoperative bleb leaks. A large, early-postoperative bleb leak may require a return to the operating room and development of a new conjunctival flap from “buttonhole-free” conjunctiva.

Remaining causes of an early-postoperative shallow chamber, other than overdrainage, are basically five, one with low IOP and four with high IOP. Most rarely, the ciliary body may shut down secondary to intense postoperative inflammation. Such eyes have flat blebs, no bleb leaks, shallow anterior chambers, low IOP, and occasionally inflammatory choroidal effusions. High-dose topical, peribulbar, and systemic corticosteroids may be helpful in these cases.

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Postoperative 5-fluorouracil injections should be considered because they may help prevent conjunctival-episcleral adhesions in the period before aqueous flow restarts.

A shallow anterior chamber associated with a high IOP results from one of four causes only:

• Pupillary block

• SCH

• Aqueous misdirection malignant glaucoma

• Ring choroidal effusion (rare)

If a full-thickness iridectomy was made at the time of surgery, pupillary block can be ruled out. However, if doubt exists with regard to the surgical iridectomy patency and the preceding scenario exists, the surgeon must perform another (laser) iridectomy as soon as possible. Only then can pupillary block be ruled out. Once pupillary block is excluded, the surgeon must examine for the presence of an SCH, which is more likely to occur in elderly, vitrectomized, aphakic, hypotonous eyes. Usually, diagnosis is made easily by indirect ophthalmoscopy, with observation of the characteristic dark choroidal swellings and the patient’s history of pain, nausea, and vomiting. If ophthalmoscopy is impossible, a B-scan ultrasound examination is carried out ( Fig. 243-9 ). If SCH is diagnosed, therapeutic options include observation and corticosteroid prescription if the patient is not too uncomfortable and there is no choroidal or lens-corneal touch. Again, 5-fluorouracil injections may be considered to prevent scarring of the sclerotomy while the SCH resolves. Otherwise, it may be best to return the patient to the operating room for evacuation of the SCH. This is best accomplished no sooner than postoperative day 7–10, at which time clot lysis has usually begun, which allows easier SCH drainage.

Another cause of a shallow anterior chamber, with associated high IOP, is aqueous misdirection. Once called malignant glaucoma, it is indeed a malignant process to treat. Aqueous misdirection

 

 

Figure 243-8 Peribleb autologous blood injection for leak.

(as discussed in Chapter 229 ) is the syndrome characterized by marked anterior displacement of the lens-iris diaphragm with a high IOP, presumably as a result of trapped misdirected posterior aqueous. If prompt treatment is initiated, perhaps 50% of mild cases resolve with intensive cycloplegic therapy (i.e., atropine 1%, one drop every 5 minutes for a total of three drops, four times a day). Also, to relieve the buildup of what is believed to be misdirected aqueous trapped behind the vitreous face, many surgeons recommend aqueous suppressants and/or osmotics. Other useful medical adjuncts include phenylephrine 2.5% four times a day and prednisolone

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acetate every 2 hours for inflammation. If this is unsuccessful and the patient is aphakic or pseudophakic, laser therapy is an option.

Finally, although rare, anterior ring choroidal effusion has been described as a cause of shallow anterior chamber associated with high IOP.[19] B-scan confirms this diagnosis.

CHOROIDAL EFFUSIONS.

Although classical posterior choroidal effusions often occur in conjunction with a shallow anterior chamber and low IOP, they may also occur in eyes that have full-depth chambers and low IOPs. Management usually consists of cycloplegia, topical corticosteroids, and observation. As long as the effusions do not touch, drainage is not required. If touch does occur centrally, because of the danger of retinal adhesion formation, many surgeons choose to perform effusion drainage via posterior sclerotomies inferiorly. The scleral flap may be revised at the time of choroidal drainage to prevent further hypotony and a recurrence of the effusions. Several permanent or releasable sutures may be enough to reduce leakage in the short term.

CORNEAL EPITHELIOPATHY.

In this era of antimetabolite use, an increased incidence of corneal epithelial toxicity and even defects occurs after 5-fluorouracil injections. Very early temporary punctal occlusion using collagen plugs optimizes the corneal wetting. Preservative-free tears are helpful. One group also reported that bandage contact lens application increased comfort and decreased inflammation.[20]

Late Postoperative Complications

LATE BLEB FAILURE.

Late bleb failure may result from heavy vascularization and healing around the bleb. Digital pressure applied by the patient to the inferior globe through the inferior lid may be useful in such cases, as this helps maintain flow through the drain and keeps the subconjunctival space expanded. If this is insufficient, needling revision of the bleb may reestablish effective filtration. The needling process alone rarely establishes long-term filtration in eyes not exposed to antimetabolites. However, if needling is followed with 5-fluorouracil injections,

 

 

Figure 243-9 B-scan of suprachoroidal hemorrhage following trabeculectomy.

 

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Figure 243-10 Neodymium:yttrium-aluminum-garnet laser bleb remodeling for bleb leak. (Courtesy of Mary Lynch, MD.)

up to an 80% success rate is possible.[21] Also, needling may help revive a failing bleb after trabeculectomy using intraoperative mitomycin.[22]

TENON’S CYST FORMATION.

A Tenon’s cyst is a high-domed, taut encapsulation of the bleb, which limits aqueous percolation. It must be differentiated from vascularized bleb failure. Once reported to occur in up to 15% of postsurgical eyes during the first postoperative month, it seems to be much less common in eyes that have received 5-fluorouracil or mitomycin. If the acute rise in IOP associated with these cysts is managed medically, with or without corticosteroid use, most of these blebs (up to 90%) continue to function later, as the bleb tissue remodels itself. If failure seems imminent (lower bleb, higher IOP), needling of the cyst, with postoperative 5-fluorouracil injections, may be helpful.

LATE BLEB LEAKS.

Initial management of these leaks involves patching, aqueous suppressants, and antibiotics. Additional management includes modalities already referred to, such as bandage contact lenses, autologous fibrin or blood, and glue. Trichloroacetic acid application and carefully applied cryotherapy may also be attempted. If these modalities fail and further management is felt necessary, neodymium:yttrium-aluminum-garnet laser bleb remodeling may be tried.[23] The laser is tuned to the continuous-wave multimode, carefully retrofocused 1.0?mm behind the bleb to the underlying sclera, and then applied in a grid pattern (3.0?J/shot) over the bleb area ( Fig. 243-10 ). Inflammation and discomfort may be intense, but up to 80% of leaks seal. Other alternatives include a return to the operating room, where free conjunctival patch grafts may be applied over the sclerotomy after excision of the cystic leaking bleb. [24] [25] Or, if scarring is minimal, local revision using conjunctival rotation may be attempted.

BLEBITIS VERSUS LATE ENDOPHTHALMITIS.

As many as 1 per 100 patients/year may develop infection of the bleb. The cystic thin blebs seen after antimetabolite application are believed to be at higher risk. When a bleb is present, the surgeon needs to treat any red eye emergency with antibiotics. Blebitis is differentiated from conjunctivitis by the presence of a murky, opalescent bleb, often with an associated bleb leak, in addition to conjunctiva injected diffusely with associated discharge ( Fig. 243-11 ). The key here is analysis of the vitreous response. If the vitreous is quiet, prompt treatment with hourly topical antibiotics may save the bleb and the eye. Topical corticosteroids after 48 hours of treatment are useful to treat the inflammation. However, if endophthalmitis is diagnosed with vitreous involvement, intravitreal cultures and antibiotics are required and eye

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Figure 243-11 Blebitis.

 

 

Figure 243-12 Intrableb injection of autologous blood for hypotony.

salvage is rare. Organisms frequently seen in these eyes include hemophilus, streptococci, and staphylococci. Thus, coverage is best initiated with fortified topical cefazolin or vancomycin and tobramycin. Alternatively, topical fluoroquinolones, perhaps in combination with systemic fluoroquinolone prescription, may cover many of these cases. Intravitreal antibiotic injections of choice are vancomycin and amikacin.

LATE HYPOTONY.

Antimetabolites have introduced a somewhat new entity, late hypotony, to the list of late postoperative trabeculectomy complications. Whereas an IOP <5?mmHg (<0.67?kPa) on a long-term basis used to be unheard of, now such eyes are not infrequent. Most commonly, the history is of high-dose mitomycin use with loose scleral flap closure, although this entity has also been seen after 5-fluorouracil injections. Characteristically, vision is decreased, the eyes are soft, blebs are large, thin, and totally avascular, retinal folds are seen in the macula (with or without the aid of fluorescein angiography), retinal vessels are tortuous, and the nerve head may be swollen. Useful treatments, as with bleb leaks, include intrableb autologous blood injection[26] ( Fig. 243-12 ) and neodymium:yttrium-aluminum-garnet bleb treatment.[23] Sometimes, a return to the operating room to revise the thin bleb and/or resuture the flap is indicated. A donor “cover” (as already discussed) may be necessary to limit aqueous egress. Alternatively, if a symptomatic cataract is present, the cataract extraction-associated inflammation frequently slows filtration through bleb healing and resolves the hypotony.[27] Some surgeons

 

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Figure 243-13 Exposure of tube in drainage seton (arrow).

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have expressed concern that if such eyes are left untreated for many months, the retinal folds may not resolve, even after successful pressure adjustment. One report exists of such an eye, finally successfully treated with pars plana vitrectomy and liquid perfluorocarbon liquid.[28]

DRAINAGE SETONS

No chapter on glaucoma surgical complications is complete without at least a mention of some of the unique problems seen with setons. Usually, with proper placement, extrusion of the plate(s) and uncontrolled intraocular inflammation are not seen. Initial hypotony may be seen with some of the valved implants. If proper tube blockage, with either a “stent” or external suture, is used with the unvalved implants, hypotony may be avoided with these devices, even after the “plug” is removed or dissolved.[29] The most frequent problems with these devices are melting of the patch graft that overlies the extraocular tube, with tube exposure ( Fig. 243-13 ), and intraocular rotation of the tube anteriorly into cornea. Melting of the graft may be monitored if conjunctival coverage is maintained. If not maintained, a new graft must be placed and conjunctiva mobilized to cover it. The other problem, tube migration, is especially common in children and young adults. At the first hint of corneal compromise (endothelial cell counts may be helpful), the tube is repositioned more posteriorly to avoid corneal failure.

 

 

REFERENCES

 

1. Riley SF, Smith TJ, Simmons RJ. Repair of a disinserted scleral flap in trabeculectomy. Ophthalmic Surg. 1993;24:349–50.

 

2. Brown SV. Management of a partial thickness scleral flap buttonhole during trabeculectomy. Ophthalmic Surg. 1994;25:732–3.

 

3. Riley SF, Lima FL, Smith TJ, Simmons RJ. Using donor sclera to create a flap in glaucoma filtering procedures. Ophthalmic Surg. 1994;25:117–18.

 

4. Hughes BA, Shin DH, Birt CM. Use of fascia lata in revision of filtration surgery. J Glaucoma. 1996;5:207–9.

 

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5. Melamed S, Ashkenazi I, Glovinski J, Blumenthal M. Tight scleral flap trabeculectomy with postoperative laser suture lysis. Am J Ophthalmol. 1990;109:303–9.

 

6. Kolker AE, Kass MA, Rait JL. Trabeculectomy with releasable sutures. Arch Ophthalmol. 1994;112:62–6.

 

7. Burchfield JC, Kolker AE, Cook SG. Endophthalmitis following trabeculectomy with releasable sutures [letter]. Arch Ophthalmol. 1996;114:766.

 

8. Rosenberg LF, Siegfried CJ. Endophthalmitis associated with releasable suture [letter]. Arch Ophthalmol. 1966;114:767.

 

9. Lundy DL, Sidoti P, Winarko T, et al. Intracameral tissue plasminogen activator after glaucoma surgery. Indications, effectiveness, and complications. Ophthalmology. 1996;103:274–82.

 

10. Tripathi RC, Tripathi BJ, Park JK, et al. Intracorneal tissue plasminogen activator for resolution of fibrin clots after glaucoma filtering procedure. Am J Ophthalmol. 1991;111:247–8.

 

11. Smith MF, Doyle JW. Use of oversized bandage soft contact lenses in the management of early hypotony following filtration surgery. Ophthalmic Surg Lasers. 1996;27:417–21.

 

12. Blok MD, Kok JH, Van Mil C, et al. Use of the megasoft bandage lens for treatment of complications after trabeculectomy. Am J Ophthalmol. 1990;110:264–8.

 

13. Osher RH, Cionni RJ, Cohen JS. Re-forming the flat anterior chamber with Healon. J Cataract Refract Surg. 1996;22:411–15.

 

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14. Asrani SG, Wilensky JT. Management of bleb leaks after glaucoma filtering surgery. Use of autologous fibrin tissue glue as an alternative. Ophthalmology. 1996;103:294–8.

 

15. Leen MM, Moster MR, Katz LJ, et al. Management of overfiltering and leaking blebs with autologous blood injection. Arch Ophthalmol. 1995;113:1050–1.

 

16. Smith MF, Magauran RG, Doyle JW. Treatment of postfiltration bleb leak by bleb injection of autologous blood. Ophthalmic Surg. 1994;25:636–7.

 

17. Smith MF, Magauran RG, Doyle JW, Betchkel J. Treatment of postfiltration bleb leaks with autologous blood. Ophthalmology. 1995;102:868–71.

 

18. Zalta AH, Wieder RH. Closure of leaking filtering blebs with cyanoacrylate tissue adhesive. Br J Ophthalmol. 1991;75:170–3.

 

19. Dugel PU, Heuer DK, Thach AB, et al. Annular peripheral choroidal detachment simulating aqueous misdirection after glaucoma surgery. Ophthalmology 1997; 104:439–44

 

20. Beckman RL, Solinski SJ, Greff LJ, et al. Bandage contact lens augmentation of 5-fluorouracil treatment in glaucoma filtration surgery. Ophthalmic Surg. 1991; 22:563–4.

 

21. Shin DH, Juzych MS, Klatana AK, et al. Needling revision of failed filter blebs with adjunctive 5-fluorouracil. Ophthalmic Surg. 1993;24:242–8.

 

22. Greenfield DS, Miller MP, Suner IJ, Palmberg PF. Needle elevation of the scleral flap for failing filtration blebs after trabeculectomy with mitomycin-C. Am J Ophthalmol. 1996;122:195–204.

 

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23. Lynch MG, Roesch M, Brown RH. Remodeling filtering blebs with the neodymium:YAG laser. Ophthalmology. 1996;103:1700–5.

 

24. Wilson MR, Kotas-Neumann R. Free conjunctival patch for repair of persistent late bleb leak. Am J Ophthalmol. 1994;117:569–74.

 

25. Buxton JN, Lavery KT, Liebmann JM, et al. Reconstruction of filtering blebs with free conjunctival autografts. Ophthalmology. 1994;101:635–9.

 

26. Wise JB. Treatment of chronic postfiltration hypotony by intrableb injection of autologous blood. Arch Ophthalmol. 1993;111:827–30.

 

27. Doyle JW, Smith MF. Effect of phacoemulsification surgery on hypotony following trabeculectomy surgery. Arch Ophthalmol. 2000;118:763–5.

 

28. Duker JS, Schuman JS. Successful surgical treatment of hypotony maculopathy following trabeculectomy with topical mitomycin C. Ophthalmic Surg. 1994; 25:463–5.

 

29. Sherwood MB, Smith MF. Prevention of early hypotony with Molteno implants. Ophthalmology. 1993;100:85–90.