Ординатура / Офтальмология / Английские материалы / Handbook of Pediatric Retinal Disease_Wright, Spiegel, Thompson_2006

same time. Patients are typically less than 30 years of age. Flashing lights commonly precede the onset of visual acuity loss. Mild vitreous inflammation is common; there may also be mild anterior chamber inflammation. A history of preexisting viral upper respiratory infection is commonly reported.

The characteristic lesions of APMPPE are cream-colored plaques at the level of the retinal pigment epithelium that tend to be oval or round with irregular edges. There are usually multiple lesions randomly distributed over the posterior pole. The presenting visual acuity is usually 20/200 or better. Central and pericentral scotomata are common. Fluorescein angiography and indocyanine green angiography (ICG) may be helpful in making the diagnosis. The cream-colored lesions seen on fundus examination tend to block fluorescence early in the angiogram and stain late. Usually, over a period of a few weeks, the lesions begin to resolve and the vision begins to improve. In most patients, the vision returns to near-normal levels. The disease has been reported to recur, but this is uncommon.

Acute posterior multifocal placoid pigment epitheliopathy may occur as a consequence of a prior viral infection. A 40-year- old man developed APMPPE following an acute group A streptococcal infection.25 Other causes probably exist. The lesions appear to be related to acute focal decreases in choroidal blood flow.58 Most cases resolve without treatment over a period of several weeks. The role of corticosteroids in treatment is controversial.

Acknowledgments. The preparation of this chapter was supported in part by an unrestricted grant from Research to Prevent Blindness, Inc.

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myopia over time.13 As can be surmised from these prevalence data, the incidence of myopia increases with increasing age. A study from the United Kingdom that analyzed refractive data from patients examined annually between the ages of 7 and 13 years found annual myopia incidence values of 3.5% to 12%, resulting in a rise in prevalence from 5% to 40% over the 6 years of the study.47

In a 1975 study, it was estimated that 5.6% of blindness in school children in the United States was secondary to myopia.21 Myopia is second only to diabetes mellitis as the most common cause of blindness in the working-age population.7,67 Lower grades of myopia, although not sight threatening, are a cause of significant morbidity.

ETIOLOGY

Myopia can be classified into three broad groups based on clinical findings and prognosis.7 The first type is physiological, or correlation, myopia. In these eyes all the components of refraction are within normal limits, but there is a lack of correlation between the refractive powers of the cornea, lens, and axial length, rendering the far point nearer than infinity. Although decreased distance vision results, these eyes are otherwise normal and there are no fundus abnormalities. The degree of myopia is usually low, but there is no “magic number” because a borderline steep cornea, a lens at the upper limit of normal, and an axial length also in the upper normal range, would be expected to yield high amounts of myopia in some cases. This form of myopia generally begins in childhood or adolescence, with a second peak of onset at the end of the second decade or beginning of the third. It usually progresses for several years, then becomes stable or increases very slowly. Some myopes experience another myopic shift in young adulthood.68

The second type is intermediate myopia.7 This form of myopia appears to be very similar to physiological myopia, although the age of onset may be slightly younger and the final amount of myopia tends to be higher. The main difference is that in these eyes the components of refraction do not fall all of within the normal range; the axial length is notably longer. Over time, fundus changes appear, often beginning in childhood. These eyes are at increased risk of developing open-angle glaucoma, retinal detachment, early cataract, and other disorders.

The third major type, and the most devastating, is pathological myopia. In this form, a highly myopic refractive error is often present from early childhood and is usually progressive.7 Increased axial length and fundus changes are evident at the earliest examination. Prognosis is poor, with legal blindness resulting from maculopathy or retinal detachment in almost 50% of eyes.8

High myopia is a term that generally refers to myopia greater than 6 diopters (D). Clinically, eyes may fit into either the intermediate or pathological category because the cause is usually at least partly axial.

The average progression in eyes with physiological or intermediate myopia in childhood is about 0.50 diopters per year.23,29,44,54 Factors associated with increased risk for progression to high degrees of myopia include fundus changes, intraocular pressure greater than 16 mm Hg, and myopia greater than3.00 diopters by 11 years of age.23 A study of children in Hong Kong found that at age 6 and 7 years, children with at least one myopic parent tended to have higher intraocular pressures than children with two non-myopic parents.11 A large study of school children in the United States found that the best predictor of juvenile-onset myopia was a cycloplegic refractive error of less than 0.75 diopters of hyperopia in the third grade (usually 8 years of age).74 Parental history of myopia also plays a role.73

There is evidence from both animal and human studies that accommodation plays a role in the development of myopia.5,51 European and North American studies have repeatedly demonstrated a higher prevalence of myopia in persons with more years of schooling; however, an Asian study failed to find a correlation between type of academic activity and myopia in children.16 A study done in Newfoundland found that near work and years of education were aspects of a common familial environment that could inflate resemblances of refraction among family members thought to be caused by genetics.4

A dramatic increase in the prevalence of myopia in Alaskan Eskimos was noted when compulsory education became mandatory, suggesting that near work was a factor.69 However, other influences, such as artificial lighting and diet changes, could also be influential.

Use of a night light in infants’ bedrooms was found to correlate with development of myopia in one study; however, these data were collected by survey and parental refractive error was not ascertained.50 A study of infant monkeys reared in continu-

ous ambient lighting,58 as well as human studies in the United States20,75 and Asia,56 failed to find a correlation in other patient populations but did find that myopic parents were more likely to use a night light, suggesting a possible heritability bias.

Although isolated myopia is the most common, it is important to remember that there are other etiologies of myopia that are less benign. Myopia may be secondary to congenital glaucoma, or systemic or ocular syndromes, as is discussed later in this chapter. Most myopia is axial, but other types of “component” myopia should always be considered, such as conditions that cause steep corneas (e.g., keratoconus, microcornea, persistent hyperplastic primary vitreous), or round or misshapen lenses (e.g., microspherophakia, ectopia lentis, posterior lenticonus). Conditions that cause deprivation in infancy may also cause myopia, such as complete congenital ptosis or dense vitreous hemorrhage. In animals such as chicks, tree shrews, and monkeys, deprivation by eyelid suture or occluder contact lens induces axial myopia.52

Ciliary spasm and night myopia may coexist with other forms. Ciliary or accommodative spasm may be caused by trauma, central nervous system abnormalities, or psychological issues. Variable esotropia and miosis are usually present. Night myopia is a small myopic shift caused by accommodation that occurs in dim illumination and may neccessitate extra correction for driving. People who have had refractive surgery may also experience decreased night vision; however, this type may be related to larger pupil size, allowing more peripheral, lesscorrected cornea to defocus the image.

CLINICAL FEATURES

Vitreous

Vitreous syneresis occurs at a younger age in myopic eyes than emmetropic eyes. The protein, hyaluronic acid, and collagen concentrations are different,6 and posterior vitreous detachment may occur up to 20 years earlier than in emmetropic eyes.14 Because onset of liquefaction is related to both the age of the patient and the degree of myopia, it may be present in childhood if the amount of myopia is very high. Examination of the vitreous with the slit lamp, 90 D lens, or direct ophthalmoscope reveals linear filaments with nodules or thickenings. In early liquefaction, there

are pockets of fluid within the vitreous gel; later, the fluid portion moves posteriorly, pushing the filaments anteriorly. If there is a posterior vitreous detachment a white ring (Vogt’s) corresponding to the vitreous condensation around the disc may be seen floating in the fluid. Patients perceive these filaments as “floaters”; on occasion dense floating particles may obscure vision.

Several systemic syndromes with vitreoretinopathies have pathognomonic vitreous abnormalities that are different than syneresis (see Chapter 6). The vitreous veils in an otherwise optically empty media seen in these disorders should not be confused with the liquefaction and filaments of isolated myopia.

Fundus

In eyes with physiological (correlation) myopia, the fundus examination is normal. There may be a tiny crescent of 1/10 diameter of the optic disc.7 The cardinal fundus findings in intermediate myopia (Fig. 12-1A–C) are optic nerve crescent formation, tessellation, and “supertraction.”7 The crescent is usually temporal to the disc and may be white, pigmented, or both7, and increases in size as myopia progresses.42 “Supertraction” appears as a rim of heaped choroid and retina slightly overhanging the disc nasally; this may occur with real or apparent tilting of the disc. Because of thinning of the retinal pigment epithelium (RPE) with axial elongation, a tigroid appearance of the fundus may be present; this is most marked in the posterior pole and is referred to as tessellation. It may not be apparent in lightly pigmented individuals. Eyes with crescents, by definition, cannot be considered to have physiological myopia.7 Although the risk of other ocular disorders is higher in these eyes than in normals, most retain good vision throughout life with optical correction.

Peripheral retinal changes such as white without pressure, lattice degeneration (Fig. 12-2), and pavingstone degeneration are found with increased frequency and at a younger age in patients with intermediate and pathological myopia.7,24 Retinal holes or tears may be associated with lattice, and this may explain the increased risk of retinal detachment in myopic eyes.

Pathological myopia is an entity distinct from the physiological and intermediate types already described; it is actually a progressive retinal dystrophy with a relatively poor prognosis for retention of good vision throughout life. The earliest signs occur in infancy or childhood, with a variable amount of myopia associated with a localized area of RPE attenuation (tessellation) in