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Myopia Induced by Vitreous Hemorrhage
Myopia Induced by Vitreous Hemorrhage Mariannette
J. Miller-Meeks, M.D., Stephen R. Bennett, M.D., Ronald V. Keech, M.D., and Christopher F. Blodi, M.D.
Six of 11 children developed myopia in one eye after vitreous hemorrhage. None had retinopathy of prematurity, glaucoma, aphakia, or scleral buckling. In seven children developing vitreous hemorrhage before 1 year of age, six exhibited a myopic anisometropia in the affected eye of 1.37 to 12.00 diopters (mean, -4.7 diopters; S.D., 4.0). The degree of myopia correlated with the age of onset and duration of media opacification. In the child without myopia, the hemorrhage did not obscure the posterior pole. None of the four children whose hemorrhage occurred after 2tf2 years of age showed myopic anisometropia (mean, +0.16 diopters; S.D., 0.24). We conclude that vitreous hemorrhage occurring in infancy is strongly associated with the development of myopia in the affected eye. ALTHOUGH MYOPIA OCCURS in approximately 33% of young adults in the western world,' its cause remains unknown. Although genetic factors have an undisputed role in the course of ocular development, the influence of environmental factors such as nutrition or accommodation are less well established. Recent investigations have suggested that a visually dependent feedback mechanism is necessary for emmetropization. It has been suggested that the deprivation of patterned visual stimulation has myopic effects on the infant eye. More specifically, it has been demonstrated that eyelid suturing of monkeys, tree shrews, cats, and chickens during infancy creates a shift
Accepted for publication Nov. 27, 1989. From the Department of Ophthalmology, University of Iowa, Iowa City, Iowa. This study was presented in part at the annual meeting of the Association for Research in Vision and Ophthalmology, Sarasota, Florida, May 3, 1989. This study was supported in part by an unrestricted grant from Research to Prevent Blindness, Inc., New York, New York. Reprint requests to Christopher F. Blodi, M.D., Department of Ophthalmology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242.
toward myopia in the deprived eye. 2.8 This myopic shift is attributed to an increase in the axial eye length presumably because of a loss of a feedback mechanism involved in the regulation of ocular growth. This phenomenon is not intrinsically related to eyelid suturing, because myopia has been induced in animals visually deprived at an early age by corneal opacification" and by translucent or optical occluders.P'" Additionally, myopia does not occur in monkeys whose eyelids are sutured at a young age but who are raised in the dark," negating the role of absolute deprivation. The relationship between deprivation of patterned visual stimulation and myopia has also been demonstrated in humans by examining the refractive error of patients with unilateral congenital cataracts, corneal opacification, blepharoptosis, and hemangiomas of the upper eyelid in infants.!4.19 It is thus hypothesized that the lack of a clear retinal image acts as a mechanism to deregulate ocular growth during maturation, which leads to myopia presumably because of an increase in axial length. If early visual stimulation is important for ocular development, then any cause of patterned visual deprivation in infancy may result in myopia. After observing an isolated case of severe myopia after neonatal vitreous hemorrhage, we decided to study the possible association of vitreous hemorrhage in childhood and myopia.
Subjects and Methods A list of patients who had a diagnosis of vitreous hemorrhage or who underwent vitrectomy seen in the pediatric eye clinic of our institution was generated by computer. If an additional diagnosis of aphakia, retinopathy of prematurity, glaucoma, or a history of a scleral buckling procedure was identified, these patients were excluded from study. On chart review, patients were also excluded if no record of refractive error was documented. Eleven eli-
©AMERICAN JOURNAL OF OPHTHALMOLOGY 109:199-203, FEBRUARY, 1990
199
200
February, 1990
AMERICAN JOURNAL OF OPHTHALMOLOGY
gible patients were identified. Those with a documented vitreous or preretinal hemorrhage occurring before the age of 1 year underwent a complete ophthalmologic examination, including visual acuity, cycloplegic refraction, indirect ophthalmoscopy, and measurement of corneal diameter. Recording of axial eye lengths by standardized A-scan ultrasonography was attempted; however, because of the young age of our subjects, reliable measurements could only be obtained in three children, and results were suboptimal in another child.
showed normal retinas with the exception of vitreous or preretinal hemorrhages. Patient 5 (Table 1) and the child whose hemorrhage was only in the periphery are the subjects who were premature. The primary causative agent in the children whose onset of hemorrhage occurred after 2V2 years of age was blunt or penetrating trauma (Table 2). Patient 10 was noted to have vitreous hemorrhage after sustaining possible blunt trauma following strabismus surgery. Of those children who acquired a vitreous or preretinal hemorrhage obscuring the posterior pole before the age of 1 year, there was a strong shift toward anisometropic myopia in the affected eye. The median difference, calculated by spherical equivalent, between the affected and unaffected eye was -4.7 diopters (range, -1.37 diopters to -10.75 diopters) (Fig. 1). The patient who had a far peripheral vitreous hemorrhage that did not obscure the posterior pole had +0.75 diopters of anisometropia in the right eye and + 1.00 diopters in the affected left eye. Those children with an acquired vitreous hemorrhage after the age of 2V2 years did not demonstrate any myopic tendency (Table 2). In this group, the median difference was +0.16 diopters (range, plano to +0.50 diopters). The degree of myopia in the affected eye also increased with the duration of media opacification (Fig. 2). Those infants with the greatest degree of anisometropic myopia also had long-
Results
Of the 11 patients included in this study, six (55%) were boys and five (45%) were girls. Six of these patients developed vitreous or preretinal hemorrhages obscuring the posterior pole between birth and 3 months of age (Table 1). An additional child who acquired a vitreous hemorrhage at birth but in whom the hemorrhage location was noted only in the far periphery is excluded from this table. The predominant cause of hemorrhage in the younger age group was birth trauma by forceps delivery or suspected birth trauma. Other sources for hemorrhage in the younger age group include Terson's syndrome and child abuse. Two subjects were premature; however, repeated examinations TABLE 1
ONSET OF HEMORRHAGE BEFORE 1 YEAR OF AGE PATIENT
AGE OF
NO.
ONSET
CAUSE
DURATION
CURRENT
SPHERICAL
CURRENT
AGE AT LAST
(MOS)
REFRACTION
EQUIVALENT
VISUAL ACUITY
FOLLOW-UP (YAS)
RE.: +4.00 L.E.: -8.00 RE.: +0.50 L.E.: -2.25 +0.50 R.E.: -2.50 -2.50
+4.00 -8.00 +0.50 -2.00 -1.25
3.3
L.E.: +2.25 +0.50
+2.50
RE.: -0.50 +0.50 L.E.: -3.00 + 1.50 RE., 4; L.E., 1 R.E.: -3.25 +2.25
-0.25 -2.25 -2.12
L.E.: -1.00 +0.50
-0.75
RE.: +3.50
+3.50
L.E.: -4.00 +1.75
-3.13
20/30 20/10020/30+ 20/30Central, steady, and unmaintained Central, steady, and unmaintained 20/30 20/800 Central, steady, and unmaintained Central, steady, and unmaintained Central, steady, and unmaintained Central, steady, and unmaintained
Birth
Forceps delivery (L.E.)
7
2
Birth
Forceps delivery (RE.)
<3
3
1 mo
Terson's syndrome (RE.)
4
3 mos
Unknown (L.E.)
5
Birth
Birth trauma (RE.>L.E.)
6
2 mos
Child abuse (L.E.)
6
2
7
3.5 3.3
4.0 2.5
2.5
Vol. 109, No.2
201
Myopia Induced by Vitreous Hemorrhage
TABLE 2 VITREOUS HEMORRHAGE ACQUIRED AFTER ONE YEAR OF AGE AGE OF PATIENT
ONSET
NO.
(YRS)
7
2Y2
AGE AT LAST DURATION
CURRENT
SPHERICAL
CURRENT
FOLLOW·UP
CAUSE
(MOS)
REFRACTION
EaUIVALENT
VISUAL ACUITY
(YRS)
Combined hamartoma (L.E.)
2
RE.: -0.25 +0.50 L.E.: +0.50 RE.: +0.50 +1.00 L.E.: +1.00 R.E.: +1.00 +0.75 L.E.: +1.50 R.E.: +0.25 +2.00 L.E.: +0.50 +1.50
Plano
20/20 20/25 20/30 20/15
6
+0.50 +1.00 +1.00 +1.37 +1.50 +1.25 +1.25
8
3
Perforating injury (RE.)
9
2Y2
Blunt trauma (RE.)
10
10
3
Blunt trauma (L.E.)
2
standing vitreous hemorrhage for many months. Those infants with a vitreous hemorrhage of greater than six months' duration had a mean anisometropia of -7.46 diopters compared with only -1.96 diopters in those with a hemorrhage for less than six months. Each child was examined for signs of glaucoma. None of the children demonstrated any significant difference in corneal diameter between the affected and unaffected eye or optic disk abnormalities commonly seen with glaucomatous nerve damage. In three patients, intraocular pressures were obtained and were equal in both eyes. Four children had axial eye length measure-
....c:: e ~
~
0
E
'-'" ~
Q)
e ~
0
c..... 0
Q)
«
CO
Hand motions
20/30 20/40
10 3Y2 12
Counting fingers
ments. Patient 3 (Table 1) displayed no difference in axial eye length measurements; however, both globes at 20.4 mm were smaller than normal for this age (average, 22.4 mm). Patient 5 (Table 1) had axial eye lengths of 22.5 mm in the right eye and 22.3 mm in the left eye. This child had bilateral vitreous hemorrhages, and the right eye, which had a longer-lasting hemorrhage, was the more myopic, and had a slightly longer axial eye length. The child who was hyperopic in both eyes and who had only a far peripheral hemorrhage had an axial length of 20.3 mm in the right eye and 20.7 mm in the left eye, which had a hemorrhage. In one other child, we were able to obtain only suboptimal
120 36 30 24 3 2 1 0 0 0 +2
Fig. 1 (Miller-Meeks and associates). Degree of anisometropia vs the age of onset of the vitreous hemorrhage.
0
-2
-4
-6
-8
-10 -12
Anisometropia (diopters)
202
AMERICAN JOURNAL OF OPHfHALMOLOGY
February, 1990
Fig. 2 (Miller-Meeks and associates). Degree of anisometropia vs the duration of vitreous hemorrhage.
+2
0
-2 -4 -6 -8 -10 -12 Anisometropia (diopters)
axial eye length measurements. Patient 2 (Table 1) had axial eye lengths of 20.7 mm in the right eye and 20.3 mm in the affected left eye, measurements which are slightly shorter than what is recognized as normal for the patient's age. Because these measurements were performed without sedation and by contact probe rather than by immersion, we are unable to comment on the lens dimensions. Three patients underwent vitrectomy for treatment of their vitreous hemorrhages. Although it is possible that the vitrectomy procedure itself contributed to the myopia, it seems unlikely. Patient 1 (Table 1) and Patients 7 and 8 (Table 2) required vitrectomy. Patient 1 developed -12.00 diopters of anisometropia and Patient 7 demonstrated +0.50 diopters of anisometropia, whereas Patient 8 had no anisometropia.
Discussion This study documents the effect of infantile vitreous hemorrhage on the refractive status of the eye. We found a strong association of vitreous hemorrhage that obscured the posterior pole and myopia in the affected eye of infants who were Visually deprived before the age of 1 year. The magnitude of the associated myopia
was also greater depending on the duration of the media opacification. One child whose onset of hemorrhage was at birth but who was hyperopic in both eyes was noted to have a hemorrhage only in the far periphery of the retina. The concept of monocular form deprivation leading to myopia in the affected eye is not new. Our data are consistent with the report by Rabin and Van Sluyters" who found less hyperopia in eyes after surgery for unilateral congenital cataract and marked myopia in eyes with other forms of monocular visual deprivation. Additionally, there appears to be a critical age at which myopia will no longer occur. In our study, those children whose vitreous hemorrhage occurred after 21h years of age did not exhibit a shift in their refractive state. Axial eye length measurements on newborn term infants show a rapid elongation of the eye to 22.01 mm by 10 months of age." and this rapid growth phase correlates well with our observations. It seems plausible that the effects of deprivation would be most detrimental at a stage of rapid growth, thus the youngest patients would be most affected. Our axial eye length measurements did not demonstrate a consistent elongation in the more myopic eye. We cannot discern, therefore, if the myopic shift is purely axial in nature or if there is a lenticular component. It is also recognized that prematurity and low birth weight are associated with an increased
Myopia Induced by Vitreous Hemorrhage
Vol. 109, No.2
incidence of myopia. 21,22 Patient 5 was premature at 32 weeks' gestation and 1,500 g, had bilateral vitreous hemorrhages, and was myopic in both eyes. The eye with the greater duration of media opacification is also the more myopic eye. The child who had a far peripheral retinal hemorrhage and a hyperopic refraction was premature at 34 weeks' gestation and 1,100 g. This does not exclude prematurity as a causative factor, but it does diminish its impact. This study supports the theory that emmetropization is a vision-dependent phenomenon and that early monocular deprivation induces a myopic shift in the affected eye. The possibility that vitreous hemorrhage may act as a mechanism for depriving formed visual stimulation in infants is strongly supported. Once identified, these children need frequent follow-up examinations that include cycloplegic refraction even long after the hemorrhage has resolved. Appropriate spectacle correction and patching therapy should be instituted as the situation mandates. The role of vitrectomy surgery is unclear in the management of infantile vitreous hemorrhage. Vitrectomy, however, should be considered in infants with longstanding vitreous hemorrhage. Sonographic axial eye length measurements may also be warranted to determine the characteristics of the induced myopia.
References 1. Angle, J., and Wissmann, D.: The epidemiology of myopia. Am. J. Epidemiol. 111 :220, 1980. 2. Wiesel, T., and Hubel, D.: Comparison of the effects of unilateral and bilateral eye closure on cortical unit responses in kittens. J. Neurophysiol. 28:1029, 1965.
3. Wiesel, T., and Raviola. E.: Myopia and eye enlargement after neonatal lid fusion in monkeys. Nature 266:66, 1977. 4. Von Noorden, G. K., and Crawford, M. L. J.: Lid closure and refractive error in macaque monkeys. Nature 272:53, 1978. 5. Sherman, S. M., Norton, T. T., and Casagrande, V. A.: Myopia in lid-sutured tree shrew (Tupaia glis). Brain Res. 124:154, 1977.
203
6. Lauber, J. K., and Oishi, T.: Lid suture in chicks. Invest. Ophthalmol. Vis. Sci. 23:135, 1982. 7. Hubel, D. H., and Wiesel, T. N.: The period of susceptibility to physiological effects of unilateral eye closure in kittens. J. Physiol. 206:419, 1970. 8. Smith, E., and Harwerth, R.: Observations on the effects of form deprivation on the refractive status of the monkey. Invest. Ophthalmol. Vis. Sci. 28:1236, 1987.
9. Wiesel, T., and Raviola, E.: Increase in axial length of the macaque monkey eye after corneal opacification. Invest. Ophthalmol. Vis. Sci. 18:1232, 1979. 10. Wallman, J., and Turkel J.: Extreme myopia
produced by modest change in early visual experience. Science 201:1249,1978. 11. Wallman, J., and Gottlieb, M.: Local retinal regions control local eye growth and myopia. Science 237:73,1987. 12. Maguire, G., and Smith, E.: Optically induced
anisometropia in kittens. Invest. Ophthaimoi. Vis. Sci. 23:253, 1982. 13. Raviola, E., and Wiesel, T.: Effect of darkrearing on experimental myopia in monkeys. Invest. Ophthaimoi. Vis. Sci. 17:485, 1978. 14. Rabin, J., and Van Sluyters, R.: Emmetropization. A vision-dependent phenomenon. Invest. Ophthalmol. Vis. Sci. 20:561, 1981. 15. Johnson, c., Post, R., Chalupa, L., and Lee, T.: Monocular deprivation in humans. A study of identical twins. Invest. Ophthalmol. Vis. Sci. 23:135, 1982. 16. Rasooly, R., and BenEzra, D.: Congenital and traumatic cataract. The effect on ocular axial length. Arch. Ophthalmol. 106:1066, 1988. 17. Gee, S., and Tabbara, K.: Increase in ocular axial length in patients with corneal opacification. Ophthalmology 95:1276,1988. 18. Von Noorden, G. K., and Lewis, R.: Ocular axial length in unilateral congenital cataracts and blepharoptosis. Invest. Ophthalmol. Vis. Sci. 28:750, 1987. 19. Hoyt, C. S., Stone, R. D., Fromer,
c.. and Billson, F. A.: Monocular axial myopia associated with neonatal eyelid closure in human infants. Am. J. Ophthalmol. 91:197,1981. 20. Grignola, A., and Rivara, A.: Observations biometriques sur l'oeil des enfants nes terme et des prematures au cours de la premiere annee. Ann. Oculist. 201:817, 1968. 21. Graham, M. V., and Gray, O. P.: Refraction of premature babies' eyes. Br. Med. J. 1:1452, 1963. 22. Curtin, B. S.: The pathogenesis of congenital myopia. Arch. Ophthalmol. 69:60, 1963.
J. Miller-Meeks, M.D., Stephen R. Bennett, M.D., Ronald V. Keech, M.D., and Christopher F. Blodi, M.D.
Six of 11 children developed myopia in one eye after vitreous hemorrhage. None had retinopathy of prematurity, glaucoma, aphakia, or scleral buckling. In seven children developing vitreous hemorrhage before 1 year of age, six exhibited a myopic anisometropia in the affected eye of 1.37 to 12.00 diopters (mean, -4.7 diopters; S.D., 4.0). The degree of myopia correlated with the age of onset and duration of media opacification. In the child without myopia, the hemorrhage did not obscure the posterior pole. None of the four children whose hemorrhage occurred after 2tf2 years of age showed myopic anisometropia (mean, +0.16 diopters; S.D., 0.24). We conclude that vitreous hemorrhage occurring in infancy is strongly associated with the development of myopia in the affected eye. ALTHOUGH MYOPIA OCCURS in approximately 33% of young adults in the western world,' its cause remains unknown. Although genetic factors have an undisputed role in the course of ocular development, the influence of environmental factors such as nutrition or accommodation are less well established. Recent investigations have suggested that a visually dependent feedback mechanism is necessary for emmetropization. It has been suggested that the deprivation of patterned visual stimulation has myopic effects on the infant eye. More specifically, it has been demonstrated that eyelid suturing of monkeys, tree shrews, cats, and chickens during infancy creates a shift
Accepted for publication Nov. 27, 1989. From the Department of Ophthalmology, University of Iowa, Iowa City, Iowa. This study was presented in part at the annual meeting of the Association for Research in Vision and Ophthalmology, Sarasota, Florida, May 3, 1989. This study was supported in part by an unrestricted grant from Research to Prevent Blindness, Inc., New York, New York. Reprint requests to Christopher F. Blodi, M.D., Department of Ophthalmology, University of Iowa Hospitals and Clinics, Iowa City, IA 52242.
toward myopia in the deprived eye. 2.8 This myopic shift is attributed to an increase in the axial eye length presumably because of a loss of a feedback mechanism involved in the regulation of ocular growth. This phenomenon is not intrinsically related to eyelid suturing, because myopia has been induced in animals visually deprived at an early age by corneal opacification" and by translucent or optical occluders.P'" Additionally, myopia does not occur in monkeys whose eyelids are sutured at a young age but who are raised in the dark," negating the role of absolute deprivation. The relationship between deprivation of patterned visual stimulation and myopia has also been demonstrated in humans by examining the refractive error of patients with unilateral congenital cataracts, corneal opacification, blepharoptosis, and hemangiomas of the upper eyelid in infants.!4.19 It is thus hypothesized that the lack of a clear retinal image acts as a mechanism to deregulate ocular growth during maturation, which leads to myopia presumably because of an increase in axial length. If early visual stimulation is important for ocular development, then any cause of patterned visual deprivation in infancy may result in myopia. After observing an isolated case of severe myopia after neonatal vitreous hemorrhage, we decided to study the possible association of vitreous hemorrhage in childhood and myopia.
Subjects and Methods A list of patients who had a diagnosis of vitreous hemorrhage or who underwent vitrectomy seen in the pediatric eye clinic of our institution was generated by computer. If an additional diagnosis of aphakia, retinopathy of prematurity, glaucoma, or a history of a scleral buckling procedure was identified, these patients were excluded from study. On chart review, patients were also excluded if no record of refractive error was documented. Eleven eli-
©AMERICAN JOURNAL OF OPHTHALMOLOGY 109:199-203, FEBRUARY, 1990
199
200
February, 1990
AMERICAN JOURNAL OF OPHTHALMOLOGY
gible patients were identified. Those with a documented vitreous or preretinal hemorrhage occurring before the age of 1 year underwent a complete ophthalmologic examination, including visual acuity, cycloplegic refraction, indirect ophthalmoscopy, and measurement of corneal diameter. Recording of axial eye lengths by standardized A-scan ultrasonography was attempted; however, because of the young age of our subjects, reliable measurements could only be obtained in three children, and results were suboptimal in another child.
showed normal retinas with the exception of vitreous or preretinal hemorrhages. Patient 5 (Table 1) and the child whose hemorrhage was only in the periphery are the subjects who were premature. The primary causative agent in the children whose onset of hemorrhage occurred after 2V2 years of age was blunt or penetrating trauma (Table 2). Patient 10 was noted to have vitreous hemorrhage after sustaining possible blunt trauma following strabismus surgery. Of those children who acquired a vitreous or preretinal hemorrhage obscuring the posterior pole before the age of 1 year, there was a strong shift toward anisometropic myopia in the affected eye. The median difference, calculated by spherical equivalent, between the affected and unaffected eye was -4.7 diopters (range, -1.37 diopters to -10.75 diopters) (Fig. 1). The patient who had a far peripheral vitreous hemorrhage that did not obscure the posterior pole had +0.75 diopters of anisometropia in the right eye and + 1.00 diopters in the affected left eye. Those children with an acquired vitreous hemorrhage after the age of 2V2 years did not demonstrate any myopic tendency (Table 2). In this group, the median difference was +0.16 diopters (range, plano to +0.50 diopters). The degree of myopia in the affected eye also increased with the duration of media opacification (Fig. 2). Those infants with the greatest degree of anisometropic myopia also had long-
Results
Of the 11 patients included in this study, six (55%) were boys and five (45%) were girls. Six of these patients developed vitreous or preretinal hemorrhages obscuring the posterior pole between birth and 3 months of age (Table 1). An additional child who acquired a vitreous hemorrhage at birth but in whom the hemorrhage location was noted only in the far periphery is excluded from this table. The predominant cause of hemorrhage in the younger age group was birth trauma by forceps delivery or suspected birth trauma. Other sources for hemorrhage in the younger age group include Terson's syndrome and child abuse. Two subjects were premature; however, repeated examinations TABLE 1
ONSET OF HEMORRHAGE BEFORE 1 YEAR OF AGE PATIENT
AGE OF
NO.
ONSET
CAUSE
DURATION
CURRENT
SPHERICAL
CURRENT
AGE AT LAST
(MOS)
REFRACTION
EQUIVALENT
VISUAL ACUITY
FOLLOW-UP (YAS)
RE.: +4.00 L.E.: -8.00 RE.: +0.50 L.E.: -2.25 +0.50 R.E.: -2.50 -2.50
+4.00 -8.00 +0.50 -2.00 -1.25
3.3
L.E.: +2.25 +0.50
+2.50
RE.: -0.50 +0.50 L.E.: -3.00 + 1.50 RE., 4; L.E., 1 R.E.: -3.25 +2.25
-0.25 -2.25 -2.12
L.E.: -1.00 +0.50
-0.75
RE.: +3.50
+3.50
L.E.: -4.00 +1.75
-3.13
20/30 20/10020/30+ 20/30Central, steady, and unmaintained Central, steady, and unmaintained 20/30 20/800 Central, steady, and unmaintained Central, steady, and unmaintained Central, steady, and unmaintained Central, steady, and unmaintained
Birth
Forceps delivery (L.E.)
7
2
Birth
Forceps delivery (RE.)
<3
3
1 mo
Terson's syndrome (RE.)
4
3 mos
Unknown (L.E.)
5
Birth
Birth trauma (RE.>L.E.)
6
2 mos
Child abuse (L.E.)
6
2
7
3.5 3.3
4.0 2.5
2.5
Vol. 109, No.2
201
Myopia Induced by Vitreous Hemorrhage
TABLE 2 VITREOUS HEMORRHAGE ACQUIRED AFTER ONE YEAR OF AGE AGE OF PATIENT
ONSET
NO.
(YRS)
7
2Y2
AGE AT LAST DURATION
CURRENT
SPHERICAL
CURRENT
FOLLOW·UP
CAUSE
(MOS)
REFRACTION
EaUIVALENT
VISUAL ACUITY
(YRS)
Combined hamartoma (L.E.)
2
RE.: -0.25 +0.50 L.E.: +0.50 RE.: +0.50 +1.00 L.E.: +1.00 R.E.: +1.00 +0.75 L.E.: +1.50 R.E.: +0.25 +2.00 L.E.: +0.50 +1.50
Plano
20/20 20/25 20/30 20/15
6
+0.50 +1.00 +1.00 +1.37 +1.50 +1.25 +1.25
8
3
Perforating injury (RE.)
9
2Y2
Blunt trauma (RE.)
10
10
3
Blunt trauma (L.E.)
2
standing vitreous hemorrhage for many months. Those infants with a vitreous hemorrhage of greater than six months' duration had a mean anisometropia of -7.46 diopters compared with only -1.96 diopters in those with a hemorrhage for less than six months. Each child was examined for signs of glaucoma. None of the children demonstrated any significant difference in corneal diameter between the affected and unaffected eye or optic disk abnormalities commonly seen with glaucomatous nerve damage. In three patients, intraocular pressures were obtained and were equal in both eyes. Four children had axial eye length measure-
....c:: e ~
~
0
E
'-'" ~
Q)
e ~
0
c..... 0
Q)
«
CO
Hand motions
20/30 20/40
10 3Y2 12
Counting fingers
ments. Patient 3 (Table 1) displayed no difference in axial eye length measurements; however, both globes at 20.4 mm were smaller than normal for this age (average, 22.4 mm). Patient 5 (Table 1) had axial eye lengths of 22.5 mm in the right eye and 22.3 mm in the left eye. This child had bilateral vitreous hemorrhages, and the right eye, which had a longer-lasting hemorrhage, was the more myopic, and had a slightly longer axial eye length. The child who was hyperopic in both eyes and who had only a far peripheral hemorrhage had an axial length of 20.3 mm in the right eye and 20.7 mm in the left eye, which had a hemorrhage. In one other child, we were able to obtain only suboptimal
120 36 30 24 3 2 1 0 0 0 +2
Fig. 1 (Miller-Meeks and associates). Degree of anisometropia vs the age of onset of the vitreous hemorrhage.
0
-2
-4
-6
-8
-10 -12
Anisometropia (diopters)
202
AMERICAN JOURNAL OF OPHfHALMOLOGY
February, 1990
Fig. 2 (Miller-Meeks and associates). Degree of anisometropia vs the duration of vitreous hemorrhage.
+2
0
-2 -4 -6 -8 -10 -12 Anisometropia (diopters)
axial eye length measurements. Patient 2 (Table 1) had axial eye lengths of 20.7 mm in the right eye and 20.3 mm in the affected left eye, measurements which are slightly shorter than what is recognized as normal for the patient's age. Because these measurements were performed without sedation and by contact probe rather than by immersion, we are unable to comment on the lens dimensions. Three patients underwent vitrectomy for treatment of their vitreous hemorrhages. Although it is possible that the vitrectomy procedure itself contributed to the myopia, it seems unlikely. Patient 1 (Table 1) and Patients 7 and 8 (Table 2) required vitrectomy. Patient 1 developed -12.00 diopters of anisometropia and Patient 7 demonstrated +0.50 diopters of anisometropia, whereas Patient 8 had no anisometropia.
Discussion This study documents the effect of infantile vitreous hemorrhage on the refractive status of the eye. We found a strong association of vitreous hemorrhage that obscured the posterior pole and myopia in the affected eye of infants who were Visually deprived before the age of 1 year. The magnitude of the associated myopia
was also greater depending on the duration of the media opacification. One child whose onset of hemorrhage was at birth but who was hyperopic in both eyes was noted to have a hemorrhage only in the far periphery of the retina. The concept of monocular form deprivation leading to myopia in the affected eye is not new. Our data are consistent with the report by Rabin and Van Sluyters" who found less hyperopia in eyes after surgery for unilateral congenital cataract and marked myopia in eyes with other forms of monocular visual deprivation. Additionally, there appears to be a critical age at which myopia will no longer occur. In our study, those children whose vitreous hemorrhage occurred after 21h years of age did not exhibit a shift in their refractive state. Axial eye length measurements on newborn term infants show a rapid elongation of the eye to 22.01 mm by 10 months of age." and this rapid growth phase correlates well with our observations. It seems plausible that the effects of deprivation would be most detrimental at a stage of rapid growth, thus the youngest patients would be most affected. Our axial eye length measurements did not demonstrate a consistent elongation in the more myopic eye. We cannot discern, therefore, if the myopic shift is purely axial in nature or if there is a lenticular component. It is also recognized that prematurity and low birth weight are associated with an increased
Myopia Induced by Vitreous Hemorrhage
Vol. 109, No.2
incidence of myopia. 21,22 Patient 5 was premature at 32 weeks' gestation and 1,500 g, had bilateral vitreous hemorrhages, and was myopic in both eyes. The eye with the greater duration of media opacification is also the more myopic eye. The child who had a far peripheral retinal hemorrhage and a hyperopic refraction was premature at 34 weeks' gestation and 1,100 g. This does not exclude prematurity as a causative factor, but it does diminish its impact. This study supports the theory that emmetropization is a vision-dependent phenomenon and that early monocular deprivation induces a myopic shift in the affected eye. The possibility that vitreous hemorrhage may act as a mechanism for depriving formed visual stimulation in infants is strongly supported. Once identified, these children need frequent follow-up examinations that include cycloplegic refraction even long after the hemorrhage has resolved. Appropriate spectacle correction and patching therapy should be instituted as the situation mandates. The role of vitrectomy surgery is unclear in the management of infantile vitreous hemorrhage. Vitrectomy, however, should be considered in infants with longstanding vitreous hemorrhage. Sonographic axial eye length measurements may also be warranted to determine the characteristics of the induced myopia.
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