Visual rehabilitation in aphakic children encounters major obstacles as a result of amblyopia, especially in monocular cataract patients. Postoperative management problems may interfere with adequate optical treatment in aphakic children wearing contact lenses. At various periods of time, the child might not wear his contact lenses. During that time, amblyopia treatment is withheld and regression of visual acuity may occur.
Implanting an intraocular lens (IOL) provides the child with an optimal permanent correction of the aphakia, thus enabling proper development of the child's visual acuity. Also, in the child with unilateral aphakia, the IOL prevents aniseikonia.
One of the main objections to IOL implantation in children, if not the most important, is the frequent and extreme changes in the child's ocular refraction during his first period of life. It has been a matter of dispute regarding which IOL power the child should receive. Some suggest >'2 that a high-power IOL should be used to achieve emmetropia or slight myopia during the child's first years. However, we still lack data about the child's ocular refraction later in Ufe following the implantation of an IOL, which results in emmetropia at the time of implantation.
Surgical Data of Eight Pseudophakie Infants (10 eyes)
Others have suggested implanting a standard adultpower lens so that the child will be emmetropic later in life.3'5 Dahan and colleagues6 undercorrect their patients because of the anticipated increase in axial length. However, the follow-up time has not been long enough to analyze the changes in the refractive status of the Pseudophakie eyes; therefore, no specific IOL power was suggested. It remains unclear whether emmetropia is preferred during the child's first years of life or later. We present our data in infants where a high-power IOL was implanted, with long-term follow up.
SUBJECTS AND METHODS
Ten eyes in eight infants were operated and followed up for at least 5 years. Clinical estimation of the cataract disturbance to vision was made by using slit lamp examination (opacity blocking at least 3 mm of the lens center) and distortion and blurring of the indirect ophthalmoscopic view of the fundus. All infants underwent extracapsular cataract extraction, posterior capsulotomy and anterior vitrectomy, and an intraocular lens (IOL) implantation.
The surgery was performed by a limbal approach. The lens material was removed using the Anis aspirating cannula (Storz, St. Louis, Mo) with the aid of an anterior chamber maintainer (Katena, Denville, NJ). A posterior capsulotomy and anterior vitrectomy was performed with the Ocutome (Coopervision, Fairport, NY). In infants where it was difficult to maintain a deep anterior chamber with the anterior chamber maintainer, sodium hyaluronate (Healon, Pharmacia, Kalamazoo, MI) was used during IOL implantation. It was our aim to fixate the IOL in the bag, however, we could not be sure it was not placed, at least in some cases, in the sulcus.
Except for cataract, all the infants were otherwise healthy, as they did not suffer from any systemic disease or congenital syndrome. Also, no other ocular syndrome was found. No biometrie calculation of IOL power was used before IOL implantation. Postoperatively, all the children underwent retinoscopy on a regular basis, and eyeglasses were prescribed accordingly. After 3 years of age bifocals were added. Patching of the good eye to treat amblyopia was recommended, although cooperation was poor in some of the children (eyes No. 1, 7, and 8). Postoperative examination of the children was performed every 3 to 6 months.
Age at surgery ranged from 2 months to 3 years. The IOL power implanted was between 27.0 D and 30.0 D in seven eyes, and 19.0 D and 23.0 D in three eyes. The follow-up period was between 5 and 11 years (median; 6.25 years). Seven eyes underwent a second surgery due to secondary cataract or posterior synechia secondary to excessive fibrin reaction in the anterior chamber (Table 1). In children with a high-power IOL, the resultant refraction after 5 to 7 years was between -5.50 and -12.0 D, and in children with lower IOL power refraction after 6 to 11 years, the resultant refraction was between -2.5 and +9.0 D (Table 2). The results were plotted on the graph: refraction (D) versus IOL power (D). Arrangement of these points in a graph (Fig) resulted in a line with a correlation coefficient of 0.885. The crossing point between this line and the X-axis shows the IOL power that may result in emmetropia when the child is older. This point is 23.2 D.
Fig: Linear refraction as function of intraocular lens power after 5 Ito 11 years' follow up (correlation coefficient is 0.885).
The change in refraction during the first 3 years of age for each child is detailed in Table 2. Emmetropization of the eyes was achieved at the following ages: In eyes No. 1 and 2 at younger than 6 months of age; in eye No. 4 at 12 months of age; in eye No. 7 at 2 years of age. Visual acuity ranged from 6/6 to 6/60. Good visual acuity (better than 6/12) was achieved in eyes No. 3, 5 and 7 (Table 2).
Studies show7 that emmetropization of the developing eye is dependent on normal visual stimulation during ocular development. Disruption of pattern vision early in life may result in myopia.6 In that study, it was also demonstrated that in aphakic patients a shift toward myopia was found in congenital cataract patients as compared with juvenile cataract patients.6 This fact also emphasizes the role of clear vision early in life on the development of normal refraction of the eye. Implanting an IOL would provide the developing eye with better conditions for emmetropization.
Implanting IOLs in infants propounds a dilemma: what IOL power should be implanted? Calculation of IOL power according to the ocular axial lens and corneal curvature is accurate and definite in adults. In contrast, in young children, a change in the refractive state of the eye is induced by the growth of the eye. Thus, implanting IOLs in infants results in only a temporary refractive state. Therefore, the decision regarding which IOL power to implant in a baby's eye is, to a certain degree, an arbitrary one. One cannot rely on the ocular biometrie parameters, because they will certainly change later in Ufe.
The main reason for early implantation of IOLs is to provide infants with an optimal visual acuity during the first 2 years of Ufe, which are of the utmost importance for vision development. The first 2 years of life constitute the main part of the critical period of vision development in humans.8 This creates an urgent need for achieving the best quality aphakic correction feasible during this period of time. Therefore, most of our children had a high power IOL implanted. Those children were emmetropic or mildly myopic during their first years of life.
Emmetropization of eyes No. 3 and 7 of our series, which developed good vision, occurred between 1 and 2 years of age. Emmetropia at that young age might have had a beneficial effect on the development of visual acuity. However, eyes No. 4 and 6 were also emmetropic at that young age, and visual acuity remained only 6/60 in those eyes. The number of eyes is too small for statistical analysis, therefore, we cannot conclude from the data whether emmetropization at that young age is crucial for visual development.
A relatively high rate of additional surgery was needed in our patients. In our opinion, this could have resulted from the implantation of an IOL. The posterior surface of the IOL may act as a site that is amenable to epitheUal cell proUferation.
In animals, anomalous patterned visual experience is considered to be a relevant factor for producing myopia experimentally. Various methods of attenuating patterned vision have been shown to induce myopia in a variety of animals.913 von Noorden and Lewis14 demonstrated that visual deprivation results in an elongated antero-posterior axis of the eye in monkeys; however, human outcome was less predictable. The axis was longer in most eyes, but shorter or unchanged in others.
Eye elongation due to visual deprivation is related to amblyopia and poor vision, but not to aphakia.18 This points to a possible role of visual perception modulating eye growth during infancy. However, two studies show that there is no significant difference in postoperative increase in axial length in phakic versus aphakic or Pseudophakie eyes in children,1617 Our results also do not support the theory of IOL-induced emmetropization with the potential for a clear retinal image being provided with IOL implantation. Ocular growth is probably regulated and maintained according to its genetic predetermined course.
During follow up, we found that implanting a highpower IOL (between 27.0 D and 30.0 D) results in high myopia (between -5.5 D and -12.0 D) after 5 to 7 years. On the other hand, implanting a lower power IOL (19.0 D to 23.0 D) results, after 6 to 11 years, in low myopia or hypermetropia. The results indicated that implanting a +23.2 D IOL and using it even at a very young age will result in an older child or adult with emmetropia. This choice may be preferred, because it avoids high refractive errors in adulthood. In our next series of patients, we are using 23.0 D IOLs. This will, however, necessitate additional refractive correction during the first years of the child's Ufe. This refractive error will diminish as the child grows older. A comparison between the visual acuity and rate of amblyopia in these two groups, such as children with high power IOLs and those with 23.0 D IOLs, will indicate to us which IOL power is preferable for implantation in infants.
Refraction and Visual Acuity in Eight Pseudophakic Infants (10 eyes)
Although no definite postoperative follow up was mentioned, a myopic shift was also found in Pseudophakie children.4 Gimbel and colleagues4 found a mean spherical equivalent of -2.45 D in the younger age group (4.7 years at surgery), as compared with -0.76 D in the older group of patients (8.4 years at surgery). In the normal infant, mild hypermetropia is usually present. The hypermetropia does not change, or slightly increases, in the first 6 or 7 years of life.18 This results from simultaneous and compensatory changes in the ocular axial length, lens power, and corneal curvature.
It was shown that the mean lens power in the full-term newborn eye is 34.4 D, which changes to about 19.0 D by age 7.19 In the Pseudophakie young infant, the eye growth- as well as corneal changes- are genetically controlled, in the presence of a fixed power aphakic correction. As a result of it, implanting a high power IOL (28.0 to 30.0 D) in the first few months of life creates emmetropia or mild myopia during their first 2 years of Ufe, and high myopia after 6 or 7 years (Table 2). Our results show that implanting an IOL with the power of 27 D to 30 D between 2 months and 3 years of age causes very high myopia (mean -8.25 D) at age 5 to 9.
According to the resultant refractions in 10 eyes, a line was drawn (correlation coefficient of 0.885). The cut point of this Une with the X-axis (Fig) indicates the lens power required to achieve emmetropia later in the child's Ufe. This cut point is 23.2 D. In this case, hypermetropic correction would be necessary during the first years of the child's life. Gordon and colleagues19 reached the same conclusion by analyzing direct measurements and data obtained in 148 normal eyes. They recommended that a 23- D to 24-D IOL should be used to create emmetropia in the adult Pseudophakie patient.
Preoperative keratometry and axial length measurements should be taken, and if the biometrie analysis falls within the age-matched normal limite, a 23-D IOL is recommended. If the measurement falls outside the normal physiological range, adjustment of the IOL power should be considered. Because of the large range of myopic shift over time in our patients (between 2.5 D and 12 D), implanting a 23-D IOL does not guarantee emmetropia in the future. However, based on the results of this series, it is the nearest estimation that can be achieved.
1 Aron JJ, Aron-Rosa D. Intraocular lens implantation in unilateral congenital cataract: a preliminary report. J Am Intraocular Implant Soc. 1983;9:306-308.
2. BenEzra D, Paez JH. Congenital cataract and intraocular lenses. Am J Ophthalmol. 1983;96:311-314.
3. Hiles DA. Intraocular lens implantation in children with monocular cataracts, 1974-1983. Ophthalmology. 1984;91:1231-1237.
4. Gimbel HV, Ferensowicz M, Raanan M, De-Luca M. Implantation in children. J Pediatr Ophthalmol Strabismus. 1993;30:69-79.
5. Burke JP, Willshaw HE, Young JDH. Intraocular lens implants for uniocular cataracts in childhood. J3r J Ophthalmol. 1989;73:860-864.
6. Dahan E, Welsh NH, Salmenson BD. Posterior chamber implants in unilateral congenital and developmental cataracts. Eur J Implant Refract Surg. 1990;2:295-302.
7. Rabin J, Van Sluyters RC, Malach R. Emmetropization: a vision-dependent phenomenon. Invest Ophthalmol Vis Sci. 1981;20:561-564.
8. Vaegan J, Taylor D. Criticai period for deprivation amblyopia in children. Trans Ophthal Soc UK. 1979;99:432-439.
9. Wiesel TN, Raviola E. Myopia and eye enlargement after neonatal lid fusion in monkeys. Nature. 1977;266:66-67.
10. Sherman SM, Norton TT, Casagrande VA. Myopia in the lidsutured tree shrew (Tupaia glis). Brain Res. 1977;124:154157.
11. Wilson JR, Sherman SM. Differential effects of early monocular deprivation on binocular and monocular segments of cat striate cortex. J Neurophysiol. 1977;40:891-903.
12. Wallman J, Türkei J, Trachtman J. Extreme myopia produced by modest change in early visual experience. Science. 1978;201:1249-1251.
13. Wiesel TN, Raviola E. Increase in axial length of the macaque monkey after corneal opacification. Invest Ophthalmol Vis Sci. 1979;18:1232-1236.
14. von Noorden GK, Lewis RA. Ocular axial length in unilateral congenital cataract and blepharoptosis. Invest Ophthalmol Vis Sci. 1987;28:750-752.
15. Rasoohy R, BenEzra D. Congenital and traumatic cataract. The effect on ocular axial length. ArcA Ophthalmol. 1988;106:1066-1068.
16. Kova Y, Shimizu K, Inatani M, Fukado Y, Ozana T. Eye growth after cataract extraction and intraocular lens implantation in children. Ophthalmic Surg. 1993;24:467-475.
17. Niederreiter P. Kiemen TJM, Leitner J. Zur ultrashall-biometrie in kindesalter (Ultrasound biometry in children). Klin Monatsb Augenheilkd. 1987;191: 355-357.
18. Duke-Elder S. System of Ophthalmology. London, England:Henry Kimpton; 1970:229.
19. Gordon RA, Donzis PB. Refractive development of the human eye. Arch Ophthalmol. 1985;103:785-789.
Surgical Data of Eight Pseudophakie Infants (10 eyes)
Refraction and Visual Acuity in Eight Pseudophakic Infants (10 eyes)