The axial length of the globe increases in a direct relationship with age until approximately 8 years old with a stronger correlation for hyperopes as compared to myopes [14]. The eyeball increases 2.86–3.25 fold between birth and adulthood [1, 15]. The most rapid portion of this growth occurs in the first 40 weeks of postnatal life [16]. Stafford and coworkers found the maximum axial length at term, as measured by ultrasound (A scan), to be 18.6 mm with a mean of 17.0 ± 0.65 standard deviation [17]. Other authors have found similar values [16]. Formulas are available for more detailed analysis of the ocular growth patterns [16]. Axial growth of the eye occurs in three phases: from birth to 18 months a rapid period from mean of 16 to 20.3 mm; a 1.1 mm increase between years 2 and 5; and 1.3 mm of growth thereafter leveling off at age 13 [18].

At birth, the mean saggital, transverse, and vertical diameters of the globe are 17.5, 17.1, and 16.5 mm respectively representing approximately 71 % of the adult equivalents [1]. The anterior segment of the infant globe is roughly 75–80 % that of adults. The posterior segment is less than half of the average adult. The total sclera surface in infants averages 822 mm² which is about 1/3 that of the average adult [19]. Therefore, a majority of the change in globe size stems from the expansion of sclera surface in the posterior segment with 50 % of growth occurring in the first 6 months of life, reaching adult averages at around 13 years [19].

Through childhood, the ocular volume increases about 300 %; from 2.5 to 7.5 cm³ [20]. Hahn and Chu performed a study showing ocular volume measured by CT scan and found that rapid eye growth occurs during the first 24 months of life and peaks between the ages of 18 and 24 years old [21]. Figure 1.1 illustrates these findings [21].

The refractive error of the eye may be measured by a variety of techniques. It is standard to use some form of cycloplegic retinoscopy in children. As the differences in the absolute level of cycloplegia which is obtained through various cycloplegic regimens is small, we will discuss the development of refractive error in the normal infant based on the reported values obtained through various cycloplegic regimens as if they were equal. However, retinoscopy in infants and young children without the use of cycloplegia may be prone to significant error. Data collected under these circumstances will not be included. Likewise, the definition of amblyopia may vary between authors. We have chosen as our definition a two line difference between each eye based on projected acuity charts, visual acuity in an eye with 6/9 acuity or worse, or any other objective test result (e.g. visual evoked potential, preferential looking) which indicates an equivalently significant difference between the eyes.

In general, there is a trend towards emmetropia throughout early childhood regardless of the initial refractive error [22]. The main changes towards emmetropia occur in the first 2 years [23, 24]. Further studies have shown that hyperopia decreases with age along with astigmatism found in infants. In a prospective study on childhood myopia ranging from −0.25D to −3.50 diopters, Ehrlich and coworkers showed that emmetropization was found to occur by 3 years old. The rate of change in myopia from age 8.5 to 38.5 months occurred at a relatively constant rate of +0.44 diopters per year [25]. Ultimately, emmetropization occurs through a combination of passive and active means. Passive means include a growth in axial length, reduction in the power of the lens, a mild reduction in power of the cornea as the radius lengthens and a lengthening of the anterior chamber [26]. The active component relies on the feedback given by the image clarity of the retina, for which the exact mechanism is unclear [27].

In 88.5 % of children, there is no significant difference between the spherical equivalent of the right and left eye [28]. One group found only 1 % of 519 children less than 48 months old to have anisometropia [29]. This group also established 99th percentile curves for normal refraction. They found the range to decrease with age, staying fairly stable after the first year. In a cross-sectional study of healthy children under the age of 5 years old, Kuo and coworkers showed that 95 % of the children had less than 1.50 D of anisometropia [24]. Deng and Gwiazda measured refractive error in children ages 6 months (n = 1120), 5 years (n = 395) and 12–15 years (n = 312) and found the mean difference in refraction between the two eyes was similar at 6, 14 months (0.11 D) and 5 years (0.15 D), increasing to 0.28 D at 12–15 years [30]. The prevalence of <1.00 D of spherical equivalent anisometropia , was 1.96 %, 1.27 %, and 5.77 % respectively [30]. Infants with significant astigmatism (≥1.00 D) in one or both eyes have an increased risk of anisometropia (p < 0.05) [30].

Over the first 3 years of life, the average spherical equivalent in normal children is −0.75 to +3.00 diopters [28, 31]. Only 7–8 % will have hyperopia (farsightedness) in excess of 2.75 diopters during this time period [28, 32] with only 2 % having greater than 4.00 diopters of hyperopia in the steepest meridian [32]. Those who have greater than 4 diopters of hyperopia at 6 months and stay hyperopic thereafter, have a very high risk of developing accommodative esotropia particularly if there is a family history of strabismus [23]. Kuo and coworkers found that greater than 95 % of children less than 5 years old had less than +3.25 diopters of hyperopia [24]. One cross sectional study involving almost 10,000 children analyzed risk factors for hyperopia and found that children whose parents had health insurance and a history of maternal smoking during pregancy were more likely to be hyperopic [33]. The relationship between hyperopia and maternal smoking appears to be linear and dose dependent with a 6 % higher prevalence of hyperopia for every increase of 10 pack-months of maternal smoking [33]. There was an unexpected higher prevalence of hyperopia in 6 year old children as compared to 1–3 year olds [33]. African-American children are significantly less at risk for hyperopia than non-Hispanic or Hispanic children [33].

Myopia (nearsightedness) is unusual in the first year of life. In the first 4 years, only 3 % of children are myopic with the incidence of myopia being less than 2 % by the age of 5 years old [29, 34]. Approximately 17 % of children will have up to 4 diopters of myopia with less than 0.5 % having more [32]. Unlike hyperopia , the prevalence of myopia is greater in children 4–6 years of age compared to those 3 years and younger [33]. Racial predilection for myopia is strongest in African-American and Hispanic children when compared to non-Hispanic white children [33]. There are two main theories regarding the development of myopia including the increased demand for near work theory and genetic disposition theory [26]. The near work theory is supported by the higher prevalence of myopia in populations with higher education levels and increased near demands [35, 36]. The genetic theory is supported both by the increased prevalence of myopia in monozygotic twins and increased prevalence of myopia in children with myopic parents [37, 38].

Most authors have found that the incidence of astigmatism is much higher in young children than in adults [28]. In the first year of life, 19 % of children will have astigmatism [28]. Myopic infants have larger astigmatism which decreases with age [25]. The incidence of astigmatism peaks at approximately 25 % between the ages of 7 to 12 months [28]. Over the first 4 years of life the incidence is still 25 % [29]. Against the rule cylinder is more common than with the rule or oblique axes (56, 29, and 14 % respectively) [29]. One group found that oblique cylinder was always a mirror image axes in the two eyes [29]. The incidence and amount of astigmatism gradually decreases after the first year [28, 32] and may even decrease after the first 4 months [29]. In fact, astigmatism in excess of 3.00 diopters is uncommon prior to 10 months or beyond 2 years [28]. Only 5.7 % of children will experience astigmatism greater than 2 diopters in the first 3 years of life [28]. The axis of astigmatism is predominately (70–90 %) against-the-rule (plus cylinder at axis 180° ± 15) [22, 28]. With-the-rule astigmatism (plus cylinder at axis 90° ± 15) represents 6–20 % of astigmatism [22, 28]. Oblique astigmatism is the least common and accounts for only 3–8 % of astigmatism in normal children [22, 28]. The axis of the two eyes is almost always symmetrical [22]. The amount of astigmatism tends to lessen in the first 4 years of life, increasing in only 10 % of patients [22]. The etiology of astigmatism in children is unknown however, like hyperopia , maternal smoking during pregnancy was found to be a risk factor. Hispanic and African American race, hyperopia and myopia are all associated with higher incident of astigmatism [39]. Children with astigmatism are more likely to come from families that have an income of <$20,000 per year and lack vision insurance [39]. The risk for amblyopia in patients with astigmatism as the only variable is only approximately 3 % although this risk may be as high as 35 % in those children with increasing astigmatism in the first 4 years of life [22]. The risk of amblyopia may also be higher for patients with oblique axis or higher hyperopic spherical equivalents [22].

At birth tear production is very close to adult levels with premature infants having a lower rate of both basal and reflex tearing [40]. As measured by Schirmer for 5 min with and without topical anesthetic respectively, the mean basal tear secretion is 6.2 ± 4.5 mm and 7.4 ± 4.8 mm for a cohort of preterm infants between 25.4–37 weeks gestation and 583–2700 g whereas for term infants the rates were 9.2 ± 4.3 and 13.2 ± 6.5 [40]. In both groups, the secretion rate was directly proportional to weight. In term infants, total tear secretion significantly increased at both 2 and 4 weeks old while in preterm infants a significant increase in tear production occurred at 4 weeks [41].

When the lids are closed, the puncta are located 6 mm lateral to the inner canthus and sit on a mound known as the lacrimal papillae [42]. Upon opening of the lids, the upper punctum shifts 0.5 mm nasal to the lower punctum [42]. The diameter of the punctum is between 0.2–0.3 mm [42]. The puncta are normally located medial to the nasal limbus positioned against the globe in primary position [43].

The proximal nasolacrimal system is normally patent at birth following the normal separation of the eyelids at 7 months gestation, followed by canalization at the level of the punctum [44]. It has been shown that the last part of the duct to canalize during development is the valve of Hasner [45]. Incidence of congenital nasolacrimal duct obstruction was found to be 73 % in a study reviewing stillbirth fetuses with all obstructions being secondary to a mucous membrane at the level of the inferior meatus [46]. The duct enters the nose within the inferior meatus under the inferior turbinate 2.5 cm posterior to the naris and is approximately 5 mm in length [42].

It should be noted that in children there can be variations in the distance within the nasolacrimal system secondary to immaturity. In children, typically the distance between the canaliculus and nasal floor is 20 mm with adult measurements being between 30–40 mm [42].

The corneal endothelium in infancy has a regular mosaic pattern of small hexagonal cells although there may be some smaller or larger cells and cells with an increased number of sides [47]. Twinning cells may also be seen [47]. Cell population density (CPD ) ranges from 2987 to 5624 (mean 4252) cells/mm² in babies less than 1 year of age without a general pattern of decline over that year [47]. However, infants with more than 5000 cells/mm² tend to be less than 2 months old [47]. The calculated endothelial surface area changes from 91.9 to 129.8 mm² from birth to 1 year of age with an assumed constant growth rate of 3.16 mm²/month [47]. Rather than loss of cells, the endothelial cells spread over this increasing area which may have led some observers to note a decline in CPD [47]. Clinically, some infant corneas show non-inflammatory retrocorneal particles on the endothelium which may represent dividing cells [47].

The cornea is steeper at birth with progressive flattening towards adult values in the first months of life. At birth, Inagaki found the mean keratometer reading to be 47.00 ± 1.19 diopters (range 45.69–49.06) [31]. By 1 and 3 months of age the cornea has flattened to 46 ± 2.15 and 44 ± 1.70 diopters respectively [31]. Isenberg and coworkers found the mean central corneal power to be 48.5 diopters (range 41.4–56.0) at birth decreasing to 43.0 diopters (range 41.3–43.1) [48]. It has been hypothesized that this relatively rapid change occurs to offset the increase in axial length which is occurring the same time therefore resulting in stabilization of the infant’s refraction [31].

The mean horizontal diameter of the term newborn cornea is 10.0 mm with a thickness of 0.8 [1]. Stafford and coworkers recorded a slightly smaller mean corneal diameter of 9.55 ± 0.5 standard deviation at term [17]. By adulthood, the diameter will have increased to a mean of 12.5 [20]. The thickness is almost 90 % of adult thickness at birth [1].

The tactile cornea reflex is present in at least one eye in only 10 % of babies at 2 days of age [49]. This increases to 25 % at 1 week, 50 % at 3.5 weeks, 75 % at 6 weeks, and 100 % by 3 months [49]. Postpartum age is more important in the development of this reflex than gestational age [49]. Birth weight also has a significant positive correlation [49]. This is particularly relevant to corneal protection only if one considers the developments of the Bell’s phenomenon: 36 % at 1–3 days old, 50 % at 4–8 weeks, and 100 % by 4 months [49]. The corneal reflex is developing more rapidly.

Portellinha and coworkers examined 74 newborn infants and found that the mean central corneal thickness and mean peripheral corneal thickness was 0.573 ± 0.052 mm and 0.650 ± 0.062 mm respectively [50]. Remon and coworkers showed an average central corneal thickness of 0.585 ±0.052 mm in 152 one day old infants. They also measured superior, inferior, nasal and temporal peripheral corneal thickness (Table 1.2) finding measurements of 0.696 ± 0.055 mm, 0.744 ± 0.062 mm, 0.742 ± 0.58 mm, and 0.748 ± 0.055 mm respectively [51]. Both studies found the corneal measurements during the first day of life to be significantly higher than the following days of life [50, 51]. They failed to find any difference between sex, gestational age, type of delivery or right and left eyes [50].

Lopez and coworkers found an average CCT in children 8 months- to 6 years old of 0.558 mm (0.489–0.614 mm) and for ages 6–17 years 0.560 mm (0.467–0.662) [52]. They failed to find any significant association between CCT and age [52]. Ehlers and coworkers found that central corneal thickness reaches adult measurements around 3 years of age [53]. They found an average CCT measurement in children ages 2–4 years old to be 520 ± 0.007 μm and ages 5–9 to be 520 ± 0.005 μm [53].

A recent review of the genetics of central corneal thickness looked at the four published studies of the heritability of central corneal thickness including twin and family pedigrees which shows that CCT is one of the most highly heritable human traits with tremendous variation amongst different ethnic groups [54]. While there is strong evidence that central corneal thickness is genetically driven, no genes have been identified to date [54].

Corneal hysteresis is the difference in the pressure required to flatten the cornea and the force at which the cornea becomes flat again which is a direct measurement of the biomechanical properties of the cornea [55]. Kirwan and coworkers studied 91 normal eyes of 42 children and found mean corneal hysteresis of 12.5 mmHg. There was no correlation between age and corneal hysteresis [56]. In a separate study, Kirwan found the average adult hysteresis was 10.8 ± 1.5 mmHg indicating corneal hysteresis reduces with age from childhood to adulthood [57]. Ortiz et al. found a mean corneal hysteresis of 10.8 ± 1.5 mmHg in 165 eyes and found hysteresis to be lower in older eyes with the difference between the younger group (9–34 years) and oldest group (60–80 years) to be statistically significant [58]. Lim and colleagues noted that in a study of 257 healthy patients (age 13.97 ± 0.9 years) in the Singapore Cohort Study, that corneal hysteresis (11.80 + 1.55 mmHg) and corneal resistance factor (11.83 + 1.72 mmHg) are associated with narrower retinal arterioles [59].

Although the newborn anterior chamber often appears relatively shallow, the depth is almost 75 % of adult values [1]. Kobayashi and coworkers evaluated the anterior chamber of 46 infants age 1–60 months and showed average anterior chamber depth was 1.724–3.743 mm with depth increasing linearly with age [60]. The iridocorneal angle is almost completely developed at birth although some further recession will gradually take place such that the infant’s ciliary body is less visible on gonioscopy than an adults [61]. Kobayashi and coworkers showed the trabecular-iris angle in infants from 1 to 60 months of age ranged from 15.35 to 44.79° and increases in angle size correlated positively with an increase in age [60].

The normal insertion of the iris and ciliary body at birth is at the level of the scleral spur. As the first year of life progresses, a posterior migration occurs forming the angle recess. Additionally, the endothelium that lines the angle becomes fenestrated while an endothelial layer of cells migrates into the underlying uveal meshwork [62]. The uveal and trabecular meshwork are relatively transparent at birth, becoming more pigmented through the first year of life [63]. While iris processes are rarely present , they are either faintly pigmented or nonpigmented [64]. The trabecular meshwork has been described as a “moist,” transparent membrane and appears somewhat translucent [65]. The peripheral iris appears to be more flat and thin than seen in adults [62]. By 1 year old, the trabecular development is complete [64–66].

Stafford and coworkers found a mean IOP of 15.2 ± 3.4 at term [17]. Giles produced higher values while using a Schiotz tonometer to measure intraocular pressures in 32 babies less than 1 h old and found the pressure approaches the upper limit of adult normal levels with 25.8 mmHg used as the upper limit of normal [67]. Six infants exceeded this level while none had measurements exceeding 30.4 mmHg [67]. Radtke and Cohan used a Perkins tonometer on 60 infants between 19 and 173 h of age and found a mean IOP of 11.4 + 2.4 mmHg (range 6–17) [68, 69]. A summary of other studies of infant intraocular pressures can be found in Table 1.3 [68, 70–74].

By the second decade, there is no significant difference between mean IOP in the sitting (16 ± 2.4 mmHg) or supine (17 ± 2.3 mmHg) position as compared to adults over 20 years [75]. Values for tonometric readings by sex and age found by Pensiero and colleagues [76] using the noncontact Keeler Pulsair tonometer and Youn and colleagues [77] using the Perkins tonometer can be found in Fig. 1.2.

These findings were used to break the increase in intraocular pressure in children into three groups. First, the neonatal phase with average value of 9.59 + 2.3 mm followed by an exponential phase up to age 7–8 years and finishing with a gradual steadying of eye pressures until the 16th year of life [76]. Jaafar and Kazi utilized regression analysis to show IOP of children and adults are equal using Perkins tonometry by age 12 [78]. Using Perkins tonometry, IOP increases gradually from infants (4.55 + 0.51 mmHg age 0–1 year) to children (7.85 + 1.27 mmHg by age 4–5 years) to adults (13.21 + 2.11 mmHg) however, there was no statistically significant different when measuring IOP with pneumotonometry [78]. Sihota and colleagues also noted in their study of 810 eyes in 405 patients ranging in age from 0 to 12 years that IOP reached adults levels by age 12 and found that IOP correlated directly with refraction (r = 0.69) and pachymetry (r = 0.39) and inversely with axial length (r = −0.1) [79].

Normal values may depend on the measurement method. One group found that the normal values using Goldmann applanation tonometry on children less than 10 years old followed the formula IOP = (0.71 × age in years) + 10 whereas the linear fit worsened after the first decade when the mean IOP was 14.6 ± 3.3 [80]. Using pneumotonometry, the same authors found no age related effects with a mean IOP of 16.8 − 3. They showed that for all ages the IOP by Goldmann was approximately equal to 1 + (pneumotonometer × 0.78). After 10 years a more accurate estimation was IOP by Goldmann = (0.94 × pneumotonometer value) − 1.2. Under general anesthesia (agent not specified) they found that readings by Perkins tonometer = 2.6 log (age) + pneumatonometer value − 10.3. Percentile charts are available in their paper. They conclude that normal adult values for IOP are reached by 10 years of age. Below this age they theorize that the lower measured values are actually artifacts due to the difference in ocular wall rigidity. Johnson and collegues showed that intraocular pressures are significantly lower when succinyl choline is used during induction which is thought to be related to a temporary increase in outflow [81].

Other options for intraocular pressure measurements include the Tono-Pen^® and ICare^® rebound tonometer. In a study of 39 children ages 3–18 months old using the ICare tonometer, the average intraocular pressure was 11.82 ± 2.67 mm with a median value of 10 mmHg with a range of 7.3–17.0 mmHg [82]. Bordon and coworkers compared IOP in children with several different methods and concluded that the Tono-Pen is reliable in children as there was no statistically significance compared to Perkins (P > .05) [83]. When evaluating the Schiötz measurements it was shown these values were significantly higher than those obtained with the Perkins and the Tono-pen tonometers (P < .05). Schiötz is an undesirable method for measuring IOP in children [83].

The pupillary size of newborns and infants is generally smaller than that of adults [84]. Average pupil sizes in neonates of 3.8 ± 0.8 mm with a range of 1.5–6 mm have been reported [84]. Wilmer and Scammon calculated that the mean pupillary size of neonates was 70 % of adult size [1]. Pupil size is significantly larger in the presence of a blue iris (4.07 ± 0.92) as compared to neonates with brown irides (3.64 ± 0.74) [84]. There are several factors that have been proposed to account for the smaller pupil in an infant. These include smaller anterior segment dimensions, loss of central inhibitory impulses to the oculomotor nucleus in a more constant state of sleep and a poorly developed iris dilator muscle [85–87]. In addition, pupil size may also be affected by the presence of quality of fixation, refractive error , amblyopia , and strabismus [6].

A difference of greater than 0.4 mm between the two eyes is a common finding in the normal population. At birth, 21 % of term neonates demonstrate physiologic anisocoria [84]. There is no significant change in this rate based on iris color [84]. Roarty found that no term neonate had anisocoria of greater than 1.2 mm and 97 % of babies with anisocoria had less than 1 mm difference between their two eyes [84].

The red reflex is one of the most important screening techniques for neonates and infants as it may reveal the presence of abnormalities along the visual axis, pupillary abnormalities, refractive errors, or strabismus [6]. When normal fixation and focusing occurs, the red reflex darkens to a dull homogeneous orange red color [6]. In neonates who fixate but do not accommodate properly (see above), the reflex will appear brilliant yellow or almost white [6]. A thin circle may also be seen normally within the red reflex [6]. However, if the reflex is not homogeneous or particularly when it is asymmetric between the two eyes, further investigation is warranted. A black or comparatively darkened reflex may indicate obstruction of the visual axis or ocular misalignment. Abnormal comparative unilateral “brightening” may be a sign of reduced visual acuity in that eye [6].

Isenberg and coworkers found that pupillary response was consistently present in 99 % of the infants studied if gestational age was >31 weeks [86]. In the full term neonate, convergence is variable with accurate and maintained convergence becoming well developed by 2–3 months old [88]. The appearance of the direct and consensual light reflexes occurs 30 weeks after conception [89].

In general, the newborn iris is paler than in older children [90]. At birth, when not controlled for race, 39 % of babies have blue irides with the remainder having brown irides [84]. In more darkly pigmented races, the iris has a darker appearance at birth due to a greater number of stromal melanocytes [90]. In all races, the iris darkens during the first 6 months of life due to increasing maturation of melanocytes [90]. Lighter colored irides may appear more vascular in the neonatal period [90]. The Louisville twin study evaluated eye color in monozygotic and dizygotic twins and showed that by 6 years of age, most individuals achieve stable eye color. They did find a subpopulation of 10–15 % of Caucasian subjects who continue to have changes in eye color throughout adolescence and adulthood thought to reflect changes in melanin content or distribution [91]. The study further illustrated the genetic influence on iris color as concordance was high (90 %) among monozygotic twins and declined among dizygotic twins from 80 % at 3 months old to 50 % by 6 years old [91].

Iris crypts are not fully developed at birth [90]. Although this process continues for several months after birth, little maturation occurs in the first 2 weeks of life [90]. Although Purtscher originally felt otherwise, there appears to be no difference in crypt development related to iris color [90]. One group of researchers found that iris vascularity and crypt development were greater in males [90]. The infant iris is flatter and thinner than the average adult. Iris thickness evaluated at the thickest part of the iris measured 249–579 μm in infants age 1–60 months and correlated positively with age [60].

At birth, the horizontal lens diameter is approximately 6 mm and continues to progress as illustrated in Fig. 1.3 [20, 92, 93]. The period of most rapid growth occurs in the first 2 years of life with moderate growth until age 4 and only a small amount of growth after age 5 [92]. The adolescent lens, with a diameter of 9–9.5 mm, is not yet at the same diameter of the adult lens which keeps increasing well into the final decades of life with an associated decrease in anterior lens curvature [94]. As the lens gets bigger, the distance between the lens edge and the ciliary sulcus decreases [94].

The thickness of the human lens has been measured in numerous studies and found to be 3.5–6.5 mm in the newborn, and 3.73–4.6 mm at 20–40 years old [95]. Using ultrasound, Larsen evaluated lens thickness from birth until puberty and found that the mean thickness of the lens decreases by 0.3 mm in the first year of life then by another 0.2 mm per year until leveling off at 8–10 years old [18].

The lens capsule remodels throughout life as the volume of the lens increases [96]. Changes to the posterior lens capsule are negligible following birth, while the anterior lens epithelium continues to secrete anterior capsule [96]. At birth, the mean diameter of the capsular bag is 7.0–7.5 mm and increases to about 9.0–9.5 mm by age 2 [97]. These values support the findings of Ohami and coworkers and Richburg and Sun who measured the capsular bag to be about 1 mm larger than lens diameter [27, 98]. There is also a change in capsular thickness with age (Fig. 1.4) [99].

When viewed with electron microscopy, the lens capsule consists of a combination of type IV collagen, as well as, types I and III collagen, laminin and fibronectin [100]. The infant anterior capsule is highly elastic in nature when compared to the adult capsule [100]. Krag and coworkers looked at the extensibility of the capsule throughout life and found its maximum extensibility was in infancy and decreased by 0.5 % every year throughout life [101]. While extensibility decreases by at least a factor of two, overall strength decreased by a factor of five [101].

Figure 1.5 displays the change in lens weight with age [96].

At birth, the accommodative power of the lens is between 14 and 16 diopters and then decreases with age (Fig. 1.6) [102].

The zonules insert less anteriorly on the lens of an adolescent as compared to adults [94]. The distance between the anterior zonular insertion and the lens edge is approximately 0.75–1 mm with a zonular free central anterior zone on the anterior capsule of 6 mm in infancy which increases to 7–9 mm s in adolescence [20, 94]. Fetal and infantile eyes have zonular fibers that are finer, less aggregated and exhibit considerably more proteoglycan staining with Alcain blue or cuprolinic blue than in adult eyes [103, 104]. The loss of size that occurs with aging has been suggested to be the result of decreased fibrillin synthesis with age, which is also seen in the aging aorta [105]. The flat zonular insertional areas attach to the thin lens equator at its periphery with the zonular bundles appearing closely packed and thick for the first two decades of life [104]. These areas of insertion become widened and displaced more centrally as the lens grows in diameter and thickness [104].

The tunica vasculosa lentis is the anterior portion of the hyaloid vascular network that surrounds and supplies the growing lens in utero [63]. The tunica is made up of multiple different vascular sources including the hyaloid artery, the vasa hyaloidae propria and from the anterior ciliary vessels by way of the major arterial circle of the iris [106]. The development of the tunica peaks at 10 weeks gestation and regresses during the fourth month of gestation [63]. Complete regression occurs in stages with the posterior part (supplied by hyaloids system) regressing completely by the seventh month of gestation and the anterior part (supplied by ciliary system) regressing completely by the 8 month of gestation [106]. Occasionally, the tunica vasculosa lentis fails to completely resolve leaving a small, 1–2 mm, area of fibrosis termed a Mittendorf dot on the back of the lens [63].

The lengths of the pars plicata and pars plana at different ages are summarized in Table 1.4 [107]. The pars plana represents 73–75 % of the total ciliary body length in infants and young children. The ciliary body is 76 % of adult size by 2 years old. Procedures designed to enter the posterior segment of the eye via the pars plana must therefore be appropriately adjusted so as to avoid unplanned violation of either the ciliary body or retina. Similar to the adult population, the temporal ciliary body is longer than the nasal ciliary body in the pediatric age group [107]. The anterior two thirds of the ciliary body houses the largest portion of the ciliary muscle with a few fibers passing posteriorly to the ora serrata [107]. In the young eye, the connective tissue between these muscle fibers is scarce [107].

After birth, the fovea continues to differentiate for the first 45 months of life [108]. From birth until 15 months old, the fovea continues to deepen as a result of the migration of cells in the inner retina toward the periphery [112]. The foveola , which measures over 1000 μm at birth, becomes progressively more narrow due to the central migration of cones reaching the adult diameter of 650–700 μm by 45 months old. It has been determined that this immature foveola accounts for 5° of visual angle [110]. This results in an increase in foveolar cone density from 18 cones/100 μm at 1 week postnatal to 42 cones/100 μm in the adult [112]. Elongation, maturation and an increase in packing density occurs in the development of the foveolar cones with cone diameter going from 7.5 μm at 5 days postnatal to 2 μm by 45 months [112]. During this time the foveolar cones develop both outer segments and basal axon processes. While foveolar differentiation is complete at 45 months of age, key factors in visual development including outer segment length and cone packing density are only half the adult values at 45 months of age [112]. The capillary free zone in the infant is similar in size to that of the adult [113].

El-Dairi and coworkers evaluated variation in macular thickness and volume with age and race (white vs. black) in children ages 3–17 years (Table 1.5) [114]. They found that perifoveolar retinal thickness and foveal thickness were both significantly greater in white than in black children as were measurements of total macular volume [114]. These racial differences were more significant in the two younger age groups, 3–6 year olds and 7–10 year olds, while only the fovea was significantly thicker in white children than black children in the older group, 11–17 year olds [114]. Huynh and coworkers studied children (mean age 6.7 years) and found a mean minimum foveal thickness of 161.1 (±19.4) μm, and mean thickness measurements of the central, inner, and outer macula of 193.6 (±17.9), 264.3 (±15.2), and 236.9 (±13.6) μm, respectively [115]. They found that the temporal quadrant was thinner than other quadrants in both the inner and outer macular regions. Total macular volume was also normally distributed, with a mean of 6.9 (±0.4) mm³ [115]. Variations in sex and ethnicity were observed with thicker measurements for the foveal minimum, central, and inner macula in white compared to East Asian children as well as in boys compared to girls [115]. Measurements of the outer macular thickness showed no significant gender-ethnic differences [115]. Changes in thickness based on axial length and spherical equivalent were noted in the inner and outer macula, but not in the central macula [115]. These changes include significant thinning with increasing axial length and significantly thicker measurements with more hyperopic spherical equivalent [115]. Huynh and coworkers went on to evaluate older children ages 11–14 years and found mean (SD) thickness of the central 1 mm, and inner and outer macular rings to be 197.4 ± 18.7, 271.9 ± 15.0, and 239.5 ± 13.5 μm, respectively with a foveal minimum thickness of 161.6 ± 19.9 μm [116]. Minimal differences between sexes were noted [116].