Eye disorders in newborn infants (excluding

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Review

Eye disorders in newborn infants (excluding retinopathy of prematurity) Michael J Wan, Deborah K VanderVeen Department of Ophthalmology, Boston Children’s Hospital, Harvard Medical School, Boston, Massachusetts, USA Correspondence to Dr Deborah K VanderVeen, Department of Ophthalmology, Boston Children’s Hospital, 300 Longwood Avenue, Fegan 4, Boston, MA 02115, USA; Deborah.VanderVeen@ childrens.harvard.edu Received 16 August 2014 Revised 17 October 2014 Accepted 22 October 2014 Published Online First 13 November 2014

ABSTRACT A screening eye examination is an essential part of the newborn assessment. The detection of many ocular disorders in newborn infants can be achieved through careful observation of the infant’s visual behaviour and the use of a direct ophthalmoscope to assess the ocular structures and check the red reflex. Early diagnosis and subspecialty referral can have a critical impact on the prognosis for many ocular conditions, including potentially blinding but treatable conditions such as congenital cataracts, life-threatening malignancies such as retinoblastoma and harbingers of disease elsewhere such as sporadic aniridia and its association with the development of Wilms tumour.

INTRODUCTION There are many important eye disorders that can affect newborn infants and most have ocular signs that can be detected on a screening eye examination. The American Academy of Pediatrics recommends that all newborns be evaluated for ocular structural abnormalities which are known to cause vision problems, such as corneal opacities, cataracts and ptosis.1 Screening early in the newborn period is crucial because the prognosis for some conditions depends on prompt detection and early treatment. The purpose of this review is to outline the components of the newborn eye examination, describe important ocular disorders and key associated findings and give general guidelines on the urgency of referral and treatment.

THE EYE EXAMINATION IN A NEWBORN Careful observation and a direct ophthalmoscope are generally all that are required to detect signs of the majority of important eye disorders in newborn infants. One systematic approach is to proceed anatomically, from external to internal structures. The facial features and periocular tissues should be examined for evidence of asymmetry, eyelid abnormalities and periocular masses. The eyelids are then gently opened and the globes inspected for symmetry and gross structural anomalies. Finally, the direct ophthalmoscope is an invaluable tool that can be used to test the infant’s visual response to light and to evaluate for abnormalities of the cornea, iris and red reflex.

EYELID AND EXTERNAL DISORDERS Cryptophthalmos To cite: Wan MJ, VanderVeen DK. Arch Dis Child Fetal Neonatal Ed 2015;100:F264–F269. F264

Cryptophthalmos is the failure of the eyelid and globe to separate during embryonic development (figure 1). It presents at birth with the eyelid skin either completely covering the eye (complete cryptophthalmos) or fusing with the conjunctiva or

cornea (incomplete/partial cryptophthalmos). In rare cases, bilateral cryptophthalmos can be associated with Fraser syndrome, an autosomal recessive condition with multiple congenital anomalies, including genital abnormalities and syndactyly.2 It is important for both physicians and parents to be aware that in essentially all cases, the eyelids and underlying eye are malformed and surgical repair, if undertaken, generally requires many procedures with a guarded prognosis for cosmesis and poor prognosis for vision.3

Ankyloblepharon Ankyloblepharon is an adhesion of the edges of the upper and lower eyelids. It is usually isolated, but can rarely be associated with oral, skeletal, digital and genitourinary anomalies.4 Unlike cryptophthalmos, the eyelid and underlying ocular structures are typically normal in ankyloblepharon and prognosis is excellent with a relatively simple excision of the bands of fibrous tissue connecting the eyelids, which can be performed in the newborn nursery.5

Eyelid coloboma An eyelid coloboma is a full-thickness defect in the lid, usually located medially in the upper lid or laterally in the lower lid (figure 2). A lid coloboma is a characteristic feature of several syndromes, including Treacher–Collins syndrome (lower lid) and Goldenhar syndrome (upper lid), but unlike colobomata of other ocular structures, there is no association with CHARGE syndrome.6 7 Although corneal exposure can occur, the majority of children do not develop corneal complications and surgical repair can usually be deferred for several months or even years.8

Congenital entropion and epiblepharon Inturning of the eyelashes at birth can be due to a true inversion of the eyelid margin (entropion) or an abnormal fold of skin that overrides a normally positioned eyelid margin (epiblepharon) (figure 3). Congenital entropion is rare, worsens over time and requires early surgical correction.9 10 In contrast, epiblepharon is much more common, usually resolves over time with facial growth and only requires surgery if there is significant corneal irritation.11

Congenital ptosis Congenital ptosis is most commonly caused by developmental dysgenesis of the levator muscle, but there are other important neurological, mechanical and syndromic aetiologies. When ptosis is severe and obstructs the visual axis, there is a high risk of amblyopia and referral to ophthalmology is urgent. However, lesser degrees of ptosis can still cause amblyopia due to strabismus or anisometropia

Wan MJ, et al. Arch Dis Child Fetal Neonatal Ed 2015;100:F264–F269. doi:10.1136/archdischild-2014-306215


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Figure 1 Infant with left-sided cryptophthalmos.

(asymmetric refractive error between eyes) and require close ophthalmology follow-up.12 Congenital ptosis is usually a sporadic and unilateral finding in an otherwise healthy infant.13 Bilateral cases may be associated with Blepharophimosis syndrome, an autosomal dominant condition that causes multiple characteristic ocular abnormalities, including telecanthus, epicanthus inversus and blepharophimosis (horizontal shortening of the palpebral fissure).14 Important neurological causes of ptosis include congenital Horner’s syndrome, cranial nerve III palsy and Marcus Gunn jaw-winking syndrome. Congenital Horner’s syndrome results from an injury to the sympathetic pathway and has a classic triad of ipsilateral ptosis, miosis and anhidrosis (figure 4). Iris heterochromia is generally not present at birth but develops over the first few months of life, with a lighter iris colour on the affected side.15 Although congenital Horner’s syndrome is most commonly idiopathic or due to birth trauma, neuroimaging of the sympathetic pathway is indicated to rule out a serious underlying process.16 A congenital cranial nerve III palsy presents with ptosis and a ‘down and out’ position of the affected eye. It is usually idiopathic but can be caused by birth trauma.17 Marcus Gunn jaw-winking syndrome presents with a combination of ptosis and excursion of the ptotic upper eyelid when the infant is chewing or sucking (often noticed during feeding).18 It is caused by a congenital synkinesis between cranial nerves III and V and neurological assessment and neuroimaging are unnecessary in typical cases. Finally, a ptotic eyelid in a newborn should always be carefully inspected and palpated for masses within the lid, which can cause mechanical ptosis.

Capillary haemangioma Capillary haemangiomas are the most common eyelid tumours in infancy and present as soft, reddish, flat or slightly elevated

Figure 2 Infant with a left upper eyelid coloboma.

Figure 3

Child with a right lower eyelid epiblepharon.

lesions that may rapidly enlarge in the first few weeks or months of life (figure 5). Infants with periocular haemangiomas need close ophthalmology follow-up to monitor for amblyopia due to refractive asymmetry, astigmatism or visual deprivation.19 Haemangiomas can be treated effectively with beta blockers or corticosteroids and surgical excision is feasible for small subcutaneous haemangiomas. Laser therapy is generally only useful for superficial vascular abnormalities.

Dacryocystocoele A congenital dacryocystocoele is a distension of the lacrimal sac that presents at birth as a cystic bluish swelling just inferior to the medial canthal area. Unlike a typical nasolacrimal duct obstruction, a congenital dacryocystocoele has a high risk of becoming infected and potentially progressing to cellulitis and sepsis.20 Early referral for surgical probing and decompression is recommended in all cases and infected dacryocystocoele require systemic antibiotic treatment. Dacryocystocoele are also associated with intranasal cysts and bilateral cases can cause neonatal respiratory distress.21

GLOBE ABNORMALITIES Congenital abnormalities of the globe are rare. Anophthalmos (complete absence of the eye) and microphthalmos (small disorganised eye) are considered to exist along the same spectrum of disease (figure 6A). When diagnosed, a systemic assessment is mandatory since there can be associated chromosomal or systemic abnormalities, and MRI may be considered since significant maldevelopment of the eye or optic nerve hypoplasia can be associated with midline brain abnormalities.22 Nanophthalmos is a rare condition in which the globe has a short axial length, enlarged lens and thickened sclera. Nanophthalmos is usually bilateral and causes a predisposition to uveal effusion and glaucoma, but there are usually no associated systemic or developmental abnormalities.23

Figure 4 Child with a right congenital Horner’s syndrome who presented with the classic triad of ptosis, miosis and anhidrosis. Heterochromia (the iris on the affected side is lighter in colour) develops in congenital Horner’s syndrome but not in acquired cases.


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Review Unilateral cataracts are generally isolated anomalies and do not require systemic investigation. One notable exception are cataracts caused by congenital rubella syndrome, which are unilateral in approximately 20% of cases.34 In contrast, bilateral cataracts that are not known to be familial (autosomal dominant inheritance) require a systemic assessment for genetic and chromosomal abnormalities, metabolic disorders and intrauterine infections.35 Figure 5 Infant with a superficial right upper eyelid capillary haemangioma. Although the visual axis is clear, the mass effect can displace the globe or cause anisometropia and refractive amblyopia.

LEUKOCORIA One of the most critical components of the newborn exam is to check for a normal red reflex, as many eye disorders can present with leukocoria (‘white pupil’) (box 1).24 This review will focus on two important causes in newborns, retinoblastoma and congenital cataracts.

Retinoblastoma Retinoblastoma is the most common primary ocular malignancy of childhood. Although sporadic cases present at a mean age of 15 months, it is not uncommon for the diagnosis to be made in newborns.25 26 It is critical to find retinoblastoma early because localised tumours are almost always curable, while disseminated disease is often fatal.27 Leukocoria is the most common clinical finding of retinoblastoma in the neonatal period (figure 7A), with strabismus being the other common clinical finding for all ages. The retinoblastoma gene is inherited in an autosomal dominant pattern and the disease manifests earlier in familial cases. Therefore, any newborn with a positive family history needs to be referred for a dilated fundus exam as soon as possible, regardless of whether leukocoria is present.28 Prenatal genetic testing or fetal ultrasound/MRI can also be performed to enable prompt treatment for affected children.29 30

IRIS ANOMALIES Iris coloboma An iris coloboma can be identified as defect in the contour of iris, typically inferonasally (giving the iris a ‘keyhole’ appearance) (figure 6A, B). An iris coloboma may be isolated or associated with microphthalmos and/or colobomata of other ocular structures.36 An iris coloboma is also a characteristic feature of many syndromes, including trisomy 13 and 18, cat eye syndrome, Klinefelter syndrome, Turner syndrome and CHARGE syndrome.

Aniridia Aniridia is characterised by hypoplasia of the iris. Vision in patients with aniridia is often poor because of other ocular abnormalities, including foveal hypoplasia, cataracts, glaucoma and corneal opacification.37 About two-thirds of affected patients have familial aniridia with autosomal dominance inheritance. It is important to identify patients with sporadic aniridia because they have a significantly increased risk of developing Wilms tumour and require genetic testing or frequent screening.38

CORNEAL OPACITY There are many potential causes of corneal opacification and all cases need urgent ophthalmological assessment.

Congenital glaucoma Congenital cataracts The most common cause of leukocoria in newborns is congenital cataracts (figures 6A and 7B).31 While not life threatening, the prognosis for vision is significantly better if congenital cataracts are diagnosed and treated before the age of 2 months.32 33 If the diagnosis is delayed, severe and irreversible amblyopia may result.

Congenital glaucoma is a potentially blinding, treatable and easily misdiagnosed cause of corneal opacification (figure 8A). While a cloudy cornea is the most readily apparent sign of congenital glaucoma, the majority of cases have no (or subtle) corneal clouding at birth.39 Therefore, it is important to be aware of other signs of congenital glaucoma, such as corneal or globe enlargement, and the classic triad of symptoms: epiphora,

Box 1 Differential diagnosis of leukocoria (a white pupillary reflex)

Figure 6 (A) Child with multiple congenital ocular anomalies, including microphthalmos of the right eye and an iris coloboma and cataract in the left eye. (B) Child with bilateral iris colobomata. F266

Retinoblastoma Congenital cataract Persistent fetal vasculature Coats’ disease Retinopathy of prematurity Retinal detachment Vitreous haemorrhage Toxocariasis Retinal dysplasia Coloboma of retina/optic nerve Myelinated nerve fibre layer Endophthalmitis Uveitis/fibrin



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Figure 7 Aetiologies of leukocoria. (A) Asymmetric red reflex with leukocoria in the right eye in a child with unilateral retinoblastoma. (B) Absent red reflex and white central opacity in a patient with a congenital cataract.

photophobia and blepharospasm. Any combination of these findings is suggestive of congenital glaucoma and warrants a prompt referral to ophthalmology.

Anterior segment dysgenesis Several developmental anomalies of the anterior eye structures can cause corneal changes, including Axenfeld-Rieger (AR) syndrome, Peters’ syndrome, sclerocornea and corneal dermoids. AR is an autosomal dominant condition with characteristic iris abnormalities and a 50% chance of developing glaucoma. Patients with AR have distinctive facial features (hypertelorism, flat nasal bridge and high forehead) and may exhibit dental anomalies, redundant periumbilical skin or other less common findings such as cardiac defects or hypospadias. Peters’ anomaly causes central corneal opacification (figure 8B), usually bilateral, and can rarely be associated with multiple systemic abnormalities, including short stature, mental retardation, abnormal ears and cleft lip and palate (Peters’-Plus syndrome).40 Sclerocornea causes bilateral opacification that is diffuse or denser in the peripheral cornea. Dermoids are choristomas (displaced tissue not normally found in the cornea) that cause unilateral corneal opacification and can often be followed conservatively (figure 8C).41

Corneal dystrophies The autosomal recessive type of congenital hereditary endothelial dystrophy (CHED) presents with severe bilateral corneal clouding at birth. CHED is associated with nystagmus and severe visual impairment and often requires corneal transplantation.42

Figure 8 Aetiologies of corneal opacification. (A) Bilateral congenital glaucoma causing corneal cloudiness and enlargement. (B) Peters’ syndrome with central corneal opacification. (C) Corneal dermoid that is sparing the visual axis.

Trauma Forceps delivery can compress the globe and cause corneal oedema. The corneal findings are unilateral and usually affect the left eye due to the typical position of the fetal head during delivery. While the corneal oedema generally resolves spontaneously, these patients still need follow-up with ophthalmology because residual scarring can cause significant astigmatism and amblyopia.44

Systemic metabolic disease

VISUAL IMPAIRMENT, NYSTAGMUS, STRABISMUS AND AMBLYOPIA Vision

Although many metabolic diseases can be associated with corneal opacification, it is extremely rare for the cornea to be cloudy at birth.43 These conditions are usually inherited in an autosomal recessive pattern and are associated with multiple systemic abnormalities.

At birth, visual acuity is poor due to immaturity of the foveal cones and visual processing centres.45 Specialised testing procedures have estimated that visual acuity is approximately 20/400 at birth and the ability to fixate on an object of interest does not develop until around 6 weeks of age. For a newborn, the most


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Review practical bedside clinical test of visual function is to check the pupillary reaction to light and to confirm a ‘blink to light’ response in both eyes.46 Diagnosing severe visual impairment on a neonatal eye exam is challenging, but early-onset nystagmus and lack of pupillary constriction or a behavioural response to a bright light are suggestive of poor vision.47 The most common cause of bilateral vision loss at birth in the developed world is cortical visual impairment (CVI).48 CVI is caused by injury to the visual cortex or cerebral visual pathways, most commonly due to hypoxic–ischaemic injury.49 Clinically, newborns with CVI present with an absent or poor response to visual stimuli, often brisk pupillary reaction to light, normal ocular examination and neurological deficits corresponding to the area of injury. Infants born prematurely will often exhibit some degree of CVI that may not be recognised until later in development.

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Nystagmus There are a number of types of nystagmus that can present in the neonatal period. Idiopathic infantile nystagmus presents early in life with bilateral conjugate nystagmus and only mildly decreased vision. Nystagmus due to poor vision (sensory deficit nystagmus) is clinically indistinguishable except that the newborn has a poor or absent behavioural response to visual stimuli. Sensory deficit nystagmus is common in ocular conditions with poor vision, most commonly albinism, achromatopsia and Leber’s congenital amaurosis. Notably, CVI almost never causes nystagmus in its pure form.50

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Strabismus Eye alignment in newborns is highly variable and transient strabismus that is comitant (ie, the angle of deviation remains the same in all fields of gaze) is not necessarily a cause for concern. Approximately 67% of infants are exotropic at birth and only 30% of newborns have straight eyes.51 While the vast majority of transient deviations resolve within the first 6 months of life, any ocular deviation that is incomitant or persists beyond 3 months of age warrants a referral to ophthalmology.52

Amblyopia Amblyopia is a loss of vision due to abnormal visual experience early in life and it is one of the leading causes of monocular blindness worldwide.53 54 There is a critical period of visual development in the first few months of life and poor visual input during this time (eg, congenital cataract) can cause severe amblyopia.55 Later in childhood, strabismus and anisometropia (asymmetric refraction between the two eyes) are the most common causes of amblyopia.

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CONCLUSION

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There are a diverse group of eye disorders that can affect newborns. The majority of disorders have signs that are detectable on a screening eye exam that is a critical component of any comprehensive newborn assessment. Therefore, it is incumbent on physicians performing newborn screening examinations to be aware of specific signs of these ocular disorders and to triage appropriately when such findings are identified. Competing interests None.

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Eye disorders in newborn infants (excluding retinopathy of prematurity) Michael J Wan and Deborah K VanderVeen Arch Dis Child Fetal Neonatal Ed 2015 100: F264-F269 originally published online November 13, 2014

doi: 10.1136/archdischild-2014-306215 Updated information and services can be found at: http://fn.bmj.com/content/100/3/F264

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