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19.3 Primary infantile glaucoma

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TOPIC OUTLINE Primary infantile glaucoma INTRODUCTION Authors Section Editors Deputy Editor EPIDEMIOLOGY Scott E O litsky, MD Evelyn A Paysse, MD Mary M Torchia, MD INHERITANCE James D Reynolds, Joseph A Garcia- PATHOGENESIS MD Prats, MD

CLINICAL FEATURES Disclosures Corneal enlargement Corneal Last literature review version 19.3: Fri Sep 30 00:00:00 GMT Optic cupping 2011 | This topic last updated: Mon Oct 05 00:00:00 GMT Ocular enlargement 2009 (More) DIAGNOSIS INTRODUCTION — Glaucoma is a group of eye diseases that DIFFERENTIAL DIAGNOSIS are traditionally characterized by elevated intraocular pressure Tearing (IOP). Increased IOP leads to damage and Corneal clouding consequent visual loss. Peripheral vision loss occurs first, but if Corneal enlargement glaucoma is untreated, central vision loss and complete blindness Cupping can occur [1]. In infants and toddlers, additional damage to the TREATMENT , including large , , Surgery , and , may occur. Early diagnosis and Medical therapy referral are crucial to ensure optimal visual outcome. SUMMARY AND Primary glaucoma may have onset at birth, in the first few years RECOMMENDATIONS of life, or later in life. A distinction sometimes is made between REFERENCES glaucoma that is present at birth (true congenital glaucoma) and glaucoma that has onset in the first two to three years of life GRAPHICSView All (infantile glaucoma) because the prognosis differs [1-4]. The later FIGURES the onset, the less severe the structural anomaly, and the more Angle anatomy likely the glaucoma will respond to treatment [4]. Impaired aqueous flow The clinical features, diagnosis, and treatment of primary infantile Angle-closure glaucoma glaucoma will be presented here. Other causes of glaucoma in PICTURES children and glaucoma in adults are discussed separately. (See Glaucoma corneal enlrgmnt "Overview of glaucoma in infants and children" and "Open-angle Glaucoma Haabs striae glaucoma: Epidemiology, clinical presentation, and diagnosis".) Glaucomatous EPIDEMIOLOGY — Primary infantile glaucoma occurs in Corneal clouding 1:10,000 live births. It is a major cause of blindness [4]. Primary infantile glaucoma is bilateral in more than two-thirds of affected patients, but may be asymmetric in onset [5]. The onset of signs Normal physiologic cupping and symptoms occurs at birth in 40 percent of affected patients

RELATED TOPICS and before one year of age in 86 percent [6]; however, the age of recognition ranges from birth until late childhood. Approach to the child with persistent tearing INHERITANCE — Primary infantile glaucoma is usually a Bacterial sporadic disease. However, a number of reports have indicated that between 10 and 27 percent of cases are inherited. Clinical features and diagnosis of Inheritance is autosomal-recessive in some cases and the mucopolysaccharidoses multifactorial in others; the penetrance is variable [4,7-9]. Congenital anomalies and Help improve UpToDate. Did UpToDate answer your question? Yes No http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?0/12/192?view=print 1/12 12/6/2017 Primary infantile glaucoma The molecular defect in the majority of familial cases is in the cytochrome P4501B1 gene (CYP1B1) on chromosome 2p21 [10]. The protein product of this gene is thought to affect a signaling pathway during the terminal stages of angle development [11]. A second locus for primary infantile glaucoma has been mapped to chromosome 1p36 [12].

PATHOGENESIS — Primary infantile glaucoma is caused by abnormal fetal development of the angle structures (figure 1), leading to impaired drainage of the aqueous fluid and elevated IOP (figure 2). Elevated IOP causes damage to the optic nerve. In addition, in children younger than approximately three years of age (who have more elastic ocular collagen), elevated IOP causes enlargement of the and distention, enlargement, and thinning of the .

The underlying cause of angle dysgenesis is not known. Proposed theories center on neural crest cell migration and development, as neural crest cells are critical in the development of the trabecular meshwork [13,14]. Some angle abnormalities that have been observed on gonioscopy include an open angle with no recess, obstruction of the trabecular meshwork by the or , an absent or rudimentary scleral spur, and fewer and smaller openings in the trabecular meshwork [1,4,8,15].

CLINICAL FEATURES — The typical infant with primary infantile glaucoma presents with chronic or intermittent tearing (ie, ), , and some degree of blepharospasm. Parents or pediatric healthcare providers also may notice a large cornea or asymmetry in the corneal diameters.

Unilateral or asymmetric cases tend to present early, as small differences in corneal diameter are detected easily on gross inspection. However, when the disease is bilateral, increased corneal size may not be recognized or may be viewed as attractive, delaying presentation to medical attention until symptoms develop. Another potential cause of delay in diagnosis is the attribution of tearing to the more common nasolacrimal duct obstruction. (See 'Differential diagnosis' below.)

Findings on physical examination include:

Corneal enlargement Corneal clouding, conjunctival injection, tearing, discharge, and blepharospasm, which are caused by corneal edema Optic nerve cupping Ocular enlargement ()

Younger children are more likely to present with corneal edema and haze, older children with corneal enlargement and buphthalmos [16].

Corneal enlargement — Increased IOP causes stretching of the cornea and increased corneal diameter in children younger than three years of age (picture 1). The normal newborn corneal diameter ranges from 9.5 to 10.5 mm. At one year of age, a diameter of 11.0 mm is typical, with the cornea reaching adult size (12.0 mm) by two or three years. As a general rule, a http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?0/12/192?view=print 2/12 12/6/2017 Primary infantile glaucoma corneal diameter that is more than 1 mm greater than average is cause for concern, and more than 2 mm is definitely abnormal [8]. Thus, a corneal diameter of 12.0 mm or more in an infant younger than one year of age should prompt urgent referral to an ophthalmologist [17,18].

Corneal enlargement has little effect on the epithelium and stroma, but injures the endothelium and basement membrane (Descemet's membrane). Corneal endothelium has little to no ability to divide after birth; it does not replicate and is a relatively static cell layer. As corneal stretching progresses, it causes breaks (called Haab's striae) in the basement membrane (picture 2). The breaks in the basement membrane leave permanent scars, which may be linear or arcuate, and are typically horizontally oriented. Haab's striae, which may be difficult to see without a slit lamp, are an important diagnostic feature found to occur in 25 and 60 percent of patients who presented at birth and six months of age, respectively [19,20].

In addition to scarring, corneal enlargement can cause astigmatism if the enlargement is irregular [1]. In one series of 102 eyes from 59 patients with primary infantile glaucoma, 24 percent had at least two diopters of astigmatism [21]. (See "Refractive errors in children", section on 'Astigmatism'.)

Corneal edema — Epithelial and stromal edema results from the absorption of aqueous fluid through Haab's striae. Corneal edema is manifest as clouding and occurs less frequently after the barrier function of the corneal endothelium matures (ie, after six months of age) [8,16].

Corneal edema causes many of the symptoms of infantile glaucoma. It is irritating, painful, and produces light scattering. The irritation causes tearing (epiphora), ocular discharge, conjunctival injection, and blepharospasm. Corneal clouding may result in unilateral or bilateral pattern deprivation, contributing to the development of amblyopia. (See "Overview of amblyopia", section on 'Deprivational'.)

Optic nerve cupping — The size of the cup, or central depression, in the head of the optic nerve is characterized by the ratio between the cup diameter and the disc diameter. Thus, a cup that has a diameter that is 50 percent of the disc diameter would be 0.5. In normal infants, the optic are symmetric with little cupping.

Elevated IOP damages the optic nerve, which takes on a hollowed-out appearance on funduscopic examination. This appearance is described as "cupping." Cupping increases as axons are damaged by elevated IOP. Axons at the superior and inferior poles of the disc are preferentially affected, increasing cupping primarily in the vertical diameter (picture 3). Asymmetry of cupping from eye to eye may be a sign of infantile glaucoma.

At a given IOP elevation, cupping increases more rapidly in infants than in adults [22]. However, in contrast to adults, infants with glaucoma may have a reduction in optic nerve cupping when http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?0/12/192?view=print 3/12 12/6/2017 Primary infantile glaucoma IOP is controlled. (See "Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis".)

Ocular enlargement — Increased IOP causes stretching of the sclera in children younger than three years of age. Stretching of the sclera increases the size of the , also called buphthalmos or "ox eye." The increased anterior-posterior diameter of the eye causes secondary axial . In one series of 102 eyes from 59 patients with primary infantile glaucoma, almost two-thirds had at least three diopters of myopia [21]. (See "Refractive errors in children", section on 'Myopia'.)

Myopic or astigmatic (unequal refractive error between the eyes) occurs in approximately one-third of children with primary infantile glaucoma (either unilateral or bilateral) [21]. Anisometropia occurs in bilateral cases because the eyes are rarely symmetrically affected. Anisometropia, if left untreated, can cause amblyopia. (See "Overview of amblyopia", section on 'Anisometropic amblyopia'.)

A rare consequence of ocular enlargement may be subluxation of the . Zonules of collagen fibers hold the lens in place behind the iris (figure 1). As the globe increases in size, the zonules are stretched, and the lens may dislocate. If it dislocates into the anterior chamber, acute angle closure glaucoma, in which the iris root completely occludes the trabecular meshwork, can develop (figure 3) [1]. Acute angle closure glaucoma requires urgent intervention to prevent permanent visual loss. (See " (dislocated lens) in children".)

DIAGNOSIS — The diagnosis of infantile glaucoma is based upon a constellation of findings that includes enlarged cornea, corneal edema, and optic nerve cupping. Infants with these findings should be referred for urgent ophthalmologic evaluation. Referral should not be delayed pending progression (eg, of optic nerve cupping), as such delay can result in permanent visual loss.

Most patients with infantile glaucoma can be diagnosed in the ophthalmologist's office, although some require an examination under anesthesia. The diagnosis usually is based upon the clinical features described above. The measurement of intraocular pressure, which some authors are able to reliably assess while the child is sleeping or feeding, is often not a vital part of the diagnostic process. However, it is helpful in following the treatment response.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of infantile glaucoma depends upon the cardinal sign(s) and/or symptom(s). When the constellation of tearing, blepharospasm, photophobia, and enlarged cornea occur together, infantile glaucoma should be the first consideration.

Tearing — Tearing (ie, epiphora) in infants can be caused by nasolacrimal duct obstruction, infectious or allergic , http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?0/12/192?view=print 4/12 12/6/2017 Primary infantile glaucoma corneal abrasions, and various metabolic disorders [1]. Nasolacrimal duct (NLD) obstruction is the most common cause, occurring in 6 percent of all normal newborns [23]. (See "Approach to the child with persistent tearing" and "Nasolacrimal duct obstruction (dacryostenosis) in children".)

The distinction between these disorders can usually be made on the basis of clinical findings. Unlike patients with infantile glaucoma, children with NLD obstruction do not have blepharospasm or photophobia. Nasal discharge is another finding that helps to distinguish glaucoma from NLD (during episodes of tearing, the nose runs in patients with glaucoma, but not in those with NLD obstruction). Among the other causes of tearing, infantile glaucoma is the only one in which enlarged cornea, corneal clouding, and optic disc cupping occur.

Children with cystinosis may have corneal deposits that cause photophobia, tearing, and blepharospasm (in addition to corneal clouding). Children with cystinosis also have extraocular manifestation (eg, growth failure, rickets). (See "Cystinosis".)

The characteristic ocular findings of tyrosinemia are corneal ulcers or dendritic , which cause photophobia, pain, excessive lacrimation, and conjunctival injection. Patients with tyrosinemia also have characteristic skin lesions. (See "Disorders of tyrosine metabolism", section on 'Hereditary tyrosinemia type 2'.)

Corneal clouding — Cloudy can be caused by congenital hereditary endothelial dystrophy (CHED), mucopolysaccharidoses, sclerocornea, and trauma.

Congenital hereditary endothelial dystrophy (CHED) presents with corneal edema at birth. The corneal edema produces epiphora and photophobia. However, the cornea is of normal size, the intraocular pressure is normal, and the optic nerve and angle are normal (albeit difficult to visualize).

Corneal clouding from structural changes in the stroma (picture 4) is a characteristic feature of mucopolysaccharidosis (MPS) type 1. Affected infants appear normal at birth; during the first year, they develop the characteristic coarse facial features, wide nasal bridge, and flattened midface. Other signs include hepatosplenomegaly, umbilical or inguinal hernias, and typical skeletal abnormalities. These infants typically present between six months and two years of age with developmental delay, recurrent respiratory infections, and chronic nasal discharge. (See "Clinical features and diagnosis of the mucopolysaccharidoses".)

Sclerocornea is a congenital malformation of the cornea in which the limits of the cornea and sclera are indistinct (picture 6). The cornea is hazy because its collagen fibrils are irregularly arranged. Additional ocular anomalies (eg, , , ) usually are present. http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?0/12/192?view=print 5/12 12/6/2017 Primary infantile glaucoma

Corneal enlargement — Primary megalocornea (picture 7) also may be confused with infantile glaucoma. Megalocornea usually is inherited as an X-linked recessive trait; as a result, it almost always occurs in males. In patients with primary megalocornea, the intraocular pressure is normal; corneal edema, epiphora, and photophobia are absent; and the optic nerve is normal.

Unilateral high myopia, proptosis, lid retraction, microphthalmos, , or can give the appearance of an enlarged cornea because one eye is larger, more prominent, or more visible than the other [1].

Cupping — In addition to glaucoma, cupping of the optic nerve can be physiologic (picture 8) or due to optic nerve anomaly. (See "Congenital anomalies and acquired abnormalities of the optic nerve", section on 'Cupping'.)

TREATMENT — The goal of infantile glaucoma therapy is preservation of vision rather than control of IOP, although IOP is used to monitor treatment success [24]. Treatment is almost always surgical, although medications have an adjunctive role.

Surgery — Surgical intervention is the mainstay of therapy for primary infantile glaucoma and most pediatric . The first-line procedures include goniotomy and trabeculotomy.

Goniotomy — Internal goniotomy involves cutting into the abnormal trabecular meshwork, which causes the iris to drop back, deepening the angle recess [25,26]. Goniotomy is limited by the need for adequate visualization, which may be impeded by corneal clouding. This limitation may be overcome with the development of endoscopic technology that provides direct visualization of the anterior chamber angle [27].

Trabeculotomy — Trabeculotomy is the procedure of choice when corneal clouding precludes visualization of angle structures [28]. It involves the insertion of a trabeculotome into Schlemm's canal to create an opening in the abnormal trabecular meshwork [29,30].

Goniotomy and trabeculotomy are successful (IOP <20 mmHg) in 80 to 90 percent of cases of primary infantile glaucoma when patients present between 1 and 24 months of age [4]. A second procedure at a different site is necessary in 20 to 30 percent of cases [24]. The success rate is decreased when patients present before two months of age (ranging from 55 to 60 percent) or after 24 months of age (76 percent) [2,4,31-34]. The visual prognosis for children treated with these procedures is good: 52 to 79 percent have visual acuity of 20/60 or better [32,33,35]. http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?0/12/192?view=print 6/12 12/6/2017 Primary infantile glaucoma Complications of goniotomy and trabeculotomy include hemorrhage, , formation, uveal or vitreous incarceration, endophthalmitis, retinal or choroidal detachment, and hypotony (abnormally low IOP).

Second-line surgical therapies include trabeculectomy, implantation of drainage devices, and cyclodestructive procedures.

Trabeculectomy — Trabeculectomy, or filtering surgery, usually is attempted if goniotomy or trabeculotomy fail. This procedure involves creation of an artificial drainage pathway through the sclera to allow excess aqueous humor to leak out of the eye through a conjunctival filtering "bleb." The long-term success rate of trabeculectomy in children is usually cited as 50 percent [36]; success has been found to increase with the use of antifibrotic agents such as topical mitomycin-C and fluorouracil [24,37,38]. Antifibrotic agents should be used with caution, as they increase the risk of leakage and late-onset endophthalmitis [38]. Severe complications (eg, infection, bleb leak, collapse of the anterior chamber) are more common after trabeculectomy than trabeculotomy or goniotomy. (See "Bacterial endophthalmitis", section on 'Bleb-related endophthalmitis'.)

Drainage devices — Glaucoma drainage devices consist of a small tube that is placed inside the eye, leading to a "reservoir" placed under the . The tube must be placed well into the anterior chamber so that retraction of the tube does not occur as the eye grows. Compared to other methods of surgical treatment, drainage devices have a higher risk of early and persistent hypotony. Success rates (IOP <20 mmHg) of 60 to 65 percent have been reported in patients who were followed for two years [24]. Complications include vitreous hemorrhage, malignant glaucoma, , erosion or recession of the implant, endophthalmitis, corneal edema, and cataract formation [39-44].

Cyclodestructive procedures — Cyclodestructive procedures aim to decrease aqueous fluid production by destroying the ciliary processes. Cyclodestructive procedures are usually recommended when other methods of control have failed or when the vision is extremely poor [45]. Cyclodestruction is performed with cryotherapy or laser application and has a success rate (IOP <20 mmHg) of approximately 50 percent [46-48]. Complications include hypotony, retinal or choroidal detachment, and inflammation.

Medical therapy — The use of topical or oral preparations of pressure-lowering agents has a limited role in primary infantile glaucoma because nearly all cases require surgery. Surgery is required because of the rapidity of ocular damage and the difficulties inherent in monitoring the disease parameters (eg, http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?0/12/192?view=print 7/12 12/6/2017 Primary infantile glaucoma IOP, visual acuity) in young children. However, medical therapy may be used postoperatively to prevent or postpone the need for a second surgical procedure.

Medications used in the treatment of glaucoma include beta blockers, alpha-2-adrenergic agonists, carbonic anhydrase inhibitors, prostaglandin analogs, miotics, and sympathomimetics [1].

Beta blockers (eg, betaxolol, carteolol, levobunolol, metipranolol, timolol) work by decreasing aqueous production. Side effects include bronchospasm, apnea, and bradycardia.

Alpha-2-adrenergic agonists (eg, apraclonidine, brimonidine) work by decreasing aqueous production. Side effects include central depression and ocular injection [49-51]. These agents are rarely used in young children and should be avoided in children younger than the age of two years, as sudden death has been reported with their use.

Carbonic anhydrase inhibitors (eg, acetazolamide, brinzolamide, dichlorphenamide, dorzolamide, methazolamide) also work by decreasing aqueous production. Side effects include paresthesias, loss of appetite, nausea, diarrhea, polyuria, and metabolic acidosis.

Prostaglandin analogs (eg, bimatoprost, latanoprost, travoprost, unoprostone) improve aqueous outflow. Side effects include iris and pigmentation, growth, and cystoid .

Miotics (eg, carbachol, echothiophate, pilocarpine) improve aqueous outflow through the trabecular meshwork. Side effects include , myopia, and prolonged (with echothiophate after pharmacologic depolarizing agents were used during anesthesia).

Sympathomimetics (eg, dipivefrin, epinephrine) improve aqueous outflow. Side effects include eye pain, headache, macular edema, and conjunctival deposits.

SUMMARY AND RECOMMENDATIONS

Glaucoma is a group of eye diseases that are characterized by elevated intraocular pressure (IOP). Increased IOP leads to optic nerve damage and consequent visual loss. Early diagnosis and referral are crucial to ensuring optimal visual outcome. (See 'Introduction' above.)

Primary glaucoma may have onset at birth, in the first few years of life, or later in life. The later the onset, the less severe the structural anomaly, and the more likely the glaucoma will respond to treatment. (See 'Introduction' above.) http://cursoenarm.net/UPTODATE/contents/mobipreview.htm?0/12/192?view=print 8/12 12/6/2017 Primary infantile glaucoma

The typical infant with primary infantile glaucoma presents with chronic or intermittent tearing (ie, epiphora), photophobia, and some degree of blepharospasm. Parents or pediatric healthcare providers also may notice a large cornea or asymmetry in the corneal diameters. (See 'Clinical features' above.)

Findings on physical examination include corneal enlargement (picture 1), corneal clouding, conjunctival injection, tearing, discharge, blepharospasm, optic nerve cupping (picture 3), and ocular enlargement (buphthalmos). (See 'Clinical features' above.)

The diagnosis of infantile glaucoma is based upon a constellation of findings that includes enlarged cornea, corneal edema, and optic nerve cupping. Infants with these findings should be referred for urgent ophthalmologic evaluation. (See 'Diagnosis' above.)

The differential diagnosis of infantile glaucoma depends upon the cardinal sign(s) and/or symptom(s). (See 'Differential diagnosis' above.)

The goal of infantile glaucoma therapy is preservation of vision rather than control of IOP, although IOP is used to monitor treatment success. Treatment is almost always surgical, although medications have an adjunctive role. (See 'Treatment' above.)

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REFERENCES

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