System Lacrimal • 25 SECTION

post-menopausal women, consistent with changes in adrogenic hormonal levels. Some reports indicate that as many as 15 million individuals in the United States may experience symptoms associated with lacrimal dysfunction.

Lymphocytic infiltration of the lacrimal gland as a result of autoimmune disease has been associated with subsequent tear film inadequacy. Dry eye syndrome can be the result of tear film dysfunction, or associated with reduced tear volume, altered tear composition, increased evaporation, or inflammatory modulators.

These conditions may coexist in varying degrees, making it difficult to establishment a precise diagnosis. Sjögren’s syndrome is a severe form of dry eye characterized by lacrimal hyposecretion, dry mouth, and arthritis, as well as immunologically modulated ocular surface inflammation.

COURSE/PROGNOSIS

The symptoms of this condition span a spectrum which extends from relatively annoying ocular discomfort to irreversible corneal scarring leading to legal blindness. In most individuals the surface irritation is chronic and associated with only minor visual disruption. Sjögren’s syndrome, ocular cicatrical pemphigoid, and Stevens–Johnson syndrome can have devastating long-term effects.

DIAGNOSIS

Isolated lacrimal hyposecretion must be differentiated from the other causes of dry eye and from chronic blepharitis and meibomian gland dysfunction.

TREATMENT

Ocular

The mainstay of therapy is the use of ocular surface lubricants, applied frequently in liquid or ointment form. When very frequent instillation is necessary, preservative-free vehicles are indicated. Concurrent use of topical anti-inflammatory or immunosuppressant agents is often necessary. Punctal occlusion or the use of protective goggles and hydrophilic contact lenses may be necessary.

COMPLICATIONS

Corneal neovascularization and scarring may result. Increased incidence of ocular surface infection is common. Corneal ulceration and secondary perforation may occur.

COMMENTS

With attention to dissecting factors in the patient’s environment, and moderate lifestyle modifications this condition can be well managed in most cases. There is no specific therapy which has been shown to consistently improve lacrimal secretion, so artificial tears are the mainstay of treatment. Severe forms need frequent involvement of a corneal subspecialist.

SUPPORT GROUP

Sjögren’s Syndrome Foundation, Inc.

333 North Broadway

Jericho, NY 11753

REFERENCES

Aquavella JV, Boghani S, Sjögren syndrome. Chapter in E-Medicine, www. emedicine.com Updated May 2005.

Lemp MA: Report of the National Eye Institute/Industry workshop on clinical trials in dry eyes. CLAO J 21:221–232, 1995.

Mircheff AK: Understanding the causes of lacrimal insufficiency: implications for treatment and prevention of dry eye syndrome. In: Research to prevent blindness science writers seminar. New York, Research to Prevent Blindness, 1993:51–54.

Sullivan PA, Sato EH: Immunology of the lacrimal gland. In: Albert DM, Jakobiec FA, eds: Principles and practice of ophthalmology: basic sciences. Philadelphia, WB Saunders, 1994:479–486.

Wang J, Aquavella JV, Zhao Y, Chung S: Tear dynamics measured with real-time otpicla cohenece tomography.[Abstract], Journal of Vision 4(11):89a, 2004.

297 UVEOPAROTID FEVER 298

(Heerfordt’s Syndrome, Uveoparotitis)

Frederick W. Fraunfelder, MD

Portland, Oregon

ETIOLOGY/INCIDENCE

Heerfordt syndrome (uveoparotid fever) consists of bilateral uveitis and parotid gland enlargement and is generally thought to be caused by sarcoidosis. It is often associated with systemic symptoms and cranial nerve palsy, usually the seventh nerve. Sarcoidosis is increasingly recognized as a cause of multifocal choroiditis and panuveitis. Severe dry eye is also a common occurrence with this condition.

COURSE/PROGNOSIS

Facial palsy and parotid swelling are usually transient and do not recur, but even with systemic steroid treatment, about onefourth of patients are left with a chronic mild uveitis that requires continuing minimal systemic or local steroid treatment. There is an increased incidence of severe sarcoidosis in the African American population. When sarcoid uveitis is severe, it is particularly likely to be associated with raised intraocular pressure during the active stage. Later, broad adhesions across the drainage angle resulting from the fibrosis of iris nodules may lead to chronic closed-angle glaucoma. As in any other case of uveitis, secondary cataracts may form.

DIAGNOSIS

Clinical signs and symptoms

The signs of the syndrome may be incomplete and are usually associated with other ophthalmic and general manifestations of sarcoidosis. Posterior uveitis frequently accompanies the

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anterior uveitis but may appear to be present alone with ‘snowball’ vitreous opacities and haze and whitish fundus lesions. Retinal vasculitis affecting the veins may be a prominent feature in some cases, but fluorescein angiography reveals that it is much more frequent than would be suspected on routine ophthalmoscopy.

Only rarely are lacrimal glands clinically swollen, but they are frequently affected as revealed by evidence of tear deficiency in 65% of sarcoid patients compared with 6% of matched control patients. The eyes feel ‘gritty,’ especially in a dry or smoke-laden atmosphere, and are prone to recurrent infection of the conjunctivae and lid margins. The hyalinized epithelial cells of the exposed conjunctiva and cornea stain with rose bengal, and especially in uveoparotid fever, mucus filaments may be attached to the corneal epithelium, causing pain and photophobia. The tear film is thinned with an accelerated break-up time of less than 10 seconds. Schirmer’s test confirms a reduction of tear flow. Conjunctival follicles with sarcoid histology are commonly present in the lower fornix and are a valuable source of biopsy material.

Both the cornea and conjunctiva may be involved in the deposition of calcium salts in exposed areas when sarcoidosis is complicated by hypercalcemia. In the cornea, this appears as a band opacity and may be associated with redness and discomfort. Some patients may become uremic from renal calcinosis. In addition to the facial palsy, in which the nerve may be involved above or below the level at which it is joined by the chorda tympani, sarcoid deposits at the base of the brain may cause other cranial nerve palsies and a variety of neurologic effects depending on the situation of the granulomas.

Diabetes insipidus and hypopituitarism from hypothalamic lesions may also occur. The optic nerve itself may be affected, with visual loss being associated with papilledema or optic atrophy. Finally, the skin of the eyelids may be disfigured by sarcoid papules.

Ocular and periocular signs include:

●Conjunctiva: follicles, hyperemia, keratoconjunctivitis sicca;

●Cornea: band keratopathy, keratoconjunctivitis sicca;

●Eyelids: sarcoid nodules in skin;

●Iris, ciliary body or choroid: sarcoid nodules, uveitis;

●Lacrimal system: decreased tear secretion, infiltration of lacrimal gland;

●Optic nerve: atrophy, papilledema, internal ophthalmoplegia;

●Retina: vasculitis, mainly affecting veins;

●Sclera: episcleral nodules, episcleritis;

●Vitreous: haze, snowball opacities;

●Other: diplopia, paralysis of seventh nerve, proptosis due to orbital sarcoid granulomas, secondary cataract, secondary glaucoma, visual loss.

Laboratory findings

●Noncaseating epithelioid cell follicles in biopsy material from the liver, skin, lymph nodes, or conjunctiva.

●Radiographic changes in the lungs.

●Low tuberculin sensitivity.

●Serum angiotensin-converting enzyme level elevated.

●Whole-body gallium isotope scans (67Ga) taken up by active cells at inflammatory sites, especially sarcoid granulomas.

●Kveim–Siltzbach skin test.

●Leukemia.

●Lymphoma.

●Tuberculosis.

●Sjögren’s syndrome.

●Mumps.

●Waldenström’s macroglobulinemia.

TREATMENT

Systemic

Systemic corticosteroid treatment is essential for all patients with Heerfordt’s syndrome. It will usually control the uveitis and retinal vasculitis, lead to resolution of the swollen parotid glands, improve the keratoconjunctivitis sicca by resolving lacrimal gland lesions, and restore a normal blood calcium level by increasing urinary excretion and decreasing intestinal absorption of calcium.

In general, the corticosteroid dose is kept as low as is possible to produce the desired response. Initially, the administration of 40 to 60 mg/day prednisone orally in conjunction with topical ophthalmic prednisolone, hydrocortisone, betamethasone, or dexamethasone may be necessary to control uveitis. This dosage may be slowly reduced over a period of months but must never be withdrawn abruptly.

Central nervous system lesions usually resist treatment and may occasionally present grave therapeutic problems, especially if a large dose is required for a long period. Skin lesions are usually resistant to corticosteroid treatment and may be disfiguring. To avoid higher corticosteroid doses, 200 mg of chloroquine may be given twice daily, although the cornea and retinal function must be reviewed regularly during treatment for signs of toxicity.

Ocular

The usual topical ophthalmic treatment for uveitis by mydriasis and cycloplegia is 1% atropine solution or ointment, 1% cyclopentolate solution, or 5% phenylephrine solutions. Corticosteroids (topical, 0.1% dexamethasone alcohol; 1.0% prednisolone acetate, or 0.5% prednisolone sodium phosphate) are used at a frequency of up to twice hourly and gradually reduced. Subconjunctival or retrobulbar injection is the initial treatment for severe uveitis, with betamethasone sodium phosphate 4 mg or a slow-release preparation of methyl prednisolone acetate 20 mg. A combined injection of corticosteroid with a mydriatic and local anesthetic may be particularly useful, for instance, Mydriacaine No. 2, a mixture containing epinephrine acid tartrate 216 μg, atropine sulphate 1 mg, procaine hydrochloride 6 mg, boric acid 5 mg, sodium metabisulphite 300 μg, sodium chloride 300 μg, and water for injection to 0.3 mL.

Keratoconjunctivitis sicca is usually treated with one of the artificial tear preparations, but in the case of filamentary keratitis, a mucolytic agent may be required at intervals, such as 5% to 10% acetylcysteine. Acute band keratopathy usually responds to reduction of the serum calcium level but may require surgical removal. EDTA (edetate disodium), chelates calcium and allows one to remove it from the surface of the cornea. The argon fluoride excimer laser, which produces an ultraviolet radiation that is readily absorbed by all tissues and penetrates by only a few micrometers, causes photoablation in which the tissues are vaporized and also can be used to remove a band opacity.

COMMENTS

The use of topical and systemic corticosteroid therapy is essential, but the possibility of corticosteroid-induced cataract or

secondary glaucoma must be borne in mind and care must be taken to exclude other diseases such as diabetes, tuberculosis, or peptic ulcer because the usual regimen may require modification. Indomethacin may be considered in acute uveitis, and azathioprine may allow a 50% reduction in the steroid dose.

Uveoparotid fever must be regarded as a potentially severe form of sarcoidosis requiring prolonged energetic systemic corticosteroid therapy and close supervision. Its duration will depend on the progress of the disease. A delicate balance must be preserved between tissue damage by sarcoidosis and the complications of corticosteroid treatment.

Local therapy with mydriatics and corticosteroids alone is unlikely to control the uveitis of uveoparotid fever; however, these medications help raise intraocular concentrations even when systemic treatment is being given, and they may be used for local ocular defense over a long period when it is considered safe or desirable to withdraw systemic corticosteroids. Such patients should always be watched for signs of corticosteroidinduced glaucoma, which is more likely to be caused by local than by systemic treatment.

It is sometimes difficult to decide whether secondary glaucoma is caused by uveitis or corticosteroids. In either case, it is usually best to continue therapy and treat the raised intraocular pressure with anti-glaucoma medications.

Corticosteroid-induced cataracts are a therapeutic risk which may require surgery in some patients.

REFERENCES

Bruins Slot WJ: Besnier-Boeck’s disease and uveoparotid fever (Heerfordt). Ned Tijdschr Geneeskd 80:2859–2863, 1936.

Blair MP, Rizen M: Heerfordt syndrome with internal ophthalmoplegia. Archives of Ophthalmology 123:1017, 2005.

Gartry G, Kerr Muir M, Marshall J: Excimer laser treatment of corneal surface pathology: a laboratory and clinical study. Br J Ophthalmol 75:258–269, 1991.

James DG, Anderson R, Langley D, Ainsley D: Ocular sarcoidosis. Br J Ophthalmol 48:461–470, 1964.

297 CHAPTERFever Uveoparotid •

298 ADULT CATARACTS 366.10

Kelly D. Chung, MD

Portland, Oregon

ETIOLOGY/INCIDENCE

Cataract is a disorder in which the crystalline lens becomes opacified. It is the leading cause of visual impairment in all but the most developed countries where cataract surgery represents one of the most common surgical procedures performed.

The etiology of the vast majority of cataracts is age-related though genetic factors probably account for around 50% of age-related cataract with systemic and environmental factors, the remainder. Diabetes mellitus, corticosteroid use, heavy alcohol use, smoking, and lifetime ultraviolet light exposure are amongst the many factors that are linked to cataract formation.

Cataract is classified according to the portion of the lens that is opacified. The major types include nuclear, cortical, and posterior subcapsular though it is common to have a mixture of these types of opacities in a given cataract. Although all types of cataract can be simply age-related cataract, posterior subcapsular cataract is commonly seen with toxicities such as uveitis or corticosteroid-induced cataracts.

DIAGNOSIS

Early cataract may not disturb vision. However, as the opacification of the lens increases, cataract can produce painless progressive decrease in visual acuity and contrast sensitivity. There may be symptoms of glare, monocular diplopia, and changing refractive error.

Cataract is diagnosed clinically, optimally with the patient’s pupil dilated and slit lamp biomicroscopy. The red reflex is reduced or completely interrupted by the opacity and the opacities are directly visualized within the lens.

COURSE/PROGNOSIS

The course of cataract is generally slowly progressive with the patient experiencing from few or no symptoms early on to blurred vision, glare and changing refractive error. There is no proven way to prevent or slow the progression of cataract.

TREATMENT

Early on, managing a change in refractive error can sometimes improve a patient’s visual function without further intervention.

When the vision is no longer adequate to meet the patient’s activities of daily living then cataract surgery is indicated. Occasionally, cataract surgery is indicated for medical rather than functional reasons if it is blocking a view to monitoring or treating the retina, leaking lens proteins, or causing narrow angle glaucoma. The prognosis for improved vision after cataract surgery in an otherwise healthy eye is excellent.

REFERENCES

McCarty CA, Taylor HR: The genetics of cataract. Invest Ophthalmol Vis Sci 42:1677–1678, 2001.

Negahban K, Chern K: Cataracts associated with systemic disorders and syndromes. Curr Opin Ophthalmol 13:419–422, 2002.

Resnikoff S, Pascolini D, Etya’ale D, et al: Global data on visual impairment in the year 2002. Bulletin of the World Health Organization 82:844– 851, 2004.

299 AFTER-CATARACTS 366.50

Christopher Graham Tinley, MBChB, MRCOphth

Devon, England

After-cataract is a term originally used to describe lens epithelial cell proliferation following cataract surgery. A broader definition may include any visually significant opacification of the intraocular lens/capsular bag complex.

ETIOLOGY/INCIDENCE

Posterior capsule opacification

By far the most common cause of after-cataract is posterior capsule opacification (PCO). Following cataract surgery, lens epithelial cells (LECs) not completely removed from the capsular bag can be divided into two entities: anterior LECs (A cells), which form a single layer on the back of the anterior capsule around the capsulorhexis and E cells, located in the equatorial region. The E cells comprise germinal cells, which are the primary cells of origin of PCO. Immediately after uncompli-

Lens • 26 SECTION

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Lens • 26 SECTION

300 CONGENITAL AND INFANTILE

CATARACTS 743.20

Krista A. Hunter, MD

Portland, Oregon

David T. Wheeler, MD

Portland, Oregon

ETIOLOGY/INCIDENCE

A cataract can be defined as any light-scattering opacity of the lens. It is estimated that congenital cataracts are responsible for 5% to 20% of blindness in children worldwide. Incidence varies from country to country. One newborn out of every 250 is estimated to have some form of cataract. One retrospective study of the prevalence of infantile cataracts in the United States showed a rate of 3–4 visually significant cataracts per 10,000 live births. This is a similar rate to a UK study which showed 3.18 per 10,000. These numbers underestimate the total number, however, since they do not take into consideration visually insignificant cataracts.

Cataracts may be unilateral or bilateral and can vary widely in size, morphology and degree of opacification from a small white dot on the anterior capsule to total opacification of the lens. Consequently, the effect on vision, course of treatment and prognosis may also be widely variable.

The causes of infantile cataracts have been the source of much speculation and research. Making a distinction between unilateral and bilateral cataracts may be useful when considering etiology.

Approximately two-thirds of bilateral congenital or infantile cataracts have an identifiable cause or are hereditary. Many genes involved in cataract formation have been identified, and inheritance is most often autosomal dominant although it can be X-linked or autosomal recessive. Within the same pedigree, there can be considerable morphologic variation. Galactosemia is an important example of an autosomal recessive condition while Lowe syndrome is the most common X-linked condition associated with cataracts.

Systemic associations with congenital cataracts include metabolic disorders such as galactosemia, Wilson disease, hypocalcemia and diabetes. Cataracts may be a part of a number of syndromes, the most common being trisomy 21. Intrauterine infections including rubella, herpes simplex, toxoplasmosis, varicella and syphilis are another cause.

In contrast, most unilateral cataracts are not inherited or associated with a systemic disease and are of unknown etiology although they do not rule out the possibility of an associated systemic disease. They are usually the result of local dysgenesis and may be associated with other ocular dysgenesis such as persistent fetal vasculature (PFV), posterior lenticonus, or lentiglobus.

Trauma is a known cause of pediatric cataracts. If there is no known history of trauma to explain an acquired cataract in this age group, investigation must be considered in children who present with other signs suggestive of child abuse.

Regardless of the etiology, prompt treatment of visually significant cataracts is necessary to allow proper development of vision.

COURSE/PROGNOSIS

The course and prognosis of pediatric cataracts is highly variable. The likelihood and rate of progression is very difficult to predict. In addition, the presence of other ocular or systemic abnormalities also contributes to the variable outcome.

The most serious complication of congenital cataracts is permanent visual impairment. When the visual axis is blocked by lens opacity during the sensitive period of visual development, irreversible amblyopia and permanent nystagmus may result. The first two months of life are the most critical for visual development; amblyopia resulting from visual deprivation after the age of 2 to 3 months can often be reversible to some degree. Visual development continues until at least 6 to 7 years of age.

Unilateral cataracts carry a less favorable prognosis than bilateral cataracts. Even a minimal opacity can create significant amblyopia. A child with a unilateral cataract is also at greater risk for anisometropia, which can complicate the picture.

In addition to clearing the visual axis by appropriate surgical technique, proper optical correction in the form of aphakic glasses, contact lenses or intraocular lens implants is essential for good visual development. This requires an ongoing commitment from both the ophthalmologist and family of the infant.

DIAGNOSIS

Clinical signs and symptoms

Cataracts present as opacities in the lens which span a spectrum from easily visible in the undilated state, and apparent to the parents or pediatrician, to much more subtle changes requiring pupillary dilation and careful examination with a slit lamp. The red reflex is an extremely useful part of the exam, as it allows the examiner to estimate the cataract’s size and location within the visual axis, even in an uncooperative child.

Cataracts are classified according to their morphological appearance and location; however, making the diagnosis of a specific type of cataract can be difficult if it spreads to involve multiple layers, obscuring the original opacity.

Cataracts may be a part of another disease or syndrome, and are sometimes the initial finding that leads to the disease diagnosis. A cataract may be accompanied by other noticeable ocular abnormalities such as microcornea, megalocornea, coloboma of the iris, aniridia, or zonular dehiscence.

Often an infant with mild cataracts appears asymptomatic, which may delay the diagnosis for years. At other times, lack of reaction to light, strabismus, a failure to notice toys and faces or an apparent delay in development becomes the cause of concern. Mild cataracts may cause photophobia only in bright lights. Dense cataracts also may be discovered if they lead to the development of sensory nystagmus.

For unilateral cataracts in an otherwise healthy child, an extensive workup is not necessary. The most critical part of the workup is a thorough ophthalmologic exam including slit lamp examination of both eyes, intraocular pressure testing, and ultrasound examination of the posterior pole if it is not visible. If the exam reveals the classic appearance of a specific diagnosis such as PFV or posterior lenticonus, no further evaluation is necessary.

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Lens • 26 SECTION

The first step in the diagnosis of a patient with bilateral cataracts should be a family history, including examination of family members. If there is a clear autosomal dominant pattern and the child is healthy, further evaluation is not necessary. In cases without clear family history, a thorough pediatric and developmental exam should be performed. Recommended lab workup includes TORCH titers, VDRL, serum calcium and phosphorus levels and urine for reducing substance. Additional systemic workup should be done in coordination with the pediatrician. Dysmorphic features may suggest the need for consultation with a geneticist.

Differential diagnosis

The differential diagnosis for leukocoria or “white pupil” includes retinoblastoma, persistent hyperplastic primary vitreous PFV, retinopathy of prematurity, chorioretinal colobomas, toxocariasis, Coats disease, vitreous hemorrhage and other retinal tumors. These can be distinguished by complete examinations of the anterior and posterior segment, often including ultrasound examination.

TREATMENT

Ocular

Not all pediatric cataracts require surgery. A small, partial or paracentral cataract can be managed by observation. Pharmacologic pupillary dilation with phenylephrine or tropicamide can be helpful. Dilation with atropine should be avoided. Parttime occlusion may be necessary in unilateral or asymmetric cases that develop or are at risk for amblyopia. These techniques may at least delay the need for surgery until a point when eye growth has stabilized and an IOL can be implanted with less refractive uncertainty. Because of the unpredictability in the progression of partial cataracts, these patients should be carefully monitored and if significant amblyopia develops and is unresponsive to treatment, surgical intervention should be performed.

Surgical

If the cataract(s) are felt to be visually significant, surgical intervention is the only option. The timing of surgery is critical for visual development. Most investigators recommend surgery within the first two months of life. There has been evidence to suggest that before one month of age, the risk of aphakic glaucoma is increased. In cases of bilateral cataracts, it may be advantageous to perform surgery on both eyes in the same intervention to allow for simultaneous initiation of visual rehabilitation as well as reducing exposure to general anesthesia. In this setting, treating each eye as a separate sterile procedure may reduce infection risk.

Removal of the lens can be approached through the limbus or the pars plana. The limbal approach has the advantage of maintaining the posterior capsule to facilitate posterior chamber intraocular lens (IOL) implantation if desired.

Several options exist for opening the anterior capsule in pediatric cataracts. The ideal anterior capsulectomy technique is one that results in low incidence of radial tears and is easily performed. In cases of dense cataract, dye can be used to stain the anterior capsule, making this step easier and safer. A manual continuous curvilinear capsulorhexis (CCC), which is the preferred method in adult eyes, can be difficult in pediatric cases due to the elasticity of the pediatric capsule. However,

when it can be controlled and completed, it creates an edge which has a low incidence of radial tears.

A mechanized circular anterior capsulectomy, known as vitrectorhexis, has been proven to be a very good, safe alternative if the CCC is not possible. The vitrector tip is placed through a stab incision at the limbus and irrigation is provided though a sleeve around the vitrector or though a separate limbal incision. A cut rate of 150 cycles per minute is recommended. The vitrector port is oriented posteriorly, and held in the center of the capsule to create an initial opening. The opening is enlarged in a circular fashion, holding the cutter just anterior to the capsule to aspirate the capsule up into the cutter. A smooth, round capsulectomy that is also resistant to radial tears can be produced. This procedure is facilitated by using a vitrector supported by a venturi pump.

Pediatric cataracts are soft, and therefore phacoemusification is generally not needed. The lens cortex and nucleus can be removed with an irrigation-aspiration or vitrector hand piece.

To reduce the risk of posterior capsule opacification, which occurs in approximately 80% of pediatric eyes, most surgeons perform a posterior capsulorhexis at the time of surgery. The lens capsule can be filled with viscoelastic and a posterior continuous capsulorhexis made slightly smaller than the anterior one. If an IOL is to be implanted, it can be placed in the capsular bag at this time and some advocate the technique of optic capture where the optic is pressed through the posterior capsulorhexis and the haptics remain in the bag.

It is controversial whether an anterior vitrectomy should be performed at the primary surgery. It can be performed either though the limbal incisions, after making the posterior capsulotomy with the vitrector hand piece, or through the pars plana. The anterior vitreous is removed and the lens epithelial cells therefore cannot grow in the vitreous face.

IOL implantation in children is felt to be safe and acceptable in children as young as one year. In those younger than one year, the decision is more controversial and research is ongoing. The refractive goal of surgery is also controversial. Most surgeons will choose to make the child hyperopic but there is currently no agreed-upon standard. These children will need bifocal glasses for the rest of their lives.

A pars plana approach can be used when no IOL implantation is intended. An attempt is made to remove the whole cataract and the adjacent vitreous with a vitreous cutter.

Care should be taken to remove the viscoelastic entirely to prevent elevated intraocular pressure following surgery and the anterior chamber should be checked carefully for vitreous. The sclera in children is soft and elastic and it is difficult to achieve a self-sealing incision; thus the incision should be closed using 10-0 nylon or Vicryl suture.

COMPLICATIONS

Opacification of the visual axis is the most common complication of cataract surgery in children. This is a serious complication because it can lead to amblyopia. A posterior capsulorhexis and anterior vitrectomy, as previously discussed, is one way to avoid this. An IOL can prevent the formation of a Sommering ‘s ring, but it is also easier for the lens epithelial cells to migrate to the center of the pupil. Others have suggested that capturing the optic by placing the haptics in the bag and pushing the optic through the posterior capsularhexis may prevent opacification. If opacification occurs, a Nd : YAG laser capsulotomy can be attempted. In this age group, general anesthesia is necessary

Cataracts300 InfantileCHAPTERand Congenital •