Delhi Journal of Ophthalmology

Pediatric Cataract

Bharat Patil, Reetika Sharma, Bhagbat Nayak, Gautam Sinha, Sudarshan Khokhar
Cataract, Refractive Surgery &
Glaucoma Services
Dr Rajendra Prasad Centre for
Ophthalmic Sciences,
All India Institute for Medical Sciences, New Delhi 110029, India

Corresponding Author:

Bharat Patil
Senior Resident,
Cataract, Refractive & Glaucoma Services
Dr Rajendra Prasad Centre for
Ophthalmic Sciences,
All India Institute of Medical Sciences, New Delhi 110029, India

Published Online: 01-MAR-2015


Paediatric cataract is one of the most important surgically treatable causes of childhood blindness. Treating pediatirc cataract has a large impact on society as ‘lost blind years’ can be saved. Various morphological types are known of which zonular has the best visual prognosis. Rubella accounts for the most common preventive cause for pediatrc cataract. Intraoperative biometry plays an important role though in coperative children optical biometry may be suitable option. Since the pediatric eye and pediatric lens is not a minature adult eye and lens repsectively, surgical steps needs to be modified. Intraocular lenses (IOL) provide the best available option for visual rehabilitation after removal of cataract because of the constant visual input provided. Poor intraocular lens power predictability, increased inflammation, postoperative complications and the technical difficulty of surgery are the main concerns for IOL implantation. Surgery is just a step towards management of pediatric cataract, amblyopia therapy, glasses correction, and log term follwup are essetinal for better outcomes. 

Keywords :pediatric cataract • Lens aspiration • Posterior capsulorhexis

According to World Health Organisation (WHO), every minute a child goes blind somewhere in the world.[1] Childhood blindness has a socioeconomic impact over child, family and the society due to ‘blind years’. Cataract being one of the leading causes of childhood blindness and being treatable, it is logical to think that an improved approach to the management of childhood cataract would have large impact on childhood blindness.[2-4] The control of childhood blindness has been identified as a priority of the WHO global initiative for the elimination of avoidable blindness by the year 2020.2 In India, lens related causes accounts for 7.4-12.3% of childhood blindness3-4global number being 14%.[5]

The prevalence of childhood cataracts has been reported to vary between 1.2 and 13.6 cases per 10000 children.[6] The wide range is due to variety of methods, case definitions, different age groups, as well as true differences between populations.

Aetiology of Childhood Cataract

Though traditionally it has been described that roughly one third childhood cataracts are inherited, one third are associated with other diseases or syndromes, and the remaining one third are idiopathic; the aetiological classification of childhood cataract is not so simple and straight forward. Different studies give varying results. Important causes of childhood cataract in younger kids include genetic aberrations,[7] metabolic disorders,[8] prematurity,[9] and intrauterine infections.[10-13] Significant causes of childhood cataract in older children include trauma,[10-12] drug-induced cataract,[14] radiation therapy,[15] and laser therapy for ROP.[16]

Angra SK10 studied 200 cases of congenital cataract and found that 31% were idiopathic, 14% were hereditary, and 21% might have been due to rubella. They didn’t examine parents and rubella was diagnosed on clinical grounds alone. Jain et al[11] prospectively enrolled 76 children with cataract from a general clinic over 1 and 1/2 years and noted that 20% of the cataracts were hereditary, 9% were due to metabolic diseases, and 5% had an associated syndrome and 46% were idiopathic. Nearly 8% had a positive rubella titre but the disease may have been acquired after birth and the significance is questionable. Michael et al[12] evaluated 514 consecutive patients of congenital cataract in a hospital based study. Of the 366 children with nontraumatic cataract, 25% were hereditary, 15% were due to congenital rubella syndrome, and 51% were undetermined. In children under 1 year of age 25% were due to rubella and cataract of nuclear morphology had a 75% positive predictive value for congenital rubella syndrome.

 In approximately 50% of bilateral cases and virtually all of the unilateral cases, the underlying cause could not be determined. Approximately 20% of cases are associated with a positive family history.[17] About one third of cases are hereditary, without a systemic disease.[18,19] Autosomal dominant transmission is responsible for 75% of congenital hereditary cataracts and affected children are usually perfectly alright. Less commonly the inheritance may be autosomal recessive and X-linked.[20,21] Rare causes of childhood cataracts are metabolic disorders such as galactosemia and hypocalcemia.[22] Galactosemia causes characteristic oil ‘droplet cataracts’. About 10 – 30% of classic galactosemia cases develop cataracts in the first few days or weeks of life, which usually clear once the baby is put on a galcatose free diet.[20] Congenital cataracts may be associated with systemic abnormalities such as trisomy[21] and Turner’s syndrome. Mental retardation is commonly associated with bilateral congenital cataract, and there are many inherited syndromes with this combination linked with other abnormalities such as craniofacial or skeletal deformities, myopathy, spasticity, or other neurological disturbances.[23] Trisomy[21] is the most common systemic association of sporadic cataract, upto 13% cases of Down’s syndrome are associated with cataract.[24]

Several intrauterine infections (toxoplasmosis, rubella, cytomegalic inclusion disease, herpes infection, varicella, and syphilis) can cause congenital cataracts.[21,25-27] Of these, rubella is the most important. Rubella cataract is usually bilateral but may be unilateral.[13] Unilateral congenital cataract is generally not associated with systemic disease and is rarely inherited; in most cases, the cause is idiopathic.[28] Some cases are associated with lenticonus or lentiglobus and persistent fetal vasculature (PFV).[21] Trauma is one of the common causes of unilateral childhood cataract in developing countries.[29,30]


Morphology of the cataract is important for several reasons: it not only gives a clue to the age of onset, heritability, and aetiology but may also be important for visual prognosis. Some morphological types have a better visual prognosis than others, with lamellar cataracts and posterior lenticonus doing well and dense central cataracts relatively poorly.[31-33] Total cataracts involving nearly the entire lens occur in Trisomy 21, acute metabolic cataracts and congenital rubella, but may be seen in familial or sporadic cases.[34]

In congenital Morgagnian cataracts, the outer zones of the lens become liquefied whilst the nucleus remains intact. This allows the nucleus to fall by gravity in any direction, depending on the position of the head. Membranous cataracts represent last stage of re-absorption of the lens, leaving either a disc of lens material or the anterior and posterior capsules fused together. It is common in PFV,[35] trauma[36] and congenital rubella.[37] Zonular cataract is the most common type of congenital cataract.[38] It involves one or more layers or zones of the lens. These cataracts are usually idiopathic or inherited as an autosomal dominant trait. Typically, they are bilateral but slightly asymmetrical, and are composed of a layer of minute white dots in a single or more layers of the lens. The embryonic nucleus is spared, but sometimes involving the foetal nucleus, and with clear cortex outside them. There is often a marked inter-ocular and intra-familial variability.[39] morphologicaly cataract is often incomplete, and may have projections from their outer edges known as ‘riders’. The visual prognosis, especially in partial cataract, is better than in many other morphological types.[34]

Sutural cataract is a special type of zonular cataract, in which there are opacities around or involving the sutures. They are often familial and range from an increased density of the sutures to a variety of whitish or cerulean dots clustered around either or both sutures. They are visually insignificant unless they progress to nuclear.[38] Anterior polar and anterior pyramidal cataracts represent abnormalities of lens vesicle detachment. Anterior pyramidal cataracts are more likely to be visually significant and to progress than anterior polar cataracts. They may become detached[40] and may form an anterior chamber foreign body. Anterior lenticonus may be sporadic or may be associated with other disorders. Bilateral anterior lenticonus is characteristic feature of Alport’s syndrome. It may be a manifestation of a basement membrane disorder.[41] It can be congenital and is found in about 10% of affected young children,[42] but may increase in frequency with time up to 30%.[43]

Posterior lenticonus is a unilateral or bilateral and asymmetrical, thinning and posterior bowing of the posterior lens capsule. Patient may either have a high degree of astigmatism, often irregular, without cataract. If cataract present it may be a progressive or localised It is not usually associated with any systemic disease, unlike anterior lenticonus. It can be sporadic, autosomal dominant[44] or X linked.[45]

Preoperative Workup


A good history can give a clue to aetiology. Presenting complaint may give clue to prognosis, as patient presenting with leucocoria may have better prognosis as compared to those with squint or abnormal eye movements. Similarly, longstanding opacity hampers prognosis due to image deprivation amblyopia. Any significant family, intranatal, postnatal history should also be noted. History of associated illness should also be elicited. Detailed history of trauma can indicate the severity of damage.

Visual assessment

Letter acuity assessment is normally possible in children from about 5 years of age. For younger children, from about 3 years of age recognition acuity can be assessed using symbols.[46] Cardiff acuity test is useful for toddlers.[47] Teller acuity test is recommended usually for infants.[48] Visual evoked potential, fixation-refixation pattern and pupillary reflexes can give idea about the child’s visual potential.

Parent Counselling

Parents should understand that surgery is one of the steps in management of the childhood cataract; in fact treatment starts after surgery. They need to come for regular follow-up visits and see that the child wears glasses or contact lenses despite the IOL implantation; the child may also need occlusion therapy following surgery. Regular follow-up is essential for the successful management of childhood cataract.

Biometry and Keratometry

Because of a lack of cooperation in the clinic setting, axial length (AL) measurements of young children often must be obtained in the operating room under general anesthesia. A-scan ultrasound biometry is the conventional method for the measurement of AL in children. Many A-scan instruments are available. For accurate measurements one must ensure calibration[49] The instrument must have an oscilloscope screen such that true echo spikes are observed in determining axiality.[49] Instruments that merely give a numerical reading of the AL do not allow clinical decision making during the examination and are fraught with potential for errors. Ultrasound biometry can be done with either contact or immersion method. In the contact method, the probe touches the cornea and may result in corneal compression and a shorter AL. Because of low corneal and scleral rigidity, corneal compression is more likely in paediatric eyes. Using the immersion technique, the ultrasound probe does not come into direct contact with the cornea, but instead uses a coupling fluid between the cornea and the probe preventing corneal indentation. Immersion A-scan has been shown to be superior to contact biometry in children.[50] Trivedi and Wilson,[51] proved that, AL measurements made with a contact technique were, on the average, 0.24–0.32 mm less than measurements made using an immersion technique. In spite of this advantage, indentation method is more commonly used, (82.4% vs. 17.6%).[51]

Optical biometry is based on partial coherence interferometry. There are currently two optical biometry devices on the market and the use of both devices in children has been reported.[52,53] Optical biometry has been used in cooperative children with reliability and accuracy. Though hand held keratometer is best for recording keratometry, manual keratometer and optical instruments can also be used.[54]

IOL Power Calculation in Children

Constant size of adult eye ensures stable refraction in postoperative period. However ocular growth has a profound effect in children causing myopic shift. Surgeons can either choose hyperopia, with expectation of myopic shift with time; or can opt for emmetropia to help with amblyopia management. Each of these approaches has advantages and disadvantages. We prefer to leave a child hyperopic, using a logical approach based on knowledge of how the refraction is likely to change with age. Various guidelines are available on residual hyperopia and IOL power undercorrection.[55] No IOL power calculation formula was found to be superior over others and there is no general consensus over the choice of formula. Andreo et al[56] found no significant difference in accuracy between SRKII, SRK-T, Holladay and Hoffer Q. Another study found that theoretic formulas were slightly more accurate than regression formulas but no IOL power calculation formula was satisfactory.[57] Errors of IOL power calculation are more if AL is <20 mm and age <36 months.[58]

Indications of Surgery

Indications for cataract surgery include visually significant central cataracts larger than 3 mm in diameter, dense nuclear cataracts, cataracts obstructing the examiner’s view of the fundus and cataracts associated with strabismus, abnormal eye movements.[59]


Paediatric eyes are not just miniature adult eyes. They differ from the adult eye in many aspects.

Applied Anatomy
  1. Capsule: The anterior capsule is thinnest at birth, increasing in thickness with age. The young anterior lens capsule is strong and very elastic. The elderly anterior lens capsule is, by comparison, weak and inelastic. Krag and coworkers[60] found that anterior lens capsule extensibility was maximal in infancy and decreased about 0.5% per year throughout life.
  2. Anterior chamber (AC): It is shallow as compared to adults. Anterior chamber is shallower in the cataractous eye in case of unilateral cataract.[61]
  3. Sclera and vitreous
    • non liquefied vitreous and thin sclera with low rigidity results in vitreous up thrust. Thus to maintain chamber stability and make a good anterior capsulorrhexis, use of high viscosity ophthalmic viscosurgical device (OVD) is must.
    • Thick vitreous gel gives protection against macular edema.
  4. Rapidly dividing lens epithelial cells (LECs), results in high incidence of visual axis opacification (VAO) necessitating primary management of the posterior capsule.
Surgery: Key Considerations

Wound construction: superior incision allows wound to be protected by eye lid and by Bell’s phenomenon in trauma prone childhood years. Adult studies showed, corneal tunnel incision has potential risk of endophthalmitis,[62] but in children the surgical incisions are sutured. This may diminish the risk of post op endophthalmitis.

Anterior capsule: Owing to the factor mentioned in applied anatomy section, anterior curvilinear capsulorrhexis (ACC) is difficult in children as compared to adults. Though various techniques (Vitrectorhexis, Fugo blade, diathermy assisted, can opener etc) have been described for paediatric ACC, manual ACC is gold standard and most preferred technique.[63] Hydro dissection: Advantages of cortical-cleaving hydrodissection, (ease, safety, and efficacy of removing lens matter) are well known. Mutiquadrant hydrodissection (at least 3 quadrants) is preferred method in paediatric group. It not only helps in lens aspiration but also ensures removal of LECs.[64]

Posterior capsulotomy and anterior vitrectomy: unlike adults, Visual Axis Opacification, VAO is more common in children. Anterior vitreous face is more closely linked to posterior capsule and more reactive in children. It acts as a scaffold for proliferating LECs and metaplastic pigment cells. Anterior vitrectomy breaks this scaffold, thus preventing VAO formation. Decision about Posterior curvilinear capsulorrhexis (PCC) and vitrectomy is based on age of patient at surgery. Posterior caapsulotomy is must for all patients less than 8 years of age. Vitrectomy can be deferred after 5 years of age.[65] IOL implantation: Primary IOL implantation is preferred, if not contraindicated.[66] The problem lies in the sizing of IOLs. Adult size IOLs are known to cause capsular bag ovaling, bag distension syndrome and displacement. Ovaling was seen least with single piece acrylic hydrophobic lenses.[67] Acrylic hydrophobic IOLs have been found to be efficacious, but long-term results are unknown.[66]

Post-operative Management

Postoperative management of Paediatric cataract surgery is unique, surgery is only a part of the management and success of the depends on the postoperative follow up, multiple examinations under anesthesia (EUA) as applicable, amblyopia management and early detection and treatment of complications.

Post-operative Medications

The regular medications post-surgery in a case of paediatric cataract surgery comprise of antibiotic eyedrops, steroid eyedrops and cycloplegics. Inflammatory response following cataract surgery is more intense in children and hence requires intensive topical steroids. The frequency and duration for their use needs to be tailored depending on the preoperative diagnosis and postoperative response. Usually it is tapered over a period of six to eight weeks. Topical antibiotics are instilled three times a day for two to three weeks. Cycloplegics stabilize the blood-aqueous barrier, relieve ciliary spasm and dilate the pupil. Hoamatropine eye drops 2% four times a day or atropine eye ointment 1% thrice a day can be used.

Follow up

These children require life-long follow up. They are seen on the first postoperative day then first week and then as and when required depending on surgeon’s protocol. EUA is planned after six to eight weeks for suture removal if non absorbable suture has been used. At each visit, visual acuity, slit lamp examination, intraocular pressure and fundus should be noted.

Correction of Refractive error

Residual refractive error should be corrected as early as possible. Options for correction of refractive error include spectacles, contact lens and epikeratophakia (outdated now due to complications). Children in the preschool-age may be provided near add incorporated in the retinoscopy where as older children should be given bifocal glasses. Need of glasses should be explained to parents. This also requires repeated refraction and change of glasses over time.

Postoperative amblyopia therapy should be instituted meticulously. Occlusion therapy for unilateral cataract after surgery should be started early as these children are at higher risk of developing amblyopia.

Post-operative Complications

Glaucoma following cataract surgery in children is well documented. It may occur in the early postoperative period or as late as decades after surgery. Various studies have found glaucoma to be observed in 10-25% of children after paediatric cataract surgery.[68-75] Early age at surgery and presence of microphthalmia are high risk factors. Trivedi et al8 have found the incidence of glaucoma to be comparable between pseudophakic and aphakic eyes. In contrast, no glaucoma was reported by Cassidy et al[76] who found a protective role of primary lens implantation against glaucoma. Visual axis opacification is the most common complication after pediatric cataract surgery with or without IOL surgery.[77,78] If not treated on time it may cause visual deprivation amblyopia. Primary posterior continuous curvilinear capsulorrhexis and anterior vitrectomy or posterior capsulotomy with endodiathermy of capsule or posterior capsulorrhexis with optic capture have been used in paediatric population and have shown to decrease VAO formation.[79-82] In a thick VAO, surgical management in the form of posterior capsulotomy combined with anterior vitrectomy is required to prevent amblyopia. Nd: YAG laser has also been used.[83]

Postoperative uveitis is a common complication due to increased tissue reactivity. This can result in posterior synechia formation leading to seclusio pupillae, iris bombe and subsequent secondary angle closure glaucoma and VAO. Due toimproved surgical techniques and frequent use of topical steroids and cycloplegics in the postoperative period uveitis and its related complications have been seen to decrease. Pupillary capture among children is high, varying from 8.5% to 33%.[38,83] In-the-bag IOL fixation decreases the incidence of this complication.[85] IOL decentration is also common which can be prevented by in the bag placement of IOL.[84]

Retinal detachment is a rare but sight threatening complication, more common in eyes with Persistent foetal vasculature Cystoid macular oedema following congenital cataract surgery has been described but is self-limiting and usually not problematic.

Financial & competing interest disclosure

The authors do not have any competing interests in any product/procedure mentioned in this study. The authors do not have any financial interests in any product / procedure mentioned in this study.

  1. WHO. Press release. Geneva: World Health Organization, 2002.
  2. Thylefors B, Negrel AD, Pararajasegaram R, et al. Global data on blindness. Bull World Health Organ 1995; 73:115–21.
  3. Gilbert C, Canovas R, Hagan M, Rao S, Foster A. Causes of childhood blindness: results from west Africa, south India and Chile. Eye 1993; 7:184-88.
  4. Rahi JS, Sripathi S, Gilbert C, Foster A.. Childhood blindness in India: causes in 1318 blind school students in nine states. Eye 1995;9:545-50.
  5. WHO. Preventing blindness in children: report of WHO/IAPB scientific meeting. Programme for prevention of blindness and deafness and International Agency for prevention of blindness. Geneva: WHO; 2000.
  6. Haargard B, Wohlfahrt J, Fledelius HC, Reosenberg T, Melbye M.  Incidence and cumulative risk of childhood cataract in a cohort of 2.6 million Danish children. Invest Ophthalmol Vis Sci 2004; 45:1316-20.
  7. Salmon JF, Wallis CE, Murray AD: Variable expressivity of autosomal dominant microcornea with cataract. Arch Ophthalmol 1988; 106:505–10.
  8. Merin S, Crawford JS: Hypoglycemia and infantile cataract. Arch Ophthalmol 1971; 86:495–98.
  9. McCormick AQ: Transient cataracts in premature infants a new clinical entity. Can J Ophthalmol 1968; 3:202–6.
  10. Angra SK. Aetiology and management of congenital cataract. Ind J Pediatr 1987; 54:673-7.
  11. Jain IS, Pillay P, Gangwar DN, Dhir SP, Kaul VK. Congenital cataract: aetiology and morphology. J Pediatr Ophthalmol Strabismus 1983; 20:238-42.
  12. Michael E, Vijayalakshmi P, Killedar M, Gilbert C, Foster A.  Aetiology of childhood cataract in south India. Br J  Ophthalmol 1996; 80:628-632.
  13. Eckstein MB, Brown DW, Foster A, et al: Congenital rubella in south India: diagnosis using saliva from infants with cataract. BMJ 1996; 312:161.
  14. Miltenyi M, Homoki J, Fazekas AK, et al: Posterior subcapsular cataracts, associated with long-term corticosteroid therapy. Prednisolone versus 6 alpha-fluor-16 alpha- methyl-1-dehydrocorticosterone. Helv Paediatr Acta 1983; 38:141–7.
  15. Henk JM, Whitelocke RA, Warrington AP, Bessell EM: Radiation dose to the lens and cataract formation. Int J Radiat Oncol Biol Phys 1993; 25:815–20.
  16. Drack AV, Burke JP, Pulido JS, Keech RV. Transient punctuate lenticular opacities as a complication of argon laser photoablation in an infant with retinopathy of prematurity. Am J Ophthalmol 1992; 13:583–4.
  17. Apple et al. Pediatric Cataract Survey of Ophthalmology , Volume 45 , S150 - S168
  18. Bardelli AM, Lasorella G, Vanni M. Congenital and developmental cataracts and multimalformation syndromes. Ophthalmic Paediatr Genet 1989; 10:293–8
  19. Merin S, Crawford JS. The etiology of congenital cataracts; a survey of 386 cases. Can J Ophthalmol 1971; 6:178–82.
  20. Sursh KP, Wilson ME Jr. Etiology and Morphology of Pediatric cataracts. In: Wilson ME Jr, Trivedi RH, Pandey SK, eds, Pediatric Cataract Surgery; Techniques, Complications, and Management. Philadelphia, PA, Lippincott, Williams & Wilkins, 2005; 6-13.
  21. Wright KW, Kolin T, Matsumoto E. Lens abnormalities. In: Wright KW, ed, Pediatric Ophthalmology and Strabismus. St Louis, MO, Mosby. 1995; 367–89.
  22. Beigi B, O’Keefe M, Bowell R, et al. Ophthalmic findings in classical galactosaemia—prospective study. Br J Ophthalmol 1993; 77:162–4.
  23. Lambert S. Lens. In: Taylor D, ed, Paediatric Ophthalmology, 2nd ed. Oxford, Blackwell. 1997; 445–76.
  24. Da Cunha RP, Moreira JB. Ocular findings in Down’s syndrome. Am J Ophthalmol 1996; 122:236–44.
  25. Lambert SR, Taylor D, Kriss A, et al. Ocular manifestations of the congenital varicella syndrome. Arch Ophthalmol 1989; 107:52–6.
  26. Cotlier E. Congenital varicella cataract. Am J Ophthalmol 1978; 86:627–9.
  27. Nahmias AJ, Visintine AM, Caldwell DR, Wilson LA. Eye infections with herpes simplex viruses in neonates. Surv Ophthalmol 1976; 21:100–5.
  28. Rahi JS, Dezateux C. Congenital and infantile cataract in the United Kingdom: underlying or associated factors. British CongenitalCataract Interest Group. Invest Ophthalmol Vis Sci 2000; 41:2108-14.
  29. BenEzra D, Cohen E, Rose L: Traumatic cataract in children: correction of aphakia by contact lens or intraocular lens. Am J Ophthalmol 1997; 123:773–82.
  30. Binkhorst CD, Gobin MH, Leonard PA: Post-traumatic artificial lens implants (pseudophakoi) in children. Br J Ophthalmol 1969; 53:518–29.
  31. Costenbader FD, Albert DG. Conservatism in the management of congenital cataracts. Arch Ophthalmol 1957; 58:426-30.
  32. Parks MM, Johnson DA, Reed GW. Long-term visual results and complications in children with aphakia: a function of cataract type. Ophthalmology 1993; 100:826-41.
  33. Crawford JS. Conservative management of cataracts. In: Hiles DA, editor. Infantile cataract surgery. Boston: Little, Brown, 1977:31-5.
  34. Amaya L, Taylor D, Russell-Eggitt I, Nischal KK, Lengyel D. The Morphology and Natural History of Childhood Cataracts. Surv Ophthalmol 2003; 48:125-44.
  35. Wegener JK, Sogaard H. Persistent hyperplastic primary vitreous with resorportion of the lens. Acta Ophthalmol (Copenh) 1968; 46:171-5.
  36. Shah MA, Shah SM, Shah SB, et al. Morphology of traumatic cataract: does it play a role in final visual outcome? BMJ Open 2011;1:e000060.
  37. Boger WP, Peterson RA, Robb RM. Spontaneous absorption of the lens in the congenital rubella syndrome. Arch Ophthalmol 1981; 99:433-4.
  38. Lambert SR, Drack AV: Infantile cataracts. Surv Ophthalmol 1996; 40:427–58.
  39. Scott MH, Hejtmancik JF, Wozencraft LA, Reuter LM, Parks MM, Kaiser Kupfer MI. Autosomal dominant congenital cataract: interocular phenotypic variability. Ophthalmology 1994; 101:866-71.
  40. Thomas R, Gopal KS, George JA. Anterior dislocation of the pyramidal part of a congenital cataract. Ind J Ophthalmol 1985; 33:51-2.
  41. Govan JA. Ocular manifestations of Alport’s syndrome: a hereditary disorder of basement membrane. Br J Ophthalmol 1983; 67:493-503.
  42. Jacobs M, Jeffrey B, Kriss A, Taylor D, Sa G, Barratt TM. Ophthalmologic assessment of young patients with Alport syndrome. Ophthalmology 1992; 99:1039-44.
  43. Arnott EJ, Crawfurd MD’A, Toghill PJ. Anterior lenticonus and Alport’s syndrome. Br J Ophthalmol 1966; 50:390.
  44. Butler TH. Lenticonus posterior: report of six cases. Arch Ophthalmol 1930; 3:425-36.
  45. Gibbs ML, Jacobs M, Wilkie AOM, Taylor DSI. Posterior lenticonus: clinical patterns and genetics. J Pediatr Ophthalmol Strabismus 1993; 30:171-5.
  46. Becker RH, Hubisch SH, Graf MH, et al. Preliminary report: examination of young children with LEA symbols. Strabismus 2000; 8:209-13.
  47. Woodhouse JM, Adoh TO, Oduwaiye KA, et al. New acuity test for toddlers. Ophthalmic Physiol Opt 1992; 12:249-51.
  48. Sharma P, Bairagi D, Sachdeva MM, et al. Comparative evaluation of teller and Cardiff acuity tests in normals and unilateral amblyopes in under two year olds. Indian J Ophthalmol 2003; 51:341-5.
  49. Hoffer KJ. IOL power. Slack Inc; 2011.
  50. Trivedi RH, Wilson ME. Prediction error after pediatric cataract surgery with intraocular lens implantation: Contact versus immersion A-scan biometry. J Cataract Refract Surg 2011; 37:501–5.
  51. Trivedi RH, Wilson ME. Axial length measurements by contact and immersion techniques in pediatric eyes with cataract. Ophthalmology 2011; 118:498–502.
  52. Lenhart PD, Hutchinson AK, Lynn MJ, Lambert SR. Partial coherence interferometry versus immersion ultrasonography for axial length measurement in children. J Cataract Refract Surg 2010; 36:2100–4.
  53. Gursoy H, Sahin A, Basmak H, Ozer A, Yldrm N, Colak E. Lenstar versus ultrasound for ocular biometry in a pediatric population. Optom Vis Sci 2011; 88:912–9.
  54. Roger DL et al.Corneal power measurements in fixating versus anesthetized nonfixating children using a handheld keratometer. JAAPOS 2010; 14:11-14
  55. Maya ET,Steve n MA, Monte ADM. Intraocular Lens Power Calculation in Children. Survey Ophthalmol 2007; 52:474-482
  56. Andreo LK, Wilson ME, Saunders RA. Predictive value of regression and theoretical IOL formulas in paediatric intraocular lens implantation. J Paditr Ophthalmol Strabismus 1997; 34:240-43.
  57. Mezer E, Rootman DS, Abdolell M, et al. Early postoperative refractive outcomes of paediatric intraocular lens implantation. J Cataract Rfract Surg 2004; 30:603-10
  58. Tromans  C, Haigh PM, Biswas S, et al. Accuracy of intraocular lens power calculation in paediatric cataract surgery. Br J Ophthalmol 2001; 85:939-41.
  59. Zetterstrom C, Lundvall A, Kugelberg M. Cataracts in children. J Cataract Refract Surg 2005; 31:824–40.
  60. Krag S, Olsen T, Andreassen TT. Biomechanical characteristics of the human anterior lens capsule in relation to age. Invest Ophthalmol Vis Sci 1997; 38:357-63.
  61. Trivedi RH, Wilson ME. Biometry data from caucasian and african-american cataractous pediatric eyes. Invest Ophthalmol Vis Sci 2007; 48:4671-8.
  62. Cooper BA, Holekamp NM, Bohigian G, et al. Case-control study of endophthalmitis after cataract surgery comparing scleral tunnel and clear corneal wounds. Am J Ophthalmol 2003; 136:300-5.
  63. Wilson ME Jr, Suresh KP. Anterior capsule management. In: Wilson ME Jr, Trivedi RH, Pandey SK, eds, Pediatric Cataract Surgery; Techniques, Complications, and Management. Philadelphia, PA, Lippincott, Williams & Wilkins, 2005; 68-76.
  64. Vasavada AR, Trivedi RH, Nihalani B. Multiquadrant hydrodissection. In: Wilson ME Jr, Trivedi RH, Pandey SK, eds, Pediatric Cataract Surgery; Techniques, Complications, and Management. Philadelphia, PA, Lippincott, Williams & Wilkins, 2005; 77-79.
  65. Trivedi RH, Wilson ME Jr. Posterior capsulotomy and anterior vitrectomy for the management of pediatric cataracts.  In: Wilson ME Jr, Trivedi RH, Pandey SK, eds, Pediatric Cataract Surgery; Techniques, Complications, and Management. Philadelphia, PA, Lippincott, Williams & Wilkins, 2005; 83-92.
  66. Trivedi RH, Wilson ME Jr. AcrySof ® Intraocular lens implantation in eye with pediatric cataracts. In: Wilson ME Jr, Trivedi RH, Pandey SK, eds, Pediatric Cataract Surgery; Techniques, Complications, and Management. Philadelphia, PA, Lippincott, Williams & Wilkins, 2005; 139-49.
  67. Pnadey SK, Werner L, Wilson ME, et al. Capsulorhexis ovaling and capsular bag stretch after rigid and foldable intraocular lens implantation: an experimental study in pediatric human eyes. J Cataract Refract Surg 2004; 30:2183-91.
  68. Egbert JE, Christiansen SP, Wright MM, et al. The natural history of glaucoma and ocular hypertension after pediatric cataract surgery. JAAPOS 2006; 10:54–57.
  69. Magnusson G, Abrahamsson M, Sjostrand J. Glaucoma following congenital cataract surgery: an 18-year longitudinal follow-up. Acta Ophthalmol Scand 2000; 78:65–70.
  70. Chen TC, Bhatia LS, Walton DS. Complications of pediatric lensectomy in 193 eyes. Ophthalmic Surg Lasers Imaging 2005; 36:6–13.
  71. Rabiah PK. Frequency and predictors of glaucoma after pediatric cataract surgery. Am J Ophthalmol 2004; 137:30–7.
  72. Watts P, Abdolell M, Levin AV. Complications in infants undergoing surgery for congenital cataract in the first 12 weeks of life: is early surgery better? JAAPOS 2003; 7:81–85.
  73. Vishwanath M, Cheong-Leen R, Taylor D, et al. Is early surgery a risk factor for glaucoma? Br J Ophthalmol 2004; 88:905–10.
  74. Lundvall A, Zetterstrom C. Complications after early surgery for congenital cataracts. Acta Ophthalmol Scand 1999; 77:677–680.
  75. Trivedi RH, Wilson Jr ME, Golub RL. Incidence and risk factors for glaucoma after pediatric cataract surgery with and without intraocular lens implantation. JAAPOS 2006; 10:117–23.
  76. Cassidy L, Rahi J, Nischal K, et al. Outcome of lens aspiration and intraocular lens implantation in children aged 5 years and under. Br J Ophthalmol 2001; 85:540–2.
  77. Morgan KS, Arffa RC, Marvelli TL, et al. Five year follow-up of epikeratophakia in     children. Ophthalmology 1986; 93:423-32.
  78. Ram J, Brar GS, Kaushik S, et al. Role of posterior capsulotomy with vitrectomy and intraocular lens design and material in reducing posterior capsule opacification after pediatric cataract surgery. J Cataract Refract Surg 2003; 29:1579-84.
  79. Vasavada A, Chauhan H. Intraocular lens implantation in infants with congenital cataract. J Cataract Refract Surg 1994; 20:592-8.
  80. Vasavada A, Desai J. Primary posterior capsulorhexis with and without anterior vitrectomy in congenital cataracts. J Cataract Refract Surg 1997; 23 (Suppl):645-51.
  81. Koch DD, Kohnen T. Retrospective comparison of techniques to prevent secondary cataract formation after posterior chamber intraocular lens implantation in infants and children. J Cataract Refract Surg (Suppl 1) 1997; 23:657-663.
  82. Parks MM. Posterior lens capsulectomy during primary cataract surgery in children. Ophthalmology 1983; 90:344-5.
  83. Atkinson CS, Hiles DA. Treatment of secondary posterior capsular membranes with the Nd: YAG laser in a pediatric population. Am J Ophthalmol 1994; 118:496-501.
  84. Apple DJ, Solomon KD, Tetz MR, et al: Posterior Capsule Opacification. Surv Ophthalmol 1992; 37:73-116.


Patil B, Sharma R, Nayak B, Sinha G, Khokhar SPediatric Cataract.DJO 2015;25:160-165


Patil B, Sharma R, Nayak B, Sinha G, Khokhar SPediatric Cataract.DJO [serial online] 2015[cited 2021 Oct 22];25:160-165. Available from: