Early management of paediatric cataract can have a significant impact on the lives of individuals, their families, communities, and the socioeconomic standing of the nation. Children with vision impairments face a lifetime of social, emotional, and financial challenges. This impacts their schooling, career, and social life. Childhood blindness causes around 70 million blindpersonyears, of which approximately 10 million blindpersonyears (14%) are related to childhood cataract [1]. There are between 280 000 and 320 000 visually handicapped children in India [2] resulting in an estimated loss of $3.5 billion. Community awareness, early detection by physicians, and timely therapy by ophthalmologists can address the issue and reach the elimination objective by 2020.

Genetics

The eye begins to mature around 22 week’s gestation. In addition to inducing migration and differentiation, fibroblast growth factor (FGF) is responsible for the polarity of the lens. During lens induction, bone morphogenetic protein interacts with FGF. The transcription factors encoded by the genes Pax6, Pitx3, c-Maf, and Foxe3 are essential for lens formation [3]. The mutations are typically autosomal dominant, and the lack of one copy's function has a devastating effect on lens development. Depending on the timing of the insult, the portion of the developing lens is affected. Cataracts with autosomal-dominant inheritance exhibit variable penetrance. Cataracts associated with autosomal dominance include hyperferritinemia cataract syndrome, Coppock-like, Volkmann-type congenital, zonular with sutural, posterior polar, anterior polar, cerulean, zonular pulverulent, crystalline aculeiform, and myotonic dystrophy 1-like cataracts. Included in autosomal-recessive cataract are Warburg micro syndrome, Hallermann-Streiff syndrome, Martsolf syndrome, Smith-Lemli-Opitz syndrome, Rothmund-Thomson syndrome, Marinesco-Sjogren syndrome, Wilson's illness, and congenital cataract facial dysmorphosis with neuropathy. Nance–Horan syndrome (NHS) and Norrie's disease are both X-linked recessive cataracts.

Idiopathic

Many unilateral and bilateral cataracts are idiopathic. Such situations are diagnosed after excluding other reasons.

• Hereditary Cataract: Most hereditary cataracts are incomplete autosomal-dominant [4]. Typically, no syndromic gene defects in crystallin and connexin are responsible

• Norrie Disease: Norrie disease, an X-linked recessive illness, causes thick congenital cataracts, retinal folds, retinal detachment, vitreous haemorrhage, and bilateral retrolental hemorrhagic vascular and glial masses. Mutations in the X-chromosome NDP gene cause the disorder. It causes developmental delay and sensorineural hearing loss [5]

• Nance–Horan Syndrome: NHS is an X-linked recessive condition in which males exhibit bilateral dense stellate or nuclear cataracts, microcornea, anteverted and simplex pinnae, and dental anomalies, sometimes known as cataract-oto-dental syndrome. Female carriers show small corneal diameter, presenile cataract, and posterior Y-suture punctate opacities [6]

• Down's Syndrome: Down's syndrome children have a 6%–50% cataract rate. They may have hyperopia, nystagmus, strabismus, or eyelid entropion [7]

• Lowe Syndrome: X-linked multisystem illness having a traditional triad of congenital cataract, mental retardation, and proximal renal tubular failure. Muscle dystonia and debilitating arthropathy are also possible. Patients rarely live past 40 [8]

Metabolic Cataract

• Galactosemia: Mutations in galactokinase (GALK1), galactose-1-phosphate uridyltransferase, or uridine diphosphate 1–4 epimerase cause galactosemia, a high serum galactose level. "Oil droplet cataract" results from galactitol accumulation. Nuclear cataracts or anterior or posterior subscapular cataracts can occur. Eliminating galactose from the diet reverses these effects. Galactokinase deficiency produces mild cataracts. It causes vomiting, failure to thrive, jaundice, and mental impairment.  Hypoglycemia and hypocalcemia also cause cataracts

• Toxoplasma, Rubella, CMV, Herpes, and Syphilis: Congenital cataracts are linked to TORCH infections, especially rubella. Pigmentary retinopathy, microphthalmos, glaucoma, iris degeneration, and chorioretinitis are also related [9]. Indian subcontinent TORCH infections are common and up to 20% are seropositive. Cataract, sensorineural hearing loss, and heart disease-usually patent ductus arteriosus-characterize congenital rubella syndrome. Most instances have bilateral cataracts, however unilateral cataracts can occur with or without salt and pepper retinopathy

• Anterior-Segment Dysgenesis: Peter's abnormality is typically characterised by central corneal opacity. Peter's abnormality could feature irido or keratolenticular characteristics. There may be further ocular malformations, such as posterior embryotoxon microcornea or chorioretinal abnormality. [10] There may be occasional family cases with autosomal-recessive inheritance, although most cases are sporadic. They may appear with lens displacement in the anterior chamber or polar and nuclear cataracts in the anterior segment [11]

• Preexisting Posterior Capsular Defect: It occurs alongside posterior polar cataract, persistent foetal vasculature (PFV), lenticonus, and lentiglobus. Due to the developmentally weak posterior capsule or tension of the regressing hyaloid artery, the fluid vitreous hydrates the lens and lens material egresses into Berger's space. The preexisting posterior capsular defect manifests as a complete cataract or occasionally as a differential opacity (whiter in the centre than the periphery), white spots on the posterior capsule or anterior vitreous, and a fish-tail sign [12]. Using ultrasonic biomicroscopy, the diagnosis can be confirmed

• Persistent Foetal Vasculature: Persistent foetal vasculature (PFV) manifests as an eccentric posterior fibrovascular plaque; for this reason, it was originally referred to as "Persistent Hyperplastic Primary Vitreous." PFV is pathognomonic for the presence of microphthalmos and an extended ciliary body. PFV is occasionally accompanied with tunica vasculosa lentis, iridohyaloid blood vessels, and persistent pupillary membrane. In contrast to patients with posterior PFV, who frequently have restricted visual potential due to associated retinal and optic nerve problems, patients with anterior PFV typically have favourable visual prognoses [13]

• Traumatic Cataract: In India, the causes of childhood traumatic cataract are distinct from those in the West. The incidence of open-globe injuries is three times that of closed-globe injuries, with bow and arrow injuries being the most common cause. Other causes include injuries from firecrackers, balls, stones, wood, and metal. Cataract is often accompanied by a shallow anterior chamber, hyphema, corneal perforation/scarring, iris distortion, posterior synechiae, vitreous haemorrhage, vitreous in the anterior chamber, and posterior capsular tear [14]

• Uveitic Cataract: Uveitic cataract in children may be related to systemic disorders, most frequently juvenile idiopathic arthritis (JIA). Due to significant intraocular inflammation, JIA is accompanied with uveitis cataract (71%). In addition to posterior subcapsular cataract, these patients frequently exhibit posterior synechiae, iris bombe, and sometimes peripheral anterior synechiae. Chronic JIA is characterized by band-shaped keratopathy and hypotony [15]. Even after cataract surgery, JIA-associated uveitis patients had a worse prognosis than non-JIA uveitis patients. Masquerade syndrome must always be ruled out in all cases of uveitis in children

History Taking

Typically, the initial complaint is leukocoria, in which the parent observes a total or progressive increase in the size of the opacity. The second is the child's failure to follow an object close to the face or make eye contact (inability to recognise mother). Parental complaints may also include eye squeezing in strong light, squinting, small eyes (microphthalmos), huge eyes (buphthalmos), and aberrant eye movement (nystagmus). A thorough medical history is obtained, including questions concerning the onset age and duration of symptoms.

Older children may have difficulties observing distant objects, the instructor may observe the child's inability to read the chalkboard, or the parent may observe the child putting objects extremely near to his or her face and watching television at close range. A pedigree chart should be created along with a search for a comparable history in siblings or family members already diagnosed with cataract. In the case of unilateral cataract, a history of fever and rash during pregnancy (TORCH), drug or alcohol use, and trauma should be sought. In addition, the history of delivery trauma, premature birth (retinopathy of prematurity), failure to thrive, and vomiting (galactosemia) should be obtained.

• Systematic Investigation: Frequently, children with cataract exhibit systemic disease and syndromic characteristics. Gross general examination may reveal dysmorphic features such as sparse eyebrows, mongoloid slant (Down's syndrome), beaked nose with dental abnormalities (Hallermann–Streiff syndrome), frontal bossing (Lowe syndrome), low-set ears, and prominent parietal and occipital eminences; skin and hair changes such as dry, scaly skin over the limbs, abdomen, and scalp with patchy alopecia; and (Weill–Marchesani syndrome). Sometimes the skull sutures are irregularly fused, the face is puffy (nephrotic syndrome), the skin may be pigmented (xeroderma pigmentosum), and the eyebrows are nonexistent (Patau's syndrome). The circumference of the head may reveal hydrocephalus or microcephaly, both of which are linked to cataracts. William's condition displays symptoms of attention deficit hyperactivity disorder (ADHD). Subnormal intelligence and mental retardation are connected with a variety of syndromes. Auscultation may detect patent ductus arteriosus (rubella) or mitral valve collapse (Ehler–Danlos syndrome) [16] 

Ophthalmic Examination

• Visual Acuity Assessment: Visual acuity testing is the most tough and difficult aspect. First, we check for fixation; central fixation indicates that the fovea is the fixation point, steady fixation indicates that there is no nystagmus component, and maintained fixation indicates that there is no squint [17]. This provides just general but vital information on optical acuity. Consequently, an unique test has been created to assess the visual acuity of preverbal children. Visual-evoked response, Catford drum, optokinetic nystagmus, and Teller's acuity cards can be used on neonates. Worth's ivory ball test, Boeck's candy test, the Screening Test for Young Children and Retards, and Cardiff's acuity test can be administered to children aged 1–2 years

• Evaluation For Cataracts: The child is most at ease on the mother's lap. Thus, the youngster is initially examined with the child's head resting on the parent's shoulder. After evaluating the patient's visual acuity and pupillary response, a distant direct examination is performed to search for anterior region anomalies. The eye may demonstrate corneal opacity, a shallow anterior chamber, peripheral anterior synechiae (Peter's anomaly), microcornea (microcornea-cataract syndrome), posterior synechiae (uveitis), a key-hole pupil (irido fundal coloboma), and dilated ciliary processes with capillaries on the lens (PFV). The red reflex screening using a direct ophthalmoscope held at 30 cm and focused on each pupil individually (Bruckner's test) assists in identifying lenticular opacity

• Refractive Mistakes: The infant is born with modest hyperopia. This hyperopia initially increases before beginning to decline [17]. The refraction of a child younger than five years is performed mostly under strong cycloplegia. Amblyopia can result from refractive errors exceeding 4 D of myopia, 5 D of hyperopia, and 2 D of astigmatism. Spherophakia and developing cataract can cause myopia to progressively worsen. If the lens is displaced from the pupillary region and the child is fundamentally aphakic, subluxation might manifest as extreme hyperopia

• Nystagmus and Posture of the Head: Nystagmus arises because the child cannot maintain fixation. Occasionally, the youngster may establish a head position that allows for optimal vision with minimal nystagmus amplitude (null position). This kind of nystagmus develops by 13 weeks of age in untreated cataract cases [18]. The presence of nystagmus is not a contraindication for surgery, as a child with nystagmus can still have functional vision if treatment is administered early

• Evaluation of Parent: Parents must be screened in order to rule out the possibility of inherited cataracts. Screening the mother can detect a sutural cataract in a child with a dense nuclear cataract who is a member of the NHS [19] 

Investigations

Ultrasonography (USG) is not only useful for intraoperative treatment, but also for prognosis, particularly in situations of unilateral cataract. USG helps us rule out retinal detachment, fundal coloboma, and retinoblastoma.  In cases of unilateral cataract, USG can detect PFV. If there is a high degree of suspicion of PFV that is missed by USG, magnetic resonance imaging can be ordered. Color Doppler additionally displays a flow image in the event of a PFV. In situations with traumatic cataract, an X-ray is taken and a computed tomography scan is performed to locate an intraocular foreign body. In the event of bilateral congenital cataract, a TORCH profile might be conducted to test for active infection. 

Echocardiography may identify aortic regurgitation, aortic root dilatation, patent ductus arteriosus, and atrial septal defect in Marfan syndrome and rubella. In cases of JIA and juvenile rheumatoid arthritis requiring immunosuppressive treatment, the opinion of a rheumatologist is sought. In cases of seizure and severe developmental delay, a neurologist must be consulted. In situations of nephrotic syndrome and Lowe syndrome, nephrology assessment is necessary [20].

Prognosis

The prognosis for congenital cataract is favourable if detected early and surgery is performed within six weeks. As a result of delayed diagnosis, ignorance, and a lack of resources, it is also common to observe delayed presentation in adulthood. Congenital cataract has a worse prognosis than developing cataract. Homocystinuria can be treated with a diet low in methionine. The existence of a unilateral cataract, nystagmus, strabismus, or any ocular abnormality, including microphthalmos and PFV, may negatively affect the surgical outcome [21].

Timing of Surgical Procedures

The essential phase of eye development extends from 2 to 6 months of age, and emmetropization is often achieved by age 9; however, the brain's flexibility can extend long beyond the first 10 years of life [22]. Surgical intervention is suggested for visually significant opacities, i.e. a central opacity greater than 3 mm. Prior to 6 weeks of age, unilateral cataracts should be surgically removed, and bilateral cataracts should be removed prior to 8 weeks of age. In symmetric cataracts, the second eye is operated on within one week after the first eye, and in children with systemic instability, both eyes can be operated on at the same time. In cases of opacities that are visually insignificant (blue-dot cataract or tiny posterior polar), the child can be checked at regular intervals.

Anesthesia

Surgery may be performed under general anaesthesia with a laryngeal mask airway or endotracheal tube. The adverse effects of opioids include vomiting and respiratory depression. The subtenon block reduces the need for postoperative analgesia, delays the onset of the first rescue analgesia, reduces the incidence of the oculo-cardiac reflex, and improves parent satisfaction ratings. Alternatives to intravenous fentanyl for perioperative analgesia include the subtenon block and topical lignocaine [23].

Surgery

The primary objective of treatment is to clear the visual axis, followed by visual rehabilitation following surgery. Children's surgery differs from that of adults due to their less rigid cornea and sclera, very elastic anterior capsule, soft lens, and well-developed vitreous. In trauma-prone childhood, a superior incision is recommended, which permits the eyelid and Bell's phenomenon to shield the wound. Either scleral or clear corneal incision may be employed, and it has been demonstrated that the type of incision makes no difference in terms of the astigmatism created by the incision. It has been demonstrated that the two-incision push–pull approach produces uniform capsulorhexis size and reduces the likelihood of run-off [24].

In the paediatric population, multiquadrant hydrodissection (at least three quadrants) is the preferable technique, followed by bimanual lens aspiration to remove lens debris. The anterior chamber is then partially underfilled with a high-viscosity, cohesive viscoelastic material. The high incidence of visual axis opacification (VAO) dictates that the posterior capsule be treated first. The cystitome is utilised to nick the posterior capsule laterally, and intravitreal forceps are used to complete posterior capsulorhexis [25]. Anterior vitrectomy destroys the framework for the proliferation of LECs and metaplastic pigment cells, hence limiting the creation of VAOs. Posterior capsulotomy is required for all patients younger than six years old. After the age of 5, vitrectomy can be postponed. In older children (with mental impairment or nystagmus) who may not cooperate with laser capsulotomy under a slit lamp, posterior capsulorhexis is typically required. 

It is difficult to insert the IOL into the bag when posterior capsulorhexis has been performed. After making a 2.75-mm incision, the IOL is inserted by placing the leading haptic against the rear surface of the anterior capsule, followed by pushing down the trailing haptic and tucking it into the bag. This procedure is risk-free and does not result in issues due to improper IOL placement [26]. The vitrectomy cutter can be used to accomplish capsulorhexis, although its tensile strength is inferior to that of curvilinear capsulorhexis. In cases of subluxation or anterior displacement in youngsters, intralenticular suction of a lens with anterior chamber IOL and peripheral iridectomy is preferable.

Postoperative Therapy

Due to the immaturity of the blood–aqueous barrier, paediatric eyes exhibit a greater number of intraocular reactions, including anterior-chamber cells, flare, fibrinous reaction, pupillary membrane creation, and posterior synechiae production. Postoperatively, patients are provided topical steroids (1% prednisolone acetate six times daily) and cycloplegics (ideally 2% homatropine). In cases of uveitis, intraocular lenses (IOLs) coated with heparin and subconjunctival injections of dexamethasone with or without triamcinolone have been shown to minimise postoperative inflammation. It has been demonstrated that postoperative single injections of hydrocortisone 5 mg/kg and dexamethasone 0.1 mg/kg are equally efficacious, without the intraocular pressure elevation found with depot steroids and the hyphema seen with heparin. The safety and efficacy characteristics of difluprednate 0.05% administered four times daily to 0–3-year-olds after cataract surgery were comparable to those of prednisolone acetate 1% [26]. Over the course of six to eight weeks, topical steroid dosages should be gradually reduced. One month after surgery, patients are followed up on every three months thereafter.

Visual Rehabilitation and Treatment for Amblyopia

Even before suture removal, surgery is promptly followed by a prescription for glasses and amblyopia treatment. Suture removal and refraction are performed one month and three months after surgery. The parent is responsible for ensuring that the youngster wears the recommended glasses and undergoes occlusion therapy (for unilateral or asymmetrical cases). As eyeglasses produce aniseikonia, contact lenses are more suitable for children with unilateral aphakia than glasses. According to the Infant Aphakia Treatment Study, there was no significant difference between primary IOL implantation and contact lens in terms of final visual acuity in infants less than 7 months. IOL-implanted youngsters experienced greater adverse events and required more reoperations to remove visual-axis opacities. In such children, contact lenses are a viable alternative to IOL implantation [28].

In younger children, near-sighted glasses are prescribed. After correcting for distance, executive bifocal glasses with near add are prescribed for school-aged youngsters. Depending on the age of children 12 months, occlusion is administered when both eyes are occluded (6-month-old child is given occlusion half of the waking hours per day in alternate eyes). A youngster older than one year receives greater occlusion in the better eye than in the poorer eye (3-year-old child is given occlusion 8 waking hours per day for 3 days in better eye and 1 day in the worse eye). To prevent the development of occlusion amblyopia in the better eye, the worse eye is occluded. Initially, patients are monitored every 4-6 weeks, and then every 3 months to assess treatment response. When the desired effect has been obtained, occlusion is gradually reduced. Levodopa, carbidopa, and citicoline have demonstrated positive modulatory effects on plasticity [29].

Complications

10%–25% of children diagnosed with glaucoma following cataract surgery. High-risk variables include younger age at surgery and the existence of microphthalmia. The intraocular pressure can be managed with medication or surgical surgery. VAO is the most common consequence of cataract surgery in children, with or without IOL surgery, and it can lead to visual deprivation amblyopia. A thick VAO necessitates posterior capsulotomy and anterior vitrectomy. Postoperative response is more prevalent in preexisting cataracts that are complex and traumatic. This can lead to the production of posterior synechia, seclusio pupillis, iris bombe, and ultimately secondary angle-closure glaucoma and VAO. Improvements in surgical methods, the frequent use of topical corticosteroids, and the administration of cycloplegics in the postoperative period have considerably reduced the incidence of problems. Posterior optic capture and in-bag IOL fixation reduce the frequency of anterior optic capture. Retinal detachment is uncommon but more prevalent in eyes affected with PFV [10].

Over the years, paediatric cataract surgery has gotten safer and more predictable. The outcomes of early detection, prompt referral, and proper treatment are positive.

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