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Year : 2004  |  Volume : 52  |  Issue : 3  |  Page : 185-98

Glaucoma in aphakia and pseudophakia after congenital cataract surgery.

Jasti V Ramanamma Children's Eye Care Centre, L V Prasad Eye Institute, L V Prasad Marg, Banjara Hills, Hyderabad - 500 034, India

Date of Submission24-Jun-2004
Date of Acceptance26-Jul-2004

Correspondence Address:
Anil K Mandal
Jasti V Ramanamma Children's Eye Care Centre, L V Prasad Eye Institute, L V Prasad Marg, Banjara Hills, Hyderabad - 500 034
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Source of Support: None, Conflict of Interest: None

PMID: 15510457

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Glaucoma is one of the most common causes of visual loss despite successful congenital cataract surgery. The overall incidence does not appear to have decreased with modern microsurgical techniques. The onset of glaucoma may be acute or insidious and notoriously refractory to treatment. Angle closure glaucoma may occur in the early postoperative period; but the most common type of glaucoma to develop after congenital cataract surgery is open angle glaucoma. Several risk factors have been identified and both chemical and mechanical theories have been proposed for its pathogenesis. Unlike children with congenital glaucoma, those with paediatric glaucoma following congenital cataract surgery are usually asymptomatic despite high intraocular pressure. They may require regular evaluation under anaesthesia, whenever there are any suspicious findings. Unlike congenital glaucoma, the first line of treatment for glaucoma in aphakia/pseudophakia may be medical. Traditional trabeculectomy in paediatric glaucoma following congenital cataract surgery has met with limited success. The addition of antimetabolites to trabeculectomy is known to inhibit fibrosis and enhance the success, but carries the lifelong risk of bleb-related endophthalmitis. Drainage implant surgery is a viable option to achieve longterm intraocular pressure control in this refractory group of patients. Cycloablative procedures may provide temporising treatment and should be reserved for patients with low visual potential. Diagnosis of glaucoma following congenital cataract surgery requires lifelong surveillance and continuous assessment of the problem. Further research is needed to understand the pathophysiology, prevention and treatment of this sight-threatening complication following successful cataract surgery in children.

Keywords: Congential cataract, glaucoma in aphakia/pseudophakia, trabeculectomy, Mitomycin C, glaucoma drainage implant, cycloablation

How to cite this article:
Mandal AK, Netland PA. Glaucoma in aphakia and pseudophakia after congenital cataract surgery. Indian J Ophthalmol 2004;52:185

How to cite this URL:
Mandal AK, Netland PA. Glaucoma in aphakia and pseudophakia after congenital cataract surgery. Indian J Ophthalmol [serial online] 2004 [cited 2023 Nov 30];52:185. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?2004/52/3/185/14592

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Many of the postoperative complications after congenital or infantile cataract surgery do not develop until years after surgery.[1] Little has been written about paediatric glaucoma in aphakia and pseudophakia, a recognised complication of congenital cataract surgery.[2] Despite improved surgical technique utilising vitreous cutting instrumentation for lens removal and vitreous management, the incidence of glaucoma following successful cataract removal remains high.[3],[4]

Transient or permanent intraocular pressure (IOP) elevation occurs in aphakic and pseudophakic eyes as a result of several mechanisms. Hence, the use of the term "aphakic glaucoma" is generally discouraged because it implies that the state of aphakia as such is the only cause of glaucoma. This group of glaucomas may be described as "glaucomas associated with aphakia and pseudophakia" or "the glaucomas in aphakia and pseudophakia," which conveys the notion that multiple mechanisms contribute to the development of elevated IOP after congenital cataract surgery.

  Ocular hypertension versus glaucoma Top

The difference between ocular hypertension (OHT) and glaucoma is poorly understood in patients with aphakia and pseudophakia following surgery for congenital or infantile cataract. Children may not be able to perform the visual field, thus precluding the use of this important diagnostic tool for glaucoma. Patients who have increased IOP without apparent disc damage must be examined for disc damage and cupping over time, without the benefit of visual field testing.

In a prospective study by Egbert et al[5] of lensectomy and anterior vitrectomy in paediatric/congenital cataract, the prevalence of glaucoma and OHT was 9.7% and 33% respectively.

Many retrospective studies on congenital or paediatric cataract suffer from short or undefined postoperative follow-up periods, and inconsistent definitions for glaucoma. Few authors have differentiated OHT and glaucoma. [5],[6],[7] If Egbert et al had defined glaucoma as IOP 26 mmHg with optic nerve head damage, the prevalence of glaucoma would have increased form 9.7% to 26%.

  Incidence of glaucoma after congenital cataract surgery Top

Prior to the use of automated lensectomy and vitrectomy (1943-1975) the incidence of glaucoma was nearly 14% [Table - 1].[8]

During the 1970s, microscopically controlled, automated lensectomy and vitrectomy gradually replaced one and two-staged needling as a method of paediatric cataract extraction. It was hoped that by removing lens and capsular remnants more effectively, postoperative inflammation and pupillary block would be minimised, so also the incidence of glaucoma. The initial experience with this technique was encouraging, and no cases of glaucoma were reported.[9] In a longer follow-up study, Keech and associates[10] found an 11% incidence of glaucoma after lensectomy and vitrectomy. Subsequent studies reported an incidence of glaucoma ranging from 6% to 26% [Table - 2]. [3],[4],[5],[9],[10],[11],[12],[13] The reported incidence varies with the duration of follow-up after cataract surgery. A longer follow-up period has been associated with a higher incidence of glaucoma.

Mills and Robb[13] followed 125 eyes of 82 patients who underwent cataract surgery before the age of 10 years. Glaucoma developed in 13 (15.8%) of them from 5 months to 13.1 years after surgery. The authors projected a 30% prevalence of glaucoma 13 years after cataract extraction. Asrani and Wilensky[2] found glaucoma in 42 eyes (65.6%) after 10 years of age, with an average interval of 12.2 years between cataract surgery and glaucoma diagnosis.

  Mean time interval at onset of glaucoma following surgery Top

Glaucoma may occur on either an acute or chronic time course. Acute glaucoma may be due to angle closure and usually presents in the early postoperative period. Lens remnants or vitreous block may prevent aqueous flow through the pupil, inducing iris bombe. In the study reported by Vajpayee et al,[14] the duration between intraocular lens (IOL) implantation and initial manifestations of pseudophakic pupillary-block glaucoma was 14 2 days. Current surgical approaches remove the lens and anterior vitreous more completely, making this complication rare. Chronic angle closure glaucoma may manifest months to years after congenital cataract surgery.

Unlike angle-closure glaucoma, which usually develops soon after surgery, open-angle glaucoma is usually not diagnosed until years later - 6.8 years in Simon et al[3] study and 2 to 45 years in the Phelps and Arafat[6] study, 5.3 years in the Parks et al[9] study and 7.4 years in the Mills and Rob study.[13] Walton analysed his data at specific time intervals following lensectomy.[15] Forty of 65 patients were not found to have glaucoma until 2 or more years after lensectomy, while 24 of 65 patients were found to have glaucoma 4 or more years after lensectomy.

Johnson and Keech[16] noted that while glaucoma developed in approximately one-third of their patients within a few months following cataract surgery in the remaining two-thirds glaucoma developed several years after surgery. The mean time onset of glaucoma following surgery in their study was 64.6 months in the persistent hyperplastic primary vitreous cataract group and 47.5 months in the infantile cataract group; this was not significant. Glaucoma following cataract surgery in children is reported after 3-6 years by Chrousos et al[11] and after an average 12.2 years by Asrani and Wilensky.[2] There is a report of lens-induced glaucoma as late as 65 years after congenital cataract surgery.[17] In this study the intraocular specimen exhibited lens material, epithelial cells, and macrophages. It may have taken years for the residual lens material to denature and break into small pieces, which resulted in phacolytic and lens-particle glaucoma.

Glaucoma can occur at any time after congenital cataract surgery; therefore, paediatric aphakic and pseudophakic patients should be routinely monitored for glaucoma throughout their lives.

  Causes of delay in diagnosis Top

Early diagnosis of glaucoma following congenital cataract surgery may be difficult for a number of reasons. The ability to measure IOP, visual field, and precise biomicroscopic examination of the optic nerve head is often difficult or impossible in these young patients. Furthermore, signs of congenital glaucoma such as epiphora, blepharospasm, photophobia, increasing corneal diameter, Haab's stria, and corneal clouding may not be seen in paediatric glaucoma following congenital cataract surgery. Usually patients with glaucoma are without symptoms despite increased IOP.

Unless the examining ophthalmologist is specifically looking for glaucoma, the diagnosis is easily missed. As a result, many children may have elevated IOPs for months or years before they are first detected. Frank signs and symptoms, such as redness and pain in the eye are rare, especially because most of the glaucoma is the open-angle type. The presence of a clear cornea and lack of ocular congestion gives the ophthalmologist a false sense of security. Also, symptoms such as loss of vision, particularly in the unilateral cases, may never manifest or may appear very late.

  Mechanism of IOP elevation and risk factors Top

Angle closure glaucoma

When needling was the treatment of choice for congenital cataract, angle-closure glaucoma most commonly occurred in the immediate postoperative period because of swelling of lens material causing pupillary block. This problem was reduced when Scheie popularised the aspiration technique. Pupillary block is also caused by a fibrin membrane extending across the pupil. Less commonly, pupillary block glaucoma may develop secondary to vitreous prolapsing into the anterior chamber. At the 24th Edward Jackson Memorial Lecture (1968), Chandler commented, "the principal cause of the loss of an eye after congenital cataract surgery is pupillary block leading to peripheral anterior synechia and intractable glaucoma."[18]

Walton[19] has described four types of glaucoma following congenital cataract surgery. They are pupillary block glaucoma, lens material blockage of the trabecular meshwork, phacolytic glaucoma, and chronic open-angle glaucoma following absorption of lens material. Uveitis also has been reported as a cause of aphakic glaucoma.

The causes of glaucoma after paediatric cataract surgery have been reviewed by Francois[8] [Table - 3]. Pupillary block glaucoma after primary IOL implantation in children in the posterior chamber secondary to irido-pseudophakic synechiae has also been reported.[14] The exact pathogenesis of pupillary-block glaucoma with posterior chamber lenses is not clear and may be related to a number of other factors, including alteration of angle anatomy, forward movement of the vitreous caused by zonular or capsular disruption, and pre-existing angle closure glaucoma. Less commonly, chronic angle closure glaucoma may develop in infantile eyes after cataract surgery. This is less frequent after a lensectomy than after lens aspiration, presumably because the lens cortex is more completely removed.

Open angle glaucoma

The most common type of glaucoma to develop following congenital cataract surgery is open-angle glaucoma.

Numerous authors have reported open angle glaucoma in paediatric patients following cataract surgery.[6],[9],[10],[20],[21] The glaucoma was detected at various time intervals and with a wide range of elevated IOP. Microcornea has been associated with glaucoma in aphakia and pseudophakia after congenital cataract surgery.[9],[12],[13],[22]

The cause of the open angle glaucoma may still remain uncertain in most of the patients. Both mechanical and chemical theories have been proposed.[23] One possibility is that release of tension on the zonules after removal of the lens may reduce traction on the trabecular meshwork, potentially decreasing the trabecular spaces and reducing outflow facility. Another possibility is the influence of lens particles or proteins, inflammatory cells, and vitreous-derived factors on the trabecular meshwork. Also, the possibility of a corticosteroid-induced glaucoma is high, because the corticosteroids are used for a longer period after cataract surgery in children who usually show increased inflammation, even with the newer techniques of cataract surgery.

  Risk factors Top

Development of glaucoma in aphakia and pseudophakia after congenital cataract surgery is multifactorial. The risk factors include the age at surgery, pre-existing ocular abnormalities, type of cataract, and the effect of lens particles, lens proteins, inflammatory cells, and retained lens material. In addition, microcornea, secondary surgery, chronic postoperative inflammation, the type of lensectomy procedure or instrumentation, pupillary block, and the duration of postoperative observation have been found to influence the likelihood of glaucoma after paediatric cataract surgery.

Young age ( 9 months), secondary membrane surgery, microcornea, and primary posterior capsulotomy with anterior vitrectomy have been identified as risk factors for glaucoma by Rabiah.[24] Vishwanath et al[25] reported that bilateral lensectomy during the first month of life was associated with a higher risk of subsequent glaucoma than with surgery performed later. The reason for this is unclear though it may be prudent, in bilateral cases, to consider delaying surgery until the infant is 4 weeks old.

  Diagnostic clues and evaluation Top

Glaucoma evaluation in aphakia and pseudophakia following congenital cataract surgery should include assessment of corneal diameter, slitlamp evaluation, applanation tonometry, and estimation of the glaucoma-tous optic nerve damage. Visual field measurements can be performed with Goldmann or automated perimetry, if the child is old enough to cooperate.

The diagnosis of glaucoma may be difficult to establish in children after congenital cataract surgery since they often lack the classical signs of congenital glaucoma, such as buphthalmos, epiphora, and blepharospasm. Moreover, the IOP may be difficult to measure with the child awake, and the view of the optic disc may be compromised by lens remnants, miosis, and nystagmus. Also, the visual fields usually cannot be accurately assessed until later in childhood. When an adequate examination cannot be obtained while a child is awake, an examination should be performed under sedation or general anaesthesia. An ideal evaluation should include measurement of the corneal diameter, IOP, cycloplegic refraction and optic nerve head evaluation. Ancillary testing should include measurement of axial length by A-scan ultrasonography and optic nerve head photographs. Measurement of corneal diameter is important, not only to identify buphthalmos, but also to detect microcornea, often associated with paediatric aphakic glaucoma.[22]

In the absence of a detailed evaluation of the eyes excessive loss of hyperopia,[26] recognition of corneal clouding, and ocular enlargement[15] could alert a physician to the possibility of glaucoma in children. The appearance of anterior chamber angle is very important in understanding the mechanism of glaucoma in the aphakic or pseudophakic eye following congenital cataract surgery. The most consistent finding in Walton's[15] series of 79 eyes with open angles, was a circumferential repositioning of the iris insertion anteriorly at the level of the posterior or mid trabecular meshwork, with resultant loss of view of the ciliary body band and scleral spur. Scattered pigment deposits were frequent but less frequent were white crystalline deposits suggestive of residual lens material caught in the meshwork.

The frequency of follow-up examinations after paediatric cataract surgery varies depending upon individual patient factors. Asrani and Wilensky[2] suggested examinations every three months during the first postoperative year, twice yearly until the 10th year, and annually thereafter.

  Treatment Top

Medical treatment

Initial medical treatment is usually tried, because the surgical options in these eyes are less successful and are associated with greater morbidity than in phakic eyes. Medical therapy with beta blocker, carbonic anhydrase inhibitor, and prostaglandin-related drugs may be used. Pilocarpine (1 or 2%), which has a better side effect profile in aphakic or pseudophakic patients compared to phakic patients, may also be helpful. But the risk of retinal detachment has to be borne in mind with pilocarpine. Epinephrine or propine are not useful because of the low efficacy of these drugs and the risk of cystoid macular oedema. In the series of Asrani and Wilensky,[2] medications alone successfully controlled the intraocular pressure in 21 (63.6%) of 33 eyes. In the series reported by Simon and colleagues,[3] six of eight eyes were controlled medically with a combination of miotics and betablockers.

Unlike primary congenital glaucoma, which responds poorly to medical therapy, it appears that at least some patients with glaucoma associated with aphakia or pseudophakia may achieve longterm control of IOP with medical therapy alone. When contemplating medical therapy in children, clinicians should evaluate the risks and benefits of the individual medications, use the minimum dosage required to achieve a therapeutic benefit, and monitor children for ocular and systemic side effects.[27],[28]

The commonly used/recommended medications are described briefly.

Beta blockers

There is variable response to adjunctive treatment with timolol in patients with a variety of paediatric glaucomas. [29],[30],[31],[32] In these reports only one-third of the patients responded to treatment with good control of IOP.

Plasma timolol levels in children after treatment with 0.25% timolol greatly exceed those in adults after instillation of 0.5% timolol.[33] Higher plasma levels of the drug would be expected to be associated with an increased risk of systemic side effects in children. In children over 5 years old, reduction in resting pulse rates have been identified and is comparable to that in adults.[29] Side effects have been reported in 4 - 13% of children,[30],[31] and timolol therapy has been discontinued in 3 - 7% of patients.[29],[30] Serious adverse events such as apnoea have been reported in younger children with smaller body mass and blood volume. [34],[35],[36] Provocation of asthma may occur with topical timolol treatment. It is not known whether betaxolol, a selective beta blocker, reduces the risk of pulmonary side effects in children. The effects of longterm use of topical beta blockers in children are not known.

Timolol in 0.25% and 0.5% solutions may be used with caution in young glaucoma patients, particularly in neonates, due to the possibility of apnoea and other systemic side effects. A detailed paediatric examination should precede use of this drug, to determine the presence of systemic abnormalities such as bronchial asthma and cardiac disease. In these cases, beta blockers are contraindicated. Use of 0.25% timolol rather than 0.5% timolol is strongly recommended in order to minimise the risk of side effects. Once daily dosing with timolol 0.25% in gel-forming solution may help simplify medical regimens.

Carbonic anhydrase inhibitors

Systemic carbonic anhydrase inhibitors would be expected to have side effects in children similar to adults. In addition, growth suppression in children has been associated with oral acetazolamide therapy,[37] and infants may experience a severe metabolic acidosis.[38] Side effects due to systemic carbonic anhydrase inhibitors in infants and young children are not commonly reported although these patients may not verbalise these side effects. Oral administration of acetazolamide suspension in a dosage of 10 mg/kg/day (range 5 to 15 mg ) given in divided doses (three times daily) is safe and well tolerated by children, lowers IOP, and may reduce corneal oedema prior to surgery.[39],[40]

Topical versus oral carbonic anhydrase inhibitor therapy has been evaluated for paediatric glaucoma in a crossover design study.[41] The mean IOP reduced by 36% and 27% from the baseline after treatment with oral acetazolamide and topical dorzolamide, respectively. All eyes showed an increase in IOP when switched from acetazolamide to dorzolamide; the mean increase was 3.7 mmHg. Although not as effective as acetazolamide in this group of patients, topical dorzolamide caused a significant reduction of IOP and was well tolerated.

At present, topical carbonic anhydrase inhibitors are more commonly prescribed that the systemic carbonic anhydrase inhibitors. Many clinicians recommend twice daily dosing, in order to minimise the discomfort associated with three times daily dosing. For older children, the fixed combination of dorzolamide with timolol may simplify medical regimens, reducing the number of drops instilled per day.

Prostaglandin-related drugs

Prostaglandin-related drugs, specifically latanoprost, has been evaluated in a variety of glaucoma including glaucoma associated with Sturge-Weber syndrome. [42],[43],[44],[45],[46]

Although the majority of children do not respond well to latanoprost, some children may have a significant ocular hypotensive effect with latanoprost treatment.[46] Side effects are infrequent and mild, and the dosage schedule is convenient. Parents and patients should be informed of the possible local side effects, including iris pigmentation change, eyelash growth, and hyperaemia. When medical therapy prior to surgery or other short-term medical therapy is planned, these local side effects are generally not a problem. The prevalence and types of side effects associated with longterm therapy are not known.

Alpha-2 agonists

Several noncomparative case series have described the use of brimonidine in paediatric glaucoma patients, but the use of apraclonidine is not described in paediatric patients. In 30 patients with a mean age of 10 years, brimonidine treatment was associated with a mean reduction of intraocular pressure by 7%.[47] Two young children (ages 2 and 4 years) were transiently unarousable after administration of brimonidine, and five other children experienced extreme fatigue.[47] In 23 patients with a mean age of 8 years, 18% had systemic adverse effects sufficient to necessitate stopping the drug.[48] Four paediatric patients are reported to develop somnolence after treatment with brimonidine.[49] A 1-month-old infant developed recurrent episodes of "coma" (unresponsiveness, hypotension, hypotonia, hypothermia, and bradycardia) following treatment with brimonidine.[50]

Alpha-2-agonists are less commonly used in paediatric patients compared to adults. The potential for central nervous system mediated side effects is greater with lipophilic drugs (e.g., brimonidine) compared with more hydrophilic drugs that are less likely to cross the blood brain barrier (e.g., apraclonidine). Iopidine may help to minimize intraoperative hyphaema in the setting of goniotomy.[51] Brimonidine should be used with caution in paediatric patients, and used only in older children.

Other Adrenergic Agonists

Although uncommonly prescribed at present, epinephrine (1%) has been used in children.[52] Lack of efficacy and the potential for systemic toxicity (tachyarrythmia, hypertension) limit the use of this drug. A reactive conjunctival hyperaemia may occur following the initial vasoconstriction. After prolonged use, melanin-like adrenochrome deposits may be noted in the conjunctiva, and occasionally in the cornea. Dipivefrin hydrochloride 0.1%, a prodrug of epinephrine, may also be used in children. Side effects may be attenuated compared to epinephrine, except for a high frequency of local allergic reactions. The drops are administered every 12-24 hours. In aphakic or pseudophakic paediatric patients, these drugs should be avoided due to the risk of cystoid macular oedema.

Cholinergic drugs

Although miotic drugs increase the facility of aqueous outflow in normal persons as well as in glaucoma patients and thus lower the intraocular pressure, these drugs are probably not as effective in developmental glaucoma because of the abnormal insertion of ciliary muscle into the trabecular meshwork. In paediatric patients, the use of pilocarpine (2% concentration, topically applied every 6-8 hours) is limited.[39] But, these drugs may be helpful in aphakic or pseudophakic children with elevated intraocular pressure. Also, cholinergic drugs may be useful in achieving miosis before and after goniotomy.[51]

The induced myopia caused by the miotics can produce disabling visual difficulties. A slow-release pilocarpine membrane delivery system (Ocusert), currently not available, was helpful in some young patients,[53] although sudden release of pilocarpine (burst effect) rarely induced myopic spasms. Ciliary spasm and angle-closure glaucoma have been precipitated by the use of phospholine iodide for esotropia in a child.[54]

The long-acting anti-cholinesterase drugs are not readily available, are associated with serious adverse effects, and offer no advantages over pilocarpine for use in children. Echothiophate iodide (Phospholine Iodide), which is instilled every 12 to 24 hours, is a potent and relatively irreversible inhibitor of cholinesterase. The systemic absorption of anticholinesterase agents can significantly reduce the serum cholinesterase and pseudocholinesterase levels. Affected children may show signs of weakness, diarrhoea, nausea, vomiting, salivation, decreased heart rate, and other evidence of parasympathetic nervous system stimulation. This becomes particularly dangerous when surgery is contemplated, since succinylcholine is commonly employed as a muscle relaxant during general anaesthesia. This drug is normally promptly hydrolysed by cholinesterase at the nerve endings. However, when the cholinesterase level is low, prolonged apnea can result.

Osmotic drugs

Glycerol or glycerine is administered in a dose of 0.75-1.5 g/kg body weight, orally, in a 50% solution.[55] The very sweet taste may be partially masked by chilling the solution and by using fruit juice (lemon or orange) or flavoured water to dilute it. This drug is rarely used in the treatment of developmental glaucomas. Mannitol (20% solution) is administered intravenously in a dose of 0.5-1.5 g/kg body weight, at approximately 60 drops per minute. A rapid fall in pressure occurs in 20-30 minutes and lasts for 4-10 hours. Mannitol may be administered to reduce the IOP before surgery in patients with developmental glaucomas when it remains very high even with standard medical therapy.

Medical therapy for paediatric glaucoma patients is often administered to reduce the IOP temporarily, to clear the cornea, and to facilitate surgical intervention. Most patients who require longterm medical therapy do usually have severe disease that has not responded to surgical therapy. Some patients with elevated IOP, however, may repond to therapy with various medications. Prior to initiating medical therapy, clinicians should carefully consider the potential for side effects. When using topical glaucoma medications, children may be at increased risk of systemic side effects compared with adults, due to reduced body mass and blood volume for drug distribution.

Laser treatment

The argon or diode lasers are usually not effective in management of glaucoma associated with aphakia or pseudophakia in children. [20]

The Nd:YAG laser is particularly useful for iridotomy in pupillary block glaucoma in children. Vajpayee and co-workers[14] reported a series of 16 children with pseudophakic pupillary-block glaucoma that was managed with neodymium:YAG laser iridotomy. After the IOP was controlled initially with medications, Nd:YAG laser iridotomy was performed within two or three days in all eyes. While the initial Nd:YAG iridotomy failed in all eyes, a repeat Nd:YAG iridotomy a week later succeeded. Satisfactory control of IOP was achieved in 13 of 16 patients (81%) after Nd:YAG iridotomy.

Surgical treatment

Surgical iridectomy
. With the advent of the Nd:YAG laser, surgical iridectomy is advisable when laser iridotomy fails repeatedly, especially in patients with severe postoperative inflammation. However, in such a situation the clinician should evaluate whether iridotomy alone will suffice or a more definitive filtering surgery will be required.

Filtering surgery with or without antifibrosis drugs. Trabeculectomy is the most commonly performed filtering surgery in aphakia and pseudophakia following infantile cataract surgery, but the success rate is variable. Barriers to success include a thick and active Tenon's capsule with rapid wound healing response in children.[56] Aphakia or pseduophakia and young age are additional risk factors for failure of trabeculectomy. [57],[58],[59]

Walton[15] assessed the results of surgical treatment for 42 eyes of 65 children. Trabeculectomy with mitomycin C was helpful for 9 of 14 eyes (64%) with paediatric aphakic glaucoma. Lichter commented that trabeculectomy with antimetabolite is probably the preferred approach in managing glaucoma in aphakia and pseudophakia following congenital and infantile cataract surgery.

Antifibrosis drugs are known to inhibit fibroblast proliferation and have been found to improve the success rate of filtering surgery in adults as well as in children.[60] Mitomycin C (MMC) and 5-fluorouracil (5-FU) are the most commonly used anti-fibrotic agents in glaucoma filtering surgery. Subconjunctival injection of 5-FU in children requires use of multiple general anaesthesias[61] and thereby is not a suitable option in children with aphakic or pseudophakic glaucoma. Additionally, several prospective randomised studies in adults with high risk glaucoma filtering surgery have shown that intraoperative MMC may be a better alternative to postoperative 5-FU because MMC results in lower overall IOP, decreased dependence on postoperative antiglaucoma medications, and decreased corneal toxicity. Several reports have been recently published on the successful use of mitomycin C in children with refractory congenital glaucoma and glaucoma following congenital cataract surgery. [62],[63],[64]

Reports of clinical experience with trabeculectomy with MMC in paediatric aphakic and pseudophakic glaucoma are summarised in [Table - 4]. [64],[65],[66],[67],[68],[69] With the exception of the report by Azuara-Blanco et al,[67] the success rate varied from 50% to 85%.

Mandal et al [64] reported the largest retrospective series of trabeculectomy both with and without MMC (0.4 mg/ml) performed in 23 Asian Indian aphakic (n=21) and pseudophakic (n=2) eyes [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8]. Overall, complete success (IOP between 6 and 21 mm Hg without medication, no further surgery and no sight-threatening complication) was achieved in only 37% after a mean follow-up of 2 years. An additional 21% patients were considered as a qualified success as the IOP was controlled with one antiglaucoma medication [Figure - 9].

The optimal dose of MMC in children is not yet known, although clinicians often use dosage ranging from 0.2 to 0.4 mg/ml for 2 to 3 minutes; we have found this safe and effective in children with aphakic and pseudophakic glaucoma. However, prospective, randomised controlled clinical studies with larger number of patients and longer follow-up period are required to determine the optimal dosage and the application time of MMC, as well as the ocular and systemic factors that may predispose the eyes with refractory glaucoma to late complications. Early complications like shallow anterior chamber, corneal epitheliopathy, and hypotony with or without choroidal detachment [Figure - 10] and [Figure - 11] are managed according to the standard treatments. Devastating complications such as late infections [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8] remain a potential danger with the use of MMC as adjunctive therapy during trabeculectomy with refractory glaucoma in aphakia and pseudophakia following congenital cataract surgery.[64],[65],[66],[69] After trabeculectomy with MMC, these children require periodic examinations and the parents should be educated about the possible late complications.[64]

  Glaucoma drainage implants Top

Glaucoma drainage implants are useful when other surgical treatments have a poor prognosis for success, prior conventional surgery fails, or when significant conjunctival scarring precludes filtration surgery. Smaller sized drainage implants have been marketed for use in paediatric patients, but adult sized devices are commonly implanted. Available types of drainage implants may be characterised as open tube (non-restrictive) devices or valved (flow-restrictive) devices. Examples of open tube implants include the Molteno and Baerveldt implants; the Krupin implant and the Ahmed Glaucoma Valve are flow-restrictive devices. The flow-restrictive devices are intended to reduce the incidence of complications associated with hypotony during the immediate postoperative period. Glaucoma drainage implants are most commonly placed in the superotemporal quadrant, but may be surgically positioned in any quadrant.

Studies of glaucoma drainage implants in paediatric patients are summarised in [Table - 5].[70],[71],[72],[73],[74],[75],[76],[77],[78],[79],[80],[81],[82],[83],[84],[85],[86] The success rate reported in these studies ranged from 56% to 95%, depending on the patient age, the definition of success, length of follow-up, and other factors. Glaucoma drainage implants may be effective in controlling the intraocular pressure, even in paediatric patients who have failed previous glaucoma surgery. Complications are reported following glaucoma drainage implants in paediatric patients. They include hypotony with shallow anterior chamber and choroidal detachments, tube-cornea touch and corneal oedema, obstructed tube, exposed tube or plate, endophthalmitis, and retinal detachment.

Postoperatively, patients often require adjunctive glaucoma medications and close monitoring for complications. Iris creep around the tube insertion site may cause correctopia with drainage implants in children.[87] Extraocular muscle imbalance has been reported after Baerveldt implant,[88] but this may occur after any type of drainage implant. Conjunctival and even transcorneal[89] tube erosion have been reported in children, which may lead to delayed endophthalmitis.[90]-[91] Episodes of postoperative hypotony are commonly reported with open-tube implants, whereas the flow-resistive implants have reduced rate of hypotony in the immediate postoperative period.

Two-stage implantation of glaucoma drainage device may be considered for eyes at high risk for complications due to hypotony.[70]-[71] In the first stage, the plate is implanted and the tube is left under the conjunctiva near the limbus. A period of 4 to 6 weeks prior to the second stage allows a pseudocapsule to form, which provides some resistance to aqueous flow in the immediate postoperative period after tube insertion. In the second stage, the tube is inserted into the anterior chamber. This approach is most commonly used for open tube implants, such as the Molteno[70]-[71] and Baerveldt[92] implants, but may also be used for flow-resistive valves. Satisfactory results have been reported using a two-stage Baerveldt implant[92] or a single stage Ahmed Glaucoma Valve.[93]

If the IOP increases after glaucoma drainage implant, most clinicians will recommend adjunctive medical therapy. If adjunctive medical therapy fails to control the IOP, supplemental laser cyclophotocoagulation may be very useful.[94] Another alternative is revision of the drainage implant, excising a portion of the pseudocapsule around the implant plate.[95] This approach is similar in concept to needling of encapsulated blebs, and has a similar success rate. Additional glaucoma drainage devices may be implanted in an unused quadrant, which may control the intraocular pressure.[96]-[97]

In the 10 - 20% of patients who fail initial surgery for paediatric glaucoma, the clinician often chooses trabeculectomy with MMC or a drainage implant as a subsequent surgical treatment. Both procedures are useful in patients with paediatric glaucoma that is refractory to initial surgical treatment.[98],[99] We often suggest trabeculectomy with MMC after failed primary surgery and, if this procedure is unsuccessful, drainage implant is indicated.

  Cyclodestructive procedures Top

Cyclodestructive procedures damage the ciliary epithelium, reduce aqueous production, and thereby lower the intraocular pressure. The most commonly performed procedures include cyclocryotherapy and cyclophotocoagulation. When available, cyclophoto-coagulation is usually the preferred procedure because it is associated with less postoperative inflammation and less discomfort for the patient compared with cyclocryotherapy. After initial and secondary surgical treatments fail to control the intraocular pressure, a cyclodestructive procedure may be considered.

It is not easy to titrate cyclodestructive procedure.[100] Retreatments are often necessary.[101],[102] But the risk of hypotony, vision loss, and even phthisis is substantial.

[Table - 6] summarises the results of studies of cyclophotocoagulation in paediatric patients.[103],[104],[105],[106],[107],[108],[109]

Cyclophotocoagulation may be performed with an endolaser and an endoscope, although this approach is not widely available. The procedure requires intraocular surgery, but the laser energy is delivered more precisely to the target tissue. [110],[111],[112],[113]

In conclusion, up to a quarter or more of paediatric patients with pseudophakia or aphakia may develop glaucoma after cataract surgery. The onset of glaucoma may occur years after cataract surgery, thus the proportion of affected children increases with longer follow-up. Patients may develop angle-closure glaucoma, but more commonly develop open-angle glaucoma. Lifelong monitoring for glaucoma is necessary. Antiglaucoma medications may be helpful in some patients, whereas laser therapy for open-angle glaucoma is generally not effective. Patients refractory to medical therapy may be treated with trabeculectomy with MMC or glaucoma drainage implant. Cyclodestructive procedures may be reserved for patients with advanced glaucoma and very minimal visual potential. Certainly, following congenital cataract surgery, lifelong surveillance for glaucoma is crucial.[114] It is clear that we need to carry out more research so that we can understand the patho-physiology and further improve the prevention and treatment of this devastating complication of paediatric cataract surgery.

  References Top

Lambert SR, Drack AV. Infantile cataracts. Surv Ophthalmol 1996;40:427-58.  Back to cited text no. 1
Asrani SG, Wilensky JT. Glaucoma after congenital cataract surgery. Ophthalmology 1995;102: 863-67.  Back to cited text no. 2
Simon JW , Mehta N , Simmons ST , Catalano RA, Lininger LL. Glaucoma after pediatric lensectomy/vitrectomy. Ophthalmology 1991;98:670-74.  Back to cited text no. 3
Miyahara S, Amino K, Tanihara H. Glaucoma secondary to pars plana lensectomy for congenital cataract. Graefe's Arch Clin Exp Ophthalmol 2002;240:176-79.  Back to cited text no. 4
Egbert JE ,Wright MM , Dahlhauser KF, Keithahn MAZ, Letson RD, Summers CG. A prospective study of ocular hypertension and glaucoma after pediatric cataract surgery. Ophthalmology 1995;102:1098-101.  Back to cited text no. 5
Phelps CD, Arafat NI. Open-angle glaucoma following surgery for congenital cataracts. Arch Ophthalmol 1977;95:1985-87.  Back to cited text no. 6
Bradford GM, Keech RV, Scott WE. Factors affecting visual outcome after surgery for bilateral congenital cataracts. Am J Ophthalmol 1994;117: 58-64.  Back to cited text no. 7
Francois J. Late results of congenital cataract surgery. Ophthalmology 1979;86:1586-89.  Back to cited text no. 8
Parks MM , Johnson DA , Reed GW. Long-term visual results and complications in children with aphakia. A function of cataract type. Ophthalmology 1993;100:826-40.  Back to cited text no. 9
Keech RV, Tongue AC, Scott WE. Complications after surgery for congenital and infantile cataracts. Am J Ophthalmol 1989;08:136-41.  Back to cited text no. 10
Chrousos GA , Parks MM ,O'Neill JF. Incidence of chronic glaucoma, retinal detachment and secondary membrane surgery in pediatric aphakic patients. Ophthalmology 1984;91:1238-41.  Back to cited text no. 11
Robb RM, Petersen RA. Outcome of treatment for bilateral congenital cataracts. Ophthalmic Surgery 1992;23:650-56.  Back to cited text no. 12
Mills MD, Robb RM. Glaucoma following childhood cataract surgery. J Pediatr Ophthalmol Strabismsus 1994;31:355-60.  Back to cited text no. 13
Vajpayee RB, Angra SK, Titiyal JS , Sharma YR, Chabbra VK. Pseudophakic pupillary-block glaucoma in children. Am J Ophthalmol 1991;111:715-18.  Back to cited text no. 14
Walton DS. Pediatric aphakic glaucoma. A study of 65 patients. Trans Am Ophthalmol Soc 1995;9:403-13.  Back to cited text no. 15
Johnson CP, Keech RV. Prevalence of glaucoma after surgery for PHPV and infantile cataracts. J Pediatr Ophthalmol Strabismus 1996;3:4-17.  Back to cited text no. 16
Barnhorst D, Meyers SM, Myers T. Lens-induced glaucoma 65 years after congenital cataract surgery. Am J Ophthalmol 1994;118:807-8.  Back to cited text no. 17
Chandler PA. Surgery of congenital cataract. Am J Ophthalmol 1968;65: 663-74.  Back to cited text no. 18
Walton DS. Glaucoma secondary to operation for childhood cataract . In :Epstein DL, editor. Chandler and Grant's Glaucoma . Philadelphia , PA : Lea & Febiger, pp 1986;521-25.  Back to cited text no. 19
Pressman SH, Crouch ER. Pediatric aphakic glaucoma. Ann Ophthalmology 1983;15:568-73.  Back to cited text no. 20
Munoz M, Parrish RK, Murray TG. Open-angle glaucoma after pars plicata lensectomy and vitrectomy for congenital cataracts. Am J Ophthalmol 1995;119:103-4.  Back to cited text no. 21
Wallace DK, Plager DA. Corneal diameter in childhood aphakic glaucoma . J Pediatr Ophthalmol Strabismus 1996;33:230-34.  Back to cited text no. 22
Asrani S, Freedman S, Hasselblad V, Buckley EG, Egbert J, Dahan E, et al. Does primary intraocular lens implantation prevent "aphakic" glaucoma in children? J AAPOS 1999;3:33-39.  Back to cited text no. 23
Rabiah PK. Frequency and predictors of glaucoma after pediatric cataract surgery. Am J Ophthalmol 2004;137:30-37.  Back to cited text no. 24
Vishwanath M, Cheong-Leen R, Taylar D, Russell-Eggitt I, Rahi J. Is early surgery for congenital cataract a risk factor for glaucoma? Br J Ophthalmol 2004;88:905-10.  Back to cited text no. 25
Egbert JE , Kushner BJ. Excessive loss of hyperopia. A presenting sign of juvenile aphakic glaucoma. Arch Ophthalmol 1990;108:1257-59.  Back to cited text no. 26
Wallace DK, Steinkuller PG. Ocular medications in children. Clin Pediatr 1998;37:645-52.  Back to cited text no. 27
Palmer EA. How safe are ocular drugs in pediatrics? Ophthalmology 1986;93:1038-40.  Back to cited text no. 28
Boger WP III, Walton DS. Timolol in uncontrolled childhood glaucomas. Ophthalmology 1981;88:253-58.  Back to cited text no. 29
McMahon CD, Hetherington J Jr, Hoskins HD Jr, Shaffer RN. Timolol and pediatric glaucomas. Ophthalmology 1981;88:249-52.  Back to cited text no. 30
Zimmerman TJ, Kooner KS, Morgan KS. Safety and efficacy of timolol in pediatric glaucoma. Surv Ophthalmol 1983;28 (Suppl):262-64.  Back to cited text no. 31
Hoskins HD Jr, Hetherington J Jr, Magee SD, Naykhin R, Migliazzo CV. Clinical experience with timolol in childhood glaucoma. Arch Ophthalmol 1985;103:1163-65.  Back to cited text no. 32
Passo MS, Palmer EA, Van Buskirk EM. Plasma timolol in glaucoma patients. Ophthalmology 1984;91:1361-63.  Back to cited text no. 33
Burnstine RA, Felton JL, Ginther WH. Cardiorespiratory reaction to timolol maleate in a pediatric patient: a case report. Ann Ophthalmol 1982;14:905-6.  Back to cited text no. 34
Bailey PL. Timolol and postoperative apnea in neonates and young infants. Anesthesiology 1984;61:622.  Back to cited text no. 35
Olsen RJ, Bromberg BB, Zimmerman TJ.: Apneic cells associated with timolol therapy in a neonate. Am J Ophthalmol 1979;88:120-22.  Back to cited text no. 36
Futagi Y, Otani K, Abe J. Growth suppression in children receiving acetazolamide with antiepileptic drugs. Pediatr Neurol 1996;15:323-26.  Back to cited text no. 37
Ritch R. Special therapeutic situations. In: Netland PA, Allen RC, eds. Glaucoma Medical Therapy: Principles and Management . San Francisco: American Academy of Ophthalmology 1999 pp. 193-211.  Back to cited text no. 38
Hass J. Principles and problems of therapy in congenital glaucoma. Invest Ophthalmol 1968;140-46.  Back to cited text no. 39
Shaffer RN. New concepts in infant glaucoma. Trans Ophthalmol Soc UK 1967;87:581-85.  Back to cited text no. 40
Portellos M, Buckley EG, Freedman SF. Topical versus oral carbonic anhydrase inhibitor therapy for pediatric glaucoma. J AAPOS 1998;2:43-47.  Back to cited text no. 41
Enyedi LB, Freedman SF, Buckley EG. The effectiveness of latanoprost for the treatment of pediatric glaucoma. J AAPOS 1999;33-39.  Back to cited text no. 42
Yang CB, Freedman SF, Myers JS, Buckley EG, Herndon LW, Allingham RR. Use of latanoprost in the treatment of glaucoma associated with Sturge-Weber syndrome. Am J Ophthalmol 1998;126:600-602.  Back to cited text no. 43
Altuna JC, Greenfield DS, Wand M, Liebmann JM, Taglia DP, Kaufman PL, Cioffi GA, Lee DA, Robin AL, Crichton A, Costa VP, Ritch R. Latanoprost in glaucoma associated with Sturge-Weber syndrome: benefits and side-effects. J Glaucoma 1999;8:99-203.  Back to cited text no. 44
Ong T, Chia A, Nischal KK. Latanoprost in port wine stain related paediatric glaucoma. Br J Ophthalmol 2003;87:1091-93.  Back to cited text no. 45
Enyedi LB, Freedman SF. Latanoprost for the treatment of pediatric glaucoma. Surv Ophthalmol 2002;(Suppl): S129-S132.  Back to cited text no. 46
Enyedi LB, Freedman SF. Safety and efficacy of brimonidine in children with glaucoma. J AAPOS 2001;281-84.  Back to cited text no. 47
Bowman RJ, Cope J, Nischal KK. Ocular and systemic side effects of brimonidine 0.2% eye drops (Alphagan) in children. Eye 2004;18:24-26.  Back to cited text no. 48
Levy Y, Zadok D. Systemic side effects of ophthalmic drops. Cloin Pediatr 2004;43:99-101.  Back to cited text no. 49
Berlin RJ, Lee UT, Samples JR, Rich LF, Tang-Liu DD, Sing KA, et al. Ophthalmic drops causing coma in an infant. J Pediatr 2001;138:441-43.  Back to cited text no. 50
Freedman SF. Medical and surgical treatments for childhood glaucomas. In: Epstein DL, Allingham RR, Schuman JS, editors: Chandler and Grant's Glaucoma , 4th ed. Baltimore, MD: Williams & Wilkins, 1997. pp 636.  Back to cited text no. 51
Raab EL. Congenital glaucoma. Persp Ophthalmol 1978;2:35-41.  Back to cited text no. 52
Pollack IP, Quigley HA, Harbin TS. The Ocusert pilocarpine system: advantages and disadvantages. South Med J 1976;69:1296-98.  Back to cited text no. 53
Jones DE, Watson DM. Angle-closure glaucoma precipitated by the use of phospholine iodide for esotropia in child. Br J Ophthalmol 1967;51:783-85.  Back to cited text no. 54
Netland PA, Kolker AE. Osmotic drugs. In: Netland PA, Allen RC, editors. Glaucoma Medical Therapy: Principles and Management . San Francisco, CA: American Academy of Ophthalmology, 1999; pp. 133-147.  Back to cited text no. 55
Beauchamp GR, Parks MM. Filtering surgery in children: Barriers to success. Ophthalmology 1979;86:170-80.  Back to cited text no. 56
Tomey KF, Traverso CE. The glaucomas in aphakia and pseudophakia. Surv Ophthalmology 1991;36:79-112.  Back to cited text no. 57
Heuer DK, Gressel MG, Parrish RK II, Anderson DR, Hodapp E, Palmberg PF. Trabeculectomy in aphakic eyes. Ophthalmology 1984;91:1045-51.  Back to cited text no. 58
Gressel MG, Heuer DK, Parrish RK II. Trabeculectomy in young patients . Ophthalmology 1984;91:1242-46.  Back to cited text no. 59
Skuta GL, Parrish RK II. Wound healing in glaucoma filtering surgery. Surv Ophthalmology 1987;32:149-70.  Back to cited text no. 60
Zalish M, Leiba H, Oliver M. Subconjunctival injection of 5-flurouracil following trabeculectomy for congenital and infantile glaucoma. Ophthalmic Surgery 1992;23:203-05.  Back to cited text no. 61
Mandal AK, Walton DS, John T, Jayagandan A. Mitomycin C augmented trabeculectomy in refractory congenital glaucoma. Ophthalmology 1997;104:996-1003.  Back to cited text no. 62
Mandal AK, Prasad K, Naduvilath TJ. Surgical results and complications of mitomycin C-augmented trabeculectomy in refractory developmental glaucoma. Ophthalmic Surg Lasers 1999;30: 473-80.  Back to cited text no. 63
Mandal AK, Bagga H, Nutheti R, Gothwal VK, Nanda AK. Trabeculectomy with or without mitomycin-C for paediatric glaucoma in aphakia and pseudophakia following congenital cataract surgery. Eye 2003;17:53-62.  Back to cited text no. 64
Wallace DK, Plager DA, Snyder SK, Raiesdana A, Helveston EM, Ellis FD. Surgical results of secondary glaucomas in childhood. Ophthalmology 1998;105:101-11.  Back to cited text no. 65
Beck AD, Wilson WR, Lynch MG, Lynn MJ, Noe R. Trabeculectomy with adjunctive Mitomycin-C in pediatric glaucoma. Am J Ophthalmol 1998;126:648-57.  Back to cited text no. 66
Azuara-Blanco A, Wilson RP, Spaeth GL, Schmidt CM, Augsburger JJ. Filtration procedures supplemented with mitomycin C in the management of childhood glaucoma. Br J Ophthalmol 1999;83:151-56.  Back to cited text no. 67
Freedman SF, McCormick K, Cox TA. Mitomycin C-augmented trabeculectomy with postoperative wound modulation in pediatric glaucoma. J AAPOS 1999;3:117-24.  Back to cited text no. 68
Sidoti PA, Belmonte SJ, Liebmann JM , Ritch R. Trabeculectomy with Mitomycin-C in the treatment of pediatric glaucomas. Ophthalmology 2000;107:422-29.  Back to cited text no. 69
Molteno AC, Ancker E, Van Biljon G. Surgical technique for advanced juvenile glaucoma. Arch Ophthalmol 1984;12:51-57.  Back to cited text no. 70
Billson F, Thomas R, Aylward W. The use of two-stage Molteno implants in developmental glaucoma. J Pediatr Ophthalmol Strabismus 1989;26:3-8.  Back to cited text no. 71
Hill RA, Heuer DK, Baerveldt G, Minckler DS, Martone JF. Molteno implantation for glaucoma in young patients. Ophthalmology 1991;98:1042-46.  Back to cited text no. 72
Munoz M, Tomey KF, Traverso C, Day SH, Senft SH. Clinical experience with the Molteno implant in advanced infantile glaucoma. J Pediatr Ophthalmol Strabismus 1991;28:68-72.  Back to cited text no. 73
Lloyd MA, Sedlak T, Heuer DK, Minckler DS, Baerveldt G, Lee MB, et al. Clinical experience with the single-plate Molteno implant in complicated glaucomas. Update of a pilot study. Ophthalmology 1992;99:679-87.  Back to cited text no. 74
Nesher R, Sherwood MB, Kass MA, Hines JL, Kolker AE. Molteno implants in children. J Glaucoma 1992;1:228-32.  Back to cited text no. 75
Netland PA, Walton DS. Glaucoma Drainage implants in pediatric patients. Ophthalmic Surg 1993;24:723-29.  Back to cited text no. 76
Fellenbaum PS, Sidoti PA, Heuer DK, Minckler DS, Baerveldt G, Lee PP. Experience with the Baerveldt implant in young patients with complicated glaucomas. J Glaucoma 1995;4:91-97.  Back to cited text no. 77
Siegner SW, Netland PA, Urban RC Jr, Williams AS, Richards DW, Latina MA, et al. Clinical experience with the Baerveldt glaucoma drainage implant. Ophthalmology 1995;102:1298-307.  Back to cited text no. 78
Coleman AL, Smyth RJ, Wilson MR, Tam M. Initial clinical experience with the Ahmed Glaucoma Valve implant in pediatric patients. Arch Ophthalmol 1997;115:186-91.  Back to cited text no. 79
Eid TE, Katz LJ, Spaeth GL, Augsburger JJ. Long-term effects of tube-shunt procedures on management of refractory childhood glaucoma. Ophthalmology 1997;104:1011-16.  Back to cited text no. 80
Donahue SP, Keech RV, Munden P, Scott WE. Baerveldt implant surgery in the treatment of advanced childhood glaucoma. J AAPOS 1997;1:41-45.  Back to cited text no. 81
Huang MC, Netland PA, Coleman AL, Siegner SW, Moster MR, Hill RA. Intermediate-term clinical experience with the Ahmed glaucoma valve implant. Am J Ophthalmol 1999;127:27-33.  Back to cited text no. 82
Englert JA, Freedman SF, Cox TA. The Ahmed valve in refractory pediatric glaucoma. Am J Ophthalmol 1999;127:34-42.  Back to cited text no. 83
Djodeyre MR, Peralta Calvo J, Abelairas Gomez J. Clinical evaluation and risk factors of time to failure of Ahmed Glaucoma Valve implant in pediatric patients. Ophthalmology 2001;108:614-20.  Back to cited text no. 84
Pereira ML, Araujo SV, Wilson RP, Azuara-Blanco A, Moster MR, Schmidt CM. Aqueous shunts for intractable glaucoma in infants. Ophthalmic Surg Lasers 2002;33:19-29.  Back to cited text no. 85
Morad Y, Donaldson CE, Kim YM, Abdolell M, Levin AV. The Ahmed drainage implant in the treatment of pediatric glaucoma. Am J Ophthalmol 2003;135:821-29.  Back to cited text no. 86
Fuller JR, Molteno AC, Bevin TH. Iris creep producing correctopia in response to Molteno implants. Arch Ophthalmol 2001;119:304.  Back to cited text no. 87
Smith SL, Starita RJ, Fellman RL, Lynn JR. Early clinical experience with the Baerveldt 350-mm2, glaucoma implant and associated extraocular muscle imbalance. Ophthalmology 1993;100:914-18.  Back to cited text no. 88
Al-Torbak A, Edward DP. Transcorneal tube erosion of an Ahmed valve implant in a child. Arch Ophthalmol 2001;119:1558-59.  Back to cited text no. 89
Al-Torbaq AA, Edward DP. Delayed endophthalmitis in a child following an Ahmed glaucoma valve implant. J AAPOS 2002;6:123-25.  Back to cited text no. 90
Gedde SJ, Scott IU, Tabandeh H, Luu KK, Budenz DL, Greenfield DS, et al. Late endophthalmitis associcated with glaucoma drainage implants. Ophthalmology 2001;108:1323-27.  Back to cited text no. 91
Budenz DL, Sakamoto D, Eliezer R, Varma R, Heuer DK. Two-staged Baerveldt glaucoma implant for childhood glaucoma associated with Sturge-Weber syndrome. Ophthalmology 2000;107:2105-10.  Back to cited text no. 92
Hamush NG, Coleman AL, Wilson MR. Ahmed glaucoma valve implant for management of glaucoma in Sturge-Weber syndrome. Am J Ophthalmol 1999;128:758-60.  Back to cited text no. 93
Semchyshyn TM, Tsay JC, Joos KM. Supplemental transscleral diode laser cyclophotocoagulation after aqueous shunt placement in refractory glaucoma. Ophthalmology 2002;109:1078-84.  Back to cited text no. 94
Tsai JC, Grajewski AL, Parrish RK II. Surgical revision of glaucoma shunt implants. Ophthalmic Surg Lasers 1999;30:41-46.  Back to cited text no. 95
Shah AA, WuDunn D, Cantor LB. Shunt revision versus additional tube shunt implantation after failed tube shunt surgery in refractory glaucoma. Am J Ophthalmol 2000;129:455-60.  Back to cited text no. 96
Burgoyne JK, WuDunn D, Lakhani V, Cantor LB. Outcomes of sequential tube shunts in complicated glaucoma. Ophthalmology 2000;107:309-14.  Back to cited text no. 97
Beck AD, Freedman S, Kammer J, Jin J. Aqueous shunt devices compared with trabeculectomy with mitomycin-C for children in the first two years of life. Am J Ophthalmol 2003;136:994-1000.  Back to cited text no. 98
Hill R, Ohanesian R, Voskanyan L, Malayan A. The Armenian Eye Care Project: s0 urgical outcomes of complicated paediatric glaucoma. Br J Ophthalmol 2003;87:673-76.  Back to cited text no. 99
Terraciano AJ, Sidoti PA. Management of refractory glaucoma in childhood. Curr Opinion Ophthalmol 2002;13:97-102.  Back to cited text no. 100
Al Faran MF, Tomey KF, Al Mutlaq FA. Cyclocryotherapy in selected cases of congenital glaucoma. Ophthalmic Surg 1990;21:794-98.  Back to cited text no. 101
Wagle NS, Freedman SF, Buckley EG, Davis JS, Biglan AW. Long-term outcome of cyclocryotherapy for refractory pediatric glaucoma. Ophthalmology 1998;105:1921-26.  Back to cited text no. 102
Phelan MJ, Higginbotham EJ. Contact transscleral Nd:YAG laser cyclophotocoagulation for the treatment of refractory pediatric glaucoma. Ophthalmic Surg Lasers 1995;26:401-3.  Back to cited text no. 103
Bock CJ, Freedman SF, Buckley EG, Shields MB. Transscleral diode laser cyclophotocoagulation for refractory pediatric glaucomas. J Pediatr Ophthalmol Strabismus 1997;34:235-39.  Back to cited text no. 104
Hamard P, May F, Quesnot S, Hamard H. Trans-scleral diode laser cyclophotocoagulation for the treatment of refractory pediatric glaucoma. J Fr Ophtalmol 2000;23:773-80.  Back to cited text no. 105
Izgi B, Demirci H, Demirci FY, Turker G. Diode laser cyclophotocoagulation in refractory glaucoma: Comparison between pediatric and adult glaucomas. Ophthalmic Surg Lasers 2001;32:100-7.  Back to cited text no. 106
Raivio VE, Immonen IJ, Puska PM. Transscleral contact krypton laser cyclophotocoagulation for treatment of glaucoma in children and young adults. Ophthalmology 2001;08:1801-7.  Back to cited text no. 107
Kirwin JF, Shah P, Khaw PT. Diode laser cyclophotocoagulation: r0 ole in the management of refractory pediatric glaucomas. Ophthalmology 2002;109:316-23.  Back to cited text no. 108
109. Autrata R, Rehurek J. Long-term results of transscleral cyclophotocoagulation in refractory pediatric glaucoma patients. Ophthalmologica 2003;217:393-400.  Back to cited text no. 109
Chen J, Cohn RA, Lin SC, Cortes AE, Alvarado JA. Endoscopic photocoagulation of the ciliary body for treatment of refractory glaucomas. Am J Ophthalmol 1997;124:787-96.  Back to cited text no. 110
Plager DA, Neely DE. Intermediate-term results of endoscopic diode laser cyclophotocoagulation for pediatric glaucoma. J AAPOS 1999;3:131-37.  Back to cited text no. 111
Neely DE, Plager DA. Endocyclophotocoagulation for management of difficult pediatric glaucomas. J AAPOS 2001;5:221-29.  Back to cited text no. 112
Barkana Y, Morad Y, Ben-nun J. Endoscopic photocoagulation of the ciliary body after repeated failure of trans-scleral diode-laser cyclophotocoagulation. Am J Ophthalmol 2002;133:405-7.  Back to cited text no. 113
Papadopoulos M, Khaw PT. Meeting the challenge of glaucoma after pediatric cataract surgery. Eye 2003;17:1-2.  Back to cited text no. 114


  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9], [Figure - 10], [Figure - 11]

  [Table - 1], [Table - 2], [Table - 3], [Table - 4], [Table - 5], [Table - 6]

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