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112.Kooner KS. Repair of Molteno implant during surgery. Am J Ophthalmol. 1994;117(5):673.

113.Smith MF, Doyle JW. Results of another modality for extending glaucoma drainage tubes. J Glaucoma. 1999;8(5):310-314.

114.Liu SM, Su J, Hemady RK. Corneal melting after avulsion of a Molteno shunt plate. J Glaucoma. 1997;6(6):357-358.

115.Raviv T, Greenfield DS, Liebmann JM, et al. Pericardial patch grafts in glaucoma implant surgery. J Glaucoma. 1998;7(1):27-32.

116.King AJ, Azuara-Blanco A. Pericardial patch melting following glaucoma implant insertion. Eye (Lond). 2001;15(pt 2):236-237.

117.Lama PJ, Fechtner RD. Tube erosion following insertion of a glaucoma drainage device with a pericardial patch graft. Arch Ophthalmol. 1999;117(9):1243-1244.

118.Brandt JD. Patch grafts of dehydrated cadaveric dura mater for tubeshunt glaucoma surgery. Arch Ophthalmol. 1993;111(10):1436-1439.

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119.Tanji TM, Lundy DC, Minckler DS, et al. Fascia lata patch graft in glaucoma tube surgery. Ophthalmology. 1996;103(8):1309-1312.

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121.Hinton R, Jinnah RH, Johnson C, et al. A biomechanical analysis of solvent-dehydrated and freezedried human fascia lata allografts. A preliminary report. Am J Sports Med. 1992;20(5):607-612.

122.Simonds RJ, Holmberg SD, Hurwitz RL, et al. Transmission of human immunodeficiency virus type 1 from a seronegative organ and tissue donor. N Engl J Med. 1992;326(11):726-732.

123.Diringer H, Braig HR. Infectivity of unconventional viruses in dura mater. Lancet. 1989;1 (8635):439-440.

124.Jacob T, LaCour OJ, Burgoyne CF, et al. Expanded polytetrafluoroethylene reinforcement material in glaucoma drain surgery. J Glaucoma. 2001;10(2):115-120.

125.Oh KT, Alward WL, Kardon RH. Myositis associated with a Baerveldt glaucoma implant. Am J Ophthalmol. 1999;128(3):375-376.

126.Fanous MM, Cohn RA. Propionibacterium endophthalmitis following Molteno tube repositioning. J Glaucoma. 1997;6(4):201-202.

127.Perkins TW. Endophthalmitis after placement of a Molteno implant. Ophthalmic Surg. 1990;21 (10):733-734.

128.Gedde SJ, Scott IU, Tabandeh H, et al. Late endophthalmitis associated with glaucoma drainage implants. Ophthalmology. 2001;108(7): 1323-1327.

129.Heher KL, Lim JI, Haller JA, et al. Late-onset sterile endophthalmitis after Molteno tube implantation. Am J Ophthalmol. 1992;114(6):771-772.

130.Melamed S, Cahane M, Gutman I, et al. Postoperative complications after Molteno implant surgery. Am J Ophthalmol. 1991;111(3):319-322.

131.Huna R, Melamed S, Hirsh A, et al. Retinal detachment adherent to posterior chamber IOL after Molteno implant surgery. Ophthalmic Surg. 1990;21(12):854-856.

132.Lotufo DG. Postoperative complications and visual loss following Molteno implantation.

Ophthalmic Surg. 1991;22(11):650-656.

133.Waterhouse WJ, Lloyd MA, Dugel PU, et al. Rhegmatogenous retinal detachment after Molteno glaucoma implant surgery. Ophthalmology. 1994;101(4):665-671.

134.Kramer T, Brown R, Lynch M, et al. Molteno implants and operating microscope-induced retinal phototoxicity. A clinicopathologic report. Arch Ophthalmol. 1991;109(3):379-383.

135.McDermott ML, Swendris RP, Shin DH, et al. Corneal endothelial cell counts after Molteno implantation. Am J Ophthalmol. 1993;115(1): 93-96.

136.Englert JA, Freedman SF, Cox TA. The Ahmed valve in refractory pediatric glaucoma. Am J Ophthalmol. 1999;127(1):34-42.

137.Asrani S, Herndon L, Allingham RR. A newer technique for glaucoma tube trimming. Arch Ophthalmol. 2003;121(9):1324-1326.

138.Zalloum JN, Ahuja RM, Shin D, et al. Assessment of corneal decompensation in eyes having undergone molteno shunt procedures compared to eyes having undergone trabeculectomy. CLAO J. 1999; 25(1):57-60.

139.Topouzis F, Coleman AL, Choplin N, et al. Follow-up of the original cohort with the Ahmed glaucoma valve implant. Am J Ophthalmol. 1999; 128(2):198-204.

140.Lim KS. Corneal endothelial cell damage from glaucoma drainage device materials. Cornea. 2003;22(4):352-354.

141.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(4):455-460.

142.Burgoyne JK, WuDunn D, Lakhani V, et al. Outcomes of sequential tube shunts in complicated glaucoma. Ophthalmology. 2000;107(2): 309-314.

143.Cardakli UF, Perkins TW. Recalcitrant diplopia after implantation of a Krupin valve with disc. Ophthalmic Surg. 1994;25(4):256-258.

144.Christmann LM, Wilson ME. Motility disturbances after Molteno implants. J Pediatr Ophthalmol Strabismus. 1992;29(1):44-48.

145.Frank JW, Perkins TW, Kushner BJ. Ocular motility defects in patients with the Krupin valve implant. Ophthalmic Surg. 1995;26(3):228-232.

146.Munoz M, Parrish RK II. Strabismus following implantation of Baerveldt drainage devices. Arch Ophthalmol. 1993;111(8):1096-1099.

147.Smith SL, Starita RJ, Fellman RL, et al. Early clinical experience with the Baerveldt 350-mm2 glaucoma implant and associated extraocular muscle imbalance. Ophthalmology. 1993;100(6):914-918.

148.Ball SF, Ellis GS Jr, Herrington RG, et al. Brown's superior oblique tendon syndrome after Baerveldt glaucoma implant. Arch Ophthalmol. 1992; 110(10):1368.

149.Dobler-Dixon AA, Cantor LB, Sondhi N, et al. Prospective evaluation of extraocular motility following double-plate Molteno implantation. Arch Ophthalmol. 1999;117(9):1155-1160.

150.Roizen A, Ela-Dalman N, Velez FG, et al. Surgical treatment of strabismus secondary to glaucoma drainage device. Arch Ophthalmol. 2008; 126(4):480-486.

151.Rhee DJ, Casuso LA, Rosa RH Jr, et al. Motility disturbance due to true Tenon cyst in a child with a Baerveldt glaucoma drainage implant. Arch Ophthalmol. 2001;119(3):440-442.

152.Sidoti PA, Minckler DS, Baerveldt G, et al. Epithelial ingrowth and glaucoma drainage implants. Ophthalmology. 1994;101(5):872-875.

153.Costa V P, Katz LJ, Cohen EJ, et al. Glaucoma associated with epithelial downgrowth controlled with Molteno tube shunts. Ophthalmic Surg. 1992;23(12):797-800.

154.Ball SF, Loftfield K, Scharfenberg J. Molteno rip-cord suture hypopyon. Ophthalmic Surg. 1990;21 (6):407-411; discussion 411-412.

155.Hyung SM, Min JP. Subconjunctival silicone oil drainage through the Molteno implant. Korean J Ophthalmol. 1998;12(1):73-75.

156.Law SK, Kalenak JW, Connor TB Jr, et al. Retinal complications after aqueous shunt surgical procedures for glaucoma. Arch Ophthalmol. 1996;114(12):1473-1480.

157.Airaksinen PJ, Aisala P, Tuulonen A. Molteno implant surgery in uncontrolled glaucoma. Acta

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158.Price FW Jr, Wellemeyer M. Long-term results of Molteno implants. Ophthalmic Surg. 1995;26 (2):130-135.

159.Broadway DC, Iester M, Schulzer M, et al. Survival analysis for success of Molteno tube implants. Br J Ophthalmol. 2001;85(6):689-695.

160.Mills RP, Reynolds A, Emond MJ, et al. Long-term survival of Molteno glaucoma drainage devices. Ophthalmology. 1996;103(2):299-305.

161.Molteno AC, Sayawat N, Herbison P. Otago glaucoma surgery outcome study: long-term results of uveitis with secondary glaucoma drained by Molteno implants. Ophthalmology. 2001;108(3):605-613.

162.Freedman J, Rubin B. Molteno implants as a treatment for refractory glaucoma in black patients. Arch Ophthalmol. 1991;109(10):1417-1420.

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167.Krishna R, Godfrey DG, Budenz DL, et al. Intermediate-term outcomes of 350-mm2 Baerveldt glaucoma implants. Ophthalmology. 2001;108(3): 621-626.

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Shields > SECTION III - Management of Glaucoma >

40 - Medical and Surgical Treatments for Childhood Glaucomas

Authors: Allingham, R. Rand

Title: Shields Textbook of Glaucoma, 6th Edition Copyright ©2011 Lippincott Williams & Wilkins

> Table of Contents > SECTION III - Management of Glaucoma > 40 - Medical and Surgical Treatments for Childhood Glaucomas

40

Medical and Surgical Treatments for Childhood Glaucomas

The successful treatment of childhood glaucoma presents many challenges, with control of intraocular pressure (IOP) as the first but not the only priority. The optimal treatment strategies for children often differ greatly from those for adults with glaucoma. Factors influencing decisions about therapy include those related not only to the type and severity of the glaucoma but also to the age and needs of the particular child.

MEDICAL THERAPY

Although surgical intervention is the primary treatment for primary congenital glaucoma and closedangle glaucomas (e.g., secondary to cicatricial retinopathy of prematurity), medications are the initial and often the mainstay of therapy for juvenile open-angle glaucoma and other secondary glaucomas (e.g., such as those occurring in aphakia or with uveitis). Medications also play an important auxiliary role even in cases of congenital glaucoma, wherein they may help clear the cornea preoperatively to facilitate goniotomy and may help control IOP postoperatively until the success of surgical intervention has been determined. Medical therapy is also indicated in managing those difficult cases in which surgery poses particular risks or has incompletely controlled glaucoma (1). Besides inadequate IOP reduction, multiple factors conspire against the success of long-term medical therapy in childhood glaucomas: the difficulties with long-term adherence, adequate ascertainment of drug-induced side effects, and potential adverse systemic effects of protracted therapy, among others.

Many medications are now available for the reduction of IOP in patients with glaucoma. The Food and Drug Administration (FDA) initially approved all of them for use without requiring data on the safety and efficacy of these drugs in pediatric patients. Ongoing study of several major new drugs is currently being undertaken by several major pharmaceutical companies, under the supervision of the FDA. For example, a randomized, double-masked, 3-month trial compared dorzolamide, 2%, three times daily with timolol, 0.25% or 0.5%, once daily in patients younger than 6 years who had glaucoma; the study found both treatments to be relatively safe and effective (2). A similarly designed study, again conducted among children with glaucoma who were younger than 6, compared use of brinzolamide, 1%, twice a day with use of levobetaxolol, 0.5%, twice a day, and it demonstrated that both drugs were well tolerated and lowered IOP (3). Nonetheless, many of the commonly used glaucoma drugs still carry a warning that “safety and efficacy in pediatric pati ents have not been established.” Furthermore, certa in drugs, such as brimonidine, carry warnings about dangerous systemic side effects in infants and young children. Because eyedrops are not downsized for pediatric use and because the plasma volume of a small child is much smaller than that of an average adult counterpart, blood levels of glaucoma drugs can reach high levels in young children at doses recommended for use in adults (4). Even topical glaucoma medication must be used with careful forethought in children, particularly in those who are very small or with special considerations such as premature birth, asthma, or other cardiac or pulmonary problems.

Table 40.1 gives information pertaining to the suggested use of various glaucoma drugs specifically in infants and children with glaucoma. (Detailed information on the use and mechanisms of these medications is provided elsewhere in this text.)

Carbonic Anhydrase Inhibitors

Oral carbonic anhydrase inhibitors, primarily acetazolamide (Diamox), have effectively reduced

elevated IOP in infants and children with primary infantile (and other types of) glaucoma for decades, often reducing the IOP about 20% to 35%. When administered orally with food or milk three or four times daily (total dosage, 10 to 20 mg/kg/day), acetazolamide is fairly well tolerated (1, 5). Caregivers should be queried specifically about the occurrence of diarrhea, diminished energy levels, and loss of appetite in children on this therapy, as such effects would necessitate a dosage adjustment or discontinuation of use. Metabolic acidosis has also been reported in infants (6), in whom it may manifest as rapid breathing and may be somewhat ameliorated with oral sodium citrate and citric acid oral solution (Bicitra, 1 mEq/kg/day) (7).

The topical carbonic anhydrase inhibitor, dorzolamide (Trusopt), offers a viable alternative to acetazolamide for many patients. In a small crossover trial, 11 children whose glaucoma was controlled on topical ß-blocker and oral acetazolamide switche d from the oral acetazolamide to topical dorzolamide, three times daily, in the study eye. Mean IOP reduction with use of the topical agent was approximately 25%, compared with approximately 35% on acetazolamide (8). Although systemic side effects occurred commonly in patients receiving the acetazolamide, no adverse effects were noted with the use of topical dorzolamide. The addition of oral acetazolamide to topical dorzolamide has been reported to reduce IOP further than when either drug is used alone (9).

A second topical carbonic anhydrase inhibitor, brinzolamide (Azopt), has also been well tolerated by children, with IOP reduction similar to that obtained with use of dorzolamide

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(Freedman SF, unpublished data). In one study of brinzolamide and levobunolol treatment in children with glaucoma younger than 6 years, both drugs were well tolerated, but brinzolamide was more effective in patients with glaucoma associated with systemic or ocular abnormalities than in patients with primary congenital glaucoma (3). The carbonic anhydrase inhibitors are useful for treating pediatric glaucoma and may be appropriate firstand second-line agents, respectively, when ß-blocker

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use is contraindicated or inadequately effective (Table 40.1; also see the following text). (The combination of a topical carbonic anhydrase inhibitor [dorzolamide] with the ß-blocker timolol is discussed further in the ß-Blockers section.)

27 - Principles of Medical Therapy and Management Page 214 of 267

patients with adverse reactions (10%) were using timolol, 0.5%. Only two patients discontinued use of timolol because of side effects—a 10-year-old who d eveloped severe asthma and a 17-year-old with symptomatic bradycardia (17). The incidence of systemic side effects reported in these studies varied from 0% to 18% (4, 14, 15, 16, 17 and 18).

The most severe systemic adverse effects in children receiving topical timolol therapy have included acute asthma attacks, bradycardia, and apneic spells (the latter in neonates) (4, 18, 19 and 20). Plasma timolol levels measured in children using 0.25% timolol (ranging from 3.5 ng/mL in a 5-year-old to 34 ng/mL in a 3-week-old) vastly exceeded those in adults using 0.5% timolol (range, 0.34 to 2.45 ng/mL)

(4). The use of punctal occlusion in adults further lowered mean 1-hour plasma timolol levels by 40% in the adult patients in this study (from 1.34 to 0.9 ng/mL). The high plasma timolol levels in children may be explained by a child's volume of distribution for the drug, which is much smaller than that of an adult.

When timolol is used in small children, treatment should always begin with 0.25% drops, excluding those children with a history of asthma or bradycardia. Topical ß-blockers should be used with extreme caution in neonates, with particular attention to the possibility of apnea. It may be reasonable to observe children for adverse systemic effects for 1 to 2 hours in the office after an initial dose of ß-blocke r has been given before prescribing the ß-blocker for out patient use (16, 20). Punctal occlusion, when feasible, should be performed by parents or other caretakers (16). There is anecdotal evidence that using timolol as Timoptic XE or timolol gel-forming solution, once daily, may result in lower plasma drug levels, compared with the same concentration of solution used twice daily.

There is little information available on the use of topical ß-blockers other than timolol in the treat ment of childhood glaucoma. A short-term, randomized, double-masked comparison of levobetaxolol and brinzolamide in children younger than 6 years demonstrated that both drugs were well tolerated and lowered IOP in this group. In children naïve to prior medication, levobetaxolol was more effective in primary congenital glaucoma than in glaucoma with associated ocular or systemic abnormalities (3). Based on experience in adults, betaxolol, as a relatively ß-1-selective ß-blocker, may be less suscept ible to precipitating acute asthma attacks (which may present as coughing) than the nonselective ß-blockers . The remaining nonselective ß-blockers should be app roached in a fashion similar to timolol regarding risks and probable efficacy. As in adults, ß-blocke rs used in children often do have an additive effect to oral and topical carbonic anhydrase inhibitors in treating children with glaucoma (1, 15).

Two combination preparations that include timolol, 0.5%, are currently available commercially in the United States. The first preparation, combining timolol, 0.5%, and dorzolamide, 2.0% (Cosopt, now also available as generic; used twice daily), is a potent IOP-reducing agent in older children, but it must be avoided in infants because of the relatively high concentration of timolol. The newer drug, Combigan, combines timolol, 0.5%, plus brimonidine, 0.2%; this potent agent must be used with caution in children and never in those for whom either ingredient alone would be contraindicated (see Adrenergic Agonists section; Table 40.1).

Topical ß-blockers, despite their contraindication in some cases, still have an important role in treating children with glaucoma and are appropriate first-line drugs for many children (Table 40.1). Adrenergic Agonists

Epinephrine compounds have been used in infants and children with glaucoma (21, 22), but there are little published data to suggest optimal dosing schedules or the magnitude of the pressure decrement to be expected from these drugs. These drugs, furthermore, are relegated to secondary importance because of their potential for systemic toxicity (e.g.,

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tachyarrhythmias, hypertension) and their ocular side effects (e.g., irritation, reactive hyperemia, adrenochrome deposits), together with their limited effectiveness. Topical dipivefrin (Propine), as an epinephrine prodrug, should theoretically have fewer systemic side effects in children than epinephrine does.

The two commercially available a2-adrenergic agonists, apraclonidine and brimonidine, have a valid