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Update in Genetics and Surgical Management of Primary Congenital Glaucoma
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Review
VOLUME: 49 ISSUE: 6
P: 347 - 355
December 2019

Update in Genetics and Surgical Management of Primary Congenital Glaucoma

Turk J Ophthalmol 2019;49(6):347-355
1. University of Illinois at Chicago, Department of Ophthalmology and Visual Sciences, Chicago, USA
No information available.
No information available
Received Date: 14.03.2019
Accepted Date: 10.06.2019
Publish Date: 31.12.2019
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ABSTRACT

Primary congenital glaucoma (PCG) continues to be an important cause of visual impairment in children despite advances in medical and surgical treatment options. The progressive and blinding nature of the disease, together with the long lifespan of the affected population, necessitates a thorough understanding of the pathophysiology of PCG and the development of long-lasting treatment options.

The first part of this review discusses the genetic features and makeup of this disorder, including all currently identified genetic loci (GLC3A, GLC3B, GLC3C and GLC3D) and relevant protein targets important for trabecular and Schlemm canal dysgenesis. These target molecules primarily include CYP1B1, LTBP2, and TEK/Tie2 proteins. Their potential roles in PCG pathogenesis are discussed with the purpose of bringing the readers up to date on the molecular genetics aspect of this disorder. Special emphasis is placed on functional implications of reported genetic mutations in the setting of PCG. The second part of the review focuses on various modifications and refinements to the traditional surgical approaches performed to treat PCG, including advances in goniotomy and trabeculotomy ab externo techniques, glaucoma drainage implant surgery and cyclodiode photocoagulation techniques that ultimately provide safer surgical approaches and more effective intraocular pressure control in the 21st century.

Keywords:
Primary congenital glaucoma, genetics, angle surgery, glaucoma drainage implants

Introduction

Primary congenital glaucoma (PCG) (OMIM 231300) is a potentially blinding ocular disease that occurs secondary to a developmental anomaly of the anterior chamber angle and which results in high intraocular pressure (IOP) with its resultant devastating consequences.1,2 It is an important global cause of pediatric visual impairment and leads to legal blindness, even with treatment.3,4,5 The underlying mechanism in PCG is trabecular dysgenesis with or without varying degrees of associated iridodysgenesis including arrested posterior migration of the peripheral iris tissue and maldeveloped trabecular angle meshwork with or without dysgenesis of the Schlemm’s canal (SC).1 Current evidence suggests that trabecular dysgenesis occurs due to mutations that impair normal trabecular meshwork development.6,7,8 However, the mechanisms through which these genes act to induce trabecular dysgenesis is not, as of yet, clearly elucidated.

Current treatment strategies for PCG revolve around surgical methods that target the abnormal trabecular angle.9 These options include goniotomy and trabeculotomy ab externo, and variations thereof, that are performed as primary procedures in patients with PCG.9,10,11,12 Many patients require more than one surgery and, in some cases, drainage procedures if these angle-based procedures do not lower the IOP to a safe level to halt glaucomatous optic neuropathy.9,13,14 Patients with PCG also frequently require adjunctive topical hypotensive medications in their postoperative course.2,4

The purpose of this review is to provide an update on the genetic basis of PCG and to summarize the current surgical options for treatment of this condition.

Study Limitations

Limitations included identifying and precisely targeting the ciliary body and titrating the laser energy to adequate uptake, especially in varying anterior segment anatomies. Post procedural complications such as inflammation and overtreatment resulting in irreversible hypotony and phthisis are also increasingly more difficult to manage in a pediatric patient.89,92

Most ophthalmologists will reserve TSCPC for patients with a limited visual potential given the adverse effect profile, especially given the potential for retinal detachment (~10%) and irreversible hypotony.88 Additionally, they will reserve this approach for patients who have glaucoma refractory to prior surgeries, elevated pressure with pain in a blind eye, or if surgical/incisional measures are too risky. Rarer complications that can occur with TSCPC involve scleral thinning, especially when too many audible laser sounds are heard. Limiting the area of ablation per session to no more than 180 degrees appears to confer increased safety to the TSCPC procedure, though the procedure may need to be repeated to achieve target IOPs.93

An intraocular procedure that has more recently been utilized in the pediatric population is ECP.93 Using a 19-23-gauge instrument, one can endoscopically visualize the ciliary body processes and treat with photocoagulation directly to the processes.94

Studies reporting results from ECP have been promising, with no sight-threatening complications of severe hypotony, intractable pain, or recalcitrant inflammation.94 At 3 year follow-ups, 50% of patients had a cumulative success rate of 43%.94 Considerations for ECP include whether the patient is phakic or aphakic and risks of introducing potential infection, causing suprachoroidal hemorrhages, or IOP spikes.

Given the propensity for glaucoma surgical procedures to fail over time in the pediatric population, secondary and tertiary surgical procedures have to be considered in these patients. Procedures that will function for the longer life expectancy of the pediatric patient are crucial. The decision to perform another tube surgery versus repeated TSCPC has been shown to be equivocal in the results, despite small powers in numbers of patients to evaluate this.95

Çalışmanın Kısıtlılıkları

Çalışmanın kısıtlılıkları şunlardır: Siliyer cismin tanımlanması ve kesin olarak hedeflenmesi ve lazer enerjisinin, özellikle değişken ön segment anatomisine uyumlu şeklide, uygun doz sağlamak için ayarlanması. Pediyatrik bir hastada, geri dönüşümsüz hipotoni ve fitizise yol açan enflamasyon ve aşırı tedavi gibi işlem sonrası komplikasyonların yönetimi de zordur.89,92

Çoğu göz hekimi, özellikle retina dekolmanı (~%10) ve geri dönüşümsüz hipotoni gibi yan etkiler göz önüne alındığında TSSFK’yi görme potansiyeli sınırlı olan hastalarda tercih edecektir.88 Ayrıca, bu yöntemi cerrahiye refrakter glokomlu hastalar, görmeyen gözde yüksek basınç ve ağrı olan olgular veya cerrahi/insizyon yapmanın çok riskli ise hastalarda kullanmayı seçeceklerdir. TSSFK’de ortaya çıkabilecek nadir komplikasyonlar arasında, özellikle çok fazla lazer sesi duyulduğunda, skleral incelme bulunmaktadır. Seans başına ablasyon alanını en fazla 180 dereceyle sınırlandırmak TSSFK’ye güvenlik kazandırır gibi görünmektedir, ancak hedeflenen GİB değerlerine ulaşmak için işlemin tekrarlanması gerekebilir.93

Pediyatrik popülasyonda daha yakın bir zamanda kullanılmaya başlanan bir diğer intraoküler girişim ESF’dir.94 Siliyer cisim uzantıları 19-23 G boyutunda bir alet kullanarak endoskopik olarak görülebilir ve fotokoagülasyon doğrudan uzantılara uygulanabilir.94

ESF’nin değerlendirildiği çalışmalarda sonuçların umut verici olduğu ve ciddi hipotoni, inatçı ağrı ya da tedaviye yanıt vermeyen enflamasyon gibi görmeyi tehdit eden komplikasyonlar izlenmemiştir.94 Üç yıllık takipte hastaların %50’sinde kümülatif başarı oranının %43 olduğu bulunmuştur.94 ESF ile ilgili akılda bulundurulması gerekenler, hastanın fakik veya afakik olup olmadığı, potansiyel enfeksiyona, suprakoroit kanamalara veya göz içi basıncında ani yükselmelere neden olma riskidir.

Pediyatrik popülasyonda glokom cerrahi girişimlerin zaman içinde başarısız olma eğilimi göz önüne alındığında, bu hastalarda sekonder ve tersiyer cerrahi girişimler yapılması gerekebilir. Pediyatrik hastalarda, daha uzun süre fonksiyonel kalacak yöntemler önem arz etmektedir. TSSFK’yi tekrarlamak veya farklı bir tüp cerrahisi yapmak arasında hangisinin tercih edilmesi gerektiği sonuçlara bakıldığında kesinlik kazanmamıştır ancak bu çalışmalarda dahil edilen hasta sayılarının yeterli olmadığı hatırlanmalıdır.95

Conclusion

PCG continues to be a challenging disease in the 21st century in that long-lasting IOP control is still difficult to achieve and the visual prognosis is somewhat guarded despite state-of-the-art treatment paradigms.3,5 Over the course of five decades, several modifications have been introduced to standard angle surgery procedures to improve IOP outcomes, increase safety of the interventions, and decrease the total number of procedures in PCG. There has been a shift away from trabeculectomy and toward GDIs to decrease the frequency of postoperative hypotony and to ensure long-term IOP control. Currently, aqueous drainage devices as well as laser cyclophotocoagulation are successfully used in current practice to lower IOP in PCG, more frequently as a secondary procedure but in select cases as a primary intervention modality. These procedures can provide a pediatric patient longevity of stable IOP and thus preservation of visual function for a longer period of time. Limitations of current studies that provide evidence of safety and efficacy are the power in numbers of patients as well as duration of follow-up. Comparative studies of various procedures are needed to further investigate efficacy, outcomes, and quality of life outcomes.

Categorizing patients as either PCG or secondary congenital glaucoma and then stratifying those with secondary congenital glaucoma by mechanism, such as trauma-related, aphakic glaucoma, or anterior segment dysgenesis-related glaucoma, could help to better understand outcomes of various procedures in these different patient groups. Additionally, the pediatric patient population is reliant on other social risk factors such as caregivers, economic, education, and distance of travel, all factors that can influence time to diagnosis, time to surgery, and postoperative care. When trying to clinically appreciate the outcomes of this literature review, a case-by-case analysis must also be performed to account for these social risk factors prior to determining a management plan for these patients. A better understanding of PCG as a disease, improved diagnostic capacity, together with advances in surgical procedures will continue to improve the outlook for PCG in the future.

References

1
Anderson DR. The development of the trabecular meshwork and its abnormality in primary infantile glaucoma. Trans Am Ophthalmol Soc. 1981;79:458-485.
2
Chang T, Brookes J, Cavuoto K, Bitrian E, Grajewski A. Primary congenital glaucoma and juvenile openangle glaucoma. In: Weinreb R, Grajewski A, Papadopoulos M, Grigg J, Freedman S, eds. Childhood Glaucoma. The 9th Consensus Report of the World Glaucoma Association. Amsterdam: Kugler; 2013:137-153.
3
Alsheikheh A, Klink J, Klink T, Steffen H, Grehn F. Long-term results of surgery in childhood glaucoma.  Graefes Arch Clin Exp Ophthalmol. 2007;245:195-203.
4
Taylor RH, Ainsworth JR, Evans AR, Levin AV. The epidemiology of pediatric glaucoma: the Toronto experience. J AAPOS. 1999;3:308-315.
5
Zagora SL, Funnell CL, Martin FJ, Smith JE, Hing S, Billson FA, Veillard AS, Jamieson RV, Grigg JR. Primary congenital glaucoma outcomes: lessons from 23 years of follow-up. Am J Ophthalmol. 2015;159:788-796.
6
Sarfarazi M, Akarsu AN, Hossain A, Turacli ME, Aktan SG, Barsoum-Homsy M, Chevrette L, Sayli BS. Assignment of a locus (GLC3A) for primary congenital glaucoma (Buphthalmos) to 2p21 and evidence for genetic heterogeneity. Genomics. 1995;30:171-177.
7
Akarsu AN, Turacli ME, Aktan SG, Barsoum-Homsy M, Chevrette L, Sayli BS, Sarfarazi M. A second locus (GLC3B) for primary congenital glaucoma (Buphthalmos) maps to the 1p36 region. Hum Mol Genet. 1996;5:1199-1203.
8
Lewis CJ, Hedberg-Buenz A, DeLuca AP, Stone EM, Alward WLM, Fingert JH. Primary congenital and developmental glaucomas. Hum Mol Genet. 2017;26:R28-R36. 
9
Chen TC, Chen PP, Francis BA, Junk AK, Smith SD, Singh K, Lin SC. Pediatric glaucoma surgery: a report by the American Academy Of Ophthalmology. Ophthalmology. 2014;121:2107-2115.
10
Papadopoulos M, Edmunds B, Fenerty C, Khaw PT. Childhood glaucoma surgery in the 21st century. Eye (Lond). 2014;28:931-943.
11
Beck AD, Lynch MG. 360 degrees trabeculotomy for primary congenital glaucoma. Archives of Ophthalmology. 1995;113:1200-1202.
12
Girkin CA, Marchase N, Cogen MS. Circumferential trabeculotomy with an illuminated microcatheter in congenital glaucomas. J Glaucoma. 2012;21:160-163.
13
Morales J, Al Shahwan S, Al Odhayb S, Al Jadaan I, Edward DP. Current surgical options for the management of pediatric glaucoma. Journal of Ophthalmology. 2013;1-16.
14
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.
15
Sarfarazi M, Stoilov I, Schenkman JB. Genetics and biochemistry of primary congenital glaucoma. Ophthalmol Clin North Am. 2003;16:543-554.
16
Ho CL, Walton DS. Primary congenital glaucoma: 2004 update. J Pediatr Ophthalmol Strabismus. 2004;41:271-288.
17
Stoilov, I.R. and Sarfarazi, M. The third genetic locus (GLC3C) for primary congenital glaucoma (PCG) maps to chromosome 14q24.3. Invest. Ophthalmol. Vis. Sci. 2002:43;3015.
18
Firasat S, Riazuddin SA, Hejtmancik JF, Riazuddin S. Primary congenital glaucoma localizes to chromosome 14q24.2-24.3 in two consanguineous Pakistani families. Mol Vis. 2008;14:1659-1665.
19
Stoilov I, Akarsu AN, Sarfarazi M. Identification of three different truncating mutations in cytochrome P4501B1 (CYP1B1) as the principal cause of primary congenital glaucoma (Buphthalmos) in families linked to the GLC3A locus on chromosome 2p21. Hum Mol Genet. 1997;6:641-647.
20
Ali M, McKibbin M, Booth A, Parry DA, Jain P, Riazuddin SA, Hejtmancik JF, Khan SN, Firasat S, Shires M, Gilmour DF, Towns K, Murphy AL, Azmanov D, Tournev I, Cherninkova S, Jafri H, Raashid Y, Toomes C, Craig J, Mackey DA, Kalaydjieva L, Riazuddin S, Inglehearn CF. Null mutations in LTBP2 cause primary congenital glaucoma. Am J Hum Genet. 2009;84:664-671.
21
Tomarev S, Wistow G, Raymond V, Dubois S, Malyukova I. Gene expression profile of the human trabecular meshwork: NEIBank sequence tag analysis. Invest Ophthalmol Vis Sci. 2003;44:2588-2596.
22
Souma T, Tompson SW, Thomson BR, Siggs OM, Kizhatil K, Yamaguchi S, Feng L, Limviphuvadh V, Whisenhunt KN, Maurer-Stroh S, Yanovitch TL, Kalaydjieva L, Azmanov DN, Finzi S, Mauri L, Javadiyan S, Souzeau E, Zhou T, Hewitt AW, Kloss B, Burdon KP, Mackey DA, Allen KF, Ruddle JB, Lim SH, Rozen S, Tran-Viet KN, Liu X, John S, Wiggs JL, Pasutto F, Craig JE, Jin J, Quaggin SE, Young TL. Angiopoietin receptor TEK mutations underlie primary congenital glaucoma with variable expressivity. J Clin Invest. 2016;126:2575-2587. 
23
Kaur K, Reddy ABM, Mukhopadhyay A, Mandal AK, Hasnain SE, Ray K, Thomas R, Balasubramanian D, Chakrabarti S. Myocilin gene implicated in primary congenital glaucoma. Clin Genet. 2005;67:335-340.
24
Chen Y, Jiang D, Yu L, Katz B, Zhang K, Wan B, Sun X. CYP1B1 and MYOC mutations in 116 Chinese patients with primary congenital glaucoma. Arch Ophthalmol. 2008;126:1443-1447.
25
Lim SH, Tran-Viet KN, Yanovitch TL, Freedman SF, Klemm T, Call W, Powell C, Ravichandran A, Metlapally R, Nading EB, Rozen S, Young TL. CYP1B1, MYOC, and LTBP2 mutations in primary congenital glaucoma patients in the United States. Am J Ophthalmol. 2013;155:508-517. 
26
Do T, Shei W, Chau PT, Trang DL, Yong VH, Ng XY, Chen YM, Aung T, Vithana EN. CYP1B1 and MYOC Mutations in Vietnamese Primary Congenital Glaucoma Patients. J Glaucoma. 2016;25:e491-e498.
27
Faiq MA, Dada R, Sharma R, Saluja D, Dada T. CYP1B1: a unique gene with unique characteristics. Curr Drug Metab. 2014;15:893-914.
28
Zhao Y, Sorenson CM, Sheibani N. Cytochrome P450 1B1 and Primary Congenital Glaucoma. J Ophthalmic Vis Res. 2015;10:60-67. 
29
Bejjani BA, Lewis RA, Tomey KF, Anderson KL, Dueker DK, Jabak M, Astle WF, Otterud B, Leppert M, Lupski JR. Mutations in CYP1B1, the gene for cytochrome P4501B1, are the predominant cause of primary congenital glaucoma in Saudi Arabia. Am J Hum Genet. 1998;62:325-333.
30
Coêlho REA, Sena DR, Santa Cruz F, Moura BCFS, Han CC, Andrade FN, Lira RPC. CYP1B1 Gene and Phenotypic Correlation in Patients From Northeastern Brazil With Primary Congenital Glaucoma. J Glaucoma. 2019;28:161-164. 
31
Doshi M, Marcus C, Bejjani BA, Edward DP. Immunolocalization of CYP1B1 in normal, human, fetal and adult eyes. Exp Eye Res. 2006;82:24-32.
32
Zhao Y, Wang S, Sorenson CM, Teixeira L, Dubielzig RR, Peters DM, Conway SJ, Jefcoate CR, Sheibani N. Cyp1b1 mediates periostin regulation of trabecular meshwork development by suppression of oxidative stress. Mol Cell Biol. 2013;33:4225-4240.
33
Narooie-Nejad M, Paylakhi SH, Shojaee S, Fazlali Z, Rezaei Kanavi M, Nilforushan N, Yazdani S, Babrzadeh F, Suri F, Ronaghi M, Elahi E, Paisán-Ruiz C. Loss of function mutations in the gene encoding latent transforming growth factor beta binding protein 2, LTBP2, cause primary congenital glaucoma. Hum Mol Genet. 2009;18:3969-3977. 
34
Azmanov DN, Dimitrova S, Florez L, Cherninkova S, Draganov D, Morar B, Saat R, Juan M, Arostegui JI, Ganguly S, Soodyall H, Chakrabarti S, Padh H, López-Nevot MA, Chernodrinska V, Anguelov B, Majumder P, Angelova L, Kaneva R, Mackey DA, Tournev I, Kalaydjieva L. LTBP2 and CYP1B1 mutations and associated ocular phenotypes in the Roma/Gypsy founder population. Eur J Hum Genet. 2011;19:326-333.
35
Hirai M, Horiguchi M, Ohbayashi T, Kita T, Chien KR, Nakamura T. Latent TGF-beta-binding protein 2 binds to DANCE/fibulin-5 and regulates elastic fiber assembly.  EMBO J. 2007;26:3283-3295. 
36
Fujikawa Y, Yoshida H, Inoue T, Ohbayashi T, Noda K, von Melchner H, Iwasaka T, Shiojima I, Akama TO, Nakamura T. Latent TGF-β binding protein 2 and 4 have essential overlapping functions in microfibril development. Sci Rep. 2017;7:43714.
37
Haji-Seyed-Javadi R, Jelodari-Mamaghani S, Paylakhi SH, Yazdani S, Nilforushan N, Fan JB, Klotzle B, Mahmoudi MJ, Ebrahimian MJ, Chelich N, Taghiabadi E, Kamyab K, Boileau C, Paisan-Ruiz C, Ronaghi M, Elahi E. LTBP2 mutations cause Weill-Marchesani and Weill-Marchesani-like syndrome and affect disruptions in the extracellular matrix. Hum Mutat. 2012;33:1182-1187.
38
Khan AO, Aldahmesh MA, Alkuraya FS. Congenital megalocornea with zonular weakness and childhood lens-related secondary glaucoma - a distinct phenotype caused by recessive LTBP2 mutations. Mol Vis. 2011;17:2570-2579.
39
Augustin HG, Koh GY, Thurston G, Alitalo K. Control of vascular morphogenesis and homeostasis through the angiopoietin-Tie system. Nat Rev Mol Cell Biol. 2009;10:165-177. 
40
Thurston G, Daly C.  The complex role of angiopoietin-2 in the angiopoietin-tie signaling pathway. Cold Spring Harb Perspect Med. 2012;2:a006550. 
41
Kizhatil K, Ryan M, Marchant JK, Henrich S, John SW. Schlemm’s canal is a unique vessel with a combination of blood vascular and lymphatic phenotypes that forms by a novel developmental process. PLoS Biol. 2014;12:e1001912.
42
Thomson BR, Heinen S, Jeansson M, Ghosh AK, Fatima A, Sung HK, Onay T, Chen H, Yamaguchi S, Economides AN, Flenniken A, Gale NW, Hong YK, Fawzi A, Liu X, Kume T, Quaggin SE. A lymphatic defect causes ocular hypertension and glaucoma in mice. J Clin Invest. 2014;124:4320-4324.
43
Anderson DR. Trabeculotomy compared to goniotomy for glaucoma in children. Ophthalmology. 1983;90:805-806.
44
Hassanein DH, Awadein A, Elhilali H. Factors associated with early and late failure after goniotomy for primary pediatric glaucoma. Eur J Ophthalmol. 2018 Oct 10:1120672118805872.
45
Barkan O. Technique of goniotomy. Arch Ophthalmol. 1938;19:217-221
46
Medical and surgical treatments for childhood glaucomas. In: Allingham RR, Shields MB, eds. Shields Textbook of Glaucoma (6th ed). Philadelphia; Lippincott Williams and Wilkins; 2011:542-564. 
47
Shaffer RN. Goniotomy technique in congenital glaucoma. Am J Ophthalmol. 1959;47:90-97.
48
Shaffer RN. Prognosis of goniotomy in primary infantile glaucoma (trabeculodysgenesis). Trans Am Ophthalmol Soc. 1982;80:321-325.
49
Gramer E, Tausch M, Kraemer C. Time of diagnosis, reoperations and long-term results of goniotomy in the treatment of primary congenital glaucoma: a clinical study. Int Ophthalmol. 1996-1997;20:117-123.
50
Russell-Eggitt IM, Rice NS, Jay B, Wyse RK. Relapse following goniotomy for congenital glaucoma due to trabecular dysgenesis. Eye (Lond). 1992;6:197-200.
51
Kulkarni SV, Damji KF, Fournier AV, Pan I, Hodge WG. Endoscopic goniotomy: early clinical experience in congenital glaucoma. J Glaucoma. 2010;19:264-269. 
52
Catalano RA, King RA, Calhoun JH, Sargent RA. One versus two simultaneous goniotomies as the initial surgical procedure for primary infantile glaucoma. J Pediatr Ophthalmol Strabismus. 1989;26:9-13.
53
Tamçelik N, Ozkiriş A. A comparison of viscogoniotomy with classical goniotomy in Turkish patients. Jpn J Ophthalmol. 2004;48:404-407.
54
Khouri AS, Wong SH. Ab Interno Trabeculectomy With a Dual Blade: Surgical Technique for Childhood Glaucoma. J Glaucoma. 2017;26:749-751.
55
Harvey MM, Schmitz JW. Use of ab interno Kahook Dual Blade trabeculectomy for treatment of primary congenital glaucoma. Eur J Ophthalmol. 2018;14:1120672118805873.
56
Smith R. A new technique for opening the canal of Schlemm. Preliminary report. Br J Ophthalmol. 1960;44:370-373.
57
Burian HM. A case of Marfan’s syndrome with bilateral glaucoma. With description of a new type of operation for developmental glaucoma (trabeculotomy ab externo). Am J Ophthalmol. 1960;50:1187-1192.
58
de Luise VP, Anderson DR. Primary infantile glaucoma (congenital glaucoma). Surv Ophthalmol. 1983;28:1-19.
59
Luntz MH. Congenital, infantile, and juvenile glaucoma. Ophthalmology. 1979;86:793-802.
60
Yalvac IS, Satana B, Suveren A, Eksioğlu U, Duman S. Success of trabeculotomy in patients with congenital glaucoma operated on within 3 months of birth. Eye (Lond). 2007;21:459-464.
61
Tamcelik N, Ozkiris A. Long-term results of viscotrabeculotomy in congenital glaucoma: comparison to classical trabeculotomy. Br J Ophthalmol. 2008;92:36-39.
62
Lim ME, Neely DE, Wang J, Haider KM, Smith HA, Plager DA. Comparison of 360-degree versus traditional trabeculotomy in pediatric glaucoma. J AAPOS 2015;19:145-149.
63
Mendicino ME, Lynch MG, Drack A, Beck AD, Harbin T, Pollard Z, Vela MA, Lynn MJ. Long-term surgical and visual outcomes in primary congenital glaucoma: 360 degrees trabeculotomy versus goniotomy. Journal of AAPOS. 2000;4:205-210.
64
Neustein RF, Beck AD. Circumferential Trabeculotomy Versus Conventional Angle Surgery: Comparing Long-term Surgical Success and Clinical Outcomes in Children With Primary Congenital Glaucoma. Am J Ophthalmol. 2017;183:17-24.
65
Neely DE. False passage: a complication of 360 degrees suture trabeculotomy. J AAPOS. 2005;9:396-397.
66
Sarkisian SR Jr. An illuminated microcatheter for 360-degree trabeculectomy in congenital glaucoma: a retrospective case series. J AAPOS. 2010;14:412-416.
67
Toshev AP, Much MM, Klink T, Pfeiffer N, Hoffmann EM, Grehn F. Catheter-assisted 360-Degree Trabeculotomy for Congenital Glaucoma. J Glaucoma. 2018;27:572-577. 
68
Shakrawal J, Bali S, Sidhu T, Verma S, Sihota R, Dada T. Randomized Trial on Illuminated-Microcatheter Circumferential Trabeculotomy Versus Conventional Trabeculotomy in Congenital Glaucoma. Am J Ophthalmol. 2017;180:158-164.
69
Mandal AK, Bhatia PG, Bhaskar A, Nutheti R. Long-term surgical and visual outcomes in Indian children with developmental glaucoma operated on within 6 months of birth. Ophthalmology. 2004;111:283-290.
70
Jalil A, Au L, Khan I, Ashworth J, Lloyd IC, Biswas S. Combined trabeculotomy trabeculectomy augmented with 5-fluorouracil in paediatric glaucoma. Clin Experiment Ophthalmol. 2011;39:207-214.
71
Sidoti PA, Belmonte SJ, Liebmann JM, Ritch R. Trabeculectomy with mitomycin-C in the treatment of pediatric glaucomas. Ophthalmology. 2000;104:422-429.
72
Giampani J Jr, Borges-Giampani AS, Carani JC, Oltrogge EW, Susanna R Jr. Efficacy and safety of trabeculectomy with mitomycin C for childhood glaucoma: a study of results with long-term follow-up. Clinics. 2008;63:421-426.
73
Fieß A, Shah P, Sii F, Godfrey F, Abbott J, Bowman R, Bauer J, Dithmar S, Philippin H. Trabeculectomy or Transscleral Cyclophotocoagulation as Initial Treatment of Secondary Childhood Glaucoma in Northern Tanzania. J Glaucoma. 2017;26:657-660.
74
Jayaram H, Scawn R, Pooley F, Chiang M, Bunce C, Strouthidis NG, Khaw PT, Papadopoulos M. Long-Term Outcomes of Trabeculectomy Augmented with Mitomycin C Undertaken within the First 2 Years of Life. Ophthalmology. 2015;122:2216-2222.
75
Nassiri N, Kouros NM, Coleman Al. Ahmed glaucoma valve in children: a review. Saudi J Ophthalmol. 2011;25:317-327.
76
Budenz DL, Gedde SJ, Brandt JD, Kira D, Feuer W, Larson E. Baerveldt glaucoma implant in the management of refractory childhood glaucomas. Ophthalmology. 2004;111:2204-2210.
77
O’Malley Schotthoefer E, Yanovitch TL, Freedman SF. Aqueous drainage device surgery in refractory pediatric glaucomas: I. Long-term outcomes. J AAPOS. 2008;12:33-39.
78
Christakis PG, Kalenak JW, Tsai JC, Zurakowski D, Kammer JA, Harasymowycz PJ, Mura JJ, Cantor LB, Ahmed II. The Ahmed Versus Baerveldt Study: Five-Year Treatment Outcomes. Ophthalmology. 2016;123:2093-2102.
79
Christakis PG, Zhang D, Budenz DL, Barton K, Tsai JC, Ahmed IIK; ABC-AVB Study Groups. Five Year Pooled Data Analysis of Ahmed Baerveldt Comparison Study and the Ahmed Versus Baerveldt Study. Am J Ophthalmol. 2017;176:118-126.
80
Englert J, Freedman S, Cox T. The Ahmed Valve in Refractory Pediatric Glaucoma. Am J Ophthalmol. 1999;127:34-42.
81
Al-Mobarak F, Khan AO.  Two-year survival of Ahmed valve implantation in the first 2 years of life with and without intraoperative mitomycin-C. Ophthalmology. 2009;116:1862-1865.
82
Morad Y, Donaldson CE, Kim YM, Abdolell M, Levin AV. The Ahmed drainage implant in the treatment of pediatric glaucoma.Am J Ophthalmol. 2003;135:821-829.
83
Coleman AL, Smyth RJ, Wilson MR, Tam M. Initial clinical experience with the Ahmed Glaucoma Valve implant in pediatric patients. Arch Ophthalmol. 1997;115:186-191.
84
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;108:614-620.
85
Souza C, Tran DH, Loman J, Law SK, Coleman AL, Caprioli J. Long-term outcomes of Ahmed glaucoma valve implantation in refractory glaucomas. Am J Ophthalmol. 2007;144:893-900.
86
Chiang MY, Camuglia JE, Khaw PT. A Novel Method of Extending Glaucoma Drainage Tube: “Tube-in-Tube” Technique. J Glaucoma. 2017;26:93-95. 
87
Britt MT, LaBree LD, Lloyd MA, Minckler DS, Heuer DK, Baerveldt G, Varma R. Randomized clinical trial of the 350-mm2 versus the 500-mm2 Baerveldt implant: longer term results: is bigger better? Ophthalmology. 1999;106:2312-2318.
88
Bock CJ, Freedman SF, Buckley EG, Shields MB. Transscleral diode laser cyclophotocoagulation for refractory pediatric glaucomas. J Pediatr Ophthalmol Strabismus. 1997;34:235-239.
89
Schlote T, Grub M, Kynigopoulos M. Long-term results after transscleral diode laser cyclophotocoagulation in refractory posttraumatic glaucoma and glaucoma in aphakia. Graefes Arch Clin Exp Ophthalmol. 2008;246:405-410.
90
Wagle NS, Freedman SF, Buckley EG, Davis JS, Biglan AW. Long-term outcome of cyclocryotherapy for refractory pediatric glaucoma. Ophthalmology. 1998;105:1921-1927.
91
Kirwan JF, Shah P, Khaw PT. Diode laser cyclophotocoagulation: role in the management of refractory pediatric glaucomas. Ophthalmology. 2002;109:316-323.
92
Hamard P, May F, Quesnot S, Hamard H. Trans-scleral diode laser cyclophotocoagulation of the treatment of refractory pediatric glaucoma. J Fr Ophthalmol. 2000;23:773-780.
93
Bezci Aygün F, Mocan MC, Kocabeyoğlu S, İrkeç M. Efficacy of 180° Cyclodiode Transscleral Photocoagulation for Refractory Glaucoma. Turk J Ophthalmol. 2018;48:299-303.
94
Neely DE, Plager DA. Endocyclophotocoagulation for management of difficult pediatric glaucomas. J AAPOS. 2001;5:221-229.
95
Sood S, Beck A. Cyclophotocoagulation versus sequential tube shunt as a secondary intervention following primary tube shunt failure in pediatric glaucoma. J AAPOS. 2009;13:379-383.