Pediatric Uveitic Glaucoma

From EyeWiki

All content on Eyewiki is protected by copyright law and the Terms of Service. This content may not be reproduced, copied, or put into any artificial intelligence program, including large language and generative AI models, without permission from the Academy.

Article initiated by:
Andrew D. Brown, Abdelrahman M. Elhusseiny, MD, MSc, Ahmed Sallam, MD PhD FRCOphth
All contributors:
Ahmad A. Aref, MD, MBA, S. Grace Prakalapakorn, MD, MPH, Ohoud A Owaidhah, MD, Allison Umfress, MD, Abdelrahman M. Elhusseiny, MD, MSc
Assigned editor:
Allison Umfress, MD, Ohoud A Owaidhah, MD
Review:
Assigned status Up to Date
 by Ohoud A Owaidhah, MD on July 12, 2024.


Background

Pediatric uveitis is a relatively rare condition with the majority of cases being idiopathic. The most common identifiable cause of pediatric uveitis is juvenile idiopathic arthritis (JIA); 14-47% of all pediatric uveitis cases are due to JIA.[1][2][3] Population-based studies in North America and Europe estimate the prevalence of pediatric uveitis to be approximately 30 cases per 100,000 population.[4]

Studies have reported that between 5-42% of those pediatric uveitis patients will develop glaucoma or ocular hypertension.[5][6][7][8][9][10] 5.3-19% of all pediatric glaucoma cases are caused by uveitis.[5][6][11]

Pathophysiology

Pediatric uveitic glaucoma progresses similarly to the adult course of the disease.[5] Chronic inflammation drives pathological changes to the iridocorneal angle, elevating intraocular pressure (IOP) which if left untreated leads to glaucomatous optic neuropathy.[12] The resulting glaucoma can be of the open-angle or closed-angle variety. In open-angle uveitic glaucoma, the cellular inflammatory materials, proteins, or chemical mediators within the eye plug the trabecular meshwork with subsequent aqueous outflow obstruction.[11] Other mechanisms include trabeculitis, altered vascular permeability, or steroid-induced ocular hypertension/glaucoma. Chronic inflammation of the trabecular meshwork leads to permanent scarring.[13] Angle-closure glaucoma results from peripheral anterior synechiae (PAS), posterior synechiae, or fibrinous membrane formation with pupillary block.[14]

Steroid-induced IOP elevation has been reported in one-fifth of children treated with different forms of corticosteroids. Steroid-induced ocular hypertension in children tends to be more aggressive with earlier and more rapid glaucomatous progression if left untreated.

Increased duration and severity of the intraocular inflammation have been associated with more severe presentations of glaucoma.[12] Less commonly, intermediate, and posterior uveitis may lead to glaucoma but infrequently compared to anterior uveitis.[12][15] Glaucomatous changes to the optic nerve can occur rapidly but often present ten or more years after the initial onset of uveitis.[9]

Management

Treating the systemic inflammatory condition and controlling the uveitis are central to preventing subsequent glaucoma and ocular hypertension. Effectively managing ocular inflammation early in the course of disease reduces the risk of secondary glaucoma.[9][10] Co-management with rheumatology will often be necessary given pediatric uveitic glaucoma’s strong correlation with systemic inflammatory conditions.

In addition to controlling inflammation, lowering IOP is the gold standard for minimizing the progression of glaucoma.[16] Data on target IOP in the pediatric patient is scarce, with most information coming from primary congenital glaucoma (PCG) treatment. Children undergoing IOP lowering surgery for PCG achieved stability of their neuropathy between 6-15 mmHg.[17] Glaucomatous changes to the optic nerve or visual field in older children can be used as evidence to modify the target IOP.[18]

In the setting of uveitis and steroid use it is difficult to determine whether the rise in IOP is a result of inflammation or steroid-induced ocular hypertension. In the presence of active inflammation the rise in IOP is usually secondary to uveitis. Steroid frequency should be increased to control inflammation and subsequently the IOP will lower. However, in absence of inflammation, ocular hypertension is most likely due to steroid response and lowering the dose or cessation of steroids may be needed.[19]

Medical Therapy

Medical therapy consists of topical eye drops in combination or monotherapy. It is essential to consider that systemic drug absorption is greater in children than in adults. Increased drug plasma levels put them at an increased risk for adverse effects. Punctal occlusion and gel formulations are recommended to minimize risk.[5][20] Studies analyzing success rates of topical medications alone in pediatric uveitic glaucoma showed success in only 17% and 26% of patients.[9][21]

Beta-blockers

(Timolol, Betaxolol)

Timolol is considered a first-line monotherapy that is generally well tolerated.[22] Timolol gel-forming solution’s once-a-day timing promotes good compliance. Systemic side effects include hypotension, bradycardia, and bronchospasms and are therefore contraindicated in children with arrhythmias, asthma, or apnea. Betaxolol is a selective β-2 antagonist that reduces the risk of side effects. β -blockers’ mechanism of action is decreased production of aqueous humor from the ciliary body.

Carbonic anhydrase inhibitors (CAI)

(Dorzolamide, Brinzolamide, Acetazolamide)

Topical CAIs Dorzolamide and Brinzolamide are most often used as an adjunct therapy in combination with a β-blocker when monotherapy does not reach the target IOP.[22] They are prescribed twice daily (BID) in combination or three times daily (TID) as monotherapy. Oral acetazolamide has also been shown to effectively lower IOP but is associated with more side effects. Contraindications include hypokalemia, hyponatremia, and sulfonamide hypersensitivity. The mechanism of action of CAIs is decreased production of aqueous humor from the ciliary body.

Prostaglandin analogs (PGA)

(Latanoprost, Travoprost)

PGAs are prescribed as once-daily topical monotherapy with a mechanism of action of increasing uveoscleral outflow.[22][23] Recent data showed that patients already affected by uveitis and glaucoma are not at an increased risk for uveitis and CME while using PGAs.[24][25][26]

A retrospective review by Bello et al. examined the use of PGAs in children with glaucoma to determine their likelihood of causing uveitis. Included in the study were 147 eyes (103 patients) with glaucoma. Of the 20 eyes (15 patients) with a history of chronic uveitis, five eyes (five patients) experienced recurrences that were explained by an improper tapering of their topical steroid or methotrexate.[27]

Alpha-adrenergic agonists

(Brimonidine, Apraclonidine)

Brimonidine is not preferred in pediatric patients due to its ability to cross the blood brain barrier and commonly causes sleepiness and lethargy.[22] It is absolutely contraindicated in children under two years old and in children with cardiovascular disorders due to potentially life-threatening complications. Children older than six years old and weighing more than 20kg have less risk of side effects. Their mechanism of action is decreased production of aqueous humor from the ciliary body and increased uveoscleral outflow. They are prescribed BID.[23] Apraclonidine is used three times daily short-term to control IOP before and after glaucoma surgeries.[23][28] In contrast to Brimonidine, several studies have demonstrated the safety of Apraclonidine use in both infants and children.[29][30]

Parasympathomimetics

(Pilocarpine)

These are primarily used before and after surgery or in patients with aphakia. They are contraindicated in active uveitis.[31]

Surgical Therapy

Angle Surgery

Goniotomy

Goniotomy utilizes an internal approach to open the trabecular meshwork with a sharp instrument or laser to improve outflow. Both goniotomy and trabeculotomy procedures have exhibited similar success rates in pediatric glaucoma dating back to 1984.[5][32]

A study conducted by Ho and colleagues evaluated the efficacy of goniotomy in 31 pediatric uveitic glaucoma patients (40 eyes).[33] Surgical success was achieved in 72% of eyes at final follow up (98.9 months).  The mean IOP in the surgical success group decreased from 35.8±5.9 mmHg to 14.7±2.9 mmHg at the final follow-up (P<.001). 22 eyes (55%) maintained an IOP of <21 without glaucoma medications at final follow-up. Predictors of success were phakic lens status (P=.004) and age <10 years old (P=.03). The main complication was intraoperative hyphema (80%) that resolved within one week.

Freedman et al. evaluated 16 eyes of 12 pediatric uveitic glaucoma patients who have undergone goniotomy.[28] The mean pre-operative IOP was 31.5±4.3 mmHg and decreased to 12±12.5 mmHg at final follow-up (mean 32.4 months) (P<.0001). Post-operative transient hyphema occurred in 9 eyes (56%).

Trabeculotomy

Wang et al. demonstrated a statistically significant decrease in IOP from 31.4±7.6 mmHg to 15.0±3.6 mmHg post-operatively (P<.001) at final follow-up (mean 31 months). [34]There was a considerable decrease in post-operative glaucoma medication requirements from 4.2±1 to 0.4±1 at final follow-up (P<.001).

Trabeculectomy

Wiese et al. studied 21 eyes (17 children) with uveitic glaucoma who underwent mitomycin-C augmented (MMC) trabeculectomy.[35] They reported that 70% of children had an IOP <15 mmHg after 1 year post-operatively. Heinz et al. presented 16 eyes (16 patients) who underwent trabeculectomy and reported a reduction in the mean IOP from 28.3±5.7 mmHg pre-operatively to 11.6±4.7 mmHg at one year post-operatively.[36]

The essential nature of tumor necrosis factor (TNF) inhibition in the trabeculectomy procedure for JIA-related uveitic glaucoma was suggested in 2015 by Leinonen et al.[37] 29 eyes (29 patients) were included in the study. Compared to trabeculectomy with MMC alone, trabeculectomy with MMC and TNF inhibitors was associated with more successful outcomes (P=.003). Success was defined as IOP ≤21mmHg without glaucoma medications and without the need for further IOP lower surgeries. By Kaplan-Meier analysis, 5-year success rates for trabeculectomy with MMC alone was only 16%, while 5-year success for trabeculectomy with MMC and TNF inhibitors was 73%.

Deep sclerectomy

A retrospective review of 8 eyes (8 patients) conducted by Heinz et al. reported a mean reduction of IOP from 30.3±6.3 mmHg to 18.5±11.4 mmHg at one-year post-operatively.[36] They compared the MMC-augmented trabeculectomy group (16 eyes) to those who underwent deep sclerectomy. The deep sclerectomy group was associated with a statistically significant higher rate of failure when compared to trabeculectomy (P=.041). Deep sclerectomy failed to achieve IOP ≤21 mmHg without medications in 50% of eyes at final follow up (mean 29.4 months) while trabeculectomy failed to achieve IOP ≤21 mmHg without medications in only 6% of eyes at final follow up (mean 21.5 months).

Glaucoma drainage devices (GDD)

The first study of GDD in JIA-associated glaucoma was conducted by Välimäki et al. including 27 eyes (19 patients) who underwent Molteno GDD.[38] The mean IOP was decreased from 38.3±5.6 mmHg pre-operatively to 14.4±4.3 mmHg (P<.001) at the final follow-up (mean 40 months). Glaucoma medications were reduced from 2.7±0.9 pre-operatively to 1.0±1.1 post-operatively (P<.001). 90% of patients achieved success which was defined as IOP ≤22 mmHg and ≥6 mmHg without loss of light perception and equal or fewer glaucoma medications at 52 months post-operatively.

Kafkala et al. evaluated the efficacy of Ahmed glaucoma valve in 7 pediatric uveitic glaucoma eyes (6 patients).[39] At the final follow-up (mean 36.8 months), all 7 eyes had an IOP between 7 and 18 mmHg. Glaucoma medications were decreased from 3±0.82 to 0.71±0.75 at final follow-up (P=.001).

A case series conducted Bohnsack et al. reported a success rate of 80% at final follow-up (mean 102 months) after GDD implantation in 5 eyes with pediatric uveitic glaucoma.[40] Success was defined as a final IOP <21 mmHg without inflammation, serious complications or need for further IOP lowering surgery. The mean IOP was decreased from 27.2±7.6 mmHg pre-operatively to 13.6±3.2 mmHg at the final follow-up (mean 57.6 months). Glaucoma medications decreased from 3.0 ±1.2 pre-operatively to 0.6 ±0.9 at final follow up. The data included both Ahmed and Baerveldt devices and reported no intraoperative complications.

In patients with co-existing corneal pathologies, combined pars-plana vitrectomy and sulcus placement of the GDD may be needed.

Cyclodestructive procedures

A retrospective review conducted by Heinz et al. included 19 pediatric uveitic open-angle glaucoma eyes who were treated with trans-scleral cyclophotocoagulation as a primary procedure.[41] IOP was decreased by 8.8 mmHg after three sessions of treatments (P=.018), but only 6 eyes (32%) achieved IOP ≤21 with glaucoma medication at the final follow-up (mean 10.1 months). None of the patients developed hypotony or serious adverse events.

Minimally invasive glaucoma surgery (MIGS)

Sachdev et al. published a case series in 2020 showing promising results from gonioscopy-assisted transluminal trabeculotomy (GATT) in JIA-associated glaucoma. Sachdev et al. presented three eyes from three patients with a 40% to 66% reduction in mean IOP following GATT.[42] The procedure resulted in one patient requiring fewer glaucoma medications post-operatively, and two patients were able to discontinue their glaucoma medications altogether.

Table Summary

Table 1: Summary of the retrospective case reviews analyzing surgical therapy outcomes specific to pediatric uveitic glaucoma.

Table 1: Summary of the retrospective case reviews analyzing surgical therapy outcomes specific to pediatric uveitic glaucoma.
Name of study, year published⬇ Procedure # of eyes (# of patients) Pre-operative IOP (Mean±SD) Post-operative IOP (Mean±SD) Pre-operative medications (Mean±SD) Post-operative medications (Mean±SD) Follow-up time, months

Mean±SD (range)

Definition of success Success Rate
Wang et al.[34], 2016 Trabeculotomy 28(22) 31.4±7.6 15±3.6 at final follow-up 4.2±1.1 0.4±1.0 31±17.8 IOP <22 and ≥6 with or without medications 81.8% at final follow-up
Leinonen et al.[37], 2015 Trabeculectomy with MMC 15(15) 96 (12-224.4) IOP ≤21, without medications or futher surgery 57% at 1 year, 16% at 5 years, and 0% 10 years
Trabeculectomy with MMC and TNF inhibitors 14(14) 87.6 (12-152.4) IOP ≤21, without medications or futher surgery 73% at 1 year, 5 years, and 10 years
Wiese et al.[35], 2014 Trabeculectomy with MMC 21(17) 31.1±6.7 10.1±4.7 at 1 year 59.5 ± 23.3 1. IOP ≤15 without medication

2. IOP ≤15 with medication

1. 55% at 1 year, 38% at 5 years.

2. 70% at 1 year, 62% at 5 years

Bohnsack and Freedman[40], 2013 GDD (Ahmed and Baerveldt) 5(5) 27.2±7.6 13.6±3.2 at final follow up 3.0±1.2 0.6±0.9 28.8±20.4 IOP <21 without inflammation, serious complications or need for further IOP lowering surgery 80% at final follow-up
Goniotomy 22(22) 34.0±7.8 13.5±4.5 at final follow up 3.3±1.1 1.5±1.4 57.6±52.8 IOP <21 without inflammation, serious complications or need for further IOP lowering surgery 76% at 1 year, 57% at 2 years, 48% at 10 years
Heinz et al.[36], 2011 Trabeculectomy 16(16) 28.3±5.7 11.6±4.7 at 1 year 3.3 21.5 1. IOP ≤21 without glaucoma meds

2. IOP ≤15 without glaucoma meds

1. 88% at last visit

2. 75% at last visit

Modified deep sclerectomy 8(8) 30.3±6.3 18.5±11.4 at 1 year 3.4 29.4 1. IOP ≤21 without glaucoma meds

2. IOP ≤15 without glaucoma meds

1. 50% at last visit

2. 38% at last visit

Heinz et al.[41], 2006 Transscleral diode laser cyclophotocoagulation 19(12) 30.2±5.5 28.7±6.4 before third treatment 3.3±0.7 2.7±1.6 after third treatment 10.1±9.3 (3–30) IOP ≤21 with medications 32% at final follow-up
Kafkala et al.[39], 2005 GDD (Ahmed) 7(6) 37 ± 8 12.1±3.4 at final follow-up 3 0.71 36.8 (6-60) IOP  <22 and >4 at final 2 follow-ups, with or without medications 100% at 3 months
Ho et al.[33], 2004 Goniotomy 40(31) 35.8±5.9* 14.7±2.9 at final follow-up* 2.9±1.1 1.6±1.1 98.9±87.8 (2-324) IOP ≤21 without medications 55% at final follow-up
Freedman et al.[28], 2002 Goniotomy 16(12) 32.3±4.6 12±2.5 at final follow-up 2.5±1.1 1.4±1.1 32.4 (6-84) IOP ≤21 after one or two goniotomies with or without medications 75% at final follow-up
Välimäki et al.[38], 1997 GDD (Molteno) 27(19) 38.3 ± 5.6 14.4 ± 4.3 at final follow-up 2.7±0.9 1.0 ± 1.1 40 (6-116) IOP  ≤22 and ≥6 at the final 2 follow-ups, with equal or fewer medications 89% at final follow-up

References

  1. ↑ Engelhard SB, Bajwa A, Reddy AK. Causes of uveitis in children without juvenile idiopathic arthritis. Clin Ophthalmol. 2015;9:1121-1128. Published 2015 Jun 25. doi:10.2147/OPTH.S83950
  2. ↑ Edelsten C, Reddy MA, Stanford MR, Graham EM. Visual loss associated with pediatric uveitis in english primary and referral centers. Am J Ophthalmol. 2003;135(5):676-680. doi:10.1016/s0002-9394(02)02148-7
  3. ↑ BenEzra D, Cohen E, Maftzir G. Uveitis in children and adolescents. Br J Ophthalmol. 2005;89(4):444-448. doi:10.1136/bjo.2004.050609
  4. ↑ Holland, Gary N, and E Richard Stiehm. “Special considerations in the evaluation and management of uveitis in children.” American journal of ophthalmology vol. 135,6 (2003): 867-78. doi:10.1016/s0002-9394(03)00314-3
  5. ↑ 5.0 5.1 5.2 5.3 5.4 Kalogeropoulos D, Kalogeropoulos C, Moschos MM, Sung V. The Management of Uveitic Glaucoma in Children. Turk J Ophthalmol. 2019;49(5):283-293. doi:10.4274/tjo.galenos.2019.36589
  6. ↑ 6.0 6.1 Paroli MP, Speranza S, Marino M, Pirraglia MP, Pivetti-Pezzi P. Prognosis of juvenile rheumatoid arthritis-associated uveitis. Eur J Ophthalmol. 2003;13(7):616-621. doi:10.1177/112067210301300704
  7. ↑ Sijssens KM, Rothova A, Berendschot TT, de Boer JH. Ocular hypertension and secondary glaucoma in children with uveitis. Ophthalmology. 2006;113(5):853-9.e2.
  8. ↑ Morelle G, Gueudry J, Uettwiller F, et al. Chronic and recurrent non-infectious paediatric-onset uveitis: a French cohort. RMD Open. 2019;5(2):e000933. Published 2019 Aug 5. doi:10.1136/rmdopen-2019-000933
  9. ↑ 9.0 9.1 9.2 9.3 Foster CS, Havrlikova K, Baltatzis S, Christen WG, Merayo-Lloves J. Secondary glaucoma in patients with juvenile rheumatoid arthritis-associated iridocyclitis. Acta Ophthalmol Scand. 2000;78(5):576-579. doi:10.1034/j.1600-0420.2000.078005576.x
  10. ↑ 10.0 10.1 Huynh E, Elhusseiny AM, Nihalani BR. Paediatric anterior uveitis management in the USA: a single-centre, 10-year retrospective chart review exploring the efficacy and safety of systemic immunomodulatory therapy [published online ahead of print, 2022 Jun 1]. Eye (Lond). 2022;10.1038/s41433-022-02121-3. doi:10.1038/s41433-022-02121-3
  11. ↑ 11.0 11.1 Kaur S, Kaushik S, Singh Pandav S. Pediatric Uveitic Glaucoma. J Curr Glaucoma Pract. 2013;7(3):115-117. doi:10.5005/jp-journals-10008-1147
  12. ↑ 12.0 12.1 12.2 Kok H, Barton K. Uveitic glaucoma. Ophthalmol Clin North Am. 2002;15(3):375-viii. doi:10.1016/s0896-1549(02)00028-7
  13. ↑ Bodh SA, Kumar V, Raina UK, Ghosh B, Thakar M. Inflammatory glaucoma. Oman J Ophthalmol. 2011;4(1):3-9. doi:10.4103/0974-620X.77655
  14. ↑ Kalogeropoulos D, Sung VC. Pathogenesis of Uveitic Glaucoma. J Curr Glaucoma Pract. 2018;12(3):125-138. doi:10.5005/jp-journals-10028-1257
  15. ↑ Engelhard SB, Patel V, Reddy AK. Intermediate uveitis, posterior uveitis, and panuveitis in the Mid-Atlantic USA. Clin Ophthalmol. 2015;9:1549-1555. Published 2015 Aug 25. doi:10.2147/OPTH.S89428
  16. ↑ Clement CI, Bhartiya S, Shaarawy T. New perspectives on target intraocular pressure. Surv Ophthalmol. 2014;59(6):615-626. doi:10.1016/j.survophthal.2014.04.001
  17. ↑ Sihota R, Sidhu T, Agarwal R, et al. Evaluating target intraocular pressures in primary congenital glaucoma. Indian J Ophthalmol. 2021;69(8):2082-2087. doi:10.4103/ijo.IJO_3473_20
  18. ↑ Sihota R, Angmo D, Ramaswamy D, Dada T. Simplifying "target" intraocular pressure for different stages of primary open-angle glaucoma and primary angle-closure glaucoma. Indian J Ophthalmol. 2018;66(4):495-505. doi:10.4103/ijo.IJO_1130_17
  19. ↑ Nuyen B, Weinreb RN, Robbins SL. Steroid-induced glaucoma in the pediatric population. J aapos. 2017;21(1):1-6.
  20. ↑ Passo MS, Palmer EA, Van Buskirk EM. Plasma timolol in glaucoma patients. Ophthalmology. 1984;91(11):1361-1363. doi:10.1016/s0161-6420(84)34141-0
  21. ↑ Heinz C, Koch JM, Zurek-Imhoff B, Heiligenhaus A. Prevalence of uveitic secondary glaucoma and success of nonsurgical treatment in adults and children in a tertiary referral center. Ocul Immunol Inflamm. 2009;17(4):243-248. doi:10.1080/09273940902913035
  22. ↑ 22.0 22.1 22.2 22.3 Coppens G, Stalmans I, Zeyen T, Casteels I. The safety and efficacy of glaucoma medication in the pediatric population. J Pediatr Ophthalmol Strabismus. 2009;46(1):12-18. doi:10.3928/01913913-20090101-0
  23. ↑ 23.0 23.1 23.2 Moore W, Nischal KK. Pharmacologic management of glaucoma in childhood. Paediatr Drugs. 2007;9(2):71-79. doi:10.2165/00148581-200709020-00001
  24. ↑ Moorthy RS, Moorthy MS, Cunningham ET Jr. Drug-induced uveitis. Curr Opin Ophthalmol. 2018;29(6):588-603. doi:10.1097/ICU.0000000000000530
  25. ↑ Heinz C, Schlote T, Dietlein T, Pillunat L. Glaukom bei Uveitis im Kindesalter [Glaucoma in childhood uveitis]. Klin Monbl Augenheilkd. 2007;224(6):511-515. doi:10.1055/s-2007-963039
  26. ↑ Chang JH, McCluskey P, Missotten T, Ferrante P, Jalaludin B, Lightman S. Use of ocular hypotensive prostaglandin analogues in patients with uveitis: does their use increase anterior uveitis and cystoid macular oedema?. Br J Ophthalmol. 2008;92(7):916-921. doi:10.1136/bjo.2007.131037
  27. ↑ Bello, Nicholas R, et al. “The Risk of Uveitis Due to Prostaglandin Analogs in Pediatric Glaucoma.” Journal of AAPOS, 2022.
  28. ↑ 28.0 28.1 28.2 Freedman SF, Rodriguez-Rosa RE, Rojas MC, Enyedi LB. Goniotomy for glaucoma secondary to chronic childhood uveitis. Am J Ophthalmol. 2002;133(5):617-621. doi:10.1016/s0002-9394(02)01344-2
  29. ↑ Wright TM, Freedman SF. Exposure to topical apraclonidine in children with glaucoma. J Glaucoma. 2009;18(5):395-398. doi:10.1097/IJG.0b013e31818624e5
  30. ↑ Eldib AA, Patil P, Nischal KK, Mitchell ER, Hiasat JG, Pihlblad MS. Safety of apraclonidine eye drops in diagnosis of Horner syndrome in an outpatient pediatric ophthalmology clinic. J AAPOS. 2021;25(6):336.e1-336.e4. doi:10.1016/j.jaapos.2021.07.011
  31. ↑ Chang L, Ong EL, Bunce C, Brookes J, Papadopoulos M, Khaw PT. A review of the medical treatment of pediatric glaucomas at Moorfields Eye Hospital. J Glaucoma. 2013;22(8):601-607. doi:10.1097/IJG.0b013e31824d1e2f
  32. ↑ Hoskins HD Jr, Shaffer RN, Hetherington J. Goniotomy vs trabeculotomy. J Pediatr Ophthalmol Strabismus. 1984;21: 153–158.
  33. ↑ 33.0 33.1 Ho CL, Wong EY, Walton DS. Goniosurgery for glaucoma complicating chronic childhood uveitis. Arch Ophthalmol. 2004;122(6):838-844. doi:10.1001/archopht.122.6.838
  34. ↑ 34.0 34.1 Wang Q, Wang J, Fortin E, Hamel P. Trabeculotomy in the Treatment of Pediatric Uveitic Glaucoma. J Glaucoma. 2016;25(9):744-749. doi:10.1097/IJG.0000000000000516
  35. ↑ 35.0 35.1 Wiese K, Heiligenhaus A, Heinz C. Trabekulektomie bei juveniler idiopathischer Arthritis-assoziierter Uveitis: Langzeitergebnisse beim kindlichen Sekundärglaukom [Trabeculectomy in uveitis associated with juvenile idiopathic arthritis: long-term results in pediatric secondary glaucoma]. Ophthalmologe. 2014;111(4):330-338. doi:10.1007/s00347-013-2888-9
  36. ↑ 36.0 36.1 36.2 Heinz C, Koch JM, Heiligenhaus A. Trabeculectomy or modified deep sclerectomy in juvenile uveitic glaucoma. J Ophthalmic Inflamm Infect. 2011;1(4):165-170. doi:10.1007/s12348-011-0039-5
  37. ↑ 37.0 37.1 Leinonen S, Kotaniemi K, Kivelä T, Majander A. Potential Effect of Tumor Necrosis Factor Inhibitors on Trabeculectomy With Mitomycin C for Patients With Juvenile Idiopathic Arthritis-Related Uveitic Glaucoma: A Retrospective Analysis. JAMA Ophthalmol. 2015;133(11):1323-1328. doi:10.1001/jamaophthalmol.2015.3387
  38. ↑ 38.0 38.1 Välimäki J, Airaksinen PJ, Tuulonen A. Molteno implantation for secondary glaucoma in juvenile rheumatoid arthritis. Arch Ophthalmol. 1997;115(10):1253-1256.
  39. ↑ 39.0 39.1 Kafkala C, Hynes A, Choi J, Topalkara A, Foster CS. Ahmed valve implantation for uncontrolled pediatric uveitic glaucoma. J AAPOS. 2005;9(4):336-340. doi:10.1016/j.jaapos.2005.04.006
  40. ↑ 40.0 40.1 Bohnsack BL, Freedman SF. Surgical outcomes in childhood uveitic glaucoma. Am J Ophthalmol. 2013;155(1):134-142. doi:10.1016/j.ajo.2012.07.008
  41. ↑ 41.0 41.1 Heinz C, Koch JM, Heiligenhaus A. Transscleral diode laser cyclophotocoagulation as primary surgical treatment for secondary glaucoma in juvenile idiopathic arthritis: high failure rate after short term follow up. Br J Ophthalmol. 2006;90(6):737-740. doi:10.1136/bjo.2005.085936
  42. ↑ Sachdev A, Khalili A, Choi J, Stead RE, Sung VCT. Gonioscopy-assisted Transluminal Trabeculotomy in Uveitic Glaucoma Secondary to Juvenile Idiopathic Arthritis. J Glaucoma. 2020;29(10):e116-e119. doi:10.1097/IJG.0000000000001641
Retrieved from "https://eyewiki.org/w/index.php?title=Pediatric_Uveitic_Glaucoma&oldid=109104"
The Academy uses cookies to analyze performance and provide relevant personalized content to users of our website.
Learn more
Powered by MediaWiki
Powered by Canasta
Powered by Semantic MediaWiki