Uveitic Glaucoma
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In 1813, Joseph Beer first reported the association of uveitis and glaucoma, describing it as arthritic iritis followed by glaucoma and blindness. In 1891, Priesley Smith proposed the first modern classification of uveitic glaucoma. Later, specific types of uveitic glaucoma were described by Fuchs in 1906 (Fuchs heterochromic uveitis) and Posner and Schlossman in 1948 (glaucomatocyclitic crisis).
The mechanisms by which uveitis leads to elevated intraocular pressure (IOP) are numerous and poorly understood. In general, iridocyclitis affects both aqueous production and resistance to aqueous outflow, with the subsequent change in IOP representing a balance between these two factors. Inflammation of the ciliary body usually leads to reduced aqueous production, and combined with increased uveoscleral outflow often seen in inflammatory states, hypotony often is a consequence.
Prostaglandins, which have been demonstrated to be present in the aqueous of eyes with uveitis, are known to cause elevated IOP without a reduction in outflow facility. Mechanisms of increased resistance to aqueous outflow with both acute and subacute forms of uveitis usually are of the open-angle type and include obstruction of the trabecular meshwork by inflammatory cells or fibrin, swelling or dysfunction of the trabecular lamellae or endothelium, and inflammatory precipitates on the meshwork. Uveitis also may be associated with secondary angle-closure glaucoma.
Alteration of the protein content of the aqueous humor may be a cause of elevated IOP in uveitis. Increased levels of protein in the aqueous are a result of increased permeability of the blood-aqueous barrier, which leads to an aqueous that more closely resembles undiluted serum. This elevated protein content may, in fact, lead to aqueous hypersecretion and IOP elevation.
The treatment of the uveitis can lead to elevated IOP. Although corticosteroids have proven to be effective in relieving inflammation, prolonged administration can result in elevated IOP. Corticosteroids increase IOP by decreasing aqueous outflow. Several theories have been proposed to explain this phenomenon, including accumulation of glycosaminoglycans in the trabecular meshwork, inhibition of phagocytosis by trabecular endothelial cells, and inhibition of synthesis of certain prostaglandins.
United States
The prevalence of uveitis has been estimated at approximately 115 people per 100,000 in the United States. Approximately 20% of uveitis patients develop glaucoma.
International
The prevalence of uveitis has been estimated at 38-730 people per 100,000 worldwide. Approximately 20% of uveitis patients develop glaucoma.
Acute iridocyclitis usually produces symptoms; however, subacute iridocyclitis produces few or no symptoms but can have serious consequences because its complications may go undetected until advanced damage has occurred. If the inflammation is not controlled promptly, posterior synechiae and peripheral anterior synechiae (PAS) can form, leading to progressive angle closure and irreversible optic nerve damage.
No known racial predilection exists.
No known sexual predilection exists.
No known age predilection exists.
Few published reports are available that address the results of surgery in patients with uveitic glaucoma.
Hoskins et al achieved successful lowering of IOP in 6 of 9 eyes undergoing trabeculectomy for uveitic glaucoma. [12]
Hill et al showed a success rate of 81% at 12 months. The success rate of trabeculectomy with antimetabolite supplementation has been reported to be higher (71-100%). [13]
Wright et al reported that 3 of 24 patients undergoing trabeculectomy with mitomycin-C required subsequent drainage implants and that 7 of 24 patients lost 2 or more lines of Snellen acuity. [14]
Hill et al reported a success rate of 79% of eyes undergoing Molteno tube implantation. [15]
Ceballos et al reported a success rate of 91.7% in eyes undergoing Baerveldt drainage device placement for uveitic glaucoma. [16]
Ozdal et al showed a 2-year success rate of 60% in eyes undergoing Ahmed drainage device placement for uveitic glaucoma. [17]
Rachmiel et al reported similar 30-month results between eyes that underwent Ahmed glaucoma valve implantation with uveitic glaucoma compared to open-angle glaucoma eyes. [18]
For patient education resources, see the Glaucoma Center and Eye and Vision Center, as well as Glaucoma Overview, Anatomy of the Eye, Glaucoma FAQs, Understanding Glaucoma Medications, and Iritis.
Callanan DG, Jaffe GJ, Martin DF, Pearson PA, Comstock TL. Treatment of posterior uveitis with a fluocinolone acetonide implant: three-year clinical trial results. Arch Ophthalmol. 2008 Sep. 126(9):1191-201. [Medline].
Bollinger K, Kim J, Lowder CY, Kaiser PK, Smith SD. Intraocular pressure outcome of patients with fluocinolone acetonide intravitreal implant for noninfectious uveitis. Ophthalmology. 2011 Oct. 118(10):1927-31. [Medline].
Hunter RS, Lobo AM. Dexamethasone intravitreal implant for the treatment of noninfectious uveitis. Clin Ophthalmol. 2011. 5:1613-21. [Medline].
Kempen JH, Altaweel MM, Holbrook JT, Jabs DA, Louis TA, Sugar EA, et al. Randomized comparison of systemic anti-inflammatory therapy versus fluocinolone acetonide implant for intermediate, posterior, and panuveitis: the multicenter uveitis steroid treatment trial. Ophthalmology. 2011 Oct. 118(10):1916-26. [Medline]. [Full Text].
Almobarak FA, Alharbi AH, Morales J, Aljadaan I. Intermediate and Long-term Outcomes of Mitomycin C-enhanced Trabeculectomy as a First Glaucoma Procedure in Uveitic Glaucoma. J Glaucoma. 2017 Feb 23. [Medline].
Dhanireddy S, Kombo NC, Payal AR, Freitas-Neto CA, Preble J, Foster CS. The Ex-PRESS Glaucoma Filtration Device Implantation in Uveitic Glaucoma. Ocul Immunol Inflamm. 2016 May 26. [Medline].
Malone PE, Herndon LW, Muir KW, Jaffe GJ. Combined fluocinolone acetonide intravitreal insertion and glaucoma drainage device placement for chronic uveitis and glaucoma. Am J Ophthalmol. 2010 May. 149(5):800-6.e1. [Medline].
Zivney M, Lin P, Edmunds B, Parikh M, Takusagawa H, Tehrani S. Combined Glaucoma TUbe Shunt (Ahmed) and Fluocinolone Acetonide (Retisert) Implantation Compared to Ahmed Alone in Uveitic Glaucoma. Ophthalmol Ther. 2016 Dec. 5:223-233. [Medline]. [Full Text].
Hennein L, Hou J, Stewart JM, Lowry EA, Jiang Z, Enanoria WT, et al. Comparison of Surgical Outcome After Ahmed Valve Implantation for Patients With and Without Fluocinolone Intravitreal Implant (Retisert). J Glaucoma. 2016 Sep. 25:[Medline]. [Full Text].
Horsley MB, Chen TC. The use of prostaglandin analogs in the uveitic patient. Semin Ophthalmol. 2011 Jul-Sep. 26(4-5):285-9. [Medline].
Markomichelakis NN, Kostakou A, Halkiadakis I, Chalkidou S, Papakonstantinou D, Georgopoulos G. Efficacy and safety of latanoprost in eyes with uveitic glaucoma. Graefes Arch Clin Exp Ophthalmol. 2009 Jun. 247(6):775-80. [Medline].
Hoskins DH, Hetherington J, Shaffer RN. Surgical management of the inflammatory glaucomas. Perspect Ophthalmol. 1977. 1:173-81.
Hill RA, Nguyen QH, Baerveldt G, et al. Trabeculectomy and Molteno implantation for glaucomas associated with uveitis. Ophthalmology. 1993 Jun. 100(6):903-8. [Medline].
Wright MM, McGehee RF, Pederson JE. Intraoperative mitomycin-C for glaucoma associated with ocular inflammation. Ophthalmic Surg Lasers. 1997 May. 28(5):370-6. [Medline].
Hill RA, Heuer DK, Baerveldt G, et al. Molteno implantation for glaucoma in young patients. Ophthalmology. 1991 Jul. 98(7):1042-6. [Medline].
Ceballos EM, Parrish RK, Schiffman JC. Outcome of Baerveldt glaucoma drainage implants for the treatment of uveitic glaucoma. Ophthalmology. 2002 Dec. 109(12):2256-60. [Medline].
Ozdal PC, Vianna RN, Deschenes J. Ahmed valve implantation in glaucoma secondary to chronic uveitis. Eye. 2006 Feb. 20(2):178-83. [Medline].
Rachmiel R, Trope GE, Buys YM, Flanagan JG, Chipman ML. Ahmed glaucoma valve implantation in uveitic glaucoma versus open-angle glaucoma patients. Can J Ophthalmol. 2008 Aug. 43(4):462-7. [Medline].
Leon Herndon, Jr, MD Professor, Department of Ophthalmology, Duke University Medical Center
Leon Herndon, Jr, MD is a member of the following medical societies: American Glaucoma Society
Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Glaukos;Aerie pharmaceuticals<br/>Received research grant from: Glaukos<br/>Received income in an amount equal to or greater than $250 from: Glaukos; Aerie.
Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society
Disclosure: Nothing to disclose.
Martin B Wax, MD Professor, Department of Ophthalmology, University of Texas Southwestern Medical School; Vice President, Research and Development, Head, Ophthalmology Discovery Research and Preclinical Sciences, Alcon Laboratories, Inc
Martin B Wax, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Society for Neuroscience
Disclosure: Nothing to disclose.
Inci Irak Dersu, MD, MPH Associate Professor of Clinical Ophthalmology, State University of New York Downstate College of Medicine; Attending Physician, SUNY Downstate Medical Center, Kings County Hospital, and VA Harbor Health Care System
Inci Irak Dersu, MD, MPH is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society
Disclosure: Nothing to disclose.
Neil T Choplin, MD Adjunct Clinical Professor, Department of Surgery, Section of Ophthalmology, Uniformed Services University of Health Sciences
Neil T Choplin, MD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, Association for Research in Vision and Ophthalmology, California Association of Ophthalmology, San Diego County Ophthalmological Society, Society of Military Ophthalmologists
Disclosure: Nothing to disclose.
Uveitic Glaucoma
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