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Science, Technology and Medicine open access publisher.Publish, read and share novel research. Uveitic GlaucomaShimon Rumelt1[1] Department of Ophthalmology, Western Galilee, Nahariya Medical Center, Nahariya, Israel1. Glaucoma is a progressive disease without a cure.  Our goal is to slow it down so much that you are never bothered by the vision loss. It causes a characteristic pattern of visual loss measured by a visual field test.  The vision loss usually starts in the periphery and slowly works its way into the center. It has a hereditary predisposition and it is common for an affected patient to have close relatives that also have the disease.
It is best detected by a dilated eye examination with detailed analysis of the optic nerve.  Routine eye pressure checks (IOP) without dilation will fail to diagnosis a large percentage of cases. It is usually treated initially with prescription eye drops that lower the eye pressure.  In patients with “Low-Pressure” Glaucoma we still lower the pressure to treat the disease. Sometimes a laser treatment called Argon Laser Trabeculoplasty (ALT) or Selective Laser Trabeculoplasty (SLT) is used to additionally lower the pressure.  These procedures do not always work and when they are effective they last only three to five years. In cases when the pressure cannot be controlled or when vision loss occurs despite medical and laser treatments, a major surgery called trabeculectomy or tube shunt may bedone.
Treated with pressure-lowering eye drops, a special type of laser surgery or major surgery to form a new drainage channel in the eye.
Strong correlation to sleep apnea, a sleep disorder in which patients cease breathing while asleep. Caused by restricted path for outflow (narrow anterior chamber angle) of eye fluid (aqueous). This can be worse after exercise or exertion.  Symptoms involve temporary blurred vision or headache. Treatment includes a variety of laser procedures (laser trabeculoplasty) and sometimes pressure-lowering prescription eye drops. Caused by a systemic condition that causes build-up of an abnormal material (exfoliative material) in the drain of the eye (trabeculum).
Secondary to another condition that reduces the normal flow of blood to the tissues in the eye.
Lack of oxygen (hypoxia) causes the tissues to release chemicals (vascular endothelial growth factor – VEGF) that promote the growth of new but abnormal blood vessels. These new defective blood vessels leak serum or blood into the tissues and results in formation of a fibrous scar tissue.  The scar tissue contracts and the resulting traction may detach the retina and cause further bleeding. Relatively common in diabetes, retinal vascular occlusions (central retinal vein occlusion, central retinal artery occlusion, ocular ischemic syndrome).
Treatment often includes laser treatment of the retina (pan-retinal photocoagulation) and injections of anti-VEGF drugs like Avastin or Lucentis. The most common method of treating glaucoma is with prescription eye drops that are put in the eye.  Newer medications only need to be put in once a day, but we often must add some other drops when the eye pressure is not sufficiently lowered. Remember to put your drops in every day.  This is the single most important thing you can do to preserve your vision. We recommend you use artificial tears 3 or 4 times per day when taking glaucoma eye drops.  This will reduce or eliminate the dry eye symptoms many patients get from the prescription medications.
Do not take any other eye drops, such as artificial tears, within 10 minutes of the glaucoma eye drops.  This will prevent the dilution of the prescription drops. It is very important to keep your appointments to monitor your eye pressure.  Sometimes the glaucoma medication loses effectiveness, if it does you will not know unless your keep your appointment.
Glaucoma has historically been considered to be the least responsive eye disease to nutritional treatment. Two new retrospective studies dealing with the effects of nutrition on glaucoma were recently published in ophthalmology journals.  Retrospective studies do not prove a causal relationship, however, they did demonstrate a strong association, showing that patients with diets high in fruits and vegetables were about 70% less likely to develop glaucoma.
Ginkgo biloba, commonly used to increase blood flow to tissue and improve memory, has shown interesting abilities to protect the nerves in some studies. Wearing a necktie with the top button buttoned will raise your eye pressure a couple of points. THE RIGHT STYLE TO FIT YOUR LOOKOUTSIDE PRESCRIPTIONS WELCOMEIN-NETWORK WITH MOST INSURANCESFIND OUT MOREAthletes, does your eye doctor understand your eyes?Dr. Artisan Optics' Eye Doctors Serve Patients in Boise, Meridian, Eagle and communities throughout Idaho.
The Boise Optometrists at Artisan Optics have served the eyecare needs of patients throughout Idaho since 1991 and are a trusted and respected part of the Boise, Meridian and Eagle communities.
GlaucomaWhat is Glaucoma?Glaucoma is a disorder that involves progressive damage to the nerve of the eye, and if left untreated the disease will result in irreversible loss of vision. IntroductionUveitis is the third leading cause of preventable blindness worldwide although its incidence is relatively infrequent. Prevalence of uveitic secondary glaucoma and success of nonsurgical treatment in adults and children in a tertiary referral center.
Expression of dominant negative Rho-binding domain of Rho-kinase in organ cultured human eye anterior segments increases aqueous humor outflow. Mechanistic basis of Rho GTPase-induced extracellular matrix synthesis in trabecular meshwork cells.
Glaucomatocyclitic crises and systemic disease: peptic ulcer, other gastrointestinal disorder, various allergies and stress. Secondary glaucoma in patients with juvenile rheumatoid arthritis-associated iridocyclitis.
Visual outcome in herpes simplex virus and varicella zoster virus uveitis: a clinical evaluation and comparison. Bilateral angle-closure glaucoma associated with uveal effusion: presenting sign of HIV infection. Latanoprost and brimonidine: therapeutic and physiologic assessment before and after oral non-steroidal anti-inflammatory therapy. Effect of non-steroidal anti-inflammatory ophthalmic solution on intraocular pressure reduction by latanoprost. Intraoperative enoxaparin minimizes inflammatory reaction after pediatric cataract surgery. Glaucoma filtering surgery with postoperative 5-fluorouracil in patients with intraocular inflammatory disease.
Preferences for glaucoma drainage device implantation and cyclodestruction in Australia and New Zealand. Molteno aqueous shunt as a primary surgical intervention for uveitic glaucoma: long-term results.
The Effect of an Ahmed glaucoma valve implant on corneal endothelial cell density in children with glaucoma secondary to uveitis. At this time wedon’t have any large prospective, double-blind studies showing significant benefit from nutrition and probably never will due to the enormous expense of such trials. Ryan Johnson is Idaho's Sports Vision ExpertATHLETE VISION ASSESSMENTSCONCUSSION MANAGEMENTSPORTS VISION TRAININGCONTACT LENSES FOR COMPETITIONSchedule your eye exam today! Artisan Optics has a Developmental Optometrist, a Pediatric Optometrist, a Neuro Optometrist and Ophthalmologist on staff. It is the second most common cause of blindness in Ireland, and is becoming more prevalent because we are living longer. Note the pigment over the crystalline lens after pupil dilation and release of posterior synechiae.5. Each Boise Optometrist provides specialized eye exams so everyone in your family can have an eye doctor who has completed advanced training within the specific area of care needed. Its prevalence in the States is estimated as 15 per 100,000 and worldwide as 38-730 per 100,000. We are dedicated to providing the best vision care possible and we provide services ranging from eye exams, eye infections and eye allergies, minor emergencies, comprehensive dry eye treatment, contact lenses and eyeglasses to Blade-free LASIK and PRK. We understand how important clear vision is to you and we're dedicated to helping you correct your vision, your way. If the IOP is higher than 21mmHg, it is defined as glaucoma and as all the secondary glaucomas, the optic disc and the visual field may be normal. Whether you choose eyewear, contact lenses or LASIK we offer all of your options right here with our team of doctors and dedicated staff who care for you every step of the way. This is in contrast to primary glaucomas, where the high IOP should be accompanied by either abnormal optic disc or visual field or both.Uveitic glaucoma refers to glaucoma that develops in uveitic patients. This is a narrow definition of uveitis and glaucoma even if since it does not include cases of uveitis that develop in glaucoma patients. Contact one of our two convenient locations today to schedule eye exam appointments for you and your family.
Uveitic glaucoma is composed of different ocular diseases of different causes and mechanisms.
Nevertheless, in glaucomatocyclitic crisis or Posner Schlossman disease, both intraocular inflammation and high IOP always concur while in others such as Fuchs’ heterochromic iridocyclitis they appear in high association or with lesser association.2.
Pathogenesis of uveitic glaucomaImbalance between aqueous humour secretion and clearance due to the intraocular inflammation may result in change in IOP. The IOP is often reduced because of hyopsecretion in conjunction with increased uveoscleral outflow. However, the IOP may be also increased due to increase in outflow resistance.Several mechanisms are involved in the pathogenesis of glaucoma and this group of diseases may be divided to open and closed angle. All of these are released from the blood vessels due to loss of aqueous-blood barrier and accumulate in the anterior chamber and the angle. Another mechanism is dysfunction of the trabeculocytes caused by toxicity of blood borne-products.
It may occur in up to one third of the patients but with impairment of the conventional outflow facility in uveitic patients, it may increase even to 70%. The development of glaucoma depends on the subject susceptibility (corticosteroid responder), dose, duration, type of medication and route of administration.
The glaucoma may develop at any time after the initiation of treatment, but usually within 6 weeks.

Trabecular cells have receptors for corticosteroids and they cause alternation of multiple gene expression leading to the production of extracellular glycosaminoglycans including fibronectin, laminin and collagen. The corticosteroids also cause inhibition of phagocytosis, proliferation and migration of the trabeculocytes, and formation of certain prostaglandins.Secondary angle closure glaucoma may occur as chronic and acute forms.
In chronic angle closure glaucoma, peripheral anterior synechiae (PAS) develop along the angle.
These PAS are broad base, trapezoid and highly pigmented bands that bridge the peripheral iris with the corneal periphery obstructing the angle. Because the angle is progressively closing, the IOP increases gradually without causing an acute stage of increased IOP and without corneal edema. The acute form of angle closure glaucoma occurs secondary to papillary block because of 360° of posterior synechiae. These synechiae develop between the posterior margin of the iris and the crystalline (or intraocular) lens secondary to accumulation of fibrin and inflammatory precipitates over the lens. When the papillary margins are completely blocked, the aqueous humour is trapped in the posterior chamber, accumulates there, resulting in anterior iris displacement (iris bombe). The peripheral iris becomes appositioned against the peripheral cornea and obstructs the angle. The glaucoma in these cases develops abruptly and may be accompanied by ocular pain and corneal edema. A third, rarer mechanism includes the anterior rotation of the lens-iris diaphragm that results in angle closure. Glaucomatocyclitic crisis (Posner-Schlossman syndrome)Glaucomatocyclitic crisis is characterized by recurrent episodes of increased IOP and anterior chamber inflammation. The disease is usually unilateral and involves the same eye.Patients complain of blurred or decreased vision and ocular discomfort.
Minimal flare and cells (usually +1 or 5-10 cells per wide field magnification of X40) are found in the anterior chamber along with increase in IOP in the range of 40-60mmHg that may reach 70mmHg. When subsequent episodes occur, the diagnosis is obvious and the patient is aware when they occur.
The disease usually appears at the 3rdto 4th decade.The pathogenesis of the disease is not well established. Viral infection by herpes and cytomegalic viruses, allergic factors and immunogenetic factors related to HLA-Bw54 have been suggested. In rare cases in which progression in optic disc and visual field damage is demonstrated, trabeculectomy or stenting procedure may be performed. The risk of developing optic disc and visual field damage is increased with the duration of the disease. Fuchs’ heterochromic iridocyclitisThe disease is characterized by iris heterochromia and chronic, low-grade iridocyclitis. On examination, heterochromia along with low-grade anterior chamber reaction (flare and cells +1) are noted. Secondary open angle glaucoma develops in 13-59% of the patients depending on the duration of the disease.
Posterior subcapsular cataract may also develop.Treatment for Fuchs’ dystrophy without glaucoma is not required since it poorly responds to corticosteroids.
Anti-glaucoma medications may be effective initially but later the medical treatment usually fails and filtration surgery is required. Glaucoma in juvenile idiopathic arthritic (JIA) uveitisSecondary glaucoma may develop in 14-42% of the patients with JIA.
However, papillary block glaucoma and chronic angle closure glaucoma may also develop.The patient is usually asymptomatic and the eye is quiet. Therefore, any child with pauciarticular arthritis should be referred to ophthalmologic examination every 6 months. In cases of uveitis, measurement of the IOP and evaluation of the optic disc are mandatory. The purpose of the treatment is to achieve remission but treatment should be continued even after its achievement.
First, topical corticosteroid (prednisolone acetate 1% every 1-2 hours) and cycloplegic (cyclopentholate 1% tid) agent are being used. Common side effects of methotrexate include nausea, anorexia, stomatitis and transient elevation of serum aminotransferase. Alopecia, hematological toxicity, headache, dizziness, fatigue, and mood changes may also occur. A “post-dosing” reaction may occur within 24 hours of receiving methotrexate and is usually characterized by malaise, fatigue, gastrointestinal upset, and occasionally central nervous system manifestations.
The patients have pulmonary hilar lymphadenopathy, peripheral lymphadenopathy and cutaneous non-caseating epithelioid granulomas. Ocular involvement occurs in 38% of the patients and may be the first manifestation of the disease. A characteristic but not pathognomonicsign is large (mutton fat) keratic precipitates (KPs) over the endothelium. The mutton fat PKs are usually encountered at this stage along with Koeppe’s nodules on the iris margins and Busacca’s nodules on the iris surface. Elevated serum angiotensin converting enzyme or a positive Kveim test will confirm the diagnosis of sarcoid.
Additional tests include Gallium [67] scan that shows high intake in the lacrimal and parotid lymph nodes with or without submandibular lymph nodes and serumlysozyme, which is increased.
Treatment includes topical corticosteroid (prednisolone acetate 1% every 1-2 hours) and cycloplegic agent. If the posterior segment is involved, sub-Tenon and or oral corticosteroids (see the section on medical treatment of uveitic glaucoma below) are added. Immunosuppressive agents such as methotrexate should replace corticosteroids if there is no response or contraindications such as steroid-induced glaucoma. In resisting cases, anti-tumor necrosis factor alpha (TNF?) such as infliximab, etanercept, or adalimumab and intravitreal anti-vascular endothelial growth factor such as bevacizumab may be employed. Herpetic keratouveitic glaucomaSecondary open angle glaucoma may develop in herpetic keratouveitis in 10-54%.
The pathogenesis is probably a complex of direct injury to the trabeculocytes by the virus, inflammatory products and response to corticosteroids.
The condition is responsive to medical treatment with topical corticosteroid and antiglaucoma medications such as ?-blockers, ?-agonists and topical and oral carbonic anhydrase inhibitors.
It may cause cataract, retinopathy, glaucoma and microphthalmia in 30-60% of the affected children. Congenital angle abnormalities, chronic iridocyclitis, papillary block and angle closure glaucoma from intumescent cataract or microphthalmia are implicated. The glaucoma may appear at any age and therefore routine follow-up that includes measurement of the IOP and evaluation of the optic disc is required for lifetime. If glaucoma is diagnosed, treatment should be aggressive and follow-up should be frequent to prevent blindness since it may occur in 44%. Glaucoma in idiopathic uveitisAny patient with chronic or recurrent anterior uveitis from unknown cause may develop glaucoma. Thus, in all patients with chronic or recurrent uveitis, IOP measurements should be obtained. Phacoanaphylactic uveitis (phacoantigenic uveitis)Phacoanaphylaxis is a granulomatous uveitis from liberated crystalline lens proteins and contact with blood circulation.
It usually causes hypotony and rarely pupillary block glaucoma or angle closure glaucoma from peripheral anterior synechiae.
Keratic precipitates may appear on the cornea and the intraocular lens (IOL), hypopion and numerous white cells in the anterior chamber and vitreous may be present.
A high suspicion index is required because the disease may be similar to infectious endophthalmitis (but without pain), sterile endophthalmitis and toxic anterior chamber reaction (fibrinoid reaction).
Uveitis-glaucoma-hyphema (UGH) syndromeUveitis-glaucoma-hyphema (UGH) syndrome is a triad classically caused by subluxated or mal-positioned IOL (usually an anterior chamber IOL) rubbing against the iris and causing release of pigment and bleeding that result in open angle glaucoma. The patient complaints are sudden (within minutes to hours) decrease in vision that gradually improves over hours to days, and sometimes, ocular pain. It is diagnosed by attacks of this triad and the presence of iris transillumination corresponding to the rubbing site. The diagnosis can be confirmed by ultrasound biomicroscopy (UBM) and anterior segment optical coherence tomography (AS-OCT) showing a contact between the optic or haptic and the iris. The complications include pseudophakic bullous keratopathy, corneal staining and cystoid macular edema (CME).
Amaurosis fugax occurs more rapidly (within seconds to minutes) and loss of light perception in at least one quadrant. Loss of light perception never occurs in UGH syndrome and there is always a history of cataract extraction and IOL implantation or iris device implantation.
The differentiation between the two is crucial because patients with amaurosis fugax may be treated with anti-coagulants that may increase the bleeding in UGH syndrome.
Other uveitic glaucomasGlaucoma has been reported in patients with pars planitis (8%), uveitic from Reiter's syndrome (1%), ankylosing spondylitis, hemorrhagic fever with renal syndrome (nephropathia epidemica) and epidemic dropsy from ingestion of sanguinarine in Argemone mexicana oil. Bilateral acute angle closure glaucoma due to uveal effusion has been described in acquired immunodeficiency syndrome (AIDS) and responded to medical treatment with cycloplegics, topical corticosteroids and anti-glaucoma medications. DiagnosisPatients with acute closed-angle glaucoma may present with ocular and brow ace, blurred vision, halos, photophobia and even nausea and vomiting.
In acute closed angle glaucoma, the cornea may be edematous and ciliary and conjunctival congestion may be present. Topical glycerin 50-100% would clear corneal edema for evaluating the angle and posterior segment. Otherwise, the corneal epithelium may be removed with a blade or 70% alcohol on a cotton-tipped applicator.
If the cornea is still cloud, UBM or AS-OCT may replace gonioscopy in evaluating is performed the angle. Optic disc evaluation by slit lamp biomicroscopy and other imaging techniques (OCT, scanning laser polarimetry (GDx) or Heidelberg retinal tomography (HRT)) when the cornea is clear.

The visual field may be abnormal due to CME (central relative scotoma) and retinitis or retinal scarring (defects corresponding to these areas).
Differentiation should be made between steroid responder (the IOP returns to normal upon discontinuation of the corticosteroids) and corticosteroid-induced glaucoma (the IOP remains high). Differentiation between increased IOP due to increased inflammation and steroid responder may be performed by replacing the corticosteroids with IOP-sparing corticosteroids. Sub-Tenon corticosteroids such as triamcinolone acetonid (Kenalog®) 20-40mg (0.5-1ml) or methylprednisolone acetate (Depo-medrol®) 40-80mg may be given to treat noninfectious uveitis and macular edema.
Intravitreal implants such as Ozurdex®, a copolymer of glycolic and lactic acid with 700?g of dexamethasone may be injected through the pars plana with 22G injector. However, they all and especially those that cannot be removed (sub-Tenon and intravitreal) should be used cautiously in patients with glaucoma and are contraindicated in steroid responders and steroid-induced glaucoma. In cases of steroid responders orcorticosteroid-induced glaucoma, topical corticosteroids may be replaced by IOP-sparing corticosteroids such as such as loteprednol etabonate 0.5% (Lotemax®) or rimexolone 1%(Vexol®) but because of low potency, they may be more frequently required. Topical immunosuppressive agent such as cyclosporine A 0.5-2% and systemic immunosuppressive drugs may be alternatives for corticosteroids and NSAID. The dosage of corticosteroids depends on the severity of inflammation and is titrated according to the response to treatment.
The corticosteroids are gradually tapered according to the response since abrupt discontinuation may cause flare-up. Prostaglandins may be added in a quiet eye but should be avoided in an inflamed eye and herpetic keratouveitis because they may exacerbate the intraocular inflammation and cause CME. The efficacy of prostaglandins and alpha adrenergic agonists may decrease with concurrent use of topical or systemic NSAID. Laser iridotomyLaser iridotomy is indicated for all cases of secondary papillary block glaucoma, chronic angle closure glaucoma and prophylactically when progressive anterior synechiae are being formed.
In some cases of papillary block glaucoma, the glaucoma may not resolve because the entrapment of aqueous in several compartments behind the iris.
In such cases, more than one iridotomy is required.The first treatment modality, which is usually the simplest, if the cornea is clear, is peripheral laser iridotomy. The spot is placed at the periphery of the iris in the superior half to avoid glare, and over a thin part of the iris (usually a crypt) avoiding blood vessels.
The procedure may be performed with contact lens such as Abraham (+66D), Wise (+103D), CGIor without it. The advantages of a contact lens are additional magnification, focusing the beam, absorbing part of the heat, stabilizing the eye and keeping the eyelids open. This procedure facilitates aqueous flow from the posterior into the anterior chamber and may result in deepening of the anterior chamber and lowering the IOP. The position of the Argon iridotomy in this case is preferably supero-nasal to prevent injury to the macula. Argon laser may increase the intraocular inflammation because it releases pigment due to a different mechanism of action (plasma creation by ionizing in cases of ND:YAG versus coagulation in Argon). Perforation of the iris is confirmed when aqueous mixed with pigment is flowing from the posterior to the anterior chamber through the iridotomy. The lens should be visible through the iridotomy, since positive transillumination is not reliable. When laser iridotomy is not feasible or is impossible to perform, surgical peripheral iridectomy should be performed. Complications include visual disturbances such as halo and glare, development and progression of cataract, transient corneal burns, temporary increase in IOP, intraocular inflammation and rarely retinal injury, CME and malignant glaucoma.Argon laser trabeculoplasty has no role in uveitic open-angle glaucoma because of its low success rate. Some authors found selective (ND:YAG) laser trabeculoplasty to be effective in 20% of the patients, [39] but the follow-up was limited and the effectiveness is expected to decline. Surgical treatmentSurgical procedures are reserved for patients who fail to respond to medical treatment.
Surgical intervention is required in 56% of the children and in 35% of the adults with uveitic glaucoma. Topical corticosteroids or other medications as indicated above should be administrated two weeks preoperatively and postoperatively to control the uveitis. Any intervention on an inflamed eye may result in exacerbation of the uveitis, failure of the procedure and complications.
Detailed description of the newer devices can be found in chapter 19 in this book, chapter 20 in Rumelt S.
TrabeculectomyAs for all secondary glaucomas, uveitic glaucoma that does not respond to medical treatment should be treated with trabeculectomy and mitomycin C (MMC) or other shunting procedure. MMC decreases the risk of scarring of the filtering bleb, which is higher in uveitic glaucoma than in primary glaucomas, because of the increased postoperative inflammation. MMC 0.04% may be applied for 3 min under the scleral flap (or the conjunctiva) avoiding the conjunctival margins. Copious BSS irrigation is performed to remove the free MMC.The cumulative probability for success of trabeculectomy with MMC or 5-fluorouracil at 1 and 2 years was 78 and 68% respectively. Non-Penetrating Glaucoma Surgery (NPGS)Non-penetrating glaucoma surgery (NPGS) is a filtration procedure in which the anterior chamber is not penetrated. Three variations of the procedure exist: canaloplasty, viscocanalostomy and deep sclerostomy.
In the first procedure, a 10-0 nylon is passed through the Schlemm’s canal while in the second, viscoelastic agent such as hyaluronic acid (Healon®) is injected into the canal. The aqueous flows through the trabeculo-Descemet’s membrane into scleral pocket and from there to surrounding blood and aqueous vessels. The NPGS with intraoperative MMC is promising showing good short-term (between one and three years) success, but a long follow-up is required.9.
Glaucoma drainage implantsDrainage implants drain the aqueous humour to the subconjunctival space. They are considered if one or two trabeculectomies with MMC fail or if extensive conjunctival scarring exists. The first type is with control of the flow (with a “valve” or flow resistance) and includes Ahmed (New World Medical, Rancho Cucamonga, CA) and Krupin-Denver (Hood Laboratories, Pembroke, MA) drainage implants. The second type is without pressure control (no valve) and includes Molteno single or double plate (IOP, Inc., Costa Mesa, CA, USA, and Molteno OpLimited, Dunedin, New Zealand), Baerveldt (Advanced Medical Optics, Santa Ana, California, USA), Shocket (self-assembled) and Eagle Vision (Eagle Vision, Inc.
The later require blocking the aqueous flow for a few days externally by temporary suture or internally passing a suture through the lumen of the tube or injecting viscoelastic agent. The implantation may also be performed as a two-stage implantation, to decrease the risk for postoperative hypotony. Ahmed and Krupin implants should be preferred over the implants without a valve, because the risk for postoperative overflow and hypotony that may result in endothelial-iris and lens touch.
This is more prevalent in patients with uveitis than without it because the aqueous production is usually low. Ahmed valve has convenient plate of variable sizes including for pediatric population.The success rate of Ahmed implant in uveitic glaucoma at one year is 77-94% and at 4 years 50%. The decrease in endothelium is related to the age of the patient, duration of the uveitis and presence of the implant and corneal-valve touch. ExPress shuntIt is expected that this device will have the advantages of trabeculectomy (guarded filtration) and other glaucoma drainage device (uniform internal opening) as long as it will not be blocked by inflammatory products.
We have found that it is beneficial in secondary glaucomas including uveitic glaucoma (in publication). The only exceptions are neovascular glaucoma and iridocorneal endothelial syndrome where it usually fails.
IStentIStent is a titanium device that is placed into the Schlemm’s canal through the anterior chamber.
This device may be effective in secondary glaucoma and may decrease the requirement for postoperative hypotensive medications.
TrabectomeTrabectome is a micro-electrical device that removes the trabecular meshwork and unroof the Schlemm's canal under gonioscopy to decrease the resistance to aqueous outflow.
CycloablationCycloablation, preferably with 810nm infrared diode laser may be applied in uncontrolled glaucoma with no potential for improvement in visual acuity in which other anti-glaucoma procedures failed. Such inflammation may result in CME with decrease in visual acuity and central scotoma, papillary and retropupillary membranes and phthisis bulbi.
The initial settings for trans-scleral cyclophotocoagulation with this laser is 1,250mW, 2sec. Following topical anesthesia and additional peribulbar lidocaine 2% 2ml, the probe is placed 1.2mmbehind the limbus.
The power is increased in 150mW increments but not over 2250mW until a “pop” sound is heard.
Prevention of CME may be possible by topical NSAID such as diclofenac sodium (Voltaren®) 0.1% qid for 6 months. Decrease in visual acuity mayoccur from CME if prophylactic treatment is refrained or in cases of advanced visual field loss (splitting of the fixation or high mean deviation) as in other surgical procedures.10. If the uveitis is active or the glaucoma is uncontrolled, the follow-up interval should be decreased. PrognosisThe prognosis depends on the etiology of the uveitis and severity of the inflammation and the glaucoma.
Early medical and surgical interventions may improve the visual outcome and obtain resolution or long-term remission of the uveitis.12.
SummaryUveitic glaucoma is a heterogeneous group of diseases in which glaucoma develops secondary to uveitis. Most of the uveitis types should be treated although uveitis in juvenile rheumatoid arthritis requires minimal medical treatment to obtain remission and the uveitis in Fuchs’ heterochromic iridocyclitis does not require any treatment.

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