**2. Pathogenesis of uveitic glaucoma**

Imbalance between aqueous humour secretion and clearance due to the intraocular inflam‐ mation 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.

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, result‐ ing 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 mecha‐ nism includes the anterior rotation of the lens-iris diaphragm that results in angle closure.

Uveitic Glaucoma

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http://dx.doi.org/10.5772/55708

Glaucomatocyclitic crisis is characterized by recurrent episodes of increased IOP and anteri‐ or chamber inflammation. Therefore, the uveitis is always accompanied by glaucoma and vice versa. In between, the eye is quiet and the IOP is normal. The disease is usually unilat‐

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. Iris heterochromia may appear after recurrent attacks. The first attack is always the most challenging to diagnose. When subsequent episodes occur, the diagnosis is obvious and the

The pathogenesis of the disease is not well established. Viral infection by herpes and cyto‐ megalic viruses, allergic factors and immunogenetic factors related to HLA-Bw54 have been suggested. [13-16] It may also be related to certain prostaglandins such as E released due to vascular incompetence. [17] Indeed, prostaglandin inhibitors, oral indomethacin and sub‐ conjunctival polyphloretin, a prostaglandin antagonist have been demonstrated to decrease

The disease responds to medical treatment with topical corticosteroid (prednisolone acetate 1% qid) and anti-glaucoma medications such as beta-blockers (timolol 0.5% bid) and carbon‐ ic anhydrase inhibitors (acetazolamide 250mg bid or tid). [19] Topical IOP sparing cortico‐ steroids and non-steroidal anti-inflammatory drugs may replace the classic corticosteroids. Prostaglandin inhibitors, oral indomethacin 75-150mg/day and subconjunctival polyphlore‐ tin, a prostaglandin antagonist, may also decrease the IOP. No preventive treatment during the remissions is known. In rare cases in which progression in optic disc and visual field damage is demonstrated, trabeculectomy or stenting procedure may be performed. The prognosis is good and some claim that the frequency of the attacks decreaseage. Unfortu‐ nately, no prophylactic treatment exists. The risk of developing optic disc and visual field damage is increased with the duration of the disease. Patients with 10 years or more of dis‐ ease have a risk of 2.8 folds to develop damage than those with duration of less than 10

patient is aware when they occur. The disease usually appears at the 3rdto 4th decade.

The forward rotation is caused by ciliary body and choroidal edema.

**3. Uveitic entities associated with glaucoma**

eral and involves the same eye.

the IOP. [17], [18]

years.

**3.1. Glaucomatocyclitic crisis (Posner-Schlossman syndrome)**

Several mechanisms are involved in the pathogenesis of glaucoma and this group of diseas‐ es may be divided to open and closed angle. Open angle is the largest group. In open angle glaucoma, increased outflow resistance is caused by obstruction of the trabecular meshwork by inflammatory cells, plasma proteins, fibrin and/ or debris. All of these are released from the blood vessels due to loss of aqueous-blood barrier and accumulate in the anterior cham‐ ber and the angle. Another mechanism is dysfunction of the trabeculocytes caused by toxici‐ ty of blood borne-products. This eventually may result in loss of trabeculocytes and scarring. Increased IOP may be caused by cytokines and prostaglandins. A role for the com‐ plement component C1qs has been implicated. [8] This component is part of the comple‐ ment system, which is activated in uveitis. Rho kinases that are released in uveitis may also result in increased IOP. [9], [10]

Corticosteroid-induced glaucoma is another mechanism for open angle glaucoma. It may oc‐ cur in up to one third of the patients but with impairment of the conventional outflow facili‐ ty in uveitic patients, it may increase even to 70%. [11] Corticosteroids are being routinely used for uveitis and they can cause this type of open angle glaucoma in any form although it is more common with topical installation. 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 treat‐ ment, but usually within 6 weeks. The glaucoma develops due to multiple mechanisms. Tra‐ becular cells have receptors for corticosteroids and they cause alternation of multiple gene expression leading to the production of extracellular glycosaminoglycans including fibro‐ nectin, laminin and collagen. [12] They also decrease the turnover of the extracellular matrix by inhibiting matrix metaloproteinases (MMPs) and tissue plasminogen activator and in‐ creasing plasminogen activator inhibitor 1 and tissue inhibitors of MMPs. Therefore, the gly‐ cosaminoglycans accumulate in the angle. 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. They are be‐ ing developed due to organization of inflammatory products in the angle. These PAS are broad base, trapezoid and highly pigmented bands that bridge the peripheral iris with the corneal periphery obstructing the angle. They may widen with time, resulting eventually in closure of the angle and increased IOP. 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 be‐ cause 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, result‐ ing 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 mecha‐ nism includes the anterior rotation of the lens-iris diaphragm that results in angle closure. The forward rotation is caused by ciliary body and choroidal edema.
