Glaucoma associated with uveitis

Increased intraocular pressure and development of glaucoma in patients with uveitis is a multifactorial process that can be considered as a complication of the intraocular inflammatory process. As a result of the inflammatory process, a direct or structurally impaired change in the dynamics of the intraocular fluid occurs, leading to an increase, decrease in intraocular pressure or its maintenance within normal values.

Optic nerve damage in glaucoma and visual field impairment in patients with uveitis are the result of uncontrolled increase in intraocular pressure. In the development of intraocular hypertension and glaucoma in patients suffering from uveitis, the inflammatory process should be eliminated first and foremost and irreversible structural impairment of intraocular fluid outflow should be prevented by anti-inflammatory therapy. Then, intraocular pressure should be reduced with medication or surgery.

This article discusses the pathophysiological mechanisms, diagnostics and treatment tactics for patients with uveitis and increased intraocular pressure or secondary glaucoma. At the end of the article, specific uveitis is described, in which increased intraocular pressure and development of glaucoma most often occur.

The term uveitis in its usual sense includes all causes of intraocular inflammation. Uveitis may result in acute, transient, or chronic increase in intraocular pressure. The terms inflammatory glaucoma or uveitis-associated glaucoma are used for all patients with uveitis with increased intraocular pressure. When elevated intraocular pressure is detected without glaucoma-related optic nerve damage or glaucoma-related visual field impairment, the terms uveitis-associated intraocular hypertension, ocular hypertension secondary to uveitis, or secondary ocular hypertension are more appropriate. Patients do not develop secondary glaucoma after resolution or adequate treatment of the inflammatory process.

The terms inflammatory glaucoma, uveitis-associated glaucoma, and glaucoma secondary to uveitis should be used only when "glaucomatous" optic nerve damage or "glaucomatous" visual field impairment occurs with increased intraocular pressure in patients with uveitis. In most uveitis-associated glaucomas, optic nerve damage occurs as a result of increased intraocular pressure. Therefore, caution should be exercised in making the diagnosis of uveitis-associated glaucoma in the absence of information about the previous level of intraocular pressure. Caution should also be exercised in making the diagnosis in patients with visual field impairment not typical of glaucoma and a normal optic disc. This is primarily due to the fact that in many forms of uveitis (especially with damage to the posterior segment of the eye), chorioretinal foci and foci in the optic nerve area develop, leading to the development of visual field defects not associated with glaucoma. It is important to distinguish the etiology of visual field disorders, since if they are associated with an active inflammatory process, then with adequate therapy they can disappear or decrease, while visual field disorders associated with glaucoma are irreversible.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ]

Epidemiology

Uveitis is the fourth most common cause of blindness in developing countries after macular degeneration, diabetic retinopathy, and glaucoma. The incidence of uveitis among all causes of blindness is 40 cases per 100,000 population, and the annual share of uveitis is 15 cases per 100,000 population. Uveitis occurs in patients of any age, most often observed in patients 20-40 years old. Children account for 5-10% of all patients with uveitis. The most common causes of vision loss in patients with uveitis are secondary glaucoma, cystoid macular edema, cataract, hypotony, retinal detachment, subretinal neovascularization or fibrosis, and optic nerve atrophy.

Approximately 25% of patients with uveitis have elevated intraocular pressure. Because inflammation in the anterior segment of the eye can directly affect the outflow pathways of intraocular fluid, intraocular hypertension and glaucoma most often develop as complications of anterior uveitis or panuveitis. Also, glaucoma associated with uveitis is more often developed in case of granulomatous uveitis than nongranulomatous uveitis. Taking into account all causes of uveitis, the incidence of secondary glaucoma in adults is 5.2-19%. The overall incidence of glaucoma in children with uveitis is approximately the same as in adults: 5-13.5%. The prognosis for the preservation of visual functions in children with secondary glaucoma is worse.

[ 6 ], [ 7 ], [ 8 ], [ 9 ], [ 10 ]

Causes of Uveitis-Associated Glaucoma

The level of intraocular pressure depends on the ratio of secretion and outflow of intraocular fluid. In most cases, several mechanisms of increasing intraocular pressure are realized with uveitis. The final stage of all mechanisms leading to an increase in intraocular pressure in uveitis is a violation of the outflow of intraocular fluid through the trabecular network. Violation of the outflow of intraocular fluid in uveitis occurs as a result of a violation of secretion and a change in its composition, as well as due to infiltration of eye tissues, the development of irreversible changes in the structures of the anterior chamber of the eye, for example, peripheral anterior and posterior synechiae, during the development of which the angle of the anterior chamber can close. With these changes, not only severe glaucoma can develop, but also glaucoma resistant to all types of drug therapy. Paradoxically, but the treatment of uveitis with glucocorticoids can also lead to an increase in intraocular pressure.

Pathophysiological mechanisms leading to increased intraocular pressure in patients with uveitis can be divided into open-angle and closed-angle. This classification is clinically justified, since the primary treatment approach in these two groups will be different.

[ 11 ]

Mechanisms leading to open-angle glaucoma

[ 12 ]

Violation of intraocular fluid secretion

Inflammation of the ciliary body usually results in decreased production of intraocular fluid. With normal outflow, intraocular pressure decreases, which is often observed in acute uveitis. However, with both impaired outflow and decreased production of intraocular fluid, intraocular pressure may remain normal or even elevated. It is unknown whether increased production of intraocular fluid and intraocular pressure occur in uveitis, where the blood-aqueous barrier is impaired. However, the most plausible explanation for increased intraocular pressure in uveitis is impaired outflow of intraocular fluid with unchanged secretion.

[ 13 ], [ 14 ], [ 15 ], [ 16 ], [ 17 ], [ 18 ]

Proteins of the intraocular fluid

One of the first assumptions regarding the cause of increased intraocular pressure in uveitis was a violation of the composition of the intraocular fluid. At the initial stage, when the blood-aqueous humor barrier is disrupted, proteins enter the intraocular fluid from the blood, which disrupts the biochemical balance of the intraocular fluid and increases intraocular pressure. Normally, the intraocular fluid contains 100 times less proteins than blood serum, and when the blood-aqueous humor barrier is disrupted, the protein concentration in the fluid can be the same as in undiluted blood serum. Thus, due to an increase in the concentration of proteins in the intraocular fluid, its outflow is disrupted by mechanical obstruction of the trabecular network and disruption of the function of the endothelial cells lining the trabeculae. In addition, with a high protein content, posterior and peripheral anterior synechiae are formed. When the barrier is normalized, the outflow of intraocular fluid and intraocular pressure are restored. However, if the permeability of the blood-aqueous humor barrier is irreversibly impaired, the flow of proteins into the anterior chamber of the eye may continue even after the inflammatory process has resolved.

[ 19 ], [ 20 ], [ 21 ], [ 22 ], [ 23 ]

Inflammatory cells

Soon after the proteins, inflammatory cells begin to enter the intraocular fluid, producing inflammatory mediators: prostaglandins and cytokines. It is believed that inflammatory cells have a more pronounced effect on intraocular pressure than proteins. An increase in intraocular pressure occurs due to the infiltration of the trabecular meshwork and Schlemm's canal by inflammatory cells, which leads to the formation of a mechanical obstacle to the outflow of intraocular fluid. Due to pronounced macrophage and lymphocytic infiltration, the likelihood of an increase in intraocular pressure in granulomatous uveitis is higher than in non-granulomatous uveitis, in which the infiltrate contains mainly polymorphonuclear cells. In chronic, severe or recurrent uveitis, irreversible damage to the trabecular meshwork and scarring of the trabeculae and Schlemm's canal occur due to damage to endothelial cells or the formation of hyaloid membranes lining the trabeculae. Inflammatory cells and their fragments in the area of the anterior chamber angle can also lead to the formation of peripheral anterior and posterior synechiae.

Prostaglandins

Prostaglandins are known to be involved in the formation of many symptoms of intraocular inflammation (vasodilation, miosis, and increased vascular wall permeability), which together can affect the level of intraocular pressure. Whether prostaglandins can directly increase intraocular pressure is unknown. By affecting the blood-aqueous humor barrier, they can increase the flow of proteins, cytokines, and inflammatory cells into the intraocular fluid, indirectly affecting the increase in intraocular pressure. On the other hand, they can lower intraocular pressure by increasing uveoscleral outflow.

[ 24 ], [ 25 ], [ 26 ], [ 27 ], [ 28 ], [ 29 ]

Trabeculitis

The diagnosis of "trabeculitis" is made in cases of localization of the inflammatory reaction in the trabecular meshwork. Clinically, trabeculitis is manifested by the deposition of inflammatory precipitates in the trabecular meshwork in the absence of other signs of active intraocular inflammation (precipitates on the cornea, opalescence or the presence of inflammatory cells in the intraocular fluid). As a result of the deposition of inflammatory cells, edema of the trabeculae and a decrease in the phagocytic activity of the endothelial cells of the trabeculae, mechanical obstruction of the trabecular meshwork is formed and the outflow of intraocular fluid is impaired. Since the production of intraocular fluid in trabeculitis, as a rule, does not decrease, then due to the disruption of its outflow, a significant increase in intraocular pressure occurs.

Steroid-induced intraocular hypertension

Glucocorticoids are considered to be the first-line drugs for treating patients with uveitis. It is known that when applied locally and systemically, as well as when administered periocularly and into the sub-Tenon space, glucocorticoids accelerate cataract formation and increase intraocular pressure. Glucocorticoids inhibit enzymes and phagocytic activity of trabecular endothelial cells, resulting in accumulation of glycosaminoglycans and inflammation products in the trabecular network, which leads to impaired outflow of intraocular fluid through the trabecular network. Glucocorticoids also inhibit prostaglandin synthesis, leading to impaired outflow of intraocular fluid.

The terms "steroid-induced intraocular hypertension" and "steroid responder" are used to describe patients who develop an increase in intraocular pressure in response to glucocorticoid treatment. It is estimated that about 5% of the population are "steroid responders" and that 20-30% of patients receiving long-term glucocorticoid treatment can be expected to develop a "steroid response". The likelihood of developing an increase in intraocular pressure in response to glucocorticoid administration depends on the duration of treatment and dosage. Patients with glaucoma, diabetes, high myopia, and children under 10 years of age are at higher risk of developing a "steroid response". Steroid-induced intraocular hypertension can develop at any time after the start of taking these drugs, but is most often detected 2-8 weeks after the start of treatment. With local use, a "steroid response" develops more often. Patients with ocular hypertension should avoid periocular administration of the drug, as a sharp increase in intraocular pressure may develop. In most cases, intraocular pressure returns to normal after glucocorticoid withdrawal; however, in some cases, especially with depot glucocorticoid administration, intraocular pressure may increase for 18 months or more. In these cases, if intraocular pressure cannot be controlled with medication, depot removal or surgery to improve outflow may be required.

When treating a patient with uveitis with glucocorticoids, it is often difficult to determine the cause of the increase in intraocular pressure: a change in the secretion of intraocular fluid, or a deterioration in its outflow due to intraocular inflammation, or the result of the development of a "steroid response", or a combination of all three causes. Similarly, a decrease in intraocular pressure when glucocorticoids are discontinued may either prove the steroid nature of intraocular hypertension or occur as a result of improved outflow of intraocular fluid through the trabecular meshwork or a decrease in its secretion due to resolution of the inflammatory process. Suspected development of a "steroid response" in a patient with active intraocular inflammation requiring systemic administration of glucocorticoids may be an indication for the use of steroid replacement drugs. If steroid-induced intraocular hypertension is suspected in a patient with controlled or inactive uveitis, the concentration, dose, or frequency of glucocorticoid administration should be reduced.

[ 30 ], [ 31 ], [ 32 ], [ 33 ], [ 34 ], [ 35 ], [ 36 ]

Mechanisms leading to oblique angle glaucoma

Morphological changes in the structures of the anterior chamber of the eye that develop with uveitis are often irreversible and lead to a significant increase in intraocular pressure, disrupting or blocking the flow of intraocular fluid from the posterior chamber of the eye to the trabecular meshwork. Structural changes that most often lead to secondary closure of the angle of the anterior chamber include peripheral anterior synechiae, posterior synechiae, and pupillary membranes, leading to the development of pupillary block and, less commonly, to anterior rotation of the ciliary body processes.

[ 37 ], [ 38 ], [ 39 ]

Peripheral anterior synechiae

Peripheral anterior synechiae are adhesions of the iris to the trabecular meshwork or cornea that may impair or completely block the flow of aqueous humor into the trabecular meshwork. Peripheral anterior synechiae are best seen with gonioscopy. They are a common complication of anterior uveitis and are more common in granulomatous than in nongranulomatous uveitis. Peripheral anterior synechiae form when inflammation products organize, causing the iris to be pulled toward the anterior chamber angle. They most often develop in eyes with an initially narrow anterior chamber angle or when the angle is narrowed by iris bombage. The adhesions are usually extensive and overlap significant segments of the anterior chamber angle, but they may also be plaque- or cord-like and involve only a small portion of the trabecular meshwork or cornea. When peripheral anterior synechiae form as a result of uveitis, despite the fact that most of the angle remains open, the patient may experience increased intraocular pressure due to the functionally defective preserved part of the angle (due to the previous inflammatory process), which may not be detected by gonioscopy.

Long-term formation of peripheral anterior synechiae in recurrent and chronic uveitis may lead to complete occlusion of the anterior chamber angle. When the anterior chamber angle closes or pronounced peripheral anterior synechiae form in uveitis, it is imperative to pay attention to possible neovascularization of the iris or the anterior chamber angle. Contraction of fibrovascular tissue in the area of the anterior chamber angle or the anterior surface of the iris can quickly lead to its complete closure. Usually, in neovascular glaucoma that develops as a result of uveitis, drug and surgical treatment are ineffective, and the prognosis is unfavorable.

[ 40 ], [ 41 ], [ 42 ], [ 43 ], [ 44 ]

Posterior synechiae

Posterior synechiae are formed due to the presence of inflammatory cells, proteins, and fibrin in the intraocular fluid. Posterior synechiae are adhesions of the posterior surface of the iris to the anterior capsule of the lens, the surface of the vitreous body in aphakia, or to the intraocular lens in pseudophakia. The likelihood of developing posterior synechiae depends on the type, duration, and severity of uveitis. In granulomatous uveitis, posterior synechiae are formed more often than in nongranulomatous uveitis. The greater the extent of posterior synechiae, the worse the pupil dilation occurs and the greater the risk of subsequent formation of posterior synechiae in case of uveitis relapses.

The term "pupillary block" is used to describe a disturbance in the flow of intraocular fluid from the posterior to the anterior chamber of the eye through the pupil as a result of the formation of posterior synechiae. The formation of seclusio pupillae, posterior synechiae over 360° around the circumference of the pupil, and pupillary membranes can lead to the development of a complete pupillary block. In this case, the flow of intraocular fluid from the posterior to the anterior chamber is completely stopped. Excess intraocular fluid in the posterior chamber can lead to iris bombage or to a significant increase in intraocular pressure, resulting in the iris bending toward the anterior chamber. Iris bombage with ongoing inflammation leads to rapid closure of the angle due to the formation of peripheral anterior synechiae, even if the anterior chamber angle was initially open. In some cases of uveitis with pupillary block, wide adhesions form between the iris and the anterior capsule of the lens, then only the peripheral part of the iris bends forward. In this situation, it is quite difficult to detect iris bombage without gonioscopy.

[ 45 ], [ 46 ], [ 47 ], [ 48 ], [ 49 ]

Anterior rotation of the ciliary body

In acute intraocular inflammation, ciliary body edema with supraciliary or suprachoroidal effusion may develop, resulting in anterior rotation of the ciliary body and closure of the anterior chamber angle unrelated to pupillary block. Increased intraocular pressure due to such closure of the anterior chamber angle most often develops in iridocyclitis, circular choroidal detachments, posterior scleritis, and in the acute stage of Vogt-Koyanagi-Harada syndrome.

[ 50 ]

Uveitis is most often associated with secondary glaucoma.

Anterior uveitis

• Juvenile rheumatoid arthritis
• Fuchs' heterochromic uveitis
• Glaucomatocyclitic crisis (Posner-Schlossman syndrome)
• HLA B27-associated uveitis (ankylosing spondylitis, Reiter's syndrome, psoriatic arthritis)
• Herpetic uveitis
• Lens-associated uveitis (phacoantigenic uveitis, phacolytic glaucoma, lens masses, phacomorphic glaucoma)

Panuveites

• Sarcoidosis
• Vogt-Koyanagi-Harada syndrome
• Behcet's syndrome
• Sympathetic ophthalmia
• Syphilitic uveitis

Moderate uveitis

• Moderate uveitis of the pars planitis type

Posterior uveitis

• Acute retinal necrosis
• Toxoplasmosis

Diagnosis of glaucoma associated with uveitis

The basis for proper diagnosis and management of patients with glaucoma due to uveitis is a complete ophthalmological examination and the correct use of auxiliary methods. A slit lamp examination is used to determine the type of uveitis, the activity of the inflammatory process, and the type of inflammatory reaction. Depending on the location of the primary inflammatory focus, anterior, middle, posterior uveitis, and panuveitis are distinguished.

The probability of developing glaucoma associated with uveitis is higher with anterior uveitis and panuveitis (with intraocular inflammation, the probability of damage to the structures that ensure the outflow of intraocular fluid increases). The activity of the inflammatory process is assessed by the severity of opalescence and the number of cells in the fluid of the anterior chamber of the eye, as well as by the number of cells in the vitreous body and the degree of its opacity. It is also necessary to pay attention to the structural changes caused by the inflammatory process (peripheral anterior and posterior synechia).

The inflammatory reaction in uveitis can be granulomatous and non-granulomatous. Signs of granulomatous uveitis: sebaceous precipitates on the cornea and nodules on the iris. Secondary glaucoma develops more often in granulomatous uveitis than in non-granulomatous uveitis.

Gonioscopy is the most important method of ophthalmological examination of patients with uveitis with increased IOP. The examination should be performed using a lens that presses the central part of the cornea, causing intraocular fluid to enter the angle of the anterior chamber. Gonioscopy reveals inflammation products, peripheral anterior synechiae, and neovascularization in the area of the angle of the anterior chamber, which allows one to differentiate between open-angle and closed-angle glaucoma.

When examining the fundus, special attention should be paid to the condition of the optic nerve. In particular, the size of the excavation, the presence of hemorrhage, edema or hyperemia, and the condition of the nerve fiber layer should also be assessed. The diagnosis of uveitis-associated glaucoma should be made only in the presence of documented damage to the optic disc and visual field impairment. Although retinal and choroidal lesions in the posterior pole of the eye do not lead to the development of secondary glaucoma, their presence and location should also be recorded, since the associated visual field impairment may lead to an erroneous diagnosis of glaucoma. Applanation tonometry and standard perimetry should be performed at each examination. Additionally, laser photometry of the opalescence of the intraocular fluid and ultrasound examination of the eye can be used for more accurate diagnosis and management of patients suffering from uveitis and increased intraocular pressure. Laser opalescence photometry can detect subtle changes in opalescence and protein content in the intraocular fluid that are not possible with slit lamp examination. Subtle changes have been shown to be helpful in assessing uveitis activity. B-scan ultrasound and ultrasound biomicroscopy in secondary glaucoma can assess the structure of the ciliary body and iridocyliary angle, which can help identify the cause of increased or excessively decreased intraocular pressure in patients with uveitis.

[ 51 ]

Treatment of glaucoma associated with uveitis

The main objective of treating patients with uveitis-related intraocular hypertension or glaucoma is to control intraocular inflammation and prevent the development of irreversible structural changes in the eye tissues. In some cases, resolution of the intraocular inflammatory process with anti-inflammatory therapy alone leads to normalization of intraocular pressure. With early initiation of anti-inflammatory treatment and provision of mydriasis and cycloplegia, it is possible to prevent the development of irreversible consequences of uveitis (peripheral anterior and posterior synechia).

The first-choice drugs for most uveitis are glucocorticoids, used in the form of instillations, periocular and systemic administration, sub-Tenon injections. Instillations of glucocorticoids are effective in inflammation of the anterior segment of the eye, but in case of active inflammation of the posterior segment in phakic eyes, instillations alone are not enough. The frequency of glucocorticoid instillations depends on the severity of inflammation of the anterior segment. Prednisolone (pred-forte) in the form of eye drops is most effective in inflammation of the anterior segment of the eye. On the other hand, the use of this drug most often leads to the development of steroid-induced ocular hypertension and posterior subcapsular cataract. When using weaker glucocorticoids in the form of eye drops, such as rimexolone, fluorometholone, medrysone, loteprednol, etabonate (lotemax), a "steroid response" develops less frequently, but these drugs are less effective in relation to intraocular inflammation. Based on experience, instillations of nonsteroidal anti-inflammatory drugs do not play a special role in the treatment of uveitis and its complications.

Periocular administration of triamcinolone (Kenalog - 40 mg/ml) into the sub-Tenon space or transseptally through the lower eyelid can be effective in the treatment of inflammation of the anterior and posterior segments of the eye. The main disadvantage of periocular administration of glucocorticoids is a higher risk of increased intraocular pressure and cataract development in patients predisposed to the development of these complications. Therefore, patients with uveitis and ocular hypertension are not recommended to undergo periocular administration of depot glucocorticoids due to their prolonged action, which is difficult to stop.

The main method of treating uveitis is oral glucocorticoids at initial doses of 1 mg/kg per day, depending on the severity of the disease. When intraocular inflammation is controlled, systemic glucocorticoids should be gradually discontinued. If intraocular inflammation is not controlled with systemic glucocorticoids due to disease resistance or drug side effects, second-line drugs may be required: immunosuppressants or steroid replacement drugs. The most commonly used steroid replacement drugs in the treatment of uveitis are cyclosporine, methotrexate, azathioprine, and, more recently, mycophenolate mofetil. For most uveitis cases, cyclosporine is considered the most effective of these drugs, so in the absence of contraindications, it should be prescribed first. If treatment with glucocorticoids, cyclosporine, or a combination of both is ineffective or has a weak effect, other drugs should be considered. Alkylating agents, cyclophosphamide and chlorambucil are reserve drugs for the treatment of severe uveitis.

In the treatment of patients with inflammation of the anterior segment of the eye, mydriatics and cycloplegic drugs are used to reduce pain and discomfort associated with spasm of the ciliary muscle and the sphincter of the pupil. When using these drugs, the pupil dilates, effectively preventing the formation and rupturing the formed synechiae, which can lead to disruption of the flow of intraocular fluid and an increase in intraocular pressure. Usually prescribed are atropine 1%, scopolamine 0.25%, homatropine methyl bromide 2 or 5%, phenylephrine 2.5 or 10% and tropicamide 0.5 or 1%.

Drug treatment of glaucoma associated with uveitis

After appropriate treatment of intraocular inflammation, specific treatment should be instituted to control intraocular pressure. Uveitis-associated ocular hypertension and secondary glaucoma are usually treated with agents that reduce aqueous humor production. Agents used to treat uveitis-associated glaucoma include beta-blockers, carbonic anhydrase inhibitors, adrenergic agents, and hyperosmotic agents to rapidly reduce intraocular pressure when it is acutely elevated. Miotics and prostaglandin analogues should not be given to patients with uveitis because these agents may exacerbate intraocular inflammation. Adrenergic receptor antagonists are the drugs of choice for lowering intraocular pressure in patients with uveitis-associated glaucoma because they reduce aqueous humor production without changing pupillary width. The following beta blockers are usually used for uveitis: timolol 0.25 and 0.5%, betaxolol 0.25 and 0.5%, carteolol, 1 and 2%, and levobunolol. In patients suffering from sarcoidosis uveitis with lung damage, betaxolol is the safest drug - the drug with the least amount of side effects from the lungs. It has been shown that when using metipranolol, granulomatous iridocyclitis develops, so it is undesirable to use this drug in patients with uveitis.

Carbonic anhydrase inhibitors are drugs that reduce intraocular pressure by reducing the secretion of intraocular fluid. They are used topically, orally, or intravenously. It has been shown that oral administration of the carbonic anhydrase inhibitor acetazolamide (diamox) reduces cystoid macular edema, which is a common cause of decreased visual acuity in patients with uveitis. Topical administration of carbonic anhydrase inhibitors does not have this effect, probably because the drug reaches the retina in a fairly low concentration.

Of the adrenergic receptor agonists, apraclonidine is used to treat secondary glaucoma, especially in cases of a sharp rise in intraocular pressure after neodymium YAG laser capsulotomy, and brimonidine 0.2% (alphagan), an a ₂ -agonist, reduces intraocular pressure by reducing the production of intraocular fluid and increasing uveoscleral outflow. Despite the fact that epinephrine 1% and dipivefrin 0.1% reduce intraocular pressure mainly by increasing the outflow of intraocular fluid, they are currently rarely used. They also cause pupil dilation, which helps prevent the formation of synechiae in uveitis.

Prostaglandin analogues are thought to reduce intraocular pressure by increasing uveoscleral outflow. Despite their effective reduction in intraocular pressure, the use of these drugs in uveitis is controversial, as latanoprost (xalatan) has been shown to increase intraocular inflammation and cystoid macular edema.

Hyperosmotic agents rapidly reduce intraocular pressure, mainly by reducing the volume of the vitreous body, so they are effective in treating patients with uveitis with acute angle closure. Glycerol and isosorbide mononitrate are used orally, and mannitol is administered intravenously.

Cholinergic drugs such as pilocarpine, echotiaphate iodide, physostigmine and carbachol are usually not used in the treatment of patients with uveitis, since the miosis that develops with the use of these drugs promotes the formation of posterior synechiae, increases spasm of the ciliary muscle and leads to prolongation of the inflammatory reaction due to disruption of the blood-aqueous humor barrier.

[ 52 ], [ 53 ], [ 54 ]