Glaucoma associated with uveitis

Increased intraocular pressure and the development of glaucoma in patients with uveitis is a multifactorial process that can be considered as a complication of intraocular inflammatory process. As a result of the inflammatory process, a change in the dynamics of the intraocular fluid occurs, directly or mediated by structural disorders, leading to an increase, a decrease in the intraocular pressure, or keeping it within normal values.

The lesion of the optic nerve in glaucoma and the violation of visual fields that occurs in patients with uveitis is the result of an uncontrolled increase in intraocular pressure. With the development of intraocular hypertension and glaucoma in patients with uveitis, first of all it is necessary to eliminate the inflammatory process and ensure the prevention of irreversible structural impairment of intraocular fluid outflow by conducting anti-inflammatory therapy. Then spend medical or surgical reduction of intraocular pressure.

This article discusses the pathophysiological mechanisms, diagnosis and tactics of treating patients with uveitis and increased intraocular pressure or secondary glaucoma. At the end of the article, specific uveitis is described, in which intraocular pressure increases and glaucoma develops most frequently.

The term "uveitis" in its usual sense includes all the causes of intraocular inflammation. As a result, uveitis may develop an acute, transient or chronic increase in intraocular pressure. The terms "inflammatory glaucoma" or "glaucoma associated with uveitis" are used in relation to all patients with uveitis with increased intraocular pressure. When an elevated intraocular pressure is detected without a “glaucomatous” lesion of the optic nerve or a “glaucomatous” visual field disorder, the terms “uveitis associated intraocular hypertension”, “ocular hypertension secondary to uveitis” or “secondary ocular hypertension” are more appropriate. Patients after the resolution or adequate treatment of the inflammatory process of development of secondary glaucoma do not.

The terms “inflammatory glaucoma”, “glaucoma associated with uveitis” and “secondary to uveitis glaucoma” should be used only with the development of “glaucomatous” optic nerve damage or “glaucomatous” visual field disorders with an increase in intraocular pressure in patients with uveitis. In most glaucomas associated with uveitis, damage to the optic nerve occurs due to an increase in intraocular pressure. Thus, a diagnosis of “glaucoma associated with uveitis” should be carefully made in the absence of data on prior intraocular pressure. You should also be wary of the diagnosis in patients with a lesion of the visual field that is not characteristic of glaucoma and the normal condition of the optic nerve head. 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 that are not associated with glaucoma. It is important to distinguish between the etiology of visual field disorders, because if they are associated with an active inflammatory process, they can disappear or decrease with adequate therapy, 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 proportion of uveitis per year is 15 cases per 100,000 population. Uveitis is found in patients of any age, more often seen in patients 20-40 years old. Children make up 5-10% of all patients with uveitis. The most common causes of vision loss in patients with uveitis are secondary glaucoma, cystic macular edema, cataracts, hypotension, retinal detachment, subretinal neovascularization or fibrosis and atrophy of the optic nerve.

Approximately 25% of patients with uveitis have an increase in intraocular pressure. Due to the fact that inflammation in the anterior segment of the eye can directly affect the outflow of intraocular fluid, most often intraocular hypertension and glaucoma develop as complications of anterior uveitis or panuveitis. Also, glaucoma associated with uveitis, often develops in the case of granulomatous uveitis than non-granulomatous. Given all the causes of uveitis, the incidence of secondary glaucoma in adults is 5.2-19%. The overall incidence of glaucoma in children with uveitis is about the same as in adults: 5–13.5%. The prognosis regarding the preservation of visual functions in children with secondary glaucoma is worse.

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

Causes of glaucoma associated with uveitis

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

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

[11]

Mechanisms leading to open-angle glaucoma

[12]

Disturbance of intraocular fluid secretion

When inflammation of the ciliary body usually decreases the production of intraocular fluid. While maintaining a normal outflow, the intraocular pressure decreases, which is often observed with acute urine. However, with simultaneous violation of the outflow and reduced production of intraocular fluid, the intraocular pressure may remain normal or even elevated. It is not known whether there is an increase in the production of intraocular fluid and intraocular pressure in uveitis, where there is a violation of the “blood-watery moisture” barrier. Nevertheless, the most plausible explanation for the increase in intraocular pressure in uveitis is a violation of the outflow of intraocular fluid with its unchanged secretion.

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

Intraocular fluid proteins

One of the first assumptions about the reason for the increase in intraocular pressure in uveitis was a violation of the composition of the intraocular fluid. At the initial stage, when the “blood-watery moisture” barrier is broken, proteins from the blood enter the intraocular fluid, which leads to disruption of the biochemical balance of intraocular fluid and an increase in intraocular pressure. Normally, intraocular fluid contains 100 times less protein than blood serum, and if the blood-to-moisture moisture barrier is broken, the concentration of proteins in the fluid may be the same as in undiluted blood serum. Thus, due to the increased concentration of proteins in the intraocular fluid, there is a violation of its outflow by mechanical obstruction of the trabecular meshwork and dysfunction of the endothelial cells lining the trabeculae. In addition, with a high content of proteins, the formation of posterior and peripheral anterior synechia occurs. With the normalization of the barrier, the outflow of intraocular fluid and intraocular pressure are restored. However, with an irreversible violation of the permeability of the blood-to-moisture moisture barrier, the flow of proteins into the anterior chamber of the eye can continue even after the resolution of the inflammatory process.

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

Inflammation cells

Soon after the proteins, inflammatory cells that produce inflammatory mediators begin to flow into the intraocular fluid: prostaglandins and cytokines. Inflammation cells are considered to have a more pronounced effect on intraocular pressure than proteins. The increase in intraocular pressure occurs due to infiltration of inflammatory cells of the trabecular network and Schlemm's canal, which leads to the formation of a mechanical obstacle to the outflow of intraocular fluid. Due to severe macrophage and lymphocytic infiltration, the likelihood of an increase in intraocular pressure during granulomatous is higher than with a non-granulomatous one, in which the infiltrate contains mainly polymorphonuclear cells. In chronic, severe, or recurrent damage due to damage to the endothelial cells or the formation of hyaloid membranes lining the trabeculae, irreversible damage to the trabecular network and scarring of the trabeculae and Schlemm's canal occurs. Inflammation 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

It is known that prostaglandins are involved in the formation of many symptoms of intraocular inflammation (vasodilation, miosis and increase in the permeability of the vascular wall), which in a complex can affect the level of intraocular pressure. Whether prostaglandins are able to directly increase intraocular pressure is unknown. By affecting the blood-to-aqueous moisture 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 response in the area of the trabecular network. Clinically, trabeculitis is manifested by deposition of inflammatory precipitates in the trabecular network 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 sedimentation of inflammatory cells, swelling of the trabeculae and reduction of the phagocytic activity of the endothelium cells of the trabeculae, mechanical obstruction of the trabecular network is formed and the outflow of intraocular fluid worsens. Since the production of intraocular fluid during trabeculitis, as a rule, does not decrease, due to the violation of its outflow, a significant increase in intraocular pressure occurs.

Steroid Induced Intraocular Hypertension

Glucocorticoids are considered the first choice drugs for treating patients with uveitis. It is known that with local and systemic use, as well as with periocular administration and introduction into the sub-tone space, glucocorticoids accelerate the formation of cataracts and increase intraocular pressure. Glucocorticoids inhibit the enzymes and phagocytic activity of trabecular endothelial cells, as a result of which glycosaminoglycans and inflammation products accumulate in the trabecular network, resulting in impaired outflow of intraocular fluid through the trabecular network. Glucocorticoids also inhibit prostaglandin synthesis, leading to impaired outflow of intraocular fluid.

The term “steroid-induced intraocular hypertension” and “steroid responder” are used to refer to patients in whom intraocular pressure has increased in response to treatment with glucocorticoids. It is estimated that about 5% of the population are "steroid responders", and in 20-30% of patients receiving long-term treatment with glucocorticoids, we can expect a "steroid response." The likelihood of an increase in intraocular pressure in response to glucocorticoid administration depends on the duration of treatment and dosage. In patients with glaucoma, diabetes, high myopia, and in children under the age of 10, the risk of developing a “steroid response” is higher. Steroid-induced intraocular hypertension may develop at any time after the start of taking these drugs, but more often it is detected 2-8 weeks after the start of treatment. When applied topically, the "steroid response" develops more frequently. Patients suffering from ocular hypertension should avoid periocular administration of the drug, as a sharp rise in intraocular pressure may develop. In most cases, after the cancellation of glucocorticoids, the intraocular pressure normalizes; nevertheless, in some cases, especially with the introduction of a depot of glucocorticoids, an increase in intraocular pressure can be observed for 18 months or more. In these cases, if it is impossible to control the intraocular pressure with drug, it may be necessary to remove the depots or conduct an operation to improve the outflow.

When treating glucocorticoid patients with uveitis, it is often difficult to identify 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 a result of the development of a “steroid response”, or a combination of all three causes. Similarly, a decrease in intraocular pressure during the cancellation of glucocorticoids can either prove the steroid nature of intraocular hypertension, or result from an improvement in the outflow of intraocular fluid through the trabecular meshwork or a decrease in its secretion due to the resolution of the inflammatory process. Suspicion of the development of a “steroid response” in a patient with active intraocular inflammation, requiring systemic administration of glucocorticoids, may be an indication for the prescription of steroid replacement drugs. If a 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 angular glaucoma

The morphological changes in the structures of the anterior chamber of the eye that develop in uveitis are often irreversible, leading 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 network. The structural changes that most often lead to the secondary closure of the anterior chamber angle include peripheral anterior synechiae, posterior synechiae and pupillary membranes leading to the development of the pupillary block and, rarely, rotation of the processes of the ciliary body anteriorly.

[37], [38], [39]

Peripheral Anterior Synechia

Peripheral anterior synechia - fusion of the iris with the trabecular network or cornea, which can disrupt or completely block the flow of intraocular fluid into the trabecular network. Best of all, the peripheral anterior synechiae are seen with gonioscopy. They are a frequent complication of anterior uveitis, more often develop with granulomatous than with non-granulomatous uveite. Peripheral anterior synechia are formed by organizing the products of inflammation, as a result of which the iris is pulled towards the anterior chamber angle. They often develop in the eyes with an initially narrow angle of the anterior chamber or when the angle is narrowed due to the bombardment of the iris. The adhesions are usually extensive and cover large segments of the anterior chamber angle, but they can also be in the form of a plaque or cord and involve only a small fragment of the trabecular meshwork or the cornea. During the formation of peripheral anterior synechias as a result of uveitis, despite the fact that most of the angle remains open, the patient may increase intraocular pressure due to the functionally inferior preserved part of the angle (due to the previous inflammatory process), which may not be revealed during gonioscopy.

Prolonged formation of peripheral anterior synechia with recurrent and chronic uveitis may lead to full cover of the anterior chamber angle. When closing the anterior chamber angle or the formation of pronounced peripheral anterior synechia with uveitis, one should always pay attention to possible neovascularization of the iris or anterior chamber angle. Reduction 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, with neovascular glaucoma that has developed as a result of uveitis, drug and surgical treatment is ineffective, the prognosis is poor.

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

Rear synechia

The formation of posterior synechia occurs due to the presence of inflammatory cells, proteins and fibrin in the intraocular fluid. Posterior synechia - adhesions of the posterior surface of the iris with the anterior capsule of the lens, the vitreous surface with aphakia or with the intraocular lens with arthifakia. The likelihood of developing back synechiae depends on the type, duration and severity of uveitis. With granulomatous, posterior synechiae form more often than with non-granulomatous. The greater the length of the posterior synechia, the worse the dilation of the pupil occurs and the greater the risk of the subsequent formation of posterior synechia with recurrences of uveitis.

The term "pupillary block" is used to refer to a violation as a result of the formation of the posterior synechias of intraocular fluid from the back to the anterior chamber of the eye through the pupil. The formation of a seclusio pupillae, posterior synechia over a 360 ° circumference of the pupil and pupillary membranes can lead to the development of a full pupillary block. In this case, the current of intraocular fluid from the back of the camera to the front completely stopped. Excess intraocular fluid in the posterior chamber can lead to bombardment of the iris or to a significant increase in intraocular pressure. As a result, the iris bends towards the anterior chamber. Iris bombing with continued inflammation leads to rapid closure of the angle due to the formation of peripheral anterior synechia, even if the anterior chamber angle was initially open. In some cases, when uveitis with the pupillary block, wide adhesions form between the iris and the anterior capsule of the lens, then only the peripheral part of the iris bends anteriorly. In this situation, it is quite difficult to detect the bombardment of the iris without the help of gonioscopy.

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

Rotation of the ciliary body anteriorly

In acute intraocular inflammation, edema of the ciliary body with supraciliary or suprahoroidal effusion may develop, resulting in rotation of the ciliary body anteriorly and closure of the anterior chamber angle, which is not associated with the pupillary block. An increase in intraocular pressure due to such a closure of the anterior chamber angle often develops with iridocyclitis, circular detachment of chorus, posterior sclerite and in the acute stage of Vogt-Koyanagi-Harada syndrome.

[50],

Uveitis most commonly associated with secondary glaucoma

Anterior uveitis

• Juvenile rheumatoid arthritis
• Heterochrome uveitis Fuchs
• Glauco-cyclic crisis (Posner-Schlossman syndrome)
• HLA B27-associated uveitis (ankylosing spondylitis, Reiter syndrome, psoriatic arthritis)
• Herpetic uveitis
• Uveitis associated with the lens (phacoantigenic uveitis, phacolytic glaucoma, lens mass, phacomorphic glaucoma)

Panuveits

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

Mean uveitis

• Partial Uveitis Average

Posterior uveitis

• Acute retinal necrosis
• Toxoplasmosis

Diagnosis of glaucoma associated with uveitis

The correct diagnosis and management of patients suffering from glaucoma due to uveitis is based on a complete ophthalmologic examination and the correct use of auxiliary methods. To determine the type of uveitis, the activity of the inflammatory process and the type of inflammatory response, a slit lamp is used. Depending on the location of the primary focus of inflammation, anterior, middle, posterior uveitis and panuveitis are distinguished.

The likelihood of developing glaucoma associated with uveitis is higher with anterior uveite and panuveitis (with intraocular inflammation, the likelihood of damage to the structures ensuring 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 and the degree of turbidity. Attention should also be paid to structural changes caused by the inflammatory process (peripheral anterior and posterior synechia).

The inflammatory reaction in uveitis is granulomatous and non-granulomatous. Signs of granulomatous uveitis: greasy precipitates on the cornea and nodules on the iris. With granulomatous wipe more often than with non-granulomatous, secondary glaucoma develops.

Gonioscopy is the most important method of ophthalmologic examination of patients with uveitis with elevated IOP. The study should be carried out using a lens that presses the central part of the cornea, as a result of which the intraocular fluid enters the anterior chamber angle. When gonioscopy revealed the products of inflammation, peripheral anterior synechia and vascular in the anterior chamber angle, which allows to distinguish between open-and close-angle glaucoma.

When examining the fundus particular attention should be paid to the state of the optic nerve. In particular, the magnitude of the excavation, the presence of hemorrhage, edema or hyperemia, also assess the condition of the nerve fiber layer. A diagnosis of glaucoma associated with uveitis should be made only if there is documented damage to the optic nerve head and visual field impairment. Despite the fact that retinal and choroidal foci 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 visual field disorder associated with them can lead to an erroneous diagnosis of glaucoma. At each inspection, applanation tonometry and standard perimetry should be performed. Additionally, you can use laser photometry of intraocular fluid opalescence and ultrasound examination of the eye in order to more accurately diagnose and manage patients with uveitis and increased intraocular pressure. Laser photometry of opalescence makes it possible to detect subtle changes in opalescence and protein content in the intraocular fluid, which cannot be done with a slit lamp. It was shown that subtle changes allow us to estimate the activity of uveitis. Ultrasound examination in B-scan mode and ultrasound biomicroscopy in secondary glaucoma allow to evaluate the structure of the ciliary body and iridociliary angle, which helps to identify the cause of increased or excessive reduction in intraocular pressure in patients with uveitis.

[51]

Treatment of glaucoma associated with uveitis

The main task of treating patients with uveitis associated with intraocular hypertension or glaucoma is to control intraocular inflammation and prevent the development of irreversible structural changes in the eye tissues. In some cases, the resolution of the intraocular inflammatory process with only anti-inflammatory therapy leads to the normalization of intraocular pressure. With the early start of anti-inflammatory treatment and with the provision of mydriasis and cycloplegia, the development of irreversible effects of uveitis (peripheral anterior and posterior synechiae) can be prevented.

The first choice drugs for most uveitis are glucocorticoids used in the form of installations, periocular and systemic injections, subtenone injections. Glucocorticoid instillations are effective in inflammation of the anterior segment of the eye, but with active inflammation of the posterior segment in the phakic eyes of the instillation alone there is little. The frequency of instillation of glucocorticoids depends on the severity of anterior segment inflammation. Most effective in the inflammation of the anterior segment of the eye is prednisone (pred-forte) in the form of eye drops. On the other hand, the use of this drug most often leads to the development of steroid-induced ocular hypertension and posterior subcapsular cataracts. When using weaker glucocorticoids in the form of eye drops, for example, rimexolone, fluorometholone, medrizone, loteprednola, etabonata (lotemax), the "steroid response" is less common, but these drugs are less effective against intraocular inflammation. Based on experience, instillation of nonsteroidal anti-inflammatory drugs does not play a special role in the treatment of uveitis and its complications.

Periocular administration of triamcinolone (Kenalog - 40 mg / ml) into the subtenone 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 the development of cataracts in patients prone to the development of these complications. Therefore, patients with uveitis and ocular hypertension are not recommended to undergo periocular depot glucocorticoid administration due to their prolonged action, which is difficult to stop.

The main method of treating uveitis is ingestion of glucocorticoids in initial doses of 1 mg / kg per day, depending on the severity of the disease. When controlling intraocular inflammation, systemic administration of glucocorticoids should be gradually abolished. If the systemic use of glucocorticoids does not control intraocular inflammation due to the resistance of the disease or the side effects of the drug, then you may need to prescribe second choice drugs: immunosuppressants or steroid replacement drugs. Steroids replacing drugs most commonly used in the treatment of uveitis are cyclosporine, methotrexate, azathioprine, and more recently mycophenolate mofetil. With most uveitis, cyclosporine is considered the most effective of these drugs, so if there are no contraindications, it should be prescribed first. In the absence or weak effect of treatment with glucocorticoids, cyclosporine, or their combination, other drugs should be taken into account. Alkylating agents, cyclophosphamide and chlorambucil are reserve drugs for the treatment of severe uveitis.

When treating patients with inflammation of the anterior segment of the eye, mydriatics and cycloplegic drugs are used to reduce the pain and discomfort associated with spasm of the ciliary muscle and the sphincter of the pupil. When these drugs are used, the pupil expands, effectively prevents the formation and rupture of the formed synechiae, which can lead to disruption of the current of the intraocular fluid and an increase in intraocular pressure. Atropine 1%, scopolamine 0.25%, gomatropine methyl bromide 2 or 5%, phenylephrine 2.5 or 10%, and tropicamide 0.5 or 1% are usually prescribed.

Drug treatment of glaucoma associated with uveitis

After appropriate treatment of intraocular inflammation, specific treatment should be prescribed to control intraocular pressure. Usually, in cases of ocular hypertension and secondary glaucoma associated with uveitis, drugs that reduce the production of intraocular fluid are prescribed. Drugs used to treat glaucoma associated with uveitis include beta-blockers, carbonic anhydrase inhibitors, adrenergic drugs, and hyperosmotic agents for rapidly reducing intraocular pressure during acute increases. You should not assign miotics and prostaglandin analogues to patients with uveitis, since these drugs can lead to an exacerbation of the intraocular inflammatory process. The drugs of choice for reducing intraocular pressure in patients suffering from glaucoma due to uveitis are adrenergic receptor antagonists, since these drugs reduce the secretion of intraocular fluid without changing the width of the pupil. Usually, the following beta-blockers are used in uveitis: timolol 0.25 and 0.5%, betaxolol 0.25 and 0.5% carteolol, 1 and 2%, and levobunolol. In patients suffering from sarcoid uveitis with lung lesions, betaxolol is the safest method of taking the drug with the least amount of side effects from the lung. Granulomatous iridocyclitis has been shown to occur when metipranolol is used, therefore the use of this drug in patients with uveitis is undesirable.

Carboanhydrase inhibitors - drugs that reduce intraocular pressure by reducing the secretion of intraocular fluid - are applied topically, by mouth or intravenously. It has been shown that cytosal macular edema, which is a common cause of reduced visual acuity in patients with uveitis, is reduced by the intake of the acetazolamide carbonic anhydrase inhibitor (diamox). With the local application of carbonic anhydrase inhibitors, there is no such effect, probably due to the fact that the drug is delivered to the retina in a fairly low concentration.

Of the adrenergic receptor agonists, apraclonidine is used for the treatment of secondary glaucoma, especially with a sharp rise in intraocular pressure after neodymium with YAG-laser capsulotomy, and brimonidine 0.2% (alfagan) - and ₂ -agonist - reduces intraocular pressure by reducing intraocular fluid and increasing uveosclerosis. Outflow. Despite the fact that epinephrine 1% and dipivefrin 0.1% reduce intraocular pressure mainly due to increased outflow of intraocular fluid, is now rarely used. They also cause pupil dilation, which helps prevent the formation of synechia in uveitis.

It is believed that prostaglandin analogues reduce intraocular pressure by increasing uveoscleral outflow. Despite the effective reduction of intraocular pressure, the use of drugs of this group in uveitis is controversial, since it has been shown that latanoprost (xalatan) increases intraocular inflammation and cystic macular edema.

Hyperosmotic drugs quickly reduce intraocular pressure, mainly due to a decrease in the volume of the vitreous body, so they are effective in treating patients with uveitis with acute closure of the anterior chamber angle. Glycerol and isosorbide mononitrate is administered orally, and mannitol is administered intravenously.

Usually, when treating patients with uveitis, cholinergic drugs, for example, pilocarpine, echothiafata iodide. Physostigmine and carbachol are not used, since the miosis that develops with the use of these drugs contributes to the formation of posterior synechiae, increases the spasm of the ciliary muscle and leads to a prolongation of the inflammatory reaction due to the violation of the blood-aqueous humor barrier.

[52], [53], [54]