Steroid-induced glaucoma: causes, symptoms, diagnosis, treatment

Secondary open-angle glaucoma can develop in almost any mode of administration of glucocorticoid drugs.

Elevation of intraocular pressure can be pronounced and prolonged.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11]

Epidemiology of steroid-induced glaucoma

The incidence of steroid-induced glaucoma in the general population is unknown. A significant increase in intraocular pressure with topical application of glucocorticoids was noted in 50-90% of patients with glaucoma and in 5-10% of patients with normal intraocular pressure. The frequency of development of such a reaction to the administration of glucocorticoids depends on the type, dose and route of administration of the drug. Increase in intraocular pressure is noted at local, nitraocular, periocular, inhalation, oral, intravenous and transdermal administration, as well as with endogenous increase in glucocorticoids in Cushing syndrome.

[12], [13], [14], [15], [16], [17]

Pathophysiology of steroid-induced glaucoma

In response to the introduction of glucocorticoids, there is an increase in the number of glycosaminoglycans in the trabecular network, which prevents a normal outflow of intraocular fluid and leads to an increase in intraocular pressure. Glucocorticoids also reduce the permeability of membranes of the trabecular network, the phagocytic activity of cells, cause the decay of extracellular and intercellular structural proteins, which leads to a further decrease in the permeability of the trabecular network. It was shown that in response to the introduction of glucocorticoids, the activation of the myocillin / TIGR gene (steroid-induced response of the trabecular network) occurs in the endothelial cells of the trabecular network. The association of the gene with glaucoma and steroid-induced increase in intraocular pressure has not yet been revealed.

Symptoms of steroid-induced glaucoma

The main fact in the anamnesis is the use of glucocorticoids in any form. The use of glucocorticoids in the distant past with the subsequent normalization of intraocular pressure can lead to the development of a typical normal pressure glaucoma. The presence of asthma, skin diseases, allergies, autoimmune diseases and similar conditions in an anamnesis indicates the possible use of glucocorticoids. Sometimes patients note a change in the quality of vision associated with a pronounced narrowing of the visual fields.

Diagnosis of steroid-induced glaucoma

Biomicroscopy

Usually, nothing is found. Even in the case of very high intraocular pressure due to a chronic process, edema of the cornea does not occur.

Gonioscopy

Usually, nothing is found.

Rear Pole

In the case of a significant and prolonged increase in intraocular pressure, the changes in the optic nerve characteristic for glaucoma are revealed.

Special researches

The elimination of glucocorticoids, if possible, leads to a steady decrease in intraocular pressure. The time required to reduce intraocular pressure is different and can be very long in cases of prolonged intake of glucocorticoids. If it is not possible to cancel the topical application of glucocorticoids (for example, at the risk of corneal transplant rejection), the steroid damage of the second eye may be manifested by increased intraocular pressure, which confirms the diagnosis.

[18], [19]

Treatment of steroid-induced glaucoma

With the elimination of glucocorticoids, complete recovery is possible. With topical application of drugs, it may be useful to switch to weaker glucocorticoids that increase intraocular pressure to a lesser degree (for example, loteprednol, rimexolone, fluorometholone). Patients with severe uveitis require special attention, since the treatment may require the use of glucocorticoids. In addition, uveitis can lead to the development of various forms of glaucoma or to mask glaucoma with a decrease in the secretion of intraocular fluid.

Treatment of steroid-induced glaucoma

Day after surgery	Intraocular pressure (mmHg)	Treatment Scheme
Operation number 1. Vitrectomy / membranectomy, subconjunctival injection of glucocorticoid depot
1	25	Prednisolone, scopolamine, erythromycin
6th	45	Timolol, yopidine, acetazolamide
16	20	Canceled acetazolamide
Thirty	29	Dorsolamide was added, a gradual withdrawal of prednisolone
48	19	Abolition of prednisolone
72	27th	Continue the appointment of timolol, apraklonidine, dorzolamide
118	44	Added latanoprost; appointment for glaucoma
154	31	The purpose of removing depot glucocorticoids
Operation number 2. Deletion of glucocorticoids
1	32	Timolol, dorzolamide
4	28	The same
23	24	The same
38	14	Abolition of dorzolamide

Note. Later, the patient discontinued the use of timolol; Since the withdrawal of the drug, intraocular pressure remained at the level of 10-14 mm Hg.

Usually, with steroid-induced increased intraocular pressure, local antiglaucoma drugs of all types are effective. In general, laser trabeculoplasty is less effective in these patients than in patients with other types of glaucoma. The results of operations aimed at increasing filtration are the same as for primary open-angle glaucoma.