Ocular Complications and Side Effects of Topical Steroid Eye Drops

Corticosteroids are important therapeutic agents that are used to treat ocular inflammation. Their complications are related to dosage and duration of therapy because usually, no serious adverse effect is observed
with short term therapy and lower dosage. The adverse effects are produced by prolonged topical or systemic steroid therapy.

The following ocular complications are usually observed in prolonged use of topical steroids.

Dermatitis

Periocular dermatitis resulting from long term use of fluorinated steroid drops or ointments have been reported. This dermatitis is similar to perioral (mouth) dermatitis and should not be confused with allergic contact dermatitis.

Delayed Wound Healing

Corneal would healing may be inhibited by proliferation of fibroblasts and new vessels.

Infection and Ulceration

Inappropriate use of topical steroids by patient and registered medical practitioners lead to infectious keratitis specially, herpetic keratitis. Reactivation of herpes simplex virus in patients who have undergone penetrating keratoplasty is specially common in patients who were previously treated with steroid antibiotic combination.

Steroid-Induced Cataracts

Posterior subcapsular cataract has been shown to occur after prolonged treatment with steroid drops and ointments. The pathophysiology of steroid induced cataract formation is by mechanism affecting water transport by increasing cation influx which leads to excess water in cells. This causes intumescence of the cells and disparity of refractive index from the surrounding medium. The steroids also bind to specific amino acids groups within the lens cell fibers. These combined factors are responsible for the lost of lens transparency. Once visual impairment has taken place, complete resolution of lenticular opacification cannot be expected.

Steroid-Induced Glaucoma

Prolonged use of corticosteroids may cause an elevation of intraocular pressure leading to optic nerve damage and visual field restriction (Changes synonymous with chronic open angle glaucoma). Intraocular pressure elevation can occur within days of starting therapy or it can occur months later. Patients with myopia greater than five diopters or a history of glaucoma are more susceptible to this complication.

The mechanism includes accumulation of glycosaminoglycans or an increase in debris in the trabecular meshwork due to inhibition of phagocytosis. The frequency and severity of intraocular pressure rise is greater with topical application than with systemic administration.

The patient is usually asymptomatic unless the intraocular pressure increases enough to cause corneal edema (Decreased vision, halos, pain, or photophobia). Clinical signs of prolonged elevation of intraocular pressure include optic nerve cupping and visual field defects.

Steroid induced intraocular pressure elevations almost always respond within days to weeks of stopping the steroids. It is not always possible to abruptly stop steroids because of underlying ocular condition being treated.

It is important to note that although most patients will respond to hypotensive agents, the hypertensive effect can occur in susceptible individuals who are already on hypotensive agents when steroids are added for either ocular or systemic diseases. In those patients in whom hypotensive agents are unable to control intraocular pressure in steroid induced glaucoma, Argon laser trabeculoplasty and glaucoma filtering surgery are necessary treatment modalities.

Systemic steroids on the other hand affect patients in many ways. The classical clinical triad that contributes to the moon-face appearance of some patients using systemic steroids comprises ptosis, chemosis and swelling of the periorbital tissues.

Eye doctors should monitor all patients on steroids, no matter what preparation or initial intraocular pressure, they should watch for any increase in intraocular pressure.