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.
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