Steroid-induced glaucoma (SIG) is an elevation of pressure inside the eye following the use of corticosteroids, whether administered as eye drops, inhaled, or taken systemically. This condition, also known as steroid-induced ocular hypertension, presents a serious risk because sustained high intraocular pressure (IOP) can damage the optic nerve. The pressure increase itself is often reversible upon stopping the steroid. However, the resulting damage to the optic nerve—the true definition of glaucoma—is permanent once it occurs.
The Mechanism of Steroid-Induced Intraocular Pressure Elevation
The rise in eye pressure is primarily caused by increased resistance to the outflow of the eye’s internal fluid, known as aqueous humor. This fluid normally drains through the trabecular meshwork, which acts like a filter. Corticosteroids interfere with the function of cells within this meshwork, causing structural and molecular changes that clog the drainage system. They promote the accumulation of extracellular matrix proteins, which thicken the meshwork tissue. This buildup prevents the fluid from draining efficiently, leading to a spike in intraocular pressure.
Not everyone who uses steroids will experience this effect; only a subset of the population is susceptible, known as “steroid responders.” About one-third of individuals may experience a moderate pressure rise, while 5% to 6% are considered high responders, showing a significant elevation. Individuals with pre-existing primary open-angle glaucoma have an even higher likelihood of experiencing a marked pressure spike. The elevation in IOP typically manifests a few weeks after starting steroid eye drops, though it can occur earlier in highly susceptible individuals. The most common forms of SIG are caused by topical administration, such as eye drops, representing about 75% of cases.
Factors Determining Irreversible Optic Nerve Damage
The most important distinction is that a steroid-induced pressure spike, or ocular hypertension, is not the same as steroid-induced glaucoma. Glaucoma involves irreversible damage to the optic nerve fibers, resulting in vision loss that cannot be recovered. The permanence of the damage is determined by three main factors: the magnitude of the pressure spike, the duration of the elevation, and the health of the individual’s optic nerve. A higher pressure over a shorter period can be just as damaging as a moderate elevation sustained over many months. If the pressure is detected and lowered quickly, the optic nerve may be protected, limiting the condition to a temporary pressure problem.
Pre-existing risk factors significantly increase the likelihood of progressing to permanent damage. Vulnerable individuals include those with a prior diagnosis of primary open-angle glaucoma, a family history of the disease, high myopia, or certain connective tissue disorders. Children, particularly those under six years of age, are also greater steroid responders and are at high risk for rapid, severe IOP elevation. In the majority of cases, once the causative steroid is discontinued, the intraocular pressure begins to return to normal levels within one to four weeks. However, in a small percentage of cases, the pressure elevation may persist, requiring ongoing medical intervention to prevent permanent optic nerve atrophy.
Management and Treatment Protocols
The primary and most effective step in managing SIG is the immediate cessation or significant reduction of the corticosteroid medication, provided the underlying medical condition allows it. If the steroid is necessary, the physician may attempt to switch to a less potent formulation, such as fluorometholone or loteprednol, which carry a lower risk of increasing eye pressure. If discontinuing the steroid is not possible or if the pressure remains dangerously high, medical management is instituted to lower the intraocular pressure using topical anti-glaucoma eye drops.
First-line medications either increase fluid outflow or decrease its production.
Medications
- Prostaglandin analogs.
- Beta-blockers.
- Carbonic anhydrase inhibitors.
When medications alone are insufficient, or if there is evidence of progressive optic nerve damage, laser or surgical treatments are considered. Selective Laser Trabeculoplasty (SLT) can be used to improve the drainage function of the trabecular meshwork.
For severe or refractory cases where medical and laser therapies fail, incisional glaucoma surgery may be required. Procedures include a trabeculectomy or the placement of a glaucoma drainage device to create a new drainage pathway for the aqueous humor. Patients who have experienced a steroid-induced pressure response require long-term monitoring of their IOP, optic nerve health, and visual fields. This vigilance is necessary because a history of steroid response suggests a higher risk of developing primary open-angle glaucoma later in life.