What Medications Can Cause Glaucoma?

Dozens of commonly prescribed and over-the-counter medications can raise the pressure inside your eye or trigger structural changes that lead to glaucoma. Corticosteroids are the most widely recognized culprits, but the list extends to antihistamines, certain antidepressants, decongestants, epilepsy drugs, sulfa-based medications, and even injections used to treat eye diseases. The mechanism varies by drug class, and so does your level of risk, which depends heavily on the anatomy of your eye and, in some cases, your genetics.

Corticosteroids Are the Best-Known Offenders

If there is one drug class that eye doctors consistently warn about, it is corticosteroids. The link between steroids and elevated eye pressure was first documented in 1950, and it has been studied extensively since then.1PubMed Central. Steroid-induced Glaucoma: An Avoidable Irreversible Blindness Steroids used as eye drops, taken by mouth, inhaled for asthma, applied as skin creams, or injected around the eye can all increase intraocular pressure (IOP). Chronic use at elevated pressure levels damages the optic nerve, producing what clinicians call steroid-induced glaucoma.2PubMed. Corticosteroids and glaucoma risk

The type of glaucoma steroids cause is open-angle glaucoma, meaning the drainage angle inside the eye looks structurally normal but the fluid outflow is impaired at a microscopic level. Steroids appear to alter the cells and tissue in the eye’s drainage system, making it harder for fluid to leave. This is a slow, pressure-building process, not a sudden emergency, which is part of what makes it dangerous. You can lose vision gradually without noticing until significant damage has occurred.

Not everyone who takes a steroid will develop elevated eye pressure. Estimates suggest that roughly 30 to 50 percent of people experience some pressure rise when steroids are applied directly to the eye, while a smaller fraction develop pressures high enough to cause glaucoma.3PubMed Central. Pharmacogenomics of steroid-induced ocular hypertension: relationship to high-tension glaucomas and new pathophysiologic insight Predisposition to steroid-induced pressure rises appears to be genetically determined. Recent pharmacogenomic work has identified specific genetic variants linked to steroid-induced ocular hypertension, with most of those variants being rare or low-frequency, which may explain why the reaction seems to strike somewhat unpredictably.3PubMed Central. Pharmacogenomics of steroid-induced ocular hypertension: relationship to high-tension glaucomas and new pathophysiologic insight A separate genome-wide study identified a gene called UBE2E3 as significantly associated with steroid-induced pressure elevation, adding another piece to the genetic puzzle.4Ophthalmology Science. Genome-Wide Association Study for Glucocorticoid-Induced Ocular Hypertension

One large population-based study of older adults found that no single route of steroid use, whether eye drops, oral pills, nasal sprays, inhalers, or skin ointments, showed a statistically significant association with open-angle glaucoma when the number of prescriptions was small.5PubMed. Corticosteroids and open-angle glaucoma in the elderly: a population-based cohort study The takeaway is that short courses at moderate doses may carry less risk than chronic use, but the evidence is hard to pin down because many people use steroids only briefly. For anyone on long-term steroid therapy, routine eye-pressure checks are standard practice.

Anticholinergics and Sympathomimetics Trigger Acute Angle Closure

While steroids cause a slow-building open-angle problem, a different set of drugs can provoke a sudden, painful emergency called acute angle-closure glaucoma (AACG). This happens when the iris shifts forward and physically blocks the drainage channel, trapping fluid and causing pressure to spike within hours. The two broad drug categories most responsible are anticholinergics and adrenergic (sympathomimetic) agents.6PubMed. Iatrogenic glaucoma secondary to medications

Anticholinergic drugs dilate the pupil by relaxing the muscle that constricts it. When the pupil widens, the iris bunches up near the drainage angle and can seal it shut. This family of drugs is enormous. It includes medications for overactive bladder, motion sickness patches, some older antihistamines, certain inhaled bronchodilators, and drugs used during anesthesia. Sympathomimetic agents, which activate the “fight-or-flight” side of the nervous system, also dilate the pupil and can trigger the same blockage.7PubMed Central. Drug-induced Acute Angle-closure Glaucoma: A Review

Even ordinary nasal decongestants can be a problem. One published case describes bilateral AACG after use of over-the-counter nasal drops containing phenylephrine and naphazoline, both sympathomimetics.8Eye. Bilateral acute angle-closure glaucoma after use of Fenoxâ„¢ nasal drops Pseudoephedrine, a decongestant found in many cold medications, has also been linked to acute angle closure in epidemiological data.9JAMA Ophthalmology. Association of Drugs With Acute Angle Closure The risk is small in absolute terms, but it is real if your eye anatomy makes you vulnerable.

Antidepressants and Other Psychiatric Medications

Selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants, and some antipsychotics have anticholinergic or serotonergic properties that can dilate the pupil. A case-control study of older adults found that recent exposure to any antidepressant was associated with roughly a 60 percent increase in the odds of acute angle-closure glaucoma.10PubMed. Short-term exposure to antidepressant drugs and risk of acute angle-closure glaucoma among older adults This does not mean antidepressants are dangerous for most people, but it does explain why the warnings appear in product labeling, particularly for people with narrow drainage angles.

Serotonergic medications are specifically flagged as a trigger class for drug-induced AACG alongside anticholinergics and adrenergic agents.7PubMed Central. Drug-induced Acute Angle-closure Glaucoma: A Review The practical implication is worth knowing: if you are starting a new antidepressant and you experience sudden eye pain, blurred vision, halos around lights, or nausea, seek emergency care. Those are signs of an acute pressure spike, not just a medication side effect you can ride out.

Topiramate Causes Glaucoma Through a Unique Mechanism

Topiramate is an anticonvulsant also prescribed for migraines and, in some cases, weight management. It stands out because it triggers angle-closure glaucoma through a pathway that has nothing to do with pupil dilation. Instead, topiramate can cause the ciliary body, the tissue behind the iris that produces eye fluid, to swell. This pushes the lens and iris forward, shallowing the front chamber of the eye and closing the drainage angle.11American Journal of Ophthalmology. Topiramate-induced ciliochoroidal effusion and acute angle-closure glaucoma associated with decreased anterior chamber depth

Detailed imaging in affected patients has confirmed that the forward displacement of the lens-iris diaphragm accounts for most of the shallowing, with actual lens thickening playing a smaller role (about 20 percent of the change).12PubMed. Bilateral acute angle closure glaucoma and myopic shift by topiramate-induced ciliochoroidal effusion: case report and literature review This mechanism means that the standard emergency treatment for angle closure, a laser procedure to create a hole in the iris, often does not work for topiramate-induced cases. The iris is not the problem; the swollen ciliary body is. Stopping the drug is the primary treatment.

A telltale clue is that topiramate-induced angle closure usually comes with sudden nearsightedness. If you started topiramate recently and the world looks blurry up close or at a distance, and your eyes ache, the drug should be high on the list of suspects.

Sulfonamide Drugs and a Similar Idiosyncratic Reaction

Sulfonamide-based medications, which include certain antibiotics, diuretics like hydrochlorothiazide and acetazolamide (ironically, acetazolamide is itself used to treat glaucoma), and other drugs, can trigger a reaction resembling the topiramate mechanism. Sulfonamides can cause swelling of the ciliary body, leading to acute myopia and angle-closure glaucoma as an idiosyncratic reaction.13PubMed. Review of sulfonamide-induced acute myopia and acute bilateral angle-closure glaucoma The reaction is not dose-dependent and can happen in patients with either open or narrow drainage angles, which distinguishes it from the anticholinergic-triggered cases that require pre-existing narrow anatomy.6PubMed. Iatrogenic glaucoma secondary to medications

Because the reaction is idiosyncratic, meaning it occurs unpredictably in certain individuals regardless of dose, there is no reliable way to predict who will be affected. The good news is that it typically reverses once the sulfonamide is discontinued.

Anti-VEGF Eye Injections

Anti-VEGF drugs like ranibizumab, bevacizumab, and aflibercept are injected directly into the eye to treat conditions such as macular degeneration and diabetic eye disease. They have become one of the most frequently performed eye procedures worldwide. Each injection introduces a small volume of fluid into the eye, and that alone causes a brief, sharp pressure spike. But the concern goes beyond the immediate post-injection moment.

A meta-analysis of randomized controlled trials found that repeated anti-VEGF injections roughly tripled the risk of sustained elevated eye pressure compared with sham injections, and the risk increased with longer follow-up.14Scientific Reports. Sustained Elevation of Intraocular Pressure Associated with Intravitreal Administration of Anti-vascular Endothelial Growth Factor: A Systematic Review and Meta-Analysis The overall pooled prevalence of sustained pressure elevation in non-randomized studies was about 5 percent. Patients who already had glaucoma before starting injections faced a higher risk than those without it.

Frequency matters. A large database study found that eyes receiving 14 or more injections within two years, or 20 or more within three years, had higher odds of needing pressure-lowering therapy or receiving a new glaucoma diagnosis.15PubMed Central. Intraocular Pressure Elevation Following Intravitreal Anti-VEGF Injections: Short- and Long-term Considerations A history of glaucoma and frequent injection schedules have both been identified as risk factors for sustained pressure elevation in these patients.16Scientific Reports. Incidence of elevated intraocular pressure after intravitreal injection in Japanese patients with age-related macular degeneration If you are receiving regular anti-VEGF injections, your eye doctor should be monitoring your pressure at each visit, and that monitoring is not optional.

Who Is Most at Risk

The single biggest risk factor for drug-induced acute angle-closure glaucoma is having anatomically narrow drainage angles, and most people who have them do not know it. The angles are part of the internal architecture of the eye and cannot be seen without a special examination. Attacks tend to strike people who are completely unaware they were vulnerable.17PubMed Central. A review of drug-induced acute angle closure glaucoma for non-ophthalmologists Narrow angles are more common in people who are farsighted, in women, in older adults, and in people of East Asian descent.

For steroid-induced glaucoma, children may be especially susceptible. A study of pediatric patients on steroid therapy found that about 39 percent were classified as steroid responders, with younger age, male sex, and higher total steroid dose per body weight independently associated with a pressure rise.18PubMed Central. Risk factors of pediatric steroid-induced ocular hypertension – Section: Results Children treated with systemic steroids for leukemia or autoimmune conditions deserve close eye-pressure monitoring.

Family history of glaucoma, high degrees of nearsightedness, and a personal history of elevated eye pressure all compound the risk from any of these drug classes. If any of these apply to you, mention them to any doctor who is prescribing a new medication, not just your eye doctor.

Anesthetic Agents and Surgical Settings

Certain drugs used during general anesthesia can temporarily raise intraocular pressure. The muscle relaxant succinylcholine, used to facilitate intubation, is known to increase IOP. The spike is brief but can be clinically relevant during eye surgery or in patients with existing glaucoma. Non-depolarizing muscle relaxants, by contrast, either have no effect on pressure or slightly lower it.19PubMed. Anesthesia and intraocular pressure Ketamine is another agent that tends to raise eye pressure and is generally avoided in patients at risk.

The choice of anesthetic induction agent also matters. Propofol-based intravenous anesthesia has been shown to be more effective than volatile (inhaled) anesthesia at keeping eye pressure down during laparoscopic surgeries, where body positioning itself forces pressure upward.20PubMed Central. Attenuation of increased intraocular pressure with propofol anesthesia: A systematic review with meta-analysis and trial sequential analysis A clinical trial comparing different anesthetic combinations during laparoscopic gynecological surgery found that propofol for induction, regardless of which inhaled agent maintained anesthesia, kept pressure closest to pre-operative levels.21PubMed Central. The effect of anesthetic agents on intraocular pressure during laparoscopic gynecological surgery performed in the Trendelenburg position: A randomized clinical trial If you have glaucoma and are scheduled for surgery, your anesthesiologist should know.

When Drug-Induced Glaucoma Reverses and When It Does Not

One of the most important things to understand about drug-induced glaucoma is that many cases resolve once the offending drug is stopped. Drug-induced secondary angle closure, the type caused by topiramate, sulfonamides, and similar agents, is described as quite common and, in the majority of cases, simply stopping the medication leads to rapid reversal.22PubMed Central. Mefenamic acid-induced bilateral transient myopia, secondary angle closure glaucoma and choroidal detachment Even an anti-inflammatory painkiller like mefenamic acid has been documented to cause transient angle closure that resolved completely after discontinuation.

Steroid-induced glaucoma is a different story. If steroids are stopped early, the pressure usually returns to normal. But if elevated pressure has persisted long enough to damage the optic nerve, that damage is permanent. The nerve fibers do not regenerate. This is why steroid-induced glaucoma has been called “an avoidable irreversible blindness” when it is not caught in time.1PubMed Central. Steroid-induced Glaucoma: An Avoidable Irreversible Blindness The window between “pressure is up” and “the nerve is damaged” can be months or years, which is plenty of time to catch it with regular monitoring, but only if someone is actually checking.

Acute angle-closure attacks triggered by anticholinergics or sympathomimetics are emergencies that require immediate treatment to bring the pressure down. The outcome depends on how quickly treatment happens. A prolonged attack can permanently damage the optic nerve and the drainage system itself, converting an acute episode into chronic glaucoma. Quick intervention, usually with pressure-lowering drops, IV medications, and often a laser procedure, prevents most permanent damage.

Herbal Supplements and Glaucoma

Many people with glaucoma turn to herbal supplements, but the evidence is thin and occasionally counterintuitive. Ginkgo biloba and bilberry may have some protective effect on retinal nerve cells, but there is no evidence yet that they change the course of glaucoma.23PubMed Central. Herbal Medicines in Glaucoma Treatment Medical marijuana does lower eye pressure in some people, but the effect lasts only a few hours, which makes it impractical as a treatment. You would need to use it around the clock to maintain any benefit, and the side effects and addictive potential make that a poor trade-off compared with conventional pressure-lowering drops.

Perhaps the more pressing concern with supplements is the one people rarely think about: some herbal products can interact with glaucoma medications or dilate the pupil. Ephedra-containing supplements, for instance, are sympathomimetic and carry the same angle-closure risk as pharmaceutical decongestants. If you have glaucoma or narrow angles, treat supplements with the same caution you would give any other medication and let your eye doctor know what you are taking.

A Practical Checklist for Protecting Yourself

The sheer number of drugs that can affect eye pressure makes it unrealistic to memorize every one. A more useful approach is knowing the patterns and your own risk factors. Here are the drug classes worth being aware of:

  • Corticosteroids: Any form, any route. Risk increases with dose and duration. Demand regular pressure checks if you are on long-term steroids.
  • Anticholinergics: Overactive bladder medications (oxybutynin, tolterodine), older antihistamines (diphenhydramine), motion sickness patches (scopolamine), certain antipsychotics.
  • Sympathomimetics: Decongestants containing pseudoephedrine or phenylephrine, stimulant medications, some appetite suppressants.
  • Antidepressants: SSRIs, SNRIs, and especially tricyclics. Risk is higher in older adults with narrow angles.
  • Topiramate: Unique swelling mechanism. Watch for sudden blurred vision within the first weeks of use.
  • Sulfonamide drugs: Certain antibiotics and diuretics. Idiosyncratic and unpredictable, but usually reversible.
  • Anti-VEGF injections: Cumulative risk with frequent injections. Ongoing pressure monitoring is essential.

If you know you have narrow angles or a family history of glaucoma, tell every prescribing physician, not just your ophthalmologist. Many of the highest-risk prescriptions come from primary care doctors, psychiatrists, neurologists, and emergency departments, none of whom will automatically check your eye anatomy before writing a script. A brief note in your medical record can prevent a preventable crisis.