What Medications Increase Eye Pressure?

Dozens of commonly prescribed and over-the-counter medications can raise the pressure inside your eyes, sometimes dramatically enough to damage the optic nerve and threaten vision. Corticosteroids are the most well-known culprits, but the list extends to antidepressants, cold remedies, ADHD drugs, certain seizure medications, and more. The way each drug raises pressure differs, and so does the level of risk it carries for any given person.

Corticosteroids Are the Single Biggest Offender

If one drug class dominates conversations about eye pressure, it is corticosteroids. The connection was first documented in 1950, when researchers noticed that long-term systemic steroid use could push intraocular pressure (IOP) upward. Since then, the link has been confirmed across every route of administration: eye drops, oral pills, injections, inhaled formulations, and even skin creams applied near the eyes.¹ Steroid eye drops carry the highest risk because the drug arrives directly at the structures that regulate fluid drainage, but any form of steroid can do it if the dose is high enough or the duration is long enough.

Steroids raise eye pressure by interfering with the meshwork of tiny drainage channels inside the eye. The tissue in that meshwork swells, debris accumulates, and fluid that normally flows out gets backed up. When the pressure stays elevated for weeks or months without treatment, it can damage the optic nerve in the same way primary glaucoma does. Chronic, unmonitored steroid use in any form can cause optic nerve damage resulting in what clinicians call steroid-induced glaucoma.¹ The problem is especially insidious with over-the-counter steroid eye drops, which are available without a prescription in some countries, because people use them for weeks without any pressure monitoring.

Glucocorticoids are also the primary drug class responsible for worsening open-angle glaucoma, the most common form of the disease.² This matters practically because many people already have mild open-angle glaucoma and do not know it. Adding a steroid, even a short course of oral prednisone for a flare of asthma or poison ivy, can tip the balance.

Anticholinergic Drugs and the Pupil-Dilation Problem

A large family of medications raises eye pressure through a completely different route than steroids. Instead of clogging the drainage system, these drugs dilate the pupil, and the physical act of the iris widening can block the narrow drainage angle in susceptible eyes. The first mechanism of drug-induced acute angle-closure glaucoma is this kind of pupillary block: the iris thickens at its base as the pupil widens, physically pushing against the drainage angle and sealing it shut.³

The drugs most likely to cause this are those with anticholinergic activity, meaning they block the neurotransmitter acetylcholine. That category is surprisingly broad. It includes:

• Bladder medications: oxybutynin, tolterodine, and similar overactive-bladder drugs
• Older antihistamines: diphenhydramine (Benadryl), chlorpheniramine
• Tricyclic antidepressants: amitriptyline, nortriptyline
• Antipsychotics: older drugs like chlorpromazine, but also some newer ones
• Anti-nausea drugs: scopolamine patches used for motion sickness
• Some muscle relaxants: cyclobenzaprine

Not everyone who takes one of these drugs will have a problem. The risk is concentrated in people with anatomically narrow drainage angles, a physical trait that is more common in older adults, women, and people of East Asian descent. In someone with wide-open angles, the same drug causes no trouble at all. Several types of drugs have the potential to precipitate acute angle-closure glaucoma, including adrenergic, cholinergic, anticholinergic, antidepressant, anticoagulant, and sulfa-based agents, but anatomical predisposition is the key variable.⁴

Antidepressants and Eye Pressure

The relationship between antidepressants and eye pressure is more complicated than a simple “they raise it.” SSRIs like fluoxetine, sertraline, and escitalopram have been linked to glaucoma in population-level studies. A large nationwide study found that people exposed to SSRIs had roughly a 28 percent higher odds of glaucoma after adjusting for other risk factors, and the risk increased with higher doses and longer use.⁵ People who used SSRIs for more than a year at higher doses had the steepest increase in risk.

Here is where the story gets counterintuitive. A meta-analysis that pooled data from clinical studies actually found that people taking SSRIs and SNRIs had lower measured IOP, not higher, compared to unexposed controls.⁶ At the same time, those antidepressant users had larger pupils. The implication is that SSRIs may not raise the steady-state pressure reading you get in a doctor’s office, but the pupil dilation they cause can trigger acute angle-closure episodes in people with narrow drainage angles. The antidepressant-associated risk of acute angle closure is thought to come from mydriasis induced by anticholinergic and adrenergic effects, as well as increases in serotonin levels; uveal effusion is also a possible mechanism.⁷ Case reports have also described acute attacks of glaucoma occurring during SSRI treatment, and a small clinical study showed that a single dose of fluoxetine increased IOP, though the effect was asymptomatic.⁸

Anxiolytics like alprazolam may also induce pupil dilation through anticholinergic effects, adding another drug class to the list of potential triggers.⁷ The practical takeaway is that if you have narrow angles and are starting an antidepressant or anti-anxiety medication, your eye doctor should know about it.

Sulfa-Based Drugs and Topiramate

Sulfa-derived medications raise eye pressure through yet another mechanism. Rather than dilating the pupil, certain sulfa drugs cause the ciliary body (the tissue behind the iris that produces eye fluid) to swell. That swelling pushes the lens and iris forward, physically narrowing or closing the drainage angle. This produces a bilateral, non-pupillary-block type of angle closure that can affect both eyes simultaneously and happens in people with either narrow or open angles.⁹ The forward displacement of the lens-iris diaphragm is the hallmark, and it distinguishes this kind of crisis from the pupil-block mechanism caused by anticholinergics.

Topiramate, a seizure and migraine-prevention drug, is the most notorious example. It can cause ciliochoroidal effusion, pushing the lens and iris forward and shallowing the front chamber of the eye, which leads to sudden-onset nearsightedness and acute angle-closure glaucoma.¹⁰ If you start topiramate and within the first few weeks notice that your distance vision has gone blurry and your eyes ache, that combination of symptoms should prompt an urgent eye exam. The good news is that stopping the drug usually reverses the process quickly.

Other sulfa-based drugs can cause the same ciliary-body swelling.¹¹ Acetazolamide, ironically used to treat glaucoma, is itself a sulfonamide, though it very rarely triggers this reaction. Hydrochlorothiazide, a common blood-pressure pill, is another sulfa-derived drug that has appeared in case reports of angle closure.

Cold Medicine and Other Over-the-Counter Products

Some of the most accessible medications on pharmacy shelves can push eye pressure to dangerous levels in the wrong person. Oral decongestants containing pseudoephedrine or phenylephrine are adrenergic agonists, meaning they stimulate the same receptors that dilate the pupil. Paired with the older antihistamines found in many combination cold products, the pupil-dilating effect is amplified. A reported case involved a 42-year-old woman with no eye or medical history who developed bilateral acute angle-closure glaucoma after five days of taking pseudoephedrine and chlorpheniramine for a common cold, with her pressures measured at 37 and 39 mmHg.¹² Normal eye pressure sits between about 10 and 21 mmHg, so those readings were nearly double the upper limit.

This is one reason you see fine-print warnings about glaucoma on the back of cold-medicine boxes. The risk, again, is primarily in people with narrow angles. But because most people have never had their angle anatomy checked, they have no way of knowing whether they are susceptible. If you have a family history of angle-closure glaucoma or have been told your angles are narrow, treat over-the-counter cold products with caution and ask your pharmacist about alternatives.

ADHD Medications

Stimulant and non-stimulant medications for ADHD have drawn increasing attention for their potential effects on eye pressure. A population-based study found that regular users of atomoxetine and amphetamines had a roughly two- to two-and-a-half times higher rate of developing angle-closure glaucoma compared to non-users, while regular methylphenidate users showed a more modest increase in the rate of open-angle glaucoma.¹³ These are relative risk numbers, not absolute ones, so the overall number of people affected is still small. But the signal is strong enough to warrant attention, particularly for amphetamine-based drugs whose adrenergic activity can dilate the pupil.

One reassuring piece of context: a study of children with ADHD found no significant differences in IOP, refraction, or corneal parameters between methylphenidate-treated patients, drug-naïve patients, and healthy controls.¹⁴ That study measured structural eye parameters at a single time point, not long-term glaucoma outcomes, but it suggests that short-to-medium-term methylphenidate use does not obviously change eye pressure in children. The population-level glaucoma risk observed with stimulants may take years to manifest or may affect primarily adults with pre-existing anatomical vulnerability.

Inhaled Respiratory Medications

People with asthma or chronic obstructive pulmonary disease (COPD) often use two types of inhaled drugs: corticosteroids and bronchodilators. You might expect inhaled corticosteroids to raise eye pressure the way systemic steroids do, but the evidence is mixed. One study of patients with chronic pulmonary disease found that inhaled or nebulized corticosteroids had no measurable effect on IOP.¹⁵ The dose reaching the eye from an inhaler is far lower than from drops or pills, which likely explains why the pressure effect is minimal in most people.

The anticholinergic bronchodilators are a different story. Tiotropium, commonly prescribed for COPD, was shown to increase eye pressure, enlarge pupil diameter, and narrow the drainage angle after three months of treatment.¹⁶ The drug works by blocking acetylcholine in the airways, but it can also reach the eye, particularly if the inhaler’s mist drifts toward the face, which is common with nebulized forms. Older COPD patients are already at higher baseline risk for narrow angles, so the combination of age-related anatomical changes and an anticholinergic bronchodilator can be a meaningful concern.

Cancer Treatment Drugs

Some drugs used in cancer therapy can raise eye pressure indirectly. Corticosteroids are a cornerstone of many chemotherapy regimens, used both to manage side effects and as direct anti-cancer agents. Beyond steroids, immune checkpoint inhibitors, a newer class of cancer drugs, can induce uveitis, an inflammatory reaction inside the eye that may in turn raise IOP.¹⁷ This connection underscores the importance of eye monitoring for patients undergoing immunotherapy, especially those receiving high-dose steroids alongside checkpoint inhibitors.

The Ketamine Myth

For decades, medical training taught that ketamine raises eye pressure, making it dangerous for patients with eye injuries or glaucoma. This belief influenced emergency-room decisions, sometimes leading doctors to avoid sedating a child with ketamine before a painful procedure if there was any concern about the eyes. The evidence, however, does not support the idea. A study measuring IOP at multiple time points during ketamine sedation found no clinically meaningful or statistically significant changes in pressure. The largest predicted change from baseline was about 1 mmHg at the 15-minute mark, and at no point did any patient reach a pressure level considered elevated.¹⁸ One clinical trial in pediatric strabismus surgery also showed that when esketamine was combined with propofol, IOP actually dropped from baseline in all groups, and only at the highest esketamine dose was a slightly higher post-induction pressure seen compared to lower-dose and control groups.¹⁹ If you have been told to avoid ketamine because of eye pressure, the current evidence suggests that concern is overblown.

Children and Steroid Sensitivity

Children appear to be especially sensitive to steroid-induced eye pressure elevation. In a study of children receiving systemic glucocorticoids, over half developed a steroid-induced ocular hypertensive response, and about 12 percent were high responders whose IOP climbed to between 32 and 44 mmHg, with net increases of 15 to 23 mmHg above baseline. Steroid responders were significantly younger than non-responders.²⁰ Those are dramatic numbers. A child whose baseline pressure is 15 mmHg reaching 38 mmHg is well into the danger zone.

This has practical implications for parents and pediatricians. Children prescribed systemic steroids for conditions like nephrotic syndrome, severe asthma, or autoimmune diseases may need periodic eye-pressure checks, especially younger children who seem to be the most reactive. The pressure typically comes back down after the steroid is tapered, but prolonged courses without monitoring can lead to irreversible optic nerve damage.

Why Anatomy Matters More Than the Drug

A recurring theme across most of these medications is that your individual anatomy determines your risk far more than the drug itself does. For every drug that triggers angle closure through pupil dilation, whether it is an antihistamine, an antidepressant, a decongestant, or an ADHD medication, the necessary precondition is narrow drainage angles. People with wide-open angles take these drugs every day without any rise in pressure. The drug is the trigger, but the anatomy is the loaded gun.

Steroids are the notable exception. They can raise pressure in anyone by directly altering the drainage tissue, regardless of angle anatomy. The degree of response varies person to person (some people are “steroid responders” and others are not), but steroid-induced pressure elevation is not limited to narrow-angle anatomy the way most other drug-induced elevations are.

Electronic health records could theoretically be used to flag patients with known narrow-angle risk factors, like family history or farsightedness, before prescribing medications known to precipitate angle-closure crises.²¹ That kind of automated screening is not yet standard practice in most health systems, which means the responsibility still falls on you to mention any history of glaucoma or narrow angles to every prescribing doctor, not just your eye doctor.

When Drug-Induced Pressure Is Reversible

The encouraging reality is that most drug-induced eye-pressure increases go away once the offending medication is stopped. Topiramate-induced angle closure typically resolves within days of discontinuation. Anticholinergic-triggered episodes can be broken with standard glaucoma emergency treatments and then prevented by switching to a different drug. Steroid-induced pressure rises also usually reverse when the steroid is tapered, though the timeline depends on how long the steroid was used and how high the pressure climbed.

The exceptions are situations where the elevated pressure has gone undetected for a long time. Optic nerve damage from sustained high pressure does not reverse. A person who uses steroid eye drops for months without monitoring, or who has repeated unrecognized angle-closure episodes triggered by a medication, can develop permanent visual field loss. The pressure itself is fixable; the nerve damage it causes is not.

If you take any of the medications discussed here and have not had a comprehensive eye exam that includes angle assessment, it is worth scheduling one. Not because these drugs are inherently dangerous to most people, but because the small group of people who are vulnerable often does not find out until after damage has started. A five-minute gonioscopy exam can tell you whether your angles are narrow, and that single piece of information changes the risk calculation for a wide range of common medications.