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What medications increase the risk of glaucoma?

4 min read

According to research, at least one-third of acute closed-angle glaucoma cases may be triggered by prescription or over-the-counter medications. Understanding what medications increase the risk of glaucoma is crucial for patients, especially those with pre-existing risk factors, to prevent potentially blinding complications.

Quick Summary

This article outlines several classes of drugs known to increase glaucoma risk through various mechanisms, from altering aqueous outflow to inducing pupillary dilation. Key culprits include corticosteroids, anticholinergics, certain antidepressants, and sulfa-containing drugs, with distinct impacts on open-angle and angle-closure glaucoma types.

Key Points

  • Corticosteroids are a major risk factor: Any form of steroid—topical, oral, inhaled, or injected—can increase intraocular pressure, typically via an open-angle mechanism.

  • Topiramate is a key cause of acute angle-closure: This migraine and seizure drug can cause rapid, bilateral angle closure through ciliochoroidal effusions, often appearing within two weeks of starting treatment.

  • Anticholinergics and decongestants can trigger angle closure: Medications with anticholinergic or sympathomimetic effects, common in cold remedies, inhalers, and motion sickness drugs, can dilate the pupil and block the drainage angle in susceptible eyes.

  • Inform your eye surgeon about tamsulosin use: This BPH drug can cause Intraoperative Floppy Iris Syndrome (IFIS) during cataract or glaucoma surgery, necessitating surgical technique modifications.

  • Not all glaucoma is the same: Drugs can induce open-angle or angle-closure glaucoma, which have different mechanisms, symptoms, and treatment approaches.

  • Regular eye monitoring is crucial: Patients on chronic medication, especially steroids, should have regular eye exams to detect pressure increases early and prevent optic nerve damage.

  • Communication is essential: Always disclose your full medication list to all healthcare providers to ensure they can evaluate potential glaucoma risks.

In This Article

Glaucoma is an optic neuropathy that can lead to irreversible vision loss, often associated with elevated intraocular pressure (IOP). While genetics and age are significant risk factors, various medications can also cause or exacerbate the condition. This phenomenon, known as drug-induced glaucoma, occurs through different mechanisms, depending on the drug and the individual's ocular anatomy.

Medications and Open-Angle Glaucoma

Open-angle glaucoma is the most common form, typically developing gradually and with few symptoms in its early stages. The primary mechanism for drug-induced open-angle glaucoma is a medication's effect on the trabecular meshwork, the eye's drainage system. The most well-documented culprits are corticosteroids.

Corticosteroids

Systemic and topical corticosteroids are widely prescribed for various inflammatory and autoimmune conditions, but they are notorious for their potential to increase IOP. The mechanism involves increasing the resistance to aqueous humor outflow at the trabecular meshwork. The risk depends on the potency, dose, and duration of steroid use. Steroid-induced ocular hypertension can occur with various routes of administration, including:

  • Topical eye drops: The most frequent cause, with potent formulations like dexamethasone and prednisolone carrying a higher risk.
  • Periocular and intravitreal injections: Used to treat eye-related inflammation, these can lead to a significant and prolonged rise in IOP.
  • Oral steroids: Long-term use of oral steroids, such as prednisone, is associated with a greater risk of glaucoma and cataracts.
  • Inhaled and nasal steroids: Used for asthma and allergies, respectively. High-dose, long-term use has been linked to increased risk, especially in the elderly.

Medications and Angle-Closure Glaucoma

Angle-closure glaucoma (ACG) is a more acute condition where the eye's drainage angle is suddenly blocked, causing a rapid and severe rise in IOP. This can cause headaches, eye pain, and blurred vision, and is considered an ophthalmic emergency. Medication-induced ACG is more likely to occur in individuals with a pre-existing narrow angle or other anatomical predispositions.

Anticholinergics and Sympathomimetics

Many medications have anticholinergic (parasympatholytic) or sympathomimetic (adrenergic) properties, which can cause pupillary dilation (mydriasis). This can trigger a 'pupillary block,' where the iris blocks the eye's drainage angle, causing pressure to build up. Culprits include:

  • Respiratory medications: Anticholinergic inhalers like ipratropium and tiotropium for asthma and COPD.
  • Cold and flu remedies: Over-the-counter decongestants and antihistamines containing pseudoephedrine or phenylephrine.
  • Urinary incontinence medications: Drugs like oxybutynin and tolterodine.
  • Psychiatric medications: Older tricyclic antidepressants and some antipsychotics.
  • Gastrointestinal medications: Antispasmodics and motion sickness drugs like scopolamine.

Sulfa-Containing Drugs

This class of drugs can cause an idiosyncratic reaction leading to swelling of the ciliary body and a forward displacement of the lens-iris diaphragm, blocking the drainage angle. This mechanism is different from pupillary block and can occur even in eyes with wide angles.

  • Topiramate (Topamax): A key example, used for migraines and seizures. Topiramate-induced ACG is typically bilateral and presents acutely within the first few weeks of treatment, often accompanied by a significant myopic shift (nearsightedness).
  • Other sulfa drugs: Includes certain antibiotics (e.g., sulfamethoxazole) and diuretics (e.g., hydrochlorothiazide).

Other Medications

Several other drug classes have been linked to increased glaucoma risk:

  • Phosphodiesterase type 5 (PDE5) inhibitors: Medications for erectile dysfunction like sildenafil (Viagra) and tadalafil (Cialis). Some studies suggest a potential link to elevated IOP, possibly by increasing blood flow to the ciliary body.
  • Tamsulosin (Flomax): Used for benign prostatic hyperplasia (BPH). While not causing glaucoma directly, it is known to cause Intraoperative Floppy Iris Syndrome (IFIS) during cataract or glaucoma surgery, complicating the procedure.
  • Anticoagulants: In rare cases, these can lead to spontaneous suprachoroidal hemorrhage, displacing the lens-iris diaphragm forward and causing angle closure.

Comparison Table: Drug-Induced Glaucoma Mechanisms

Feature Open-Angle Mechanism Angle-Closure (Pupillary Block) Angle-Closure (Non-Pupillary Block)
Primary Drug Class Corticosteroids (topical, oral, inhaled) Anticholinergics, sympathomimetics, tricyclic antidepressants Sulfa-containing drugs (e.g., Topiramate)
Underlying Pathophysiology Increased resistance to aqueous outflow at the trabecular meshwork. Pupillary dilation causes the iris to block the trabecular meshwork. Ciliochoroidal effusion or anterior rotation of the ciliary body displaces the iris-lens diaphragm.
Onset Gradual, often over weeks or months. Rapid, often within hours of taking the medication. Rapid, usually within the first two weeks of treatment.
Effect on Pupil No direct effect on pupil size. Causes pupillary dilation (mydriasis). Mydriasis may or may not be present.
Typical Presentation Asymptomatic until significant optic nerve damage occurs. Severe eye pain, headache, blurred vision, and halos. Blurred vision (myopic shift), eye pain, and headache.
Patient Risk Factors Pre-existing glaucoma, family history, high myopia, diabetes. Narrow anterior chamber angles. Idiosyncratic reaction, can occur even in eyes with wide angles.

The Importance of Physician Communication

Managing medication-related glaucoma risk requires close collaboration between patients and healthcare providers. It is crucial to inform all doctors, including ophthalmologists, about your complete medication list, including over-the-counter drugs, herbal supplements, and injections.

If you have a history of glaucoma or have been identified with narrow drainage angles, this information is critical for any physician prescribing new medication. A comprehensive eye exam, including an evaluation of the anterior chamber, is the best way to assess risk.

Conclusion

Many medications, from commonly used steroids to specific antidepressants and decongestants, carry a risk of inducing or worsening glaucoma. While steroid-induced glaucoma typically follows an open-angle mechanism, numerous other systemic drugs can trigger acute angle-closure glaucoma, particularly in susceptible individuals. The key to prevention is awareness, open communication with your healthcare team, and regular eye monitoring, especially when starting a new medication. For example, the American Academy of Ophthalmology offers valuable resources detailing medication-induced angle-closure glaucoma and other ocular adverse effects. Understanding the specific mechanism by which a drug affects eye pressure is vital for correct diagnosis and management, protecting vision from potential harm.

Frequently Asked Questions

Yes, many over-the-counter cold and flu remedies contain antihistamines and decongestants (e.g., pseudoephedrine) that have anticholinergic or sympathomimetic effects. These can cause pupillary dilation, triggering acute angle-closure glaucoma in individuals with narrow drainage angles.

No, the risk varies by potency, dose, and administration route. Topical eye drops and injections carry the highest risk, but oral, inhaled, and nasal steroids can also increase IOP, particularly with high-dose or long-term use.

While steroids can cause open-angle glaucoma, acute angle-closure glaucoma is more commonly triggered by systemic medications, especially in individuals with narrow anterior chamber angles.

Certain antidepressants, including selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), and older tricyclic antidepressants, have been associated with an increased risk of acute angle-closure glaucoma, especially in elderly, female patients with narrow angles.

No, you should never stop or change your medication without consulting your doctor. If you are concerned about glaucoma risk, talk to your prescribing physician and an ophthalmologist. They can assess your individual risk and recommend appropriate management or alternative medications.

The symptoms depend on the type. For open-angle glaucoma, symptoms may be non-existent until the disease is advanced. For acute angle-closure glaucoma, symptoms can include severe eye pain, headache, nausea, sudden blurred vision, and seeing halos around lights.

Doctors can prevent drug-induced glaucoma by taking a complete medical and medication history, assessing risk factors like narrow eye angles, and monitoring patients on high-risk medications with regular eye exams. They may also consider prophylactic laser iridotomy for high-risk patients starting certain medications.

Even topical steroids applied to the skin, especially near the eyes, can be absorbed and increase intraocular pressure. It is crucial to inform your eye doctor about any steroid use so they can monitor your eye pressure.

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.