Steroid-induced glaucoma (SIG) occurs in up to 8% of the general population, with higher, clinically significant, or severe responses (IOP > 31 mmHg) affecting 4%–6% of individuals. The risk increases significantly to 46%–92% in patients with pre-existing primary open-angle glaucoma. It is more common in males (4.34%) than females (2.88%) and is strongly associated with high-potency, long-term topical steroid use.
Key Prevalence and Risk Data:
- General Response Rates: About 30%–33% of the population are “moderate responders” (IOP increase of 6-15 mmHg), while 4%–6% are “high responders” (IOP > 15 mmHg).
- Population at Risk: Studies show that 90% of patients with pre-existing open-angle glaucoma may experience a steroid response.
- High-Risk Groups: Individuals with pre-existing glaucoma, a strong family history of glaucoma, or high myopia are at higher risk.
- Children and Young Adults: Children, particularly those with conditions like vernal keratoconjunctivitis (VKC), are at a high risk of rapid, severe pressure elevation.
- Incidence in Specific Studies: One study found a 3.92% prevalence in a sample group, with higher rates (6.57%) in those aged 61 to 70. Another study reported a 5.5% prevalence of SIG.
Factors Influencing Prevalence:
- Route of Administration: Topical eye drops pose the highest risk, though inhaled and systemic steroids can also cause increased IOP.
- Potency and Duration: High-potency steroids used for more than 3-6 weeks significantly increase the likelihood of developing ocular hypertension.
- Demographics: Studies have shown a higher prevalence of steroid-induced cataracts and glaucoma in males.
Signs of Steroid-Induced Glaucoma:
- Elevated intraocular pressure (IOP).
- Glaucomatous disc changes and field defects.
- Increased cup-to-disk ratio (0.5 to 0.7).
Management:
- The primary treatment for steroid-induced ocular hypertension (SIOHT) or glaucoma is the discontinuation of the steroid, which usually reverses the pressure elevation.
- In cases of high IOP, 62.9% of eyes required glaucoma medication (AGM), and 24.9% required surgery in one study.
Steroid-Induced Glaucoma Flashcards
Clinical Knowledge Match: SIG
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Technical Insight
Steroid-induced glaucoma (SIG) is a secondary open-angle glaucoma caused by increased resistance to aqueous outflow at the level of the trabecular meshwork (TM). This occurs due to the accumulation of extracellular matrix proteins like fibronectin and glycosaminoglycans.
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In uveitis, corticosteroids increase IOP by increasing outflow resistance and also improving aqueous production, which can be decreased in eyes with intraocular inflammation.
(according to aao references).
Pathophysiology of Steroid-Induced Glaucoma (Increased TM Resistance)
caused by structural and functional changes in the TM.
The mechanisms :
1. Extracellular Matrix Accumulation
Glucocorticoids activate specific receptors in TM cells, leading to increased synthesis and deposition of ECM components such as collagen, fibronectin, and glycosaminoglycans .This “thickening” of the matrix—particularly in the Juxtacanalicular Tissue significantly reduces the permeability.
2. Inhibition of Matrix Degradation
Steroids disrupt the natural turnover of the ECM by decreasing the production of Matrix Metalloproteinases and increasing the levels of Tissue Inhibitors of Metalloproteinases .This imbalance prevents the breakdown of debris
3. Impaired TM Phagocytosis
4. Cytoskeletal Reorganization
Steroids induce the formation of Cross-Linked Actin Networks within TM cells. This reorganization increases cellular stiffness and alters the shape of TM cells, which negatively impacts their ability to regulate aqueous humor egress.
5. Upregulation of Myocilin :
Steroid exposure leads to the over-expression of the Myocilin protein Excessive Myocilin can interfere with the normal physiology of TM cells and is strongly associated with the mechanical obstruction of the outflow facility.