Secondary glaucoma (SG) is a specialized form of glaucoma where increased fluid pressure within the eye results from a separate, identifiable health condition, injury, or medication. Unlike primary open-angle glaucoma, which develops without a clear underlying cause, SG has a clear etiology for the outflow blockage. The condition arises when the eye’s drainage system, the trabecular meshwork, becomes overwhelmed or obstructed. This disruption leads to an accumulation of aqueous humor, causing intraocular pressure (IOP) to rise and potentially damage the optic nerve, resulting in permanent vision loss.
How Secondary Glaucoma Develops
Secondary glaucoma develops when a mechanism impairs the outflow of aqueous humor through the trabecular meshwork. This impairment can be caused by physical debris, the growth of abnormal tissues, or inflammatory processes. Understanding the source of the blockage dictates the specific type of secondary glaucoma.
Inflammatory secondary glaucoma (uveitic glaucoma) occurs when inflammation (uveitis) releases cells and proteins into the aqueous fluid. This cellular debris congests the trabecular meshwork, slowing drainage. Prolonged inflammation can also cause the iris to adhere to the drainage angle, forming scar tissue (synechiae) that completely blocks the outflow pathway.
Neovascular glaucoma is frequently associated with advanced systemic diseases like severe diabetes or retinal vascular occlusions. Poor oxygen supply triggers the growth of new, fragile blood vessels (neovascularization) on the iris and over the drainage angle. These abnormal vessels form a dense, fibrous membrane that seals off the trabecular meshwork, causing a rapid elevation in intraocular pressure.
Certain syndromes cause materials to accumulate and clog the drainage system. Pseudoexfoliative glaucoma develops when a flaky, dandruff-like protein material is deposited throughout the anterior segment of the eye. These deposits flake off and obstruct the pores of the trabecular meshwork. Similarly, pigmentary glaucoma results from pigment granules rubbing off the back of the iris and dispersing into the fluid, gradually blocking the meshwork’s filtering ability.
Physical trauma, such as a blunt injury, can cause traumatic glaucoma by directly damaging drainage structures or initiating a delayed inflammatory response. The impact can tear the ciliary body, leading to angle recession, where scarring impedes fluid flow years later. Certain medications, particularly long-term topical corticosteroids, can induce steroid-induced glaucoma. These steroids alter the cells in the trabecular meshwork, increasing resistance to outflow and causing pressure to rise.
Identifying the Warning Signs
The symptoms of secondary glaucoma vary depending on the underlying cause and the speed at which intraocular pressure rises. When pressure increases slowly, such as with chronic pigmentary or pseudoexfoliative types, the condition is often asymptomatic in its early stages. Patients may not notice any change until significant, irreversible peripheral vision loss has occurred.
A sudden, rapid increase in pressure, common in acute angle-closure or advanced neovascular glaucoma, triggers severe symptoms. These acute signs include intense eye pain, a throbbing headache, and noticeable redness. Patients may also experience blurred or hazy vision and see rainbow-colored halos around lights due to corneal swelling.
In acute situations, the reaction to sudden pain and pressure can include nausea and vomiting. These sudden, severe symptoms constitute a medical emergency requiring immediate attention to prevent permanent damage to the optic nerve. In less acute cases, a subtle, progressive loss of peripheral vision may be the only warning sign, emphasizing the need for routine eye examinations.
Diagnostic Procedures and Treatment Strategies
Diagnosing secondary glaucoma requires investigation to confirm elevated pressure and identify the underlying cause. The process begins with tonometry to measure intraocular pressure (IOP). This is followed by gonioscopy, which uses a specialized lens to examine the drainage angle for obstruction by debris, pigment, or new vessels. Visual field testing (perimetry) maps the patient’s vision to detect areas of loss indicative of optic nerve damage. Imaging techniques, such as Optical Coherence Tomography (OCT), provide high-resolution scans of the optic nerve head to assess nerve fiber layer damage and monitor progression.
Treatment for secondary glaucoma follows a dual strategy: lowering intraocular pressure to prevent further optic nerve damage and addressing the underlying cause of the blockage. Pressure reduction often starts with prescription eye drops that either decrease the production of aqueous humor or enhance its drainage. Oral medications may be used temporarily to manage dangerously high pressures.
Managing the primary condition is equally important; for example, uveitic glaucoma requires anti-inflammatory treatment to clear the debris from the meshwork, while neovascular glaucoma demands aggressive control of underlying systemic disease. When medications are insufficient, surgical options are explored to create a better outflow pathway. Laser procedures, such as Selective Laser Trabeculoplasty (SLT), can improve the meshwork’s function in some open-angle types. More advanced or refractory cases may require incisional surgery, like trabeculectomy, to create a new drainage channel, or the placement of a tube shunt to permanently divert fluid.