Glaucoma is a group of eye conditions characterized by damage to the optic nerve, which transmits visual information from the eye to the brain. This damage is most often linked to an increase in intraocular pressure (IOP), caused by an imbalance in the production and drainage of the fluid inside the eye, known as aqueous humor. Secondary glaucoma is a specific classification where this pressure increase is directly traceable to another underlying medical condition, eye injury, or external factor. Effective management requires addressing both the elevated eye pressure and the root cause of the problem.
How Secondary Glaucoma Differs from Primary Glaucoma
The fundamental difference between primary and secondary glaucoma lies in the presence of an identifiable cause. Primary glaucoma, such as Primary Open-Angle Glaucoma, develops without any known, pre-existing condition that triggers the pressure rise. It is often attributed to age-related changes or inherent issues within the eye’s drainage system.
Secondary glaucoma is a direct complication of a known event, disease, or medical intervention. This precursor disrupts the normal flow or drainage of aqueous humor, leading to a pathological rise in IOP. The elevated pressure is a consequence, or a “secondary” effect, of the initial problem.
Secondary forms can manifest as either open-angle or angle-closure glaucoma, depending on how the underlying condition affects the eye’s drainage angle where the iris and cornea meet. The underlying condition can physically obstruct the trabecular meshwork, the eye’s primary drain, or cause inflammation that damages this filtration tissue. The presence of a distinct trigger defines the secondary classification.
Common Conditions That Cause Secondary Glaucoma
A diverse range of conditions and external factors can initiate secondary glaucoma, each employing a unique mechanism to raise intraocular pressure.
Uveitic Glaucoma
Inflammation inside the eye, known as uveitis, is a common cause. Inflammatory cells and protein debris accumulate and clog the delicate pores of the trabecular meshwork, significantly impeding the outflow of aqueous humor.
Traumatic Glaucoma
This results from a physical injury, such as blunt force trauma to the eye, which can tear the tissue behind the drainage angle, a condition called angle recession. This damage can lead to chronic glaucoma years later due to scarring and reduced drainage capacity. Bleeding within the eye after an injury, known as hyphema, can also cause red blood cells and clot material to block the meshwork temporarily or permanently.
Steroid-Induced Glaucoma
Certain medications, particularly corticosteroids administered as drops, pills, or injections, are a well-documented cause. These steroids can cause physical changes within the drainage structures, increasing the resistance to fluid outflow in susceptible individuals. The mechanism involves changes in the genetic expression of cells within the trabecular meshwork, which alters the structure of the tissue.
Neovascular Glaucoma
Vascular issues can lead to this severe form, often associated with systemic diseases like advanced diabetes or central retinal vein occlusion. These conditions cause a lack of oxygen in the retina, stimulating the growth of abnormal new blood vessels on the iris and over the drainage angle. These fragile vessels subsequently block the trabecular meshwork, causing a rapid increase in intraocular pressure.
Pigmentary and Pseudoexfoliation Glaucoma
These syndromes involve the mechanical clogging of the drainage system. In pigmentary glaucoma, pigment granules from the iris rub off and disperse into the aqueous humor, accumulating in the meshwork. Pseudoexfoliation involves the production of a flaky, abnormal protein material that deposits on structures throughout the front of the eye, physically obstructing the outflow channels.
Recognizing Symptoms and Confirming Diagnosis
The symptoms of secondary glaucoma vary widely, depending on the speed of the pressure increase and the underlying cause. If pressure rises gradually, similar to chronic primary glaucoma, the individual may experience no early symptoms. The only noticeable change may be a slow, progressive loss of peripheral vision, often missed until significant optic nerve damage has occurred.
Underlying causes like acute inflammation or neovascularization can lead to a sudden and severe spike in intraocular pressure. This acute presentation may cause symptoms like intense eye pain, redness, blurred vision, headaches, and the perception of rainbow-colored halos around lights. Nausea and vomiting can also accompany an acute pressure spike due to the severity of the ocular pain.
Confirming the diagnosis involves a comprehensive eye examination using specialized instruments. Tonometry measures the intraocular pressure, providing quantitative data on the pressure elevation. Gonioscopy uses a special contact lens to directly visualize the eye’s drainage angle, allowing the doctor to identify the specific cause blocking the outflow, such as pigment, inflammatory debris, or abnormal vessels.
The extent of optic nerve damage is assessed through ophthalmoscopy, where the doctor examines the optic nerve head for characteristic signs of damage. Visual field testing is also performed to map the patient’s peripheral vision and quantify any existing vision loss. These tools collectively determine the type of secondary glaucoma and the severity of the damage.
Treatment Strategies for Managing Secondary Glaucoma
Effective management requires a two-pronged strategy that addresses both the elevated intraocular pressure and the specific underlying cause. The first step is to control the primary condition responsible for the pressure increase. For example, uveitic glaucoma necessitates aggressive treatment of the inflammation, often with topical or systemic steroids, to reduce debris clogging the drainage angle.
Standard glaucoma treatments are simultaneously employed to lower the damaging intraocular pressure. Medicated eye drops are the initial line of defense, including classes such as prostaglandin analogues and beta-blockers that decrease fluid production or enhance drainage. Oral medications, such as carbonic anhydrase inhibitors, may be temporarily used to rapidly reduce pressure in acute situations.
If medications are insufficient, laser procedures like selective laser trabeculoplasty can improve the function of the drainage meshwork. When the eye’s natural drainage system is severely compromised, surgical intervention becomes necessary. Procedures like trabeculectomy create a new bypass channel for fluid to drain from the eye, while the implantation of glaucoma drainage devices, or tube shunts, acts as an artificial drainage system to maintain a lower, safer pressure.