What makes a glaucoma 'secondary'?

A glaucoma is secondary when the raised intraocular pressure and optic nerve damage can be traced to an identifiable cause — such as neovascularisation, inflammation, trauma, pigment dispersion, or corticosteroid use — rather than arising without an evident underlying process.

Why can steroids cause glaucoma?

In susceptible individuals, corticosteroids can increase resistance to aqueous outflow at the trabecular meshwork, raising intraocular pressure; a systematic review documented this rise after intravitreal steroid administration, which is why pressure monitoring is discussed in that context.

Secondary Glaucoma

Secondary glaucoma refers to glaucomatous optic neuropathy in which raised intraocular pressure results from an identifiable ocular or systemic cause rather than arising primarily, encompassing forms driven by neovascularisation, inflammation, pigment dispersion, trauma, lens changes, or drugs such as corticosteroids. The unifying feature is that another process disrupts aqueous outflow or angle anatomy.

Definition

Secondary glaucoma is glaucoma in which elevated intraocular pressure and consequent optic nerve damage are caused by an identifiable ocular or systemic condition, mechanism, or agent, distinguishing it from primary glaucoma where no such cause is found.

Scope

The topic groups the diverse glaucomas attributable to a recognisable underlying cause, organised by whether the secondary process produces an open or a closed drainage angle. It treats secondary glaucoma as a clinical-entity reference grouping; named subtypes such as neovascular and steroid-induced glaucoma illustrate the mechanisms. It offers no individualised diagnostic or treatment guidance.

Core questions

What distinguishes secondary from primary glaucoma?
How are secondary glaucomas usefully classified into open-angle and angle-closure mechanisms?
How does retinal ischaemia lead to neovascular glaucoma?
Why do corticosteroids raise intraocular pressure in susceptible eyes?

Key concepts

Identifiable underlying cause
Secondary open-angle versus secondary angle-closure mechanism
Neovascular glaucoma
Steroid-induced ocular hypertension
Pigment dispersion
Inflammatory (uveitic) glaucoma
Traumatic and lens-related glaucoma

Mechanisms

Secondary glaucomas share the final pathway of impaired aqueous outflow but differ in cause. In secondary open-angle forms, material or change at the level of the trabecular meshwork raises outflow resistance: pigment liberated from the iris, inflammatory cells and protein in uveitis, or trabecular dysfunction induced by corticosteroids. In secondary angle-closure forms, the angle is mechanically obstructed, for example by a fibrovascular membrane in neovascular glaucoma, by synechiae from chronic inflammation, or by anterior displacement of ocular structures. Neovascular glaucoma typically follows retinal ischaemia, which drives growth of new vessels and a fibrovascular membrane across the angle (Hayreh 2007); steroid-induced pressure rise reflects altered trabecular outflow in susceptible individuals (Kiddee 2013; Weinreb 2014).

Clinical relevance

Recognising that a glaucoma is secondary matters because the course is shaped by the underlying cause, and conditions such as neovascular glaucoma can be aggressive and sight-threatening. Understanding these mechanisms is part of comprehensive ophthalmic knowledge and of appraising why certain systemic diseases and medications carry ocular risk. This entry is descriptive and a reference resource, not a basis for individual diagnosis or treatment decisions.

Evidence & guidelines

Society terminology frameworks classify secondary glaucomas by the responsible mechanism and by whether the angle is open or closed (European Glaucoma Society 2021). Subtype-specific evidence includes long-standing reviews of neovascular glaucoma describing its ischaemic basis (Hayreh 2007) and a systematic review documenting the intraocular pressure rise associated with intravitreal corticosteroids (Kiddee 2013).

History

As the primary glaucomas were defined by the configuration of an otherwise normal drainage system, a parallel understanding grew of glaucomas attributable to identifiable insults — inflammation, trauma, lens disease, neovascularisation, and later iatrogenic causes such as corticosteroids. Hayreh's work consolidated the ischaemic model of neovascular glaucoma, and recognition of steroid responsiveness clarified an important drug-related secondary form (Hayreh 2007; Kiddee 2013).

Key figures

Sohan Singh Hayreh
Robert N. Weinreb
Jost B. Jonas

Seminal works

hayreh-2007
weinreb-2014
kiddee-2013

Frequently asked questions

What makes a glaucoma 'secondary'?: A glaucoma is secondary when the raised intraocular pressure and optic nerve damage can be traced to an identifiable cause — such as neovascularisation, inflammation, trauma, pigment dispersion, or corticosteroid use — rather than arising without an evident underlying process.
Why can steroids cause glaucoma?: In susceptible individuals, corticosteroids can increase resistance to aqueous outflow at the trabecular meshwork, raising intraocular pressure; a systematic review documented this rise after intravitreal steroid administration, which is why pressure monitoring is discussed in that context.