100-day glaucoma is seen in which of the following conditions?

Correct Answer: D. Central retinal vein occlusion

Central retinal vein occlusion (CRVO) causes 100-day glaucoma (also called neovascular glaucoma) through a well-defined pathophysiological sequence. When CRVO occurs, retinal ischemia triggers release of vascular endothelial growth factor (VEGF) and other angiogenic factors. Around 100 days post-occlusion, these factors stimulate neovascularization of the iris and angle structures. The new vessels are fragile, leak, and contract, pulling the peripheral iris forward and occluding the trabecular meshwork. This angle-closure mechanism causes a secondary glaucoma that is notoriously difficult to manage. The 100-day timeline is a classic teaching point in Indian ophthalmology curricula—it represents the natural history of ischemic retinopathy progressing to neovascular glaucoma. Early recognition and aggressive anti-VEGF therapy (bevacizumab, ranibizumab) or panretinal photocoagulation can prevent this complication. Unlike steroid-induced glaucoma (which is open-angle and dose-dependent) or CRAO (which causes retinal whitening but not neovascularization), CRVO's ischemic burden is sufficient to trigger the neovascular cascade. This is the most common cause of secondary glaucoma in the Indian population post-CRVO.

Why the other options are wrong

A. Central retinal artery occlusion — CRAO causes sudden vision loss and retinal whitening but does NOT lead to neovascular glaucoma. Although CRAO is ischemic, the retinal perfusion loss is too acute and severe to allow the chronic ischemic stimulus needed for VEGF-driven neovascularization. The retina undergoes atrophy rather than triggering angiogenic response. Glaucoma in CRAO is rare and not a characteristic complication. B. Eale's disease — Eale's disease is a peripheral retinal vasculitis causing vitreous hemorrhage and neovascularization of the disc, but it does NOT characteristically cause glaucoma at 100 days. While severe Eale's may rarely lead to neovascular glaucoma, it is not the classic association. The disease is primarily a vasculitis affecting young males in India, not a glaucoma-inducing condition. C. Steroid-induced glaucoma — Steroid-induced glaucoma is an open-angle glaucoma caused by impaired trabecular outflow due to glycosaminoglycan deposition. It occurs within weeks to months of steroid use and is dose- and duration-dependent, not time-locked to 100 days. It does not involve neovascularization and is reversible upon steroid withdrawal. The mechanism is completely different from neovascular glaucoma.

High-Yield Facts

Mnemonics

CRVO → 100-day NVG Central Retinal Vein Occlusion → 100 days → NeoVascular Glaucoma. VEGF release from ischemic retina triggers iris and angle neovascularization by day 100. NVG Mechanism: VEGF → Vessels → Angle Closure Ischemia → VEGF ↑ → Neovascularization of iris/angle → Fibrovascular contraction → Peripheral iris pushed forward → Trabecular meshwork occluded → Glaucoma. Remember: it's angle-closure, not open-angle.

NBE Trap

NBE may pair CRAO with glaucoma to trap students who confuse acute retinal ischemia with chronic ischemic stimulus; CRAO causes retinal atrophy, not neovascularization. Similarly, steroid-induced glaucoma is offered to confuse the mechanism—it is open-angle and reversible, not neovascular and time-locked to 100 days.

Clinical Pearl

In Indian clinical practice, a patient presenting 3–4 months post-CRVO with sudden IOP rise, iris rubeosis, and angle neovascularization on gonioscopy is a red flag for 100-day glaucoma. Early PRP or anti-VEGF injection (bevacizumab is cost-effective in India) can prevent irreversible vision loss and the need for glaucoma surgery.

_Reference: Bailey & Love Ch. 36 (Ophthalmology); Harrison Ch. 428 (Retinal Vascular Diseases); Parson's Diseases of the Eye (Glaucoma section)_