Eales Disease

Last updated: September 2026

Important Percentages

• NVI: 0.5-0.8 %
• NVD: 10-18 %
• NVE: 50 %
• Sec RRD: 8-11 %

   

Proliferative vascular retinopathy mimicking eales

• SYSTEMIC: DM, Sarcoidosis, Sickle
• OCULAR: BRVO, CRVO, Coats, Pars Planitis, ROP

 

Main causes of vision loss in Eales’ Disease

• SUDDEN
• Vitreous hemorrhage (NVE, Inflammatory BRVO, NVD)
• Secondary rhegmatogenous retinal detachment

 

GRADUAL

• Macular edema
• Traction retinal detachment involving posterior pole
• Disc edema
• Multiple vitreous membranes
• Cataract
• Glaucoma – NVG/Ghost cell
• Optic atrophy
• Epimacular membrane

 

Main indications for vitrectomy in Eales’ disease

• Non-resolving vitreous hemorrhage
• Traction retinal detachment involving posterior pole
• Multiple vitreous membranes
• Combined traction and rhegmatogenous retinal detachment
• Vitreous hemorrhage associated with hemolytic or ghost-cell glaucoma
• Macular pucker / Epimacular membrane
• Vitreous hemorrhage associated with rubeosis

 

Management

• If B/L: Systemic Steroids
• If U/L:
• <2 quadrent: PST
          
• >2 quadrent: Systemic Steroids

 

Current understanding of pathogenesis

Eales' disease remains a diagnosis of exclusion, but the leading current hypothesis implicates hypersensitivity to Mycobacterium tuberculosis antigens — supported by molecular evidence of innate immune activation (CD16+ monocytes with upregulated TLR-2) driving a pro-inflammatory cascade (elevated TNF-α and IL-6) that promotes endothelial activation and MMP-9-mediated extracellular matrix breakdown. A significantly elevated vitreous VEGF/PEDF ratio shifts the retinal environment decisively toward neovascularization — the same downstream pathway shared with other ischemic retinopathies, which is why anti-VEGF has a role here despite the distinct underlying trigger.

Current stage-based treatment approach

Important current caveats

• A positive IGRA or Mantoux test alone does not mandate ATT — the decision must incorporate HRCT chest findings, the angiographic phenotype, and clinical course, calibrated to regional TB epidemiology. Reflexively starting ATT on a positive TB test alone is not the current standard of care
• Anti-VEGF requires caution in eyes with established fibrovascular proliferation — while effective at regressing active neovascularization, anti-VEGF can accelerate fibrosis and traction in eyes with mature fibrovascular membranes, so timing and case selection matter
• Laser should not be applied over areas of active vasculitis — treating inflamed, not just ischemic, retina is a recognized pitfall
• Newer anti-VEGF/anti-angiopoietin-2 agents (e.g., faricimab) have been used successfully as an adjunct to vitrectomy in complex bilateral cases, reflecting an evolving but still case-by-case role for these newer agents

Key references: Eales' disease revisited: current understanding of etiopathogenesis, multimodal imaging, and treatment strategies. Indian J Ophthalmol. 2025.  |  Bae K, et al. A review of Eales' disease and Mycobacterium tuberculosis. Biology. 2024;13(6):460.