OP7.4 | Secondary Glaucoma: Cause Framework — Summary & Reflection

KEY TAKEAWAYS

Secondary glaucoma is IOP elevation due to an identifiable underlying cause. The mechanistic scaffold: open-angle (trabecular meshwork drainage impaired by pre-trabecular membrane, trabecular clogging, or post-trabecular venous pressure) vs closed-angle (angle physically closed, with or without pupil block). Key named types: pseudoexfoliation (PXF material on lens + TM — commonest secondary OAG worldwide); pigmentary (Krukenberg spindle, young myopic male, exercise-induced IOP spike); neovascular (rubeosis iridis from retinal ischaemia in PDR/CRVO — anti-VEGF + PRP); steroid-induced (reversible on stopping steroid — IOP rise in 2–6 weeks); uveitic (both open-angle trabeculitis and closed-angle pupil block — complex); phacomorphic (swollen lens CLOSES angle — B2; treat with lens extraction); phacolytic (leaking hypermature cataract OPENS angle with protein + macrophages — A2; treat with lens extraction); angle recession (unilateral traumatic, gonioscopic widening of angle — delayed glaucoma). Management is two-pronged: IOP-lowering (same drug ladder, with cause-specific contraindications) PLUS treatment of the underlying cause. Normal IOP = 10–21 mmHg; all secondary glaucomas raise IOP above this.

REFLECT

Return to the three patients in the hook. Patient A (young myopic male with a Krukenberg spindle and IOP 28 mmHg) has pigmentary glaucoma — his concave iris is rubbing pigment onto his trabecular meshwork every time he exercises. Patient B (diabetic with IOP 46 mmHg and new iris vessels) has neovascular glaucoma from proliferative diabetic retinopathy — his ischaemic retina has been secreting VEGF, which has grown new vessels across his drainage angle. Patient C (on prednisolone eye drops with IOP 34 mmHg from a baseline of 14 mmHg) has steroid-induced glaucoma. Now reflect: in all three cases, the glaucoma is a window into a systemic or local disease. What does this tell you about the importance of asking about medications and systemic conditions in every glaucoma patient? And how does the model of 'treat the cause' differ from the lifetime of IOP-lowering drops that a POAG patient faces?