Secondary Glaucoma

Secondary glaucoma is glaucomatous optic neuropathy with raised intraocular pressure caused by an identifiable ocular or systemic condition, rather than primary trabecular dysfunction or primary angle crowding. It is classified by the mechanism of outflow obstruction.

• Open angle mechanisms:
  • Pre-trabecular (a membrane covers the meshwork): neovascular glaucoma, iridocorneal endothelial syndrome, epithelial downgrowth, fibrous ingrowth, inflammatory membranes.
  • Trabecular: pigment dispersion, pseudoexfoliation, uveitis (cells, protein), steroid response, red blood cells (hyphaema, ghost cell glaucoma), macrophages (haemolytic glaucoma), lens protein (phacolytic), tumour cells, viscoelastic or silicone oil, alkali burns, angle recession.
  • Post-trabecular (raised episcleral venous pressure): carotid cavernous fistula, cavernous sinus thrombosis, Sturge-Weber syndrome, thyroid eye disease, superior vena cava obstruction, orbital varices.
• Closed angle mechanisms:
  • With pupillary block: seclusio or occlusio pupillae in uveitis, swollen or dislocated lens, microspherophakia, aphakic or pseudophakic pupillary block, vitreous or silicone oil in the anterior chamber.
  • Without pupillary block (anterior pulling or posterior pushing): neovascular membrane contraction, iridocorneal endothelial syndrome, peripheral anterior synechiae after inflammation or surgery, ciliochoroidal effusion (topiramate, sulpha drugs), malignant (aqueous misdirection) glaucoma, ciliary body or iris tumours, retinopathy of prematurity, large posterior segment masses, scleral buckle, and panretinal photocoagulation.
• Aqueous misdirection (malignant glaucoma): after intraocular surgery in short eyes, aqueous flows posteriorly into the vitreous, pushing the lens iris diaphragm forward, producing a uniformly shallow or flat chamber with high pressure despite a patent iridotomy.

• Features of the primary cause: ocular pain, redness, photophobia, hyphaema, uveitis, trauma history, rubeosis, pigment on the corneal endothelium or iris, pseudoexfoliation material, lens dislocation, prominent episcleral vessels.
• Raised pressure that is often higher and more variable than in primary disease, with early disc damage and corneal oedema.
• Unilateral or asymmetric disease commonly suggests a secondary cause.
• Aqueous misdirection: pain, blur, flat chamber after surgery or after miotic or laser treatment in an angle closure eye.

• Detailed history: trauma, steroid or other drug use, previous eye surgery or inflammation, systemic disease.
• Slit lamp, tonometry, gonioscopy (compare both eyes; look for neovascularisation, pigment, recession, synechiae, tumour), dilated optic disc and retinal examination.
• Anterior segment optical coherence tomography and ultrasound biomicroscopy for ciliary body pathology, lens position, and effusion; B-scan for posterior segment masses.
• Special tests for the cause: cultures or PCR of aqueous for viral uveitis, specific blood tests for uveitis, fluorescein angiography for ischaemia, orbital imaging and angiography for vascular fistula.

• Treat the underlying cause first, while lowering intraocular pressure in parallel.
• Medical: aqueous suppressants as first line (timolol 0.5 percent twice daily, dorzolamide 2 percent three times daily, brimonidine 0.2 percent twice daily, acetazolamide 250 mg four times daily or 500 mg intravenously for acute rises). Prostaglandin analogues are less effective or contraindicated in some conditions (active uveitis, herpetic disease, neovascular disease, and aphakia with macular oedema). Avoid miotics in pupillary block, uveitis and neovascular disease.
• Laser: peripheral iridotomy for pupillary block, laser trabeculoplasty only for selected open angle types (pigment, pseudoexfoliation).
• Surgery for refractory pressure: trabeculectomy with mitomycin C, glaucoma drainage devices (preferred in neovascular, uveitic, and scarred eyes), and cyclodestructive procedures (transscleral diode laser, endoscopic cyclophotocoagulation) for blind painful or end stage eyes.
• Aqueous misdirection: intensive cycloplegia (atropine 1 percent twice daily and phenylephrine 10 percent), aqueous suppressants, hyperosmotics (mannitol 20 percent 1 to 1.5 g/kg), and stop miotics; if no response in 2 to 5 days, Nd:YAG posterior capsulotomy and anterior hyaloidotomy in pseudophakic eyes, or pars plana vitrectomy with zonulohyaloidectomy and iridectomy.
• Elevated episcleral venous pressure: treat the vascular lesion (embolisation of the fistula), and use aqueous suppressants.
• Follow regularly with visual fields and optic nerve imaging.