This page summarises the secondary causes of open-angle glaucoma. These conditions involve clogging of the trabecular meshwork where the angle is still open. This blocks aqueous outflow and leads to increased IOP, which subsequently leads to glaucoma.
Posner-schlossman Syndrome
Recurrent unilateral episodes of acute IOP elevation
Pathology
- Idiopathic episodic disease
- Associations: CMV + H.pylori + HLA BW5
Diagnostics
Presentation
- 20yr male + Unilateral + blurred vision + recurrent attacks + white eye
Investigations
- IOP (40-80mmhg) + open angle + no synechiae
Management
- Topical steroids
- IOP lowering(high → IV acetazolamide, medium/low → topical timolol)
Pseudoexfoliation Syndrome
Grey white fibrillar deposits block the anterior chamber angle leading to secondary open-angle glaucoma
Pathology
- Linked to a mutation in the LOXL1 (an enzyme that contributes to elastin formation) in Chr 15q24.1
- Associations: hearing loss + Alzheimers + high homocysteine + low folate intake
Diagnostics
Presentation
- Scandinavian female of 50 years
Investigations
- Elevated IOP + Glaucomatous vision changes + anterior lens capsule white deposits + sampaolesi line
Management
- As for POAG
Pigment Dispersion Syndrome
An inherited autosomal dominant condition characterised by clogging of the trabecular meshwork by iris pigment.
Pathology
- Pigment dispersion syndrome = shedding of iris pigment throughout the anterior chamber
- Pigment dispersion glaucoma = iris pigment clogs trabecular meshwork and leads to open-angle glaucomatous vision changes
Diagnostics
Presentation
- Blurred vision on exertion
Investigation
- Elevated IOP + Glaucomatous damage + TM pigmentation + Krukenberg spindles + Mid peripheral spoke like pigmentation
Management
- Conservative: avoid exertion
- Medical: Topical prostaglandins or pilocarpine before exercise
- Surgical: Trabeculoplasty or trabeculectomy
Phacolytic Glaucoma
Debris from hypermature cataracts can break off and clog the trabecular meshwork. This can lead to secondary open-angle glaucoma
Diagnostics
Presentation
- Painful red eye
- Pseudohypopyon
Investigations
- AC tap → lens proteins and foamy macrophages
- Slit-lamp → Anterior chamber flare + hypermature cataract
Management
- Medical → topical IOP lowering medications following the same protocol as POAG
- Definitive → cataract extraction
Angle Recession Glaucoma
Ciliary body damage caused by blunt trauma can lead to chronic open-angle glaucoma. This is called angle recession glaucoma.
Pathology
- Blunt ocular trauma can rupture the ciliary body between the root of the iris and the scleral spur.
- Glaucoma is caused by damage to the trabecular meshwork and only develops in around 10% of patients over 10 years.
Diagnostics
Presentation
- History of ocular trauma
Investigations
- Gonioscopy shows irregular widening of the ciliary body
Red Cell and Ghost Cell Glaucoma
Cells can get trapped within the trabecular meshwork and lead to aqueous outflow obstruction, raised IOP and open-angle glaucoma.
Red cell |
Ghost cell |
|---|---|
Fresh red cells blocking the TM |
Degenerated old red cells blocking the TM |
Typically occurs acutely after hyphema and blunt trauma |
Typically occurs a few weeks after vitreous haemorrhage |
Characteristic tan coloured degenerating red cells can be seen in the anterior chamber in patients with ghost cell glaucoma.
Sturge-weber Syndrome
A congenital neurocutaneous disorder which leads to glaucoma
Pathology
- Anterior chamber malformation → glaucoma within first year of life
- Increased episcleral venous pressure → glaucoma later in life
Causes of raised episcleral venous pressure can also lead to raised IOP.
Diagnostics
Presentation
- Port Wine stain + seizures + + choroidal hemangiomas
- Glaucomatous eye is ipsilateral to the stain
Port Wine stains are non-blanching pink/purple patches that do not cross the midline.
Management
- Early-onset → Goniotomy or trabeculectomy or combined trabeculectomy-trabeculectomy.
- Late-onset → Medical therapy first, then trabeculectomy if medical therapy fails.
