SECONDARY GLAUCOMA
SECONDARY GLAUCOMA
- Glaucoma that occurs as a complication of various other ocular conditions.
Important secondary glaucoma are described below:
LENS INDUCED GLAUCOMA
- Patients are usually elder.
Following types of lens induced glaucoma are:
1. Phacomorphic glaucoma:
- Occurs in intumescent stage of cataract.
- The swollen lens leads to relative pupillary block (pupillary block glaucoma).
- It is a type of angle closure glaucoma & anterior chamber is very shallow.
- Also seen in anterior subluxation/dislocation of lens & spherophakia (congenital small spherical lens).
2. Phacolytic glaucoma:
- In hypermature stage lens proteins leak out into the anterior chamber & are engulfed by macrophages.
- These swollen macrophages clog the trabecular meshwork.
- It is a type of open angle glaucoma.
3. Phacotopic glaucoma:
- In hypermature stage, subluxation or dislocation of lens cause angle closure glaucoma.
4. Phacoanaphylactic uveitis & phacotoxic glaucoma:
- It is chronic uveitis.
- Occurs 1-14 days following cataract extraction or lens trauma.
- Lens matter induces hypersensitivity uveitis .
- The open angle glaucoma may be precipitated by clogging of trabecular meshwork by inflammatory cells & lens matter.
5. Lens particle glaucoma:
- Type of open angle glaucoma.
- Occurs due to blockade of trabecular meshwork by lens particle.
NEOVASCULAR GLAUCOMA (Rubeosis iridis)
- It is a secondary angle closure glaucoma
- Results due to formation of neovascular membrane over the iris i.e. neovascularisation of iris (rubeosis iridis).
Causes of rubeosis iridis are:
i) Common:
- Diabetic retinopathy (m/c cause)
- Central retinal vein occlusion
- Eale’s disease
- Sickle-cell retinopathy
ii) Rare causes:
- Central retinal artery occlusion
- Intraocular inflammation (uveitis)
- Retinoblastoma
- Fusch’s heterochromatic iridocyclitis
- In CRVO, glaucoma manifests about 100 days after thrombosis of central vein c/d 100 days glaucoma.
- Treatment of choice is panretinal photocoagulation.
PIGMENTORY GLAUCOMA
- Type of secondary open angle.
- Occurs in young myopic males.
Characterstic feature is the deposition of pigment granules in antetrior segment such as:
- posterior surface of cornea (Krukenberg’s spindle)
- Trabecular meshwork
- ciliary zonules
- Crystalline lens
- Iris transillumination shows radial slit-like transillumination defects in the mid periphery (pathognomonic features)
- Treatment is as for primary open angle glaucoma.
GLAUCOMA SECONDARY TO INTRAOCULAR HAMORRHAGE
Intraocular hemorrhage (vitreous Hg/ hyperemia) may cause:
i) Red cell glaucoma:
- Caused by blockade of trabeculae by RBCs .
ii) Haemolytic glaucoma:
- Caused by an obstruction of trabecular meshwork by macrophagesladen with pigment, RBCs & debris.
iii) Ghost cell glaucoma:
- Caused by blockage of pores of trabeculae by deformed RBCs.
iv) Hemosiderotic glaucoma:
- Caused by sclerosis of trabecular meshwork caused by the iron (Siderosis).
IRIDOCORNEAL ENDOTHELIAL SYNDROME
Spectrum of conditions of eye where the corneal endothelium is abnormal which causes:
- Iris atrophy
- Secondary glaucoma
- Corneal edema
- The main histological finding is the alteration in corneal endothelium that leads to deposition of collagen on posterior surface of Descemet’s membrane.
Three clinical variants are:
- Progressive iris atrophy (Essential iris atrophy)
- Chandler’s Syndrome: Changes in iris are minimal & corneal edema predominates.
- Cogan Rees Syndrome: These are nodular or diffuse pigmented lesions of the iris, also c/d iris naevus syndrome.
Exam Important
- Intractable secondary glaucoma is seen in Diffuse iris melanoma.
- Secondary glaucoma following corneal perforation is due to Peripheral anterior synechiae.
- Secondary glaucoma associated with angle recession is seen in Concussion injury.
- Iridocorneal endothelial syndrome is associated with Progressive atrophy of iris stroma.
- Most common cause of neovascular glaucoma is Diabetes.
- Rubeosis Iridis is most commonly seen in Diabetes mellitus.
- Intumescent cataract is associated with Phacomorphic glaucoma.
