secondary glaucoma, classification, open angle glaucoma, angle closure glaucoma, pseudoexfoliative glaucoma, pigmentary glaucoma, neovascular glaucoma.

1. Secondary Glaucoma

2. Secondary Glaucoma: Group of disorders in which
the raised IOP is associated with a primary ocular
or systemic disease.
Classifications
 Open-angle Glaucoma
 Angle-closure Glaucoma

3. Open-angle Glaucoma
Secondary open-angle glaucoma can be
subdivided on the basis of the site of aqueous
outflow obstruction:
• Pre-trabecular
• Trabecular
• Post-trabecular

4. Pre-trabecular:- in which aqueous outflow is
obstructed by a membrane covering the
trabeculum, which may consist of:
 Fibrovascular tissue (neovascular glaucoma).
 Endothelial cellular membranous proliferation
(iridocorneal endothelial syndrome).
 Epithelial cellular membranous proliferation
(epithelial ingrowth).

5. Trabecular:- in which the obstruction occurs as a result of
‘clogging up’ of the meshwork and secondary degenerative
changes.
○ Pigment particles (pigmentary glaucoma).
○ Red blood cells (red cell glaucoma).
○ Degenerate red cells (ghost cell glaucoma).
○ Macrophages and lens proteins (phacolytic glaucoma).
○ Proteins (probably an element in hypertensive uveitis).
○ Pseudoexfoliative material (pseudoexfoliation glaucoma).
○ Trabecular glaucomas. trabeculitis in hypertensive uveitis)
or scarring (e.g. post-traumatic angle recession).

6. Post-trabecular:- in which the trabeculum itself is
normal but aqueous outflow is impaired as a
result of elevated episcleral venous pressure.
○ Carotid-cavernous fistula.
○ Sturge–Weber syndrome.
○ Obstruction of the superior vena cava.

7. Angle-closure Glaucoma
• With pupillary block:
○ Seclusio pupillae (360° posterior synechiae),
usually secondary to recurrent iridocyclitis.
○ Subluxated lens.
○ Phacomorphic glaucoma.
○ Capsular block syndrome with 360° iris–capsule
adhesion in a pseudophakic eye.
○ Aphakic pupillary block.
○ Anterior chamber lens implant without a patent
iridotomy.

8. • Without pupillary block:
○ Secondary causes of PAS such as advanced neovascular
glaucoma and chronic anterior uveitis.
○ Cilio-choroidal effusion.
○ Capsular block syndrome without iris–capsule adhesion.
○ Ciliary body/iris cyst or other ciliary body or posterior
segment tumour.
○ Contraction of retrolenticular fibrovascular tissue such as
in proliferative vitreoretinopathy and retinopathy of
prematurity.
○ Malignant glaucoma (cilio-lenticular block).

10. Pseudoexfoliative Glaucoma
 a common cause of secondary open-angled
glaucoma.
 rare before 50 years.
 more common in women.
Trabecular blockage by the exfoliative material.
 Diagnosis; usually incidental
Present with chronic angle gluacoma
Treatment :medical like POAG
Laser trabeculoplasty
Phacoemulsification
Filtration surgery
Trabecular aspiration

12. Pigmentary glaucoma
• Clogging up of trabecular meshwork by the
pigment particles
• Patients with Pigment Dispersion Syndrome
• Pigment release caused by mechanical rubbing
of the posterior pigment layer of iris with zonular
fibrils
Clinical features :–
 Young myopic males
 Glaucomatous features similar to POAG
 Deposition of pigment granules in the anterior
segment

13. Diagnosis
• Gonioscopy – pigment accumulation along the
Schwalbe’s line especially inferiorly (Sampaolesi’s
line).
• Iris transillumination – radial slit – like
transillumination defects in the periphery.
Treatment
•Life style measures
•Medical : miotic (pilocarpine)
•Laser trabeculoplasty
•Laser iridotomy
•Filtration surgery

15. NEOVASCULAR GLAUCOMA
glaucoma results due to formation of
neovascular membrane involving the angle of
anterior chamber
Etiology – Neovascularization of iris following retinal
ischaemia, feature of
 Proliferative diabetic retinopathy
 Central retinal vein occlusion
 Sickle – cell retinopathy
 Rare causes (intraocular tumours and long standing
retinal detachment).

16. Clinical features
• pain, decreased vision, redness and
photophobia.
• Cornea ;Elevated IOP leads to corneal oedema.
• IOP may be normal early, but is extremely high
later on.
• Anterior chamber: Flare, cells and posterior
synechiae.
Pupillary margin: Subtle vessels at the pupillary
margin.
• Iris surface. New vessels grow radially over the
surface of the iris towards the angle haemorrhage

17. Treatment :
Medical : like POAG but miotic and prostaglandine
derivative should be avoided.
Panretinal photocoagulation.
Goniophotocoagulation.
Intraocular VEGF inhibitors.
RD repair
Ciliary body ablative procedures: cyclodiode
Filtration surgery
Pars plana vitrectomy
Retrobulbar alcohol injection
Enucleation

19. INFLAMMATORY GLAUCOMA
Open -angle inflammatory glaucoma
Angle- closure inflammatory glaucoma

20. Open - angled inflammatory glaucoma
Chronic open – angle
inflammatory glaucoma
Acute open – angle
inflammatory glaucoma
Chronic trabeculitis and
trabecular scarring
Trabecular obstruction
Acute trabeculitis
Mechanism of rise
in IOP
Raised IOP, open angle, no
active inflammation but
signs of previous episode
of uveitis present
Features of acute
iridocyclitis associated with
raised IOP with open-angle
of anterior chamber
Clinical features
Medical therapy
Trabeculectomy
Cyclodestructive
procedures
Treatment of iridocyclitis
and medical therapy to
lower IOP by use of
hyperosmotic agents,
acetazolamide and beta –
blockers eye drops
Treatment

21. Angle – closure inflammatory glaucoma
 Mechanism of rise in IOP –
• Secondary angle – closure with pupil block
caused by posterior synechiae (selusio
pupillae),iris bombe and shallow anterior
chamber
•Secondary angle – closure without pupil
block:- chronic anterior uveitis causes the
deposition of inflammatory cells and debris
in the angle gradually leads to synechial
angle closure.

24. :
Treatment
Medical :
•Beta blockers 1st line of choice
•Miotic and prostaglandine should be avoided
Laser iridotomy
Surgery:
Trabeculectomy with mitomycin C enhancement
of glaucoma drainage device implantation.
 Cyclodestructive

25. Lens – induced glaucoma
 phacolytic glaucoma: secondary open –
angle glaucoma occurring in association with
hyper mature cataract, caused by leaking
high molecular weight proteins.
C/F :pain, poor vision, corneal oedema.
Deep anterior chamber and aqueous may
contain fine white protein particles, which
settle down as pseudohypopyon.
RX: after IOP controlled medically cataract
should be remove.

27. Phacomorphic Glaucoma
 Causes :-
 Intumescent lens.
 Anterior subluxation or dislocation of the lens and
spherophakia.
 Pathogenesis :– Swollen lens pushes iris forwards,
obliterating the angle.
 Presentation :– Acute congestive glaucoma and shows
features of acute primary angle closure glaucoma.
Treatment: medical ; like POAG but miotic should be
avoided ,systemic hyper osmotic agent may be use
Laser iridotomy (for both eyes )
Laser iridoplasty
Cataract extraction

29. Pupillary block from disruption of lens position
Causes:
 blunt ocular trauma.
 congenitally small lens
Diagnosis: A lens fully or partially dislocated into the anterior
chamber will usually be evident. Acute pupillary block will cause a
sudden severe elevation of IOP with associated visual impairment
Treatment : supine posture with dilated pupil
Lens extraction.

30. Traumatic Glaucoma
 Hyphaema: IOP elevation from trabecular obstruction by red
blood cells or from angle closure due to pupillary occlusion by a
blood clot
Treatment :
A coagulation abnormality, haemoglobinopathy, should be
excluded
Any current anticoagulant medication should be
Discontinued ,NSAIDs should not be used for analgesia.
medical : (miotic and prostaglandine should be avoided) A beta-
blocker and/or a topical or systemic CAI
Topical steroid , atropin can be use
Laser photocoagulation
Surgical evacuation

31.  Angle recession glaucoma: Angle recession involves
rupture of the face of the ciliary body, the portion between
the iris root and the scleral spur, due to blunt trauma.
Diagnosis: Presentation is with unilateral chronic glaucoma.
• Slit lamp examination may show signs of previous blunt
trauma; these may be mild, such as a small sphincter
rupture.
• Gonioscopy may initially reveal irregular widening of the
ciliary body face. In long-standing cases, the cleft may become
obscured by fibrosis and the angle may show
hyperpigmentation
Treatment :
medical therapy usually unsatisfactory
Laser trabeculoplasty is of little beneficial
Trabeculetomy with adjunctive antimetabolite
Filtaration shunt or cyclodiode .

33. Glaucoma associated with Iridocorneal
endothelial (ICE) Syndrome
3 entities :–
o Progressive iris atrophy
o Chandler’s syndrome
o Cogan – Reese syndrome
Presence of abnormal corneal endothelial cells
which proliferate to form an endothelial
membrane in the angle of anterior chamber.

34. Clinical features :– Affects middle – aged women
 Progressive iris atrophy – iris features predominates
with corectopia, atrophy and hole formation.
 Chandler’s syndrome – Mild iris changes and
corneal oedema predominates.
Cogan – Reese syndrome – nodular and diffuse
pigmented lesions of iris, may or may not be
associated with corneal changes
Treatment :–
 Medical treatment
 Trabeculectomy
 glaucoma drainage device and cyclodiode

35. Glaucoma associated with intraocular tumours
• Trabecular block.
○ Angle invasion by a solid iris melanoma.
○ Trabecular infiltration by neoplastic cells originating from an
iris melanoma. Rarely, tumour seeding from a retinoblastoma
may also invade the trabeculum.
○ Melanomalytic glaucoma may occur in some eyes with iris
melanoma; it is due to trabecular blockage by macrophages
that have ingested pigment and tumour cells, similar to
phacolytic glaucoma.
• Secondary angle closure
○ Neovascular glaucoma is the most common mechanism in
eyes with choroidal melanoma or retinoblastoma.
○ Anterior displacement of iris–lens diaphragm may occur in
an eye with a ciliary body melanoma or a large tumour of the
posterior segment.

37. Glaucoma secondary to epithelial ingrowth
a rare but potentially blinding complication of
anterior segment surgery or trauma, occurring
when conjunctival or corneal epithelial cells migrate
through a wound and proliferate in the anterior
segment.
Diagnosis:
• Persistent postoperative anterior uveitis.
• Diffuse epithelialization characterized by a greyish
translucent membrane .
• Cystic and fibrous proliferative
• Pupillary distortion.

38. Treatment :
Block excision
 Cryotherapy
 5_flurouracil
 Glaucoma drainage device

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