A review for medical students.

1. SECONDARY
GLAUCOMA
By: Qurat-ul-ain
Ophthalmic Medical
Technologist/ MBA Health
& Hospital management

2. Secondary
glaucoma
Lens-induced
glaucoma
Phacomorphic
Phacolytic
Lens particle
Ectopia lentis
Phacoantigenic
uveitis
Aphakic

3. HMW lens
proteins
• Released through microscopic
defects in the intact capsule of
hypermature lens
Causes
obstruction
of outflow
pathways Results in
blockage at
the angle of
AC
• Leads to  IOP
MECHANISM OF
PHACOLYTIC
GLAUCOMA

4. SYMPTOMS:
Acute ocular pain
Slow vision loss
history prior to the
acute onset of pain
Inaccurate light
perception due to
the density of
cataract
SIGNS:
Conjunctival hyperemia
Corneal edema
AC depth normal or deep
AC containing flare,
aqueous cells
Precipitate on the corneal
endothelium
Sluggish pupil
Hypermature/
morgagnian cataract
TREATMENT & MANAGEMENT:
Acute lowering of IOP by:
Combination of topical &
systemic IOP lowering agents.
Hyperosmotic agents
Systemic carbonic anhydrase
inhibitors
Topical beta blockers
Prednisolone acetate eye drops
Cycloplegic drugs
Cataract extraction under
mannitol followed by steroid
cover
CLINICAL PICTURE & PRINCIPLES
OF MANAGEMENT

5. Acute angle-
closure
glaucoma
• By an intumescent cataract
Slackens the
suspensory
ligaments &
allows lens to
move anteriorly Leads to the
iridolenticular
contact by ant-post
lens growth.
MECHANISM OF
PHACOMORPHIC
GLAUCOMA
• Equatorial age related growth of the lens
• Potentiates pupillary
block & iris bombe’
formation.

6. SYMPTOMS:
Similar to
PACG
SIGNS:
Shallow anterior
chamber
Mid dilated pupil
Dense white
cataract is
evident.
TREATMENT & MANAGEMENT:
Reduce IOP
Cataract extraction
Should be handled as an
emergency
Combination of topical &
systemic IOP lowering agents.
Topical steroids
Prednisolone acetate 1%
CLINICAL PICTURE & PRINCIPLES
OF MANAGEMENT

7. IOP
elevation
• By obstruction of aqueous outflow
d/t retained lens matter.
Secondary open
angle glaucoma
May occur after cataract
surgery, trauma or YAG
posterior capsulotomy
MECHANISM OF LENS-
PARTICLE GLAUCOMA:
• Grossly disrupted lens material in the
anterior chamber

8. SYMPTOMS:
Acute rise in
IOP
SIGNS:
TM blocked by
the lens particles
floating in
aqueous humor
Diagnosis from
history of trauma
and surgery
TREATMENT &
MANAGEMENT:
Topical & systemic pressure
lowering drugs.
Mydriatics to inhibit
posterior synechia
formation.
Topical steroids
Surgical removal of retained
lens matter if IOP not
controlled by medical
management.
CLINICAL PICTURE & PRINCIPLES
OF MANAGEMENT

9. Acute
inflammatory
reaction due to
antigen-antibody
• Rarest type of lens-induced glaucoma
Granulomatous
inflammation
Raised IOP
MECHANISM OF
PHACO-ANTIGENIC
GLAUCOMA:
• Preceding disruption of lens capsule by
cataract extraction, penetrating injury
• Due to inflammatory
reaction of uveal tissue

10. SYMPTOMS:
Sensitized
with own
lens proteins
SIGNS:
Eyelid edema
Conjunctival
injection
Corneal edema
An intense AC
reaction
Post. Synechiae
Mutton fat keratitic
precipitates
Ant. uveitis
TREATMENT &
MANAGEMENT:
Topical steroid therapy
Anti-glaucoma medication
Surgical intervention if
necessary
CLINICAL PICTURE & PRINCIPLES
OF MANAGEMENT

11. Lens
displacement
Pupillary block
resulting in iris
bombe
Shallowing of
ACA resulting
in  IOP
MECHANISM OF
ECTOPIA LENTIS
GLAUCOMA:
TREATMENT:
Lensectomy to
restore vision
& reduce the
risk of
recurrent
pupillary
block

12. Intact
vitreous face
Block the pupil
or an iridotomy
site Leads to
sec. angle
closure
glaucoma
MECHANISM OF
APHAKIC/
PSEUDOPHAKIC
GLAUCOMA:
TREATMENT:
IV hyperosmotic
agents
Removal of
viscoelastic
substances
PC-IOL
Anti-
cholinesterase
agents
intraoperatively
Iridotomy

13. NEOVASCULAR GLAUCOMA
CAUSES:
Ischemic CRVO
DM
Arterial retinal
vascular disease
Long standing
retinal detachment
Intraocular tumors
SIGNS:
Corneal edema
Raised IOP
Flares & cells in AC
Subtle vessels on the pupillary
margin
New vessels on surface of the
iris
TREATMENT:
Medical treatment
of raised IOP
Panretinal
photocoagulation
RD surgery 3PPPV
Anti-VEGF
Trab with shunts
Ciliary body
ablation
Enucleation

14. INFLAMMATORY GLAUCOMA
Sec. ANGLE CLOSURE
CAUSES:
As a result of ocular
inflammation.
Fibrin &  aqueous
proteins d/t
breakdown of blood-
aqueous barrier
Posterior synechiae
TYPES:
Pseudoexfoliation
syndrome
Pigment dispersion
syndrome
Posner schlossman
syndrome
FUCHS heterochromia
uveitis
Traumatic hyphema
Hemolytic & ghost cell
glaucoma
Angle recession
glaucoma
Steroid induced
glaucoma
Sec. OPEN ANGLE
CAUSES:
Edema of trabecular
meshwork
Endothelial cell
dysfunction
Fibrin or
inflammatory cells
blocking aqueous
outflow

15. THANK YOU!