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SECONDARY
GLAUCOMA
By: Qurat-ul-ain
Ophthalmic Medical
Technologist/ MBA Health
& Hospital management
Secondary
glaucoma
Lens-induced
glaucoma
Phacomorphic
Phacolytic
Lens particle
Ectopia lentis
Phacoantigenic
uveitis
Aphakic
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
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
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.
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
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
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
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
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
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
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
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
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
THANK YOU!

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15. Secondary glaucoma.pptx

  • 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