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Secondary Glaucoma
Definition
• Secondary Glaucoma
A group of disorders in which rise in
intraocular pressure(leading to glaucoma) is
associated with some primary ocular or
systemic disease.
2
Classification of secondary glaucoma's
• Based on mechanism of IOP rise
Secondary open angle glaucoma
Secondary angle closure glaucoma
3
Classification of secondary glaucoma's
• Depending on causative primary disease
– Phacogenic (Lens induced) glaucoma
– Pigmentary glaucoma
– Neovascular glaucoma
– Inflammatory glaucoma (Uveitic)
– Traumatic glaucoma
– Steroid induced glaucoma
– Pseudoexfoliative glaucoma
– Glaucomas associated with intraocular tumours
(Malignant melanoma, retinoblastoma)
4
Lens induced glaucoma
• Raised IOP secondary to a disorder of crystalline lens
• Secondary angle closure Secondary open angle
Phacomorphic glaucoma Phacolytic glaucoma
Phacotopic glaucoma Lens particle glaucoma
Phacoanaphylactic
glaucoma
5
Phacomorphic glaucoma
• Causes -
• Intumescent lens
• Anterior subluxation or dislocation of the lens
and spherophakia (Phacotopic variant)
• Pathogenesis – Swollen lens pushes iris
forwards, obliterating the angle
• Presentation – Acute congestive glaucoma
6
• Treatment –
• Medical treatment –
Control of IOP by
iv mannitol, systemic
acetazolamide and
topical beta blockers
• Surgical
Cataract extraction
with implantation of
PCIOL
7
Phacolytic glaucoma
• Trabecular meshwork is clogged
by lens proteins and
macrophages which
phagocytose the lens
proteins and inflammatory
debris
• Treatment
• Medical therapy to lower IOP
followed by extraction of
cataractous lens with PCIOL
implantation. 8
Lens particle glaucoma
• Trabecular meshwork is
blocked by lens
particles floating in
aqueous humour.
• Management
• Medical therapy to lower
IOP and
irrigation – aspiration of
lens particles from
anterior chamber
9
Phacoanaphylactic glaucoma
• Fulminating acute inflammatory
reaction due to antigen – antibody
reaction
• Granulomatous inflammation in
involved eye
• Preceding disruption of lens capsule
and leakage of proteins from capsule
• IOP is raised due to inflammatory
reaction of uveal tissue excited by lens
matter.
10
• Management includes
medical therapy to
lower IOP.
Treatment of iridocyclitis
with steroids and
cycloplegics .
Irrigation – aspiration
of lens matter from
anterior chamber ( if
required).
11
Pigmentary glaucoma
• Clogging up of trabecular
meshwork by pigment particles
in patients with Pigment
Dispersion Syndrome(PDS)
• Pigment released by mechanical
rubbing of posterior pigment
layer of iris with zonular fibrils
• Clinical features –
• Young myopic males
• Features similar to POAG
• Deposition of pigment granules
in anterior segment
Pigment deposition on lens zonules and
equatorial region. The deposits are clearly
visible in full mydriasis.
12
REVERSE PUPILLARY BLOCK IN
PIGMENTARY GLAUCOMA
13
CLASSIC DIAGNOSTIC TRIAD
• Krukenberg spindle (Pigment deposition on
the endothelium, in a vertical spindle-shaped
distribution).
• Midperipheral iris transillumination defects
• Dense trabecular meshwork pigmentation
14
Pigmentary glaucoma
• Gonioscopy – pigment
accumulation along
the Schwalbe’s line
especially inferiorly
(Sampaolesi’s line)
• Iris transillumination –
radial slit – like
defects in the periphery
• Treatment is similar to
that of POAG
15
Neovascular glaucoma
• Intractable glaucoma due to neovascularisation of
iris and angle of anterior chamber.
• 90 day glaucoma
• Due to retinal ischaemia
Diabetic retinopathy
CRVO
Sickle cell retinopathy
Eales’ disease
Chronic intraocular inflammation
16
PATHOGENESIS
• CHRONIC RETINAL ISCHAEMIA
• ANGIOGENIC FACTORS RELEASED
• NEOVASCULARISATION ON IRIS AND ANGLE
• NEOVASCULAR GLAUCOMA
17
Stages of neovascular glaucoma
• Pre-glaucomatous stage
• Open angle glaucoma
stage
• Secondary angle closure
glaucoma
18
TREATMENT
• Panretinal photocoagulation
• Intra- vitreal Anti -VEGF
• Mydriatics and Corticosteroids
• Filtering surgeries
• Glaucoma drainage devices
• Cyclodestructive procedures
19
INFLAMMATORY GLAUCOMA
• Non specific inflammatory glaucoma
• Open angle
• Angle closure
• Specific hypertensive uveitis syndromes
• Fuchs’ uveitis syndrome
• Glaucomatocyclitic crisis (Posner Schlossman
syndrome)
20
21
Open angle inflammatory glaucoma
Acute open – angle
inflammatory glaucoma
Chronic open – angle
inflammatory glaucoma
Mechanism of rise in
IOP
Trabecular clogging ,
trabecular oedema and
prostaglandin – induced
rise in IOP
Chronic trabeculitis and
trabecular scarring
Clinical features Features of acute
iridocyclitis associated with
raised IOP with open-angle
of anterior chamber
Raised IOP, open angle, no
active inflammation but
signs of previous episode
of uveitis present
Management Treatment of iridocyclitis
Medical therapy to
lower IOP by use of
hyperosmotic agents,
acetazolamide and beta –
blockers eye drops
Medical therapy
Trabeculectomy
Cyclodestructive
procedures
22
Angle closure inflammatory glaucoma
• Mechanism of rise in IOP –
• Secondary angle – closure with pupillary block
• Secondary angle – closure without pupillary block
• Clinical features – Raised IOP, seclusio papillae,
shallow anterior chamber
• Management –
• Prophylaxis – Local steroids and atropine to
prevent formation of synechiae
• Curative treatment – Medical therapy, surgical or
laser iridotomy and filtration surgery
23
Specific hypertensive uveitis
syndromes
• Glaucomatocyclitic crisis
(Posner Schlossman
syndrome)
• Recurrent attacks of
unilateral, acute mild
uveitis with secondary
open angle glaucoma.
• Glaucoma is out of
proportion to
inflammation.
• Due to accompanying
acute trabeculitis.
• Fuchs’ uveitis syndrome
• Chronic low grade anterior
uveitis.
• Occurs unilaterally in middle
aged persons
• Heterochromia of iris
• No posterior synechia.
• Associated with cataract
and secondary glaucoma
24
Blunt Trauma
25
26
Causes of glaucoma after trauma
• Inflammatory glaucoma
• Glaucoma due to hyphema
• Lens induced glaucoma
• Angle recession glaucoma
• Epithelial or fibrous ingrowth
• Angle closure due to PAS
27
Angle recession glaucoma
• Rupture in ciliary body
face
• Bimodal onset at 1 year
and 10 year post
trauma
• 270 degree recession-
risk of glaucoma- 5%
• 360 degree recession-
risk of glaucoma- 24%
Gonioscopic view of angle recession,
demonstrated by a widened ciliary body band.
There is a disruption in the ciliary body
between the external longitudinal muscle
fibers and the internal oblique and circular
muscle fibers.
28
Traumatic glaucoma
• Management
• Medical therapy with topical 0.5% timolol and
oral acetazolamide
• Surgical intervention needs to be
individualized according to nature and site of
trauma
29
Steroid induced glaucoma
• Secondary open angle glaucoma following steroid therapy
• In the general population:
• High steroid responders – 5%
• Moderate steroid responders – 35%
• Non steroid responders – 60%
(IOP rise after six weeks of steroid therapy)
Precise mechanism of IOP rise not known
Prevented by judicious use of steroids and regular IOP
monitoring
Treated by stopping steroids gradually and anti glaucoma
medications
30
Pseudoexfoliative glaucoma
• Pseudo exfoliation
syndrome(PES)/Glaucoma
capsulare is associated
with Secondary OAG in
50% of the cases.
• Deposition of an
amorphous grey dandruff
– like material on the
pupillary border,
posterior surface of iris
and ciliary processes
• Trabecular blockage by
exfoliative material
• Managed on the same
lines as POAG
31
Causes of elevated IOP post cataract surgery
• Early phase
• Inflammation
• Haemorrhage
• Retained viscoelastic/lens matter
• Late phase
• Tight suture
• Excessive cautery
• Pupillary block(IOL/Vitreous)
• Aqueous misdirection
• Epithelial/Fibrous down growth
32
Glaucoma associated with iridocorneal endothelial
syndromes
• Three clinical entities:
• Progressive iris atrophy
• Chandler’s syndrome
• Cogan-Reese syndrome/Iris
nevus syndrome
• Pathogenesis: Abnormal
corneal endothelial cells
proliferate to form a
membrane in angle of AC.
Contraction of membrane
leads to secondary angle
closure
• Treatment: Difficult and
usually surgical 33
Other causes of secondary glaucoma
• Glaucoma in aphakia/pseudophakia
• Ciliary block glaucoma
• Glaucoma associated with intraocular
haemorrhage
Red cell glaucoma
Haemolytic glaucoma
Ghost cell glaucoma
Hemosiderotic glaucoma
34
35
36
37
38

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Secondary-glaucoma-Final.pptx

  • 2. Definition • Secondary Glaucoma A group of disorders in which rise in intraocular pressure(leading to glaucoma) is associated with some primary ocular or systemic disease. 2
  • 3. Classification of secondary glaucoma's • Based on mechanism of IOP rise Secondary open angle glaucoma Secondary angle closure glaucoma 3
  • 4. Classification of secondary glaucoma's • Depending on causative primary disease – Phacogenic (Lens induced) glaucoma – Pigmentary glaucoma – Neovascular glaucoma – Inflammatory glaucoma (Uveitic) – Traumatic glaucoma – Steroid induced glaucoma – Pseudoexfoliative glaucoma – Glaucomas associated with intraocular tumours (Malignant melanoma, retinoblastoma) 4
  • 5. Lens induced glaucoma • Raised IOP secondary to a disorder of crystalline lens • Secondary angle closure Secondary open angle Phacomorphic glaucoma Phacolytic glaucoma Phacotopic glaucoma Lens particle glaucoma Phacoanaphylactic glaucoma 5
  • 6. Phacomorphic glaucoma • Causes - • Intumescent lens • Anterior subluxation or dislocation of the lens and spherophakia (Phacotopic variant) • Pathogenesis – Swollen lens pushes iris forwards, obliterating the angle • Presentation – Acute congestive glaucoma 6
  • 7. • Treatment – • Medical treatment – Control of IOP by iv mannitol, systemic acetazolamide and topical beta blockers • Surgical Cataract extraction with implantation of PCIOL 7
  • 8. Phacolytic glaucoma • Trabecular meshwork is clogged by lens proteins and macrophages which phagocytose the lens proteins and inflammatory debris • Treatment • Medical therapy to lower IOP followed by extraction of cataractous lens with PCIOL implantation. 8
  • 9. Lens particle glaucoma • Trabecular meshwork is blocked by lens particles floating in aqueous humour. • Management • Medical therapy to lower IOP and irrigation – aspiration of lens particles from anterior chamber 9
  • 10. Phacoanaphylactic glaucoma • Fulminating acute inflammatory reaction due to antigen – antibody reaction • Granulomatous inflammation in involved eye • Preceding disruption of lens capsule and leakage of proteins from capsule • IOP is raised due to inflammatory reaction of uveal tissue excited by lens matter. 10
  • 11. • Management includes medical therapy to lower IOP. Treatment of iridocyclitis with steroids and cycloplegics . Irrigation – aspiration of lens matter from anterior chamber ( if required). 11
  • 12. Pigmentary glaucoma • Clogging up of trabecular meshwork by pigment particles in patients with Pigment Dispersion Syndrome(PDS) • Pigment released by mechanical rubbing of posterior pigment layer of iris with zonular fibrils • Clinical features – • Young myopic males • Features similar to POAG • Deposition of pigment granules in anterior segment Pigment deposition on lens zonules and equatorial region. The deposits are clearly visible in full mydriasis. 12
  • 13. REVERSE PUPILLARY BLOCK IN PIGMENTARY GLAUCOMA 13
  • 14. CLASSIC DIAGNOSTIC TRIAD • Krukenberg spindle (Pigment deposition on the endothelium, in a vertical spindle-shaped distribution). • Midperipheral iris transillumination defects • Dense trabecular meshwork pigmentation 14
  • 15. Pigmentary glaucoma • Gonioscopy – pigment accumulation along the Schwalbe’s line especially inferiorly (Sampaolesi’s line) • Iris transillumination – radial slit – like defects in the periphery • Treatment is similar to that of POAG 15
  • 16. Neovascular glaucoma • Intractable glaucoma due to neovascularisation of iris and angle of anterior chamber. • 90 day glaucoma • Due to retinal ischaemia Diabetic retinopathy CRVO Sickle cell retinopathy Eales’ disease Chronic intraocular inflammation 16
  • 17. PATHOGENESIS • CHRONIC RETINAL ISCHAEMIA • ANGIOGENIC FACTORS RELEASED • NEOVASCULARISATION ON IRIS AND ANGLE • NEOVASCULAR GLAUCOMA 17
  • 18. Stages of neovascular glaucoma • Pre-glaucomatous stage • Open angle glaucoma stage • Secondary angle closure glaucoma 18
  • 19. TREATMENT • Panretinal photocoagulation • Intra- vitreal Anti -VEGF • Mydriatics and Corticosteroids • Filtering surgeries • Glaucoma drainage devices • Cyclodestructive procedures 19
  • 20. INFLAMMATORY GLAUCOMA • Non specific inflammatory glaucoma • Open angle • Angle closure • Specific hypertensive uveitis syndromes • Fuchs’ uveitis syndrome • Glaucomatocyclitic crisis (Posner Schlossman syndrome) 20
  • 21. 21
  • 22. Open angle inflammatory glaucoma Acute open – angle inflammatory glaucoma Chronic open – angle inflammatory glaucoma Mechanism of rise in IOP Trabecular clogging , trabecular oedema and prostaglandin – induced rise in IOP Chronic trabeculitis and trabecular scarring Clinical features Features of acute iridocyclitis associated with raised IOP with open-angle of anterior chamber Raised IOP, open angle, no active inflammation but signs of previous episode of uveitis present Management Treatment of iridocyclitis Medical therapy to lower IOP by use of hyperosmotic agents, acetazolamide and beta – blockers eye drops Medical therapy Trabeculectomy Cyclodestructive procedures 22
  • 23. Angle closure inflammatory glaucoma • Mechanism of rise in IOP – • Secondary angle – closure with pupillary block • Secondary angle – closure without pupillary block • Clinical features – Raised IOP, seclusio papillae, shallow anterior chamber • Management – • Prophylaxis – Local steroids and atropine to prevent formation of synechiae • Curative treatment – Medical therapy, surgical or laser iridotomy and filtration surgery 23
  • 24. Specific hypertensive uveitis syndromes • Glaucomatocyclitic crisis (Posner Schlossman syndrome) • Recurrent attacks of unilateral, acute mild uveitis with secondary open angle glaucoma. • Glaucoma is out of proportion to inflammation. • Due to accompanying acute trabeculitis. • Fuchs’ uveitis syndrome • Chronic low grade anterior uveitis. • Occurs unilaterally in middle aged persons • Heterochromia of iris • No posterior synechia. • Associated with cataract and secondary glaucoma 24
  • 26. 26
  • 27. Causes of glaucoma after trauma • Inflammatory glaucoma • Glaucoma due to hyphema • Lens induced glaucoma • Angle recession glaucoma • Epithelial or fibrous ingrowth • Angle closure due to PAS 27
  • 28. Angle recession glaucoma • Rupture in ciliary body face • Bimodal onset at 1 year and 10 year post trauma • 270 degree recession- risk of glaucoma- 5% • 360 degree recession- risk of glaucoma- 24% Gonioscopic view of angle recession, demonstrated by a widened ciliary body band. There is a disruption in the ciliary body between the external longitudinal muscle fibers and the internal oblique and circular muscle fibers. 28
  • 29. Traumatic glaucoma • Management • Medical therapy with topical 0.5% timolol and oral acetazolamide • Surgical intervention needs to be individualized according to nature and site of trauma 29
  • 30. Steroid induced glaucoma • Secondary open angle glaucoma following steroid therapy • In the general population: • High steroid responders – 5% • Moderate steroid responders – 35% • Non steroid responders – 60% (IOP rise after six weeks of steroid therapy) Precise mechanism of IOP rise not known Prevented by judicious use of steroids and regular IOP monitoring Treated by stopping steroids gradually and anti glaucoma medications 30
  • 31. Pseudoexfoliative glaucoma • Pseudo exfoliation syndrome(PES)/Glaucoma capsulare is associated with Secondary OAG in 50% of the cases. • Deposition of an amorphous grey dandruff – like material on the pupillary border, posterior surface of iris and ciliary processes • Trabecular blockage by exfoliative material • Managed on the same lines as POAG 31
  • 32. Causes of elevated IOP post cataract surgery • Early phase • Inflammation • Haemorrhage • Retained viscoelastic/lens matter • Late phase • Tight suture • Excessive cautery • Pupillary block(IOL/Vitreous) • Aqueous misdirection • Epithelial/Fibrous down growth 32
  • 33. Glaucoma associated with iridocorneal endothelial syndromes • Three clinical entities: • Progressive iris atrophy • Chandler’s syndrome • Cogan-Reese syndrome/Iris nevus syndrome • Pathogenesis: Abnormal corneal endothelial cells proliferate to form a membrane in angle of AC. Contraction of membrane leads to secondary angle closure • Treatment: Difficult and usually surgical 33
  • 34. Other causes of secondary glaucoma • Glaucoma in aphakia/pseudophakia • Ciliary block glaucoma • Glaucoma associated with intraocular haemorrhage Red cell glaucoma Haemolytic glaucoma Ghost cell glaucoma Hemosiderotic glaucoma 34
  • 35. 35
  • 36. 36
  • 37. 37
  • 38. 38