This document discusses various types and causes of glaucoma, including: - Angle closure glaucoma which can be pre-trabecular, trabecular, or post-trabecular - Neovascular glaucoma which involves the growth of new blood vessels in the angle - Pigmentary and pseudoexfoliation glaucoma caused by pigment dispersion and buildup - Lens-induced glaucoma from phacolytic mechanisms, particles, or phacoanaphylaxis - Glaucoma caused by trauma, hemorrhage, tumors, corticosteroids, and after cataract surgery Treatment options vary depending on the type and stage of glaucoma but

1. Dr. Samarth Mishra

2. introductionCharacterized by-
o Raised IOP
o Open angles
o A/w underlying disorder leading to
alteration in aq. humor dynamics
o A/w OD & VF changes

3. classification
SOAG
Pre-
trabecular
Trabecular
Post-
trabecular

5. pretrabecular
 Aq. Flow obstructed by a membrane covering TM
 Consists of –
6. Fibrovascular memb.--neovascular glaucoma
7. Descement like memb.—IEC, trauma
8. Epithelial downgrowth
9. Fibrous downgrowth
10. Inflammatory memb– Fuch,s cyclitis

6. Neovascular glaucomaNeovacular tissue arbourise in the angle
Form a fibrovascular memb.
Blocks TM
SOAG

7. Stages of neovascular glaucoma.
(A)Pre-glaucoma stage with new vessels appearing at pupillary margin
and in angle.
(B) Open-angle glaucoma stage with new vessels spreading and
fibrovascular tissue covering angle.
(C) Heavy neovascularization and extensive peripheral anterior
synechiae.
(D) Regression stage with angle sealed and vessels less visible.

9. Treatment options of neovascular glaucoma
• Atropine and steroids to decrease inflammation
• Beta-bockers
•intravitreal VEGF inhibitor injection
Panretinal photocoagulation
- in early cases
Artificial filtering devices
- in very advanced cases
Cyclodestructive procedures
- to relieve pain
Retrobulbar alcohol
injection to relieve pain
Topical

11. (A)Membrane forms in one area of angle.
(B) Additional areas of angle are involved, and contraction of
membrane displaces pupil.

12. Trabecular causes
CLOGGING
 Erythrocytes: haeme, ghost cell
 Macrophages: phacolytic,
hemolytic, melanolytic
 Neoplastic: melanoma, NF,
naevus of Ota, JXG
 Pigment: PDS, Uveitis,
melanoma
 Proteins: PXF, uveitis, lens
particle
 Mucopolysaccharides: vitreous,
viscoelastic
 Gas & oil: C3F8, SF6, Air,
silicone oil
 Retinal photoreceptors :
Swartz’s syn
TM ALTERATION
 Edema/ inflammation
 Chemical burn
 Blunt trauma, angle recession
 Fe IOFB, siderosis of TM
 Steroid induced

13. Pigmentary glaucoma
 B/L condition due to pigment dispersion in AC
 Risk factors is young adolescent male, whites, high
myopic, AD located at 7q35-36
 Pathogenesis is rubbing of pig. Epi. Of iris against
zonules -> liberation of pig -> deposited in angle by
convection current in aq.
 Signs are:- cornea – krukenberg’s spindle
AC – deep, homogeneous fine hyperpig.
over post. Trabeculum
Iris – radial, spoke like, mid peripheral
transillumination defect, concave iris
Lens – Scheie’s line/Zentmayer’s ring
Zonules - pigmentation

15. Contd…
 Management ->
1) medical—beta blockers, adrenaline, dipivefin, CA
inhibitor, miotic
2) Laser – ALT, PI, Peri. Iridoplasty
3) Surg - trabeculectomy

16. Exfoliation glaucoma
 TM clogging up by PXF material &/or pig. From iris
 Risk factors are –fem, in Scandinavia, mutation in
LOXL1 gene at 15q22 locus
 Patho ---grey-white fibrillary extracellular material
composed of protein core surrounded by GAGs
produced by abnormal BM of ageing epi. Cells of
TM, equatorial lens capsule & CB.
 Signs –cornea -> dandruff like deposi, in endo.
AC -> Sampolesi’s line
iris -> absence of pupi. Ruff, moth-eaten
trans illumination defect
lens -> cataract, exfo. Deposi. As central
disk with peri. Band & a clear zone in
middle

17. Pseudoexfoliation glaucoma
Pseudoexfoliative material Iris sphincter atrophy Gonioscopy
Central disc with
peripheral band
Trabecular hyperpigmentation
- may extend anteriorly
(Sampaolesi line)
On retroillumination

18. Contd..
 T/T ---
1) Medical - beta blockers, epinephrine, miotics
2) Laser – ALT
3) Surg – trabeculectomy
4) Trabecular aspiration

19. Lens induced glaucoma
1) PHACOLYTIC:-
. Due to protein leakage from mat./hypermat. cat
. mechanism is –a) high molecular wt. soluble
protein directly block
b)macrophages engulf the
proteins & block
. c/f – seen in elderly with h/o poor vision for mons
- acute onset of uniocular pain, redness & watering
- grossly decres. Vision & raised IOP
- signs of uveitis
-hypermat/ morgagnian cat
- AC shows heavy flare a/w hyper refringent crystals which are
ca++ oxalate / cholesterol crystals
. t/t – medical (hyperosmotic, CA inhi.,topical b-blockers & steroids
- surg ( ECCE with PCIOL)

20. Phacolytic glaucoma
Pathogenesis Signs
• Deep anterior chamber
• Control IOP medically
• Remove cataract • Floating white particles
Treatment

21. Calcium oxalate crystal in the lens of a
patient with glaucoma associated with
hypermature cataract. (Hematoxylin and
eosin stain.)
Phacolytic glaucoma with bloated
macrophages and lens material
obstructing the trabecular
meshwork.

22. Contd…
2) LENS PARTICLE:-
. k/a phacotoxic uveitis
. Mechanism is – due to trauma/ surg.retained lens material
disruption of lens capsule
lens material liberation raised IOP
inflammatory response
raised IOP
. c/f – features of uveitis, rai IOP, chunky white particles in AC,
hypopyon
. Diag. by paracentesis
. t/t – medical as phacolytic
- surg. ( removal of lens material)

23. Contd…
3)PHACOANAPHYLAXIS :-
. occur when patients become sensitized to their own lens
protein k/a endophthalmitis anaphylactica
. typically develops after penetrating trauma or
extracapsular cataract extraction
. granulomatous inflammation of the lens with
polymorphonuclear leukocytes, lymphocytes, epithelioid
cells, and giantcells.
. t/t is surg. Removal of residual lens material

24. Glaucoma after trauma
1) CHEMICAL :-
. Alkali>acid
. caused by scleral shrinkage and release of active
substances, including prostaglandins
. IOP measured more accurately with the
pneumatic or MacKay-Marg tonometers
.managed by – medical ( topical and systemic
medications)
2) ELECTRIC :-
. pressure rise to venous dilation, contraction of
the extraocular muscles, and pigment dispersion
. No therapy due to transient rise of IOP

25. Contd…
3) RADIATION :-
. Mechanism are neovascularization/ ghost-cell
glaucoma associated with radiation retinopathy and
vitreous hemorrhage.
4) PENETRATING :-
. Due to retained organic material / FB / severe
inflammation / TM damage
5) CONTUSION :-
. can cause hyphema, iridocyclitis, iris sphincter tears,
iridodialysis, cyclodialysis, lens subluxation, retinal
tear or dialysis, retinal detachment, vitreous
hemorrhage, choroidal rupture, and glaucoma.

26. Contd…

27. Glaucoma a/w intraocular
haemorrhage
1) GHOST CELL:-
.mecha. - retinal disease/ trauma/surgery /snake poisoning
vitreous haem.
degenerated RBC’s travel thr. Disruped ant
hyaloid face
obstructs TM
. Diag. by paracentesis & cyto. Exam. which shows HEINZ bodies
i.e. RBCs in the vitreous degenerate to tan-colored spheres
(ghost cells), which appear empty except for clumps of
denatured hemoglobin
. t/t is AC wash / pars plana vitrectomy to remove remaining ghost
cells

28. Contd…
2) HEMOLYTIC :-
. Due to macrophages laden with pigments, RBC’s &
debris
3) HEMOSIDEROSIS :-
. Due to iron liberted from Hb causing siderosis of
TM
4) HYPHEMA :-
. Due to blood & blood products
. Total hyphema changing color from red to black
(black-ball or eightball hyphema)
. t/t – topical anti glaucoma
- surgical removal of hyphema

29. Glaucoma a/w uveitis
. Mechanism are-
(1) increased viscosity of aqueous humor;
(2) obstruction of the trabecular meshwork by
inflammatory cells and debris
(3) swelling and dysfunction of the trabecular
meshwork;
(4) liberation of active substances such as
prostaglandins;
(5)scarring of the outflow channels;
(6) development of a cuticular endothelial membrane
over the angle;
(7) neovascularization;
(8) elevation of episcleral venous pressure;

30. Contd…
Causes are:-
1) FUCH’S HETEROCHROMIC
IRIDOCYCLITIS
. Mild form of anterior uveitis associated with
cataract and glaucoma.
.c/f – mild uveitis, fine filaments on the
endothelium between the keratic precipitates, a
patchy loss of the iris pigment epithelium,
hypochromia, grey-white nodules on the anterior
iris, a few opacities in the anterior vitreous, and
chorioretinal scars
. Gonioscopy reveals fine vessels that bridge the
angle

31. Contd…
2) GLAUCOMATOCYCLITIC CRISIS:-
. k/a POSNER – SCHLOSSMAN SYNDROME
. young to middle-aged adults and consists of
recurrent episodes of mild anterior uveitis and
marked elevations of IOP
. mild ciliary flush, a dilated or sluggishly reactive
pupil, corneal epithelial edema, IOP in the range
of 40–60 mmHg, decreased outflow facility, open
angles, faint flare, and 1–20 fine
keratic precipitates

32. Contd…
3) JRA:-
. most common in young girls with iridocyclitis and
monoarticular or pauciarticular involvement
. Due to inflammation of the trabecular meshwork
4) HERPES :-
. Due to trabeculitis , inflamm. Of TM
. Commonly in disciform & necrotising sromal type
5) SYPHILIS:-
. Due to acute interstitial keratitis

33. Contd…
6) SARCOIDOSIS:-
. swelling and dysfunction of the trabecular meshwork,
obstruction of the trabecular meshwork by inflammatory
cells and debris
7) PRECIPITATES IN THE TM
Diag. by lab. & imaging technique
t/t- medical ( topical, sys. & periocular steroids, cycloplegics,
NSAIDS, immunomodulators, anti glaucoma)
- surg (ALT, filtering procedure, tube shunts, cycloablative,
Nd:YAG laser cyclophotocoag.)

34. Glaucoma a/w intraocular
tumors
 Mechanisms are:-
(1) direct extension of the tumor into the trabecular
meshwork
(2) seeding of tumor cells into the outflow channels
(3) pigment dispersion
(4) inflammation
(5) Hemorrhage,inducing hemolytic glaucoma, and
suprachoroidal hemorrhage
(6) neovascularization of the angle
(7) obstruction of the trabecular meshwork by
macrophages containing melanin released by a
necrotic tumor (melanomalytic glaucoma)

35. Contd…
 Tumors causing rai. IOP:-
1) Iris- neavus, melanocytoma, malignent
melanoma, metastatic
2) CB- medullocytoma, melanocytoma, malignent
melanoma
3) Choroid- malignent melanoma, metastatic
4) ON- melanocytoma, metastatic
5) Retina – retinoblastoma
6) Metastatic CA
7) Others- leukemia, lymphoma, multiple
myeloma, juvenile xanthogranuloma

36. Contd…
 Diag. by- gonio., indirect & direct ophthalmoscope, USG,
MRI, FNAC, Aq. Aspiration, excisional biopsy
 t/t –medical (anti glaucoma with surg./radiation/ chemo/a
combination)
- surg—
. smaller tumor ( observation till growth)
. Iridectomy / iridocyclectomy for smaller tumor
. Ant. Tumor ( argon laser trabeculopexy)
. Post. Tumor ( local resection/ photocoagulation/ episceral
radiopaque therapy / enucleation/exenteration)

37. Corticosteroid glaucoma
 Seen in steroid responders who use topical, creams, oientment
on eyelids, systemic, periocular, inhaled steroids
 Steroid responders are those who showed rai. IOP to topical
steroids in 4-6 wks as compared to general population
 3 groups- low (manifest with no change in IOP)
intermediate ( mod. Elevation of IOP to 22-30)
high ( marked rise to >30)
Patho.:- stabilize lysosomal memb. Prevents polymerization of
GAG GAG accumulation in TM
t/t :- dicontinuation of drug
- anti glaucoma medication
- trabeculectomy / seton implantation in uncontrolled

38. Glaucoma after cataract surgery Mechanism are:-
1. Inflammation with the release of active
substances, including prostaglandins and the
formation of secondary aqueous humor.
2. A watertight wound closure with multiple fine
sutures limiting the ‘safety valve’ leak of aqueous
humor.
3. Deformation of the limbal area, reducing
trabecular outflow.
4. Obstruction of the trabecular meshwork by
pigment, blood,lens particles, inflammatory cells,
and viscoelastic substances.

39. Contd…A. Early onset (within first postoperative week)
 1. Pre-existing chronic open-angle glaucoma
 2. alpha- Chymotrypsin-induced glaucoma
 3. Hyphema/debris
 4. Viscoelastic material
 5. Idiopathic pressure elevation
B. Intermediate onset (after first postoperative week)
 1. Pre-existing chronic open-angle glaucoma
 2. Vitreous in the anterior chamber
 3. Hyphema
 4. Inflammation
 5. Lens particle glaucoma
 6. Corticosteroid-induced glaucoma
 7. Ghost-cell glaucoma
C. Late onset (more than 2 months postoperatively)
 1. Pre-existing chronic open-angle glaucoma
 2. Ghost-cell glaucoma
 3. Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser capsulotomy
 4. Vitreous in the anterior chamber
 5. Late-occurring hemorrhage
 6. Chronic inflammation

40. 1.alpha-Chymotrypsin
Glaucoma
 used widely to facilitate intracapsular cataract
extraction.
 mechanism for alpha-chymotrypsin glaucoma
is that zonular fragments obstruct the outflow
channels
 t/t by using a lesser concentration of the drug (1:10 000
instead of 1:5000) in a lower volume(0.25–0.5 ml
instead of 2 ml)
 anterior chamber should be irrigated before lens
extraction to remove zonular fragments

41. Scanning electron micrograph of the zonular fragments
obstructing the trabecular meshwork after alpha-
chymotrypsin administration

42. 2. Glaucoma From Viscoelastic
Substances
 Sodium hyaluronate blocks TM
 tiny ruby-like globs of hemorrhage on the iris surface
or suspended in the anterior chamber

43. 3. Glaucoma with Pigment
Dispersion from Intraocular
Lenses
 Mechanism:-
Decentered, tilted, excessively mobile, too small, or
reversed in position
excess friction between the optic or haptic and the iris
pigment epithelium
Pigment particles block TM
c/f :- geographical loss of iris pigment

44. 4. Uveitis-Glaucoma-Hyphema
Syndrome
 Seen in iris supported ACIOL / PCIOL
 c/f:- rai.IOP, iridocyclitis & recurrent hyphema for wks
to mons after surg.
 Due to excessive chafing of the iris by the
pseudophakics because the lenses are too mobile

45. 5.Glaucoma After nD: yag Laser
Posterior Capsulotomy
 occurs within 2–4 hours of the laser treatment and
then abates spontaneously over the next 24 hours
 usually associated with particulate debris clogging the
trabecular meshwork
 Pretreatment with apraclonidine 1% 1 hour prior to
surgery and one drop 1 hour after surgery has been
shown to decrease the number and severity of
postoperative pressure spikes

46. 6. Glaucoma from Vitreous in
the Anterior Chamber
 Common in aphakic eyes
 after a spontaneous rupture of the hyaloid face or after
an extensive posterior vitreous detachment.

47. Retinal detachment and glaucoma
 Due to vitreous loss
 Schwartz Syndrome- RD + Rai. IOP + decrea.
Outflow + open angles + cells & flare in AC
 Mechanism:- a)angle recession,inflammation,
pigment granules released by the retinal pigment
epithelium, and glycosaminoglycans synthesized by
the photoreceptors blocks TM
- b) photoreceptor outer segments migrate through
the retinal hole and obstruct the trabecular meshwork

48. Glaucoma after vitrectomy
Pre-existing glaucoma
 Angle recession
 Ghost cell
 Primary open-angle glaucoma
 Pigmentary glaucoma
Associated with intraocular hemorrhage
 Hyphema
 Ghost cell
 Hemolytic
 Hemosiderosis
Related to lens material
 Phacolytic
 Lens particle
 Phacoanaphylactic
Neovascular
Inflammatory
Corticosteroid induced
Intraocular gas or liquid
 Air
 Viscoelastic substances
 Perfluorocarbons
 Silicone

49. Post- trabecular causes
 TM is normal but aq. Flow is impaired due to elevated
episcleral venous pressure
 For every 1mm rise in EVP-> 0-8 mm rise in IOP
 Causes are :-
I. Obstruction of venous drainage
A. Episcleral-1. Chemical burns 2. Radiation
B. Orbital -1. Retrobulbar tumors 2. Thyroid eye disease
3. Pseudotumor 4. Phlebitis
C. Cavernous sinus thrombosis
D. Jugular vein obstruction
E. Superior vena cava obstruction
F. Pulmonary venous obstruction
II. Arteriovenous fistulas
A. Orbital
B. Intracranial-1. Carotid-cavernous fistula 2. Dural fistula
3. Venous varix 4. Sturge-Weber syndrome
III. Idiopathic

50. Superior Vena Cava
Obstructions
 Mainly due to tumors, aortic aneurysms,
mediastinal masses, hilar adenopathy, and
intrathoracic goiter
 produces edema and cyanosis of the face and
neck (pumpkinhead appearance) as well as
dilated vessels in the head, neck, chest, and upper
extremities
 ocular findings include exophthalmos,
papilledema, and prominent blood vessels in the
conjunctiva, episclera, and retina
 IOP is elevated mainly in supine position

51. Arteriovenous Fistulas
 Carotid-cavernous fistulas-
- It provide a free communication between the
internal carotid artery and the surrounding
cavernous sinus in high blood flow and high
mean pressure in the shunt
- reversal of blood flow in the vessels leads to
congestion of the orbital veins and soft tissues
- c/f--- pulsating exophthalmos, chemosis, lid edema,
vascular engorgement, and restriction of ocular
motility

52. Carotid-cavernous fistula.

53. Contd…
 Sturge-Weber Syndrome
- k/a enchephalotrigeminal angiomatosis
- Congenital, sporadic oculocutaneous disorder
- Glaucoma is seen in 30% of pt’s having
ipsilateral facial hemangiomata during first
2yrs of life
- Patho isolated trabeculogenesis
-> raised episcleral venous pressure
- t/t medical (topical PG’s)
 goniotomy
 combined trabeculotomy &
trabeculectomy

54. THE END