Precise theory with picture to understand and to learn with ease

1. Secondary glaucoma
Dr.B.Lakshmi Preethi
Post graduate M.S.,ophthal (2nd yr)

2. categorized aS
 Pigment dispersion syndrome
• Pigmentary glaucoma
• Exfoliation syndrome
 Lens induced glaucoma

3. • Malignant glaucoma
• Glaucoma associated with retinal disorders
• Glaucoma associated with intraocular tumors
• Glaucoma associated with inflammation
• Steriod induced glaucoma

4. Lens induced
 Lens particle glaucoma
 Phacoanaphylactic glaucoma
 Phacolytic glaucoma
 Phacomorphic glaucoma

5. Phacolytic Glaucoma
• Lens induced glaucoma due to protein leakage from
mature or hypermature cataract is termed as phacolytic
glaucoma.
• It was first described by Gifford in 1900

6.  Mechanism of Glaucoma
 Theort 1:release of lens particle into aqueous which is
engulfed by macrophages blocks trabecular meshwork
 Theory2: high molecular weight soluble protein released
from the lens directly block the trabecular meshwork

7.  Clinical Features
acute form with sudden onset of pain, redness and
watering in the eye.
typically have sudden, high rise in IOP ( similar to acute
angle closure glaucoma)

8. Slit-lamp examination:
shows diffuse corneal edema
Soluble lens proteins, and aggregates of white
material leaked from cataractous lens are seen in
the anterior chamber
heavy flare in the anterior chamber -calcium
oxalate or cholesterol crystles

9.  The lens is mature, hypermature or Morgagnian with
wrinkling of the anterior lens capsule due to release of
lens material
 Gonioscopy: open angle is seen ( angle recession in 25
percent cases)

11.  Differential Diagnosis
I. phacomorphic glaucoma
II. acute angle closure glaucoma
III. primary open angle glaucoma
IV. glaucoma associated with uveitis.

12.  Management
 Immediate treatment( medical mx):
a) hyperosmotic agents
b) carbonic anhydrase inhibitors
c) topical beta blockers
d) Topical corticosteroids can be used to decrease the
inflammatory component

13.  Treatment of choice : cataract extraction
AC should be washed thoroughly to avoid post operative
complication
ECCE with PCIOL implantation shows good result

14. Lens Particle Glaucoma
 Previously thought as phacotoxic uveitis leading to
glaucoma
 Now , this term has been proposed for cases when lens
particle and debris are liberated in the anterior chamber
after disruption of lens capsule

15.  Clinical Features
Slit lamp examination : heavy flare in AC ,
cellular reaction –lens particles are seen in
anterior chamber
Gonioscopy : open angle , lens pareicles at angle

16.  Mechanism of Glaucoma :
The lens material obstructs the trabecular meshwork
inflammation due to trauma ,surgery ,retained lens
material
Differential Diagnosis
 phacoanaphylaxis,
 phacolytic glaucoma
 uveitis associated with primary open angle glaucoma

17.  Management
 Medical therapy – same as phacolytic glaucoma
however, steroids should be used only in moderate amount
as it delays absorption of lens material
 Surgical treatment- surgical removal of lens material

18. Phacoanaphylactic Glaucoma
Rupture of lens capsule can lead to intraocular inflammation
in individuals who are hypersensitive to lens protein.
This is also known as “endophthalmitis
phacoanaphylactica”.
It was first reported by Verhoeff and Lemoine in 1922.

19.  Clinical Features
There is usually a preceding disruption of the lens
capsule by cataract surgery or penetrating injury.
The duration of latent period and the severity of uveitis
are not associated with the quantity of free lens material.

20.  Slit lamp examination:
cornea – keratic precipitates
AC – anterior uveitis with hypopyon
Iris –anterior & posterior synechiae
complication :
Patient may develop pupillary block or chronic angle
closure glaucoma

21.  Mechanism of Glaucoma
Phacoanaphylaxis represents an immune complex
disease that develops when normal tolerance to lens protein
is lost, rather than a cell mediated rejection of foreign
tissue.
Glaucoma can also develop due to accumulation of
inflammatory cells which block the trabecular meshwork

22.  Differential Diagnosis
 sympathetic ophthalmia
 phacolytic glaucoma
 lens particle glaucoma

23.  Management
 Medical therapy: does not respond to any steroids.
topical betablockers and carbonic
anhydrase can be helpful
 Surgical treatment:
Surgical removal of residual lens material is
required.
The intraocular lens and the capsule can also be
removed.

24. Phacomorphic Glaucoma
 Reduction in the anterior chamber angle due to swollen or
intumescent lens in advanced cataract which leads to
increase in the IOP is known as phacomorphic glaucoma
 Mechanism of Glaucoma
Angle closure may be caused by pupillary block mechanism
or by forward displacement of the lens iris diaphragm.

25.  Clinical Features
 Conjuctiva -hyperemia
 Cornea edema (if iop is high)
 AC- shallow
 Lens –pearly white with aqueous filled spaces or vacuoles
filled inside the lens
Gonioscopy : angle closed
 Management : same as phacolytic glaucoma

26. Malignant glaucoma
High iop
Slit lamp examination –flat or uniformly shallow anterior
chamber following incisional surgery
Other names :
“ciliary block” glaucoma
“aqueous misdirection syndrome”.
this has got its name as it is difficult to treat due to poor
treatment responds

27. Mechanism of Glaucoma:
 aqueous is misdirected posteriorly into the vitreous
cavity- Shaffer
 Trigger not known
 Relative block to anterior movement of aqueous near the
lens equator, ciliary processes and anterior vitreous face
may be the starting event

28. Predisposing Conditions
 incisional surgery - peripheral iridectomy ,
trabeculectomy,cataract extraction , laser iridotomy,YAG
capsulotomy
Differential Diagnosis:
 Choroidal Detachment –follows filtration surgery ,peripheral
cleaved choroid seen
 Pupillary Block- peripherally shallow anterior chamber
 patent peripheral iridectomy rule out pupillary
block
 Suprachoroidal Hemorrhage - choroidal elevation are dark reddish
in colour

29. Management
 Medical Therapy
 one percent atropine four times a day
 ten percent phenylephrine four times daily.
 mydiatric-cycloplegic drops,
 0.5 percent timolol maleate twice daily,
 oral acetazolamide 500 mg twice,
 oral glycerol 1.5 to 2 ml/kg/day is administered in two to
three divided doses

30.  Laser Treatment
Nd:YAG laser hyaloidotomy-for aphakic and pseudophakic
malignant glaucoma, there is immediate formation of
anterior chamber.
Argon laser treatment of ciliary processes-. Two to four
ciliary processes should be lasered. The size of ciliary
processes may shrink with laser treatment. Medical
treatment has to be continued simultaneously

31.  Surgical Treatment -Pars plana vitrectomy should be done
in cases where medical and laser therapy is unsuccessful
- iridozonulovitrectomy is also done.
 video
 Fellow Eye -Nd:YAG laser iridotomy must be done, Miotic
therapy should be avoided .

32. GLAUCOMAS ASSOCIATED WITH
DEGENERATED OCULAR BLOOD
 Ghost Glaucoma
 Hemolytic Glaucoma
 Hemosiderotic glaucoma

33. Ghost Cell Glaucoma
 In 1976, Campbell and coworkers described a form of
glaucoma in which degenerated red blood cells (ghost
cells) develop in the vitreous cavity and subsequently
enter the anterior chamber, where they temporarily
obstruct aqueous outflow

34. Mechanism
 Having entered the vitreous cavity by one of several
mechanisms (trauma, surgery, or retinal disease), fresh
erythrocytes are transformed from their typical
biconcave, pliable nature to tan- or khaki-colored,
spherical, less-pliable structures, referred to as ghost
cells . Unlike fresh red blood cells, ghost cells do not pass
readily through a 5-µm Millipore filter or human
trabecular meshwork.

35.  The ghost cells develop within 7 to 10 days and may
remain in the vitreous cavity for many months, until a
disruption of the anterior hyaloid allows them to enter the
anterior chamber. Once in the anterior chamber, the
abnormal cells accumulate in the trabecular meshwork,
where they may cause a temporary, but occasionally
marked, elevation of IOP.
 Histologically- Heinz bodies ( denatured hemoglobin
)present.

36. Specific Causes
 cataract extraction (3 ways- VH before,during ,after
obstruct trabecular meshwork as ghost cells)
 vitrectomy (not completely removed VH)
 Vitreous Hemorrhage without Surgery
o Trauma –hyphema
o snake bite ( eg ; crotalids have proteolytic enzyme
which disrupts vascular integrity act as hemorrhagic factor

37.  Clinical Features
IOP –Normal to marked elevation with pain
and corneal edema depanding on number of
ghost cells in anterior chamber.
Slit lamp examination –
khaki-colored cells in the aqueous and
on the corneal endothelium

38.  in large quantities- appears as
pesudohypopyon
 With layer of fresher red blood cells
(known as a “candy-stripe sign”)
Gonioscopy : open

39.  Differential Diagnosis - hemolytic and hemosiderotic
glaucomas
 econfirmed by –aqueous aspirate, phase contrast
microscopy, elight microscopy
 Management –It is a temporary condition last for months
Medical management –anti glaucoma drugs
Surgical management –AC irrigation OR vitrectomy ( after
removal of ghost cells IOP returns to normal in most cases)

40. Hemolytic Glaucoma
 intraocular hemorrhage in which macrophages ingest
contents of the red blood cells and then accumulate in
the trabecular meshwork
 Slit lamp examination : red tinted cells in AC
 Cytology :macrophage containing golden brown pigment
 Gonioscopy : open
 Ultrasound – phacocytized blood and pigment in
trabecular spaces , endothelial cells of trabecular
meshwork were degenerated and had phacocytized blood
 Treatment –self limiting

41. Hemosiderotic Glaucoma
 Hemoglobin from lysed red blood cells in the anterior
chamber is phagocytized by endothelial cells of the
trabecular meshwork in this rare condition.
 Iron in the hemoglobin subsequently causes siderosis,
produce tissue alterations in the trabecular meshwork,
resulting in obstruction to aqueous outflow
 Hyphema in sickle cell hemoglobinopathies requires
aggressive management, as moderately elevated IOP
can produce rapid damage to the optic nerve.

42. NEOVASCULAR GLAUCOMA
 In 1906, Coats described new vessel formation on the iris
in eyes with central retinal vein occlusion.
 Rubeosis iridis is frequently associated with a severe form
of glaucoma.
 rubeotic glaucoma or neovascular glaucoma, which was
proposed by Weiss and colleagues

43. Factors Predisposing to Rubeosis Iridis
 hypoxic disease of the retina rubeosis iridis
 Causes includes-diabetic retinopathy,CRVO,carotid
ischemic diseases
 Intracapsular cataract surgery ,ECCE,Primary capsulotomy,
laser capsulotomy in eyes with diabetic retinopathy has
been associated with an increased incidence of
postoperative rubeosis iridis and neovascular glaucoma
 Optic disc cupping was reported to be a significant risk
factor for central and branch retinal vein occlusions in the
Beaver Dam Eye Study

44.  acute onset or exacerbation of rubeosis iridis after
diabetic vitrectomy can indicate the presence of a
peripheral traction retinal detachment
 Intraocular silicone oil also reduces the incidence of
anterior segment neovascularization

45. Conditions Predisposing to Rubeosis
Iridis and Neovascular Glaucoma
 Retinal Ischemic Disease :
Diabetic retinopathy
Central retinal vein occlusion
Central retinal artery occlusion
Branch retinal vein occlusion
Branch retinal artery occlusion
Retinal detachment
Hemorrhagic retinal disorders
Coat exudative retinopathy

46.  Eales disease
 Leber congenital amaurosis
 Retinopathy of prematurity
 Persistent hyperplastic primary vitreous
 Sickle-cell retinopathy
 Syphilitic retinal vasculitis
 Retinoschisis Stickler syndrome (inherited vitreoretinal
degeneration)
 Optic nerve glioma with subsequent venous stasis
retinopathy

47. Irradiation:
 Photoradiation
 External beam
 Charged particle: proton, helium ion radiation
 Plaques
Tumors
 Choroidal melanoma
 Ring melanoma of the ciliary body
 Iris melanoma
 Retinoblastoma Large-cell lymphoma

48. Inflammatory Diseases
 Uveitis: chronic iridocyclitis, Behçet disease
 Vogt-Koyanagi-Harada syndrome
 Sympathetic ophthalmia
 Endophthalmitis
 Crohn disease with retinal vasculitis
Extraocular Vascular Disorders
 Carotid artery obstructive disease (3rd m/c cause)
 Carotid-cavernous fistula
 Internal carotid artery occlusion

49. Theories of Neovasculogenesis
1. Retinal Hypoxia-rubeosis iridis involve diminished
perfusion of the retina, retinal hypoxia may be one factor
in the formation of new vessels on the iris and anterior
chamber angle and on the retina and optic nerve head.
2. Angiogenesis Factors (1948)-Four VEGF isoforms
(VEGF121, VEGF165, VEGF189, and VEGF206) have been
identified, which are generated by alternative mRNA
splicing from the same gene. VEGF165 is the most
abundant form in the majority of tissues. under
conditions of retinal ischemia, Müller cells appear to be
the primary source

50.  Vasoinhibitory Factors - The vitreous and lens are possible
sources of these vasoinhibitory factors , which could
explain why vitrectomy or lensectomy increases the risk
for rubeosis iridis in eyes with diabetic retinopathy.
Retinal pigment epithelial cells release an inhibitor of
neovascularization

51. Clinicopathologic Course
A –PREGLAUCOMA
STAGE:
A-new vessels in iris
B-new vessels in
anterior chamber
angle

52. B OPEN ANGLE
GLAUCOMA STAGE :
C-membrane on the iris
D-membrane in angle

53. C-ANGLE CLOSURE
GLAUCOMA STAGE :
e -ectropian uvea
F-flattening iris
G-peripheral anterior
synechiae

55. Clinical Features
 A- preglaucoma stage
I. IOP- Normal
II. Gonio- neovascularization of iris ,
single vascular trunks crossing the
ciliary body band and scleral spur and
arborizing on the trabecular meshwork.
III. Slit lamp -dilated tufts of preexisting
capillaries and fine on the surface of
the iris near the pupillary margin

56. 4.FFA – leakage of new vessels seen
5.Histopathologic Features - The rubeosis iridis begins
intrastromally and then develops on the surface of the iris
The silicone-injection studies also show that new vessels in
the angle run circumferentially in the trabecular meshwork,
with branches coursing into the fibrosed Schlemm canal and
occasionally into collector channels

57.  B-Open-Angle Glaucoma Stage :
It has been called 90- day glaucoma because the
average time interval was thought to be 3 months
IOP- Elevated ,sometimes acute attack is seen
Gonio – open
Slit lamp - aqueous often reveals an inflammatory
reaction and sometimes a hyphema
Histopathologic Features- a fibrovascular membrane
that covers the anterior chamber angle and anterior
surface of the iris

58.  Angle-Closure Glaucoma Stage
The glaucoma in this stage is typically
severe and usually requires surgical
intervention.
Slit lamp –
the stroma of the iris has become flattened,
with a smooth, glistening appearance
Ectropion uvea
peripheral anterior synechia, with eventual
total synechial closure of the angle

59. Histopathologic Features:
peripheral anterior synechiae and flattening of the anterior iris
surface by a confluent fibrovascular membrane
Overlying the new vessels is a clinically inapparent, superficial layer
of myofibroblasts (i.e., fibroblastic cells with smooth-muscle
differentiation), which may be responsible for the tissue contraction

60. Differential Diagnosis
 In the open-angle stage- acute onset, such as
angleclosure glaucoma and glaucoma associated with
anterior uveitis .
 Fuchs heterochromic iridocyclitis also typically have new
vessels in the anterior chamber angle.
 In the angle - closure stage - iridocorneal endothelial
syndrome

61. Management
 Panretinal Photocoagulation- Ablation of the peripheral
retina with laser (usually argon) photocoagulation
 significantly reduce or eliminate anterior segment
neovascularization
 related to decreasing the retinal oxygen demand, reduce
the stimulus for release of an angiogenesis factor or may
reduce the hypoxia in the anterior ocular segment
 It is done as prophylactic therapy in CRVO patients with
prerubeosis stage
 endophotocoagulation in conjunction with pars plana
vitrectomy for diabetic retinopathy

62.  Panretinal Cryotherapy- When cloudy media preclude
panretinal photocoagulation, transscleral panretinal
cryotherapy, often combined with cyclocryotherapy, in
eyes with neovascular glaucoma can control the IOP and
reduce or abolish the neovascularization
 Anti-VEGF Agents-bevacizumab as an adjunctive
treatment of iris neovascularization (regression within 48
hours)

63.  Medical Management of Glaucoma and Inflammation:
o The mainstay of the therapy - reduce aqueous production,
such as carbonic anhydrase inhibitors, topical (ß-blockers,
and a2 - agonists.
o Prostaglandin analogues are rarely effective because
access to the uveoscleral route is generally compromised
from angle closure, and there is a theoretical concern
regarding exacerbation of inflammation.
o Topical corticosteroids- inflammation and pain
o Hyperosmotic agents - control of marked IOP elevation.

64.  Glaucoma Surgical Procedures
 Cyclodestructive Procedures
 Filtering Surgery
 Glaucoma Drainage-Device Surgery (drainage tubes or
valves )
 Other Surgical Procedures : Endoscopic
cyclophotocoagulation,IVTA.

65. Schwartz Syndrome
 A rhegmatogenous retinal
detachment+ slight reduction
in the IOP
 patient presents with
unilateral pressure elevation, a
retinal detachment, and an
open anterior chamber angle
with aqueous cells and flare

66.  Theories of Mechanism :
1. Photoreceptor outer segments with few inflammatory
cells in the aqueous (Matsuo and collegues)
2. ocular trauma with concomitant damage to the
trabecular meshwork
3. anterior uveitis from the retinal detachment
4. obstruction of the trabecular meshwork by pigment
from the retinal pigment epithelium, or glycosaminoglycans
from the visual cells

67.  Management
 Treatment of rhegmatogenous retinal detachment and
glaucomais to repair detachment .
 DD- retinal detachment + glaucoma harbour malignant
melanoma

68. KEY POINTS
 Neovascular glaucoma is a relatively common and serious
complication of several retinal disorders, especially
diabetic retinopathy, central retinal vein occlusion, and
ocular ischemia, as well as certain other ocular and
extraocular conditions
 The pathophysiology of neovascular glaucoma involves
abnormally high levels of VEGF within the eye and growth
of a fibrovascular membrane on the iris surface and in the
anterior chamber angle, which initially obstructs aqueous
outflow in an open-angle glaucoma and then contracts to
produce an angle-closure form of glaucoma

69.  The most effective long-term treatment of
neovascularization of the iris or neovascular glaucoma is
pan retinal photocoagulation in the early stages of the
disease to reduce the stimulus for anterior segment
neovascularization.
 Intravitreal or intracameral injection of anti-VEGF agents
cause regression of anterior segment neovascularization
and can thus be a very useful short-term adjunct

70.  Retinal detachments are usually associated with a
reduction in IOP, although some patients may have
concomitant retinal detachment and glaucoma, which
may or may not have a cause-and effect relationship.
 A group of conditions in which angle-closure glaucoma
may be associated with a retinal, choroidal, or vitreous
disorder include central retinal vein occlusion,
nanophthalmos, retinopathy of prematurity, persistent
hyperplastic primary vitreous, and retinal dysplasia.