Glaucoma is an optic neuropathy characterized by damage to the optic nerve and visual field defects that is frequently associated with elevated intraocular pressure (IOP). It can be primary or secondary. Primary glaucoma involves elevated IOP without another cause, while secondary glaucoma occurs when another eye condition alters aqueous outflow leading to elevated IOP. Glaucoma is classified as open-angle or angle-closure depending on whether the angle between the iris and cornea is open or closed. Pseudoexfoliation glaucoma is a secondary open-angle glaucoma caused by deposits of pseudoexfoliative material clogging the trabecular meshwork. Neovascular glaucoma is also secondary, occurring

1. Glaucoma
BY
Dr. Amr Mounir , Lecturer of Ophthalmology
Sohag university

2. GlaucomaGlaucoma
DefinitionDefinition::
Glaucoma is an optic neuropathy withGlaucoma is an optic neuropathy with
characteristic appearcharacteristic appear­­ances of the optic disc andances of the optic disc and
specific pattern of visual Held defects that isspecific pattern of visual Held defects that is
associated frequently but not invariably withassociated frequently but not invariably with
raised IOPraised IOP

3. AnatomicalAnatomical
BackgroundBackground

4. The Angle of the anteriorThe Angle of the anterior
chamber (AC)chamber (AC)
It is the angle between the posterior surface of theIt is the angle between the posterior surface of the
cornea and the anterior surface of the iris.cornea and the anterior surface of the iris.
Closed Angle:Closed Angle:
It is the condition in which there is contact betweenIt is the condition in which there is contact between
the posterior surface of the peripheral corneathe posterior surface of the peripheral cornea
and the anterior surface of the peripheral iris.and the anterior surface of the peripheral iris.
Open Angle:Open Angle:
It is the condition in which there is wide separationIt is the condition in which there is wide separation
between the posterior surface of the peripheralbetween the posterior surface of the peripheral
cornea and the anterior surface of the peripheralcornea and the anterior surface of the peripheral
iris.iris.

5. GonioscopyGonioscopy

6. GonioscopyGonioscopy
It is the method of examination used toIt is the method of examination used to
examine the angle of the AC.examine the angle of the AC.
Indications:Indications:
1) Diagnostic: to determine whether it is1) Diagnostic: to determine whether it is
closed or open & detect abnormal angleclosed or open & detect abnormal angle
structures.structures.
2) Surgical: to visualize the angle during2) Surgical: to visualize the angle during
surgical procedures (e.g. Goniotomy).surgical procedures (e.g. Goniotomy).

8. Schlemm CanalSchlemm Canal
- It is a circumferential channel in the- It is a circumferential channel in the
perilimbal sclera.perilimbal sclera.
- Lined by endothelium.- Lined by endothelium.
- Drained by the- Drained by the collector channelscollector channels to theto the
episcleral veinsepiscleral veins..

10. PhysiologicalPhysiological
backgroundbackground

11. Aqueous HumourAqueous Humour
It is the fluid which fills the anterior and posteriorIt is the fluid which fills the anterior and posterior
chamber.chamber.
Formation:Formation:
1) Active secretion1) Active secretion: By the non-pigmented epithelium of: By the non-pigmented epithelium of
the ciliary processes in the posterior chamber,the ciliary processes in the posterior chamber,
depending on several enzyme systems (e.g. Na/Kdepending on several enzyme systems (e.g. Na/K
ATPase pump & Carbonic anhydrase).ATPase pump & Carbonic anhydrase).
2) Passively2) Passively: (minor role) the water contents diffuse: (minor role) the water contents diffuse
passively along osmotic gradient.passively along osmotic gradient.

13. CirculationCirculation:: Aqueous flows fromAqueous flows from
the posterior chamber via the pupil into thethe posterior chamber via the pupil into the
anterior chamber, from where it exits theanterior chamber, from where it exits the
eye (Drained).eye (Drained).

14. DrainageDrainage::
By two different routes:By two different routes:
1) Trabecular1) Trabecular (conventional) route: (90%) The(conventional) route: (90%) The
aqueous flows through the trabeculum intoaqueous flows through the trabeculum into
Schlemm canal and is then drained by theSchlemm canal and is then drained by the
episcleral veins.episcleral veins.
2) Uveoscleral2) Uveoscleral (unconventional) route: (10%)(unconventional) route: (10%)
The aqueous passes across the face of the ciliaryThe aqueous passes across the face of the ciliary
body into the suprachoroidal space and is drainedbody into the suprachoroidal space and is drained
by the venous circulation in the ciliary body,by the venous circulation in the ciliary body,
choroid and sclera.choroid and sclera.

15. DrainageDrainage

16. The intraocular pressureThe intraocular pressure
(IOP(IOP((
The Normal IOP:The Normal IOP:
- The IOP within the general population has a range of- The IOP within the general population has a range of 11-11-
21 mmHg21 mmHg..
- However, in some patients glaucoma occurs with IOP less- However, in some patients glaucoma occurs with IOP less
than 21 mmHgthan 21 mmHg (normal- tension glaucoma)(normal- tension glaucoma), while others, while others
remain unaffected with IOP up to 50 mmHgremain unaffected with IOP up to 50 mmHg (ocular(ocular
hypertension)hypertension)..
Fluctuation in IOP:Fluctuation in IOP:
Normal IOP varies with the time of day, with a tendency toNormal IOP varies with the time of day, with a tendency to
be higher in the morning and lower in the afternoon andbe higher in the morning and lower in the afternoon and
evening. The value of diurnal pressure variation is:evening. The value of diurnal pressure variation is:
1) In normal eyes : 5 mmHg.1) In normal eyes : 5 mmHg.
2) In ocular hypertensive or glaucomatous eyes : wider2) In ocular hypertensive or glaucomatous eyes : wider
fluctuation (> 5 mmHg).fluctuation (> 5 mmHg).
3) In normal-tension glaucoma the fluctuations are the3) In normal-tension glaucoma the fluctuations are the
same as in normalssame as in normals..

17. Measurement of IOPMeasurement of IOP
(Tonometry(Tonometry((
* Principle:* Principle: Tonometry is the objectiveTonometry is the objective
measurement of IOP, based on one of themeasurement of IOP, based on one of the
following principles:following principles:
1) Applanation tonometry:1) Applanation tonometry: measuring the forcemeasuring the force
required to flatten the cornearequired to flatten the cornea
2) Indentation tonometry:2) Indentation tonometry: measuring the degreemeasuring the degree
of corneal indentation produced by a fixed forceof corneal indentation produced by a fixed force

18. IOP MeasurementIOP Measurement

19. ClassificationClassification::
Classification intoClassification into open-angleopen-angle andand angle-closureangle-closure types istypes is
based on the mechanism by which aqueous outflow isbased on the mechanism by which aqueous outflow is
impaired.impaired.
The glaucoma may also beThe glaucoma may also be primaryprimary oror secondarysecondary. In. In
primary glaucomas, the elevation of IOP is notprimary glaucomas, the elevation of IOP is not
associated with any other ocular disorder whereas inassociated with any other ocular disorder whereas in
secondary glaucomas a recognizable ocular or non-secondary glaucomas a recognizable ocular or non-
ocular disorder alters aqueous outflow which, in turn,ocular disorder alters aqueous outflow which, in turn,
results in elevation of IOP.results in elevation of IOP.

20. Secondary glaucomaSecondary glaucoma

21. 11((Angle ClosureAngle Closure
GlaucomaGlaucoma::
A) With pupillary block:A) With pupillary block:
1) 1ry Angle Closure Glaucoma with pupillary block.1) 1ry Angle Closure Glaucoma with pupillary block.
2) 2ry Angle Closure Glaucoma with pupillary block:2) 2ry Angle Closure Glaucoma with pupillary block:
- Miotic induced.- Miotic induced.
- Swollen lens induced glaucoma (Phacomorphic glaucoma).- Swollen lens induced glaucoma (Phacomorphic glaucoma).
- Mobile lens induced glaucoma (ectopia lentis, microspherophakia).- Mobile lens induced glaucoma (ectopia lentis, microspherophakia).
- Posterior synechiae (to lens, vitreous, or IOL).- Posterior synechiae (to lens, vitreous, or IOL).
A) Without pupillary block:A) Without pupillary block:
1) 1ry Angle Closure Glaucoma without pupillary block (plateau iris).1) 1ry Angle Closure Glaucoma without pupillary block (plateau iris).
2) 2ry Angle Closure Glaucoma without pupillary block:2) 2ry Angle Closure Glaucoma without pupillary block:
a) Anterior pulling mechanism: pulling the iris forward by contraction of aa) Anterior pulling mechanism: pulling the iris forward by contraction of a
membrane e.g. late neovascular glaucoma and inflammatory membrane.membrane e.g. late neovascular glaucoma and inflammatory membrane.
b) Posterior pushing mechanism: pushing the iris forward by a condition in theb) Posterior pushing mechanism: pushing the iris forward by a condition in the
posterior segment e.g. Malignant glaucoma (ciliary block glaucoma) andposterior segment e.g. Malignant glaucoma (ciliary block glaucoma) and
intraocular tumours.intraocular tumours.

22. 22((Open AngleOpen Angle
glaucomaglaucoma::
A) 1ry open Angle glaucoma:A) 1ry open Angle glaucoma:
- With IOP higher than normal range.- With IOP higher than normal range.
- With IOP within normal range (normal tensionWith IOP within normal range (normal tension
glaucoma)glaucoma)
B) 2ry open angle glaucoma:B) 2ry open angle glaucoma:

23. B) 2ry open angle glaucoma:B) 2ry open angle glaucoma:
Subdivided on the basis of the site of aqueousSubdivided on the basis of the site of aqueous
outflow obstruction.outflow obstruction.
1)1) Pre-trabecular glaucoma:Pre-trabecular glaucoma: in which aqueous outflowin which aqueous outflow
is obstructed by a membrane covering theis obstructed by a membrane covering the
trabeculum, which may consist of:trabeculum, which may consist of:
- Fibrovascular tissue (e.g. early neovascular- Fibrovascular tissue (e.g. early neovascular
glaucoma).glaucoma).
- Endothelial cells (e.g. iridocorneal endothelial- Endothelial cells (e.g. iridocorneal endothelial
synsyn­­drome).drome).
- Epithelial cells (e.g. epithelial ingrowth).- Epithelial cells (e.g. epithelial ingrowth).

24. 2)2) Trabecular glaucoma:Trabecular glaucoma: in which the obstruction occurs as ain which the obstruction occurs as a
result of:result of:
a) 'clogging up' of the meshwork by:a) 'clogging up' of the meshwork by:
- Pigment particles (e.g. pigmentary glaucoma).- Pigment particles (e.g. pigmentary glaucoma).
- Red blood cells (e.g. red cell glaucoma).- Red blood cells (e.g. red cell glaucoma).
- Degenerated red cells (e.g. ghost cell glaucoma).- Degenerated red cells (e.g. ghost cell glaucoma).
- Macrophages and lens proteins (e.g. phacolytic glau- Macrophages and lens proteins (e.g. phacolytic glau­­
coma).coma).
- Proteins (e.g. hypertensive uveitis).- Proteins (e.g. hypertensive uveitis).
- Pseudoexfoliative material (e.g. pseudoexfoliation- Pseudoexfoliative material (e.g. pseudoexfoliation
glaucoma).glaucoma).
b) Alteration of the trabecular fibres themselves by:b) Alteration of the trabecular fibres themselves by:
- Oedema (e.g. herpes zoster iritis).- Oedema (e.g. herpes zoster iritis).
- Scarring (e.g. post-traumatic angle recession glau- Scarring (e.g. post-traumatic angle recession glau­­coma).coma).

25. 3)3) Post-trabecular glaucomaPost-trabecular glaucoma in which the trabeculumin which the trabeculum
itself is normal but aqueous outflow is impaireditself is normal but aqueous outflow is impaired
as a result of elevated episcleral venous pressureas a result of elevated episcleral venous pressure
due to:due to:
- Carotid-cavernous fistulae.- Carotid-cavernous fistulae.
- Obstruction of the superior vena cava.- Obstruction of the superior vena cava.

26. Important types ofImportant types of
secondarysecondary
GlaucomasGlaucomas

27. PseudoexopholiationPseudoexopholiation
GlaucomaGlaucoma::
Pathogenesis:Pathogenesis:
Pseudoexopholiation (PEX) syndrome: a condition characterized byPseudoexopholiation (PEX) syndrome: a condition characterized by
deposition of grey-white, fibrillogranular material in the anteriordeposition of grey-white, fibrillogranular material in the anterior
lens capsule, zonules, ciliary body, iris, trabeculum, anteriorlens capsule, zonules, ciliary body, iris, trabeculum, anterior
vitreous face and conjunctiva.vitreous face and conjunctiva.
Pseudoexopholiation Glaucoma occurs when 2ry trabecular blockPseudoexopholiation Glaucoma occurs when 2ry trabecular block
occur by clogging up of the trabeculum by Pseudoexopholiationoccur by clogging up of the trabeculum by Pseudoexopholiation
material.material.
Clinical picture:Clinical picture:
1) Cornea: PEX materials on the posterior surface.1) Cornea: PEX materials on the posterior surface.
2) Iris: Atrophy2) Iris: Atrophy –– PEX material.PEX material.
3) Lens: PEX materials forming central disc and peripheral band3) Lens: PEX materials forming central disc and peripheral band ––
cataractcataract –– subluxation.subluxation.
4) Gonioscopy: trabecular hyperpigmentation and PEX materials.4) Gonioscopy: trabecular hyperpigmentation and PEX materials.
Treatment:Treatment: as POAG.as POAG.

29. Neovascular GlaucomaNeovascular Glaucoma
Pathogenesis:Pathogenesis:
Retinal ischemiaRetinal ischemia  vasoproliferative growth factorvasoproliferative growth factor  retinalretinal
neovascularization, rubeosis iridis & neovascularizationneovascularization, rubeosis iridis & neovascularization
at the angle of AC.at the angle of AC.
Causes:Causes:
1) Ischemic CRVO and CRAO.1) Ischemic CRVO and CRAO.
2) DM.2) DM.
3) OLD RD.3) OLD RD.
4) IO Tumours.4) IO Tumours.

30. Clinical pictureClinical picture
3 stages:3 stages:
1) Rubeosis iridis: iris new vessles.1) Rubeosis iridis: iris new vessles.
Treatment : Argon laser photocoagulation of the ischemic retina.Treatment : Argon laser photocoagulation of the ischemic retina.
2) 2ry open angle glaucoma:2) 2ry open angle glaucoma: due to neovascular membrane in front ofdue to neovascular membrane in front of
the trabeculum.the trabeculum.
Treatment:Treatment:
1) Medical: antiglaucoma (avoid Miotics)1) Medical: antiglaucoma (avoid Miotics) –– steroidssteroids –– atropine.atropine.
2) Argon laser photocoagulation of the ischemic retina.2) Argon laser photocoagulation of the ischemic retina.
3) 2ry angle closure glaucoma3) 2ry angle closure glaucoma: due to contraction of the membrane.: due to contraction of the membrane.
Treatment:Treatment:
1) Medical: usually fails.1) Medical: usually fails.
2) Argon laser photocoagulation of the ischemic retina.2) Argon laser photocoagulation of the ischemic retina.
3) Surgery: trabeculectomy with adjunctive mitomycin OR artificial shunt.3) Surgery: trabeculectomy with adjunctive mitomycin OR artificial shunt.
4) Cyclodestruction: destruction of the ciliary processes by laser.4) Cyclodestruction: destruction of the ciliary processes by laser.
5) Blind painful eye: enucleation or retrobulbar alcohol.5) Blind painful eye: enucleation or retrobulbar alcohol.

32. Lens inducedLens induced
GlaucomaGlaucoma::

33. A) Phacolytic GlaucmaA) Phacolytic Glaucma
Pathogenesis:Pathogenesis:
Hypermature cataractHypermature cataract  lens proteins leak through intact capsulelens proteins leak through intact capsule 
blockage of the trabeculum with proteins and macrophages ladenblockage of the trabeculum with proteins and macrophages laden
with proteins.with proteins.
Clinical picture:Clinical picture:
- Corneal edema.- Corneal edema.
- Deep AC with floating white particles (pseudohypopyon).- Deep AC with floating white particles (pseudohypopyon).
- Gonioscopy: open angle.- Gonioscopy: open angle.
Treatment:Treatment:
- 1st : Control IOP medically.- 1st : Control IOP medically.
- Then: cataract surgery.- Then: cataract surgery.

34. B) PhacoanphylacticB) Phacoanphylactic
glaucoma:glaucoma:
Rupture of lens capsuleRupture of lens capsule  autoimmune reaction to lens proteinsautoimmune reaction to lens proteins 
uveitis and glaucoma.uveitis and glaucoma.
C) PhacomorphicC) Phacomorphic
glaucoma:glaucoma:
Pathogenesis:Pathogenesis:
Intumescent cataract (Swollen lens)Intumescent cataract (Swollen lens)  pupillary blockpupillary block  iris bombeiris bombe 
angle closure.angle closure.
Treatment:Treatment:
1) Control of IOP as in PACG.1) Control of IOP as in PACG.
2) Cataract surgery.2) Cataract surgery.

36. Primary open-Primary open-
angle glaucomaangle glaucoma

37. DefinitionDefinition
Primary open-angle glaucoma (POAG), alsoPrimary open-angle glaucoma (POAG), also
referred to asreferred to as chronic simple glaucomachronic simple glaucoma, is a, is a
generally bilateral, but not always symmetricalgenerally bilateral, but not always symmetrical
disease, characterized by:disease, characterized by:
1- Adult onset.1- Adult onset.
2- An IOP > 21 mmHg at some point in the course2- An IOP > 21 mmHg at some point in the course
of the disease.of the disease.
3- An open angle of normal appearance.3- An open angle of normal appearance.
4- Glaucomatous optic nerve head damage.4- Glaucomatous optic nerve head damage.
5- Visual Held loss5- Visual Held loss..

38. IncidenceIncidence
-- The commonestThe commonest type of glaucoma.type of glaucoma.
-- Population:Population: Affecting 1% of the generalAffecting 1% of the general
population > 40 years.population > 40 years.
-- Sex:Sex: It affects both sexes equally.It affects both sexes equally.
-- Age:Age: most cases > 65 years. It is unusual < 40most cases > 65 years. It is unusual < 40
years.years.
-- Race:Race: more common, develops earlier, and ismore common, develops earlier, and is
more severe, in black people.more severe, in black people.
-- Laterality:Laterality: Bilateral (usually one eye before theBilateral (usually one eye before the
other).other).

39. Risk factors and associationsRisk factors and associations::
1) Family history and inheritance:1) Family history and inheritance:
POAG is frequently inherited, probably in aPOAG is frequently inherited, probably in a
multifactorial manner. First-degree relatives aremultifactorial manner. First-degree relatives are
at increased risk of developing POAG.at increased risk of developing POAG.
2) Myopia:2) Myopia: is associated with an increasedis associated with an increased
incidence of POAG.incidence of POAG.
3) Retinal disease:3) Retinal disease: - Central retinal vein- Central retinal vein
occlusion.occlusion.
- Rhegmatogenous retinal detachment.- Rhegmatogenous retinal detachment.
- Retinitis pigmentosa.- Retinitis pigmentosa.

40. Pathogenesis ofPathogenesis of
glaucomataus damageglaucomataus damage
Elevation of IOP in POAG is caused byElevation of IOP in POAG is caused by increased resistance to aqueousincreased resistance to aqueous
outflowoutflow in the trabecular meshwork. Retinal ganglion cell deathin the trabecular meshwork. Retinal ganglion cell death
occurs predominantly through apoptosis (prooccurs predominantly through apoptosis (pro­­grammed cellgrammed cell
death) rather than necrosis.death) rather than necrosis.
The factors that influence the rate of cell death are multiple, butThe factors that influence the rate of cell death are multiple, but
current opinion is polarized between ischemic and mechanicalcurrent opinion is polarized between ischemic and mechanical
etiologies of damage:etiologies of damage:
1) The ischemic theory1) The ischemic theory postulates that compromise of thepostulates that compromise of the
microvasculature with resultant ischemia in the optic nerve headmicrovasculature with resultant ischemia in the optic nerve head
is responsible.is responsible.
2) The direct mechanical theory2) The direct mechanical theory suggests that raised IOP directlysuggests that raised IOP directly
damages the retinal nerve fibers as they pass through the laminadamages the retinal nerve fibers as they pass through the lamina
cribrosa.cribrosa.

41. ClinicalClinical
PicturePicture

42. SymptomsSymptoms
1) Early1) Early: Asymptomatic: Asymptomatic
2) Late2) Late: Significant loss of visual field occurs: Significant loss of visual field occurs
gradually and fixation is involved late in thegradually and fixation is involved late in the
course of the disease.course of the disease.
3) Bilaterality3) Bilaterality: Although the disease is almost: Although the disease is almost
invariably bilateral, progression is ofteninvariably bilateral, progression is often
asymmetrical. Patients therefore frequentlyasymmetrical. Patients therefore frequently
present with significant visual field loss in onepresent with significant visual field loss in one
eye and less advanced disease in the other.eye and less advanced disease in the other.

43. SignsSigns
A) IOP:A) IOP:
1) Raised IOP:1) Raised IOP:
- Approximately 2% of the general population over the age of 40- Approximately 2% of the general population over the age of 40
years have IOPs > 24 mmHg and 7% have IOPs > 21 mmHg.years have IOPs > 24 mmHg and 7% have IOPs > 21 mmHg.
However, only about 1% of these have glaucomatous visual fieldHowever, only about 1% of these have glaucomatous visual field
loss.loss.
2) Diurnal fluctuations:2) Diurnal fluctuations:
- In normal individuals: Diurnal fluctuations up to 5 mmHg occur- In normal individuals: Diurnal fluctuations up to 5 mmHg occur
in approximately 30%.in approximately 30%.
- In POAC: this fluctuation is exaggerated and occurs in about 90%- In POAC: this fluctuation is exaggerated and occurs in about 90%
of cases.of cases.
3) Asymmetry of the IOP between the two eyes3) Asymmetry of the IOP between the two eyes
If 5 mmHg or more, should arouse suspicionIf 5 mmHg or more, should arouse suspicion

44. B) Optic disc changes:B) Optic disc changes:
1) Baring of the curve linear blood vessels (blood1) Baring of the curve linear blood vessels (blood
supply of the optic disk) due to loss of thesupply of the optic disk) due to loss of the
neuroglial fibrous tissue as a result of ischemia.neuroglial fibrous tissue as a result of ischemia.
Leaving the blood vessels unsupported.Leaving the blood vessels unsupported.
2) Optic disc hemorrhage (Splinter or flame2) Optic disc hemorrhage (Splinter or flame
shaped) in 2-4% of cases. It is due to easyshaped) in 2-4% of cases. It is due to easy
rupture of the non-supported curve linearrupture of the non-supported curve linear
vessels.vessels.
3) Nasalization of central blood vessels.3) Nasalization of central blood vessels.
4) Enlargement of the physiological cup.4) Enlargement of the physiological cup.
5) Asymmetry cup / disc ratio between both eyes.5) Asymmetry cup / disc ratio between both eyes.
6) Specific glaucomatous cupping:6) Specific glaucomatous cupping:

45. 6) Specific glaucomatous cupping:6) Specific glaucomatous cupping:
- Narrow opening.- Narrow opening.
- Size: large.- Size: large.
- Depth: very deep (Can be measured by- Depth: very deep (Can be measured by
ophthalmoscope by focusing the blood vesselsophthalmoscope by focusing the blood vessels
at the edge and at the floor of the cupping).at the edge and at the floor of the cupping).
- Edges: overhanging with marked interruption of- Edges: overhanging with marked interruption of
the vessels.the vessels.
- Marked sliding of the side wall, so vessels come- Marked sliding of the side wall, so vessels come
out from edge like a head of snake.out from edge like a head of snake.
- Increase cup/disc ratio (normal = 0.3).- Increase cup/disc ratio (normal = 0.3).
- In advanced cases lamina cribrosa can be seen.- In advanced cases lamina cribrosa can be seen.
7) Post-glaucomatous optic atrophy: show cupping7) Post-glaucomatous optic atrophy: show cupping
and pallorand pallor

46. NormalNormal

50. C) Visual fields (Perimetry):C) Visual fields (Perimetry):
A) Central changes:A) Central changes:
1) Paracentral scotomata: Are isolated scotomata which later1) Paracentral scotomata: Are isolated scotomata which later
becomes connected with the blind spot to form the arcuatebecomes connected with the blind spot to form the arcuate
scotoma.scotoma.
2) Baring of the blind spot: Is exclusion of the blind spot from the2) Baring of the blind spot: Is exclusion of the blind spot from the
central field (due to localized contraction of the temporal edgecentral field (due to localized contraction of the temporal edge
of the central field)of the central field)
3) Siedel scotoma: Is a tapering wing like elongation of the upper3) Siedel scotoma: Is a tapering wing like elongation of the upper
and/or lower pole of the blind spot.and/or lower pole of the blind spot.
4) Bjerrum (arcuate) scotoma: Upper and/or lower bundle defect4) Bjerrum (arcuate) scotoma: Upper and/or lower bundle defect
around and joining the blind spot and is concentric with thearound and joining the blind spot and is concentric with the
fixation point.fixation point.
5) Annular scotoma: By fusion of the 2 (upper and lower) Bjerrum5) Annular scotoma: By fusion of the 2 (upper and lower) Bjerrum
scotomata in the nasal field.scotomata in the nasal field.

51. B) Peripheral field defects:B) Peripheral field defects:
1) Nasal field contraction: Occurs earlier than the1) Nasal field contraction: Occurs earlier than the
temporal field because the temporal retinaltemporal field because the temporal retinal
fibres are more dense and so suffer more.fibres are more dense and so suffer more.
2) Roenne's nasal step: Is a sectorial nasal field2) Roenne's nasal step: Is a sectorial nasal field
defect (upper or lower) with a sharply horizontaldefect (upper or lower) with a sharply horizontal
edge.edge.
3) Concenteric contraction.3) Concenteric contraction.
4) Tubular vision.4) Tubular vision.
C) End Stage:C) End Stage: Total Field loss.Total Field loss.

56. D) Gonioscopy:D) Gonioscopy:
Shows a normal open angle.Shows a normal open angle.

57. ManagementManagement

58. Aim:Aim:
- The primary aim of treatment is to prevent- The primary aim of treatment is to prevent
functional impairment of vision within thefunctional impairment of vision within the
patient's lifetime by slowing the rate of ganglionpatient's lifetime by slowing the rate of ganglion
cell.cell.
- Method of achieving this goal is- Method of achieving this goal is by lowering ofby lowering of
IOP.IOP.
-- Target pressureTarget pressure: It is an IOP level below which: It is an IOP level below which
further damage is unlikely. Therapy shouldfurther damage is unlikely. Therapy should
maintain the IOP at or below the target level.maintain the IOP at or below the target level.
-- MonitoringMonitoring is performed of the optic nerve andis performed of the optic nerve and
visual fields. In the event of further damage thevisual fields. In the event of further damage the
target IOP is reset at a lower level.target IOP is reset at a lower level.

59. Patient instructionPatient instruction
Including:Including:
1) A simple explanation of the nature of the disease.1) A simple explanation of the nature of the disease.
2) The patient should be taught how to instil drops and2) The patient should be taught how to instil drops and
the intervals between medications should be specified.the intervals between medications should be specified.
3) In order to minimize systemic absorption the patient3) In order to minimize systemic absorption the patient
should be instructed either to perform lacrimal sacshould be instructed either to perform lacrimal sac
occlusion (by applying pressure at the medial canthus)occlusion (by applying pressure at the medial canthus)
or to close the eyes for about 3 minutes afteror to close the eyes for about 3 minutes after
instillation.instillation.
4) Potential adverse effects should be explained and4) Potential adverse effects should be explained and
subsequently asked for at follow-up visits.subsequently asked for at follow-up visits.

60. Lines of treatmentLines of treatment::
1) Medical.1) Medical.
2) Laser.2) Laser.
3) Surgical3) Surgical..

61. 11((Medical therapyMedical therapy
Basic principlesBasic principles
1) Any chosen drug should be used in its lowest1) Any chosen drug should be used in its lowest
concentration and as infrequently as possible.concentration and as infrequently as possible.
2) Initial treatment is usually with one drug.2) Initial treatment is usually with one drug.
3) Follow-up3) Follow-up

62. Antiglaucoma DrugsAntiglaucoma Drugs
1) B-blockers1) B-blockers
Timolol – Betaxolol – Levobunolol – MetipranololTimolol – Betaxolol – Levobunolol – Metipranolol
2) Alpha-2 Agonist2) Alpha-2 Agonist
Brimonidine – ApraclonidineBrimonidine – Apraclonidine
3) Prostaglandin analogues3) Prostaglandin analogues
Latanoprost – Travoprost – BimatoprostLatanoprost – Travoprost – Bimatoprost
4) Miotics:4) Miotics: PilocarpinePilocarpine
5) Topical Carbonic anhydrase inhibitors5) Topical Carbonic anhydrase inhibitors
Dorzolamide – BrinzolamidDorzolamide – Brinzolamid
6) Systemic Carbonic anhydrase inhibitors:6) Systemic Carbonic anhydrase inhibitors:
AcetazolamideAcetazolamide
7) Hyperosmotic agents:7) Hyperosmotic agents: Manitol - GlycerolManitol - Glycerol

63. 22((Laser treatmentLaser treatment
Laser trabeculoplastyLaser trabeculoplasty
Principle:Principle: In this procedure discrete argon orIn this procedure discrete argon or
diode laser burns are applied to the trabeculumdiode laser burns are applied to the trabeculum
to enhance aqueous outflow and lower IOP.to enhance aqueous outflow and lower IOP.
The therapeutic effectThe therapeutic effect ::
- Often transient, lasting a few years, so that laser- Often transient, lasting a few years, so that laser
therapy may merely defer the need for filtrationtherapy may merely defer the need for filtration
surgery.surgery.
- IOP reduction is seldom greater than 30%. So,- IOP reduction is seldom greater than 30%. So,
an IOP > 28 mmHg isan IOP > 28 mmHg is
unlikely to be adequately controlled by laserunlikely to be adequately controlled by laser
alone.alone.

64. 33((Surgical treatmentSurgical treatment::
TrabeculectomyTrabeculectomy
Principle:Principle:
This involves the surgical creation of a fistula between the angle ofThis involves the surgical creation of a fistula between the angle of
the anterior chamber and the sub-Tenon space, which allowsthe anterior chamber and the sub-Tenon space, which allows
egress of aqueous from the anterior chamber into a 'drainageegress of aqueous from the anterior chamber into a 'drainage
bleb' under the upper eyelid.bleb' under the upper eyelid.
Indications:Indications:
1) Failed medical therapy and/or laser trabeculoplasty.1) Failed medical therapy and/or laser trabeculoplasty.
2) Unsuitability for laser therapy due to poor patient cooperation or2) Unsuitability for laser therapy due to poor patient cooperation or
inadequate visualization of the trabeculum (narrow angle, conicalinadequate visualization of the trabeculum (narrow angle, conical
opacification).opacification).
3) Advanced disease requiring a very low target pressure.3) Advanced disease requiring a very low target pressure.

65. Normal-tensionNormal-tension
glaucomaglaucoma
Is a variant of POAC. It is characterized by;Is a variant of POAC. It is characterized by;
1) A mean IOP equal to or less than 211) A mean IOP equal to or less than 21
mmHg on diurnal testing.mmHg on diurnal testing.
2) Glaucomatous optic disc damage and2) Glaucomatous optic disc damage and
visual field loss.visual field loss.
3) Open drainage angle on gonioscopy.3) Open drainage angle on gonioscopy.
4) Absence of secondary causes for4) Absence of secondary causes for
glaucomatous optic disc damage.glaucomatous optic disc damage.

66. Primary angle-closurePrimary angle-closure
glaucomaglaucoma
Definition:Definition:
Primary angle-closure glaucoma (PACG) is aPrimary angle-closure glaucoma (PACG) is a
condition in which elevation of IOP occurs as acondition in which elevation of IOP occurs as a
result of obstruction of aqueous outflow byresult of obstruction of aqueous outflow by
partial or complete closure of the angle by thepartial or complete closure of the angle by the
peripheral iris.peripheral iris.

67. ClassificationClassification::
Based on the mechanism of angle closure, twoBased on the mechanism of angle closure, two
forms of PACG arc recognized:forms of PACG arc recognized:
(a) Pupillary block.(a) Pupillary block.
(b) Plateau iris syndrome.(b) Plateau iris syndrome.

68. 11((Primary angle-closurePrimary angle-closure
glaucoma with pupillary blockglaucoma with pupillary block
Anatomical predisposing factorsAnatomical predisposing factors
1) Relatively anterior location of the iris-lens1) Relatively anterior location of the iris-lens
diaphragm.diaphragm.
2) Shallow anterior chamber.2) Shallow anterior chamber.
3) Narrow chamber angle.3) Narrow chamber angle.

69. PathogenesisPathogenesis
- Contraction of the dilator pupillae exerts a posterior- Contraction of the dilator pupillae exerts a posterior
vector. This increases the amount of appositionvector. This increases the amount of apposition
between the iris and the anteriorly located lens,between the iris and the anteriorly located lens,
enhancing the degree of physiological resistance at theenhancing the degree of physiological resistance at the
pupil (pupil block).pupil (pupil block).
- Dila- Dila­­tation of the pupil renders the peripheral iris moretation of the pupil renders the peripheral iris more
flaccid.flaccid.
- The pupil block causes the pressure in the posterior- The pupil block causes the pressure in the posterior
chamcham­­ber to increase and the peripheral iris bowsber to increase and the peripheral iris bows
anteriorly (iris bombe).anteriorly (iris bombe).
- Eventually the iris touches the posterior corneal surface,- Eventually the iris touches the posterior corneal surface,
obstructing the angle and the IOP rises.obstructing the angle and the IOP rises.

71. ClassificationClassification
Although PACG can be divided intoAlthough PACG can be divided into overlapping stagesoverlapping stages thethe
condition does not necessarily progress from onecondition does not necessarily progress from one
stage to the next in an orderly sequence:stage to the next in an orderly sequence:
1.1. Latent.Latent.
2.2. Subacute (intermittent).Subacute (intermittent).
3.3. Acute congestive.Acute congestive.
4.4. Chronic.Chronic.
5.5. Absolute is the end-stage of acute congestive PACGAbsolute is the end-stage of acute congestive PACG
in which the eye is completely blindin which the eye is completely blind

72. 11((Latent angle-closureLatent angle-closure
glaucomaglaucoma
Implies an anatomically predisposed eye. It can only beImplies an anatomically predisposed eye. It can only be
suspected prospectivelysuspected prospectively
Clinical featuresClinical features
1) Symptoms are absent.1) Symptoms are absent.
2) The eclipse sign2) The eclipse sign
3) Slit-lamp biomicroscopy:3) Slit-lamp biomicroscopy:
- Axial anterior chamber depth is less than normal.- Axial anterior chamber depth is less than normal.
- Convex-shaped iris-lens diaphragm.- Convex-shaped iris-lens diaphragm.
- Close proximity of the iris to the cornea- Close proximity of the iris to the cornea
Gonioscopy shows an 'occludable' angle.Gonioscopy shows an 'occludable' angle.
TreatmentTreatment
Prophylactic peripheral laser Iridotomy: If the other eye hasProphylactic peripheral laser Iridotomy: If the other eye has
had acute or subacute PACG.had acute or subacute PACG.

74. 22((Subacute angle-Subacute angle-
closure glaucomaclosure glaucoma
Pathogenesis:Pathogenesis:
Subacute (intermittent) PACG occurs in a predisposed eye with anSubacute (intermittent) PACG occurs in a predisposed eye with an
occludable angle in association with intermittent pupillary block.occludable angle in association with intermittent pupillary block.
Rapid closure of the angle results in sudden increase in IOP. TheRapid closure of the angle results in sudden increase in IOP. The
pupillary block is then spontaneously relieved, the angle openspupillary block is then spontaneously relieved, the angle opens
and the IOP returns to normal.and the IOP returns to normal.
Precipitating factorPrecipitating factor
Attacks may be precipitated by:Attacks may be precipitated by:
1) Physiological mydriasis (watching television in a dark room).1) Physiological mydriasis (watching television in a dark room).
2) Physiological shallowing of the anterior chamber when the2) Physiological shallowing of the anterior chamber when the
patient assumes a prone or semiprone position (when sewing orpatient assumes a prone or semiprone position (when sewing or
reading).reading).
3) Emotional stress.3) Emotional stress.

75. DiagnosisDiagnosis
Between attacks the eye looks normal although the angle is narrow.Between attacks the eye looks normal although the angle is narrow.
Diagnosis is based on a characteristic history of:Diagnosis is based on a characteristic history of:
1) Transient blurring of vision associated with haloes around lights1) Transient blurring of vision associated with haloes around lights
due to corneal epithelial edemadue to corneal epithelial edema
2) Ocular discomfort or frontal headache.2) Ocular discomfort or frontal headache.
3) The attacks are recurrent and are usually broken after 1-2 hours3) The attacks are recurrent and are usually broken after 1-2 hours
by physiological miosis (exposure to bright sunlight or sleep).by physiological miosis (exposure to bright sunlight or sleep).
The clinical courseThe clinical course
Without treatment is variable. Some eyes develop an acute attackWithout treatment is variable. Some eyes develop an acute attack
and others may develop chronic angle closure.and others may develop chronic angle closure.
TreatmentTreatment
Prophylactic peripheral laser iridotomy.Prophylactic peripheral laser iridotomy.

76. 33((Acute congestiveAcute congestive
angle-closureangle-closure
glaucomaglaucomaThis is a sight-threatening emergency, involving painfulThis is a sight-threatening emergency, involving painful
loss of vision, due to sudden and total closure of theloss of vision, due to sudden and total closure of the
angle.angle.
Clinical featuresClinical features
SymptomsSymptoms
1) Rapidly progressive unilateral visual loss1) Rapidly progressive unilateral visual loss
2) Periocular pain and congestion.2) Periocular pain and congestion.
3) Nausea and vomiting may occur in severe cases.3) Nausea and vomiting may occur in severe cases.
4) History of transient blurring and haloes characteristic4) History of transient blurring and haloes characteristic
of previous intermittent attacks is often absent.of previous intermittent attacks is often absent.

77. Signs:Signs:
1) Conjunctiva: "Ciliary" flush (Ciliary injection) due to injection of1) Conjunctiva: "Ciliary" flush (Ciliary injection) due to injection of
the limbal and conjunctival blood vessels.the limbal and conjunctival blood vessels.
2) Cornea: Corneal oedema with epithelial vesicles and stromal2) Cornea: Corneal oedema with epithelial vesicles and stromal
thickening.thickening.
3) AC: Shallow anterior chamber with peripheral iridocorneal3) AC: Shallow anterior chamber with peripheral iridocorneal
contact. Aqueous flare may be seen once the corneal oedema hascontact. Aqueous flare may be seen once the corneal oedema has
resolved.resolved.
5) The pupil: is vertically oval, fixed in the semi-dilated position5) The pupil: is vertically oval, fixed in the semi-dilated position
and unreactive to both light and accommodation.and unreactive to both light and accommodation.
6) The iris: blood vessels are dilated.6) The iris: blood vessels are dilated.
7) The IOP: is severely elevated (50-100 mmHg).7) The IOP: is severely elevated (50-100 mmHg).
8) Gonioscopy: may need to be deferred until the corneal oedema8) Gonioscopy: may need to be deferred until the corneal oedema
has resolved. It is, however, vital to perform this examination inhas resolved. It is, however, vital to perform this examination in
the fellow eye. which usually exhibits characteristics of latentthe fellow eye. which usually exhibits characteristics of latent
angle closure. The affected eye shows complete peripheralangle closure. The affected eye shows complete peripheral
iridocorneal contact.iridocorneal contact.
9) Ophthalmoscopy: shows optic disc oedema and hyperaemia.9) Ophthalmoscopy: shows optic disc oedema and hyperaemia.

81. Treatment:Treatment:
[I] Control of the attack:[I] Control of the attack:
A) Immediate treatment:A) Immediate treatment:
1) Systemic:1) Systemic: Acetazolamide 500 mg intravenously and 500 mg orally.Acetazolamide 500 mg intravenously and 500 mg orally.
2) Topical:2) Topical:
- Pilocarpine 2% two drops to both eyes.- Pilocarpine 2% two drops to both eyes.
- Dexamethasone (or equivalent).- Dexamethasone (or equivalent).
- Beta-blocker.- Beta-blocker.
3) Analgesia and anti-emetics3) Analgesia and anti-emetics. Patient to. Patient to lie supinelie supine for 1 hour.for 1 hour.
B) After 1 hour:B) After 1 hour:
PilocarpinePilocarpine 2% should be repeated, by which time reduction of iris2% should be repeated, by which time reduction of iris
ischemia and lowering of IOP allows the sphincter papillae toischemia and lowering of IOP allows the sphincter papillae to
respond to the drug.respond to the drug.

82. C) After further 30 minutes:C) After further 30 minutes:
If IOP has not fallen to below 35 mmHg:If IOP has not fallen to below 35 mmHg:
1) Glycerol1) Glycerol 50% Orally (1 g/kg) (with caution in diabetics)50% Orally (1 g/kg) (with caution in diabetics)
and fluid intake limited for maximum effect.and fluid intake limited for maximum effect.
2) Mannitol2) Mannitol 20% (1-2 g/kg) may be given intravenously20% (1-2 g/kg) may be given intravenously
over 45 minutes, if the patient is unable to tolerate oralover 45 minutes, if the patient is unable to tolerate oral
glycerol.glycerol.
D) A high IOP unresponsiveD) A high IOP unresponsive to medito medi­­cation maycation may
sometimes respond to axial corneal indentation, thissometimes respond to axial corneal indentation, this
allows aqueous humour to force its way between the irisallows aqueous humour to force its way between the iris
and cornea to the angle, thus opening it and gainingand cornea to the angle, thus opening it and gaining
access to the trabecular meshwork.access to the trabecular meshwork.

83. [II] Surgical treatment:[II] Surgical treatment:
1) Nd:YAG laser iridotomy:1) Nd:YAG laser iridotomy:
The purposeThe purpose: to re-establish communication between the posterior: to re-establish communication between the posterior
and anterior chambers by making an opening in the peripheraland anterior chambers by making an opening in the peripheral
iris.iris.
IndicationIndication: This will be successful only if less than 180o of the: This will be successful only if less than 180o of the
angle is closed by permanent peripheral anterior synechiae.angle is closed by permanent peripheral anterior synechiae.
TimingTiming: when the corneal edema and iris congestion have settled: when the corneal edema and iris congestion have settled
(usually 48 hours).(usually 48 hours).
2) Trabeculectomy2) Trabeculectomy::
Laser iridotomy is effective in about 75% of eyes. UnresponsiveLaser iridotomy is effective in about 75% of eyes. Unresponsive
cases (more than 180o of the angle is closed) may requirecases (more than 180o of the angle is closed) may require
trabeculectomy.trabeculectomy.
[III] Prophylactic treatment for the other eye:[III] Prophylactic treatment for the other eye:
Laser iridotomy.Laser iridotomy.

84. 44((Chronic angle-Chronic angle-
closure glaucomaclosure glaucoma
PathogenesisPathogenesis
1) Type 1 (creeping): is caused by gradual and1) Type 1 (creeping): is caused by gradual and
progressive angle closure.progressive angle closure.
2) Type 2: is caused by angle closure as a result of2) Type 2: is caused by angle closure as a result of
intermittent subacute attacks.intermittent subacute attacks.
3) Type 3 (mixed): is caused by a combination of3) Type 3 (mixed): is caused by a combination of
POAG with narrow angles usually associatedPOAG with narrow angles usually associated
with the long-term use of miotics.with the long-term use of miotics.

85. Clinical featuresClinical features
1) These are similar to POAG.1) These are similar to POAG.
2) Shallow AC.2) Shallow AC.
3) Gonioscopy shows a variable degree of angle closure3) Gonioscopy shows a variable degree of angle closure
TreatmentTreatment
1) Type I: initially treated by laser iridotomy to eradicate1) Type I: initially treated by laser iridotomy to eradicate
any element of pupil block. Any residual elevation ofany element of pupil block. Any residual elevation of
IOP is then treated medically. If this fails.IOP is then treated medically. If this fails.
trabeculcctomy will be required.trabeculcctomy will be required.
2) Type 2: will already have undergone iridotomy. Medical2) Type 2: will already have undergone iridotomy. Medical
therapy should be added as necessary.therapy should be added as necessary.
3) Type 3 (mixed) will already be on medical therapy for3) Type 3 (mixed) will already be on medical therapy for
POAG and should be treated by laser iridotomy.POAG and should be treated by laser iridotomy.

86. 22((Primary angle-closure glaucomaPrimary angle-closure glaucoma
without pupillary block (Plateauwithout pupillary block (Plateau
irisiris((
Plateau iris configuration:Plateau iris configuration:
Characterized by a closed anterior chamber angle in association withCharacterized by a closed anterior chamber angle in association with
a flat iris plane and a deep central anterior chamber.a flat iris plane and a deep central anterior chamber.
Plateau iris glaucoma:Plateau iris glaucoma:
Acute angle closure occurs with pupillary dilatation despite a patentAcute angle closure occurs with pupillary dilatation despite a patent
iridotomy. When the pupil dilates, the peripheral iris becomesiridotomy. When the pupil dilates, the peripheral iris becomes
bunched up and occludes the trabeculum.bunched up and occludes the trabeculum.
Clinically:Clinically:
All the features of acute congestive angle closure are present exceptAll the features of acute congestive angle closure are present except
that the axial anterior chamber depth is normal and the iris planethat the axial anterior chamber depth is normal and the iris plane
is flat rather than convex.is flat rather than convex.
TreatmentTreatment
1) Laser peripheral iridotomy.1) Laser peripheral iridotomy.
2) Pilocarpine 1% drops.2) Pilocarpine 1% drops.

87. Congenital GlaucomasCongenital Glaucomas
1) Primary Congenital Glaucomas.1) Primary Congenital Glaucomas.
2) Secondary Congenital Glaucomas:2) Secondary Congenital Glaucomas:
- Tumours such as retinoblasloma and juvenile- Tumours such as retinoblasloma and juvenile
xanthogranuloma.xanthogranuloma.
- Persistent hyperplastic primary vitreous.- Persistent hyperplastic primary vitreous.
- Retinopathy of prematurity.- Retinopathy of prematurity.
- Intraocular inflammation.- Intraocular inflammation.
- Trauma.- Trauma.
- Ectopia lentis.- Ectopia lentis.

89. 11((Primary CongenitalPrimary Congenital
GlaucomaGlaucoma
PathogenesisPathogenesis
(isolated trabeculodysgenesis)(isolated trabeculodysgenesis)..
Classification:Classification:
1) True congenital glaucoma (40%)1) True congenital glaucoma (40%)
2) Infantile glaucoma (55% of cases)2) Infantile glaucoma (55% of cases)
3) Juvenile glaucoma, the least common3) Juvenile glaucoma, the least common

90. Clinical pictureClinical picture::
1) Corneal haze associated with lacrimation, photophobia and1) Corneal haze associated with lacrimation, photophobia and
blepharospasm.blepharospasm.
2) Buphthalmos is a large eye as a result of stretching due to2) Buphthalmos is a large eye as a result of stretching due to
elevated IOP prior to the age of 3 years.elevated IOP prior to the age of 3 years.
- Sclera: stretches & becomes thinner and translucent. the eye then- Sclera: stretches & becomes thinner and translucent. the eye then
takes on a blue appearance due to enhanced visualization of thetakes on a blue appearance due to enhanced visualization of the
underlying uvea.underlying uvea.
- The anterior chamber deepens.- The anterior chamber deepens.
- The zonular fibres stretch and the lens may rarely subluxate.- The zonular fibres stretch and the lens may rarely subluxate.
- The increased axial length- The increased axial length
- Breaks in Descemet membrane- Breaks in Descemet membrane
- Optic disc cupping- Optic disc cupping

91. TreatmentTreatment
SurgerySurgery
1) Goniotomy is performed at the initial examination if1) Goniotomy is performed at the initial examination if
the diagnosis is confirmed. Provided there is sufficient,the diagnosis is confirmed. Provided there is sufficient,
corneal clarity and the angle can be visualized.corneal clarity and the angle can be visualized.
2) Trabeculotomy may be necessary if corneal clouding2) Trabeculotomy may be necessary if corneal clouding
prevents visualization of the angle or when repeatedprevents visualization of the angle or when repeated
goniotomy has failed.goniotomy has failed.
3) Trabeculectomy is often successful, particularly when3) Trabeculectomy is often successful, particularly when
combined with trabeculotomy and adjunctivecombined with trabeculotomy and adjunctive
anti-metabolites.anti-metabolites.

92. GoniotomyGoniotomy

93. TrabeculotomyTrabeculotomy

94. Follow-upFollow-up
Patients should be reviewed 1 month after initialPatients should be reviewed 1 month after initial
surgery. The IOP and corneal diameters shouldsurgery. The IOP and corneal diameters should
be monitored at regular intervals becausebe monitored at regular intervals because
progressive enlargement of the corneal diameterprogressive enlargement of the corneal diameter
is ay important a sign of uncontrolled congenitalis ay important a sign of uncontrolled congenital
glaucoma.glaucoma.

95. Thank youThank you