The document provides information on the anatomy and physiology of the anterior segment of the eye. It discusses the ciliary body, anterior chamber, structures within the anterior chamber angle like the scleral spur, trabecular meshwork, Schlemm's canal, and how aqueous humor is produced and drained from the eye. It also provides definitions and classifications of glaucoma, risk factors for primary angle closure glaucoma, stages of primary angle closure glaucoma attacks, clinical features and diagnosis. Treatment of early stage primary angle closure involves miotic eye drops or laser iridotomy.

1. PRESENTED BY
DR.MD.HASAN SHAHRIAR

2.  Ciliary Body:
◦ 6-7 mm wide
◦ Has 2 parts:
 Pars plana:
 Avascular, smooth pigmented
 4 mm wide
 From ora serrata to ciliary process
 Pars plicata:
 Vascularized
 Has around 70 radial folds (ciliary process)
 Zonular fibers attachment

3. ◦ Lined by 2 layers of epithelial cells
 Nonpigmented Epithelium (NPE)
 Pigmented Epithelium (PE)
◦ The apices of NPE and PE are fused together by a
system of junctions and cellular interdigitations
(Blood Aqueous Barrier)

5.  Anterior Chamber
◦ Between Cornea (front) and Iris (back)
◦ AC Angle lies at the corner of Cornea-Iris junction,
consists of:
 Schwalbe Line
 Schlemm Canal and TM
 Scleral Spur
 Ciliary Process
 Iris

7.  Schwalbe’s Line
◦ Is the anatomical line found on the interior surface
of the cornea, and delineates the outer limit of
corneal endothelium layer.
◦ It represents the termination of Descemet’s
membrane

8.  Trabecular Meshwork
◦ Is a circular spongework of connective tissue lined
by trabeculocytes, that have contractile properties
and may influence outflow resistance
◦ 3 portions:
 Uveal Portion
 Corneoscleral Meshwork
 Juxtacanalicular Tissue

10.  Schlemm Canal
◦ Circular tube resembling a lymphatic vessel
◦ Contribute to the pressure-dependent outflow of
aqueous

11.  Aqueous Humor
◦ Clear fluid that fills the PC and AC
◦ Secreted by ciliary epithelium (NPE)
◦ Flow rate 2-3 µL/mn
◦ Functions:
 Provide nutrients to avascular zones
 Remove metabolic wastes
 Maintain IOP
 Clear medium for transmission of light

13.  AH secretion into the PC result from:
◦ Active Secretion: Na/K ATPase pump
◦ Ultrafiltration: Hydrostatic/Oncotic pressure
◦ Simple Diffusion: Different concentration

14.  Outflow: 0,22-0,30µL/mn/mmHg
◦ Pressure-dependant:
 Trabecular-Schlemm canal pathway
 80-95 % of outflow
◦ Pressure-independent:
 Non-trabecular or uveal pathway
 8-15 % of outflow

15.  Composition of AH
◦ Inorganic Ions:
 Na+, K+, Mg
 Ca+
 Cl-, HCO3-
 Iron, copper, zinc
◦ Organic Ions:
 Lactate and Ascorbic Acid
◦ Carbohydrates
◦ Glutathione and Urea
◦ Proteins
◦ Enzymes

16.  IOP: 11-21mmHg
 Balance between the aqueous inflow and
outflow
 Fluctuation:
◦ Higher in morning, lower in noon and evening
◦ Heart rate
◦ Blood pressure
◦ Respiration

17. Definition:
Glaucoma is a complex ocular disorder
characterized by structural and functional
defect of eye in the form of cupping of the
optic disk and visual field defect, related
frequently but not absolutely with increased
intraocular pressure.

18. Glaucoma can be classified as
A.Congenital or developmental- It may be
. Primary which includes both true and infantile
glaucoma.
.Secondary or juvenile glaucoma.
B.Aquired –It may be
.Primary
.Secondary
Primary glaucoma may be classified as
1. Primary open angle glaucoma(POAG)
2. Primary angle closure glaucoma(PACG)
Secondary glaucoma is associated with some ocular
or systemic disease.

19.  Angle Closure
◦ Refers to the occlusion of the TM by the
peripheral iris (Iridotrabecular Contact or ITC)
 Obstructing the aqueous outflow
◦ Can be divided into two types:
 Primary
 Secondary

20. Primary angle closure glaucoma is a
condition in which there is elevation of IOP
occurs as a result of obstruction of aqueous
outflow by partial or complete closure of
the angle by the peripheral iris.

24. 1.Age:
The average age at presentation is
about 60years and the prevalence increases
thereafter.
2.Gender:
Females are commonly affected than
males by a ratio of 4:1.

25. 3.Race:
In whites the rate is about 6% of all types of
glaucoma and approximately 1 in 1ooo individuals
over the age of 40.PACG is more common in South
east asians ,Chinese and Eskimos but uncommon
in blacks.
4.Family history:
First degree relatives are at increased risk as
ocular anatomical features are inherited.

26. 1.Relatively anterior location of the iris-lens
diaphragm.
2.Shallow anterior chamber.
3.Narrow entrance of the chamber angle due
to-
.Smaller cornea
.Bigger size of the lens
.Bigger size of the ciliary body

27. .1.Pupillary block mechanism:
The initial event is thought to be a functional
pupillary block (between pupillary portion of the iris
and the anterior surface of lens) in mid-dilated
position.
The pupillary block causes accumulation of
aqueous in the posterior chamber
Increased pressure in posterior chamber

28. Forward bowing of the peripheral
iris, resembling an iris bombe
Closure of anterior chamber angle
Sharp rise in intraocular pressure

29. 2.Plateau-iris mechanism:
It is due to an abnormal anatomical
configuration of the anterior chamber
angle.
The angle is closed by infolding of the
iris into the angle in association with
pupillary dilatation , but without a
significant pupillary block component.

30.  The changes that occur in ACG can be divided
into different stages . Stages are as follow
1.Prodromal or latent stage
2.Stage of constant instability
3.Acute attack which divided into 2
stages congestive and postcongestive
glaucoma
4.Chronic congestive attack
5.Stage of absolute glaucoma

31. Usually asymptomatic
Signs:
. Slit lamp bio microscopy shows -
shallow anterior chamber which
can be demonstrated by ‘eclipse sign’
convex shaped iris-lens diaphragm
close proximity of the iris to the
cornea
Gonioscopy shows –
Shows an occludable angle in
which pigmented trabecular meshwork is
not visible.
.sudden rise in IOP up to 40/6o mm hg.

32. Also called intermittent or subacute stage
It occurs in a predisposed eye with an
occludable angle in association with
intermittent pupillary block.
A rapid closure of the angle results in a
sudden rise in IOP .

33. The pupillary block may be
spontaneously broken, the angle
opens and IOP returns to normal
level during sleep as the pupil
becomes constricted.
The attacks may be precipitated by
physiological mydriasis like
watching television in a dark room.

34.  Diagnosis based on a characteristic history
of transient blurring of vision associated
with haloes around the light due to corneal
epithelial edema.
 There may also be associated eye ache or
frontal headache.
 The attacks are usually recurrent lasts for
1-2 hours and are usually broken by
physiological miosis.

35. Acute congestive attack occurs as a
result of complete closure of anterior
chamber angle resulting in acute ischemia.
If the attack lasts for several hours or days
causes irreversible damage may occur at
ocular tissues.

36.  Accumulation of fluid results in raised IOP
 Circumcorneal congestion and chemosis
due to stasis with increased permeability of
the capillaries
 Pupil is mid-dilated and oval . Iris shows
atrophic changes.

37.  Glaucom-fleckens are small
greyish-white anterior subcapsular
opacities occurs in the pupillary
zone . These are diagnostic for
previous attack of ACG and due to
atrophy of the newly formed lens
fibers.
 Optic nerve head is usually
edematous and hyperemic. cupping
of optic disc is usually evident after
2weeks.

38. 1.Acute, intense, unbearable pain,
radiating along the distribution of 5th
cranial nerve.
2.Severe headache often with nausea
and vomiting often mistaken for acute
abdomen.
3.Marked dimness of vision, is mainly
due to ischemic optic neuropathy and partly
due to corneal edema.
4.Redness, lacrimation and
photophobia.

39.  Tender eyeball
 Slitlamp biomicroscopy shows
-Eyelids are edematous narrowing of
palpebral aperture.
-Both ciliary and conjunctival congestion
with chemosis.
-Cornea steamy and insensetive.
-Anterior chamber is shallow cells and
flare may be present.

40. -iris pattern is lost and discolored.
-Pupil mid-dilated and vertically oval.
Reaction to light and accommodation are
absent.
-IOP markedly elevated.
-Visual acuity may reduced to PL PR.
 Gonioscopy shows complete peripheral
iridocorneal contact.
 Ophthalmoscopy when possible shows
optic disc edema and hyperemic.

41. Postcongestive angle closure glaucoma may be
found in case of –
1. Postsurgical – in which the IOP is normalized
by successful peripheral iridotomy or
trabeculectomy.
After peripheral iridotomy IOP may be still
elevated in some eyes due to associated
trabecular damage despite the fact that 50% 0r
more of the angle is open.
2.Sponteneous angle reopening – without
treatment may occur in few cases.

42. 3.Cilliary body shutdown – Here a
temporary decrease in aqueous secretion
occurs as a result of ischemic damage to
the secretory cilliary epithelium in the
presence of complete angle closure. In
this case a subsequent recovery of cilliary
function may lead to chronic elevation of
IOP with optic disk cupping and visual
field loss. So it is to be confirm that the
angle is open after peripheral iridotomy
even if the IOP is normal.

43. Patient will give history about acute attack or
surgery.
1.Slitlamp biomicroscopy shows –
.IOP may be normal, elevated or
subnormal
.Folds in descemet membrane if the IOP
reduced so rapidly
.Fine pigment granules on the corneal
endothelium

44.  Stromal iris atrophy with spiral-
like configuration and fine
pigment granules on its surface
 A fixed and semidilated pupil
due to combination of paralysis
of sphincter and posterior
synechiae.
 Aqueous flare and cells.
 Glaukomflecken

45. 2.Gonioscopy shows angle is
narrow open or partly closed.
3.Ophthalmoscopy may show
congestion of the optic disk
and choroidal folds if the IOP
is very low

46. This is sometimes called ‘creeping
angle closure’ as the angle becomes slowly
and progressively closed.
Clinical features:
.Visual acuity is always impaired.
.Congested and irritable eye.
.IOP remains permanently elevated.
.Cupping of the disk appears.

47.  Peripheral anterior synechiae develop, mostly
in the upper part of the angle, but gradually
spread around the whole circumference.
 Typical glaucomatous field defects become
evident. The chronic congestive phase, if
untreated, gradually passes into the final
stage of absolute glaucoma

48. 1.Type 1 – creeping angle closure or
progressive synechial angle closure.
2.Type 2 – caused by synechial angle closure
as a result of intermittent or subacute
attacks secondary to pupillary block.
3.Type 3 – caused by a combination of POAG
with narrow angle usually associated with
long term use of miotics.

49. Absolute glaucoma is the end stage of any
glaucoma whether congenital or acquired ,
primary or secondary charecterized by
extremely high IOP with no PL.
 Ultimately may lead to
 Staphyloma formation
 Increased danger of rupture from slight
injury.
 Atrophic bulbi

50.  Painful blind eye with no PL
 Reddish-blue zone surrounding the limbus
due to dilated anterior ciliary vein.
 Cornea is cloudy and insensetive;there may
be associated bullous keratopathy or
filamentary keratopathy .
 Anterior chamber is very shallow.

51.  Iris patches of atrophy ectropion
of the uveal pigments.
 Pupil dilated and greyish in
appearance no light reaction.
 Optic disc large and deep
cupping with atrophic changes.
 Tension extremely high like stony
hard.

52. In acute and chronic congestive stages, the
nature of the condition is usually obvious.
But the diagnosis of angle closure glaucoma
is really difficult in the prodromal stage and
is of immense importance.

53. Diagnostic criteria in early stages:
1.The history of seeing “coloured
halos’’.
2.The presence of a “narrow angle’’ of
the anterior chamber.
3.Inducement of a rise of
tension(positive provocative test)

54. Coloured halos:
Coloured halos are due to accumulation
of fluid in the corneal epithelium alteration
in the refractive condition of the corneal
lamellae.This halos are seen around the
lighted bulb.

55. Gonioscopy:
To identify the abnormalities of the
angle and to estimate the width of the angle.
It may be direct or indirect.
When gonioscope are not available slit
lamp technique of van Herick may be used.
Here the depth of the peripheral anterior
chamber is estimated by comparing it to the
adjacent corneal thickness which is 1cm
near the limbus.

56. Grade 4 - PAC > 1CT wide open angle
Grade 3 – PAC = 1/4 – 1/2 CT mild
narrow angle
Grade 2 – PAC = 1/4 CT moderately
narrow angle
Grade 1 – PAC < ¼ CT extremely narrow
angle

57. Tonometry:
Measurement of IOP.
Normal IOP is about 12-21 mm hg
In glaucoma >21mmhg.
Provocative tests:
. Physiological provocative test –
Dark room test
Prone test
Prone dark room test

58.  Pharmacological (Mydriatic) provocative test -
short acting topical mydriatic is instilled
causes rise in IOP about 8mmhg considered
to be positive.
 Mapstone’s test – Pilocarpine and 10%
phenylephrine are instilled simultaneously
every minute for 3 applications to achieve
mild dilated pupil. A pressure rise >8mmhg
is considered to be positive.

59. Usually
blurred
Markedly
blurred
Slightly
blurred
No effect on
vision
Vision
Moderate to
severe
SevereModeratevariablePain
Watery or
purulent
NoneNoneModerate to
copious
(mucopurulent
)
Discharge
CommonUncommonCommonExtremely
common
Incidence
Corneal
trauma or
infection
Acute
congestive
glaucoma
Acute
iridocyclitis
Acute
conjunctivitis

60. Organisms
found only in
corneal ulcers
due to
infection
No organismsNo organismsCausative
organisms
Smear
NormalElevatedNormalNormalIntraocular
pressure
NormalNonePoorNormalPupillary light
response
NormalSemidilated
and fixed
SmallNormalPupil size
Change in
clarity related
to cause
HazyUsually clearClearCornea
DiffuseDiffuseMainly
circumcorneal
Diffuse, more
toward
fornices
Conjunctival
injection

61. A . In early stage
1. Miotic therapy: Instillation of
pilocarpine 2% every 5 minutes is usually
effective in pulling the iris from the angle
and aborting the attack. The fellow should
be treated with 2% pilocarpine 3times
daily.
2. Peripheral iridectomy and Laser
iridotomy should then be performed in
both eyes.

62. Medical therapy:
1.Tab. Acetazolamide(250mg) – initially 2tab. Stat
then 1tab 4 times daily with potassium
supplement.
2.Corneal indentation – simple repeated indentation
of central part of cornea with a squint hook or a
sterile swab-stick may be effective in opening the
angle. This is only effective in absence of
significant synechial closure of the angle.

63. 3.Hyperosmotic agents – act by drawing
water out of the eye and reduce IOP. eg.
 Inj. Manitol(2o%) – 1-2gm/kg body wt
i.e.300-500ml is given iv over a period of
30-40 minutes
 Oral glycerol – (50% solution) 30ml of
pure glycerol with equal amount of fruit
juice stat and 3times daily.
 Isosorbide

64. 4.Pilocarpine(2% or 4%) eye drop is instilled
every 5minutes till the pupil gets
constricted and then 3-4 times daily. The
fellow eye should be treated with 2%
pilocarpine 3times daily.
5.Strong analgesics(even Ing. Pethidine) and
anti-emetic may be needed to reduce the
pain and vomiting.

65. 6.Steroid-antibiotic drops frequently instilled to
reduce the congestion.
Once the IOP has been reduced medically
and eye becomes quite, the further
management is
. Continue the medical treatment with
pilocarpine2% 3-4 times daily. This is only
indicated for old patient with poor general
health and where laser is not available.

66. .Surgery
(1). Laser iridotomy or
peripheral iridectomy and if
necessary
(2).Filtration surgery.

67. If the angle closure is less than 50% then a
surgical peripheral iridectomy or laser
iridotomy should done.
If the angle closure is more than 50%
then a filtration operation is indicated that
is Trabeculectomy.
Treatment of the fellow eye:
The fellow eye should be treated by
surgical peripheral iridectomy or laser
iridotomy as soon as possible.

68. 1.A laser iridotomy may be tried initially. If
this is unsuccessful a filtration operation
i.e. trabeculectomy should be performed.
Miotics are not useful in this stage

69. 1.Cyclocryotherapy – this is to reduce the
aqueous secretion and thereby reduce the
IOP.
2.Retrobulber injection of 70% alcohol to
destroy the cilliary ganglion.
3.If the pain is still unbearable then the eye
may be enucleated.

70. THANK
YOU