CLASSIFICATION OF

GLAUCOMA
Primary adult glaucomas
Primary open angle glaucomas (POAG)
Primary angle closure glaucoma (PACG)
Primary mixed mechanism glaucoma

Secondary glaucomas
Congenital and developmental glaucomas
Primary congenital glaucoma (w/o associated
anomalies)
Developmental glaucoma (with associated
anomalies)

PRIMARY GLAUCOMA

PRIMARY OPEN ANGLE GLAUCOMA

(POAG)
No obvious systemic or ocular cause of rise in
IOP
Occurs in eyes with open angle of the
anterior chamber.
also known as chronic simple glaucoma of
adult onset
Characterized by slowly progressive raised
intraocular pressure
associated with optic disc cupping and
specific visual field defects.

PRIMARY OPEN-ANGLE GLAUCOMA

(POAG)
EPIDEMIOLOGY

Most common in black and whites

1.29% - 2% over age 40

4.7% over age 75

4x more common and 6x more likely to

cause blindness in blacks
Strong familial tendency and close
relatives affected must undergo regular
screening

PRIMARY OPEN ANGLE GLAUCOMA

(POAG)
PATHOLOGIC FEATURE

Degenerative process in the trabecular

meshwork
With deposition of extracellular material
within meshwork or beneath endothelial
lining of Schlemms canal
As a consequence there is reduction in
aqueous drainage leading to high IOP
In Juvenile-onset OAG, 5% familial and 3%
non-familial. Associated with mutation in
myocilin gene in Chromosome 1

PRIMARY OPEN ANGLE GLAUCOMA

(POAG)
PREDISPOSING AND RISK FACTORS:

Heredity
Age
Race
Myopes
Diabetics
Cigarette smoking
High blood pressure
Thyrotoxicosis

 SYMPTOMS
Insidious and usually asymptomatic,
until it has caused a significant loss of
visual field. Periodic eye examination
is required after middle age.
Mild headache and eye ache.
May notice a defect in the visual field.
Accommodative failure
Development of delayed dark
adaptation

 SIGNS
I. Anterior segment signs
May reveal normal anterior segment.
In late stages pupil reflex becomes sluggish and
cornea may show slight haze.
II. Intraocular pressure changes
In the initial stages the IOP may not be raised
There is an exaggeration of the normal diurnal
variation. Repeated observations of IOP (every 3-4
hour), for 24 hours is required during this stage
(Diurnal variation test).
III. Optic disc changes.
Important clue for suspecting POAG. These are
typically progressive, asymmetric and present
avariety of characteristic clinical patterns .

 DIFFERENTIAL DIAGNOSIS
OCULAR HYPERTENSION GLAUCOMA
High IOP without optic nerve damage or visual
field defects.
Some will continue to have elevated IOP but
will not develop glaucomatous lesions;
Others will develop primary open angle
glaucoma.
Increase risk:
increasing IOP and age, greater disk cupping,
(+) family history, myopia, DM, cardiovascular
dse,
development of disk hemorrhage

 DIFFERENTIAL DIAGNOSIS
LOW-TENSION GLAUCOMA
Exhibit typical progressive glaucomatous
changes in the optic disc and visual field
without high IOP
They are very difficult to treat because
management cannot focus on the control
of intraocular pressure.
Often these patients will have a history of
hemodynamic crises such as GI or uterine
bleeding with significant loss of blood, low
blood pressure, and peripheral vascular
spasms (cold hands and feet).

 SCREENING
Start early/ Active screening
COURSE AND PROGNOSIS
Without treatment progress to BLINDNESS
TREATMENT
Medical management
Anti-glaucoma drops
IOP control slows disk damage and field loss. For
every 1 mmHg reduction 10% decrease risk of
progression.
Surgery
Trabeculectomy

PRIMARY
ANGLE- CLOSURE GLAUCOMA
Elevated IOP due to obstruction of aqueous
outflow of occlusion of trabecular meshwork
by peripheral iris resistant to ON damage
and VF loss
Can be an ophthalmic emergency or
asymptomatic until visual loss
Risk factors:
Increasing age, female sex, (+) family
history, SE Asian, Chinese or Inuit
background

ACUTE ANGLE CLOSURE

Iris bombe develops causing occlusion of AC angle by
the peripheral iris
PREDISPOSING RISK FACTORS.
ANATOMICAL FACTORS
Eyes anatomically predisposed to develop (PACG)
include:
Hypermetropic eyes with shallow anterior chamber.
Eyes in which iris-lens diaphragm is placed
anteriorly
Eyes with narrow angle of anterior chamber
due to: small eyeball
relatively large size of the lens
smaller diameter of the cornea
bigger size of the ciliary body
Plateau iris configuration

 GENERAL FACTORS
Age
Sex - M:F is 1:4
Type of personality
Season
Family history
Race.
PRECIPITATING FACTORS
Dim illumination
Emotional stress
Use of mydriatic drugs like atropine,
cyclopentolate, tropicamide and
phenylephrine

CLINICAL
MANIFESTATIONS:
Sudden visual
loss
Excruciating pain
Halos
Nausea
Vomiting
High IOP
Shallow AC
Steamy cornea
Fixed round
dilated pupil
Ciliary injection

DIFFERENTIAL DIAGNOSIS:
Acute Iritis
Acute conjunctivitis
COMPLICATIONS
Delayed treatment will cause:
Peripheral iris may adhere to trabecular
meshwork (Anterior synechiae)
Produce irreversible occlusion of AC
angke requiring surgery
ON damage

 MEDICAL TREATMENT
1. Systemic hyperosmotic agent
2. Acetazolamide
3. Analgesics and anti-emetics as required
4. Pilocarpine eyedrops
5. Beta blocker eyedrops
6. Corticosteroid eyedrops

 SURGICAL TREATMENT

1.
2.
3.
4.

Peripheral iridotomy
Laser iridotomy
Filtration surgery
Clear lens extraction by
Phacoemulsification

PROPHYLACTIC TREATMENT IN THE NORMAL

FELLOW EYE
Prophylactic laser iridotomy (preferably) or surgical
peripheral iridectomy should be performed on the
fellow asymptomatic eye.

SUB ACUTE ANGLE CLOSURE

occurs an attack of transient rise of IOP

(40-50 mmHg) which may last for few

minutes to 1-2 hours.
attack in a patient with occludable or
narrow angle is usually precipitated
by :
Physiological mydriasis

Physiological shallowing of anterior

chamber after lying in prone
position.

 SYMPTOMS

unilateral episodes of
transient blurring of vision, pain,
redness
colored halos around light
headache
brow ache

eye ache on the affected side

attacks occur at night which resolves
DIAGNOSIS
Gonioscopy
TREATMENT
Laser peripheral iridotomy

 CHRONIC ANGLE CLOSURE

results from gradual synechial closure of
the angle of anterior chamber in
following circumstances:
Creeping synechial angle-closure.
Attacks of subacute angle-closure
glaucoma may eventually end up in
chronic angle-closure glaucoma.
Mixed mechanism, (a combination of
POAG with narrow angles. It presents as
chronic angle closure glaucoma)

 CLINICAL FEATURES
Increase IOP
Narrow AC angle
Variable amounts of anterior synechiae
OP disk cupping
VF defects
MANAGEMENT
Laser peripheral iridotomy
Medical control of IOP
Drainage surgery
Cataract extraction

CONGENITAL /DEVELOPMENTAL
GLAUCOMAS
Types
1. Primary developmental/congenital
glaucoma.
2. Developmental glaucoma with
associated ocular anomalies.

PRIMARY DEVELOPMENTAL /
CONGENITAL GLAUCOMA
Refers to abnormally high IOP which
results due to developmental anomaly
of the angle of the anterior chamber,
not associated with any other ocular or
systemic anomaly.
Rare

 TRUE CONGENITAL GLAUCOMA

o IOP is raised during intrauterine life and
child is born with ocular enlargement.
o It occurs in 40% of cases.

INFANTILE GLAUCOMA
o Manifests prior to the child's 3rd
birthday.
o It occurs in about 50 % of cases.

JUVENILE GLAUCOMA
o 10% cases who develop pressure rise
between 3-16 years of life.

CLINICAL FINDINGS

50% dx at the first 6 months

80% dx at the first year
Epiphora earliest and most
common symptom
Photophobia and decrease
corneal luster
Increase IOP cardinal sign
Early glaucomatous cupping
most important change
Increase corneal dm > 11.5
mm
Epithelial edema
Tears of Descemets membrane
Edema and opacity of cornea

Congenital glaucoma
(Buphthalmos)

DIFFERENTIAL DIAGNOSIS

Megalocornea
Corneal clouding
Mucopolysaccharidoses
Traumatic rupture of Descemets membrane

COURSE AND PROGNOSIS

If untreated , blindness occurs early
TREATMENT
Always surgical
Goniotomy or Trabeculectomy

ANTERIOR SEGMENT
ANOMALIES
AXENFELD SYNDROME
Hypoplasia of anterior stroma of the iris with bridging
filaments occuring peripherally and connecting
to
a prominent, axially displaced Schwalbes line
RIEGERS SYNDROME
Broader iridocorneal adhesions associated with with
disruption of iris, with polycoria, skeletal and dental
abnormalities
PETERS ANOMALY
Adhesions are between the central iris and the central
posterior surface of the cornea

Axenfeld

Peters
anomal
y

Riegers syndrome

ANIRIDIA
Distinguishing feature is vestigial iris
Thin iris margin is present
Rare and can be AD or AR in inheritance
Glaucoma develops before adolescence and
can be refractory to medical and surgical
treatment