PRIMARY

GLAUCOMA
PRESENTER- MONAZZAH AND ARPITA
MODERATOR – SWEETY MA’AM
 GLAUCOMA

• Glaucoma is not a single disease but group of

disorders characterized by progressive optic
neuropathy resulting in characteristic appearance of
the optic disc and a specific pattern of irreversible
visual field defects that are associated frequently but
not invariably with raised intraocular pressure (IOP).
ETIOLOGICAL CLASSIFICATION

• A. Congenital/developmental glaucoma
• 1. Primary congenital/ developmental glaucoma {without associated anomalies).
2. Secondary congenital/developmental glaucoma (with associated anomalies).
• B. Primary adult glaucomas
1. Primary open-angle glaucomas (POAG
2. Primary angle-closure glaucoma (PACG)
• C. Secondary glaucomas
PRIMARY OPEN ANGLE GLAUCOMA

As the name implies, it is a type of primary glaucoma, where there is no obvious systemic
or ocular cause of rise in the intraocular pressure. Primary open-angle glaucoma (POAG),
also known as chronic simple glaucoma of adult onset, is typically characterized by:
• Slowly progressive raised intraocular pressure (>21 mm Hg recorded on at least few
occasions) associated with,
• Open normal appearing anterior chamber angle,
• Characteristic optic disc cupping, and
• Specific visual field defects.
RISK FACTOR

• intraocular pressure (IOP)

• Age : commonly seen after 5th and 7th decade
• Race: more common in black people than in whites
• Diabetics have a higher prevalence of POAG than nondiabetics.
• Cigarette smoking is also thought to increase its risk.
• High blood pressure is not the cause of rise in IOP, however, the prevalence of POAG is
more in hypertensive than the normotensives.
SYMPTOMS

• Asymptotic
• Headache and eye ache of mild intensity
• Difficulty in reading and close work
• Delayed dark adaptation may develop
• Scotoma (defect in the visual field) may be noticed occasionally by some observant
patients.
• Significant loss of vision and blindness is the end result of untreated cases of POAG.
SIGN

• Anterior segment: may be normal

• IOP – diurnal variation seen
- in late stages IOP is permanently raised above 21 mm of Hg and ranges between 30
and 45 mm of Hg.
• Glaucomatous disc changes
INVESTIGATION

• Tonometry.
• Central corneal thickness (CCT)
• Diurual variation test is especially useful in detection of early cases
• Gonioscopy. It reveals a wide open angle of anterior chamber.
• Check for optic disc changes
• Perimetry
• OCT
MANAGEMENT

• Medical therapy-Antiglaucoma drugs

1. Prostaglandin- Bimatoprost, Travoprost
2. Adrenergic drugs. – Brimonidine
3. Beta blockers- timilol melonate
4. Dorzolamide
PRIMARY ANGLE-CLOSURE DISEASE

Primary angle closure disease, is characterized by apposition of peripheral iris against the
trabecular meshwork resulting in obstruction of aqueous outflow by closure of an already
narrow angle of the anterior chamber.
Clinical classification
• Primary angle closure suspect
• Primary angle Closure
• Primary angle closure glaucoma
RISK FACTOR

• Gender. Male to Female ratio is 1:3

• Age: 6th and 7th decade
• Race: It is more common in South-East Asians, Chinese and Eskimos but uncommon in
Blacks.
• Heredity
• Hypermetropic eye with shallow anterior chamber and short axial length.
PRIMARY ANGLE-CLOSURE SUSPECT

Primary angle- closure suspect (PACS), can be considered analogous to the term ‘latent
primary angle-closure glaucoma’ of clinical classification.
• Symptoms are absent in this stage.
• Gonioscopy should reveal irido-trabecular contact in greater than 270° angle and no
peripheral anterior synechiae (PAS absent).
• IOP should be normal.
• Optic disc should show no glaucomatous change.
• Visual feild should be normal.
PRIMARY ANGLE-CLOSURE

• lrido-trabecular contact noted on gonioscopy in greater than 270° angle,

• IOP elevated and/or peripheral anterior synechiae (PAS) present,
• Optic disc: normal, and
• Visual field: Normal.
• Symptoms- Colored halo
-Transient loss of vision
PRIMARY ANGLE-CLOSURE GLAUCOMA

PACG) as per ISGEO classification is:

• lrido-trabecular contact is noted on gonioscopy in greater than 270° of angle,
• PAS are formed,
• IOP is elevated,
• Optic disc shows glaucomatous damage or cupping, and
• Visual fields show typical glaucomatous defects.
Clinical features
• lntraocular pressure (IOP) remains constantly raised.
• Eyeball remains white (no congestion) and painless.
• Optic disc shows glaucomatous cupping.
• Visual field defects similar to POAG occur
• Gonioscopy reveals more than 270° of angle closure along with peripheral anterior synechiae (PAS)
Treatment
• Laser iridotomy alone or along with medical therapy similar to POAG should be tried first.
• Trabeculectomy (filtration surgery) is needed when the above treatment fails to control IOP.
• Prophylactic laser iridotomy in fellow eye must also be performed. L
TREATMENT

Medical therapy ( antiglaucoma drugs) to lower IOP

Laser iridotomy alone or along with medical therapy similar to POAG should be tried first.

Trabeculectomy (filtration surgery) is needed when the above treatment fails to control
IOP.
• Prophylactic laser iridotomy in fellow eye must also be performed.