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)

CLASSIFICATION OF GLAUCOMA

PRIMARY GLAUCOMA

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 Schlemm’s 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

PRIMARY OPEN ANGLE GLAUCOMA (POAG)

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

SIGNSI. Anterior segment signsMay reveal normal anterior segment. In late stages pupil reflex becomes sluggish and cornea may show slight haze.II. Intraocular pressure changesIn 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 aretypically 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 dropsIOP control slows disk damage and field loss. For every 1 mmHg reduction 10% decrease risk of progression.

SurgeryTrabeculectomy

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

PRIMARY ANGLE- CLOSURE GLAUCOMA

ACUTE ANGLE CLOSURE Iris bombe develops causing occlusion of AC angle

by the peripheral irisPREDISPOSING 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 anteriorlyEyes with narrow angle of anterior chamber

due to: small eyeballrelatively 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

COMPLICATIONSDelayed 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. Peripheral iridotomy2. Laser iridotomy3. Filtration surgery4. 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

Types

• 1. Primary developmental/congenital glaucoma.

• 2. Developmental glaucoma with associated ocular anomalies.

CONGENITAL /DEVELOPMENTAL GLAUCOMAS

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

PRIMARY DEVELOPMENTAL /CONGENITAL GLAUCOMA

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 Descemet’s

membrane Edema and opacity of cornea

Congenital glaucoma (Buphthalmos)

DIFFERENTIAL DIAGNOSIS Megalocornea Corneal clouding Mucopolysaccharidoses Traumatic rupture of Descemet’s

membrane

COURSE AND PROGNOSIS If untreated , blindness occurs early

TREATMENT Always surgical

Goniotomy or Trabeculectomy

AXENFELD SYNDROME

Hypoplasia of anterior stroma of the iris with bridging filaments occuring peripherally and connecting to a prominent, axially displaced Schwalbe’s line

RIEGER’S SYNDROME

Broader iridocorneal adhesions associated with with disruption of iris, with polycoria, skeletal and dental abnormalities

PETER’S ANOMALY

Adhesions are between the central iris and the central posterior surface of the cornea

ANTERIOR SEGMENT ANOMALIES

AxenfeldPeter’s anomaly

Rieger’s 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