By: Ahmad Al-Zu’bi & Saja Aloran

It is a group of eye diseases in which damage to the optic nerve (optic neuropathy) is usually “ not always” caused by raised ocular pressure (normal IOP is 15.5 mmHg) acting

on the nerve head.

Its optic neuropathy and visual field defect

with or without increase intraocular pressure .

1.Conventional pathway

2.Uveo-scleral pathway

IOP: Depends on the balance between production and removal of aqueous humour .

Conventional pathway :

Aqueous humour is secreted by the ciliary processes in the posterior chamber, then it passes through the pupil into the anterior chamber and leaves the eye via Trabecular meshwork, Schlemm’s canal, and episcleral veins.

:Uveo-scleral pathway

Drains a small proportion of aqueous (4%).

It drains it across the ciliary body into the supra-coroidal space, and into the venous circulation across the sclera.

Two theories :

1 Raised intraocular pressure causes

mechanical damage to the axons.

2 Raised intraocular pressure causes ischaemia of the nerve axons by reducing

blood flow at the nerve head

-Family history of glaucoma

-Age 60 and older.

-Eye injury , certain eye surgeries or chronic eye inflammation.

-Diabetes, high blood pressure, heart disease or hypothyroidism .

-steroids for long periods of time .

In open angle glaucoma the trabecular

meshwork appears normal on gonioscopy but functionally, it offers an increased resistance the outfl ow of aqueous

:The causes of outflow obstruction include

• Thickening of the trabecular lamellae, which reduces pore size.

• Reduction in the number of lining trabecular cells.

• Increased extracellular material in the trabecular meshwork spaces

Open irido-corneal angle

(Trabecular meshwork is not covered)

It is the most common type of glaucoma

It is the 3rd cause of blindness in the UK.

It is also called chronic open angle glaucoma.

It causes SLOW damage to the optic nerve, causing gradual loss of vision.

The patient first loses the peripheral visual field then it progress to total blindness if left untreated.

.Symptoms :

1.Because the vision loss is gradual, usu. Bilateral and asymmetrical the patient usually present when severe damage has occurred & Its painless .

2.Most patients are detected by optometrist routine examination. Other sign is disck cupping .

3. Visual field defect : Gradual loss of peripheral vision, usually in both eyes, Tunnel vision in the

advanced stages

Risk group :

1.Affects 1 in 200 of population over the age of 40.

2.Males and females are equally affected.

3.There maybe family history but the exact mode of inheritance is not clear.

4.Myopic patient .

1.IOP

2.Visual field changes

3.Optic nerve damage (cupping)

Cupping takes place first then the visual field changes.

Visual field changes:

1) nasal step 2) arcuate scotoma

3)tuunle vision 4)blurring in central vision

C:D(cup:disk) ratio 0.4; visual acuity changes take place after cupping reaches 0.8 { normal is 0.0.-0.8)

Note: *visual acuity is

the least affected in

glaucoma. Don’t mix

between

v. field and v. acuity.

The optic disc marks the exit point of the retinal nerve fibers from the eye. With a sustained rise in IOP the nerve fibers atrophy, leaving the characteristic sign of chronic

glaucoma—the cupped, pale optic disc.

Aim of treatment is to decrease the IOP Amount of decrease depends on the level at

which no more damage to the optic nerve happens . This level differs from patient to other

Modalities :

1- Medical Treatment 2- Laser Treatment

3- Surgical Treatment

Topical eye drops five families:

1.Prostaglandins analogues Latanoprost (1st line of Rx)

2.B-blocker Timilol (2nd line of Rx) contraindicated in asthma .we can use bate 1 selective but with caution in asthmatic patient.

3.Carbonic anhydrase inhibitors Dorsolamide

4.Alpha 2 agonist

5.Cholinergic agonist

MOA :

1+4+5 > increase aqueous humor outflow .

2+3+4 > decrease aqueous secretion

Systemic (IV / oral)

1.CAI (Acetazolamide ) S/E: hypokalemia, metabolic acidosis, renal stones, nephritis,

parasthesia (m. common S/E)

2.Manitol {hyperosmotic} S/E: rebound increased IOP.

Adding additional medical treatment

Laser treatment

Surgical drainage procedures

1) Open angle glaucoma

2) Retintis pigmentosa : ( "classic triad" seen on fundoscopic exam of bony spicule pigmentation, vascular narrowing, and abnormal pallor of the optic disc)

-The condition occurs in small eyes (as in hyperopoia) with shallow anterior chambers.

-In the normal eye the point of contact between the pupil margin and the lens offers a resistance to aqueous fl ow from the posterior into the anterior chamber (relative

.(pupil block

Sometimes when the pupil is dilated, the lens sticks to the back of the iris causing obstruction of fluid flow from posterior to anterior chambers. Fluid will accumulate behind the iris and pushes it on to the Trabecular meshwork preventing drainage of aqueous from the eye. This causes rapid increase in IOP.

Hypermetropia : closed angle glaucoma

Myopia : open angle

Symptoms:

1) The eyes becomes red and

painful due to rapid increase

in IOP & ischemic

tissue damage.

2) Blurred vision; because

the cornea becomes edematous.

3.Patient may notice haloes (circles of light(rainbow)) around light due to dispersed light in waterlogged cornea.

4.Headache

5.Nausea and vomiting due to vagal

stimulation

6.Photophobia.

Red eye

Increase IOP .

mid dilated fixed ( reacted poorly to the light) pupil

shallow anterior chamber

Cloudy cornea

#Gonioscopy : Gonioscopy is the gold-standard

method of diagnosing angle closure ,This technique involves using a special lens for the slit lamp, which allows the ophthalmologist to visualizethe angle and diagnose angle closure

#Slit lamp grading of anterior chamber depth

#Ultrasound biomicroscopy

Urgent Treatment is necessary

All efforts to decrease IOP

For the acute attack

-IV/oral acetazolamide. If nausea and vomiting are not tolerated switch to manitol.

-Topical antiglaucoma Pilocarpine, B-blockers

For prevention of subsequent attacks:

Laser ( iridotomy )

Surgery (iridectomy )IS THE MAIN STEP IN TREATMENT .

Prophylactic to the fellow eye.