By: noor majeed rehani

Definition: It is a heterogenous group of 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.range (11-21)

Definition Its optic neuropathy and visual field defect with or

without increase intraocular pressure .

So glaucoma doesn't always equal increase IOP

Basic physiology of aqueous humour:

1. Conventional pathway

2. Uveo-scleral pathway

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

•Aqueous humour is secreted by the ciliary processes in the

posterior chamber. Then it passes through the pupil into the

anterior chamber.

•It is drained in posterior chamber through the Trabecular

meshwork, Schlemm’s canal, and episcleral veins.

1. Conventional Pathway:

Supra-choroidal space

choroid

•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.

2. Uveo-scleral pathway

Mechanism of Optic nerve fiber damage Mechanical damage To optic nerve axons by the raised

IOP

Ischemia of nerve fibers caused by impaired perfusion pressure (reducing blood flow at optic nerve head)

Risk factors of glaucoma Over age 60

family member with glaucoma

Are nearsighted

diabetes, high blood pressure, heart disease or hypothyroidism

injury to the eye, certain eye surgeries or chronic eye inflammation

steroids for long periods of time

Asian-American descent – this puts you at increased risk for angle-closure glaucoma

Classification of Glaucoma: 1. Primary glaucoma:

1. Chronic open angle

2. Acute and chronic closed angle

2. Congenital glaucoma: 1. Primary

2. Rubella

3. Seconday to other inherited ocular disorders (e.g. an-iridia; absense of iris)

3. Secondary glaucoma (causes): 1. trauma

2. Ocular surgery

3. Associated with other ocular diseases (uveitis) by { hypopyon , posterior synechea , steriod tt }

4. Raised episcleral venous pressure

5. Steroid induced

Primary Glaucoma: Is the iris:

Covering the Trabecular meshwork

NOT covering the Trabecular meshwork

OPEN angle glaucoma CLOSED angle glaucoma

Primary OPEN angle glaucoma Pathogenesis:

Resistance of drainage of aqueous through the Trabecular meshwok, due to:

1. Thickening of Trabecular lamellae (reduces pore size).

2. Reduction in number of lining Trabecular cells.

3. Increased extracellular material in the Trabecular meshwork spaces.

Open irido-corneal angle (Trabecular meshwork is not covered)

Primary OPEN angle glaucoma:

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.

As fluids accumulates in the anterior chamber due to

decreased drainage, intra-ocular pressure increases and

cases damage to the optic nerve.

Primary OPEN angle glaucoma 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 dick cupping .

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

Risk groups:

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 .

POAG criteria: (you need 2 out of 3) 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) tunnel vision

4) blurring in central vision.

C:D(cup:disk) ratio 0.4; visual acuity changes take place after cupping reaches 0.9 { normal is 0.0.-0.9)

Note: *if IOP reaches 30 mmHg then its enough to diagnose POAG. If IOP

<30 with no v. field changes or optic nerve damage its considered ocular hypertension.

*visual acuity is the least affected in glaucoma. Don’t mix between v. field and v. acuity.

Optic disc cupping 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.

Normal disc diameter is 1.5

High C:D ratio with smaller disc is more likely to be glaucoma than high C:D ratio with large disc , because the large disc permits higher number of neuron to pass through and achieve good vision .

Rapid progression of C:D ratio even is small increase / time is more significant that higher but steady C:D ratio.

Normal tension glaucoma: Some (dr said 60%)open angle glaucoma have

normal intra-ocular pressure called low-tension or normal-tension glaucoma.(glucomatous change)

In these cases, there will be damage to the optic nerve even though the intra-ocular pressure is within normal range.

The eyes of the normal tension glaucoma have normal angles, so its features are similar to that of primary open angle glaucoma.

The causes of normal tension glaucoma is still unknown. The optic nerve is susceptible to damage even from normal IOP.

Normal-tension glaucoma is thought to be related, at least in part, to poor blood flow to the optic nerve.

Normal tension glaucoma (cont.): Risk factors:

1. Family history of glaucoma.

2. Cardiovascular diseases (migraine , raynaud’s phenomena )

3. F>M (dr said that )

Treatment:

1. Even though the IOP is normal but medication to decrease IOP as much as possible are used.

TESTS FOR SCREENING AND DIAGNOSIS: Exclude other systemic diseases. 1. Tonometer IOP (20 – 44 mmHg) Parameters for referral :

IOP > 40 mm Hg: Emergency referral IOP 30 to 40 mm Hg: Urgent referral (within 24 hours) if no symptoms suggesting

acute glaucoma IOP 25 to 29 mm Hg: Evaluation within one week IOP 23-24 warrants repeat measurement to confirm and/or referral for

comprehensive eye examination 5. Visual field testing (perimetry) scotomata Optic disk measure vertical ratio (cup to disk) 0.4 (0-0.8) 2. Gonioscopy iridocorneal angle to see if its open or closed , not seen

in slit lamp . 3. Pachymetry corneal thickness , normal corneal thickness is 54o

Micrometer , The lower the thickness the higher risk for glaucoma . When corneal thickness is low u overestimate the IOP and vise versa .

4. Fundus examination : cupping , splinter hemorrhage of nerve fiber

Management:

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

Medical 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 .

3. Carbonic anhydrase inhibitors Dorsolamide

4. Alpha 2 agonist Brimonidine.

5. Cholinergic agonist Pilocarpine

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.

MOA :

1+4+5 > increase aqueous humor outflow .

2+3+4 > decrease aqueous secretion .

If IOP remains elevated the choice lies between:

Adding additional medical treatment

Laser treatment

Surgical drainage procedures

Laser treatment

laser burns in the trabecular meshwork to improve

aqueous flow

Laser trabeculoplasty indications:

1.Failed medical therapy.

2. Avoidance of polypharmacy

3. Avoidance of surgery in elderly

4. As primary therapy in patients who are expected not to

comply with medical treatment

Surgery

Drainage surgery ( Trabeculectomy ) by creating a fistula between

the anterior chamber and the subconjunctival space

1. Conjenctival incision.

2. Sclerostomy.

3. Iridectomy.

Ahmed valve implant: The device works by bypassing the trabecular meshwork and redirecting the outflow of aqueous humour through a small tube into an outlet chamber or bleb. The IOP generally decreases from around 33 to 10 mmHg by removing aqueous on average 2.75 microliters/min

Ddx of tunnel vision Open angle glaucoma

Retintis pigmentosa

Acute angle closure glaucoma: The condition occurs in small eyes (as in hyperopoia)

with shallow anterior chambers.

Normally there is some resistance between the pupil margin when its in the mid-dilated stage and the lens this resistance disturb the drainage of aqueous humor so increase IOP .

But sometimes….

Acute angle closure glaucoma (cont.):

Sometimes when the iris 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.

Risk factors

1. Hypermetropia : small eye, big lens

2. Age 55 – 70 yrs

3. Female ( have smaller anterior chamber)

4. Common in asians

5. Family history of glaucoma

6. Mature cataracts

7. Shallow anterior chamber

8. Pupil dilation ( topical and systemic

anticholinergics, stress, darkness)

Types of angle-closure glaucoma: Primary angle closure — Patients are anatomically predisposed to

this type of glaucoma; there is no identifiable secondary cause.

Secondary angle closure — A secondary process is responsible for narrowing or closure of the anterior chamber angle. Same causes of synecia uvietis , NVD. (at first lead to 2ry open then progresses to 2ry closed).

Examples of secondary causes are a fibrovascular membrane that grows over the angle to pull it closed, as in neovascular glaucoma, or a mass or hemorrhage in the posterior segment of the eyeball that pushes the angle closed

Acute angle closure glaucoma Symptoms:

1. The eyes becomes red and painful due to rapid increase in IOP & ischemic tissue damage .

Acute angle closure glaucoma

2. Blurred vision; because the cornea becomes edematous.

Acute angle closure glaucoma 3. Patient may notice haloes (circles of light)

around light due to dispersed light in waterlogged cornea.

4. Headache (unilateral)

5. Nausea and vomiting due to vagal stimulation .

6. Photophobia.

DDX : Migraine

Sings Red eye

Increase IOP .

mid dilated fixed ( reacted poorly to the light) pupil

shallow anterior chamber

Cloudy cornea

Acute angle closure glaucoma They may have similar

symptoms in the past that are aborted by going to sleep, because sleeping constricts the pupils pulling it from the lens.

Most common mechanism by which glaucoma happens is when susceptible patient awakes from sleep and gets exposed to faint light.

Diagnostic tests 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 visualize

the angle and diagnose angle closure

Slit lamp grading of anterior chamber depth — In this technique, the

width of the angle is estimated by shining a light beam from the slit

lamp on the peripheral anterior chamber. It is not as reliable as

gonioscopy for diagnosing angle closure.

Ultrasound biomicroscopy — Specialized ultrasound of the anterior

chamber can show angle closure and help to define the mechanism.

The ultrasound biomicroscope instrument is costly and thus not

widely available. This technique also requires specialized

interpretation of the results.

Management 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. Incase of occludable angle or 2ry closed angle glaucoma perform trabeculectomy or

Ahmed valve implant.

Note: acetazolamide + B-blocker reduce aqueous secretion pilocarpine constricts the pupil and draws the peripheral iris out of the angle

This is an elargement of an optic nerve with glaucoma .

ENLARGED OPTIC NERVE

Notice the large cupping or large white area within the nerve

The red vessel located at about 11 o'clock should not be there. This is called a

Drance Hemorrhage and shows up in glaucoma .

Risk factors Hypermetropia : closed angle glaucoma

Myopia : open angle

By definition, primary congenital glaucoma is present at birth; however, its manifestations may not be recognized until infancy or early childhood.

It is characterized by improper development of the eye's

aqueous outflow system, leading to increased intraocular pressure (IOP), with consequent damage to ocular structures, resulting in loss of vision..

Early recognition and appropriate therapy of the glaucoma can significantly improve the child's visual future.

This type of glaucoma is due to the abnormal development of the anterior chamber angle before birth.

This causes a decrease in aqueous outflow through the trabecular meshwork.

Congenital glaucoma may be found in association with congenital cataract extraction, inflammation, injury, or in conjunction with other syndromes or diseases.

History : This 15-day-old infant was presented with a history of having cloudy corneas

since birth. The child is fussy and her eyes watery. Two older siblings are normal and

there is no family history of a similar eye condition. Intraocular pressure is 50 in each eye

and the corneal diameters are 12.5 mm in each eye

Diagnosis : congenital glaucoma

Symptoms

Tearing

Light sensitivity

Bupthalmus due to epithelial oedema.(increase corneal diameter ).

Cloudy cornea.

Spilts in descement’s membrane ( habbs stria = horizontal stretch marks )

Treatment

Usually surgical :1. Goniotomy (surgical incision into the trabecular meshwork to increase aqueous drainage OR

2.Trabeculectomy

Medical and laser treatment may be needed later

.

Secondary Glaucoma (intro) Much rarer than Primary Glaucoma

S&S depend on rate at which IOP ↑

Mostly symptomless..

Tx : most of underlying cause are not treatable if they are treatable treat them first --Difficult cases : removal of ciliary processes ↓ aqueous production.. by laser / cryoprobe to d’ sclera overlying d’ processes

--Endoscopic techniques ?

Blood. (Hyphema) this block the trabecular meshwork and increased IOP

Following blunt trauma

This hyphema has almost completely layered while the patient's head was tilted. Note the hazy greenish area at 6 o'clock in contrast to the remainder of the blue iris. This represents blood circulating in the anterior chamber that has not yet layered

Inflammatory cells(Uveitis), block the meshwork .

Uveitis. Left: This African American patient has severe uveitis from

sarcoidosis. The episcleral vessels are dilated, the corneal endothelium is covered with inflammatory precipitates, and the iris is indistinct due to the anterior chamber cellular reaction. There is a mixed hypopyon (layered white blood cells) and hyphema (hemorrhage) within the inferior anterior chamber. The pupil has scarred in places to the lens by posterior synechiae, which causes the irregular appearance of the pupil. Right: This man with spondyloarthritis presented with bloody diarrhea and a red painful eye. He was diagnosed with ulcerative colitis complicated by spondyloarthropathy and uveitis. Note the ciliary flush.

Pigment from the iris (Pigment despersion syndrom)

Glaucoma may develop as a result of the breakdown and flaking off of the coloring (pigment) found in the iris and the part of the eye that produces fluid (ciliary body). These flakes of pigment block the fluid drainage system of the eye. This type of secondary glaucoma is called pigmentary glaucoma

Pseudoexfoliative glaucoma

Another type of common secondary glaucoma can occur when a different type of flaky material is produced in the eye. The origin of this white, flaky material is not clearly known but it can block the fluid drainage system of the eye. This type of secondary glaucoma is called pseudoexfoliation glaucoma or exfoliation syndrome.

Diagnosis of PXFG is made by identifying the abnormal material, which looks a bit like dandruff flakes, on the iris or lens. It is important to have the pupils dilated, as the material may be missed otherwise. Visualizing the material can be difficult, particularly early on in the disease, and it may not be found until years after the diagnosis of glaucoma is made. The presence of pseudoexfoliation, and the associated risk of glaucoma, increases with age.

Secondary glaucoma can develop as a complication of a disease, such as diabetes.

Diabetes can cause new blood vessels to grow into the drainage angle of the eye (trabecular meshwork) and create scarring.

This scarring can limit drainage of the fluid (aqueous humor) out of the eye.

This blood vessel problem is called neovascular glaucoma

Angle closure – for some cases

Rubeosis iridis

--(Abnormal iris blood vessel may obstruct the angle cause the iris to adhere to periph. Cornea closing the angle

Large choroidal melanoma

push iris forward acute attack of angle closure glaucoma

Cataract : may swell, push iris forward & closing the drainage angle

Drugs

Certain medications (corticosteroids) may cause secondary glaucoma when they are used to treat eye inflammation and other diseases. They unintentionally cause a rise in pressure within the eye

secondary glaucoma treated as other types since most of the underlying causes are NOT treatable