GLAUCOMA- THE BASICS

DR. MOSURO ADEDAMOLA LAMEEDCONSULTANT OPHTHALMOLOGIST

GENERAL HOSPITAL, LAGOS

Glaucoma

• The second most common cause of blindness worldwide

• The leading cause of irreversible blindness worldwide

• 70 million with the condition• 7 million bilaterally blind (6/60 or worse vision)

Definition of Glaucoma

• “Glaucoma is an optic neuropathy often, but not always, associated with elevated intra-ocular pressure, having characteristic optic nerve-head cupping and visual field loss on conventional perimetry.”

Epidemiology

Affected Blind

Developmental 300000 200000

Open angle 13.5M 3.0M

Angle closure 6.0M 2.0M

Total 5.2M

Glaucoma suspects 105M

Second leading cause of blindness Leading cause of irreversible blindness

Ocular Hypertension

• “A disorder characterized by a statistically elevated intra-ocular pressure”

• “≥ 21 mm Hg in patients with normal looking optic discs and normal findings using conventional perimetry.”

Glaucoma Suspect

• Includes those with “Ocular Hypertension”

• Suspicious, but no definite optic nerve damage (e.g., large C/D or asymmetry)

• Suspicious, but no definite visual field loss (e.g., suspicious Bjerrum scotomas)

• One or more major “Risk Factors”,– eg., race, age, documented family history

Primary Open Angle Glaucoma (POAG)

• A bilateral disease• Usually appears after age 40 years

• No symptoms until the disease reaches an advanced stage - thus, in the early and mid-stages it must be looked for by a doctor or nurse

• There is treatment but no cure (usually for the rest of a patient’s life)

Primary Open Angle Glaucoma (contd)

– A family of diseases– Have progressive optic neuropathy– Show as loss of optic nerve tissue and excavation

of the disc– Over time, defects of retinal sensitivity– Detected in decline of peripheral vision and

ultimate loss of central visual function– Open angles on gonioscopy

POAG Risk Factors (Classic and Strong)

• IOP• Family history - glaucoma in a sibling or

parent–must be a history of visual loss, not just

“glaucoma”– increases risk of glaucoma by 5—10X

• Self-management ability (compliance)– the most important single risk factor

• Race - African heritage (especially Afro-Caribbean)

POAG Risk Factors (Classic and Strong)

• Age - (causing a 2X prevalence of POAG in year 2020)

• Pseudoexfoliation• Pigment dispersion syndrome

• Age – Risk for OAG increases 4-5 times between ages 40-70– Prevalence is less than 0.1% below 30yrs but rises

above 10% or more in elderly• Race– Blacks 3-4 times more likely than whites to develop

glaucoma– Prevalence of glaucoma in persons of African descent

up to more than 4 times other world populations

• Family history– Previous family history imparts a 5 times risk of

developing glaucoma– 10-15% first degree relatives of POAG patients

likely to develop glaucoma– 40% risk in offspring of glaucoma patients– AD and AR modes of inheritance with incomplete

penetrance and environmental influences have been described

• Myopia – An association has been established– Possibly poor supporting structure for optic nerve

head in myopia• Diabetes mellitus– Higher prevalence of OAG among diabetics?– Small vessel damage in diabetes may make optic

nerve head susceptible to damage from IOP rise

• Cardiovascular disease (hyper/hypotension)– Microcirculatory changes in hypertension could make

optic nerve head susceptible to damage with longer duration of raised BP and vascular changes making damage poor likely

– Hypotension and reduced optic nerve head perfusion has effects on ON head (low perfusion pressure)

– Migraine, peripheral vascular disease, stroke and vasospasm with poor auto regulation to ON head may predispose to damage

Other Risk Factors

• Sedentary life style (aerobic exercise is good for glaucoma patients; it increases blood flow to the optic nerve)

• Smoking• Obesity• Diet?

Combination of Risk Factors

• Risk factors are additive• The appearance of a new risk factor in a patient with stable glaucoma is suggested by the loss of IOP control or a change in the optic disc or visual field after a long period of stability

• Examples: atrial fibrillation, nocturnal hypotension, anemia

Risk Factors for Those With African Heritage

• Much greater chance - – to have glaucoma– to have greater damage at presentation– for medications not to work as well– to have trabeculectomy not work as long

– to progress while receiving therapy– not to be offered filtration surgery– to have routine surgery fail– to be blinded by the disease

Clinical features- Presentation

• Early – Usually asymptomatic– Incidental finding

• Late– Poor vision– Bumping into objects– Heaviness in the eyes– Frequent change of

reading glasses

Clinical Signs

• Visual acuity is reduced but may be normal• Pupillary reaction: normal, RAPD, amaurotic• Disc– Abnormal cupping– Asymmetry ≥ 0.2 – Disc hemorrhage– Notching /thinning of neuro-retinal rim

• IOP is normal or raised• Open angles on gonioscopy• Visual field changes- characteristic

Medical Treatment

• Reduce aqueous humor production– β-adrenergic blockers

• Non-selective: timolol, levobunolol 0.5% (betagan), metipranolol 0.3%, cateolol hydrochloride 1.0%

• β 1- selective with less tendency for lung or CV problems: betaxolol 0.5% (betoptic)

– Adrenergic agonists (cause vasoconstriction of ciliary blood vessels thus reducing ultrafiltration) • Non-selective: epinephrine, dipivefrin• α selective: apraclonidine (iopidine)- also reduces episcleral

venous pressure; brimonidine (alphagan) increases uveoscleral outflow

Medical Treatment (contd)

• Reduce aqueous humor production– Carbonic anhydrase inhibitors (inhibit conversion

of carbondioxide to bicarbonate)• Oral or IV: acetazolamide (diamox), dichlorphenamide,

methazolamide• Topical: dorzolamide 2% (trusopt), brinzolamide 1%

Medical Treatment (contd)

• Increase outflow through trabecular meshwork– Adrenergic agonists:- mediated by α and β

stimulation– Cholinergic agonists:- open up trabecular

meshwork by causing contraction of longitudinal muscles• Direct acting: acetylcholine (miochol)• Cholinesterase inhibitors: echothiopate (phospholine

iodide), physostigmine (eserine)

Medical Treatment (contd)

• Increase uveoscleral outflow– Hypotensive lipids• Prostaglandin analogues: latanoprost 0.005%,

travoprost 0.004%• Prostamide: bimatoprost 0.03%• Decasanoid : unoprostone isopropyl 0.15%

– Hyperosmotic agents: increase blood osmolality• Oral: glycerol, lsosorbide• IV: 20% mannitol, urea

Medical Treatment (contd)

• Neuroprotection – Prevent glutamate excitotoxicity: memantine– Inhibition of apoptosis: caspase inhibitors– Calcium homeostasis: calcium channel blockers-

betaxolol, brimonidine (possible effects on blood vessel stability or preventing vasoconstriction)

Surgical Treatment

– Primary surgical treatment gives better long term results

– Better ways of handling conjunctiva and use of releasable sutures give better results

– Use of antimetabolites (5FU, MMC, β-irradiation) have also improved outcome

– Previous medical treatment with adrenaline and pilocarpine reduce the prognosis for successful medical treatment

Surgical Treatment (contd)

• Trabeculectomy– Most common– Creates alternative drainage channel (fistula)

• Laser trabeculoplasty• Destruction of the ciliary body– Cyclocryotherapy– Cyclodiode treatment

• Shunts

Primary Angle Closure Glaucoma (PACG)

• May be more common than POAG, prevalence vary widely in different populations

• Main form of glaucoma in Mongolian races (Mongols, Eskimos, Mainland China, Vietnamese, 80-90% of glaucoma in Myanmar

• Has been recognized in various parts of Africa (Somalia, Nigerians, south Africa)

• Need for gonioscopy in all patients

Risk factors

• Age– Angle get more narrow with age and PAS increases– Steep and plateau iris profile increases with age– Rate of PAS increases as angle narrows– PAS is more common in eyes with steep iris

• Race – More common in Inuit and Asians– Acute forms seem to be more in whites while

blacks present with the chronic asymptomatic form

Risk Factors (contd)

• Gender – More common in females– Females may have smaller anterior segments and axial

lengths than men• Refractive error

– May be more common in hyperopes– May just be an indication of anterior segment dimensions

• Family history– First degree relatives at greater risk– Smaller dimensions of anterior segment may be inherited

Mechanism of angle closure

• Relative pupil block– Maximum in mid-dilated position– Iris hugs the lens over a greater surface area and

impedes the flow of aqueous from posterior to anterior chamber

• Peripheral iris crowding– Bulky peripheral roll– Plateau iris– Anteriorly rotated ciliary body

Clinical features

• Acute PAC– Sudden onset– Severe ocular pain– Headache– Blurred vision– Haloes around light– Nausea– Vomitting

• Chronic – Assymptomatic– Similar to POAG– Differentiated by

gonioscopy

Treatment

• Acute attack: reduce IOP immediately– Topical anti-glaucoma medications: topical beta

blockers and alpha-2 adrenergic blockers. Pilocarpine

– Acetazolamide– Osmotic agents

Treatment (contd)

• Surgical treatment:- mainstay– Surgical iridectomy– Argon or YAG laser iridectomy– Trabeculectomy • Chronic phase• Trabecular damage from previous acute or sub-acute

attacks

– Prophylactic iridotomy/iridectomy

Congenital Glaucoma

• Primary congenital– Accounts for 50-70% of congenital glaucomas– Incidence vary from 1:2000- 1:20,000– Usually present at age of 6/12– 75% bilateral involvement– Majority are sporadic with sibling risk of less than 2%– 10% are hereditary with AR mode of inheritance– Immature drainage angle development-

trabeculodysgenesis

Congenital Glaucoma Types

• Glaucoma associated with anterior segment dysgenesis– Axenfield Rieger syndrome– Peter’s anomaly– Aniridia

• Aphakic glaucoma• Sturge-Weber syndrome• Uveitic glaucoma

Presentation

• Symptoms– Watery eyes– Blepharospasm– Photophobia– Eye rubbing – Reduced vision and

nystagmus

• Signs– Reduced VA– Bupthalmos– Corneal edema– Haab’s striae– Asymmetric eye size– Rapidly increasing

myopia– Strabismus

Assessment

• History• General exam and examination of parents and

siblings• Orthoptic assessment• USS for biometry and posterior sement anomalies• EUA– IOP– Horizontal corneal diameter– Optic disc assessment

Treatment

• Medical– Usually temporising

• Surgical– Goniotomy– Trabeculotomy– Trabeculectomy– Tube drainage?– Transcleral cyclophotocoagulation

Others

• Secondary glaucomas• Traumatic glaucomas• Irido-corneal syndromes• Epithelial in-growth• Pseudoexfoliation syndrome• Pigment dispersion• Post surgical (aphakic or psuedophakic)• Glaucomas resulting from Complicated cataracts