1. GLAUCOMA- THE BASICS DR. MOSURO ADEDAMOLA LAMEED
CONSULTANT OPHTHALMOLOGIST
GENERAL HOSPITAL, LAGOS

2. 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)

3. 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.”

6. Epidemiology Affected Blind Developmental 300000 200000 Open angle
Angle closure
6.0M
2.0M
Total
5.2M
Glaucoma suspects
105M
Second leading cause of blindness
Leading cause of irreversible blindness

7. 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.”

8. 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

10. 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)

11. 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

12. 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)

13. POAG Risk Factors (Classic and Strong)
Age - (causing a 2X prevalence of POAG in year 2020)
Pseudoexfoliation
Pigment dispersion syndrome

14. Age Race 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

15. 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

16. Myopia Diabetes mellitus 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

17. 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

18. Other Risk Factors
Sedentary life style (aerobic exercise is good for glaucoma patients; it increases blood flow to the optic nerve)
Smoking
Obesity
Diet?

19. 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

20. 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

21. Clinical features- Presentation
Early
Usually asymptomatic
Incidental finding
Late
Poor vision
Bumping into objects
Heaviness in the eyes
Frequent change of reading glasses

22. 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

25. 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

26. 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%

27. 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)

28. 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

29. 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)

30. 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

31. Surgical Treatment (contd)
Trabeculectomy
Most common
Creates alternative drainage channel (fistula)
Laser trabeculoplasty
Destruction of the ciliary body
Cyclocryotherapy
Cyclodiode treatment
Shunts

32. 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

35. Risk factors Age Race 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

36. Risk Factors (contd) Gender Refractive error Family history
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

37. 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

38. Clinical features Acute PAC Chronic Sudden onset Severe ocular pain
Headache
Blurred vision
Haloes around light
Nausea
Vomitting
Chronic
Assymptomatic
Similar to POAG
Differentiated by gonioscopy

39. Treatment Acute attack: reduce IOP immediately
Topical anti-glaucoma medications: topical beta blockers and alpha-2 adrenergic blockers. Pilocarpine
Acetazolamide
Osmotic agents

40. 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

41. Congenital Glaucoma Primary congenital
Accounts for 50-70% of congenital glaucomas
Incidence vary from 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

44. Congenital Glaucoma Types
Glaucoma associated with anterior segment dysgenesis
Axenfield Rieger syndrome
Peter’s anomaly
Aniridia
Aphakic glaucoma
Sturge-Weber syndrome
Uveitic glaucoma

45. Presentation Symptoms Signs 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

46. 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

47. Treatment Medical Surgical Usually temporising Goniotomy Trabeculotomy
Trabeculectomy
Tube drainage?
Transcleral cyclophotocoagulation

48. 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