Glaucoma

Dr. Matyas T
 Introduction to Glaucoma
Terminology, Epidemiology

Definitions:
• OLD VIEWS-Glaucoma was widely known as
the disease related to the rise in intraocular
pressure(IOP) >21mmhg
• Glaucoma: A group of disease that have in
common a characteristic optic neuropathy
with associated visual field loss for which
elevated IOP is one of primary risk factors.
• Glaucoma is the second leading cause of
blindness worldwide
• Around 50% of patients do not know that they
have the disease, because of which it is called

– “The silent Blinder” or “The Sneak Thief of Sight”

 Pathogenesis of glacomatous damage

Glaucomateous optic neuropathy:means death

of the neurons of the retina and optic nerve
• Mechanical theory:
– direct compression of axonal fibers with distribution of
lamina cribosa plates
– interuption of axoplasmic flow => death of RGCs.

• Ischemic theory:
– decrease optic nerve perfusion=> intraneural ischemia
 Clinical evaluation

History and general examination

• Pain
• Redness
• Alteration or loss of vision
• Alteration of visual field
• Family history of glaucoma
• History of DM, trauma
• Past surgical history
• Medication history
 Clinical evaluation
Physical examination
• Visual acuity: The VA of glaucoma patient ranges from
normal to NLP in advanced or terminal disease.
– A normal VA does not rule out glaucoma
• Tonometry:
– The normal IOP ranges from 10-22 mmhg
• but normal tension range does not always rule out glaucoma
• Conversely, high measurement of IOP (greater than 22) does not
always tell a glaucoma (especially when IOP is less than 30)
– All eyes do not respond the same to given pressure level
• The factors that determine the IOP level are:
1. Rate of aqueous humor production by ciliary
body
2. Resistance to aqueous outflow across the
Trabecular meshwork-Schlemm’s canal system
3. The level of episcleral venous pressure
 IOP measurement / Tonometry

Goldmann applanation tonometer: Gold standard

 Tonometers

Goldmann Perkins Schiotz

Contact applanation Portable contact applanation Contact indentation

Air-puff Pulsair 2000 (Keeler) Tono-Pen

Non-contact indentation Portable non-contact applanation portable contact applanation
 Clinical evaluation
• Slit lamp microscopy
 Ciliary injection in AACG
 Cornea could be steamy (cloudy) in AACG
 Anterior chamber reaction
 Anterior chamber could be shallow in AACG
 Pupil could be dilated and fixed
 Clinical evaluation
• The optic nerve:
• Examined with slit lamp combined with 60,78 or 90
D lens
• Normal disc
– neural rim : ISN’T rule
– color : orange to pink
– vertical C:D : 0.1-0.4
 Clinical evaluation

• GLAUCOMA: OPTIC NERVE HEAD

CHANGES
– Increased size of the cup
– Thinning of disc rim
– Progressive loss of neural rim tissue
– Disc hemorrhages
 OPTIC NEUROPATHY
.
Effect of glaucoma on visual field
SHRINKING OF VISUAL FIELD.
 Classification of glaucoma

Based on the angle

1. Open angle glaucoma
2. Angle closure glaucoma
Differentiation of open-angle form closed-angle glaucoma is
essential from a therapeutic stand point.
Based on the cause
1.primary
2. secondary
• The primary glaucomas are not associated with known ocular or systemic
disorders that cause increased resistance to aqueous outflow.
– usually affect both eyes and may be inherited.
– Primary open angle glaucoma
– Primary angle closure glaucoma
• Secondary glaucomas are associated with ocular or systemic disorders
responsible for decreased aqueous outflow.
– often unilateral, and familial occurrence is less common.
– Secondary open angle glaucoma
– Secondary angle closure glaucoma
 Open-angle glaucoma

• Primary open angle glaucoma(POAG):Clinical feature:-

– insidous onset
– slow progression
– painless
– bilateral, can be asymmetrical
– IOP >22 mmHg.
– glaucomatous optic neuropathy
– visual field loss
– gonioscopy: open angle
• Risk factors for POAG:
– age
– race : black > white
• Blindness = 3-4 times more common
• Age > 70 = 10% prevalence (2% for whites > 70)
• POAG occurs at earlier age
• POAG more advanced when discovered
– family history
– controversy: myopia, DM, cardiovascular disease
CRVO
 Secondary open-angle glaucoma:

• Pseudoexfoliative glaucoma
– deposition of a distinctive fibrillar material in anterior segment
• Lens-induced glaucoma
• Uveitic glaucoma secondary to ocular inflammation
• Accidental and surgical trauma:
– Hyphema
– Retained viscoelastic substance after cataract surgery
• Steroid induced glaucoma
 Angle-closure glaucoma
• Risk factor:
1. race : East Asians
2. ocular biometrics : -shallow anterior chamber
-thick lens
- short axial length
3. age
4. gender: women 2-4 times common than men
5. family history
6. hyperopic
 Angle-closure glaucoma
• 5

Acute primary angle closure glaucoma:

-symptoms:-Redness, ocular pain, headache, decrease vision,
nausea and vomiting
- sign: - high IOP
- mid dilated, sluggish and often irregular pupil
- corneal epithelial edema
- congested episcleral and conjunctival blood vessels
- shallow anterior chamber

- Diagnosis: gonioscopy closed angle

Acute angle closure glaucoma
Chronic angle closure glaucoma:
• major cause of blindness in Asia
• mechanism: creeping angle closure ( slow formation of PAS )
– PAS: peripheral anterior synechiea is an adhesion between
peripheral part of the cornea with the iris causing closure of the
angle structure
• Sign
– permanent PAS
– rise IOP
– progressive cupping
– loss of visual field
Secondary angle closure glaucoma
• Lens induced angle closure
– Phacomorphic glaucoma
– Ectopia lentis
• Neovascular glaucoma:
– most common causes: DM, CRVO
– neo-vascularization of iris and TM. => PAS
Secondary angle closure glaucoma
• Inflammation - formation of posterior synechiae
and peripheral anterior synechiae
• Trauma- peripheral anterior synechiae
• Drug induced secondary angle closure
glaucoma:
– antiepileptic, antidepressant
Phacomorphic glaucoma
General Management of Glaucoma
Glaucoma is a progressive disease, & any visual loss
is permanent.

Early diagnosis and early treatment are therefore

essential to prevent permanent blindness!
The goal of currently available glaucoma therapy is
to preserve visual function by lowering IOP below a
level that is unlikely to produce further damage to
the nerve.
Lifelong follow up!
 Management of Glaucoma
• Medical Management
• Surgical management
 Medical Management
• Ocular hypotensive agents are divided into several groups
based on chemical structure and pharmacologic action.
1) Prostaglandin analogs
2) β-adrenergic antagonists(nonselective and selective)
3) Adrenergic agonists (nonselective and selective α2–
agonists)
4) Parasympathomimetic (miotic) agents, including
cholinergic and anticholinesterase agents
5) Carbonic anhydrase inhibitors( oral and topical)
6) Hyperosmotic agents
7) Combination medication
 Medical Agents
• Prostaglandin analogs
– E.g . Latanoprost(Xalatan) 0.005% once perday at
night
• Mechanism of Action: Increase uveoscleral outflow
• Decrease IOP by 25% - 32%
 Medical Agents
• β-adrenergic antagonists( beta-blockers)
– Mechanism of action: Decrease aqueous production
– Nonselective
• Timolol 0.5% bid Decrease IOP by 20%-30%
– Selective
• Betaxolol 0.25% bid Decrease IOP by 15-20%
 Medical Agents
• Carbonic anhydrase inhibitors
– Mechanism of action decrease aqueous production
– Oral: Acetazolamide( Diamox) bid to qid =>
– Topical: IOP by 15%-20%
• Dorzolamide 2% bid, tid
• Brinzolamide 1% bid, tid
 Medical Agents
• Hyperosmotic agents
– Mechanism of action: osmotic gradient dehydrates the vitreous
e.g., Manitol ( IV), Glycerin( oral)
– Useful in acute increased IOP
 Medical Agents
• Fixed combinations  IOP by 25-30%
– Timolol/Dorzolamide (cosopt)
– Tomolol/Latanoprost
– Timolol/Travoprost
– Timolol/Bimatoprost
– Timolol/Brimonidine
 Surgical Therapy
• Usually undertaken when medical therapy is not appropriate,
not tolerated, not effective, or not properly utilized by a
particular patient, & the glaucoma remains uncontrolled with
either documented progressive damage or a very high risk of
further damage.
• Surgery is the primary approach for both congenital glaucoma
and pupillary block glaucoma.
• In patients with POAG , surgery is considered when medical
therapy is failed.
 Surgical Therapy
• Surgery for OAG
– Laser Trabeculoplasty
– Trabeculectomy
• Surgery for ACG
– Laser Iridectomy
– Surgical iridectomy
• Other procedures to lower IOP
– Aqueous shunt Implantation
– Ciliary Body Ablation Procedures
• Surgery for congenital glaucoma
– Goniotomy
– Trabeculotomy
Trabeculectomy
 Childhood glaucoma

• Classified
– Primary congenital/infantile glaucoma
– Glaucoma associated with congenital anomalies
– Secondary glaucoma. E.g Seconadary to
retinoblastoma
• Asymptomatic in early stages
• Can result in total optic nerve atrophy and
blindness
 Congenital glaucoma
• Symptoms (Triad)
– Tearing
– Photophobia (Painful oversensitivity to light)
– Blepharospasm (Involuntary protective closing of the
eyelids)
• Sign
– High IOP
– Large cornea that could be cloudy
– Enlarged globe
– Optic nerve cupping
• Diagnosis
– Examination under anesthesia
 Clinical features Congenital glaucoma

• Parents may notice enlargement of the eye

and may initially consider the large eyes an
attractive feature rather than a warning sign
of glaucoma
• If an infant or a young child shows any of
these symptoms, parents or caregivers should
seek medical care as soon as possible from an
ophthalmologist because they might be signs
of glaucoma.
 Management of congenital glaucoma

• Medical treatment to lower IOP is a temporary measure till the

child is ready for surgery
• Surgery to open the drainage of aqueous humor or by pass
surgeries are definitive treatment for glaucoma
• After glaucoma surgery, long-term follow up is essential, to
make sure the intraocular pressure is controlled and vision is
developing as normally as possible
Thank you