The document covers glaucoma, detailing its anatomy, physiology, types, pathogenesis, symptoms, diagnosis, and treatment. It explains various classifications, including congenital glaucoma, primary open angle glaucoma, and angle-closure glaucoma, highlighting their etiologies and clinical presentations. Treatment options range from medical therapies to surgical interventions depending on the specific type and severity of glaucoma.

1. GLAUCOMA
NTHEMBE C MWANZA
BSc Human Biology
Lusaka Apex Medical University
6th year

2. OUT LINE
• Relevant anatomy and Physiology
• Definition
• Pathogensis
• Classification
• Congenital glaucoma
• Primary glaucoma
• POAG
• PACG
• Secondary glaucoma
• Other types of Glaucoma

3. ANTOMY AND PHYSIOLOGY
• Pathophysiology of glaucoma revolves around the aqueous humor
dynamics.
The principal ocular structures concerned with it are
1. The pars plicata part of the ciliary body,
2. The angle of anterior chamber
3. The aqueous outflow system

4. 1. Ciliary Body
It is the main site of aqueous production
Ciliary body has two parts namely:
a) Pars plicata—The anterior one-third of ciliary body (about 2 mm) is
known as pars plicata. The ciliary processes are attached to this
part. Pars plicata part of the ciliary body secretes aqueous humor.
b) Pars plana—The posterior two-third of ciliary body (about 4 mm) is
known as pars plana. It is relatively avascular therefore posterior
segment of the eye is entered through the pars plana incision 3-5
mm behind the limbus.

5. 2. Angle of Anterior Chamber
• It plays an important role in the process of aqueous drainage. It is
formed by the root of iris, anterior
• most part of the ciliary body, scleral spur, trabecular meshwork and
Schwalbe’s line (prominent end
• of Descemet’s membrane of cornea)

6. 3. Aqueous Outflow System
It includes the trabecular meshwork, canal of Schlemm, aqueous veins and the episcleral veins.
• 1. Trabecular meshwork—It is a sieve-like structure through which aqueous humor gets filtered
• into the canal of Schlemm.
• 2. Canal of Schlemm—This is an endothelial lined oval channel present circumferentially in the
• scleral sulcus.
• 3. Aqueous veins—These are about 25-35 in number. They leave the canal of Schlemm at oblique
• angles to terminate into episcleral veins.
• 4. Episcleral veins—These are branches of anterior ciliary veins. There is pressure difference of
• about 5 mm Hg between the anterior chamber and the episcleral veins so that the aqueous drains
• continuously in them.

7. Mechanism of aqueous formation, flow and
outflow pathways in the normal eye

8. DEFINATION
Glaucoma is a chronic, progressive optic neuropathy caused by a group
of ocular conditions which lead to damage of optic nerve with loss of
visual function. The most common risk factor known is raised
intraocular pressure.
• Normal intraocular pressure = 10–20 mm Hg (Schiotz)
• Suspicious case = 20–25 mm Hg (Schiotz)
• Glaucoma = Above 25 mm Hg (Schiotz)
• Hypotony = Below 10 mm Hg (Schiotz

9. Etiology
Etiology
• The most important factor which causes rise of intraocular pressure is
obstruction to the drainage
• of the aqueous humor through the:
• i. Angle of the anterior chamber
• ii. At the pupil.

10. Pathogenesis
The glaucomatous damage is attributed to a combination of factors
which affect perfusion of optic nerve head.
1. Mechanical changes—The coats of the eye can withstand raised
intraocular pressure except at the lamina cribrosa which is pushed
backwards. This squeezes the nerve fibres within its meshes to disturb
the axoplasmic flow.
2. Vascular factors—The perfusion of optic nerve head may be affected
due to decreased blood flow in the capillaries and in annulus of Zinn
which supply nutrition to the laminar and postlaminar optic nerve
head.

11. Classification of Glaucoma

12. CONGENITAL OR INFANTILE GLAUCOMA
(BUPHTHALMOS, HYDROPHTHALMOS)
It is defined as glaucoma appearing between birth and the age of 3-4
years.
There is raised intraoculartension present since birth. When the
glaucoma presents at puberty, it is known as Juvenile glaucoma.

13. Etiology
It is usually of a simple obstructive type due to congenital abnormality
at the angle of anterior chamber. It is transmitted as an autosomal
recessive trait.
1. The iris is not completely separated from the cornea.
2. Persistence of embryonic mesodermal tissue at the angle.
3. Absence of canal of Schlemm.

14. Types
• 1. Congenital glaucoma—It manifests at birth.
• 2. Infantile glaucoma—It presents between 1-3 years.
• 3. Juvenile glaucoma—It presents around puberty.
Syndromes Associated with Infantile Glaucoma.
1. von Recklinghausen’s disease, i.e. generalised neurofibromatosis.
2. Sturge-Weber syndrome—The capillary naevus of face is associated
with angiomatous ,conditions of the choroid and the brain.

15. Symptoms
• 1. Lacrimation - due to corneal oedema and erosion.
• 2. Photophobia - associated with corneal involvement.
• 3. There is defective vision- due to corneal oedema leading to hazy
cornea.
• 4. There is enlargement of cornea and the eye as a whole, due to
stretching of the sclera.

16. Signs
• 1. Enlargement of the eyeball as a whole is present with globular cornea.
• 2. There is corneal oedema and opacities due to endothelium damage and
rupture of Descemet’s membrane (Haabs’ striae). These occur because
Descemet’s membrane is less elastic than the corneal stroma. Tears are
situated in the periphery and are concentric with the limbus.
• 3. Deep anterior chamber with iridodonesis may be seen due to backward
displacement of the lens . Iris may have atrophic patches in the late stages.
• 4. Lens is flattened and displaced backwards due to stretching of the zonule
of Zinn.
• 5. Sclera becomes thin and bluish as the uveal tissue shines through it.

18. Diagnosis
1 . Raised intraocular pressure—It is not raised markedly due to:
I . Extensibility or stretching of the sclera
ii . Uveoscleral outflow.
2 . Measurement of corneal diameter—Corneal enlargement occurs along
with the enlargement of the globe—buphthalmos (Bull-like eyes), specially
when the onset is before the age of 3 years.
A normal infant’s cornea measures about 10.5 mm in diameter.
3 . Fundus examination—The cupping of optic disc is seen due to stretching
of the lamina cribrosaand raised tension. Optic atrophy usually sets in after
the third year.
4. Gonioscopy—The angle of anterior chamber shows certain abnormalities.

19. Differential Diagnosis
i. Keratoglobus (megalocornea)—It is present since birth.
ii. Very high myopia—The eyeball is large as a whole.
iii. Raised intraocular pressure (IOP) in infants may be associated with:
• Retinoblastoma.
• Retinopathy of prematurity.
• Aniridia or absence of iris.
• Persistent primary hyperplastic vitreous.

20. Treatment
The treatment of congenital or infantile glaucoma is always surgical.
1. Medical Treatment
Systemic acetazolamide and mannitol IV along with local beta blockers,
e.g. timolol maleate control the intraocular pressure preoperatively.
Miotics are useless as they do not help in aqueous outflow.
2. Operative Treatment
i. Goniotomy
ii. Trabeculotomy
iii. Trabeculectomy

22. PRIMARY OPEN ANGLE GLAUCOMA (POAG)
It is a chronic, slowly progressive condition with an insidious onset. This
presents an entirely different clinical picture from the acute closed
angle glaucoma.
Etiology:
It has a genetic basis. There is sclerosis of the trabecular meshwork in
any type of eye. The endothelial lining of the canal of Schlemm may
also be sclerosed.

23. Mechanism of Primary Open Angle Glaucoma
There is increased resistance to the outflow of the aqueous humor
offered by:
1. The sclerosed trabecular meshwork—Electron microscopic picture
shows following changes in the trabecular meshwork.
(i) Proliferation of endothelial lining with thickening of the basement
membrane.
(ii) Narrowing of intertrabecular spaces.
(iii) Deposition of amorphous material in the juxtacanalicular tissue.
2. The sclerosed endothelium lining of the canal of Schlemm—This
leads to narrowing or collapse of canal of Schlemm.

24. Associated Ocular Pathology
Following ocular diseases may be present in association with primary
open angle glaucoma:
• High myopia
• Fuchs endothelial dystrophy
• Retinitis pigmentosa
• Retinal vessel occlusion
• Retinal detachment.

25. Symptoms
1. There is painless, progressive loss of vision. Due to its insidious onset, it is
usually noticed when vision is completely lost in one eye and the other eye is
seriously impaired.
2. Mild headache and eyeache may be present.
3. A defect in the visual field (noticed by an intelligent patient) is often
present.
4. There is increasing difficulty in doing near work. Reading or close work is
often difficult due to accommodative failure as a result of pressure upon the
ciliary muscle and its nerve supply.
5. Light sense is defective. Light minimum is raised and dark adaptation is
slowed.

26. Signs
1. Visual acuity decreases gradually. However, it remains good till the
late stage as the central field of vision persists.
2. Cornea is usually clear.
3. Anterior chamber depth and angle are normal.
4. Pupillary reactions remain normal until the late stage when they
become sluggish.

27. Diagnosis
The diagnosis depends on the classical triad signs:
1. Raised intraocular pressure
↓
2. Cupping of the optic disc
↓
3. Visual field defects

32. NORMAL

37. 1. Baring of the blind spot 2. Small scotomatous areas 3. Seidel’s sign
4. Bjerrum’s arcuate scotoma 5. Double arcuate scotoma or 6. Temporal-central island
annular scotoma

39. Treatment POAG
Methods
The treatment options available at present are medicines, laser or
surgery to lower the intraocular pressure.
1. Medical—It is always the treatment of choice in the early stages.
2. Surgical—It is considered to be the last resort.
3. Argon or diode laser trabeculoplasty (ALT or DLT)—It is the most
advanced technique.
4. Recent advanced procedures—These include laser filtration, seton
valves, deep sclerotomy and viscocanalostomy.

40. Treatment POAG
• β-blockers (Timolol)
• Parasympathomimetics [Miotics] (Pilocarpine)
• Carbonic Anhydrase inhibitors (Dorzolamide)
• Adrenergic Agonists (Dipivefrin, Brimonidine)
• Prostaglandin analogues (Latanoprost)
• Hyperosmotic Agents (Mannitol, Glycerine, Isosorbide)

41. Treatment Con.
• In the event of failure of medical treatment of glaucoma
• Trabeculectomy (filtration surgery)

45. PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG
This is a condition in which the intraocular tension is raised due to the
narrow or closed angle of the anterior chamber. There is obstruction to
the outflow of the aqueous humor.
RISK FACTORS
It has a genetic basis. It is typically seen in eyes which are:
I . Small and hypermetropic eye common in adults
II . Anatomical narrow angle of the anterior chamber
III. Shallow anterior chamber
IV . Iris—lens diaphragm is pushed forwards

47. Convex Iris Lens Diaphragm | Shallow anterior chamber | Narrow entrance to chamber angle
Small and hypermetropic eye

48. Mechanism of Angle-
closure Glaucoma
• Pupillary Block
• Iris Bombé
• Angle Closure

49. Stages
The clinical course of the disease has been divided into five stages. The
condition however does not necessarily progress from one stage to the
other in an orderly sequence.
1. Primary angle-closure glaucoma suspect (latent)
2. Subacute or intermittent primary angle-closure glaucoma ( slight
emergency)
3. Acute primary angle-closure glaucoma
4. Chronic primary angle-closure glaucoma
5. Absolute primary angle-closure glaucoma

50. Acute Attack
• Pain
• Nausea and Vomiting clinical signs
• Photophobia
• Semi dilated pupil
• Injected eye
• Cornea edam (haze)
• Iris Bombé

51. • Diagnosed by doing gonioscopy
• Goniolens
• Knowledge of normal angle is crucial

53. Absolute Glaucoma
When chronic stage is not treated with or without sub-acut attackes
• Blind
• Painful
• Treatment :
• Pain relief with med and surgical procedures, if does not work
other options such as :
• Enucleation
• Laser/Cryotherapy
• Absolute alcohol

54. SECONDARY GLAUCOMA
• Secondary glaucoma occurs due to a specific anomaly or disease of the
eye.
Lens
• Intumescence
• Dislocation
• Phacolytic
Trauma
Uveitis
Neovascular
Pigmentary

55. Treatment
• Treat the basic underlying cause of raised tension.

56. NORMAL TENSION GLAUCOMA (NTG)
Definition:
The term normal tension glaucoma, also referred to as low tension
glaucoma is characterized by typical glaucomatous disc changes with
visual field defects, with an intraocular pressure remaining constantly
below 21 mm of Hg.
• It is a variant of primary open angle glaucoma

57. OTHER TYPES OF GLAUCOMA
APHAKIC GLAUCOMA
• It is a type of secondary glaucoma which occurs following extraction of the
lens.
Etiology
• It occurs after cataract surgery due to:
i. Delayed formation of anterior chamber—This results in the formation of
peripheral anterior synechiae. It may occur due to choroidal detachment or
leaking section
ii. The vitreous protruding through the pupil in the anterior chamber may
cause pupillary block
iii. Presence of vitreous in the anterior chamber blocks the angle.

58. OTHER TYPES OF GLAUCOMA
MALIGNANT GLAUCOMA
• Malignant glaucoma is a rare condition which may occur as a
complication of any intraocular surgery.
Etiology
Malignant glaucoma occurs typically in patients with
I . Primary narrow angle glaucoma operated for peripheral buttonhole
iridectomy or trabeculectomy (ciliolenticular block)
II . Aphakic eyes following vitreous phase disturbance (ciliovitreal block)

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