GLAUCOMA.pdf

Glaucoma is not a single disease process but a group of disorders characterized by a progressive optic neuropathy resulting in a irreversible visual field defects that are associated frequently raised intraocular pressure (IOP).
IOP is the most common risk factor but not the only risk factor for development of glaucoma.

1. GLAUCOMA
BY -MS. MEGHNA VERMA
ASSISSTANT PROFESSOR
DEPARTMENT OF OPTOMETRY
RAMA UNIVERSITY

2. CONTENTS
•Formation of aqueous humour
•Drainage of aqueous
•Intra ocular pressure
•Ocular hypertension
•Normal tension glaucoma
•Developmental glaucoma
[Buphthalmos]
•Primary narrow angle glaucoma
•Primary open angle glaucoma
•Secondary glaucoma

3. FORMATION
OF
AQUEOUS
HUMOUR

4. Aqueous humour is derived from capillary network of cilliaryprocesses.
The normal aqueous production rate is 2.3 µl/min.
The 3 mechanisms ultra filtration, diffusion, and secretion (active
transport).
ULTRAFILTRATION
By ultra filtration, most of the plasma substances pass out from the capillary
wall, loose connective tissue and pigment epithelium of the cilliary
processes.
Thus, the plasma filtrate and accumulates behind the non pigment
epithelium of cilliaryprocesses.

5. SECRETION
•The tight junctions between the cells of the non-pigment epithelium create part
of blood aqueous barrier.
•Certain substances are actively transported (secreted) across this barrier into the
posterior chamber.
•The active transport is brought about by Na+ K+ activated ATP pump and carbonic
anhydraseenzyme system.
•Substances that are actively transported include sodium, chlorides, potassium,
ascorbic acid, amino acids and bicarbonates.
DIFFUSION
•Active transport of these substances across the non-pigmented cilliaryepithelium
results in an osmosis leading to the movement of other plasma constituents into
the posterior chamber by ultra filtration and diffusion.
•Sodium is primarily responsible for the movement of water into the posterior
chamber.

6. DRAINAGE
OF
AQUEOUS
HUMOUR

7. Aqueous humour flows from the posterior chamber into the anterior
chamber through the pupil. The aqueous is drained out by two routes –
1.TRABECULAR (CONVENTIONAL) OUTFLOW.
•Trabecularmeshwork is the main part for aqueous outflow.
•Approx. 90 % aqueous is drained out via this route.
•Freely flow of aqueous occurs from trabecularmeshwork up to inner
wall of Schlemm'scanal.
•Mechanism of aqueous transport across inner wall of Schlemm’scanal.
•There are transcellularspaces in the endothelial cells forming inner
wall of Schlemm'scanal.
•These open as a system of vacuoles and pores, primarily in response to
pressure, and transport the aqueous from the juxtacanalicular
connective tissue to Schlemm’scanal.

8. •From Schlemm'scanal the aqueous is transported via 25-35 external
collector channels into the episcleralveins by direct and indirect
systems.
•A pressure gradient between intraocular pressure and intrascleral
venous pressure is responsible for unidirectional flow of aqueous.
2. UVEOSCLERAL (UNCONVENTIONAL) OUTLOW.
It is responsible for about 10 percent of the total aqueous outflow.
Aqueous passes across the ciliarybody into the suprachoroidalspace
and is drained by the venous circulation in the ciliarybody, choroid
and sclera.

11. INTRA
OCULAR
PRESSURE

12. •The intraocular pressure (IOP) refers to the pressure exerted by intraocular
fluids on the coats of the eyeball.
•The normal IOP varies between 10 and 21 mm of Hg (mean 16 ±2.5 mm
of Hg).
•The normal level of IOP is maintained by a balance between the formation
and outflow of the aqueous humour.
•Various factors influencing intraocular pressure can be grouped as under:
Local factors
•Rate of aqueous formation influences IOP levels.
•Increased episcleralvenous pressure may result in rise of IOP.
•Dilatation of pupil in patients with narrow anterior chamber angle may
cause rise of IOP owing due to obstruction of the aqeuousdrainage by the
iris.

14. General factors
•Heredity
•Age. IOP increases after the age of 40 years due to reduced facility
of aqueous outflow.
•Postural variations. IOP increases when changing from the sitting to
the supine position.
•Osmotic pressure of blood. An increase in plasma osmolarityis
associated with a fall in IOP, while a reduction in plasma osmolarity
is associated with a rise in IOP. 8. General anaesthetics and many
other drugs also influence IOP .

15. GLAUCOMA

16. •Glaucoma is not a single disease process but a group of
disorders characterized by a progressive optic neuropathy
resulting in a irreversible visual field defects that are
associated frequently raised intraocular pressure (IOP).
•IOP is the most common risk factor but not the only risk factor
for development of glaucoma.
•The term ‘ocular hypertension’ is used for constantly raised
IOP without any glaucomatous damage.
•The term ‘normal or low tension glaucoma’ (NTG/LTG) is used
for the cupping of the disc and/or visual field defects
associated with a normal or low IOP.

18. OCULAR
HYPERTENSION

19. •Ocular hypertension or glaucoma suspect, when a patient has
an constantly increased IOP more than 21 mmHg but no optic
disc or visual field changes.
•These patients should be carefully monitored and should be
treated as cases of POAG.
High risk factors include:
•Significant diurnal variation -a difference of more than 8 mmHg
b/w the lowest & highest values of IOP.
•Positive water drinking provocative test.
•IOP constantly more than 28 mmHg.

20. •NFL defects & Central corneal thickness < 555 µm.
•Asymmetry in the cup size of the two eyes, i.e., a difference of
more than 0.2.
•Strong family history of glaucoma.
•When associated with high myopia, diabetes or pigmentary
changes in the anterior chamber.
TREATMENT
•Patients with high-risk factors, should be to reduce IOP by 20%.
•Patients with no high risk factors should be annually followed
by examination of optic disc, perimetryand record of IOP.
Treatment is not required till glaucomatous damage is
documented

21. NORMAL
TENSION
GLAUCOMA

22. When typical glaucomatous disc changes with or without
visual field defects are associated with an IOP constantly below
21 mmHg.
ETIOLOGY
•It is associated with more common in NTG than in POAG :
peripheral vascular spasm on cooling, Migraine, Nocturnal
systemic hypotension and overtreated systemic hypertension.
•Reduced blood flow velocity in the ophthalmic artery.

23. CLINICAL FEATURES
•Optic disc changes & visual field defects are similar to POAG,
but the IOP is below 21mm Hg
TREATMENT
•Medical treatment to lower IOP. [Betaxolol]
•Other beta blockers and adrenergic drugs (such as
dipiverafrine) should better be avoided (as these cause systemic
hypotension and are the optic nerve perfusion).
•Trabeculectomy, Systemic calcium channel blockers (e.g.,
nifedipine) may be useful in patients with peripheral vasospasm.
And Monitoring of systemic blood pressure should be done for
24 hours.

25. CONGENITAL GLAUCOMA
OR
BUPHTHALMOS

26. •The congenital glaucoma are a group of disorders in
which abnormal high intraocular pressure.
•It results due to abnormalities of the angle of anterior
chamber obstructing the drainage of aqueous humour.
•It is not associated with any other ocular or systemic
anomaly.
•Sometimes, glaucoma may not occur until several years
after birth, but after some time, the term is
developmental glaucoma.

27. 1. True congenital glaucoma -IOP is raised during
intrauterine life.
2.Infantile glaucoma -the disease seen on child's third
birthday.
3.Juvenile glaucoma –IOP rise between 3-16 years of life.
➢when the disease seems to age of 3 years, the
eyeball enlarges and so the term
buphthalmos(bull-like eyes) is used.

29. CLINICAL FEATURES
•Photophobia, blepharospasm, lacrimationand eye rubbing.
•Corneal signs -oedema, enlargement and Descemet’sbreaks.
•Sclera -thinning and appears blue in colour.
•Anterior chamber becomes deep.
•Iris may show iridodonesis.
•Lens becomes flat due to stretching of zonulesand may
subluxate.
•Optic disc may show cupping and atrophy.
•IOP is raised.
•Axial myopia may give rise to anisometropicamblyopia.

30. EXAMINATION
•Measurement of IOP with Schiotzor Applanationtonometer.
•Measurement of corneal diameter.
•Ophthalmoscopy-to evaluate optic disc.
•Gonioscopicexamination -angle of anterior chamber.
TREATMENT
•Congenital glaucoma is primarily surgical.
•IOP must be lowered by use of hyperosmoticagents,
acetazolamideand beta-blockers till surgery is taken up.
•Mioticsare of no use in such cases.

31. PRIMARY
OPEN ANGLE
GLAUCOMA

32. •It occurs in eyes with open angle of the anterior chamber.
•Primary open angle glaucoma (POAG) also known as chronic simple
glaucoma
•It is characterised by slowly progressive raised intraocular pressure (>21
mmHg ) associated with optic disc cupping and visual field defects.
ETIOLOGY
(A)Predisposing and risk factors.
1.Heredity.
2.Age. The risk increases with increasing age.
3.Race. POAG is more severe in black people than in white.
4.Myopic are more predisposed than the normal.
5. Diabetics, smoking & High blood pressure is the prevalence of POAG.

34. Pathogenesis of rise in IOP.
•It is rise in IOP occurs due to decrease in the aqueous outflow
facility caused by age-related thickening and sclerosis of the
trabecularmeshwork.
CLINICAL FEATURES
Symptoms
•Significant loss of visual field,
•Mild headache and eye ache.
•Reading and close work difficulties due to accommodative failure
•Frequent changes in presbyopicglasses, delayed dark adaptation.

35. Signs
❑Anterior segment signs -
•Ocular examination by slit-lamp, may reveal normal anterior segment. In
late stages pupil reflex becomes sluggish and cornea show slight hazy.
❑Intraocular pressure changes -
•Initially, the IOP may not be raised permanently. Therefore, repeated
observations of IOP (every 3-4 hour), for 24 hours is required during this
stage (Diurnal variation test). In most patients IOP falls during the evening.
•A variation in IOP of over 5 mm Hg (Schiotz) is suspicious and over 8 mm
of Hg is diagnostic of glaucoma.
•In later stages, IOP is permanently raised above 21 mm of Hg and ranges
between 30 and 45 mm of Hg.

36. ❑Optic disc changes -
•Optic disc changes, usually observed on routine fundusexamination,
provide an important clue for suspecting POAG.
❑Visual field defects -
•Visual field defects usually run parallel to the changes at the optic nerve
head and continue to progress if IOP is not controlled.
* Progression of visual field defects
•Isoptercontraction.
•Baring of blind spot
•Small wing-shaped paracentralscotoma
•Seidel’s scotoma
•Arcuateor Bjerrum’sscotoma
•Ring or double arcuatescotoma
•Roenne'scentral nasal step.

37. INVESTIGATIONS
1. Tonometry. Applanationtonometryshould be preferred
over Schiotztonometry.
2. Diurnal variation test is especially useful in detection of
early cases.
3. Gonioscopy. It reveals a wide open angle of anterior
chamber.
5. Slit-lamp examination of anterior segment to rule out causes
of secondary open angle glaucoma.
6. Perimetryto detect the visual field defects.
7. Nerve fibre layer analyzer (NFL) helps in detecting the
glaucomatous damage to the retinal nerve fibres.

38. ❑Water drinking test.
•In it after an 8 hours fast, baseline IOP is noted and the patient is
asked to drink one litre of water and IOP is noted every 15 min. for 1
hour.
•The maximum rise in IOP occurs in 15-30 min. and returns to baseline
level after 60 minutes in both normal and the glaucomatous eyes.
•A rise of 8 mm of Hg or more is said to be diagnostic of POAG.
MANAGEMENT
Therapeutic choices include:
•Medical therapy
•Argon or diode laser trabeculoplasty
•Filtration surgery

39. PRIMARY
CLOSURE ANGLE
OR
NARROW ANGLE
GLAUCOMA

40. •It is a type of glaucoma in which rise in intraocular pressure occurs due to
blockage of the aqueous humour outflow by closure of a narrower angle of
the anterior chamber.
ETIOLOGY
(A) Predisposing risk factors
➢Anatomical factors
•Hypermetropiceyes with shallow anterior chamber.
•Eyes with narrow angle, which may be due to: small eyeball, large size of
the lens and smaller diameter of the cornea or bigger size of the ciliary
body.
➢General factors
•Age -PACG is comparatively more common in 5th decade of life.
•Gender -male to female ratio is 1:4.

42. Mechanism of rise in IOP.
•First of all due to the effect of precipitating factors there occurs
mid dilatation of the pupil which & between iris and anteriorly
placed lens increases pressure.
•Consequently the aqueous collects in the posterior chamber
and pushes the peripheral iris, resulting angle closure due to
iridocornealcontact.
•The angle closure is converted into synechialangle closure.
➢There are two main type of angle closure glaucoma -
1.Acute primary angle-closure glaucoma
2.Chronic primary angle-closure glaucoma

43. ACUTE PRIMARY ANGLE CLOSURE GLAUCOMA
•It occurs due to a sudden angle closure leading to severe rise in IOP.
CLINICAL FEATURES
Symptoms
•Severe pain in the eye.
•Nausea, vomiting and prostrations are frequently associated with pain.
•Sudden loss of vision, redness, photophobia and watering.
Signs
•Lids may be oedematous
•Conjunctiva is chemosed, and congested and Corneal oedema and
insensitive.
•AC is very shallow & Aqueous flare or cells may be seen in anterior
chamber.

44. •Angle of anterior chamber is completely closed as seen on gonioscopy.
•Iris may be discoloured.
•Pupil is semi-dilated and non-reactive to light
•IOP is markedly elevated, usually between 40 and 70 mm of Hg.
•Optic disc is oedematous and hyperaemic.
•Fellow eye shows shallow anterior chamber and a narrow angle (latent
angle closure glaucoma).
MANAGEMENT
1.Medical therapy
2.Surgical treatment
•Peripheral iridotomy
•Filtration surgery

45. CHRONIC PRIMARY ANGLE CLOSURE GLAUCOMA
Pathogenesis
It results from gradual synechialclosureof the angle of anterior
chamber.
Clinical features
•Intraocular pressure (IOP) remains constantly raised.
•Eyeball remains white (no congestion) and painless
•Optic disc may show glaucomatous cupping.
•Gonioscopyreveals a permanent peripheral anterior synechiae.
Treatment
•Laser iridotomyalone or along with medical therapy should be tried.
•Trabeculectomy(filtration surgery) is needed when the above
treatment fails to control IOP.

46. SECONDARY
GLAUCOMA

47. Secondary glaucoma is not a disease entity, but a group of disorders in
which rise of IOP is associated with primary ocular or systemic disease.
1.Lens-induced glaucoma.
2.Inflammatory glaucoma (due to intraocular inflammation/uveitis).
3.Pigmentary glaucoma.
4.Neovascular glaucoma.
5.Glaucoma associated with intraocular haemorrhage.
6.Steroid-induced glaucoma.
7.Traumatic glaucoma.
8.Glaucoma-in-aphakia.
9.Glaucoma associated with intraocular tumours.

48. PHACOLYTIC GLAUCOMA (LENS PROTEIN GLAUCOMA)
Pathogensis. in which trabecular meshwork is blocked by the lens
proteins and macrophages which have phagocytosed the lens proteins.
Leakage of the lens proteins occurs in hypermature cataract .
Clinical features
Features of congestive glaucoma due to an acute rise of IOP in an eye
having hypermature cataract.
Anterior chamber may become deep and aqueous may contain fine
white protein particles.
Management
It consists of medical therapy to lower the IOP followed by extraction of
the hypermature cataractous lens with PCIOL implantation.

49. LENS INDUCED GLAUCOMA
Pathogenesis
It is a type of glaucoma, in which trabecularmeshwork is
blocked by the lens particles floating in the aqueous humour.
It may occur due to lens particles left after accidental or
planned ECCE surgery or traumatic rupture of the lens.
Clinical featuresRaised IOP associated with lens particles in
the anterior chamber.
Managementincludes medical therapy to lower IOP and
irrigation-aspiration of the lens particles from the anterior
chamber

50. GLAUCOMAS DUE TO UVEITIS or INFLAMMATORY GLAUCOMA
The IOP can be raised by inflammations of the uveal tissue (iridocyclitis).
other ocular inflammations such as keratitis and scleritis.
Types -Itcan be divided into two main groups:
1.Hypertensive uveitis.
2. Post-inflammatory glaucoma.
Hypertensive uveitis
It refers to acute inflammation of the anterior uvea associated with
raised IOP.
It includes:
i. Non-specific hypertensive uveitis
ii) Specific hypertensive uveitis

51. i. Non-specific hypertensive uveitis.
•It includes inflammation of the anterior uvealtract associated with
raised IOP.
•Mechanisms of rise in IOP -occurs due to trabecular clogging
(blocking) by inflammatory cells and trabecular oedema due to
trabeculitis), and prostaglandin–induced rise in IOP.
Management -It includes treatment of iridocyclitisand medical
therapy to lower IOP by use of hyperosmoticagents, acetazolamide
and beta-blocker eye drops.
ii. Specific hypertensive uveitis
These include: Fuchs’ uveitissyndrome and Glaucomatocycliticcrisis.

52. 2. Post-inflammatory glaucoma
•IOP is raised due to after-effects of the iridocyclitis.
Mechanisms of rise in IOP
•Pupillary block due to annular synechiae,
•Secondary glaucoma with pupil block following iris bombe
formation.
•Secondary glaucoma due to inflammatory debris in the
angle.
•Secondary glaucoma due to trabecular scarring and
obstruction of the meshwork.

53. Management.
It includes prophylaxis and curative treatment.
1.Prophylaxis -Acute iridocylitisshould be treated with local
steroids and atropine to prevent formation of synechiae.
2.Curative treatment -It consists of medical therapy to lower
IOP (mioticsare contraindicated). Surgical or laser
iridotomymay be useful in pupil block without angle
closure

54. PIGMENTARY GLAUCOMA
It is a type of glaucoma in which blocking of trabecularmeshwork by the
pigment particles.
Pathogenesis
Some pigment release is caused by mechanical rubbing of the posterior
pigment layer of iris with the zonular fibrils.
Clinical features
The condition typically occurs in young myopic males.
It is associated with deposition of pigment granules in the anterior segment
structures such as iris, posterior surface of the cornea, trabecular
meshwork, ciliary zonules and the crystalline lens.
Gonioscopy shows pigment accumulation along the Schwalbe’s line.
Treatment
Same as primary open angle glaucoma.

55. NEOVASCULAR GLAUCOMA (NVG)
It occurs due to formation of neovascular membrane involving
the angle of anterior chamber.
Etiology
•It is usually associated with neovascularization of iris. [rubeosis
iridis]
•Neovascularization develops following retinal ischaemia, which
is a common feature of :
•Diabetic retinopathy, Central retinal vein occlusion, Sickle-cell
retinopathy and Eales’disease.
•Other rare causes are chronic intraocular inflammations,
intraocular tumours, retinal detachment and central retinal
artery occlusion.

56. Clinical profileNVG occurs in three stages :
1.Pre-glaucomatous stage (stage of rubeosisiridis);
2.Open-angle glaucoma stage—due to formation of a
pretrabecularneovascularmembrane
3.Secondary angle closure glaucoma—due to goniosynechiae
resulting from contracture of the neovascularmembrane.
Treatment
•Panretinalphotocoagulation, prevent further neovascularization.
•Medical therapy are usually not effective in controlling the IOP.
•Artificial filtration shunt (Seton operation) may control the IOP

57. GLAUCOMAS DUE TO INTRAOCULAR HAEMORRHAGES
Intraocular haemorrhagesinclude hyphaemaor vitreous haemorrhage due to
multiple causes.
1.Red cell glaucoma -It is associated with fresh traumatic hyphaema. It is
caused by blockage of trabeculae by RBCs in patients with hyphaema
(anterior chamber full of blood).
2.Haemolyticglaucoma -It occurs due to the obstruction of the trabecular
meshwork caused by macrophages.
3.Ghost cell glaucoma -It occurs in aphakic or pseudo phakic eyes with
vitreous haemorrhage.
After about 2 weeks of haemorrhage the RBCs degenerate, lose
their pliability and become khaki-color cells (ghost cells) which
pass from the vitreous into the anterior chamber, and block the
pores of trabeculae leading to rise in IOP.

58. STEROID-INDUCED GLAUCOMA
It is a type of glaucoma which develops following topical, and
sometimes systemic steroid therapy.
Etiopathogenesis.
•It develop marked rise of IOP after about 6 weeks of steroid
therapy.
Following theories have been put forward :
•Glycoaminoglycans(GAG) theory
•Endothelial cell theory
•Prostaglandin theory

59. Clinical features
Steroid-induced glaucoma usually develops following weeks of
topical therapy with strong steroids and months of therapy
with weak steroids.
Management
It can be prevented by a proper use of steroids and a regular
monitoring of IOP.
Its treatment consists of -Discontinuation of steroids

60. TRAUMATIC GLAUCOMA
A secondary glaucoma may complicate perforating as well as blunt
injuries.
Mechanisms
Traumatic glaucoma may develop by -
•Inflammatory glaucoma due to iridocyclitis
•Glaucoma due to intraocular haemorrhage
•Lens-induced glaucoma due to ruptured, swollen or dislocated lens.
•Angle-closure due to peripheral anterior synechiae formation
following perforating corneal injury producing adherent leucoma.
•Angle recession (cleavage) glaucoma due to disruption of
trabecular meshwork followed by fibrosis.

61. Management
It consists of medical therapy with topical timololand
oral acetazolamide.
Treatment of associated causative mechanism (e.g.
atropine and steroids for control of inflammation) and
surgical intervention according to the situation.

62. GLAUCOMA-IN-APHAKIA/PSEUDOPHAKIA
It includes following conditions:
•Raised IOP with deep anterior chamber in early postoperative
period, may be due to hyphaema, inflammation, vitreous filling
the anterior chamber.
•Secondary glaucoma due to flat anterior chamber.
•Secondary glaucoma due to pupil block due to formation of
annular synechiae.

63. GLAUCOMA ASSOCIATED WITH INTRAOCULAR TUMOURS
Secondary glaucoma due to intraocular tumourssuch as malignant
melanoma (iris, choroid, ciliary body) and retinoblastoma may occur
by -
•Trabecular block due to clogging [blocking] by tumourcells or
direct invasion by tumourseedlings.
•Neovascularization of the angle.
•Venous stasis following obstruction of the vortex veins.
•Angle closure due to forward displacement of iris-lens diaphragm
by increasing tumourmass.
Treatment
Enucleation of the eyeball should be carried out as early as possible.

64. ANTI
GLAUCOMA
DRUGS

65. A.Parasympathomimetic
drugs (Miotics/cholinergic
drugs) –
•Pilocarpine
•Carbachol
•Echothiophate
•Demecariumbromide
•Physostigmine
B. Sympathomimeticdrugs
(Adrenergic agonists) –
•Epinephrine
•Dipivefrine
•Clonidinehydrochloride
•Brimonidine
•Apraclonidine

66. C. Carbonic anhydrase
inhibitors
•Acetazolamide(diamox)
•Methazolamide
•Ethoxzolamide
•Dorzolamide
•Brinzolamide
D. β-blockers –
•Timolol
•Betaxolol
•Levobunolol
•Carteolol
•Metipranolol
E. Hyperosmoticagents –
•Glycerol
•Urea
•Mannitol
•Isosorbide
F. Prostaglandins–
•Latanoprost
•Bimatoprost
•Travoprost
G. Calcium channel blockers
•Nifedipine,
•Diltiazem,
•Verapamil