GLAUCOMA

American Academy of Ophthalmology

_____________________GLAUCOMA_____________________ CLASSIFICATION OF GLAUCOMA________________________________

A. OPEN-ANGLE GLAUCOMA
DEFINITION: A group of disease that have in common 1. Primary open-angle glaucoma (POAG)
• a characteristic optic neuropathy • not associated with known ocular or systemic disorders that cause
• associated visual field loss increased resistance to aqueous outflow or damage to optic nerve
• elevated IOP is one of the primary risk factors • usually associated with elevated IOP
NORMAL IOP: commonly range in general population is 10-22 mmHg. 2. Normal-tension glaucoma
THREE FACTORS DETERMINE THE IOP • considered in continuum of POAG; often used when IOP is not elevated
1. The rate of aqueous humor production by the ciliary body 3. Juvenile open-angle glaucoma
2. Resistance of aqueous outflow across the trabecular meshwork – • used when open-angle glaucoma diagnosed at young age (typically 10-30
Schlemm’s canal system (in most cases) years of age)
3. The level of episcleral venous pressure. 4. Glaucoma suspect
FACTORS ASSOCIATED WITH THE DEVELOPMENT OF GLAUCOMA • normal optic disc and visual field associated with elevated IOP
1. Increased IOP • suspicious optic disc and/or visual field with normal IOP
2. Advanced age 5. Secondary open-angle glaucoma
3. Racial background • increased resistance to trabecular meshwork outflow associated with
4. Positive family history other conditions (e.g. pigmentary-, phacolytic-, steroid-induced-)
Optic nerve and visual field changes seen in glaucoma are determined by: • increased posttrabecular resistance to outflow secondary to elevated
1. the level of IOP episcleral venous pressure (e.g. carotid cavernous sinus fistula)
2. the resistance of the optic nerve axons to pressure damage B. ANGLE-CLOSURE GLAUCOMA
PRIMARY GLAUCOMA 1. Primary ACG with relative pupillary block
• not associated with known ocular or systemic disorders that cause the • movement of aqueous humor from posterior chamber to anterior chamber
increased resistance to aqueous outflow restricted
• usually affects both eyes • peripheral iris in contact with trabecular meshwork
• may be inherited 2. Acute angle closure
SECONDARY GLAUCOMA • occurs when IOP rises rapidly as a result of relatively sudden blockage of
• associated with ocular or systemic disorders responsible for decreased the trabecular meshwork
aqueous outflow 3. Subacute angle closure (intermittent angle closure)
• the causal diseases are often unilateral • repeated, brief episodes of angle closure with mild symptoms and
• family occurrence is less common elevated IOP, often a prelude to acute angle closure
4. Chronic angle closure

1 Sengdy Chandra Chauhari

 • IOP elevation caused by variable portions of anterior chamber angle 2. Trabecular
being permanently closed by PAS • idiopathic (chronic open-angle glaucoma, juvenile open-angle glaucoma)
5. Secondary ACG with pupillary block • “clogging” of trabecular meshwork
• e.g. swollen lens, secluded pupil 1. red blood cells (hemorrhagic-, ghost cell-, sickled red blood cells)
6. Secondary ACG without pupillary block 2. macrophages (hemolytic-, phacolytic-, melanomalytic-)
• posterior pushing mechanism: lens-iris diaphragm pushed forward (e.g. 3. neoplastic cells (primary ocular tumors, neoplastic tumors, juvenile
posterior segment tumor, scleral buckling procedure, uveal effusion) xanthogranuloma)
• anterior pulling mechanism: anterior segment process pulling iris forward 4. pigment particles (pigmentary-, exfoliation syndrome / glaucoma
to form PAS (e.g. iridocorneal endothelial syndrome, neovascular capsulare, malignant melanoma)
glaucoma, inflammation) 5. protein (uveitis, lens-induced glaucoma)
7. Plateau iris syndrome 6. viscoelastic agents
• primary angle closure with or without component of pupillary block, but 7. α-chymotrypsin-induced glaucoma
pupillary block is not predominant mechanism of angle closure 8. vitreous
C. CHILDHOOD GLAUCOMA • alterations of the trabecular meshwork
1. Primary congenital/infantile glaucoma 1. steroid-induced glaucoma
• primary glaucoma present from birth to first few years of life 2. edema (uveitis, scleritis, episcleritis, alkali burns)
2. Glaucoma associated with congenital anomalies 3. trauma (angle recession)
• associated with ocular disorders (e.g. anterior segment dysgenesis, 4. intraocular foreign bodies (hemosiderin, chalcosis)
aniridia) 3. Posttrabecular
• associated with systemic disorders (e.g. rubella, Lowe syndrome) • obstruction of Schlemm’s canal (e.g. collapse at canal)
3. Secondary glaucoma in infants and children • elevated episcleral venous pressure
• e.g. glaucoma secondary to retinoblastoma or trauma 1. carotid cavernous fistula
2. cavernous sinus thrombosis
CLASSIFICATION OF THE GLAUCOMAS 3. retrobulbar tumors
________based on MECHANISM of OUTFLOW OBSTRUCTION________ 4. thyroid ophthalmopathy
OPEN-ANGLE GLAUCOMA MECHANISMS 5. superior vena cava obstruction
1. Pretrabecular (membrane overgrowth) 6. mediastinal tumors
• fibrovascular membrane (neovascular glaucoma) 7. Sturge-Weber syndrome
• endothelial layer, often with Descemet-like membrane (iridocorneal 8. familial episcleral venous pressure elevation
endothelial syndrome, posterior polymorphous dystrophy, penetrating ANGLE-CLOSURE GLAUCOMA MECHANISMS
and non-penetrating trauma) 1. Anterior (“pulling”)
• epithelial downgrowth • contracture of membranes
1. neovascular glaucoma
• fibrous ingrowth
2. iridocorneal endothelial syndrome
• inflammatory membrane (Fuchs heterochromic iridocyclitis, luetic
3. posterior polymorphous dystrophy
interstitial keratitis)

2 Sengdy Chandra Chauhari

 4. penetrating and non-penetrating trauma
ƒ consolidation of inflammatory products
2. Posterior (“pushing”)
• with pupillary block
1. pupillary block glaucoma
2. lens-induced mechanisms (phacomorphic lens, ectopia lentis)
3. posterior synechiae (iris-vitreous block, pseudophakia, uveitis)
• without pupillary block
1. ciliary block (malignant) glaucoma
2. lens-induced mechanisms (phacomorphic lens, ectopia lentis)
3. following lens extraction (forward vitreous shift)
4. anterior rotation of ciliary body (following scleral buckling or
panretinal photocoagulation, central retinal vein occlusion)
5. intraocular tumors (retinoblastoma, malignant melanoma)
6. cysts of the iris and ciliary body
7. retrolenticular tissue contracture (retinopathy of prematurity,
persistent hyperplastic primary vitreous)
DEVELOPMENTAL ANOMALIES OF ANGLE
• incomplete development of trabecular meshwork / Schlemm’s canal
1. congenital (infantile) glaucoma
2. Axenfeld-Rieger syndrome
3. Peter’s anomaly
4. glaucomas associated with other developmental anomalies
• iridocorneal adhesions
1. broad strands (Axenfeld-Rieger syndrome)
2. fine strands that contract to close angle (aniridia)
COMBINED-MECHANISM GLAUCOMA
• Combination of two or more forms of glaucoma present either sequentially or
simultaneously
• IOP elevation can occur as a result of either or both of the following:
1. the intrinsic resistance of the trabecular meshwork to aqueous outflow in
open-angle glaucoma
2. the direct anatomic obstruction of the filtering meshwork by synechiae in
ACG
3 Sengdy Chandra Chauhari
• Treatment is modified based on the proportion of open angle to closed angle
and the etiology of the angle-closure component
RISK FACTORS for POAG
• IOP, age, race and positive family history
• Myopia, sex, various systemic factors (diabetes, systemic hypertension,
arteriosclerotic and ischemic vascular disease)
RISK FACTORS for PACG
• Race: acute PACG is relatively uncommon in blacks
• Sex: women develop acute PACG 3-4 times more often than do men
• Age: acute PACG is most common between the ages of 55 and 65 years
• Refraction: PACG is typically associated with hyperopia
• Inheritance: some of the anatomic features of the eye that predispose to
pupillary block (such as forward position of the lens and greater than
average lens thickness) are inherited.
GENES known to be associated with GLAUCOMA
TIGR/Myocilin 1q23 (GLC1A) juvenile and adult open-angle glaucoma
CYP1B1 2p21 (GLC3A) congenital glaucoma
PITX2 4q25 (RIEG1) Rieger syndrome
FKGL7 6p25 (IDYS1) iridodysgenesis
LMX1B 9q34 (NPS1) glaucoma, with nail-patella syndrome
PAX6 11p13 (AN1) aniridia
INTRAOCULAR PRESSURE and AQUEOUS HUMOR DYNAMICS______
Aqueous outflow: posterior chamber → pupil → anterior chamber → trabecular
meshwork → Schlemm’s canal → collector channels →
venous system
Goldmann equation: Po = (F/C) + Pv
Po = the IOP (mmHg)
F = the rate of aqueous formation (uL/min)
C = the facility of outflow (uL/min/mmHg)
Pv = the episcleral venous pressure (mmHg)
Aqueous humor is formed by the ciliary processes
• Each of which is composed of a double layer of epithelium over a core of
stroma and a rich supply of fenestrated capillaries.
• The apical surfaces of both the outer pigmented and the inner non-pigmented
layers of epithelium face each other and are joined by tight junctions, which
are probably an important part of the blood-aqueous barrier.
• The inner non-pigmented epithelial cells contain numerous mitochondria and
microvilli. These cells are thought to be the site of aqueous production.
Aqueous humor formation involves the combination of several processes:
1. Active transport (secretion)
• Consumes energy to move substances against an electrochemical gradient
and is independent of pressure.
• Accounts for the majority of aqueous production and involves activity of
the enzyme carbonic anhydrase.
2. Ultrafiltration
• Pressure-dependent movement along a pressure gradient (hydrostatic
pressure and oncotic pressure, between capillary pressure and IOP)
3. Simple diffusion
• The passive movement of ions across a membrane related to charge.
Suppression of aqueous formation
• Carbonic anhydrase inhibitors (CAIs) → inhibits the active secretion of
bicarbonate or hydrogen ions
• Beta-blockers → may affect active transport by causing a decrease in either
the efficiency of the Na+/K+ pump or in the number of pump sites.
4 Sengdy Chandra Chauhari
• Alpha2-agonists
Rate of aqueous formation
• Normal flow is approximately 2-3 uL/min or a 1% turnover in aqueous
volume per minute.
• Varies diurnally and drops during sleep. Decreases with age.
• Affected by a variety of factors:
1. the integrity of the blood-aqueous barrier
2. blood flow to the ciliary body
3. neurohumoral regulation of vascular tissue and the ciliary epithelium
• Decreases when the eye is injured or inflamed and following the
administration of certain drugs. Decreases with carotid occlusive disease.
Facility of outflow (C in the Goldmann equation)
• The mean value reported ranges from 0.22-0.28 uL/min/mmHg.
• Decreases with age and is affected by surgery, trauma, medications and
endocrine factors.
TRABECULAR OUTFLOW
• Trabecular meshwork (uveal, corneoscleral, juxtacanalicular) – Schlemm’s
canal – venous system
• Trabecular meshwork functions as a one-way valve that permits aqueous to
leave the eye by bulk flow but limits flow in the other direction independently
of energy. Aqueous moves both across and between the endothelial cells
lining the inner wall of Schlemm’s canal. Once in Schlemm’s canal, aqueous
enters the episcleral venous plexus by way of scleral collector channels.
UVEOSCLERAL OUTFLOW
• Anterior chamber → ciliary muscle → supraciliary and suprachoroidal spaces
→ exits the eye through the intact sclera or along the nerves and the vessels
that penetrate it.
• Pressure-independent.
• Influenced by age. Increased by cycloplegic, adrenergic, and prostaglandin
agents and certain forms of surgery (e.g. cyclodialysis). Decreased by miotics
Tonography • Measures the force necessary to flatten an area of the cornea of 3.06 mm
• This measurement can be taken using a Schiotz tonometer of known weight, diameter. At this diameter, the resistance of the cornea to flattening is
which is placed on the cornea, suddenly elevating IOP. counterbalanced by the capillary attraction of the tear film meniscus for
• The rate at which the pressure declines with time is related to the ease with the tonometer head.
which the aqueous leaves the eye. The decline in IOP over time can be used • Relatively unaffected by ocular rigidity.
to determine outflow facility. • Excessive fluorescein leads to high reading, whereas inadequate
fluorescein leads to low reading.
Episcleral venous pressure • Measurements are affected by corneal edema or scar, alteration in scleral
• Relatively stable, except when alterations in body position and certain rigidity and central corneal thickness.
diseases of the orbit, head and neck obstruct venous return to the heart or 2. Perkins tonometer
shunt blood from the arterial to the venous system. • Using a split-image device and fluorescein staining of the tears.
• The usual range of values is 8-12 mmHg. 3. Non-contact (air-puff) tonometer
• In acute conditions IOP rises approximately 1 mmHg for every 1 mmHg • Measuring the time necessary for a given force of air to flatten a given
increase in episcleral venous pressure. area of the cornea.
4. Portable electronic applanation devices
Factors influencing IOP 5. Pneumatic tonometer
• Time of day, heartbeat, respiration, exercise, fluid intake, systemic • Has a pressure-sensing device that consists of a gas-filled chamber
medications, topical drugs. covered by a Silastic diaphragm.
• Alcohol ↓. Caffeine ↑. Cannabis ↓. 6. Schiotz tonometer
• IOP is higher when the patient is recumbent rather than upright. • Measuring the indentation of the cornea produced by a known weight.
• IOP usually increases with age and is genetically influenced.
Diurnal variation of IOP
• In normal individuals IOP varies 2-6 mmHg over a 24-hour period, as
aqueous humor production changes.
• The higher the pressure, the greater the fluctuation.
• A diurnal fluctuation of greater than 10 mmHg is suggestive of glaucoma.

Imbert-Fick principle
The pressure inside an ideal dry, thin-walled sphere equals the force necessary to
flatten its surface divided by the area of the flattening.
P = F/A (P=pressure, F=force, A=area)

Tonometer
1. Goldmann applanation tonometer

5 Sengdy Chandra Chauhari

CLINICAL EVALUATION_____________________________________ • massive episcleral venous dilation → chronic elevated IOP
The goal of glaucoma management is the preservation of patient’s visual function • black adrenochrome deposits → chronic use of epinephrine derivative drops
and quality of life. • use of topical antiglaucoma medication → decreased tear production, allergic
reactions, foreshortening of the conjunctival fornices, scarring.
--------------------HISTORY and GENERAL EXAMINATION-------------------- • filtering bleb: size, height, degree of vascularization, integrity
History Episclera and sclera
1. The patient’s current complaint • dilation of the episcleral vessels → elevated episcleral venous pressure
2. Symptoms, onset, duration, severity, location • sentinel vessels → intraocular tumor
3. Ocular history • thinning or staphylomatous areas
4. History of present illness Cornea
5. Past ocular medical and surgical history • enlargement of the cornea, breaks in Descemet’s membrane (Haab’s striae)
6. General medical history → developmental glaucoma
7. Past systemic medical history (including medications and allergies) • punctate epithelial defects (especially in the inferonasal interpalpebral region)
8. Review of systems → medication toxicity
9. Social history • microcystic epithelial edema → acute elevated IOP
10. History of ethanol and tobacco
• endothelial abnormalities → underlying associated secondary glaucoma
11. Occupation, avocation, interests
1. Krukenberg spindle in pigmentary glaucoma
12. Family history
2. deposition of exfoliation material in exfoliation syndrome
Refraction
3. keratic precipitates in uveitic glaucoma
• neutralizing any refractive error is crucial for accurate perimetry 4. guttae in Fuchs endothelial dystrophy
• hyperopic eyes → increased risk of ACG 5. irregular and vesicular lesions in posterior polymorphous dystrophy
• myopic eyes → increased risk for pigment dispersion, associated with disc 6. ‘beaten bronze’ appearance in the iridocorneal endothelial syndrome
morphologies that can be clinically confused with glaucoma. • anteriorly displaced Schwalbe’s line → Axenfeld-Rieger syndrome
External adnexae • traumatic or surgical corneal scars, corneal thickness
Its examination and assessment is useful in determining the presence of a variety
Anterior chamber
of conditions associated with secondary glaucomas as well as external ocular
• width of the chamber angle → van Herick method (A narrow slit beam is
manifestations of glaucoma therapy.
directed at an angle of 60˚ onto the cornea just anterior to the limbus. If the
Pupils
distance from the anterior iris surface to the posterior surface of the cornea is
Pupillary responses are one measure of compliance in patients who are on miotic
less than one fourth the thickness of the cornea, the angle may be narrow)
therapy. Corectopia, ectropion uveae and pupillary abnormalities may be observed
• uniformity of depth of the anterior chamber (iris bombe, iris masses)
in some forms of glaucoma. Testing for a RAPD may detect asymmetric optic
nerve damage in glaucoma. • inflammatory cells, red cells, ghost cells, fibrin, vitreous
Conjunctiva Iris
• conjunctival injection → acute elevated IOP, chronic use of sympatho- • heterochromia, iris atrophy, transillumination defects, ectropion uveae,
mimetic drops corectopia, nevi, nodules, exfoliative material

6 Sengdy Chandra Chauhari

 • early stages of neovascularization of the anterior segment → fine tufts around • Grade II 20˚ Angle closure possible
the pupillary margin, fine network of vessels on the surface of the iris. • Grade I 10˚ Angle closure probable in time
• evidence of trauma (sphincter tear, iridodonesis), iris pigmentation • Slit <10˚ Angle closure very likely
Lens • O (the iris is against the trabecular meshwork; angle closure is present)
• exfoliative material, phacodonesis, subluxation, dislocation 2. Spaeth system → describes the peripheral iris contour, the insertion of the
• lens size, shape and clarity iris root, and the effects of indentation gonioscopy on the
• posterior subcapsular cataract → chronic corticosteroid use angle configuration.
• presence, type and position of an IOL • Ordinarily, Schlemm’s canal is invisible by gonioscopy. Occasionally during
Fundus gonioscopy in normal eyes, blood refluxes into Schlemm’s canal where it is
• careful assessment of the optic disc seen as a faint red line in the posterior portion of the trabecular meshwork.
• hemorrhage, effusion, masses, inflammatory lesion, retinovascular occlusion, Blood enters Schlemm’s canal when episcleral venous pressure exceeds IOP,
diabetic retinopathy, retinal detachment most commonly because of compression of the episcleral veins by the lip of
the goniolens. Pathological causes include hypotony and elevated episcleral
---------------------------------------GONIOSCOPY--------------------------------------- venous pressure (e.g. carotid-cavernous fistula, Sturge-Weber syndrome)
• Under normal conditions the anterior chamber angle cannot be viewed • Normal blood vessels in the angle include:
directly through the cornea, because light coming from the angle undergoes 1. radial iris vessels, portions of the arterial circle of the ciliary body
total internal reflection at the tear film-air interface. 2. vertical branches of the anterior ciliary arteries
• Because the index of refraction of glass or plastic is similar to that of the → oriented either radially along the iris or circumferentially (in a serpentine
cornea and tears, gonioscopy eliminates this interface and replaces it with a manner) in the ciliary body face
new lens-air interface set at a different angle to the emerging rays. Fuchs heterochromic iridocyclitis → fine, branching, unsheathed, meandering
• Indirect goniolens: Goldmann-type, Zeiss-type Neovascular glaucoma → trunklike vessels crossing the ciliary body and
• Direct goniolens: Koeppe, Barkan, Wurst, Richardson. scleral spur and arborizing over the trabecular meshwork.
• Angle landmarks: Schwalbe’s line and scleral spur → inferior portion • Gonioscopic examination
Posterior cornea pigmentation, guttata
• The width of the angle is determined by :
Schwalbe’s line thickening, anterior displacement
1. the site of insertion of the iris on the ciliary face
2. the convexity of the iris Trabecular meshwork pigmentation, PAS, inflammatory or neovascular
membranes, keratic precipitates
3. the prominence of the peripheral iris roll
Scleral spur iris processes
• The best method for describing the angle is a description or drawing of the
Ciliary body band width, regularity, cyclodialysis cleft
iris contour, the location of the iris insertion, and the angle between the iris
Iris contour, rubeosis, atrophy, cysts, iridodonesis
and the trabecular meshwork.
Pupil, lens exfoliation syndrome, posterior synechiae, position
• Gonioscopic grading systems and regularity, sphincter rupture, ectropion uveae
1. Shaffer system→ describes the angle between the iris and the surface of the
Zonular fibers pigmentation, rupture
trabecular meshwork
• Iris processes → follow the normal curve of the angle; the angle structures
• Grade IV 45˚
are visible in the open spaces between the processes
• Grade III 20-45˚

7 Sengdy Chandra Chauhari

 PAS → more solid or sheetlike; composed of iris stroma and obliterate the
angle recess
• Pigmentation of the trabecular meshwork
• increases with age; more marked in individuals with darkly pigmented iris
• can be segmental; most marked in the inferior angle; dynamic over time
• Conditions that cause increased anterior chamber angle pigmentation are
pigment dispersion, exfoliation syndrome, malignant melanoma, trauma,
surgery, inflammation, hyphema.
• Posttraumatic angle recession may be associated with monocular open-
angle glaucoma.
• Gonioscopic criteria for diagnosing angle recession
1. an abnormality wide ciliary body band
2. increased prominence of the sclera spur
3. torn iris processes
4. sclera visible through disrupted ciliary body tissue
5. marked variation of ciliary face width and angle depth in different
quadrants of the same eye
• Others findings that may be visible gonioscopically are microhyphema or
hypopyon, retained anterior chamber foreign body, iridodialysis, angle
precipitates suggestive of glaucomatocyclitic crisis, pigmentation of the lens
equator, other peripheral lens abnormalities, ciliary body tumors
The optic nerve
• Consists of approximately 1.2 million axons that are separated into fascicles,
with the intervening spaces occupied by astrocytes. The cell bodies of these
axons lie in the ganglion cell layer of the retina
Retinal ganglion cells
1. Magnocellular neurons (M cells)
• Approximately 10% of all ganglion cells.
• Have larger-diameter axons. Synapse in the magnocellular layer of the lateral
geniculate body.
• Are sensitive to luminance changes in dim illumination (scotopic conditions)
2. Parvocellular neurons (P cells)
• Approximately 90% of all ganglion cells
8 Sengdy Chandra Chauhari
• Have smaller-diameter axons, smaller receptive fields and slower conduction
velocity. Synapse in the parvocellular layer of the lateral geniculate body.
• Subserve color vision; are most active under higher luminance conditions;
discriminate fine detail.
Anatomy of retinal nerve fiber distribution
• Peripheral fibers run closer to choroid and exit in periphery of optic nerve,
while fibers originating closer to the nerve head are situated closer to the
vitreous and occupy a more central portion of the nerve.
The optic nerve branches of the short posterior ciliary artery (differ from its
branches in the choriocapillaries)
• They are surrounded by pericytes; lack fenestrations; have tight junction;
have the ability to autoregulate.
------------------------------THE OPTIC NERVE HEAD--------------------------------
• Composed of neural tissue, glial tissue, extracellular matrix and blood vessels
1. Nerve fiber layer
• Supported by astrocytes. Can be viewed with the ophthalmoscope using the
red-free (green) filter.
• Blood supply: the central retinal artery; the short posterior ciliary arteries
2. Prelaminar layer
• The depression in the center of the optic disc.
• Blood supply: the short posterior ciliary arteries
3. Laminar layer
• A fenestrated area of connective tissue (lamina cribrosa), through which
nerve fibers exit from the eye.
• Blood supply: the short posterior ciliary arteries.
• Lamina cribrosa appears as a series of approximately 10 stacked plates of
fenestrated connective tissue whose septae contain small blood vessels. The
gray dots that can sometimes be seen ophthalmoscopically in the depths of
the optic cup are the superficial openings of the lamina.
4. Retrolaminar layer
• The addition of the myelin sheath produced by oligodendrocytes doubles the
diameter of the nerve at this point.
• Blood supply: branches of the meningeal arteries and centrifugal branches
of the central retinal artery.

Early glaucomatous cupping
• Consists of loss of axons, blood vessels, and glial cells → seems to start at the
level of the lamina cribrosa (associated with compaction and fusion of the
laminar plates), most pronounced at the superior and inferior poles of the disc
More advanced glaucoma
• Tissue destruction extends behind the cribriform plate. Lamina bows
backward. The optic nerve head takes on an excavated and undermined
appearance.
Glaucomatous cupping in infants and children
• accompanied by an expansion of the entire scleral ring
→ may explain why cupping seems to occur earlier in children
→ may explain why reversibility of cupping is more prominent with
successful treatment in these cases
Theories of glaucomatous damage
1. Mechanical theory → direct compression of the optic nerve fibers against the
lamina cribrosa with interruption of axoplasmic flow
2. Ischemic theory → effects of IOP on the blood supply to the nerve
3. Disturbance of autoregulation (the optic nerve vessels normally increase or
decrease their tone to maintain a constant blood flow independent of IOP)
Examination of the optic nerve head
1. Direct ophthalmoscope
• Simple to learn. Inexpensive. Can provide a view of the optic disc through a
small pupil. Can provide a view of the nerve fiber layer on the posterior pole
(with red-free filter). Does not provide sufficient stereoscopic detail.
2. Indirect ophthalmoscope
• Is used for examining the optic disc in young children, uncooperative
patients, highly myopic individuals, and individuals with substantial opacities
of the media.
• The magnification is often inadequate for detecting subtle or localized details
important in the evaluation of glaucoma.
3. Slit-lamp biomicroscope combined with a Hruby lens; a posterior pole contact
lens; or a 60-, 78-, or 90- diopter lens.
9 Sengdy Chandra Chauhari
• Best method of examination for the diagnosis of glaucoma
• Provides high magnification, excellent illumination, and a stereoscopic view
of the disc. Require patient cooperation and moderate pupil size.
Early changes of glaucomatous optic neuropathy
1. Generalized enlargement of the cup
• By progressive posterior collapse and compaction of the remaining viable
nerve fibers
2. Focal enlargement of the cup
• Notching or narrowing of the rim
• Acquired optic disc pit formation (deep localized notching where the lamina
cribrosa is visible at the disc margin)
3. Superficial splinter hemorrhages
• Usually appears as a linear red streak on or near the disc surface
• Clears over several weeks to months. Repeated episodes.
• Individuals with NTG are particularly likely to have disc hemorrhages
• An important prognostic sign for the development or progression of visual
field loss
4. Loss of nerve fiber layer
• Appears as a pattern of striations that radiate toward the optic disc
• May be diffuse or localized to specific bundles
• With the development of glaucoma, the nerve fiber layer thins and becomes
less visible. Can be seen most clearly in high-contrast black-and-white
photographs
5. Translucency of the neuroretinal rim
• Can be observed in the early stages of nerve fiber loss
6. Development of vessel overpass
• Can be observed in circumstances where the neuroretinal tissue, but not the
overlying nerve head vasculature, has collapsed. The blood vessels overlying
the collapsed neural rim tissue appear like a highway overpass suspended
over, but not in contact with, the underlying tissue.
7. Asymmetry of cupping between the patient’s two eyes
Other less specific signs of glaucomatous damage include:
• Nasal displacement of the vessels
 • Narrowing of peripherally retinal vessels 7. Visually evoked cortical potentials (VECP) and electroretinography (ERG)
• Baring of the circumlinear vessels
With advanced damage the cup becomes pale and markedly excavated. Brief definitions of some of the major perimetric terms
Retinal nerve fiber layer defects • Threshold → the differential light sensitivity at which a stimulus of given size
1. Focal abnormalities: slitlike grooves or wedge defects and duration of presentation is seen 50% of the time (in practice, the dimmest
2. Diffuse nerve fiber loss → more common in glaucoma spot detected during testing)
• Suprathreshold → above the threshold (brighter than the threshold stimulus). A
---------------------------------THE VISUAL FIELD--------------------------------- stimulus may also be made suprathreshold by increasing the size or duration of
Visual field is “an island hill of vision in a sea of darkness” presentation.
The island of vision is usually described as a three-dimensional graphic • Kinetic testing → perimetry in which a target is moved from an area where it is
representation of differential light sensitivity at different positions in space. not seen toward an area where it is just seen.
Perimetry refers to the clinical assessment of the visual field. It has two major • Static testing → a stationary stimulus is presented at various locations (the
purposes in the management of glaucoma: brightness, size and duration of the stimulus can be varied at each location to
1. Identification of abnormal fields determine the threshold)
2. Quantitative assessment of normal or abnormal fields to guide follow-up care. • Isopter → a line on a visual field representation connecting points with the
Variety of methods to test visual functions same threshold
1. Differential light perimetry with white light • Depression → a decrease in retinal sensitivity
2. Blue/yellow perimetry • Scotoma → an area of decreased retinal sensitivity within the visual field
• Projects a blue stimulus onto a yellow background. surrounded by an area of greater sensitivity
• Sensitive in the early identification of glaucomatous damage.
3. High-pass resolution perimetry Typical glaucomatous defects
• The stimulus is a ring-shaped target that varies in size. It is made up of a dark 1. Paracentral scotoma
annulus with bright center and dark borders. The average luminance of this 2. Arcuate or Bjerrum scotoma
target is the same as the background. 3. Nasal step
• To determine spatial resolution thresholds. 4. Altitudinal defect
4. Frequency doubling perimetry 5. Temporal wedge
• Uses a low spatial frequency sinusoidal grating undergoing rapid phase-
reversal flicker. Variables in perimetry
• More sensitive in the detection of early glaucomatous loss. 1. Patient
5. Contrast sensitivity 2. Perimetrist
• Measures a subject’s ability to detect a pattern of alternating light and dark 3. Fixation
bands presented at varying frequencies and degrees of contrast. 4. Background luminance (4.0-31.5 apostilbs) → the luminance of the surface
6. Flicker sensitivity onto which the perimetric stimulus is projected affects retinal sensitivity and
• Measures the ability of the subject to recognize the difference between a thus the hill of vision.
flickering light from one that is constantly on. The contrast can be varied.

10 Sengdy Chandra Chauhari

5. Stimulus luminance → The brighter the stimulus, the more visible a given
stimulus
6. Size of stimulus (0 = 1/16 mm2; I = ¼ mm2; II = 1 mm2; III = 4 mm2; IV =
16 mm2; V = 64 mm2) → The larger the stimulus, the more likely it is to be
perceived.
7. Presentation time → The longer the presentation time, the more visible a
given stimulus
8. Patient refraction → Proper neutralization of refractive error is essential for
accurate perimetry
9. Pupil size → Testing with pupils smaller than 3 mm in diameter may induce
artifacts.
10. Wavelength of background and stimulus
11. Speed of stimulus movement → Temporal summation occurs over a time
period as long as 0.5 second
Automated static perimetry
• Computerized perimeter must be able:
1. To determine threshold sensitivity at multiple points in the visual field
2. To perform an adequate test in a reasonable amount of time
3. To present results in a comprehensive form.
• The best instruments currently available are bowl perimeters that project stimuli
in programmed locations
• Four general categories of testing strategy are currently in common use:
1. Suprathreshold testing. A stimulus, usually one expected to be a little
brighter than threshold, is presented at various locations and recorded as seen
or not seen. Sometimes, if it is not seen, it is presented again, and if not seen a
second time, is recorded as not seen. Then the stimulus may be presented at
maximum brightness to determine if a defect is relative or absolute. This type
of test is designed to screen for moderate to severe defects.
2. Threshold-related screening strategy records tested points as seen or not
seen. Screening is done at an intensity 6 dB brighter than the expected
threshold, and points missed twice at that level are recorded as defects. This
type of test will detect moderate to severe defects.
3. Full-threshold strategy determines retinal sensitivity at each tested point by
altering the stimulus intensity in 4-dB steps until the threshold is crossed.
11
This type of test is the current standard for automated perimetry in glaucoma
management.
4. SITA
Interpretation of a single field
1. Quality → The percentage of fixation losses, the false positives and false
negatives, and the fluctuations of doubly determined points (less than 2 dB in a
normal field, less than 3 dB in a field with early damage, less than 4 dB in a
field with moderate damage). Patient reliability can be evaluated by looking at
the least damaged areas in badly damaged visual field.
2. Normality or abnormality. When tested under photopic conditions, the normal
field demonstrates the greatest sensitivity centrally, with sensitivity falling
steadily toward the periphery. A cluster of two or more points depressed ≥5 dB
compared with surrounding points is suspicious. Corresponding points above
and below the horizontal midline should not vary markedly; normally the
superior field is depressed 1-2 dB compared with the inferior field.
3. Artifacts
• Lens rim
• Incorrect corrective lens
• Cloverleaf field. The Humphrey visual field perimeter test is designed so that
four circled points are checked initially and the testing in each quadrant
proceeds outward from these points. If the patient ceases to respond after only
a few points have been tested, the result is some variation of the cloverleaf
field.
• High false-positive rate. When a patient responds at a time when no test
stimulus is being presented, a false-positive response is recorded. False-
positive rates greater than 33% suggest unreliability of the test.
• High false-negative rate. When a patient fails to respond to a stimulus
presented in a location where a dimmer stimulus was previously seen, a false-
negative response is recorded. False-negative rates greater than 33% suggest
unreliability of the test.
Interpretation of a series of fields
1. Separating real change from ordinary variation
Sengdy Chandra Chauhari
2. Using the information from the field testing to determine the likelihood that a
change is related to glaucomatous progression.
Visual field progression
1. Deepening of an existing scotoma is suggested by the reproducible depression
of a point in an existing scotoma by ≥7 dB.
2. Enlargement of an existing scotoma is suggested by the reproducible depression
of a point adjacent to an existing scotoma by ≥9 dB.
3. Development of a new scotoma is suggested by the reproducible depression of a
previously normal point in the visual field by ≥11 dB, or of two adjacent
previously normal points by ≥5 dB.
Correlation of changes in the visual field with the optic disc is important if:
1. The patient’s optic disc seems less cupped than would be expected for the
degree of field loss
2. The pallor of the disc is more impressive than the cupping.
3. The progression of the visual field loss seems excessive
4. The pattern of visual field loss is uncharacteristic for glaucoma.

Manual perimetry
Goldmann perimetry using the Armaly-Drance screening technique
• Combines a kinetic examination of the peripheral isopters with a
suprathreshold static examination of the central field

Other tests
1. Fluorescein angiography
2. Corneal pachymetry
3. Measurement of episcleral venous pressure
4. Ophthalmodynamometry
5. Carotid noninvasive vascular studies
6. Ocular blood-flow measurements
7. Ultrasonography

12 Sengdy Chandra Chauhari

OPEN-ANGLE GLAUCOMA_____________________________
----------------PRIMARY OPEN-ANGLE GLAUCOMA (POAG) -----------------
• Chronic, slowly progressive optic neuropathy characterized by atrophy and
cupping of the optic nerve head and associated with characteristic patterns of
visual field loss.
• Clinical features: usually insidious in onset, slowly progressive and painless;
usually bilateral, quite asymmetric; visual loss generally progresses without
symptoms.
• Risk factors: elevated IOP, race (black), advanced age (>50), family history,
associated disorders (myopia, diabetes mellitus, cardiovascular disease, CRVO)
• Periodic evaluation of the optic disc and visual field is vital.
• Repeated gonioscopy is indicated to detect possible progressive angle closure
caused by miotic therapy or age-related lens changes (especially in hyperopic
patients), when the chamber becomes shallow, when strong miotics are
prescribed, after laser trabeculoplasty or iridectomy, and when IOP rises.
----------------------------THE GLAUCOMA SUSPECT-------------------------------
• Definition: an adult who has normal open angle on gonioscopy and one of the
following findings in at least one eye:
• An optic nerve or nerve fiber layer suggestive of glaucoma (enlarged cup/disc
ratio, asymmetric cup/disc ratio, notching or narrowing of the neural rim, disc
hemorrhage, or diffuse or local abnormality in the nerve fiber layer)
• A suspicious visual field abnormality
• An elevated IOP consistently greater than 22 mmHg.
• Usually, if two or more of these findings are present, the diagnosis of POAG is
supported, especially in the presence of other risk factors.
• Ocular hypertension: elevated IOP in the absence of identifiable optic nerve
damage or visual field loss.
--------------------NORMAL TENSION GLAUCOMA (NTG) ----------------------
• Elevated IOP is not the only risk factors in the development of glaucoma, but
other risk factors, most of which are currently unknown, may play a more
important role.
13
• Local vascular factors! Higher prevalence of vasospastic disorders such as
migraine headache and Raynaud phenomenon, ischemic vascular diseases,
autoimmune diseases and coagulopathies.
• Vascular autoregulatory defects!
• Reducing IOP by greater than 30% reduced the rate of visual field progression.
However, since progression was not affected in all patients, other factors may
be operative as well. Progression of the visual field loss tended to be slow.
• The temporal and inferotemporal neuroretinal rim are most affected early in
NTG, although other patterns of disc damage may also be observed.
• Classification of NTG based on disc appearance:
• A senile sclerotic group with shallow, pale sloping of the neuroretinal rim
(primarily in older patients with vascular disease)
• A focal ischemic group with deep, focal, polar notching in the neuroretinal
rim
• The visual field defects in NTG tend to be more focal, deeper and closer to
fixation, especially early in the course of the disease.
• Differential diagnosis
• Undetected high-tension glaucoma: POAG with diurnal IOP variation,
intermittent IOP elevation (ACG, glaucomatocyclitic crisis), previously
elevated IOP (old secondary glaucoma, normalized IOP in an eye with
previously elevated IOP), use of medication that may cause IOP lowering
(systemic beta blocker), tonometric error (reduced corneal thickness, low
scleral rigidity)
• Nonglaucomatous optic nerve disease: vascular occlusion, optic nerve head
drusen, optic nerve head pits and colobomas, chorioretinitis, retinal
detachment, retinoschisis, chiasmal tumors, anterior ischemic optic
neuropathy.
• Diagnostic evaluation: medical history, measurement of IOP by applanation
tonometry at various times during the day, gonioscopy, careful stereoscopic disc
evaluation. Medical and neurological evaluation.
• Criteria for initiating therapy: visual field loss threatening fixation, disc
hemorrhage, and documented visual field or optic nerve progression.
• Therapy: medications. If medications is inadequate in controlling the disease →
laser trabeculoplasty, glaucoma filtering surgery with or without antifibrotic
agent (5-fluorouracil or mitomycin-C)
Sengdy Chandra Chauhari
• Role of ‘neuroprotective’ agents such as calcium channel blockers, alpha2-
agonists, and NMDA (N-methyl-D-aspartate receptor) antagonist??
--------------------SECONDARY OPEN-ANGLE GLAUCOMA--------------------
• Exfoliation syndrome (pseudoexfoliation)
• Pigmentary glaucoma
• Lens-induced glaucoma (phacolytic glaucoma, lens particle glaucoma,
phacoanaphylaxis)
• Intraocular tumors
• Ocular inflammation (glaucomatocyclitic crisis, Fuchs heterochromic
iridocyclitis)
• Raised episcleral venous pressure
• Accidental and surgical trauma (hyphema, angle recession glaucoma,
cyclodialysis cleft, hemolytic and ghost cell glaucoma)
• Drugs
-----------EXFOLIATION SYNDROME (PSEUDOEXFOLIATION) -----------
• Characterized by the deposition of a distinctive fibrillar material in the anterior
segment of the eye (in and on the lens epithelium and capsule, pupillary margin,
ciliary epithelium, iris pigment epithelium, iris stroma and blood vessels,
inferior anterior chamber angle or Sampoelesi’s line, corneal endothelium and
subconjunctival tissue)
• This material probably arises from multiple sources as part of a generalized
basement membrane disorder. Histochemically, the material resembles amyloid.
• Other findings: targetlike pattern of deposits on the anterior lens capsule,
heavily pigmented trabecular meshwork, shallow chamber angle, peripupillary
atrophy, diffuse depigmentation of iris, phacodonesis, iridodonesis, zonular
weakness, abnormalities of the iris vessels.
• Monocular (the unvolved fellow eye may develop the syndrome at a later time)
or binocular with varying degrees of asymmetry. Age related (>70)
• The open-angle glaucoma associated with exfoliation syndrome is thought to be
caused by the fibrillar material obstructing flow through and causing damage to
the trabecular meshwork.
14
• Exfoliation syndrome with glaucoma differs from POAG in often being
monocular and showing greater pigmentation of the trabecular meshwork and
higher IOP. The overall prognosis is worse.
• Laser trabeculoplasty → effective, but the response may not be long lasting.
• Lens extraction → does not alleviate the condition.
• Trabeculectomy → an increase in postoperative inflammation.
• Increased ocular inflammation can be seen following all ocular surgery in
patients with this condition.
-----------------------------PIGMENTARY GLAUCOMA------------------------------
• Occurs in approximately 25-50% of patients with pigment dispersion syndrome
• Occurs most commonly in myopic males between the ages of 20 and 50 years.
• Affected females tend to be older than affected males.
• Characterized by wide fluctuations in IOP.
• High IOP often occurs when pigment is released into the aqueous humor, such
as following exercise or pupillary dilation.
• Symptoms: haloes, intermittent visual blurring, ocular pain.
• Treatment: medication, laser trabeculoplasty, filtering surgery
• Laser iridectomy can minimize posterior bowing of the iris; most often applied
in eyes with pigment dispersion and ocular hypertension or early glaucomatous
optic neuropathy.
Pigment dispersion syndrome________________________________________
• Pigment deposition on the corneal endothelium in a vertical spindle pattern
(Krukenberg spindle), in the trabecular meshwork, and on the lens periphery.
• Classic spokelike iris transillumination defects
• The spindle pattern on the posterior cornea is caused by the aqueous convection
currents and subsequent phagocytosis of pigment by the corneal endothelium.
• Krukenberg spindle may occur in other diseases such as exfoliation syndrome.
• With age, the signs and symptoms of pigmentary dispersion may decrease in
some individual. Possible causes are normal growth the lens, increase in
physiologic pupillary block, and loss of accommodation.
Gonioscopy
1. Homogenous, densely pigmented trabecular meshwork with a speckled ring
of pigment at or anterior to Schwalbe’s line
Sengdy Chandra Chauhari
 2. Posterior bowing of the midperipheral iris with ‘reverse pupillary block’
(→ greater contact of the zonular fibers with the posterior iris surface →
increase of pigment release)
3. When dilated, pigment deposits can be seen on the lens zonules and both
the anterior and posterior lens capsule.
------------------------------PHACOLYTIC GLAUCOMA------------------------------
• Pathogenesis: leakage of high-molecular weight lens protein through the
capsule of a mature or hypermature cataract → the proteins precipitate an
inflammatory reaction → lens material-filled macrophages and other
inflammatory debris obstruct the trabecular meshwork → secondary glaucoma
• Clinical picture: usually involves an elderly patient with a history of poor
vision who has sudden onset of pain, conjunctival hyperemia, and worsening
vision.
• Examination reveals an elevated IOP of 30-50mmHg, microcystic corneal
edema, prominent cell and flare reaction without KP, and open anterior chamber
angle. Wrinkling of the anterior lens-capsule. Cellular debris and white particles
can be seen in the anterior chamber angle. Hypopyon may be present.
• The lack of KP helps distinguish phacolytic glaucoma from phacoanaphylaxis.
• Therapy: medications and cataract extraction.
----------------------------LENS PARTICLE GLAUCOMA----------------------------
• Occurs when the lens cortex obstructs the trabecular meshwork following
cataract extraction, capsulotomy or ocular trauma.
• The extent of the glaucoma depends on:
1. The quantity of lens material released
2. The extent of inflammatory response
3. The preexisting ability of the trabecular meshwork to clear the lens material
4. The functional status of the ciliary body which is often altered following
surgery or trauma.
• Usually occurs within weeks of the initial surgery or trauma, but it may occur
months or years later.
• Clinical findings: free cortical materior in the anterior chamber, elevated IOP,
moderate anterior chamber reaction, microcystic corneal edema, and with time,
the development of posterior and peripheral anterior synechia.
15
• Therapy: medications while the residual lens material resorbs (aqueous
suppressants, mydriatics to inhibit PAS, and topical corticosteroids). If the
glaucoma can’t be controlled, surgical removal of the lens material is necessary.
--------------------------------PHACOANAPHYLAXIS----------------------------------
• Pathogenesis: sensitization to own lens protein following surgery or penetrating
trauma → granulomatous inflammation.
• Clinical pictures: moderate anterior chamber reaction with KP on both the
corneal endothelium and the anterior lens surface; low-grade vitritis, synechial
formation, residual lens material in the anterior chamber.
• Treatment: corticosteroids, aqueous suppressants. If medical therapy is
unsuccessful, residual lens material should be removed.
• Glaucoma, while it may occur, is not common in eyes with phacoanaphylaxis.
------------------------------INTRAOCULAR TUMORS--------------------------------
• Glaucoma can result from several different mechanisms:
1. Direct tumor invasion of the anterior chamber angle (e.g., primary or
metastatic tumors of the ciliary body0
2. Angle closure by rotation of the ciliary body or by anterior displacement
of the lens-iris diaphragm (e.g., choroidal melanomas, other choroidal
and retinal tumors)
3. Intraocular hemorrhage
4. Neovascularization of the angle (e.g., choroidal melanomas, medulloepi-
theliomas, retinoblastomas)
5. Deposition of tumor cells, inflammatory cells, and cellular debris within
the trabecular meshwork
• Tumors causing glaucoma in adults include uveal melanoma, metastatic
carcinoma, lymphomas, and leukemia.
• Glaucoma in children is associated with retinoblastoma, juvenile
xanthogranuloma, and meduloepithelioma.
---------------------------INFLAMMATORY GLAUCOMA---------------------------
• A secondary glaucoma that often combines components of open-angle and
angle-closure disease
Sengdy Chandra Chauhari
• Occurs when the trabecular dysfunction exceeds the accompanying ciliary body
hyposecretion seen with acute inflammation.
• Causes by a variety of mechanisms
1. Edema of the trabecular meshwork
2. Endothelial cell dysfunction
3. Blockage of the trabecular meshwork by fibrin and inflammatory cells
4. Prostaglandin-mediated breakdown of the blood-aqueous barrier.
• The presence of KP and a miotic pupil suggests iritis as the cause of IOP
elevation.
• Gonioscopic evaluation may reveal subtle trabecular meshwork precipitates.
• Sometimes, PAS or posterior synechia with iris bombe may develop, resulting
in angle closure.
• Treatment: corticosteroid → may raise IOP
• Miotic agents should be avoided in patients with iritis, because they may
aggravate the inflammation and cause posterior synechia.
GLAUCOMATOCYCLITIC CRISIS (POSNER-SCHLOSSMAN syndrome)
• Characterized by:
1. Recurrent bouts of markedly increased IOP. The IOP is usually markely
elevated, in the 40-50 mmHg range. In between bouts the IOP usually
returns to normal, but with increasing numbers of attacks, a chronic
secondary glaucoma may develop.
2. Low-grade anterior chamber inflammation. The iritis is mild with few
KP that are small, discreet, and round in nature and usually resolve
spontaneously within a few weeks. KP may be seen on the trabecular
meshwork on gonioscopy, suggesting a ‘trabeculitis’.
• Affects middle-aged patients and usually presents with unilateral blurred vision
and mild eye pain.
• The etiology remains unknown. Prostaglandin-mediated mechanism!
-----------------FUCHS HETEROCHROMIC IRIDOCYCLITIS-------------------
• Characterized by:
1. Iris heterochromia (with loss of iris pigment in the affected eye)
2. Low-grade anterior chamber reaction with small, stellate KP
3. Posterior subcapsular cataracts
16
4. Secondary open-angle glaucoma
• The condition is insidious and unilateral, affecting the hypochromic eye, and
presents equally in middle-aged men and women.
• The secondary open-angle glaucoma occurs in approximately 15% of cases.
• Gonioscopy reveals multiple fine vessels that cross the trabecular meshwork.
These vessels do not appear to be associated with a fibrous membrane and
usually do not lead to PAS and secondary angle closure. They are fragile and
may cause an anterior chamber hemorrhage.
• The glaucoma does not correspond to the degree of inflammation and may be
difficult to control. Corticosteroids are generally not effective. Aqueous
suppressants and alpha2-agonists are the agents of choice.
-------------------RAISED EPISCLERAL VENOUS PRESSURE-------------------
• Normal episcleral venous pressure is approximately 9 mmHg.
• Causes of increased episcleral pressure
1. Arteriovenous malformations (arteriovenous carotid-dural fistula,
orbital varix, Sturge-Weber syndrome).
2. Venous obstruction (retrobulbar tumor, thyroid ophthalmopathy).
3. Superior vena cava syndrome
• Clinical features: tortuous, dilated episcleral veins. Anterior segment appears
normal in most of these patients, except for elevated IOP and the gonioscopic
finding of blood in Schlemm’s canal.
• Medications that reduce aqueous humor formation are more effective than
drugs that increase aqueous outflow. Laser trabeculoplasty is not effective
unless there are secondary changes in the outflow channels. Glaucoma filtering
surgery may be complicated by ciliochoroidal effusions or suprachoroidal
hemorrhage.
----------------------ACCIDENTAL and SURGICAL TRAUMA--------------------
• Nonpenetrating, or blunt, trauma to the eye causes a variety of anterior segment
injuries: hyphema, angle recession (cleavage), iridodialysis, iris sphincter tear,
cyclodialysis, and lens subluxation.
• Elevated IOP after blunt trauma may occur by several mechanisms
1. Posttraumatic inflammation
2. Presence of blood and degenerative red blood cells (ghost cells)
Sengdy Chandra Chauhari
 3. Direct injury to the trabecular meshwork.
This elevation tends to be short in duration but may be protracted with the risk
of corneal blood staining and glaucomatous optic nerve damage.
• Acute secondary glaucoma caused by chemical injuries may result from:
1. Inflammation
2. Shrinkage of scleral collagen
3. Release of chemical mediators such as prostaglandins
4. Direct damage to the chamber angle
5. Compromise of the anterior uveal circulation
Trabecular damage or inflammation may cause glaucoma to develop months or
years after a chemical injury.
• Open-angle glaucoma is one of the long-term sequelae of siderosis or chalcosis
from a retained intraocular metallic foreign body in penetrating or perforating
injuries.
--------------TRAUMATIC or ANGLE-RECESSION GLAUCOMA--------------
• An angle recession, or cleavage, is a tear in the ciliary body that splits between
the longitudinal and circular muscle fibers. Angle recessions are often
associated with tears in the trabecular meshwork as well.
• Angle-recession glaucoma is a chronic, unilateral secondary open-angle
glaucoma that usually occurs months to years following ocular trauma.
• Classic gonioscopic findings
1. Broad angle recess
2. Absent or torn iris process
3. White glistering scleral spur
4. Depression in the overlying trabecular meshwork
5. Localized PAS at the border of the recession.
• The development of secondary glaucoma depends on:
1. The degree of angle involvement
2. Underlying patient predisposition
• Treatment: aqueous suppressants, alpha2-agonists. Miotics may be useful, but
paradoxical responses with increased IOP may occur. Laser trabeculoplasty has
a limited role and a low chance of success but may be considered prior to
filtering surgery.
17
-------------------------------CYCLODIALYSIS CLEFT--------------------------------
• Definition: focal area of separation of the ciliary body from its attachment to
the scleral spur.
• When a cyclodialysis cleft is present, the eye is often hypotonus. The
mechanism of hypotony is:
1. Increased uveoscleral outflow through the cleft into suprachoroidal space
2. Possibly reduced aqueous production as a result of vascular compromise
to the ciliary processes.
• Closure of a cyclodialysis cleft may cause long-term elevation of IOP and
glaucoma. Treatment is similar to POAG.
----------------------------------------HYPHEMA-------------------------------------------
• Increased IOP is a result of:
1. Obstruction of the trabecular meshwork with red blood cells,
inflammatory cells, debris and fibrin
2. Direct injury to the trabecular meshwork from the blunt trauma
• Increased IOP is more common following recurrent hemorrhage or rebleeding
following a traumatic hyphema. Rebleeding usually occurs within 5-7 days after
the initial hyphema and may be related to normal clot retraction and lysis. The
size of the hyphema associated with rebleeding is greater than the primary
hyphema. The larger the hyphema, the higher the incidence of increased IOP.
• Individuals with sickle cell hemoglobinopathies have an increased incidence of
glaucoma following hyphema. The RBCs tend to sickle in the aqueous humor,
and these more rigid cells have great difficulty passing out of the eye through
the trabecular meshwork. The optic discs of these patients are much more
sensitive to elevated IOP and are prone to ischemic injury as a result of
compromised microvascular perfusion.
• Management of uncomplicated hyphema
1. Eyeshield (patching), limited activity (bed rest), head elevation.
2. Topical and systemic corticosteroids → may reduce associated
inflammation
3. Cycloplegic agents → if significant ciliary spasm or photospasm occurs
4. Aminocaproic acid → reduce rebleeding
• Management of elevated IOP in hyphema
1. Aqueous suppressants
Sengdy Chandra Chauhari
 2. Alpha2-agonists
3. Hyperosmotic agents
• CAIs should be avoided in sickle cell hemoglobinopathies because they
may increase the sickling tendency in the anterior chamber by increasing
aqueous levels of ascorbic acid.
• Adrenergic agonists with significant alpha1 effects (apraclonidine,
dipivefrin, epinephrine) should be avoided in sickle cell disease.
• Parasympathomimetic agents should be avoided in all hyphema patients.
• Management of persistently elevated IOP
1. Anterior chamber irrigation or washout procedure.
2. Iridectomy → if a total hyphema is present, to relieve pupillary block.
3. Trabeculectomy.
-----------------HEMOLYTIC and GHOST CELL GLAUCOMA------------------
• May develop after vitreous hemorrhage.
• Hemolytic glaucoma
→ hemoglobin-laden macrophages block the trabecular outflow channels
→ red-tinged cells are seen floating in the anterior chamber
→ a reddish brown discoloration of the trabecular meshwork is often present
• Ghost cell glaucoma is a transient secondary open-angle glaucoma caused by
degenerated RBCs (ghost cells) blocking the trabecular meshwork
• Ghost cell
1. RBCs that have lost their intracellular hemoglobin and appear as small
khaki-colored cells that are less pliable than normal RBCs → Obstruction
of the trabecular meshwork → Secondary glaucoma.
2. The cells develop within 1-3 months following a vitreous hemorrhage.
3. They gain access to the anterior chamber through a disrupted hyaloid
face, which can occur from previous surgery (pars plana vitrectomy,
cataract extraction, or capsulotomy), trauma, or spontaneous disruption.
• Clinical features of ghost cell glaucoma
1. Increased IOP and history of a recent vitreous hemorrhage resulting from
trauma, surgery, or preexisting retinal disease.
2. The anterior chamber is filled with small circulating tan-colored cells.
3. The cellular reaction appears out of proportion to the aqueous flare.
18
4. The conjunctiva tends not to be inflamed unless the IOP is markedly
elevated.
5. Gonioscopically, the angle appears normal except for the layering of
ghost cells over the trabecular meshwork inferiorly.
6. The vitreous has the appearance of old hemorrhage with characteristic
khaki coloration and clumps of extracellular pigmentation from
degenerated hemoglobin.
• Both are generally self-limiting and resolve once the hemorrhage has cleared.
• Treatment: Aqueous suppressants. If failed, consider irrigation of the anterior
chamber, pars plana vitrectomy, and/or trabeculectomy.
-----------------------------------SURGICAL TRAUMA----------------------------------
• Operative procedures and laser surgery may be complicated by posttreatment
IOP elevation. This elevation is usually transient, lasting from a few hours to a
few days.
• Mechanisms of elevated IOP following surgery
1. Pigment release.
2. Presence of inflammatory cells and debris
3. Mechanical deformation of the trabecular meshwork and angle closure
• Agents used as adjuncts to intraocular surgery such as viscoelastic substances
may cause secondary IOP elevations. Dispersive viscoelastics (sodium
hyaluronate) may be more likely to cause IOP increases than retentive
viscoelastic agents (chondroitin sulfate).
• Elevated IOP may increase the risk of retinal and optic nerve ischemia and
cause damage in susceptible individual even in a short time. Thus, measurement
of IOP soon after surgery or laser treatment is important. If a substantial rise in
IOP does occur, therapy with beta-blockers, alpha2-agonists, or CAIs is
required.
• The implantation of an intraocular lens (IOL) can lead to a variety of
secondary glaucomas
1. Uveitis-hyphema-glaucoma syndrome (UGH syndrome)
2. Secondary pigmentary glaucoma
3. Pseudophakic pupillary block
Sengdy Chandra Chauhari
• UGH syndrome
1. A form of secondary inflammatory glaucoma caused by chronic irritation
that is usually the result of a malpositioned anterior chamber IOL (the
chafing of the iris by the IOL or erosion of the lens haptics through the iris
or ciliary body).
2. Characterized by chronic inflammation, secondary iris neovascularization,
and recurrent hyphemas.
3. May also occur following implantation of a posterior chamber or suture-
fixated IOL.

-------------GLAUCOMA and PENETRATING KERATOPLASTY-------------

• Mechanisms of secondary glaucoma following penetrating keratoplasty
1. Open angle: inflammatory, corticosteroid induced, viscoelastic, wound
distortion of trabecular meshwork, fibrous/epithelial ingrowth
2. Closed angle: chronic PAS (angle closure), pupillary block, in
association with corticosteroid use, fibrous/epithelial ingrowth,
inflammatory
• Attempts to minimize these secondary glaucomas
1. Oversized donor grafts
2. Peripheral iridectomies
3. Surgical repair of the iris sphincter

--------------------------------DRUGS and GLAUCOMA--------------------------------

• Corticosteroid-induced glaucoma
• An open-angle glaucoma caused by prolonged use of topical, periocular,
inhaled, or systemic corticosteroids.
• It mimics POAG in its presentation and clinical course.
• The duration of time before the IOP rises and the extent of this rise depends
on: 1. the type and potency of the agent
2. the means and frequency of its administration
3. the susceptibility of the patient
• The elevated IOP is a result of an increased resistance to aqueous outflow in
the trabecular meshwork.
• Cycloplegic drugs can increase IOP in individuals with open angles.

19 Sengdy Chandra Chauhari

ANGLE-CLOSURE GLAUCOMA_________________________
------MECHANISMS and PATHOPHYSIOLOGY of ANGLE CLOSURE-----
• Angle closure develops because apposition of the iris to the trabecular
meshwork blocks the drainage of aqueous humor.
• The mechanisms of angle closure fall into 2 general categories
1. Mechanisms that push the iris forward from behind
2. Mechanisms that pull the iris forward into contact with the trabecular
meshwork
• The most frequent cause of angle closure is pupillary block.
Pupillary block → obstruction of aqueous flow from the posterior chamber
through the pupil → pressure gradient between the posterior and anterior
chambers → forward bowing of the peripheral iris against the trabecular
meshwork → closure of the anterior chamber angle.
• Angle closure may also occur without pupillary block. The lens-iris diaphragm
can be pushed or rotated forward by several mechanisms:
1. Ciliary body swelling, inflammation, or cysts.
2. Aqueous misdirection (malignant or ciliary block glaucoma)
3. Posterior segment tumors
4. Contracting retrolental tissue
5. Scleral buckling procedures
6. Conditions predisposing to ciliochoroidal effusions (panretinal
photocoagulation and nanophthalmos)
Angle closure can occur when the iris is pulled forward by contraction of a
membrane or fibrovascular tissue, as with inflammation, neovascularization, or
endothelial proliferation closing the anterior chamber angle.
-------------------PRIMARY ANGLE-CLOSURE GLAUCOMA--------------------
• Pathophysiology
1. small anterior segments and short axial length → relative pupillary block
2. age heightens the risk of relative pupillary block, as the lens grows and
iridolenticular contact increases
An angle-closure attack is often precipitated by some minor event, such as
pupillary dilation. The dilation to midposition relaxes the peripheral iris so
that it may bow forward, coming into contact with the trabecular meshwork;
20
in this position lens-iris apposition is maximal, setting the stage for pupillary
block and subsequent angle closure.
ACUTE PRIMARY ANGLE-CLOSURE GLAUCOMA__________________
• Occurs when IOP rises rapidly as a result of relatively sudden blockage of the
trabecular meshwork by the iris.
• Symptoms: pain, blurred vision, rainbow-colored haloes around lights, nausea
and vomiting.
• Signs: high IOP; middilated, sluggish and often irregular pupil; corneal
epithelial edema; congested episcleral and conjunctiva blood vessels; shallow
anterior chamber; a mild amount of aqueous flare and cells.
• Definitive diagnosis depends on the gonioscopic verification of angle closure.
Compression gonioscopy is required to determine if the iris-trabecular
meshwork blockage is reversible (appositional closure) or irreversible
(synechial closure) and it may be therapeutic in breaking the attack of acute
angle closure.
• Acute attack (high IOP) may cause:
1. glaucomatous optic nerve damage and/or retinal vascular occlusion
2. peripheral anterior synechiae (PAS)
3. sector atrophy of the iris → releases pigment and causes pigmentary
dusting of the iris surface and corneal endothelium.
4. ischemia of the iris sphincter muscle → causes the pupil to become
permanently fixed and dilated.
5. glaukomflecken (small anterior subcapsular lens opacities)
• Treatment
• Definitive treatment is an iridectomy, laser or surgical.
• Mild attacks may be broken by cholinergic agents (pilocarpine 1%-2%),
which induce miosis that pulls the peripheral iris away from the trabecular
meshwork.
• Stronger miotics should be avoided, as they may increase the vascular
congestion of the iris or rotate the lens-iris diaphragm more anteriorly,
increasing the pupillary block. However, when the IOP is quite elevated, the
pupillary sphincter may be ischemic and unresponsive to miotic agents alone.
• The patient should be treated with some combination of a topical beta-
blockers; alpha2-agonists; an oral, topical, or intravenous CAI; and, when
Sengdy Chandra Chauhari
 necessary, a hyperosmotic agent. This treatment is used to reduce IOP to the
point where the miotic agent will constrict the pupil and open the angle.
• Globe compression and compression gonioscopy may also treat acute ACG.
• Nonselective adrenergic agonists or medications with significant alpha1-
adrenergic activity (apraclonidine) should be avoided to prevent further
pupillary dilation and iris ischemia.
• Laser iridectomy is the treatment of choice for angle closure glaucoma
secondary to pupillary block. Surgical iridectomy is indicated when laser
iridectomy cannot be accomplished. Once an iridectomy has been performed,
pupillary block is relieved and the iris is no longer pushed forward into
contact with the trabecular meshwork, as the pressure gradient between the
posterior and anterior chambers approaches zero. If a laser iridectomy cannot
be performed, the acute attack may rarely be stopped by flattening the
peripheral iris through iridoplasty or by relieving pupillary block with laser
pupilloplasty.
• Once the attack is broken, a peripheral iridectomy should be performed as
soon as possible. Following resolution of the acute attack, it is important to
reevaluate the angle by gonioscopy for persistent residual angle closure that
may be amenable to laser gonioplasty.
• The IOP may remain low for weeks following acute ACG because of ciliary
body ischemia and poor aqueous production, and it is a poor indicator of
angle function or anatomy. Repeat or serial gonioscopy is therefore
essential.
• Fellow eye
• Shares the anatomic predisposition for increased pupillary block. Gonioscopy
usually reveals a narrow, occludable angle. At high risk for developing acute
angle closure.
• The pain and emotional upset resulting from the involvement of the first eye
may increase sympathetic flow to the fellow eye and produce pupillary
dilation.
• Peripheral iridectomy is recommended if a similar angle configuration is
present. If it is not, specific secondary ACGs must be strongly considered in
the differential diagnosis.
• An untreated fellow eye has a 40%-80% chance of developing an acute attack
of angle closure over the next 5-10 years.
21
SUBACUTE (INTERMITTENT, PRODROMAL) ANGLE-CLOSURE GLAUCOMA
• Characterized by episodes of blurred vision, haloes, and mild pain caused by
elevated IOP. These symptoms resolve spontaneously, especially during sleep-
induced miosis. IOP is usually normal between the episodes, which occur
periodically over days or weeks.
• The typical history and the gonioscopic appearance of a narrow chamber angle
help establish the diagnosis
• Laser iridectomy is the treatment of choice.
• This condition can progress to chronic ACG or to an acute attack that does not
resolve spontaneously.
CHRONIC ANGLE-CLOSURE GLAUCOMA_________________________
• May develop either after acute angle closure in which synechial closure persists
or when the chamber angle closes gradually and IOP rises slowly as enough
angle is compromised.
• The clinical course resembles that of open-angle glaucoma in its lack of
symptoms, modest elevation of IOP, progressive cupping of the optic nerve
head, and characteristic glaucomatous loss of visual field.
• Permanent PAS are present, as determined by indentation gonioscopy.
• Even if miotics and other agents lower IOP, iridectomy is necessary to relieve
the pupillary block and prevent further permanent synechial angle closure.
Without iridectomy, closure of the angle progresses and becomes irreversible.
• Laser iridectomy is the treatment of choice.
• Argon laser gonioplasty or goniosynechialysis may be helpful in extensive
PAS and elevated IOP following acute angle closure.
THE NARROW ANTERIOR CHAMBER ANGLE_____________________
• Provocative tests are designed to precipitate a limited form of angle closure,
which can then be detected by gonioscopy and IOP measurement. The methods
commonly used include pharmacologic pupillary dilation and prone-darkroom
testing. An IOP increase of 8 mmHg or more is considered positive. An
asymmetric pressure rise between the two eyes with a corresponding degree of
angle closure is also considered a positive sign.
• Various factors that cause pupillary dilation may induce ACG
Sengdy Chandra Chauhari
 1. Drugs: mydriatics and miotics.
2. Pain, emotional upset, or fright.
• The effect of miotics is to pull the peripheral iris away from the chamber angle.
However, miotics also cause the zonular fibers of the lens to relax, allowing the
lens to come forward. Furthermore, their use results in an increase in the
amount of iris-lens contact, thus potentially increasing pupillary block.
• Alpha-blockers (moxisylyte or thymoxamine, dapiprazole) can reverse the
effects of sympathomimetic dilating agents and minimize the chances of angle
closure → used as a diagnostic test for combined-mechanism glaucoma.
--------------------------------------PLATEAU IRIS----------------------------------------
• Caused by anteriorly positioned ciliary processes that critically narrow the
anterior chamber recess by pushing the peripheral iris forward. Following
dilation of the pupil, the peripheral iris bunches up and obstructs the trabecular
meshwork.
• Should be suspected if:
1. The central anterior chamber seems unusually deep and the iris plane
appears rather flat for an eye with angle closure.
2. Angle closure occurs in younger myopic patients.
• Can be confirmed with ultrasound biomicroscopy.
• Treatment
1. Iridectomy → for plateau iris configuration.
2. Long-term miotic therapy → for plateau iris syndrome.
3. Laser peripheral iridoplasty → for plateau iris syndrome, to thin the
peripheral iris.
----SECONDARY ANGLE-CLOSURE GLAUCOMA with PUPILLARY BLOCK-----
• Lens-induced ACG
1. Phacomorphic glaucoma
2. Ectopia lentis
3. Aphakic or pseudophakic ACG
• Nonrhegmatogenous retinal detachment
PHACOMORPHIC GLAUCOMA____________________________________
• Definition: secondary ACG arises from a swollen lens.
22
• The process is much more rapid and is precipitated by marked lens swelling
(intumescence) as a result of cataract formation and the development of
pupillary block in an eye anatomically not disposed to closure.
• (PACG → the process tends to occur slowly in hyperopes who undergo
progressive shallowing of the anterior chamber as a result of increasing
anterior-posterior lens diameter)
• Disparities between the two eyes in the anterior chamber depths and degree of
cataract should suggest a phacomorphic process.
ECTOPIA LENTIS_________________________________________________
• Definition: displacement of the lens from its normal anatomic position.
• Common causes: trauma, Marfan syndrome, homocystinuria, microsphero-
phakia, Weill-Marchesani syndrome.
• Anterior displacement of the lens → pupillary block → iris bombe →
shallowing of the anterior chamber → secondary ACG.
• May present clinically as acute or chronic ACG.
• Laser iridectomy is the treatment of choice.
• Lens extraction is indicated if pupillary block is not relieved or when the
anterior chamber progressively shallows following laser iridectomy.
APHAKIC or PSEUDOPHAKIC ANGLE-CLOSURE GLAUCOMA_______
• Pupillary block in aphakic and pseudophakic eyes
1. An intact vitreous face can block the pupil and/or an iridectomy in aphakic or
pseudophakic eyes or in phakic eyes with dislocated lenses.
2. Shallow anterior chamber and iris bombe
3. Mydriatics → may restore the aqueous flow through the pupil
4. Topical beta blockers, alpha-2 agonists, CAIs and hyperosmotic agents →
can be effective in reducing the IOP
5. Laser iridectomy!
• Pupillary block with anterior chamber IOL
1. Pupillary block develops with apposition of the iris, vitreous face, and/or lens
optic. The lens haptic or vitreous may obstruct the iridectomy or the pupil,
and the peripheral iris bows forward around the anterior chamber IOL to
occlude the chamber angle. The central chamber remains deep in this
Sengdy Chandra Chauhari
 instance, because the lens haptic and optic prevents the central portions of the NEOVASCULAR GLAUCOMA______________________________________
iris and vitreous face from moving forward. • Characterized by fine arborizing blood vessels on the surface of the iris and
2. Laser iridectomies trabecular meshwork, which are accompanied by a fibrous membrane. The
• Pupillary block after extracapsular cataract extraction contraction of the fibrovascular membrane results in the formation of PAS,
1. if an iridectomy has not been performed at the time of surgery → when the leading to the development of secondary ACG.
iris forms adhesions to a posterior chamber IOL or to the residual anterior or • Disorders predisposing to neovascularization of the iris and angle
posterior capsule. 1. Systemic vascular disease: carotid occlusive disease, carotid artery ligation,
2. when retained viscoelastic or fluid in the capsular bag pushes a posterior carotid cavernous fistula, giant cell arteritis, Takayasu (pulseless) disease
chamber IOL anteriorly 2. Ocular vascular disease: diabetic retinopathy, CRVO, CRAO, BRVO, SCR,
Coats disease, Eales disease, ROP, PHPV, syphilitic vasculitis, anterior
NONRHEGMATOGENOUS RETINAL DETACHMENT________________ segment ischemia
• The subretinal fluid accumulates and progressively pushes the retina forward 3. Other ocular disease: chronic uveitis, chronic retinal detachment, endophthal-
against the lens like a hydraulic press. The fluid or hemorrhage may accumulate mitis, Stickler syndrome, retinoschisis
rapidly, and as it pushes the bullous retinal detachment forward to a retrolenti- 4. Intraocular tumors: uveal melanoma, metastatic carcinoma, retinoblastoma,
cular position, it can flatten the anterior chamber completely. reticulum cell sarcoma
5. Ocular therapy: radiation therapy
------------------SECONDARY ANGLE-CLOSURE GLAUCOMA --------------- 6. Trauma
without PUPILLARY BLOCK • Classic pattern of neovascularization of the anterior segment: Fine vascular
Mechanisms of secondary angle closure tufts at the pupil that then extend radially over the iris, crosses the ciliary body
1. Contraction of a membrane, band, or exudate in the angle, leading to PAS and scleral spur as fine single vessels that then branch as they reach and involve
2. Forward displacement of the lens-iris diaphragma, often accompanied by the trabecular meshwork (reddish coloration). With contraction of the
swelling and anterior rotation of the ciliary body fibrovascular membrane, PAS develop and coalesce, gradually closing the
• Neovascular glaucoma angle. The PAS end at Schwalbe’s line because the fibrovascular membrane
• Iridocorneal endothelial (ICE) syndrome cannot grow over healthy corneal endothelium (distinguishing this condition
• Tumors from other secondary ACGs that result from an abnormal corneal endothelium
• Inflammation such as ICE syndrome)
• Aqueous misdirection • Clinical features: often present with an acute glaucoma.
• Epithelial and fibrous downgrowth • The most common cause of iris neovascularization is ischemic retinopathy.
• Trauma 1. Panretinal photocoagulation is the treatment of choice when the ocular
• Retinal surgery and retinal vascular disease media are clear. The resulting decrease in neovascularization after retinal
• Nanophthalmos ablation may reduce or normalize the IOP, depending on the degree of
synechial closure that has occurred. This procedure may improve the success
• Fuchs corneal endothelial dystrophy
rate of filtering surgery by eliminating the angiogenic stimulus and decrease
• Retinopathy of prematurity
the risk of hemorrhage at the time of surgery.
• Flat anterior chamber

23 Sengdy Chandra Chauhari

 2. Medical therapy (topical beta blockers, alpha2-agonists, CAIs, cycloplegics
and corticosteroids) may be useful in reducing IOP and decreasing
inflammation.
3. Filtering surgery has a better chance of success once neovascularization has
regressed after panretinal photocoagulation. The use of the antimetabolites 5-
fluorouracil and mitomycin-C may increase the success rate. Tube-shunt
operations can also be effective in controlling the IOP.
4. Cyclodestructive procedure.
IRIDOCORNEAL ENDOTHELIAL (ICE) SYNDROME_________________
• Definition: a group of disorders characterized by abnormal corneal endothelium
that causes variable degrees of iris atrophy, secondary ACG, and corneal
edema.
• Three clinical variants
1. Chandler syndrome
2. Progressive iris atrophy
3. Cogan-Reese syndrome
→ The corneal endothelium appears abnormal and takes on a beaten bronze
appearance. Specular microscopy!
• Clinical features: Unilateral, presents between 20 and 50 years of age, occurs
more often in women. Decreased vision, pain or abnormal iris appearance.
Microcystic corneal edema may be present without elevated IOP, especially in
Chandler syndrome. The unaffected eye may have subtle changes of the corneal
endothelium without other manifestations of the disease.
• High PAS are characteristic of ICE syndrome (often extend anterior to
Schwalbe’s line). The PAS are caused by the contraction of the single layer of
endothelial cells and surrounding collagenous-fibrillar tissue that extend from
the peripheral cornea over the trabecular meshwork and iris. The PAS result in
synechial closure of the anterior chamber and lead to an ACG
• Progressive iris atrophy
1. Characterized by severe iris atrophy
2. Resulting in heterochromia, corectopia, ectropion uveae, iris stromal and
pigment epithelial atrophy, and hole formation.
• Chandler syndrome
1. Minimal iris atrophy and corectopia occurs
24
2. The corneal and angle findings predominate
• Cogan-Reese syndrome
1. The iris atrophy tends to be less severe
2. Tan pedunculated nodules or diffuse pigmented lesions on the anterior iris
surface
• Causes: virus? (Epstein-Barr and herpes simplex viruses)
• Therapy
1. Hypertonic saline solutions
2. Aqueous suppressants
3. Filtering surgery (trabeculectomy or tube-shunt procedures)
TUMORS_________________________________________________________
• The most common type is uveal melanomas.
• Mechanisms of angle-closure: forward displacement of the lens-iris diaphragm,
and neovascularization
INFLAMMATION_________________________________________________
• Pathogenesis
1. Breakdown of the blood-aqueous barrier → fibrin and increased aqueous
proteins → posterior synechiae → iris bombe → secondary angle closure
2. PAS are formed through peripheral iris edema, organization of inflammatory
debris in the angle, and the bridging of the angle by large KP. PAS from
inflammatory disease occur most frequently in the inferior angle, and tend to
be nonuniform in shape and height (PAS from primary angle closure → in the
superior angle, uniform in shape and height)
3. Ischemia secondary to inflammation may rarely cause rubeosis iridis and
neovascular glaucoma
• Posterior uveitis → massive exudative retinal detachment → forward displace-
ment of the lens-iris diaphragm → ACG. Treatment is aqueous suppressants
and corticosteroids.
• Interstitial keratitis → chronic inflammation, PAS formation, multiple cysts of
the iris pigment epithelium → ACG.
Sengdy Chandra Chauhari
AQUEOUS MISDIRECTION________________________________________
• Synonyms: malignant glaucoma, ciliary block glaucoma, posterior aqueous
diversion syndrome
• Cause: anterior rotation of the ciliary block and posterior misdirection of the
aqueous in association with a relative block to aqueous movement at the level of
the lens equator, vitreous face, and ciliary processes.
• Usually presents following ocular surgery in patients with a history of angle
closure or PAS. May also occur spontaneously in eyes with an open angle
following cataract surgery or various laser procedures.
• Uniform flattening of the anterior chamber and elevated IOP.
• Clinical features
1. The anterior chamber is shallow or flat with anterior displacement of the lens,
pseudophakos, or vitreous face.
2. Ciliary processes are seen to be rotated anteriorly and may be seen through an
iridectomy to come in contact with the lens equator.
3. Optically clear “aqueous” zones may be seen in the vitreous highlighting the
underlying pathology.
• Differential diagnosis: choroidal effusion, pupillary block, suprachoroidal
hemorrhage. Often the level of IOP, time frame following surgery, patency of
an iridectomy, or presence of a choroidal effusion or suprachoroidal
hemorrhage help the clinician make the appropriate diagnosis and initiate
treatment.
• Medical management
1. cycloplegic therapy
2. beta blockers
3. alpha2-agonists
4. carbonic anhydrase inhibitors (CAIs)
5. hyperosmotic agents
• Miotics should not be used and can make aqueous misdirection worse.
• Prostaglandin analogues would appear to be contraindicated, as they may
increase inflammation.
• In aphakic and pseudophakic eyes, the anterior vitreous can be disrupted with
the Nd:YAG laser.
• Surgical treatment: vitrectomy combined with anterior chamber deepening.
25
EPITHELIAL and FIBROUS DOWNGROWTH________________________
• Epithelial proliferation
1. ‘pearl’ tumors of the iris
2. epithelial cysts → translucent, nonvascular anterior chamber cysts that
originate from the surgical or traumatic wound
3. epithelial ingrowth → grayish sheetlike growth on the trabecular meshwork,
iris, ciliary body, and posterior surface of the cornea; often associated with
wound incarceration, wound gape, ocular inflammation, and corneal edema.
→ The argon laser produces characteristic white burns on the epithelial
membrane on the iris surface, which helps to confirm the diagnosis of
epithelial downgrowth and to determine the extent of involvement.
→ Cytologic examination of an aqueous aspirate can be performed to
confirm the diagnosis
→ Radical surgery is recommended to remove the intraocular epithelial
membrane and the affected tissues and to repair the fistula.
• Fibrovascular tissue proliferation
1. Fibrous ingrowth progresses slowly and is often self-limited; appears as a
thick, gray-white, vascular, retrocorneal membrane with an irregular border.
2. Fibrous ingrowth is a common cause of corneal graft failure
3. Fibrous ingrowth often involves the angle, resulting in PAS and the
destruction of the trabecular meshwork. The resultant secondary angle-
closure is treatment by medication, although surgical intervention may be
required
TRAUMA_________________________________________________________
• Mechanisms of ACG without pupillary block following ocular trauma
1. Formation of PAS associated with angle recession
2. Contusion, hyphema and inflammation.
RETINAL SURGERY and RETINAL VASCULAR DISEASE____________
• Scleral buckling operations (especially encircling bands)
1. Can produce shallowing of the anterior chamber angle and frank ACG. Often
accompanied by choroidal effusion and anterior rotation of the ciliary body,
causing a flattening of the peripheral iris with a relatively deep central
anterior chamber.
Sengdy Chandra Chauhari
 2. Medical management: cycloplegics, anti-inflammatory agents, beta blockers,
CAIs, and hyperosmotic agents.
3. If medical management is unsuccessful, argon laser gonioplasty, drainage of
suprachoroidal fluid, or adjustment of the scleral buckle is required.
4. If scleral buckle compresses a vortex vein, increased episcleral venous
pressure and IOP occurs. This can be treated permanently only by shifting the
scleral buckle or releasing the band.
• Following pars plana vitreous surgery
1. ACG may result from the injection of air, long-acting gases such as sulfur
hexafluoride and perfluorocarbons (perfluoropropane and perfluoroethane), or
silicone oil. These substances are less dense than water and rise to the top of
the eye.
2. An iridectomy should be located inferiorly to prevent obstruction of the
iridectomy site by the oil or gas.
3. Eyes that have undergone complicated vitreoretinal surgery and have
developed elevated IOP require individualized treatment plans. Treatment
options include removal of silicone oil, releasing of the encircling element,
removal of expansile gases, filtering surgery including tube-shunts,
cilioablation.
• Following panretinal photocoagulation
1. The ciliary body is thickened and rotated, and often an anterior annular
choroidal detachment occurs.
2. Generally, this glaucoma is self-limited, and therapy is directed at temporary
medical management with cycloplegic agents, topical corticosteroids, and
aqueous suppressants.
• Central retinal vein occlusion (CRVO)
1. Sometimes causes early shallowing of the chamber angle, presumably
because of swelling of the choroid and ciliary body.
2. Medical treatment of the glaucoma is topical corticosteroids and cycloplegia.
3. If the contralateral eye of a patient with CRVO has a potentially occludable
anterior chamber angle, an underlying pupillary-block mechanism must be
considered and bilateral iridectomy is needed.
26
NANOPHTHALMOS_______________________________________________
• Definition: normal eye in shape, but unusually small, with a shortened antero-
posterior diameter, a small corneal diameter, and a relatively large lens for the
eye volume.
• Thickened sclera may impede drainage from the vortex veins.
• These eyes are markedly hyperopic and highly susceptible to PACG.
• Intraocular surgery is frequently complicated by choroidal effusion and non-
rhegmatogenous retinal detachment. Choroidal effusion may occur sponta-
neously, and it can induce ACG.
• Therapy for the glaucoma: laser iridectomy, argon laser peripheral iridoplasty,
and medical therapy.
FUCHS CORNEAL ENDOTHELIAL DYSTROPHY____________________
• Mechanism of glaucoma: gradual thickening of the cornea from edema →
eventual closure of the anterior chamber angle.
RETINOPATHY OF PREMATURITY________________________________
• Mechanism of glaucoma: contracting retrolental tissue → progressive
shallowing of the anterior chamber angle.
• The onset of this complication usually occurs at 3-6 months of age during the
cicatricial phase of the disease. However, the ACG may occur later in
childhood.
PERSISTENT HYPERPLASTIC PRIMARY VITREOUS (PHPV)________
• Usually unilateral; often associated with microphthalmos and elongated ciliary
processes
• Mechanism of glaucoma: contracture of the hyperplastic primary vitreous and
swelling of a cataractous lens → shallowing of the anterior chamber angle
FLAT ANTERIOR CHAMBER______________________________________
• Following cataract surgery
1. Hypotony with postoperative flat chamber often indicates a wound leak. A
Seidel test should be performed to locate the leak.
2. Simple pressure patching or bandage contact lens application will often
causes the leak to seal and the anterior chamber to re-form.
Sengdy Chandra Chauhari
3. If not, it should be repaired surgically to prevent permanent synechial closure
of the angle.
4. Some ophthalmologists repair the wound leak and re-form a flat chamber
following cataract surgery within 24 hours. Others prefer corticosteroid
therapy for several days to prevent synechiae formation.
5. The chamber should be re-formed without delay if:
• The hyaloid face or an IOL is in contact with the cornea
• There is corneal edema, excessive inflammation, or posterior synechiae
formation

27 Sengdy Chandra Chauhari

CHILDHOOD GLAUCOMA_____________________________
DEFINITIONS____________________________________________________
• Primary congenital or infantile glaucoma is evident either at birth or within
the first few years of life. Both conditions are caused by dysplasia of the
anterior chamber angle without other ocular or systemic abnormalities.
• Secondary infantile glaucoma is associated with inflammatory, neoplastic,
hamartomatous, metabolic, or other congenital abnormalities of the eye.
• Juvenile glaucoma is recognized later in childhood (after 3 years of age) or in
early adulthood.
• Developmental glaucoma includes primary congenital glaucoma and glaucoma
associated with other development anomalies, either ocular or systemic.
Glaucoma associated with other ocular or systemic abnormalities may be
inherited or acquired.
• Buphthalmos (cow’s eye) refers to enlargement of the globe. This condition
appears when the onset of elevated IOP occurs before the age of 3 in primary
congenital or infantile glaucoma or in the pediatric glaucomas associated with
other ocular and/or systemic abnormalities.
EPIDEMIOLOGY and GENETICS___________________________________
• Congenital glaucoma → 50%-70% is isolated.
• Pediatric glaucoma cases → 60% are diagnosed by the age of 6 months and
80% within the first year of life; 65% are male, 70% are bilateral.
• Pattern of inheritance: autosomal dominant (chromosome 1q21-31), autosomal
recessive?
• Some patients may also have Axenfeld-Rieger syndrome, aniridia, or a
multisystem genetic disorder.
PATHOPHYSIOLOGY_____________________________________________
• Cellular or membranous abnormality in the trabecular meshwork → either an
anomalous impermeable trabecular meshwork or a Barkan membrane covering
the trabecular meshwork.
• Abnormal insertion of the ciliary muscle.
→ Developmental anomaly of the angle structures of 11-week fetus.
28
CLINICAL FEATURES____________________________________________
• Characteristic findings of infantile glaucoma
1. Epiphora
2. Photophobia
3. Blepharospasm
• Diagnosis of infantile glaucoma depends on careful clinical evaluation
1. IOP measurement
2. Measurement of corneal diameter
3. Gonioscopy
4. Measurement of axial length of ultrasonography
5. Ophthalmoscopy
• External eye examination
1. Buphthalmos with corneal enlargement greater than 12 mm in diameter
during the first year of life (The normal horizontal corneal diameter is 9.5-
10.5 mm in full-term newborns and smaller in premature newborns)
2. Corneal edema (from mild haze to dense opacification of the corneal stroma)
→ present in 25% of affected infants at birth and in more than 60% by the
sixth month.
3. Haab’s striae (tears in Descemet’ membrane) → occurs acutely; results from
corneal stretching; typically oriented horizontal or concentric to the limbus.
• Reduced visual acuity → caused by optic atrophy, corneal clouding,
astigmatism, amblyopia, cataract, lens dislocation, or retinal detachment.
• Amblyopia → caused by corneal opacity or by refractive error.
• Myopia → caused by enlargement of the eye
• Large astigmatism → caused by tears in Descemet’s membrane
• IOP measurement
1. Most general anesthetic agents and sedatives lower IOP. In general anesthesia
the infant may become dehydrated and the IOP may be reduced. As
anesthesia becomes deepens, IOP falls.
2. The only exception to this rule is ketamine, which may raise IOP.
3. The normal IOP in an infant under anesthesia may range from 10 to 20mmHg
depending on the tonometer. A significant IOP elevation may occur in one
eye only in 25%-30% of cases.
• Gonioscopy
1. Under anesthesia, using a direct gonioscopic lens
Sengdy Chandra Chauhari
 2. Isolated childhood glaucoma → deep anterior chamber with normal iris
structure, high and flat iris insertion, absence of angle recess, peripheral iris
hypoplasia, tenting of the peripheral iris pigment epithelium, thickened uveal
trabecular meshwork.
3. The angle is typically open with a high insertion of the iris root that forms a
scalloped line as result of abnormal tissue with a shagreened, glistening
appearance. This tissue holds the peripheral iris anteriorly. The angle is
usually avascular, but loops of vessels from the major arterial circle may be
seen above the iris root.
4. The normal anterior chamber angle in childhood is different from the adult
angle.
• Examination of the optic disc
1. Using a direct ophthalmoscope and a direct gonioscopic or fundus lens on the
cornea. Photographic documentation of the optic disc is recommended.
2. The optic nerve head of a normal infant is pink with a small physiologic cup.
3. Glaucomatous cupping in childhood resembles the cupping in adulthood, with
preferential loss of neural tissue in the superior and inferior poles.
4. In childhood the scleral canal enlarges in response to elevated IOP, causing
enlargement of the cup. Cupping may be reversible if IOP is lowered, and
progressive cupping indicates poor control of IOP.
• Ultrasonography may be useful in documenting progression of glaucoma by
recording increasing axial length. Increase in axial length may be reversible
following reduction of IOP.
DIFFERENTIAL DIAGNOSIS_______________________________________
• Excessive tearing: nasolacrimal duct obstruction, corneal epithelial defect or
abrasion, conjunctivitis.
• Corneal enlargement or apparent enlargement: X-linked megalocornea, high
myopia, exophthalmos, shallow orbits (e.g., craniofacial dysostoses)
• Corneal clouding: birth trauma, inflammatory corneal disease, congenital
hereditary corneal dystrophies, corneal malformations (dermoid tumors,
sclerocornea), keratomalacia, metabolic disorders with associated corneal
abnormalities (mucopolysaccharidoses, corneal lipidosis, cystinosis, and von
Gierke disease), skin disorders affecting the cornea (congenital ichthyosis and
29
congenital dyskeratosis), optic nerve abnormalities (optic nerve pit, optic nerve
coloboma, optic nerve hypoplasia, physiologic cupping)
LONG-TERM PROGNOSIS and FOLLOW-UP________________________
• Medications have limited long-term value for congenital or infantile glaucoma
in most cases, and the preferred therapy is surgical.
• The initial procedures of choice are:
1. goniotomy if the cornea is clear
2. trabeculectomy ab externo if the cornea is hazy
• Trabeculectomy and shunt procedures should be reserved for those cases
where goniotomy or trabeculotomy has failed.
• Beta blockers, alpha2-agonists, or CAIs may be used as temporizing therapy
prior to surgery to control IOP and help clear a cloudy cornea. These drugs must
be used with caution and at doses appropriate for the child’s weight to prevent
systemic side effects. The parents should be instructed to occlude the
nasolacrimal drainage system for at least 2 minutes immediately after
administering topical beta-blockers or alpha2 agonists and to be alert for apnea
and hypotension. Young children on CAIs require assessment for possible
acidosis, hypokalemia, and feeding problems.
• Long-term prognosis has greatly improved with the development of effective
surgical techniques, particularly for patients who are asymptomatic at birth and
present with onset of symptoms before 24 months of age. When symptoms are
present at birth or when the disease is diagnosed after 24 months of age, the
outlook for surgical control of IOP is more guarded.
DEVELOPMENTAL GLAUCOMAS with ASSOCIATED ANOMALIES___
Glaucoma associated with systemic congenital syndromes, with reported
chromosomal abnormalities
• Trisomy 21 (Down syndrome, trisomy G syndrome)
→ Mental deficiency, short stature, cardiac anomalies, hypotonia, atypical
facies
• Trisomy 13 (Patau syndrome)
→ Mental retardation, deafness, heart disease, motor seizures
• Trisomy 18 (Edwards syndrome, trisomy E syndrome)
Sengdy Chandra Chauhari
 → low-set ears, high-arched hard plate, ventricular septal defects, rocker- • Cockayne syndrome
bottom feet, short sternum, hypertonia. → Autosomal recessive disorder, dwarfism, mental retardation, progressive
• Turner (XO/XX) syndrome wasting, “birdlike” facies
→ Short stature, postadolescent females with sexual infantilism, webbed neck, → Retinal degeneration, cataracts, corneal exposure, blepharitis, nystagmus,
mental retardation, congenital deafness, and multiple systemic anomalies. hypoplastic irides, irregular pupils
Glaucoma associated with systemic congenital disorders • Fetal alcohol syndrome
• Lowe (oculocerebrorenal) syndrome → Teratogenic effects of alcohol during gestation, facial abnormalities, mental
→ X-linked recessive disease, mental retardation, renal rickets, aminoaciduria, retardation, anterior segment involvement resembling Axenfeld-Rieger
hypotonia, acidemia, cataracts syndrome and Peters anomaly, optic nerve hypoplasia
• Stickler syndrome (hereditary progressive arthro-ophthalmopathy) Glaucoma associated with ocular congenital disorders
→ Autosomal dominant connective tissue dysplasia; ocular, orofacial, and • Congenital ectropion uveae
generalized skeletal abnormalities with high myopia; open-angle glaucoma; • Congenital corneal staphyloma
cataracts; vitreoretinal degeneration; retinal detachment • Cornea plana
• Zellweger (cerebrohepatorenal) syndrome • Iridoschisis
→ Congenital autosomal recessive syndrome; abnormal facies, cerebral • Megalocornea
dysgenesis, hepatic interstitial fibrosis, polycystic kidneys, CNS • Microcoria
abnormalities • Microcornea
→ Nystagmus, corneal clouding, cataracts, retinal vascular and pigmentary • Microphthalmos
abnormalities, optic nerve head lesions
• Persistent hyperplastic primary vitreous (PHPV)
• Hallermann-Streiff syndrome (dysephalic mandibulo-oculofacial syndrome, • Retinopathy of prematurity
Francois dysephalic syndrome)
• Sclerocornea
→ Micrognathia, dwarfism, microphthalmos, cataract, aniridia, optic atrophy
• Rubinstein-Taybi (broad-thumb) syndrome
Secondary glaucoma in infant and children
→ Mental and motor retardation, typical congenital skeletal deformities of
• Trauma
large thumbs and first toes
• Inflammation
→ Bushy brows, hypertelorism, epicanthus, anti-mongoloid slant of eyelids,
hyperopia, strabismus. • Retinopathy of prematurity with secondary ACG
• Oculodentodigital dysplasia (Meyer-Schwickerath and Weyers syndrome) • Lens-induced glaucoma
→ Autosomal dominant inheritance, hypoplastic dental enamel, microdontia, • Corticosteroid-induced glaucoma
bilateral syndactyly, thin nose, microcornea, microphthalmos • Pigmentary glaucoma
• Prader-Willi syndrome • Glaucoma secondary to intraocular tumors (retinoblastoma, juvenile
→ Chromosome 15 deletion, muscular hypotonia, hypogonadism, obesity, xanthogranuloma, medulloepithelioma)
mental retardation
→ Ocular albinism, congenital ectropion uveae, iris stromal hypoplasia, angle Children often develop glaucoma within 3 years following surgery for congenital
abnormalities cataract

30 Sengdy Chandra Chauhari

MEDICAL MANAGEMENT OF GLAUCOMA______________
• Two decisions arise in choosing an appropriate glaucoma therapy:
1. when to treat
2. how to treat
• Primary angle-closure and infantile glaucoma are treated as soon as the
diagnosis is made.
• Open-angle glaucoma is treated:
1. when damage to the optic nerve has been demonstrated in the form of
progressive pathologic cupping and/or characteristic visual field defects
2. when IOP is elevated to an extent that it is likely to cause damage to the optic
nerve
• The goal of currently available glaucoma therapy
1. To preserve visual function by lowering IOP below a level that is likely to
produce further damage to the nerve.
2. The treatment regimen should have lowest risk, fewest side effects, and least
disruption of the patient’s life
• Target pressure goal
1. Should actually be a range with an upper IOP limit that is unlikely to lead to
further damage of the nerve in a given patient
2. The more advanced the glaucomatous process on initial presentation, the
lower the target pressure generally needs to be prevent further progression.
3. An initial reduction in the IOP of 20%-30% from baseline is suggested, but
those patients who have progressive NTG may require a decrease of at least
30% from baseline.
4. The target pressure range needs to be reassessed or changed as comparisons
of IOP fluctuations, optic nerve changes, and/or visual field progression
dictate.
• The anticipated benefits of any therapeutic regimen should justify the risks, and
regimens associated with substantial side effects should be reserved for patients
with a high probability of eventual severe visual dysfunction.
• Ocular hypotensive agents are divided into several group based on chemical
structure and pharmacologic action:
1. Beta-adrenergic antagonists (nonselective and selective)
31
2. Parasympathomimetic (miotic) agents, including cholinergic and
anticholinesterase agents
3. Carbonic anhydrase inhibitors (oral, topical)
4. Adrenergic agonists (nonselective and selective alpha2 agonists)
5. Prostaglandin analogues
6. Combination medications
7. Hyperosmotic agents
BETA-ADRENERGIC ANTAGONISTS (BETA BLOCKERS)____________
• Mechanism of action of topical beta blockers
Inhibition of cAMP production in ciliary epithelium → reduction of aqueous
humor secretion 20%-50% (2.5 ml/min to 1.9 ml/min) → IOP reduction of
20%-30%.
• The effect of beta blockers on aqueous production occurs within 1 hour of
instillation and can be present for up to 4 weeks after discontinuation.
• As systemic absorption occurs, a contralateral effect with lowering of the IOP in
the unilateral eye can also be observed.
• Beta blockers are additive in combination with miotics, adrenergic agonists,
CAIs (oral, topical) and prostaglandin analogues.
• Approximately 10%-20% of the patients treated with topical beta blockers fail
to respond with significant lowering of the IOP.
• If a patient is on systemic beta-blocker therapy, the addition of topical beta
blockers may be significantly less effective.
• Use of beta blockers for more than months to years may reduce their
effectiveness, as the response of beta receptors is affected by constant exposure
to an agonist (long-term drift, tachyphylaxis). Similarly, receptor saturation
(drug-induced upregulation of beta receptors) may occur within a few weeks,
with loss of effectiveness (short-term escape)
• Six topical beta blockers are approved for use for the treatment of glaucoma in
the US. All except betaxolol are noncardioselective beta1 and beta2 anta-
gonists. Beta1 activity is largely cardiac and beta2 activity largely pulmonary.
1. Betaxolol → 0.25%, bid
2. Carteolol hydrochloride → 1.0%, qd, bid
3. Levobunolol → 0.25%, 0.5%, qd, bid
4. Metipranolol → 0.3%, bid
Sengdy Chandra Chauhari
 5. Timolol maleate → 0.25%, 0.5%. qd, bid
6. Timolol hemihydrate → 5.12 mg/ml, qd, bid
• Since betaxolol is a selective beta1 antagonist, it is significantly safer than the
nonselective beta blockers when pulmonary, CNS, or other systemic conditions
are considered. Betaxolol may be useful in patients with a history of
bronchospastic disorders, although other therapies should be tried in lieu of
betaxolol, as beta selectivity is only relative and not absolute, and some beta2
effect can therefore remain. In general, the IOP-lowering effect of betaxolol is
less than the nonselective beta blockers.
• Carteolol demonstrates intrinsic sympathomimetic activity, which means that,
while acting as a competitive antagonist, it also causes a slight to moderate
activation of receptors. Thus, even though carteolol produces beta-blocking
effects, these may be tempered, reducing the effect on cardiovascular and
respiratory systems. Carteolol may also be less likely to adversely affect the
systemic lipid profile when compared with other beta blockers.
• Ocular and systemic side effects of beta blockers are bronchospasm,
bradycardia, increased heart block, lowered blood pressure, reduced exercise
tolerance, and CNS depression. Diabetic patients may experience reduced
glucose tolerance and masking of hypoglycemic signs and symptoms. Abrupt
withdrawal of ocular beta blockers can exacerbate symptoms of
hyperthyroidism. Other side effects include lethargy, mood changes, depression,
altered mentation, light-headedness, syncope, visual disturbance, corneal
anesthesia, punctate keratitis, impotence, reduced libido, allergy and alteration
of serum lipids.
PARASYMPATHOMIMETIC AGENTS______________________________
• Classifications
1. Direct-acting cholinergic agonists (e.g., pilocarpine)
• Affect the motor end plates in the same way as acetylcholine, which is
transmitted at postganglionic parasympathetic junctions, as well as at other
autonomic, somatic, and central synapses.
2. Indirect-acting anticholinesterase agents (e.g., echothiophate iodide,
demecarium bromide)
• Inhibit the enzyme acetylcholinesterase, thereby prolonging and enhancing
the action of naturally secreted acetylcholine.
32
→ Because of the potential for significant ocular and systemic side effects,
indirect-acting parasympathomimetic agents are used less commonly.
• Carbachol has both direct and indirect actions, although its primary mechanism
is direct.
• Mechanism of IOP reduction by both direct- and indirect-acting agents
Contraction of the ciliary muscle, which pulls the scleral spur to tighten the
trabecular meshwork, increasing the outflow of aqueous humor.
• These agents can reduce the IOP by 10%-20%.
• The currently accepted indications for miotic therapy
1. Chronic treatment of increased IOP in patient with at least some filtering
angle
2. Prophylaxis for ACG prior to iridectomy
• Other actions of the parasympathomimetic agents
1. Reduce uveoscleral outflow. This action may actually worsen the glaucoma if
miotics are used in patients with little to no trabecular outflow.
2. Cause the pupillary sphincter to contract, stimulate secretory activity in the
lacrimal and salivary glands, and disrupt the blood-aqueous barrier. These
actions have little bearing on the IOP-lowering effect, except in ACG, where
the mechanical action of the contracting pupillary sphincter may pull the iris
away from the trabecular meshwork.
• Side effects of miotic agents
1. Retinal detachment, especially in patients with peripheral retinal disease.
2. Induced myopia, brow ache, alteration of vision in dim light and in
patients with lens opacities.
3. Paradoxical angle closure (indirect-acting miotics or the stronger direct-
acting agents), caused by the contraction of ciliary muscle leads to forward
movement of the lens-iris diaphragm, an increase in the anteroposterior
diameter of the lens, and a very miotic pupil. The concomitant administration
of an alpha-adrenergic agonist such as phenylephrine may cause a larger pupil
without interfering with the reduction of IOP.
4. Generalized cataract formation in addition to anterior subcapsular
opacity (indirect-acting miotics). Direct-acting agents may also be weakly
cataractogenic.
5. Formation of iris pigment epithelial cysts (indirect-acting miotics)
6. Ocular surface changes (pseudopemphigoid) (indirect-acting miotics)
Sengdy Chandra Chauhari
 7. Increased inflammation following surgery (stronger miotics) → Anti-
cholinesterase agents should be discontinued and other agents substituted at
least 2-4 weeks prior to ocular surgery, because they cause significant
bleeding during surgery and severe fibrinous iridocyclitis postoperatively.
8. Breakdown of the blood-aqueous barrier. Thus, their use in treating uveitic
glaucoma should be limited.
9. Systemic parasympathetic stimulation such as diarrhea, abdominal cramps,
increased salivation, bronchospasm and enuresis (indirect-acting miotics).
Since cholinesterase is suppressed throughout the body, depolarization agents
such as succinylcholine should be avoided while the patient is using these
eyedrops and for 6 weeks after discontinuation.
• Preparations
1. Pilocarpine HCl 0.2%, 0.5%, 1.0%, 2.0%, 3.0%, 4.0%, 6.0%, bid-qid
2. Pilocarpine nitrate 1.0% - 4.0%, bid-qid
3. Pilocarpine membrane 20ug, 40ug, q5-7d → releases drug at a steady rate for
approximately 1 week; the induced myopia is more stable and the miosis is
less marked than with eyedrop therapy; the release of drug and the induced
symptoms are greatest during the first 24 hours; tolerated better when
administered at bedtime.
4. Pilocarpine gel 4.0% qhs → loss of drug effect after 18-20 hours; induced
myopia and miosis are less prominent than with drops.
5. Carbachol 1.5%, 3.0%, bid, tid
6. Echothiophate iodide 0.03%, 0.06%, 0.125%, 0.25%, qd, bid
7. Physostigmine 0.25%, 0.5%, qd, bid
8. Demecarium bromide 0.125%, 0.25%, qd, bid
• Pilocarpine membrane and pilocarpine gel may be useful:
1. In some younger patients.
2. In patients bothered by variable myopia or intense miosis.
3. In older patients with lens opacities.
4. In patients who have difficulty complying with more frequent dosing regimen
• Indirect-acting agents are usually reserved for treatment of glaucoma:
1. In aphakic and pseudophakic eyes when IOP is not controlled by less toxic
agents
2. In phakic eyes when filtering surgery has failed.
33
CARBONIC ANHYDRASE INHIBITORS_____________________________
• Mechanism of action
1. Direct antagonist activity upon ciliary epithelial carbonic anhydrase
2. Producing a generalized acidosis (?)
• The enzyme carbonic anhydrase is also present in many other tissues, including
corneal endothelium, iris, retinal pigment epithelium, brain and kidney.
• Over 90% of the ciliary epithelial enzyme activity must be abolished to
decrease aqueous production and lower IOP.
SYSTEMIC AGENTS
• Most useful in acute situations (e.g., acute ACG). Can be given orally,
intramuscularly, and intravenously.
• Because of the side effects of the systemic CAIs, chronic therapy with these
agents should be reserved for patients whose glaucoma cannot be controlled by
alternative topical therapy.
• The oral agents most commonly used are acetazolamide and methazolamide.
The lowest dose that reduces the IOP to an acceptable range should be used.
Methazolamide → has longer duration of action; less bound to serum protein;
metabolized by liver, thereby decreasing the risk of systemic side effects; 25-50
mg 2-3 times daily.
Acetazolamide → not metabolized; excreted in urine; may be started at 62.5mg
every 6 hours, and higher doses may be used if tolerated.
• Side effects are usually dose related. They include paresthesias of the fingers or
toes, lassitude, loss of energy, anorexia, weight loss, abdominal discomfort,
diarrhea, loss of libido, impotence, unpleasant taste in the mouth, several mental
depression, increased risk in formation of calcium oxylate and calcium
phosphate renal stones, allergic reactions (sulfa derivatives), cross reactivity,
hypokalemia, aplastic anemia, thrombocytopenia, agranulocytosis.
• Preparations:
1. acetazolamide 62,5mg, 125mg, 250mg, 500mg, bid-qid (oral)
2. acetazolamide 500mg (parenteral) 5-10mg/kg, usually ≤ 1qd q6-8hrs
3. methazolamide 25mg, 50mg, 100mg, bid, tid
4. dichlorphenamide 50mg, bid, tid
TOPICAL AGENTS
• Dorzolamide and brinzolamide are topical CAI agents available for chronic
treatment of IOP elevation. They reduce IOP (monotherapy) by 14%-17%.
Sengdy Chandra Chauhari
• Common adverse effects include bitter taste, blurred vision, punctate
keratopathy, and systemic lassitude. Ocular surface irritation with dorzolamide
may be a result of the relative greater acidity (lower pH) when compared with
brinzolamide. The brinzolamide solution may cause more blurring than the
dorzolamide solution.
• Preparations:
1. dorzolamide 2.0%, bid, tid
2. brinzolamide 1%, bid, tid
NONSELECTIVE ADRENERGIC AGONISTS_________________________
• Mechanism of action: increase conventional trabecular and uveoscleral outflow
• Epinephrine-related agents may initially increase aqueous production; with
chronic use, they decrease it.
• Systemic side effects include headache, increase blood pressure, tachycardia,
arrhythmia, and nervousness.
• Ocular side effects
1. Epinephrine causes adrenochrome deposits from oxidized metabolites in the
conjunctiva, cornea and lacrimal system. It may stain soft contact lenses.
2. Pupillary dilation as a consequence of alpha-agonist action that stimulates
norepinephrine receptors may precipitate or aggravate angle closure in
susceptible individuals.
3. Allergic blepharoconjunctivitis
4. Cystoid macular edema may be precipitated or exacerbated in aphakic and
pseudophakic eyes without intact posterior capsules.
5. Rebound conjunctiva hyperemia is common when they are discontinued.
EPINEPHRINE (alpha and beta agonist)
• Epinephrine and related compounds have less hypotensive effect in eyes with
dark irides.
• The IOP-lowering effect begins at 1 hour and is maximal at 2-6 hours.
• IOP reduction (monotherapy) by 15%-30%.
• Tolerance, or tachyphylaxis, is common with long-term use.
• Epinephrine salts
1. epinephrine hydrochloride → 1.0%, 2.0%, bid
2. epinephrine borate → 0.5%, 1.0%, 2.0%, bid
3. epinephrine bitartrate → 2.0%, bid
34
DIPIVEFRIN
• A pro-drug that is chemically transformed into epinephrine by esterase enzymes
in the cornea. Has greater corneal penetration, and its activity is relatively low.
• Two major advantages over epinephrine salt
1. A lower topical concentration of dipivefrin has an intraocular effect similar to
a higher dosage of epinephrine salt.
2. Therapeutic effectiveness in they eye can be achieved with fewer topical and
systemic side effects.
• Tolerated by some patients who are allergic to epinephrine salt.
• Its effectiveness may be diminished if an anticholinergic agent is added because
anticholinergic agent may prevent dipivefrin’s cleavage and activation by
corneal esterases.
• Preparation: 0.1%, bid
ALPHA2-ADRENERGIC AGONISTS_________________________________
• Alpha1 effects include vasoconstriction, pupillary dilation, and eyelid
retraction, while alpha2 effects are primarily IOP reduction and possible
neuroprotection.
• Apraclonidine and brimonidine are relatively selective alpha2 agonists that have
been developed for glaucoma therapy. Brimonidine is much more highly
selective for the alpha2 receptor than apraclonidine. Apraclonidine has a much
greater affinity for alpha1 receptor than does brimonidine.
• Caution is recommended when using them in patients on a MAO inhibitor or
tricyclic antidepressant therapy, in patients with severe cardiovascular disease,
and concomitant with beta blockers, antihypertensives, and cardiac glycosides
(ophthalmic and systemic)
APRACLONIDINE HYDROCHLORIDE (PARA-AMINOCLONIDINE)
• Mechanism of action
1. Prevents release of norepinephrine at nerve terminals.
2. Decreases aqueous production and episcleral venous pressure
3. Improves trabecular outflow
• May be effective for the short-term lowering of IOP (e.g., following argon laser
iridectomy, argon laser trabeculoplasty, Nd:YAG laser capsulotomy, and
cataract extraction)
Sengdy Chandra Chauhari
• Development of topical sensitivity and tachyphylaxis often limits long-term use.
More likely to produce vasoconstriction and can prolong iris sphincter ischemia
• Preparation: 0.5%, 1.0%. bid, tid
BRIMONIDINE TARTRATE
• Encounters less tachyphylaxis in long-term use, and allergenicity such as
follicular conjunctivitis and contact blepharitis-dermatitis is also lower. Cross
sensitivity to brimonidine in patient with known hypersensitivity to
apraclonidine is minimal. Less likely to induce vasoconstriction.
• Actions:
1. IOP reduction, by:
• Decreased aqueous production
• Increased uveoscleral outflow
→ Its peak IOP reduction is approximately 26% (2 hour postdose)
2. Neuroprotection, independent of IOP reduction by:
• Upregulation of a neurotrophin, basic fibroblast growth factor
• Cellular regulatory genes
• Preparation: 0.2%, bid, tid
PROSTAGLANDIN ANALOGUES_(PGF2α)___________________________
LATANOPROST
• A pro-drug that penetrates the cornea and becomes biologically active after
being hydrolyzed by corneal esterase.
• Mechanism of action: enhancing uveoscleral outflow.
• Can reduce IOP by 25%-35%.
• Advantages of this agent:
1. Once-daily dosing
2. Lack of cardiopulmonary effects
3. The additivity to other antiglaucoma medications except, perhaps, higher
concentration miotic agents
• Ocular side effects:
1. Darkening of the iris and periocular skin
→ Caused by increased numbers of melanosomes within the melanocytes.
→ The risk of iris pigmentation correlates with baseline iris pigmentation.
Blue irides may experience increased pigmentation in 10%-20% of eyes
in the initial 18-24 months of therapy, whereas nearly 60% of eyes that
are light brown, blue-green, or two-toned may experience increased
pigmentation over the same time period.
2. Hypertrichosis of the eyelashes
3. Cystoid macular edema, uveitis, and possible herpetic keratitis.
• Topical application is performed at night to mitigate the conjunctival injection
and perhaps potentiate hypotensive effect.
• Preparation: latanoprost 0.005%, qd
COMBINED MEDICATIONS_______________________________________
• Potential benefits:
1. improved efficacy, convenience, and compliance
2. reduced cost
• Adrenergic agonists & parasympathomimetic agent (epinephrine & pilocarpine)
• Adrenergic agonists & beta blockers (dipivefrin & levobunolol)
• Beta blockers & parasympathomimetic agent (timolol & pilocarpine)
• Beta blockers & CAIs (timolol & dorzolamide)
HYPEROSMOTIC AGENTS________________________________________
• Common hyperosmotic agents include:
1. Oral glycerin → 50% soln, 4-7oz
2. Oral isosorbide → particularly useful oral agent for diabetic patient because it
is not metabolized into sugar; 45% soln, 4-7 soln
3. Intravenous mannitol → 5.25% soln, 2 g/kg body wt
• Used to control acute episodes of elevated IOP.
• Mechanism of action: Increasing the blood osmolarity → creating an osmotic
gradient between the blood and the vitreous humor → drawing water from the
vitreous cavity → reduction in IOP.
• They are rarely administered for longer than a few hours because the effects of
hyperosmotic agents are transient as a result of the rapid reequilibration of the
osmotic gradient. They become less effective over time, and rebound elevation
in IOP may occur if the agent penetrates the eye and reverses the osmotic
gradient.
• The larger the dose and the more rapid the administration, the greater the
reduction in IOP because of the increased gradient.

35 Sengdy Chandra Chauhari

• The substance distributed only in the extracellular water (e.g., mannitol) is more ANGLE-CLOSURE GLAUCOMA____________________________________
effective than a drug distributed in total body water (e.g., urea). • Medical treatment for acute ACG is aimed at preparing the patient for laser
• When the blood-aqueous barrier is disrupted, the osmotic agent enters the eye iridectomy. The goals of medical treatment are:
faster than when the blood-aqueous barrier is intact, thus reducing both the 1. To reduce IOP rapidly to prevent further damage to the optic nerve
effectiveness of the drug and its duration of action. 2. To clear the cornea
• Side effects include headache, mental confusion, backache, acute congestive 3. To reduce intraocular inflammation
heart failure, myocardial infarction, subdural and subarachnoid hemorrhage, 4. To allow pupillary constriction
hyperglycemia and ketaacidosis (glycerin → sugar + ketone bodies). 5. To prevent formation of posterior and PAS
• Treatment of chronic ACG is the same as POAG, although miotics may
--------------GENERAL APPROACH TO MEDICAL TREATMENT------------ induce a paradoxical increase in IOP if the angle is closed and the trabecular
meshwork is nonfunctional.
OPEN-ANGLE GLAUCOMA________________________________________
• Treatment is usually initiated with a single topical medication, unless the
starting IOP is extremely high, in which case combination therapy may be
indicated.
• A beta blocker is commonly the drug of choice for initial therapy, assuming
there is no medical contraindication. Initiation with a selective alpha2 agonist,
topical CAI, or PG analogue can also be considered.
• If one drug is not adequate to reduce IOP to the estimated desired safe level,
another agent should be tried, preferably as a therapeutic trial in one eye.
• If no single agent controls the pressure, a combination of topical agents should
be used. A beta blocker with an alpha2 agonist, topical CAI, or PG analogue
should be considered as second-line agents, and then miotic therapy followed
by systemic CAI may be used.
• Information for patients
1. How to space medications. Instructional charts.
2. How to administer eyedrops properly. Assistive drop device.
3. Eyedrops to given at the same time should be separated by at least 5 minutes
to prevent washout of the first by the second.
4. Nasolacrimal occlusion or gentle eyelid closure for 1 full minute after
instillation of the drop helps to promote corneal penetration and reduce
systemic absorption.
5. Topical and systemic side effects.
6. Compliance.

36 Sengdy Chandra Chauhari

SURGICAL THERAPY OF GLAUCOMA__________________
• Surgery therapy of glaucoma is undertaken when:
1. medical therapy is not appropriate, not tolerated, not effective, or not properly
utilized by a particular patient
2. the glaucoma remains uncontrolled with either documented progressive
damage or a very high risk of further damage.
• Surgery is usually the primary approach for infantile and pupillary-block
glaucoma.
• When surgery is indicated, the clinical setting must guide the selection of the
appropriate procedure.
1. trabeculectomy and its variations
2. non-penetrating filtration procedures
3. glaucoma drainage tube implants
4. angle surgery for congenital glaucoma
5. ciliary body ablation.
6. iridectomy
7. gonioplasty
SURGERY FOR OPEN-ANGLE GLAUCOMA_________________________
• Surgery is indicated when IOP cannot be maintained by nonsurgical therapies at
a level considered low enough to prevent further pressure-related damage to the
optic nerve or visual field loss. Surgery has traditionally been considered only
when medical therapy has failed and is associated with long-term risks of bleb-
associated problems, cataracts, and infection.
• The glaucoma may be uncontrolled for various reasons:
1. Maximal medical therapy fails to adequately reduce IOP
2. The amount of medical therapy necessary to control IOP is not well tolerance
or places the patient at unacceptable risk
3. Optic nerve cupping or visual field loss is progressing despite apparent
“adequate” reduction of IOP with medical therapy.
4. The patient cannot comply with the necessary medical regimen
37
------------------------LASER TRABECULOPLASTY (LTP) ------------------------
• Mechanism of action
LTP stimulates the growth of trabecular meshwork endothelial cells → restores
trabecular meshwork function → improves the outflow facility
• Indications
1. Patients with glaucoma on maximum tolerated medical therapy who require
lower IOP and in whom the angle is open on gonioscopy.
2. LTP effectively reduces IOP in patients with POAG, pigmentary glaucoma,
and exfoliation syndrome. Aphakic and pseudophakic eyes may respond less
favorably than phakic eyes; therefore, LTP may be more effective before than
after cataract surgery.
3. The role of initial LTP in POAG is at least as effective as medications for the
first 2 years. LTP may postpone the need for conventional surgery or
additional medications.
→ When effective, LTP is expected to lower IOP 20%-25%.
• Relative contraindications
1. Inflammatory glaucoma
2. Membrane in the angle
3. Young patients who have developmental defects.
4. The lack of effect in the fellow eye
• Preoperative evaluation
1. Optic nerve evaluation
2. Visual field examination
3. Gonioscopy → the angle must be open. The amount of pigment in the angle
will help determine the laser settings for argon laser; a more pigmented angle
responds to lower laser energy
• Argon laser procedure
1. Set at 300-1000 mW, 50 um, and 0.1 second.
2. Laser beam is focused through a goniolens at the junction of the anterior
unpigmented and the posterior pigmented edge of the trabecular meshwork.
Laser energy was applied to the entire circumference (360˚) of the trabecular
meshwork. End point: blanching of the trabecular meshwork or production of
a tiny bubble. If a large bubble appears, the power is reduced.
3. Application to the posterior trabecular meshwork tends to produce
inflammation, pigment dispersion, prolonged elevation of IOP, and PAS.
Sengdy Chandra Chauhari
• Diode laser procedure: is similar; set at 600-1000 mW, 75 um, and 0.02
second.
• Complications
1. Transient rise in IOP (occurs in 20% of patients) → usually evident within the
first 2-4 hours after treatment. Topical medications shown to blunt the IOP
spikes include alpha2-agonists, beta blockers, pilocarpine, and topical CAIs.
Hyperosmotic agents, oral CAIs, and ice packs may be helpful in eyes with
IOP spikes not responsible to topical medication.
2. Low-grade iritis
3. Persistent elevation of IOP requiring filtering surgery
4. Hyphema
5. Formation of PAS
• Re-treatment of an angle that has been fully treated has a lower success rate and
a higher complication rate than does primary treatment. If initial LTP fails to
bring IOP under control, a trabeculectomy should be considered.
-------------------SELECTIVE LASER TRABECULOPLASTY --------------------
• Q-switched 532 nm Nd:YAG laser trabeculoplasty
• The laser targets intracellular melanin
--------INCISIONAL SURGERY FOR OPEN-ANGLE GLAUCOMAS --------
• The goal of filtering surgery (fistulizing procedure) is to create a new pathway
(fistula) for the bulk flow of aqueous humor from the anterior chamber through
the surgical defect in the sclera into the subconjunctival and sub-Tenon’s space.
• The filtering procedure most commonly used is guarded trabeculectomy.
• Indications: a patient with glaucoma on maximum tolerable medical therapy
(MTMT) who has had maximal laser benefit and whose optic nerve function is
failing or is likely to fail.
• The physician can determine that the patient is at MTMT only by advancing
therapy beyond the tolerated level and documenting intolerance. An alternative
concept is core therapy, in which treatment consists of those medications likely
to work well in combination.
• Relative contraindications
1. Blind eye → ciliary body ablation is a better alternative for lowering IOP
38
2. Active anterior segment neovascularization (rubeosis iridis) or active iritis →
the underlying problem should be addressed first, or a surgical alternative
such as tube implant surgery should be considered.
3. Sustained extensive conjunctival injury or extremely thin sclera from
extensive prior surgery or necrotizing scleritis.
4. Younger or aphakic/pseudophakic patients. Black patients.
5. Patients with uveitic glaucoma or with previously failed filtration procedures
• Preoperative evaluation
1. The patient must be medically stable for an invasive ocular procedure under
local anesthesia.
2. Control of preoperative inflammation with corticosteroids helps to reduce
postoperative iritis and scarring of the filtering bleb.
3. Anticholinesterase agents should be discontinued if possible and replaced
temporarily by alternative medications at least 2-3 weeks before surgery to
reduce bleeding and iridocyclitis.
4. IOP should be reduced as close as possible to normal levels before surgery is
performed, to minimize the risk of expulsive choroidal hemorrhage.
5. Antiplatelet medications should be discontinued.
6. Systemic hypertension should be controlled.
7. Patient should be informed:
• The purpose and expectations of surgery: to arrest or delay progressive
visual loss caused by their glaucoma.
• Glaucoma surgery alone rarely improves vision.
• Glaucoma medications may still be required postoperatively
• Surgery may fail completely
• Vision could be lost as a result of surgery
• Glaucoma may progress despite successful surgery
• Patients with far advanced visual field loss or field loss that is impinging on
fixation are at risk for total loss of central acuity following a surgical
procedure. The possible mechanism of this phenomenon include:
1. Cystoid macular edema
2. Early postoperative IOP spiking
3. Shifting of the lamina, further compromising remaining axons
4. Optic nerve ischemia, possibly related to regional anesthesia
Sengdy Chandra Chauhari
• Trabeculectomy
1. A guarded partial-thickness filtering procedure performed by removing a
block of limbal tissue beneath a scleral flap. The scleral flap provides
resistance and limits the outflow of aqueous, thereby reducing the
complications associated with early hypotony (such as flat anterior chamber,
cataract, serous and hemorrhagic choroidal effusion, macular edema, and
optic nerve edema)
2. The use of antifibrotic agents (such as mitomycin-C and 5-fluorouracil),
combined with techniques of releasable sutures or laser suture lysis, enhances
the longevity of guarded procedures.
3. Succesful trabeculectomy surgery:
• Involves reducing IOP and avoiding or managing complications
• Depends on appropriate and timely postoperative intervention to influence
the functioning of the filter.
4. Complete healing of the epithelial and conjunctival wound with incomplete
healing of the scleral wound is the goal of this procedure.
• Trabeculectomy procedures
1. Preoperative evaluation
2. Exposure. A corneal traction suture or superior rectus bridle suture can rotate
the globe down, giving excellent exposure of the superior sulcus and limbus.
3. Conjunctival wound.
• Fornix-based conjunctival flap → provides better exposure at the limbus;
• Antifibrotic agents
more difficult to achieve a water-tight closure.
• Limbal-based conjunctival flap → technically more challenging but allows
for a secure closure well away from the limbus.
4. Scleral flap (3-4 mm trapezoidal or rectangular flap).
• The flap is dissected anteriorly into clear cornea.
5. Paracentesis
• To control the anterior chamber through instillation of BSS or viscoelastic
• Allows for gradual lowering of IOP
• Intraoperative testing of the patency of the filtration site as well as of the
integrity of the conjunctival closure.
6. Sclerotomy (with a punch or with sharp dissection).
• The size of the ostomy is determined by the scleral flap and the amount of
overlap desired by the surgeon.
39
• A small amount of tissue should remain at the edges of the ostomy to allow
for resistance to outflow from the flap.
7. Iridectomy
• To lessen the risk of iris occluding the ostomy
• To reduce the risk of pupillary block
8. Closure of scleral flap
• With the advent of laser suture lysis and releasable sutures, many surgeons
close the flap relatively tightly to avoid early shallow chambers. After a
few days, flap sutures are released to promote filtration.
• Flow should be tested around the flap before closing the conjunctiva.
• Leakage around the flap may be adjusted intraoperatively by the placement
of additional sutures, removal of sutures, or application of cautery to shrink
the wound edges.
9. Closure of conjunctiva
• Fornix-based flap → conjunctiva is secured at the limbus
• Limbal-based flap → conjunctiva and Tenon’s capsule are closed
separately or in a single layer.
10. Postoperative management
• Topical antibiotics and corticosteroids
• Topical cycloplegic agents or mydriatics
• Sub-Tenon’s corticosteroids or a short course of systemic corticosteroids
1. 5-fluorouracil (5-FU), a pyrimidine analogue
• 5-FU → deoxynucleotide 5-fluoro-2’-deoxyuridine 5’-monophosphate
(FdUMP) → interferes with DNA synthesis through its action on
thymidylate synthetase
• Inhibits fibroblast proliferation; reduces scarring after filtering surgery.
• 50 mg/ml on a surgical sponge is used intraoperatively.
• A total of 5 mg in 0.1-0.5 cc can be injected postoperatively.
2. Mitomycin-C (MMC), derived from Streptomyces caespitosus
• Acts as an alkylating agent after enzyme activation resulting in DNA cross-
linking.
• Most commonly administered intraoperatively by placing a surgical sponge
soaked in MMC within the subconjunctival space in contact with sclera at
the planned trabeculectomy site.
Sengdy Chandra Chauhari
 • Concentrations are typically between 0.2 and 0.4 mg/ml with a duration of
application from 1 to 4 minutes
3. They should be used with caution in primary trabeculectomies on young
myopic patients because of an increased risk of hypotony.
• Techniques allowing tighter initial wound closure of the scleral flap help to
prevent early postoperative hypotony.
1. The use of releasable flap sutures
2. The placement of additional sutures that can be cut postoperatively.
3. Laser suture lysis
• Early complications: infection, hypotony, flat anterior chamber, aqueous
misdirection, hyphema, formation or acceleration of cataract, transient IOP
elevation, cystoid macular edema, hypotony maculopathy, choroidal effusion,
suprachoroidal hemorrhage, persistent uveitis, dellen formation, loss of vision
• Late complications: leakage or failure of the filtering bleb, cataract, blebitis,
endophthalmitis (bleb infection), symptomatic bleb (dysesthetic bleb), bleb
migration, hypotony.
• When an initial filtering procedure is not adequate to control the glaucoma and
resumption of medical therapy is not successful, revision of original surgery,
repeat filtering surgery at a new site, and possibly cyclodestructive procedures
may be indicated.
----------------------FULL-THICKNESS SCLERECTOMY -------------------------
• A block of limbal tissue is removed with a punch, trephine, laser or cautery.
• Advantages: IOP can be lowered and maintained at a lower level for long
periods of time.
• Disadvantages: higher incidence of postoperative flat anterior chamber, cataract,
hypotony, choroidal effusion, leakage of filtering blebs, and
endophthalmitis.
-----------COMBINED CATARACT AND FILTERING SURGERY ------------
• Indications
1. Glaucoma that is uncontrollable either medically or after laser trabeculoplasty
when visual function is significantly impaired by a cataract
2. Cataract requiring extraction in a glaucoma patient who has advanced visual
field loss
40
3. Cataract requiring extraction in a glaucoma patient requiring medications to
control IOP in whom medical therapy is poorly tolerated
4. Cataract requiring extraction in a glaucoma patient who requires multiple
medications to control IOP
• Contraindications
1. Glaucoma that requires a very low target IOP
2. Advanced glaucoma with uncontrolled IOP and immediate need for
successful reduction of IOP
→ Glaucoma surgery alone is preferred.
SURGERY FOR ANGLE-CLOSURE GLAUCOMA_____________________
• The first clinical decision point following the diagnosis of ACG is to distinguish
between angle closure based on a pupillary block mechanism and angle closure
based on another mechanism.
• The treatment of pupillary-block glaucoma, whether primary or secondary, is a
laser or an incisional iridectomy
• For eyes with secondary angle closure not caused by pupillary block, an attempt
should be made to identify and treat underlying conditions.
---------------------------------LASER IRIDECTOMY-----------------------------------
• Indications
1. The presence of pupillary block
2. The need to determine the presence of pupillary block
3. To prevent pupillary block in an eye considered at risk, as determined by
gonioscopic evaluation or because of an angle-closure attack in the fellow eye
→ This procedure provides an alternative route for aqueous trapped in the
posterior chamber to enter the anterior chamber, allowing the iris to recede
from its occlusion of the trabecular meshwork.
• Contraindications: active rubeosis iridis, systemic anticoagulants consumption,
angle closure not caused by a pupillary block mechanism
• Preoperative consideration
1. The glaucoma attack should be attempted medically, then proceed to surgery.
2. Care should be taken to keep the iridectomy peripheral and covered by eyelid,
if possible, to avoid monocular diplopia.
3. Pilocarpine may be helpful by stretching and thinning the iris
Sengdy Chandra Chauhari
 4. Apraclonidine or other agents can help blunt IOP spikes
• Technique ----------------INCISIONAL SURGERY FOR ANGLE-CLOSURE---------------
1. Set the argon laser at 800-1000 mW, 50 um, 0.02-0.1 second, using a • Peripheral iridectomy may be required if a patent iridectomy cannot be
condensing contact lens. There are a number of variations in technique, and achieved with a laser (cloudy cornea, flat anterior chamber, insufficient patient
iris color dictates which technique is chosen. Complications include localized cooperation)
lens opacity, acute rise in IOP, transient or persistent iritis, early closure of • Cataract extraction might be considered when pupillary block is associated
the iridectomy, and corneal and retinal burns with a visually significant cataract.
2. Q-switched Nd:YAG laser generally requires fewer pulses and less energy. • Chamber deepening and goniosynechialysis may break PAS.
The effectiveness of this laser is not affected by iris color. With a condensing
contact lens, the typical initial laser setting is 2-8 mJ. Complications include -----------------------------GLAUCOMA TUBE SHUNT-------------------------------
corneal burns, disruption of the anterior lens capsule or corneal endothelium, • Types of glaucoma drainage devices
bleeding, postoperative IOP spike, inflammation, and delayed closure of the 1. Resistance (valved) or flow-restricted devices: Krupin, Ahmed
iridectomy. 2. Nonresistance (nonvalved) devices: Molteno, Baelveldt
• Postoperative care 3. Anterior chamber tube shunt to an encircling band (ACTSEB) – Schocket
1. Bleeding → particularly with Nd:YAG laser; compression of the eye with the procedure
laser lens will tamponade the vessel, or argon laser can be used to coagulate • Indications
the vessel. 1. Trabeculectomy failure
2. IOP spikes → can be treated as described in the section on LTP 2. Failed trabeculectomy with antifibrotics
3. Inflammation → topical corticosteroids 3. Active uveitis
• Complications 4. Neovascular glaucoma
1. Focal lens damage → can be avoided by ceasing the procedure as soon as the 5. Inadequate conjunctiva
iris is penetrated 6. Impending need for penetrating keratoplasty
2. Retinal detachment → very rare, associated with Nd:YAG laser. 7. Others: poor candidate for trabeculectomy, potential for visual acuity, need
3. Bleeding and IOP spike for lower IOP
• Contraindications
----------LASER GONIOPLASTY or PERIPHERAL IRIDOPLASTY---------- 1. Eyes with very poor visual potential
• Indications 2. Patients unable to comply with self-care in the postoperative period.
1. ACG resulting from plateau iris syndrome and nanophthalmos. 3. Borderline corneal endothelial function
2. To open the angle temporarily, in anticipation of a more definitive laser or • Preoperative considerations
incisional iridectomy. 1. The status of the conjunctiva
• Contraindications: same as those for laser iridectomy 2. The health of the sclera at the anticipated tube and external reservoir sites
• Technique 3. The location of vitreous in the eye
1. Set the argon laser at 200-500 mW, 200-500 um, 0.1-0.5 second • Technique for implantation:
2. Stromal burns are created in the peripheral iris to cause contraction and 1. The superotemporal quadrant is preferred.
flattening.

41 Sengdy Chandra Chauhari

 2. The extraocular plate or valve mechanism is sutured between the vertical and
horizontal rectus muscles posterior to the muscle insertions.
3. The tube is routed anteriorly to enter in the chamber angle or through the pars
plana for posterior implantation in eyes that have had a vitrectomy.
4. The tube is covered with tissue such as sclera, pericardium, or dura to help
prevent erosion.
• Postoperative management: topical steroids, antibiotics, and cycloplegics; IOP
monitoring
• Complications: tube-corneal touch, flat chamber and hypotony, tube occlusion,
tube migration, valve malfunction, tube or plate exposure or erosion
--------------------CILIARY BODY ABLATION PROCEDURES------------------
• Procedures: cyclocryotherapy, diathermy, therapeutic ultrasound, thermal lasers
(continuous Nd:YAG, argon, diode)
• Goal: To reduce aqueous secretion by destroying a portion of the cilary body.
• Indications
1. Eyes that have poor visual potential or are poor candidates for incisional
surgery → generally reserved for eyes that have been or are likely to be
unresponsive to other modes of therapy.
• Contraindications: eyes with good vision
• Preoperative evaluation: same as for incisional glaucoma surgery
• Postoperative management: analgesics, narcotics
• Complications: prolonged hypotony, pain, inflammation, cystoid macular
edema, hemorrhage, phthisis bulbi
------------------------------------CYCLODIALYSIS--------------------------------------
• Indications: aphakic patients who have not responses to filtering surgery.
• Techniques
1. A small scleral incision is made approximately 4 mm from the limbus.
2. A fine spatula is passed under the sclera into the anterior chamber.
3. This spatula disinserts a portion of the ciliary muscle from the scleral spur
and creates a cleft in the angle, providing direct communication between the
anterior chamber and the suprachoroidal space.
• Complications: bleeding, inflammation, cataract, stripping of Descemet’s
membrane, profound hypotony.
42
------------------------NONPENETRATING PROCEDURES-------------------------
1. Deep sclerectomy with collagen implant
2. Deep sclerectomy with injection of viscoelastic into Schlemm’s canal
(viscocanalostomy)
• Involve creation of a superficial scleral flap and a deeper scleral dissection
underneath to leave behind only a thin layer of sclera and Descemet’s
membrane.
CONGENITAL OR INFANTILE GLAUCOMA________________________
----------------------GONIOTOMY and TRABECULOTOMY-----------------------
• Indications: childhood glaucoma
• Contraindications: infants with unstable health, multiple anomalies with poor
prognosis and a grossly disorganized eye.
• Technique
1. The anterior chamber should be filled with viscoelastic to prevent collapse
and to tamponade bleeding.
2. Goniotomy → A needle-knife is passed across the anterior chamber, and a
superficial incision is made in the anterior aspect of the trabecular meshwork
under gonioscopic control.
3. Trabeculotomy → A fine wirelike instrument (trabeculotome) is inserted into
Schlemm’s canal from an external incision, and the trabecular meshwork is
torn by rotating the trabeculotome into the anterior chamber.
• Goniotomy is possible only in an eye with a relatively clear cornea, whereas
trabeculotomy can be performed whether the cornea is clear or cloudy.
Sengdy Chandra Chauhari