3

CHAPTER II
LITERATURE REVIEW
2.1 Physiology of Aqueous Humour
Intraocular pressure is determined by the rate of aqueous production and the
resistance to outflow of aqueous from the eye.
2
2.1.1 Composition of Aqueous
The aqueous is a clear liquid that fills the anterior and posterior chambers of
the eye. Its volume is about 250 microL, and its rate of production, which is
subject to diurnal variation, is about 2.5 microL/min. The osmotic pressure is
slightly higher than that of plasma. The composition of aqueous is similar to
that of plasma except for much higher concentrations of ascorbate, pyruvate,
and lactate and lower concentrations of protein, urea, and glucose.
2
2.1.2 Formation & Flow of Aqueous
Aqueous is produced by the ciliary body. An ultrafiltrate of p lasma produced
in the stroma of the ciliary processes is modified by the barrier function and
secretory processes of the ciliary epithelium. Entering the posterior chamber,
the aqueous passes through the pupil into the anterior chamber (Figure 111)
and then to the trabecular meshwork in the anterior chamber angle. During this
period, there is some differential exchange of components with the blood in the
iris.
4


Picture 2.1 Anterior segment structures. Arrows indicate direction of flow of aqueous.

2.1.3 Outflow of Aqueous
The trabecular meshwork is composed of beams of collagen and elastic tissue
covered by trabecular cells that form a filter with a decreasing pore size as the
canal of Schlemm is approached. Contraction of the ciliary muscle through its
insertion into the trabecular meshwork increases pore size in the meshwork and
hence the rate of aqueous drainage. Passage of aqueous into Schlemm's canal
depends on cyclic formation of transcellular channels in the endothelial lining.
Efferent channels from Schlemm's canal (about 30 collector channels and 12
aqueous veins) conduct the fluid directly into the venous system. Some aqueous
passes between the bundles of the ciliary muscle into the suprachoroidal space
and then into the venous system of the ciliary body, choroid, and sclera
(uveoscleral flow).
The major resistance to aqueous outflow from the anterior chamber is the
juxtacanalicular tissue adjacent to the endothelial lining of Schlemm's canal,
5

rather than the venous system. But the pressure in the episcleral venous network
determines the minimum level of intraocular pressure that can be achieved by
medical therapy.
2.2 Patophysiology of Glaucoma
The major mechanism of visual loss in glaucoma is retinal ganglion cell
apoptosis, leading to thinning of the inner nuclear and nerve fiber layers of the
retina and axonal loss in the optic nerve. The optic disk becomes atrophic, with
enlargement of the optic cup.
2
The pathophysiology of intraocular pressure elevationwhether due to open-
angle or to angle-closure mechanismswill be discussed as each disease entity is
considered. The effects of raised intraocular pressure are influenced by the time
course and magnitude of the rise in intraocular pressure. In acute angle-closure
glaucoma, the intraocular pressure reaches 6080 mm Hg, resulting in acute
ischemic damage to the iris with associated corneal edema and optic nerve
damage. In primary open-angle glaucoma, the intraocular pressure does not
usually rise above 30 mm Hg and retinal ganglion cell damage develops over a
prolonged period, often many years. In normal-tension glaucoma, retinal ganglion
cells may be susceptible to damage from intraocular pressures in the normal
range, or the major mechanism of damage may be optic nerve head ischemia.
2

2.3 Classification of Glaucoma
Two major forms of glaucoma exist: open-angle glaucoma, in which aqueous
humor has free access to the trabecular meshwork, and angle-closure glaucoma, in
which access of the aqueous humor to the trabecular meshwork is obstructed.
Both forms of glaucoma demonstrate a progressive optic neuropathy with visual
field loss and characteristic structural changes, including thinning of the retinal
nerve fiber layer and excavation of the optic nerve head. Intraocular pressure
6

(IOP) does not define glaucoma, and many with glaucoma have IOP
measurements that are also found in individuals without glaucoma.
3
The nomenclature of angle closure has undergone significant changes in the
last decade. The most commonly used definitional system is one proposed by
Foster and colleagues, in which subjects are defined based on examination
findings.

Primary angle-closure suspects (PACS) have 270 degrees or more of
iridotrabecular contact without elevated IOP or peripheral anterior synechiae
(PAS). Persons with primary angle closure (PAC) have 270 degrees or more of
iridotrabecular contact and elevated IOP, PAS or both. These individuals are felt
to have suffered adverse sequelae of the iridotrabecular contact, but do not have
glaucoma. Finally, persons with primary angle-closure glaucoma (PACG) have
270 degrees or more of iridotrabecular contact and characteristic optic nerve
damage. In addition, there is a group of patients who suffer an acute, symptomatic
elevation of IOP in association with angle closure, referred to as acute angle
closure (AAC).
3

Both open-angle and angle-closure glaucoma can occur secondary to other
ocular conditions though this chapter will mostly focus on primary open-angle
glaucoma (POAG) and PACG. While the optic neuropathies resulting from
POAG and PACG may differ in some ways,

even more distinct is the
epidemiology of these two conditions, which will be discussed separately below.
3
2.3.1 Primary glaucoma
a. Primary open-angle glaucoma (broad definition)
Primary open-angle glaucoma (broad definition) is a disease concept
including both conventional primary open-angle glaucoma (in the following,
this will denote the conventional concept of primary open-angle glaucoma
unless broad definition is specified) and normal-tension glaucoma. The risk
7

of the development and progression of primary open-angle glaucoma (broad
definition) increases with increasing IOP.
Moreover, there are differences in the vulnerability of the optic nerve to IOP,
and because primary open-angle glaucoma and normal-tension glaucoma
cannot be distinguished based on specified IOP values, the term primary open
angle glaucoma (broad definition) was developed as a concept encompassing
both disease types. Primary open-angle glaucoma (broad definition) can be
conveniently subdivided in the clinical setting into an ocular hypertension
group (primary open-angle glaucoma) and a normal IOP group (normal-
tension glaucoma). It was reported in the Tajimi Study that the IOP was 14.6
2.7 mmHg and 14.5 2.7 mmHg (mean standard deviation) in the right
eye and in the left eye, respectively, in Japanese. Thus, the upper normal limit
is 19.9-20.0 mmHg when we define normal IOP as mean value 2 standard
deviations. Accordingly, dividing this disease in Japanese subjects into the
two clinical disease types of primary open-angle glaucoma and normal-
tension glaucoma, taking IOP of 20 mmHg as a boundary, appears to be fairly
reasonable.
Primary open-angle glaucoma (broad definition) is characterized by
chronic progressive optic neuropathy in which the optic disc and retinal nerve
fiber layer show particular morphological characteristics (thinning of the optic
disc margin, retinal nerve fiber layer defects), and it is a disease type in which
other illnesses and congenital anomalies are absent and in which gonioscopy
shows a normal anterior chamber angle (although the presence of functional
anomalies of the anterior chamber angle cannot be ruled out). This is
accompanied by progressive retinal ganglion cell loss and corresponding
visual field defects. In cases of discrepancies between optic nerve findings
and visual field findings, if the optic disc is found to show pallor relative to
the degree of cupping, the visual field and optic nerve should be retested, and
8

brain imaging studies should be conducted in order to detect intracranial
diseases, etc. Moreover, among cases of primary openangle glaucoma (broad
definition), genetic variations in myocilin or optineurin gene may be detected.
b. Normal-tension glaucoma, normal-pressure glaucoma
In this subtype of primary open-angle glaucoma (broad definition),
IOP constantly remains within the statistically determined normal range
during the development and progression of glaucomatous optic neuropathy.
However, this does not necessarily mean that abnormal IOP does not play a
role in the development of optic neuropathy in normal-tension glaucoma. In
many cases, moreover, as another etiological factor, findings indicate that
factors independent of IOP (such as circulatory damage) may also play a role.
As IOP is known to be subject to diurnal and seasonal fluctuations, it is often
quite difficult to establish that it is always within the normal range, and tests
such as diurnal fluctuation measurements are frequently necessary.
c. Primary Angle-Closure Glaucoma
Primary angle closure occurs in anatomically predisposed eyes without
other pathology. Elevation of intraocular pressure is a consequence of
obstruction of aqueous outflow by occlusion of the trabecular meshwork by
the peripheral iris. The condition may manifest as an ophthalmic emergency
or may remain asymptomatic until visual loss occurs. The diagnosis is made
by examination of the anterior segment and careful gonioscopy. Primary
angle-closure glaucoma is the term that should be used only when primary
angle closure has resulted in optic nerve damage and visual field loss. Risk
factors include increasing age, female gender, family history of glaucoma, and
South-East Asian, Chinese, or Inuit ethnic background.

9

d. Acute Angle Closure
Acute angle closure ("acute glaucoma") occurs when sufficient iris
bomb develops to cause occlusion of the anterior chamber angle by the
peripheral iris. This blocks aqueous outflow, and the intraocular pressure
rises rapidly, causing severe pain, redness, and blurring of vision. Angle
closure develops in hyperopic eyes with preexisting anatomic narrowing of
the anterior chamber angle, usually when it is exacerbated by enlargement
of the crystalline lens associated with aging. The acute attack is often
precipitated by pupillary dilation. This occurs spontaneously in the
evenings, when the level of illumination is reduced. It may be due to
medications with anticholinergic or sympathomimetic activity (eg, atropine
for preoperative medication, antidepressants, nebulized bronchodilators,
nasal decongestants, or tocolytics). It may occur rarely with pupillary
dilation for ophthalmoscopy. If pupillary dilation is necessary in a patient
with a shallow anterior chamber (easily detected by oblique illumination
with a penlight [Figure 114]), it is best to rely on short-acting mydriatics,
avoid constricting the pupil with pilocarpine, and advise the patient to seek
attention immediately in the event of ocular pain or redness or increasingly
blurred vision.
1) Clinical Findings
Acute angle closure is characterized by sudden onset of visual loss
accompanied by excruciating pain, halos, and nausea and vomiting.
Patients are occasionally thought to have acute gastrointestinal disease.
Other findings include markedly increased intraocular pressure, a
shallow anterior chamber, a steamy cornea, a fixed, moderately dilated
pupil, and ciliary injection. It is important to perform gonioscopy on the
10

fellow eye to confirm the anatomic predisposition to primary acute
angle closure.
2) Differential Diagnosis
Acute iritis causes more photophobia than acute glaucoma. Intraocular
pressure is usually not elevated; the pupil is constricted or irregular in
shape and the cornea is usually not edematous. Marked flare and cells
are present in the anterior chamber, and there is deep ciliary injection.
Acute conjunctivitis is usually bilateral, and there is little or no pain
and no visual loss. There is discharge from the eye and an intensely
inflamed conjunctiva but no ciliary injection. The pupillary responses
and intraocular pressure are normal, and the cornea is clear.
3) Complications & Sequelae
If treatment is delayed, the peripheral iris may adhere to the trabecular
meshwork (anterior synechiae), producing irreversible occlusion of the
anterior chamber angle requiring surgery. Optic nerve damage is
common.
4) Treatment
Acute angle closure is an ophthalmic emergency!
Treatment is initially directed at reducing the intraocular pressure.
Intravenous and oral acetazolamidealong with topical agents, such as
beta-blockers and apraclonidine, and, if necessary, hyperosmotic
agentswill usually reduce the intraocular pressure. Pilocarpine 2%
should be instilled one-half hour after commencement of treatment, by
which time reduction of iris ischemia and lowering of intraocular
11

pressure allow the sphincter pupillae to respond to the drug. Topical
steroids may also be used to reduce secondary intraocular
inflammation. Once the intraocular pressure is under control, laser
peripheral iridotomy should be undertaken to form a permanent
connection between the anterior and posterior chambers, thus
preventing recurrence of iris bomb. This is most often done with the
neodymium:YAG laser (see above). Surgical peripheral iridectomy is
the conventional treatment if laser treatment is unsuccessful, but ALPI
may be performed. The fellow eye should always undergo prophylactic
laser iridotomy.
e. Subacute Angle Closure
The same etiologic factors operate in subacute as in acute angle closure
except that episodes of elevated intraocular pressure are of short duration and
are recurrent. The episodes of angle closure resolve spontaneously, but there
is accumulated damage to the anterior chamber angle, with formation of
peripheral anterior synechiae. Subacute angle closure will occasionally
progress to acute closure.
There are recurrent short episodes of unilateral pain, redness, and blurring
of vision associated with halos around lights. Attacks often occur in the
evenings and resolve overnight. Examination between attacks may show only
a narrow anterior chamber angle with peripheral anterior synechiae. The
diagnosis can be confirmed by gonioscopy. Treatment consists of laser
peripheral iridotomy.
f. Chronic Angle-Closure Glaucoma
Patients with the anatomic predisposition to anterior-chamber angle
closure may never develop episodes of acute rise in intraocular pressure but
12

form increasingly extensive peripheral anterior synechiae accompanied by a
gradual rise in intraocular pressure. These patients present in the same way as
those with primary open-angle glaucoma, often with extensive visual field
loss in both eyes. Occasionally, they have attacks of subacute angle closure.
On examination, there is elevated intraocular pressure, narrow anterior
chamber angles with variable amounts of peripheral anterior synechiae, and
optic disk and visual field changes.
Laser peripheral iridotomy should always be undertaken as the first step in
the management of these patients. Intraocular pressure is then controlled
medically if possible, but the extent of peripheral anterior synechia formation
and sluggish outflow through the remaining trabecular meshwork make
pressure control very difficult, so that drainage surgery is often required.
Cataract extraction with intraocular lens implantation can be effective in
controlling the intraocular pressure, provided no more than two quadrants of
synechial angle closure are present. Epinephrine and strong miotics must not
be used unless peripheral iridotomy or iridectomy has been performed
because they will accentuate angle closure.
2.4 Clinical Assessment in Glaucoma
2.4.1 Tonometry
Tonometry is measurement of intraocular pressure. The most widely used
instrument is the Goldmann applanation tonometer, which is attached to the
slitlamp and measures the force required to flatten a fixed area of the cornea.
Corneal thickness influences the accuracy of measurement. Intraocular pressure
is overestimated in eyes with thick corneas and underestimated in eyes with thin
corneas. This difficulty may be overcome by the Pascal dynamic contour
tonometer. Other applanation tonometers are the Perkins tonometer and the
13

Tono-Pen, both of which are portable, and the pneumatotonometer, which can
be used with a soft contact lens in place when the cornea has an irregular
surface. The Schiotz tonometer is portable and measures the corneal indentation
produced by a known weight.
The normal range of intraocular pressure is 1021 mm Hg (Figure 112). The
distribution is Gaussian, but with the curve skewed to the right. In the elderly,
average intraocular pressure is higher, giving an upper limit of 24 mm Hg. In
primary open-angle glaucoma, 3250% of affected individuals will have a
normal intraocular pressure when first measured. Conversely, isolated raised
intraocular pressure does not necessarily mean that the patient has primary
open-angle glaucoma, since other evidence in the form of a glaucomatous optic
disk or visual field changes is necessary for diagnosis. If the intraocular
pressure is consistently elevated in the presence of normal optic disks and visual
fields (ocular hypertension), the patient may be observed periodically as a
glaucoma suspect.
2.4.2 Gonioscopy
The anterior chamber angle is formed by the junction of the peripheral cornea
and the iris, between which lies the trabecular meshwork. The configuration of
this angleie, whether it is wide (open), narrow, or closedhas an important
bearing on the outflow of aqueous. The anterior chamber angle width can be
estimated by oblique illumination with a penlight or by slitlamp observation of
the depth of the peripheral anterior chamber, but it is best determined by
gonioscopy, which allows direct visualization of the angle structures. If it is
possible to visualize the full extent of the trabecular meshwork, the scleral spur,
and the iris processes, the angle is open. Being able to see only Schwalbe's line
or a small portion of the trabecular meshwork means that the angle is narrow.
Being unable to see Schwalbe's line means that the angle is closed. Large
14

myopic eyes have wide angles, and small hyperopic eyes have narrow angles.
Enlargement of the lens with age narrows the angle and accounts for some cases
of angle-closure glaucoma.
Picture 2.2 Composite illustration showing anatomic (left) and gonioscopic
(right) view of normal anterior chamber angle.

Picture 2.3 Estimation of depth of anterior chamber by oblique illumination
(diagram).
15

2.4.3 Optic Disk Assessment
The normal optic disk has a central depressionthe physiologic cupwhose
size depends on the bulk of the fibers that form the optic nerve relative to the
size of the scleral opening through which they must pass. In hyperopic eyes, the
scleral opening is small, and thus the optic cup is small; the reverse is true in
myopic eyes. Glaucomatous optic atrophy produces specific disk changes
characterized chiefly by loss of disk substancedetectable as enlargement of
the optic disk cupassociated with disk pallor in the area of cupping. Other
forms of optic atrophy cause widespread pallor without increased disk cupping.
In glaucoma, there may be concentric enlargement of the optic cup or
preferential superior and inferior cupping with focal notching of the rim of the
optic disk (Figure 115). The optic cup also increases in depth as the lamina
cribrosa is displaced backward. As cupping develops, the retinal vessels on the
disk are displaced nasally. The end result of glaucomatous cupping is the so-
called "bean pot" cup in which no neural rim tissue is apparent.

Picture 2.4 Early glaucoma showing inferior focal notching of the neuroretinal
rim (arrow).
16

The "cupdisk ratio" is a useful way of recording the size of the optic disk in
glaucoma patients. It is the ratio of cup size to disk diameter, eg, a small cup is
0.1 and a large cup 0.9. In the presence of visual field loss or elevated
intraocular pressure, a cupdisk ratio greater than 0.5 or significant asymmetry
between the two eyes is highly suggestive of glaucomatous atrophy.
Clinical assessment of the optic disk can be performed by direct
ophthalmoscopy or by examination with the 78-diopter lens or special corneal
contact lenses that give a three-dimensional view.
Other clinical evidence of neuronal damage in glaucoma is atrophy of the
retinal nerve fiber layer, which precedes the development of optic disk changes.
It is detectable by ophthalmoscopy or fundal photography, both aided by using
red-free light, optical coherence tomography, scanning laser polarimetry, or
scanning laser tomography.
2.4.5 Visual Field Examination
Regular visual field examination is essential to the diagnosis and follow-up of
glaucoma. Glaucomatous field loss is not in itself specific, since it consists of
nerve fiber bundle defects that may be seen in other forms of optic nerve
disease; but the pattern of field loss, the nature of its progression, and the
correlation with changes in the optic disk are characteristic of the disease.
Glaucomatous field loss involves mainly the central 30 degrees of field. The
earliest change is baring of the blind spot. Contiguous extension into Bjerrum's
area of the visual fieldat 15 degrees from fixationproduces a Bjerrum
scotoma and then an arcuate scotoma. Focal areas of more pronounced loss
within Bjerrum's area are known as Seidel scotomas. Double arcuate
scotomasabove and below the horizontal meridianare often accompanied
by a nasal step (of Roenne) because of differences in size of the two arcuate
17

defects. Peripheral field loss tends to start in the nasal periphery as a
constriction of the isopters. Subsequently, there may be connection to an arcuate
defect, producing peripheral breakthrough. The temporal peripheral field and
the central 510 degrees are affected late in the disease. Central visual acuity is
not a reliable index of progress of the disease. In end-stage disease, there may
be normal central acuity but only 5 degrees of visual field in each eye. In
advanced glaucoma, the patient may have 20/20 visual acuity and be legally
blind.
Various ways of testing the visual fields in glaucoma include the automated
perimeter (for example, Humphrey, Octopus, or Henson), the Goldmann
perimeter, the Friedman field analyzer, and the tangent screen. (For testing
techniques, see Chapter 2.) Conventional automated perimetry, most commonly
using the Humphrey perimeter, employs a white stimulus on a white
background (white-on-white perimetry). Visual field defects are not detected
until there is about 40% retinal ganglion loss. Refinements to detect earlier
visual field changes include blue-on-yellow perimetry, also known as short-
wavelength automated perimetry (SWAP), frequency-doubling perimetry
(FDP), and high-pass resolution perimetry.
2.5 Treatment of Raised Intraocular Pressure
2.5.1 Medical Treatment
- Suppression of Aqueous Production
a. Topical beta-adrenergic blocking agents may be used alone or in combination
with other drugs. Timolol maleate 0.25% and 0.5%, betaxolol 0.25% and 0.5%,
levobunolol 0.25% and 0.5%, metipranolol 0.3%, and carteolol 1% solutions
twice daily and timolol maleate 0.1%, 0.25%, and 0.5% gel once daily in the
morning are the currently available preparations. The major contraindications to
18

their use are chronic obstructive airway diseaseparticularly asthmaand
cardiac conduction defects. Betaxolol, with its relatively greater selectivity for
receptors, less often produces respiratory side effects, but it is also less effective
at reducing intraocular pressure. Depression, confusion, and fatigue may occur
with the topical beta-blocking agents. The frequency of systemic effects and the
availability of other agents has reduced the popularity of the beta-adrenergic
blocking agents.
b. Apraclonidine (0.5% solution three times daily and 1% solution before and after
laser treatment) is an alpha
2
-adrenergic agonist that decreases aqueous humor
formation without effect on outflow. It is particularly useful for preventing rise of
intraocular pressure after anterior segment laser treatment and can be used on a
short-term basis in refractory cases. It is not suitable for long-term use because of
tachyphylaxis (loss of therapeutic effect over time) and a high incidence of
allergic reactions. Epinephrine and dipivefrin have some effect on aqueous
production but are rarely used these days.
c. Brimonidine (0.2% solution twice daily) is an alpha-adrenergic agonist that
primarily inhibits aqueous production and secondarily increases aqueous outflow.
It may be used as a first-line or adjunctive agent, but allergic reactions are
common.Dorzolamide hydrochloride 2% solution and brinzolamide 1% (two
or three times daily) are topical carbonic anhydrase inhibitors that are especially
effective when employed adjunctively, although not as effective as systemic
carbonic anhydrase inhibitors. The main side-effects are a transient bitter taste
and allergic blepharoconjunctivitis. Dorzolamide is also available combined with
timolol in the same solution.
d. Systemic carbonic anhydrase inhibitorsacetazolamide is the most widely
used, but dichlorphenamide and methazolamide are alternativesare used in
chronic glaucoma when topical therapy is insufficient and in acute glaucoma
when very high intraocular pressure needs to be controlled quickly. They are
capable of suppressing aqueous production by 4060%. Acetazolamide can be
19

administered orally in a dosage of 125250 mg up to four times daily or as
Diamox Sequels 500 mg once or twice daily, or it can be given intravenously
(500 mg). The carbonic anhydrase inhibitors are associated with major systemic
side effects that limit their usefulness for long-term therapy.
- Facilitation of Aqueous Outflow
a. The prostaglandin analogsbimatoprost 0.003%, latanoprost 0.005%, and
travoprost 0.004% solutions, each once daily at night, and unoprostone 0.15%
solution twice dailyincrease uveoscleral outflow of aqueous. They are highly
effective first-line or adjunctive agents. In many countries but not the United
States, latanoprost is available combined with timolol in the same solution for use
once daily in the morning. All the prostaglandin analogs may produce
conjunctival hyperemia, hyperpigmentation of periorbital skin, eyelash growth,
and permanent darkening of the iris (particularly in green-brown and yellow-
brown irides). These drugs have also been rarely associated with reactivation of
uveitis and herpes keratitis and can cause macular edema in predisposed
individuals.
b. Parasympathomimetic agents increase aqueous outflow by action on the
trabecular meshwork through contraction of the ciliary muscle. Pilocarpine is not
commonly used since the advent of prostaglandin analogs but can be useful in
some patients. It is given as 0.56% solution instilled up to four times a day or as
4% gel instilled at bedtime. Carbachol 0.753% is an alternative cholinergic
agent. Parasympathomimetic agents produce miosis with dimness of vision,
particularly in patients with cataract, and accommodative spasm that may be
disabling to younger patients. Retinal detachment is a serious but rare occurrence.
c. Epinephrine, 0.252% instilled once or twice daily, increases aqueous outflow
with some decrease in aqueous production. There are several external ocular side
effects, including reflex conjunctival vasodilation, adrenochrome deposits,
20

follicular conjunctivitis, and allergic reactions. Dipivefrin is a prodrug of
epinephrine that is metabolized intraocularly to its active state. Neither
epinephrine nor dipivefrin should be used in eyes with narrow anterior chamber
angles. Both agents have an adverse effect on the outcome of subsequent
glaucoma drainage surgery.
- Miotics, Mydriatics, and Cycloplegics
Constriction of the pupil is fundamental to the management of primary angle-
closure glaucoma and the angle crowding of plateau iris. Pupillary dilation is
important in the treatment of angle closure secondary to iris bomb due to
posterior synechiae. When angle closure is secondary to anterior lens
displacement, cycloplegics (cyclopentolate and atropine) are used to relax the
ciliary muscle and thus tighten the zonular apparatus in an attempt to draw the
lens backward.
- Surgical & Laser Treatment
a. Peripheral Iridotomy, Iridectomy, and Iridoplasty
Pupillary block in angle-closure glaucoma is most satisfactorily
overcome by forming a direct communication between the anterior and
posterior chambers that removes the pressure difference between them. Laser
peripheral iridotomy is best done with the neodymium:YAG laser, although
the argon laser may be necessary in dark irides. Surgical peripheral iridectomy
is performed if YAG laser iridotomy is ineffective. YAG laser iridotomy is
preventive when used in patients with narrow angles before closure attacks
occur.
In some cases of acute angle closure when it is not possible to control
the intraocular pressure medically or YAG laser iridotomy cannot be
21

performed, argon laser peripheral iridoplasty (ALPI) can be undertaken. A
ring of laser burns on the peripheral iris contracts the iris stroma,
mechanically pulling open the anterior chamber angle. There is a 30% risk of
peripheral anterior synechiae and chronically elevated intraocular pressure,
but this may reflect the refractory nature of the cases treated.
b. Laser Trabeculoplasty
Application of laser (usually argon) burns via a goniolens to the
trabecular meshwork facilitates aqueous outflow by virtue of its effects on the
trabecular meshwork and Schlemm's canal or cellular events that enhance the
function of the meshwork. The technique is applicable to many forms of
open-angle glaucoma, and the results are variable depending on the
underlying cause. The pressure reduction usually allows decrease of medical
therapy and postponement of glaucoma surgery. Treatments can be repeated
(see Chapter 24). Laser trabeculoplasty may be used in the initial treatment of
primary open-angle glaucoma. In most cases, the intraocular pressure
gradually returns to the pretreatment level 25 years later. The outcome of
subsequent glaucoma drainage surgery may be adversely affected.
c. Glaucoma Drainage Surgery
The increased effectiveness of medical and laser treatment has reduced
the need for glaucoma drainage surgery, but surgery is able to produce a more
marked reduction in intraocular pressure.
Trabeculectomy is the procedure most commonly used to bypass the
normal drainage channels, allowing direct access from the anterior chamber to
the subconjunctival and orbital tissues (Figure 119). The major complication
is fibrosis in the episcleral tissues, leading to closure of the new drainage
22

pathway. This is most likely to occur in young patients, in blacks, in patients
with glaucoma secondary to uveitis, and in those who have previously
undergone glaucoma drainage surgery or other surgery involving the
episcleral tissues. Perioperative or postoperative adjunctive treatment with
antimetabolites such as 5-fluorouracil and mitomycin C reduces the risk of
bleb failure and is associated with good intraocular pressure control but may
lead to bleb-related complications like persistent ocular discomfort, bleb
infection, or maculopathy from persistent ocular hypotony. Trabeculectomy
markedly accelerates cataract formation.