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DISTURBANCES IN VISION
GLAUCOMA

Norman M. Aquino M.D.

Marissa N. Valbuena M.D., MHPEd

INTRODUCTION

Glaucoma is a neurodegenerative disease characterized by death of retinal ganglion cells and loss of
their axons. This leads to the formation of defects within the nerve fiber layer of the retina (RNFL) with
subsequent cupping, or excavation, of the optic nerve head. As a result, functional visual field disturbance or
visual field loss occur.

OBJECTIVES

After reading this material, the medical student in ophthalmology is expected to:
1. discuss the pathophysiology of glaucoma
2. given a patient with glaucoma, be able to extract a complete history and perform an ocular
examination.
3. discuss the examinations for glaucoma.
4. discuss the principles of management of glaucoma

RECOMMENDED PREPARATION

The student is advised to review the anatomy and physiology of the anterior chamber angle, retina and optic
nerve before going through this material. He is also advised to review the parts of a clinical history and the
method of conducting a complete eye examination.

CONTENT

Glaucoma and The Optic Nerve

The assessment of the morphologic features of the optic disc are essential in glaucoma. (Table 1).
The optic disc can be examined clinically with a direct ophthalmoscope, an indirect ophthalmoscope, or a
posterior fundus lens (with a slit lamp). The direct ophthalmoscope, although providing high magnification,
does not provide sufficient stereoscopic detail. The main disadvantage of the indirect ophthalmoscope is the
small image size. The best method to examine the optic disc is with the posterior fundus lens with a slit lamp.
This system provides high magnification, excellent illumination and a stereoscopic view of the disc.

Table 1: Clinical Evaluation of the Optic Nerve Head

1. Size and shape of the optic disc;
2. Size, shape, and pallor of the neuroretinal rim;
3. Size of the optic cup in relation to the area of the optic disc;
4. Configuration and depth of the optic cup;
5. Cup-to-disc diameter ratio and cup-to-disc area ratio;
6. Position of the exit of the central retinal vessel trunk on the lamina cribrosa surface;
7. Presence and location of splinter-shaped hemorrhages;
8. Occurrence, size, configuration, and location of parapapillary chorioretinal atrophy;
9. Diffuse and/or focal decrease ot the diameter of the retinal arterioles; and
10. Visibility of the RNFL

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The optic disc is usually round or slightly oval in shape and contains a central cup. The tissue between the
cup and the disc margin is the neuroretinal rim (Fig.1). In normal patients, this rim has a uniform width and a
color that ranges from orange to pink.

It is common practice to grade an optic disc by comparing the diameter of the cup to the diameter of
the disc in both the horizontal and vertical meridians. This is usually expressed as a ratio such as 2/10 or 0.2.
Usually, a horizontal cup-to-disc ratio of 3/10 or 0.3 is considered normal. Cup-to-disc ratio increases slightly
with age. There are also racial differences in cup-to-disc ratios.

Fig.1- Normal Optic Nerve. Arrows show borders of optic disc and cup

Elevated intraocular pressure was traditionally considered to be solely responsible for the anatomic
damage in glaucoma. However, it has now been shown that there are other factors which play a role in the
production of these morphologic changes seen in the glaucomatous optic nerve. Inherent structural defects,
genetic predisposition, vascular and biochemical insults have been found to play a significant role in the
pathogenesis of the disease. (Fig.2)

Fig.2- Concept of proposed pathogenesis of glaucoma. European Glaucoma Society

The appearance of the optic disc often provides essential information about the existence, the stage, and
course of the disease (Table 2).

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Table 2: Optic Disc Signs of Glaucoma

Generalized Signs
1. Large optic cup
2. Asymmetry of the cups
3. Progressive enlargement of the cups
Focal Signs
1. Localized narrowing of the neuroretinal rim (notching)
2. Vertical elongation of the cup
3. Cupping to the rim margin
4. Regional pallor
5. Splinter hemorrhage
6. Nerve fiber layer loss
Less Specific Signs
1. Exposed lamina cribrosa
2. Nasal displacement of vessels
3. Baring of circumlinear vessels
4. Peripapillary atrophy

Generalized enlargement of the cup may be the earliest change detected in glaucoma (Fig. 3). This
may be difficult to appreciate unless previous clinical records, diagrams or photographs are available. It is also
useful to compare one eye to the fellow eye as disc asymmetry is unusual in normal individuals. Focal
enlargement of the cup appears as localized notching or narrowing of the rim (Fig. 4). If this occurs at either
(or both) the superior or inferior pole of the disc, the cup becomes vertically oval. In more advanced
glaucoma, the tissue destruction extends behind the cribriform plate and the lamina bows backward. The
optic nerve head then takes on an excavated and undermined appearance that has been likened to a
“beanpot” (Fig. 5). Splinter hemorrhage usually appears as a linear red streak on or near the disc surface (Fig.
6). The hemorrhage clears over several weeks but is often followed by localized notching and pallor of the
rim with subsequent visual field loss.

Fig. 3- Enlarged optic cup with narrow neuroretinal rim.

Fig. 4 - Localized loss of neuroretinal rim (notching)

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F
Fig. 5 - Glaucomatous disc damage: Eye of patient; of a cadaver; and a histologic section showing
excavation or cupping of the optic disc

Fig. 6 - Splinter Hemorrhage in the disc

In the normal eye, the nerve fiber layer can be best visualized with red-free illumination, and appears
as a pattern of striations that radiate toward the optic disc. With the development of glaucoma, the nerve
fiber layer thins and becomes less visible. Diffuse loss of the nerve fiber layer may be a very important sign of
early glaucomatous damage (Fig.7).

Fig. 7 - Nerve fiber bundles

The Normal Visual Field

With the eye open and looking straight, the visual field of that eye is defined as all the space that it
can see. The dimensions of the normal field of vision are defined relative to fixation. The normal visual field
extends approximately 60 degrees superior and nasal, 70 degrees inferior, and 90-100° temporal to fixation

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(Fig. 8). . The blindspot occupies the area defined by the optic nerve head and is typically located 15 degrees
temporal to fixation. Visual sensitivity is greatest in the center, the fovea, and decreases toward the periphery.
By convention, the visual field of each eye is plotted as the patient sees it.

Fig. 8 - Normal limits of the visual field of the right eye

Traquair graphically described the visual field as a three-dimensioned “island of vision surrounded by
a sea of blindness” (Fig. 9). He described the variable slope of the island, the “peak” of sensitivity at fixation,
and the normal blind spot as a “gorge” that drops to sea level at a location approximately 15° to the temporal
side of the highest peak.

Fig. 9 - Traquiar’s Island of vision/ Hill of vision

The size and contour of a visual field can be influenced by other factors in addition to glaucoma.
These include facial structure, eyelid anatomy, pupil size, clarity of the ocular media, and refraction. Many
neurologic and neuro-ophthalmologic conditions also alter the visual field.

Testing the Visual Field

Visual field testing, or perimetry, is an important diagnostic tool in glaucoma. It likewise plays a
critical role in monitoring the disease’s progression. There are various ways of testing and mapping out a
patient’s visual field.

The confrontational method of visual field testing will quickly demonstrate gross field defects. It may
be the only practical method to evaluate patients who are unable to perform well using the more sophisticated

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instruments used in perimetry testing. The detection of small field defects in early glaucoma may be missed
using this technique.

Kinetic visual field testing is performed, as the name implies, with a moving test object. The object,
usually a light of variable size and intensity projected on an evenly illuminated surface, is moved from a non-
seeing area toward a seeing area. The location is recorded when the patient sees the object. The process is
repeated until a boundary of seeing and non-seeing is determined. This boundary line is called an isopter.
Several isopters are usually obtained using test objects of different size and or intensity (Fig. 10). The
Goldmann perimeter is an example of a manual kinetic perimeter.

Fig. 10 - Kinetic perimetry

Fig. 11 - Static perimetry

Static visual field testing involves the use of non-moving test spots. Fixed test spots of varying
intensity of light are presented for a short period of time. The patient responds when light is perceived in
each test spot. Static testing attempts to find the light sensitivities of the eye at preselected locations in the
visual field. It describes the contour of the hill of vision (Fig. 11). The Humphrey Visual Field Analyzer and
the Octopus are examples of automated static perimeters.

The Glaucomatous Visual Field

Glaucomatous optic nerve damage produces characteristic changes in the contour and shape of the
visual field. It is important to correlate changes in the visual field with changes in the optic disc. If an
appropriate correlation is not present, other causes of visual field loss must be considered.

Visual field changes seen in glaucoma reflect retinal and optic nerve anatomy. Retinal nerve fibers
radiate from the optic nerve head and are distributed in an arcuate manner around the foveal region (Fig. 12).
Glaucomatous damage at the optic nerve head produces visual field defects in the region subserved by the

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affected nerve fibers. The location, distribution, size and shape of the resulting visual field defect, called a
scotoma, is therefore determined by the location and extent of the anatomic defect. Typical glaucomatous
visual field defects include localized paracentral scotomas, arcuate defects, nasal steps, and temporal defects.

Fig. 12 - Distribution of retinal nerve fibers

The most common location of glaucomatous visual field defects occurs within an arcuate area
commonly referred to as Bjerrum’s area which includes that portion of the arcuate region that extends from
the blindspot to the median raphe, where it extends 10-20 degrees nasally from fixation (Fig. 13) The arcuate
scotoma often begins as a single area of relative loss which become larger, deeper and multi-focal (Fig. 14). In
its full form, the scotoma arches from the blind spot and ends at the nasal raphe, becoming wider and closer
to fixation on the nasal side (Fig. 15). Later in the disease, the arcuate scotoma may break through the nasal
periphery.

A paracentral scotoma is a discrete area of absolute or relative visual loss within 10° of fixation. The
scotoma can be single or multiple and can occur as an isolated finding or can be associated with other visual
field defects. Paracentral scotomas may be missed because of their location and small size. With progression,
paracentral scotomas become deeper and larger and may gradually coalesce forming an arcuate or Bjerrum
scotoma.

A nasal step is a depression in the superior or inferior nasal field near the horizontal raphe. It can
occur as an isolated finding in early glaucoma or can be associated with a paracentral or arcuate defect.

A temporal defect is a wedged-shaped defect extending from the periphery toward the central visual
field (Fig. 16). These defects are produced by damage to the nasal neuroretinal rim. Nerve fibers radiate
without deviation from the optic nerve; therefore wedge-shaped defects develop. Temporal defects are
usually found as a late manifestation of glaucomatous visual field loss.

Fig. 13 - Bjerrum’s area

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Fig. 14 - Beginnings of an arcuate scotoma

Fig. 15 - Full arcuate scotoma

Fig. 16 - Temporal wedge defect

Summary: The Optic Nerve and The Visual Field

The visual field is the functional correlate of the anatomical change brought about by the
glaucomatous damage to the optic nerve. Visual field examination, or perimetry, is useful in assessing optic
nerve function. Correlating the information obtained by careful examination of the optic nerve with its
function is far superior to using either piece of information alone.

Primary Open Angle Glaucoma

The chief pathologic feature of primary open angle glaucoma is a degenerative process in the trabecular
meshwork resulting in reduction of aqueous drainage leading to a rise in intraocular pressure. Raised
intraocular pressure preceded the optic disc and visual field changes by months to years.

Many patients are asymtopmatic. They may have blurring of vision which they attribute to an error of
refraction. Focal loss of vision such as in scotoma, unless severe is rarely noticed by the patient. Diagnosis is
established when glaucomatous optic disc or visual field changes are associated with elevated intraocular
pressure, a normal appearing anterior chamber angle by gonioscopy and no other reason for elevated
intraocular pressure.

Normal Tension Glaucoma

(Low Tension Glaucoma)

Some patients may have glaucomatous optic disc of visual field changes But have IOP consistently below 22
mm Hg. Pathogenesis of low tension glaucoma may involve abnormal sensitivity to IOP because of vascular
or mechanical abnormalities in the optic nerve head, or this may be a purely vascular disease.

Although intraocular pressure is within the normal range, reduction of intraocular pressure may still be
beneficial.

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Primary Acute Angle Closure Glaucoma

When sufficient iris bombe develops to cause occlusion of the anterior chamber angle by the peripheral iris.
Aqueous outflow is blocked and IOP rises causing severe pain, redness and blurring of vision. Attack is
precipitated by papillary dilatation, which can occur spontaneously, by reduced illuminations in the evenings
or due to medications.

Patients complain of sudden severe blurring of vision, with severe pain, nausea and vomiting. Ocular findings
include ciliary injection, a hazy cornea, shallow anterior chamber and an elevated IOP.

Acute angle closure glaucoma is an emergency. Treatment is directed at reducing IOP. Laser peripheral
iridotomy , which creates a permanent connection between the posterior and anterior chamber is the
definitve treatment. In many cases, the fellow eye should receive a prophylactic laser iridotomy.

Chronic Angle Closure Glaucoma

Some patients with anatomic predisposition for angle closure do not develop acute rises in intraocular
pressure but develop instead progressive peripheral synechia resulting in gradual rise in intraocular pressure.
They may have attacks of subacute angle closure.
Patients maybe asymptomatic or may have recurrent short episodes of unilateral pain, redness and blurring of
vision associated with halos around lights. Attacks may resolve spontaneously.

On examination, patients have elevated intraocular pressure, narrow or closed anterior chamber angle with
varying amounts of peripheral anterior syneechia, optic disc and visual field changes.

Intraocular pressure is controlled medically if possible. Extensive peripheral synechia may require drainage
surgery.

Treatment of Raised Intraocular Pressure

I. Medical Treatment
A. Suppression of aqueous production
1. beta adrenergic blocking agents – timolol, betaxalol, levobunolol
2. alpha adrenergic agonists- apraclonidine, brimonidine
3. carbonic anhydrase inhibitors- dorzolamide, oral acetazolamide

B. Facilitation of aqueous outflow.

1. Parasymathomimetic agents – pilicarpine
2. Prostaglandin analogs – bimatoprost, latanoprost, travaprost

C. Reduction of vitreous volume

1. Hyperosmotic agents – oral glycerol, IV mannitol

II. Surgical and Laser Treatment

A. Peripheral iridotomy, Iridectomy
B. Laser trabeculoplasty
C. Glaucoma Drainage Surgery
1. Trabeculectomy
2. Glaucoma valves
D. Cyclodestructive Psocedures

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SUMMARY

Glaucoma is an important ocular disorder that can cause preventable blindness. It results from ganglion cell
loss with resultant optic nerve damage and functional visual field loss.

REFERENCES

1. American Academy of Ophthalmology Basic and Clinical Science Course Glaucoma Section 10,
2004-2005.
2. Epstein, David L. (ed). Chandler and Grant's Glaucoma. Williams and Wilkins. 1997.
3. Riordan-Eva, Whitcher, John. Vaughn and Ashbury’s General Ophthalmology , 16th Edition, New York:
Lange Medical Books/ McGraw Hill, 2004
4. Ritch, R.; Shields, B.M.; Krupin, T. (eds) The Glaucomas. Mosby. 1996.

SELF-TEST

1. Signs of acute angle closure glaucoma include the following, EXCEPT

A. Ciliary injection
B. Irregular miotic pupil
C. Hazy cornea due to bedewing
D. Ocular pain
E. Blurring of vision

2. The following are methods for viewing the optic disc, EXCEPT
A. indirect ophthalmoscopy
B. Schiotz tonometry
C. Direct ophthalmoscopy
D. Use of posterior fundus lens and slit lamp

3. You were assigned to see 4 patients at the OPD. Which of the following findings in your patients will
make you suspect that he has glaucoma ?
A. 20 year old ; C/D ratio 0.5 OU, IOP = 15 mm OU
B. 45 year old ; C/D ratio 0.3 OU, IOP = 22 mm OU
C. 60 year old, C/D ratio 0.3 OD, 0.8 OS, IOP =12 mm OD, 28 mm OS
D. 60 year old, C/D ratio 0.3 OD. 0.4 OS, IOP=16 mm OD, 18 mm OS

4. Using the direct ophthalmoscope , you will be able to examine the following EXCEPT
A. scotoma
B. cup disc ratio
C. nerve fiber layer
D. pallor of the optic nerve

5. The typical visual field defect in glaucoma is a/an

A. arcuate scotoma
B. nasal hemianopsia
C. quadrantanopia
D. any of the above, depending on the severity of the disease.

ANSWERS TO SELF-TEST
1. B 2. B 3. C 4. A 5. A

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