C h a p t e r 3 8
Disorders of Special Sensory Function: Vision, Hearing, and Vestibular Function
967
develop suddenly at any time. Careful monitoring for
metamorphopsia, or distorted vision of straight lines,
can aid in the early detection of retinal damage.
Neovascular Degeneration.
The neovascular form of
AMD is characterized by the formation of a choroidal
neovascular membrane. These new blood vessels have
weaker walls than normal and are prone to leakage;
thus, this form is commonly referred to as “wet.” The
leakage of serous or hemorrhagic fluid into the subreti-
nal space causes separation of the pigmented epithelium
from the neurosensory retina. Over time, the subretinal
hemorrhages organize to form scar tissue, causing death
of the underlying retinal tissue and loss of all visual func-
tion in the corresponding macular area (see Fig. 38-10B).
Although some subretinal neovascular membranes may
regress spontaneously, the natural course is toward irre-
versible loss of central vision.
Diagnosis and Treatment.
The early stages of
subretinal neovascularization may be difficult to detect
with an ophthalmoscope. Therefore, there is a need to
be alert for recent or sudden changes in central vision,
blurred vision, or scotomata (visual field areas in which
vision is depressed or absent). Persons with late-stage
disease often find it difficult to see at long distances
(e.g., in driving), do close work (e.g., reading), see faces
clearly, or distinguish colors. However, they may not
be severely incapacitated because the peripheral retinal
function usually remains intact.
Effective therapies for neovascular macular degen-
eration include thermal laser photocoagulation, pho-
todynamic therapy, and intravitreal injections of VEGF
inhibitors.
23,31–33
Conventional retinal laser photoco-
agulation can achieve direct destruction of a choroidal
neovascular membrane. Photodynamic laser therapy
involves the intravenous injection of a dye that is subse-
quently activated by retinal laser irradiation to produce
selective vascular damage. Recognition of the key role
that VEGF plays in choroidal neovascularization patho-
genesis led to development of VEGF inhibitors, a class
of drugs that has now become the preferred treatment
for neovascular macular degeneration. These drugs are
given by intravitreal injection.
In addition to currently used and forthcoming
treatments, there is interest in the so-called preventative
category of treatments.
21,31–33
Tobacco smoking is
consistently identified as a preventable age-related
macular degeneration risk; thus, its elimination should
be one of the first therapeutic recommendations.
Preventative recommendations also include dietary
supplementation containing high-dose antioxidants and
minerals (vitamins E and C, zinc, and
β
-carotene) for
persons at risk for developing macular degeneration
and for slowing the progression of age-related macular
degeneration in persons with the disease.
30
However,
more experimental data and randomized clinical trials
are needed to support their therapeutic value, the most
effective composition in terms of single- or multiple-
supplement combinations, and dosing of the particular
supplements.
Disorders of Intraocular Pressure
The intraocular pressure reflects that of the aqueous
humor that fills the anterior and posterior chambers of
the eye. The aqueous humor is produced by the ciliary
body and passes from the posterior chamber through
the pupil into the anterior chamber
6,25,34,35
(Fig. 38-11A).
Aqueous humor leaves through the trabecular mesh-
work at the iridocorneal angle between the anterior iris
and the cornea. It then drains into the canal of Schlemm,
a thin-walled vein that extends circumferentially around
the iris, for return to the venous circulation. Intraocular
pressure results from a balance of several factors,
including the rate of aqueous humor production by the
ciliary body, the resistance to flow between the iris and
ciliary body, and its rate of removal by the drainage
system (trabecular meshwork and canal of Schlemm).
Normally, the rate of aqueous humor secretion is equal
to the rate of outflow, and the intraocular pressure is
maintained within a normal range of 10 to 21 mm Hg.
34
Glaucoma is a chronic, pressure-induced degen-
erative neuropathy that produces changes in the optic
nerve and visual field loss (see Fig. 38-1D). Glaucoma
is commonly classified as open-angle or angle-closure
glaucoma depending on the appearance of the iridocor-
neal angle, and according to whether it is a primary or
secondary disorder.
6,25,34,35
Open-Angle Glaucoma
Open-angle glaucoma, which is the most common
form of glaucoma, results from an abnormality of the
trabecular meshwork that controls the flow of aqueous
humor into the canal of Schlemm without obstruction
at the iridocorneal angle
34–36
(see Fig. 38-11B). Open-
angle glaucoma is usually asymptomatic and chronic,
causing progressive damage to the optic nerve and
vision loss unless it is appropriately treated. Elevated
intraocular pressure is a primary factor; however, some
eyes tolerate elevated intraocular pressure without
developing disk or visual field changes, whereas others
develop glaucomatous changes with consistently normal
intraocular pressures (normal-tension glaucoma).
Clinical Manifestations.
Because open-angle glaucoma
is usually asymptomatic, it is often suspected when
abnormal intraocular pressure measurements or optic disk
abnormalities are found during a routine eye examination.
The normal optic disk has a central depression called the
optic nerve cup
(Fig. 38-12). In glaucoma, the neuroretinal
rim of the optic nerve becomes progressively thinner,
thereby enlarging the optic nerve cup, a phenomenon
referred to as
optic nerve cupping
. Its cause is loss of
retinal ganglionic cell axons, along with supporting glia
and vasculature.
6
Because changes in the optic cup precede
visual field loss, regular ophthalmoscopic examinations
are important to detect damage to retinal ganglion axons
before visual field loss occurs.
Diagnosis and Treatment.
Diagnostic methods include
applanation tonometry (measurement of intraocular
