Diabetes mellitus is a disorder that is caused by a deficiency
in insulin (Type 1) or an inability of existing insulin (Type
2 ) to keep blood sugars under control. Over time patients
with diabetes, especially those with poorly controlled blood
sugar may develop eye, kidney, heart, nerve and skin problems.
In the eye, diabetes mainly affects the retina and causes diabetic
retinopathy. Diabetes affects small blood vessels all over
the body and makes them abnormally leaky. In the retina, capillaries
(the tiniest of blood vessels) that supply nutrients and remove
waste products become leaky and allow contents of blood (serum,
lipids, and blood cells) to leak into the retina, causing the
retina to swell (edema). This stage of retinopathy is called
non-proliferative or background retinopathy. When swelling
occurs in the macula (the part of the retina responsible for
color and fine vision), vision becomes blurred and permanent
damage can occur to the retina. Your retina specialist will
examine your eye to determine if there is swelling in the macula
that requires treatment (clinically significant macular edema).
Treatment can be performed with laser in the office and may
be repeated one or more times over the course of the lifetime
of the patient. In some cases injections of steroid into the
eye may be performed to help reduce swelling. In severe cases,
vitrectomy surgery (removal of the vitreous gel) may be necessary,
especially if laser and steroids have failed.
In more severe cases of diabetic retinopathy, leaky capillaries
may become permanently damaged and may not work at all. This
capillary damage results in lack of blood flow to sections
of the retina (ischemia). Ischemia results in the production
of chemical messengers in the retina that lead to development
of abnormal new blood vessels (retinal neovascularization)
that can grow out of the retina and into the vitreous (the
jelly like substance that fills the eye). This stage of retinopathy
is called proliferative diabetic retinopathy. These blood vessels
use the vitreous gel as scaffolding and grow along its back
surface (posterior hyaloid). Since the gel is in motion when
the eye moves and these blood vessels are pulled on by the
gel and in turn pull on the retina, they can lead to vitreous
hemorrhage. Vitreous hemorrhage causes string like floaters
that worsen and result in severe haze. The hemorrhage can become
severe enough to cause severe vision loss and blindness. The
pulling on the retina also can cause retinal detachment and
result in severe visual loss and blindness. Your retina specialist
will examine your eye for neovascularization. It is best to
detect and treat neovascularization early with scatter laser
treatment. (Yes, you can have 20/20 vision and still have abnormal
retinal vessels!) This type of laser treatment destroys the
damaged retina that is making the chemicals that cause these
abnormal blood vessels to grow. After laser treatment, abnormal
blood vessels shrink and are less likely to result in vitreous
hemorrhage and retinal detachment. If vitreous hemorrhage or
retinal detachment is severe or sight threatening, vitrectomy
surgery may be necessary to restore vision and stabilize the
retinopathy.
The most important way to prevent visual loss in diabetes
to keep blood sugars and blood pressures under good control.
Keeping the Hemoglobin A1C (long term measure of sugar control)
under 7.0 is extremely important. Tight blood sugar control
reduces the risk of developing diabetic retinopathy. Even if
retinopathy develops, patients with tight control tend to have
mild and non-sight threatening retinopathy. Annual check-ups
by your eye doctor or retina specialist after the diagnosis
of diabetes and every 6 month follow-up evaluation once diabetic
retinopathy develops is important. Women who have diabetes
and become pregnant may need very close monitoring during pregnancy.
The eye is like a complex hollow ball. The back 2/3rds of
this hollow ball are filled with a gel like tissue called the
vitreous. The vitreous has the consistency of solid gelatin
at birth and is important for the normal maturation and development
of the eye. After age 4 or 5, the eye matures to its adult
size and the vitreous begins a long process of degeneration
(liquefaction) and becomes more jelly like in consistency.
Small pockets of liquefaction occur in the central vitreous
and, between age 50-70, these pockets combine together and
form one large pocket of liquefied gel. The peripheral gel
is still solid and attached firmly to the retina and optic
disc but there is no support from the central liquefied vitreous.
The peripheral gel eventually and suddenly collapses and pulls
away from the retina. This event is called a Posterior Vitreous
Detachment (PVD). The tugging of the vitreous on the retina
causes streaks of flashing lights in the peripheral visual
field. The collapse of the vitreous results in one or more
large floaters. When the PVD occurs, the vitreous may tug hard
enough on the peripheral retina to tear it. A tear in the retina
may be associated with hundreds or thousands of tiny, dot-like
floaters. A tear the retina should be treated prompted with
laser or cryotherapy (freezing treatment) to decrease the risk
of retinal detachment.
A retinal detachment occurs when a tear
or hole in the retina allows the liquid vitreous to get under
the retina and accumulate. The retina separates from the
back wall of the eye. This detachment causes symptoms of a
gradually enlarging veil or dark shadow in the peripheral visual
field. When the detachment extends into the central part of
the retina (macula) the central vision is lost. Retinal detachments
should generally be fixed or complete loss of vision will result.
Ideally the retinal detachment should be repaired prior to
the involvement of the macula. If the macula becomes detached,
the vision is unlikely to be as good as it was prior to the
retinal detachment even with successful surgical re-attachment.
Retinal detachments may be fixed in the office in some selected
cases by using a gas bubble and laser treatment called pneumatic
retinopexy. More complex detachments commonly require sleral
buckling or vitrectomy surgery in a hospital setting with anesthesia.
In scleral buckling surgery, the retinal tear or tears (there
may be several or many) are treated with cryotherapy (freezing
treatment) and a band is sutured around the eyeball that indents
the eye wall inward against the detached retina. This bump
seals the retinal tears and the fluid under the retina is absorbed
by the body. Thus, the retina becomes reattached to the back
wall of the eye. A third way to fix retinal detachments is
to perform vitrectomy surgery. The vitreous is removed using
small needle like microinstruments. The tear is identified
and treated with laser. The fluid under the retina removed
with a straw like instrument. All of the fluid in the eye is
then removed, and a gas bubble that usually lasts 2-6 weeks
is placed in the eye. The bubble acts as an internal splint
keeping the retina in place while the laser heals. The body
absorbs the gas bubble slowly and the eye replaces the bubble
with its own fluid. The vitreous does not grow back and is
not necessary for the normal functioning of the eye. Remember
that the collapsing vitreous gel actually caused the tear(s)
that led to the detachment. Your retina surgeon will decide
which of these three procedures is the best way to fix each
retinal detachment.
ARMD is the leading cause of legal blindness in persons over
the age of 55. Early symptoms include a reduction in reading
speed, inability to read fine print, and skipping letters or
lines when reading. Later symptoms can include distortion of
straight lines or dark or missing areas in the central vision.
The macula is the central part of the retina and allows us
to read fine print clearly and see colors vividly. It is this
area of the retina that deteriorates in ARMD. There are 2 forms
of ARMD. Everyone who has macular degeneration starts out with
the dry type and 20% progress to the wet type over the course
of a lifetime. Macular degeneration in its most severe forms
almost never causes total blindness. Usually only central vision
is lost. It is a disease that leaves older persons unable to
read and drive. However, nearly all patients will still have
enough vision to care for themselves
As the macula ages, the retinal cells cannot remove their
own waste products and begin to die. Deposits of these waste
products, called drusen, build up under the retina. Drusen,
when large in number and size, are the first signs of macular
degeneration that an eye doctor sees on examination. Collections
of drusen can crowd out other cells in the retina and can cause
further damage to the retina and the pigmented cell layer underneath
the retina called the retinal pigment epithelium. Eventually,
clumping pigment and punched out areas of pigment loss called
geographic atrophy are seen. These areas can cause blind spots
in vision. These areas of atrophy progress slowly over years
but can result in severe central vision loss. Currently there
is no specific treatment for dry macular degeneration.
20% of patients with dry degeneration will eventually develop
abnormal blood vessels under the retina that can bleed and
leak fluid. Patients often have abrupt vision loss with distortion
of straight lines, or a stationary, dark or blurry spot in
the central vision of one eye. The vision can worsen rapidly
in a few days or weeks. Treatment can include traditional laser,
injection of steroids into the eye, and/or ocular photodynamic
therapy (cold laser). Each treatment has its risks and benefits
and is individualized for the patient by the retina specialist.
Multiple treatments may be necessary to control the disease.
The treatments usually only slow down the disease and neither
cure the disease nor commonly make the vision better.
Since macular degeneration cannot be cured, much research
has been done on its prevention. Genetics play a role in ARMD.
Persons who have relatives with ARMD, especially parents
or siblings, are at greater risk for developing macular
degeneration. Exposure to ultraviolet light radiation may aggravate
ARMD. Persons with ARMD should wear sunglasses that block 100%
of UVA and UVB light when outdoors. Patients with ARMD
should eat 2 to 3 servings daily of darkly pigmented fruits
(red or black grapes, blueberries, cantaloupes, strawberries,
etc.) and dark green leafy vegetables (spinach, broccoli,
mustard or turnip or collard greens). Eating these foods
daily has been scientifically shown to protect the macula
and slow down the progression of macular degeneration.
Also, the Age-Related Eye Diseases Study (AREDS) has shown
that daily dietary intake of high doses of Vitamin A, C, E
, and the minerals zinc and copper can also slow down macular
degeneration and prevent severe vision loss especially in those
with advanced ARMD. Most important of all, patients should
monitor the central vision in each eye daily with an Amsler
grid to determine if there are any distorted lines or dark
spots. If any changes are present, contact the retina specialist
within 24-48 hours. These symptoms may be a sign that wet macular
degeneration has started or recurred after treatment and indicate
the need for urgent evaluation and possible treatment.
Histoplasmosis is an infectious disease caused by Histoplasma
capsulatum, a yeast like fungal organism that lives in the
gastrointestinal tract of birds and is spread to humans by
inhalation of dried and airborne dust containing spores. Almost
everyone who lives or spends time in the Ohio and Mississippi
River valleys has had systemic Histoplasmosis (almost 80 million
people).
Most of us get exposed to histoplasmosis and develop a flu-like
illness and heal from it without problems. About 10% of persons
who get this flu-like illness can develop scars in the back
of the eye affecting the retina and a vascular layer under
the retina called the choroid (Ocular Histoplasmosis). Sometimes
these scars can occur around the optic nerve or near the macula.
The scars themselves do not cause any visual problems. Many
years later and generally in the prime of life (ages 20 to
55) these scars can be sites for the development of new blood
vessels under the retina called choroidal neovascularization.
Depending on where these blood vessels grow, they may or may
not cause vision loss. The closer they are to the macula the
more likely they are to cause vision loss. These new vessels
are most often treated with laser, which can produce a blind
spot at the site of treatment but will prevent further vision
loss. Even with successful laser treatment, choroidal neovascularization
may come back 25% of the time in the first five years in the
treated eye. In some cases the abnormal blood vessels grow
directly under the very center of the macula (fovea) and cannot
be treated with laser because the resulting blind spot would
be in the center of vision. In these cases, medical therapy
with steroids (prednisone), cold laser treatment (ocular photodynamic
therapy), or simply conservative observation may be recommended.
In some very severe cases, surgical removal of blood vessels
may be performed.
It is very important to monitor central vision in both eyes
using an Amsler grid daily if you have ocular histoplasmosis
and especially if the vision has been affected in one eye.
Patients who develop choroidal neovascularization in one eye
have a 25% chance of developing the same in the fellow eye
within 3 years if they have histo scars close to the macula.
|
