Eye Problems Associated With Graves' Disease
Introduction
Involvement of the eyes can be an unpredictable accompaniment of
thyroid disorders, producing a spectrum of symptoms ranging from
eye irritation, swelling, light sensitivity, and a staring appearance
to the less frequent but more severe problems of double vision,
cornea erosion, and optic nerve compromise. The initial symptoms
are common and annoying. The more advanced symptoms can evolve into
permanent eye changes and threaten vision, but these occur in only
a small percentage of people with thyroid disorders.
This discussion addresses the questions patients most
frequently ask.
- What causes the eyes to be irritated, to swell and to bulge?
- How long will it last, and when will the eyes return to normal,
or at least stop getting worse?
- Why do the eyes worsen after the thyroid gland has been cured?
- Why is it happening to me and not to everyone with thyroid disease?
- Will my vision be impaired?
- Can it be prevented?
- Can it be arrested or reversed?
- What treatments are available, and what is the expectation
for improvement?
- How should my eyes be monitored?
To understand the answers to these questions, one needs some information
about the autoimmune basis of the disorder, the several degrees
of eye changes, and the expected disease course.
Background of eye problems and Graves' disease
Eye problems developing with hyperthyroidism were described over
160 years ago by Dr. Robert Graves of Dublin. That is why it is
called Graves’ disease. It is now known to be an autoimmune disorder.
By "autoimmune," we mean that the body's immune system produces
a reaction to its own tissues -- in the case of Graves' disease
react not only against thyroid cells, but also commonly react against
tissues behind the eyes (muscles and fat) and rarely react against
skin tissues of the legs and hands. The reasons for this autoimmune
reactivity to several tissues is not fully understood, but probably
relates to similar tissue antigens in these areas, or perhaps to
neighboring genetic locations for these tissues.
The eye involvement, like the thyroid disorder, is mediated in
part by white blood cells (lymphocytes) that accumulate in the targeted
tissues. These cells produce the antibodies that cause local tissue
inflammation and fluid accumulation, resulting in abnormal functioning
of the affected tissues.
Connective tissue cells (fibroblasts) also react by releasing
complex proteins.
For the thyroid gland, this usually causes overactivity and increased
release of thyroid hormones. For the eyes, the immune reaction causes
swelling of muscles and fat behind the eyes (orbital tissues), resulting
in retraction of the eyelids, forward protrusion of the eyes (proptosis
or exophthalmos), and sometimes dysfunction of the eye muscles and
optic nerve.
Patterns of involvement
Most of the eye problems develop, if they are going to occur at
all, within eighteen months of the hyperthyroidism. Since the autoimmune
process may selectively affect the thyroid gland, the eyes, or the
skin, variants of Graves’ disease are seen in which one, two, or
all three of these tissues are affected. Thus, the thyroid may be
overactive while the eyes and skin remain normal. Alternatively,
eyes or skin may be affected while the thyroid continues to release
normal amounts of thyroid hormone.
While most people with overactive thyroid due to Graves’ disease
probably have some mild eye changes that do not cause them any symptoms,
about three per cent of them with more severe disease will require
some form of treatment. Although clinicians speculate that the type
of treatment given to control thyroid overactivity may influence
the development of eye problems, there is as yet not clear consensus
that one form of treatment is superior in preventing the later emergence
of eye involvement.
Although the fundamental cause of Graves’ eye disease remains
unknown, we do understand the immediate cause of the symptoms and
findings that patients experience. The eye socket is a cone and
the globe of the eye sits in it like a scoop of ice cream. The walls
of the cone are made of bone that resists expansion. The muscles
that move the eyes partially fill the space in the cone behind the
globe and the rest of that space is filled with vessels and loose
connective tissue. Through this space runs the optic nerve.
In Graves’ eye disease the eye muscles and connective tissue swell
for reasons that are still not fully understood. Regardless of why
they swell however they increase the pressure in the space behind
the globe of the eye and force the globe forward in the orbital
cone. As the globe moves forward more of the sensitive cornea is
exposed. The eyes become red and congested and the eyelids fail
to cover the protruding globe. If the pressure behind the eye is
high enough the function of the optic nerve may be impaired and
this can cause blurring of vision and loss of color vision. The
swollen eye muscles move sluggishly and when they do not move in
concert the patient experiences double vision. Thus one can accurately
state that ALL the clinically apparent manifestations of Graves’
eye disease stem from either swelling in the space behind the globe
of the eye or from restriction of the motion of the muscles that
move the globe of the eye. It follows that effective treatment for
Graves eyes will either reduce the swelling, expand the space, or
improve the range or coordinate the movement of the eye muscles.
Treatments that aim to reduce swelling
For many years cortisone derivatives such as prednisone or prednisolone
have been used to reduce the swelling and congestion in Graves’
eyes. These agents are effective but when used long term or in high
dosage they evoke undesirable side effects such as weight gain,
high blood sugar and thin bones. Other immunosuppressive agents
such as azathioprine have been tried but have not been widely accepted
as being both safe and effective. External beam radiotherapy has
been employed for the same purpose but its usefulness has recently
been challenged and its place in the treatment of Graves’ eyes is
currently being reassessed.
Treatments that expand the orbital space include many varieties
of orbital decompression which vary only in where the incision is
made, from which orbital wall bone is removed and how much new space
is actually created. Different medical centers tend to specialize
in different procedures so it is wise to ask your surgeon for the
information that supports the choice you have been offered.
Treatments that affect the movement of the eye muscles are almost
entirely surgical. There may be some role for exercises intended
to strengthen the eye muscles. Some patients are very much benefited
by the addition of prisms to their glasses. These prisms can correct
for minor degrees of double vision. Severe degrees of double vision
require repositioning the shortened swollen eye muscles so they
can at least keep the eye straight in the resting position and while
reading.
In approaching surgical treatment of Graves’ eye disease the desired
sequence is to first perform orbital decompression if it is needed.
Eye muscle surgery is next and surgery that is intended to improve
eyelid position is done last. As is true of most surgical procedures
the training, skill and experience of your surgeon are important
determinants of outcome.
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