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Thyroid Eye Disease (also known as T.E.D.) goes by many names including Graves' Associated Opthalmopathy (G.A.O.) and Thyroid-associated orbitopathy (T.A.O.). Thyroid Eye Disease is an autoimmune condition that, while separate from thyroid gland disease, is often seen in conjunction with an overactive thyroid gland (also known as Graves' Disease or hyperthyroidism).
Despite the association with an over-active thyroid gland the condition can occur in people with no other evidence of thyroid dysfunction, and occasionally in patients who have other forms of thyroid gland disease including Hashimoto's thyroiditis. The vast majority of patients with thyroid gland dysfunction will not develop signs or symptoms of thyroid eye disease, and if they do, the symptoms are usually mild.
Both the eye disease and the glandular disease are autoimmune in origin. Autoimmune diseases occur when the cells that normally protect the body from infection develop a glitch and begin to recognize the thyroid gland as foreign material and attack it. This stimulates the thyroid gland to produce extra thyroid hormones. This attack may spill over to the cells behind the eye causing them to swell. It is not yet known why immune cells develop the glitch that causes them to attack the thyroid gland or why only some patients with over-activity of the thyroid develop thyroid eye disease.
Active autoimmune disease within the eye socket leads to inflammation that results in swelling of the muscles that move the eyes and open the eyelids along with swelling and scarring of soft tissues that envelop and support the eyes. Because the eye socket is a boney socket incapable of expansion, the swollen tissues behind the eyeball causes the eyes to become pushed forward and more prominent. In addition there is retraction, or tightening and stiffening of the muscles that open the eyelids which forces the lids apart leading to an inability to fully close the eyelids and an abnormally large amount of the front of the eyes is exposed. This entire process results in wide, prominent eyes, a fixed staring expression, and infrequent blinking of the eyelids.
In more severe cases the swelling may cause stiffness of the muscles that move the eyes. This can result in "squint" or misalignment between the two that may result in double vision. Occasionally the swelling behind the eyeball may be so severe that the enlarged muscles press on the nerve from the eye to the brain and disrupt vision. Prolonged pressure on the delicate optic nerve may result in permanent vision loss.
Most people with thyroid eye disease have or had or will subsequently develop an overactive thyroid gland. In 20% the thyroid eye disease develops in people who do not have an overactive thyroid at the time (but may subsequently develop this years later). In 40% thyroid eye disease occurs while the thyroid is overactive and in 40% can occur years after the overactive thyroid has been treated successfully.
Severe thyroid eye disease associated with permanent vision loss is rare and probably only occurs in about 2% of patients with an overactive thyroid. For reasons that are poorly understood, smoking increases the risk of developing thyroid eye disease 8 fold and is associated with a more severe course of disease.
Thyroid eye disease mostly affects persons of 30 to 50 years of age. Females are four times more likely to develop the condition than males. When males are affected, they tend to have a later onset and a more severe course of eye disease.
Signs and Symptoms of Thyroid Eye Disease
Patients with thyroid eye disease may experience pain or pressure in or behind the eyes, pain when looking up and down or sideways, itching, difficulty wearing contact lenses, inflammation and swelling of the eyelids and the surrounding tissues, bloodshot eyes, double vision, and swelling in the orbital tissues which causes the eye to be pushed forward. The condition when the eyes begin to bulge from the eye socket is referred to as proptosis or exophthalmos. In combination with a widening of the eyelids, this forward displacement of the eyeballs can make thyroid eye disease sufferers appear to have a wide-eyed or bulging stare. Overexposure of the eyes during the day and an inability to completely close the eyelids at night can result in injury or damage to the cornea (the front of the eye) and irritation of the conjunctiva (the mucous membrane that lines the eye) resulting in considerable discomfort, and visual problems, such as blurred vision, foreign body sensation, excessive tearing or light sensitivity. In extreme cases corneal ulceration and scarring may occur that can result in permanent vision loss. In a small percentage of patients the disease may lead to progressive pressure on the optic nerve that can result in permanent vision loss due to neurologic injury in one or both eyes if left untreated.
The eye symptoms usually occur at the same time as the thyroid disease, however they may precede or follow the obvious symptoms of the thyroid gland abnormality. Although the incidence of eye disease associated with thyroid dysfunction is higher and more severe in smokers, there is no way to predict which thyroid patients will be affected.
Thyroid Eye Disease is known to go through varying degrees of severity, and can go into periods of remission as well. Once inflamed, the eye disease may remain active from several months to as long as three years. Subsequently, there may be a gradual or, in some cases, a complete improvement. In addition, while eye disease may have its onset during a period of thyroid gland dysfunction, successful treatment of the thyroid gland does not guarantee that the eye disease will improve, and no particular thyroid treatment can guarantee that the eyes will not continue to deteriorate. While rare, recurrence of the eye disease after a period of inactivity can happen and may coincide with inadequate control of thyroid hormone levels. When thyroid eye disease has been inactive for a period of about six months to one year, it is less likely to recur.
Thyroid eye disease is most commonly diagnosed clinically by the presence of classic ocular signs and symptoms, but positive tests for antibodies (anti-thyroglobulin, anti-microsomal and anti-thyrotropin receptor) and abnormalities in thyroid hormone levels (T3, T4 and TSH) can help in supporting the diagnosis. Orbital imaging using computerized tomography (CT), magnetic resonance imaging (MRI) and ultrasonography can be useful tools for the diagnosis of thyroid eye disease and also aids in monitoring patients for progression of the disease. On orbital imaging the most characteristic findings are thick extra-ocular muscles and proptosis.
Medical Management of Thyroid Eye Disease
Patients who have not already done so should be strongly encouraged to stop smoking. In addition careful checks of the thyroid blood level may help to prevent eye problems getting worse but despite this other treatment is sometimes required.
Thyroid eye disease ironically can be made worse during the actual treatment of the overactive thyroid gland and so certain preventative measures are taken to reduce this risk. If radioactive iodine therapy is used to treat an over active thyroid gland then patients may be asked to take prednisolone (a steroid) for up to 3 months after therapy to reduce the risk of onset or progression of thyroid eye disease.
Treatment of the symptoms of active thyroid eye disease
Irritation and Redness of the eyes is best treated with artificial tears (hypromellose drops). These drops are harmless and can be applied as often as required during the day. Because the eyelids may not close fully when sleeping, a lubricating ointment applied to the surface of the eyes when sleeping may be necessary to control nocturnal dryness. The use of plastic shields known as moisture chambers at night can help prevent drying of the cornea if the eyelids cannot close during sleep. Tarsorrhaphy (surgical sewing the upper and lower eyelids together) is an alternative option when the complications of ocular exposure can't be avoided solely with the drops.
Puffiness around the eyes is more difficult to treat. Using extra pillows at night may help or sometimes a water tablet (diuretic) may be prescribed for you. The swelling usually improves as the eyes begin to settle down. Tinted glasses with side guards will help protect the eyes and minimize light sensitivity.
If Double vision only occurs from time to time then no treatment is necessary. If the double vision begins to interfere with normal activity then treatment may be needed. Special glasses with lenses called prisms may be useful and if the double vision remains after the disease enters remission then eye surgery, known as strabismus surgery may be considered.
If deteriorating vision occurs quite rapidly specialist treatment with powerful (immunosuppressive) drugs may be needed to damp down the inflammation around the eyes. Alternatively surgery called orbital decompression or radiotherapy treatment may be considered.
If the inflammation around the eyes is very severe powerful drugs may be required to suppress the autoimmune process that is attacking the eyes. Currently daily steroid tablets or periodic infusions of intravenous steroids are used in this situation. Steroids are very effective in reducing swelling around the eyes and protecting the eyes from deteriorating vision but may cause weight gain, thinning of the bones and skin and diabetes if continued for a long time at high dosage. Steroids are therefore reserved for more severe cases and used only under specialist supervision. Newer therapies on the horizon may provide the same degree of immune suppression seen with steroids but without the negative side effects.
Radiotherapy (the use of radiation to treat disease) may also be used to control inflammation within the eye sockets. This treatment targets radiation to the tissues behind the eyeball. It involves usually 10 dosages given over 2 weeks. Two thirds of patients find significant benefit but regrettably one third do not and require other therapy such as orbital decompression. Often radiotherapy is combined with steroids and other forms of immunosuppression.
In severe cases urgent surgical orbital decompression may be necessary to provide more room in the orbit for the swollen eye muscles by removal of a portion of the boney walls that make up the eye socket. Although this surgery is usually delayed until after the disease has entered remission, it may become necessary to operate while the disease is still active if the pressure from the enlarging extraocular muscles compromises optic nerve function.
Surgical options for the treatment of stable thyroid eye disease
If your eyes are mildly affected they may return to nearly normal. This can take between 12 and 36 months. If the eyes have been more severely affected it is less likely that the changes will go away. In this situation surgical treatment is required and carefully planned surgery can be very effective in improving the appearance of the eyes. This may require squint (strabismus) surgery to minimize double vision or visible misalignment of the eyes, orbital decompression to reduce the prominence of the eyeball by expanding the boney eye socket through the removal of a portion of the walls that surround the eye and eyelid surgery to improve eyelid closure by the lengthening of the eyelid opening muscles as well as reducing the bags and wrinkles around the eye by the removal of excess fatty tissue and redundant eyelid skin. No surgery is 100% effective in reversing the changes brought about by thyroid eye disease but surgery can certainly help to greatly improve the situation.
The particular surgical techniques and the order in which they are performed will depend on the type and severity of the eye problems.
Risk factors of progressive and severe thyroid eye disease are:
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