Thyroid orbitopathy

Your doctor thinks you have thyroid orbitopathy. This is an autoimmune disease, in which a person’s own immune system attacks the tissues of that person. In thyroid orbitopathy the immune system produces factors that enlarge the muscles that move the eyes. In this condition there may be eye prominence, eyelid retraction, double vision, visual loss, and eye irritation. Abnormalities in the functioning of the thyroid gland (hyperactivity in Graves’ disease or hypoactivity in Hashimoto’s thyroiditis) may
accompanied by ocular involvement. In most cases there is no close relationship between treatment of the thyroid disorder and the ocular manifestations which may persist despite good control of thyroid function. Thyroid orbitopathy may be present in the absence of clinical manifestations of thyroid involvement.

The movement of each eye is controlled by six muscles.
Four of these muscles, the inferior rectus, superior rectus, external rectus, and internal rectus are the most commonly affected. These muscles originate behind the eye at the tip of the orbital cavity, and attach to the eye just behind the cornea (the clear portion covering the coloured part of the eye). The muscles are not visible on the surface of the eye as they are covered by a thin layer of tissue (the conjunctiva) except when the blood vessels on their foremost part become prominent. Stimulation by the immune system of the fibroblasts, the supporting cells inside the muscles, causes the muscles to enlarge and become stiffer.
The enlargement of the muscles pushes the eyeball forward. The stiffness of the muscles that raise the upper eyelids causes the eyelids to retract over the coloured part of the eye. The eye can become red as a result of the poor closure of the eyelids as well as because of the prominence of the blood vessels.

When the muscles become too large, they can compress, and therefore damage, the optic nerve. As the optic nerve is essential for the transmission of information from the eye to the brain, its damage results in loss of vision. Fortunately, this complication only occurs in approximately 5% of patients with thyroid orbitopathy, and is reversible if the pressure on the optic nerve is removed quickly.

We do not know exactly how and why the immune system
attacks the eye muscles. The consequence of the attack is to cause an enlargement
of these muscles. The progressive enlargement of the muscles can cause: a forward displacement of the eyeball, rigidity of the muscles (causing impairment of eye movement), and abnormal pressure on the optic nerve. The inferior rectus muscle (located
under the globe) is most frequently affected. When this muscle becomes rigid, the eyeball cannot move upwards normally. This often results in double vision, with one image above the other.
If the optic nerve is compressed, the patient may develop blurred or dark vision.
Visual blur or distortion of vision may also be the result of abnormalities of the surface of the eye due to dryness or exposure or it may be due to compression of the optic nerve. It is important to distinguish between these two causes of visual impairment.

The diagnosis of optic nerve damage is made from the examination of the vision, pupils and visual field as well as from the appearance of the optic discs on fundus examination.


Although thyroid orbitopathy is typically preceded by abnormalities in thyroid function, occasionally ocular symptoms may appear first or in the presence of normal thyroid function.
The link between the eye and the thyroid gland is through the immune system. The same conditions that cause the immune system to attack the eye muscles will cause it to attack the thyroid gland first. At the level of the thyroid gland the autoimmune attack has the effect of causing an overproduction of thyroid hormones and thus a state of hyperthyroidism. Hyperthyroidism is characterised by tremors, restlessness, weight loss, increased heart rate, palpitations, nervousness, and heat intolerance. More rarely, the immune attack on the thyroid gland will lead to a decrease in thyroid hormone production. Antibodies that attack the thyroid gland can be detected in the blood.

Patients with thyroid orbitopathy often experience blurred or double vision. Due to the forward displacement of the eyeball there is frequently redness of the conjunctiva (the white of the eye) as well as symptoms of eye irritation such as tearing or a feeling of sand in the eye. Although patients with thyroid orbitopathy do not usually experience pain, they may complain of a feeling of heaviness in the eye socket. Other discomforts such as tightness, irritation and increased sensitivity to light may also be present.
Double vision is often perceived as “one image above the other”. The two images may also be next to each other. When double vision occurs, the position of one image in relation to the other may vary with the direction of gaze. The separation between the two images is often more pronounced when looking upwards or to the sides. Sometimes patients are only aware of the symptoms produced by the overactive thyroid gland (nervousness, tremors, palpitations, heat intolerance, weight loss, diarrhoea) or the underactive thyroid gland (fatigue, weight gain, constipation, skin thickening). These symptoms may precede the ocular symptoms by months or even years.

Thyroid orbitopathy can be suspected from
the patient’s appearance. Excessive elevation of the upper eyelids, particularly in downward gaze
especially in downward gaze, the exorbitant appearance and the prominence of blood vessels on either side of the pupil. Other signs include incomplete closure of the eyelids during sleep, increased resistance when trying to push the eyeballs backwards, abnormal reaction of the pupils and limitation of the normal excursion of the eyeballs. The pressure inside the eye may be too high, especially in certain gaze positions.

As with other autoimmune diseases, the active phase of thyroid orbitopathy begins and ends on its own.
thyroid orbitopathy begins and ends on its own. There is frequently only one episode of acute inflammation, the effects of which may, unfortunately, persist for years or permanently. Even when the inflammation is resolved, things do not return to normal. The prominence of the eyes may decrease but the abnormal eye movements and the abnormal position of the eyelids persist indefinitely. Eyelid closure may also remain abnormal.
The aim of treatment is to improve the symptoms of orbital involvement. When the orbital involvement is mild, consisting mainly of a sensation of eye irritation and a foreign body in the eye, the use of artificial tears and lubricating ointment at bedtime may be sufficient. If the eyelids do not close completely, tape can be used to hold them closed at night. For serious corneal problems it may be necessary to close the eyelids or elevate the lower eyelid surgically. In cases of marked retraction of the eyelids
In cases of marked eyelid retraction, surgery is often recommended to reduce the restraining effect of the retractor muscle, thus allowing better eye closure. Smoking aggravates the symptoms of thyroid orbitopathy and should be discontinued.
There is no medication to improve eye muscle function and thus treat double vision. Recent studies suggest that good control of thyroid function may reduce double vision without making it normal.
Double vision can be easily controlled by closing one eye (any eye). It can also be eliminated by realigning the eyes with prisms. When double vision cannot be corrected with prisms, eye muscle surgery is used. In most cases, the surgeon will ensure that the degree of double vision is stable before performing surgery. It is not recommended to perform surgery on a patient with fluctuations in the degree of double vision as any improvement will only be temporary. Often, since several eye muscles are involved, the desired result cannot be achieved in a single operation and must be addressed several times. Perfect correction of double vision may not be possible with any treatment. The aim is to eliminate diplopia in the positions in which it is most troublesome, i.e. straight ahead and in the reading position.

Fortunately, it is rare that the visual impairment is due to damage to the optic nerves. When such damage does occur, it is due to the pressure of the eye muscles on the nerve. The aim of treatment in this situation is to reduce the size of the muscles with steroids (prednisone). For patients who do not tolerate such treatment, muscle irradiation may be beneficial. When the size of the muscles cannot be reduced sufficiently to reduce nerve compression and improve vision, the orbital cavity must be surgically enlarged. This is done by removing one or more of the bony walls of the orbit. Since the optic nerve is typically compressed in the back of the orbit, it is the back of the orbit on the side of the nose that must be resected. This can be done directly (through the soft tissue or skin surrounding the eye), through the sinus under the eye, or through the nose.
In order to reduce the prominence of the eye, the floor, outer wall and even the roof of the orbit may have to be removed. One of the problems encountered following surgical decompression of the orbit is an impairment of ocular motility, either by changing the characteristics of existing double vision or by inducing double vision in someone who did not have it.

Frequently asked questions

The doctors tell me that they have treated my thyroid gland properly and that it is functioning normally. Why do I still have problems with my eyes?
In Graves’ disease, due to stimulation by the immune system, the thyroid gland secretes too many hormones. The excess of hormones is responsible for various symptoms such as nervousness, palpitations, weight loss, diarrhoea, tremors, and intolerance of the thyroid gland.
tremors, and heat intolerance. Treatment is aimed at limiting the production of hormones by the gland. Treatment modalities include medication, thyroid surgery, and radioactive iodine administration.
Following these treatments, which may require the addition of thyroid hormone, there is a return to normal function of the gland. However, none of these treatments affect the autoimmune process that causes the disease. The immune system can therefore continue to attack tissues other than the thyroid gland and in particular the eye muscles. Damage to the eye should therefore be treated separately (as detailed above) from the treatment. Orbital symptoms may worsen after treatment of the thyroid gland with radioactive iodine.
Steroids make my eyes more comfortable. Can I continue to take them?
Treatment with steroids can reduce the duration of the inflammatory phase associated with thyroid orbitopathy and reduce muscle enlargement, however prolonged use of steroids is frequently accompanied by potentially serious side effects. In a patient with persistent impairment of eye movement, eye exposure problems (eye irritation and foreign body sensation), or vision loss, surgical treatment should be considered.
Why can’t my eyelid disorder be corrected with surgery now?
Surgery on the muscles responsible for vertical eye movements can affect the position of the eyelids. It is therefore best to wait until the eye muscle surgery is done before addressing the eyelids.
Can’t I just put my eyes back in the socket?
We can reduce the prominence of your eyes by performing a surgical orbital decompression. If you already have stiff muscles, orbital decompression may produce double vision. Double vision can be treated with eye muscle surgery. However, if you do not currently have double vision it is possible to improve the appearance of your eyes with surgery confined to the eyelids, thus eliminating the risk of double vision.
Why is it necessary to operate on my good eye as well?
Surgery on the muscles of the eye can improve the function of a muscle that has become rigid due to disease. However, as a result of enlargement and fibrosis, such a muscle is often unable to move the eye in a normal way. If we operate only on the most affected eye, it will have limited movement and you will be left with double vision when looking away from the front. By limiting the eye movements of the other eye, we can maximise the area of single vision.

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