Thyroid eye disease: symptoms, treatments, and recommendations

Thyroid eye disease – also known as ophthalmopathy or thyroid orbitopathy– refers to eye and periocular changes resulting from thyroid disease. This pathology causes an increase in the volume of the extraocular muscles and orbital fat, which causes proptosis or bulging eyes, said in a colloquial way.

Thyroid eye disease has an annual incidence of 16 women and 3 men per 100,000 inhabitants per year. It is one of the most common anatomical eye conditions, as it represents 70% of orbital pathologies.

The Basics of Thyroid Eye Disease

Thyroid eye disease is an autoimmune disease. As indicated by the portal NanosWeb (North American Neuro-Ophthalmology Society), the immune system of the patient with this condition produces factors that stimulate the enlargement of the muscles that move the eye.

4 of the facial muscles are the most affected. Among them, the upper rectum, the lateral rectum, the lower rectum and the median rectum.

All these musculature originate in the posterior part of the ocular apparatus – at the bottom of the orbit – and adhere to the eye behind the cornea. In normal situations, they are not directly visible.

For reasons that we will see in later lines, the patient's immune system attacks fibroblasts. These are cell types of connective tissue that synthesize fibers – collagen and glycosaminoglycans – and maintain the extracellular matrix of tissues.

When the immune system damages fibroblasts there is a generalized inflammation of the eye muscles. With its enlargement, the eyeball is pushed forward, which generates proptosis. Difficulty closing the eyes and bulging blood capillaries lead to widespread redness.

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What are the symptoms?

The Institute of Ocular Microsurgery (IMO) shows us the most common symptoms of this condition. Thyroid eye disease manifests as orbital inflammation that presents as swelling of the eyelids, bulging of the eyeball, eyelid retraction, and occasionally strabismus.

Once the pathology has started, the period of inflammation can be extended for up to 2 years. In addition, in the most severe cases, vision is compromised – in 5% of patients.

Some of the most common clinical signs are the following:

  • Foreign body sensation in the eye apparatus, irritation and tearing from exposure of the cornea.
  • Double vision by strabismus.
  • Decreased visual acuity. This happens due to a compression of the optic nerve.

The manifestation is usually bilateral – in both eyes – but sometimes there is a clear asymmetry in the progression between one eye and the other. In addition to all the clinical signs described, the patient may manifest photophobia and intense pain in the retrobulbar area.

It is the thyroid disease that is at the base of the ocular alterations that we are describing.

Why is it produced?

Although it may seem like a simple clinical entity, answering this question is a task that is still under development. The journal of Endocrinology and Nutrition tells us that everything indicates that the cause of thyroid eye disease is autoimmune for 3 reasons:

  1. In all patients an immune abnormality is found at the level of the thyroid gland. From 25% to 50% of people with Graves' hyperthyroidism present with manifestations of ophthalmopathy.
  2. Many patients they respond well to the administration of immunosuppressants.
  3. There is usually a closeness in time between the development of hyperthyroidism and thyroid eye disease.

The most widely accepted hypothesis is that the immune system recognizes some antigens – substances that activate antibodies – common between the thyroid and orbital tissues. Although the antigen responsible for this response has not yet been identified, sources already cited indicate that it is the receptor for TSH (thyrotropin hormone).

Thyroid eye disease and hyperthyroidism

As we said, the antibodies involved in ophthalmopathy are the same as in hyperthyroidism. Specifically, they are TRAb or TSI, also known as anti-TSH receptor antibodies. Fibroblasts of the orbital muscles present these receptors.

Up to 50% of patients with Graves' hyperthyroidism will end up developing this ophthalmopathy. Other signs that accompany ocular involvement, due to thyroid malfunction, are nervousness, fatigue, muscle weakness, weight loss, sleep problems, and tremors.

How is it diagnosed?

The Navarra University Clinic (CUN) shows us the protocol that must be followed to quantify the ocular involvement in the patient. Among the most common methods we find the following:

  • First, it must be verified that there is no corneal involvement. It is necessary to rule out clinical entities such as keratitis.
  • A CT (computed tomography) scan and MRI can help elucidate how inflamed the eye muscles are.
  • These imaging methods also they will help assess the level of optic nerve involvement. It is very important to detect if this clinical sign is present, since it causes partial or total loss of vision.
  • Depending on the degree of involvement of the eyes, tests of visual acuity, visual field and color vision can be performed.

Anyway, the diagnosis is multidisciplinary, since it requires the evaluation of an ophthalmologist and an endocrinologist alike. The TSH, T3 and T4 test and thyroid antibody blood test will help detect the presence of this problem at the systemic level.

Treatment of thyroid eye disease

Usually, thyroid eye disease has a positive prognosis. It is estimated that up to 2/3 of patients suffer spontaneous improvement, 22% remain stable and only 13.5% get worse. Furthermore, in most cases the ophthalmopathy is mild.

General treatment of mild cases

When it is mild patients are advised to wear eye protectors (glasses), artificial tears during the day and eye lubricants at night, as indicated by the Endocs portal. In addition, it is also indicated to raise the head of the bed to sleep in an upright position.

Endocrinological control

Antithyroid and beta-blocker medications help reduce the overproduction of thyroid hormones and symptoms associated with hyperthyroidism. You can also go to treatment with active iodine and, in the most severe cases, to surgery to remove part or most of the thyroid gland.

Corticosteroid pulses

They are administered to the patient high doses of intravenous corticosteroids. This approach lasts for about 6 weeks and is only considered in those patients with optic nerve impingement.

Behind the eyeball is the optic nerve, which if compressed puts the patient's ability to see at risk.

Surgical treatments for proptosis

The bulging of the eyeball can be treated surgically. Some of the medical approaches to this clinical sign are as follows:

  • Orbital decompression: To treat severe exophthalmia, the space in the orbital cavity can be increased (bone decompression) and its fat content reduced (fat decompression).
  • Eyelid retraction correction: For this, the muscles responsible for lifting the eyelid are weakened.
  • Strabismus surgery: focused on correcting double vision caused by exophthalmia.

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Thyroid eye disease is treatable

As you may have seen, thyroid eye disease is a common clinical entity in those who suffer from hyperthyroidism. Although it is determined by aesthetically alarming clinical signs, only 3-5% of cases are considered serious and many remit spontaneously.

As a last point, it is necessary to emphasize that scientific sources highlight that smoking increases the chances of severe forms. Quitting smoking is a necessity so that the pathology does not progress quickly.