Thyroid Eye Disease 101: What Is It, How to Diagnose, Treatment Options and More.

Diseases and Condition
Written by Harsha Sharma
February 14, 2024

Thyroid eye disease may seem to be related to thyroid. In a way it is related to thyroid, more specifically, the production of the hormone – thyroid. The condition is also usually related to Graves’ Disease.

The latter causes Graves’ Eye Disease (GED) or more commonly known as Thyroid Eye Disease or TED.

The condition, as the name suggests, includes adipocytes, fibroblasts, optic nerve, extra-ocular nerves and the orbital vasculature (which is just the collection of arteries and veins.) The other names that are associate themselves with thyroid eye disease are: Graves’ ophthalmology and Graves’ orbitopathy.

The condition is known to be an autoimmune condition that is a complex inflammatory disorder of the eyes. It also involves the systemic thyroid status which can unpredictably affect the progression of TED.

The following article delves deeper into the condition, emphasizing the causes, symptoms that can help you recognize it and the treatment options among others.

Contents

What Is Thyroid Eye Disease?

The immune system is a sophisticated biological system that protects an organism’s body from diseases. The system is known to detect any threat that enters the body and knocks it down before any harm can be done. In thyroid eye disease, the immune system attacks the muscles and tissues around the eyes.

As per the recent reports, the prevalence rate of the condition is nearly 19/100, 000. The prevalence of TED in the United States is nearly 63, 726 in a population of 335, 401, 864. In addition, the condition affects around 155 to 250 people per 100, 000 of the overall populaces.

The frequent symptoms that may be experienced with the condition are quite a handful. However, these symptoms help in recognizing the signs that point towards the condition.

The following section will also address “how to reduce swelling from thyroid eye disease?” as it involves a lifestyle change.

Who Are Affected?

As per a study, nearly 50% of the people with Graves’ disease develop thyroid eye disease. The condition annually affects 16 out of 100,000 females, and just 2.9 or 3 males out of 100,000 within the US population.

Apart from an apparent gender discrimination in the prevalence, there are also other risk factors:

Age: This is prominent in age groups such as 40-44 years and 60-64 years in females. Along with 65-69 years in males. The severity of the condition is seen prominently in elderly people.
Moreover, there are higher chances of people with dysthyroid optic neuropathy and restrictive myopathy being affected with TED.
Ethnicity: It is also known that African American populace is at an elevated risk than White and Asian, that follow up quite closely.
Genetics: Genetics plays a big role in the determination of several diseases. The condition, TED, is also dependent on the family history. Such that, if there is a history of the condition or if the parents may be a carrier of the condition, it is most likely to affect that person as well.
Genes such as the CTLA-4, HLA-DRB-1 and TNF-alpha genes. These genes are more prominently associated with thyroid eye disease.
Environmental factors: The environmental factors that can promote the development of this condition include smoking. The toxic products that are present in cigarettes or tobacco-based products can worsen the symptoms of hypothyroidism.
Dysthyroid status: The dysthyroid status determines the dis-balance from the normal thyroid conditions. People who receive a diagnosis of TED usually have a presence of hyperthyroid (around 90%), 6% have euthyroid, 3% show Hashimoto thyroiditis symptoms while 1% have hypothyroid.

Euthyroid is a condition where the serum levels of thyroid hormones are low, however, they have nonthyroidal systemic illness.
Radioactive iodine therapy: RAIT can lead to exacerbation in nearly 24% TED cases.
Pregnancy: During the post-partum period, it is necessary to take care of the new mother as they are 30% more likely to develop the signs of Graves’ disease.
Stress: Stress aggravates several diseases and conditions. The condition is also known to elevate the chances of a person developing TED.
Stress is known to cause rebound immune hyperactivity that follows corticosteroid-induced immune suppression.

Apart from these, trauma can also affect the extent to which the condition can spread. Trauma can trigger ana autoimmune cascade in the orbit (space that holds the eyeball.) In addition, high cholesterol can act as a significant risk factor for the condition.

How Does Thyroid Eye Disease Occur?

The development of thyroid eye disease occurs in three phases. The initial phase is when there’s a steep rise in the severity of the disease and it lasts six months. The stage can also last from a couple of years to 5 years.

Next is the inflammatory phase where TED is active. There is no specific duration of this. The final stage of the condition is the stable, inactive phase where the condition stabilizes. By this time, the TED regresses beyond 18 months (about 1 and a half years) of activity.

The condition does not return to the baseline and there are changes that stay persistent in the orbit. Limiting the condition requires aggressive immunosuppressive management during the initial phase when it is active. This helps in stopping the fibrotic and destructive consequences of the immune cascade.

In addition, the inactive phase is when the medical management does not perform well, thus needing surgical intervention.

There is a famous model that helps understand the progression of the disease in an enhanced manner. The Cone Model helps explain the condition by expanding the muscle cone against a rigid bony orbit in three phases.

The first, circumferential cone expansion displaces the extraconal fat outwards.
Second, the axial elongation of the cone leads to proptosis and muscle strain.
The final phase is muscle stiffness and cone hypertension that impedes the orbital venous drainage.

The Cone model clarifies the difference between the normal state of the eyes and when thyroid eye disease occurs.

Normally, the rectus muscles anchor the globe to the orbital apex with the connective tissue encapsulating the joints and muscles. This is the intermuscular septa, defining the muscle cone.
Extraconal fat surrounds the cone, while the venous drainage to the cavernous sinus passes superior and inferior ophthalmic veins.
However, in case of thyroid eye disease, the circumferential enlargement of the muscle cone leads to the displacement of extraconal fat. This causes the rectus muscles to stretch, consequently elevating the cone pressure. Finally, the high pressure stops the venous drainage to the cavernous sinus.

Changes To Anticipate During Thyroid Eye Disease

The condition can lead to several changes that are obviously not pleasant. This section describes these changes, further discussing the prominent changes such as eyelid changes, surface and orbital changes among others.

The usual changes that occur are:

Dryness
Photophobia
Excessive watering
Pain behind the eyes
Redness

There may even be visual disturbances such as:

Double vision
Blurring, both of which require immediate intervention

In most cases of Graves’ disease, the onset precedes the diagnosis in around 20% of the cases. The condition can also lead to retraction of eyelids, which is characteristic of proptosis.

5 Major changes due to thyroid eye disease:

Eyelid changes

Orbital changes

Ocular surface changes

Optic nerve changes

EOM changes

1. Eyelid Changes

Changes here are obvious in this condition and are also one of the primary signs that indicate this condition’s development.

There may be an alteration of the upper eyelid contour which is a characteristic sign. This is known as “lateral flare,” and occurs due to scarring between levator aponeurosis and lacrimal gland fascia.

There’s also lid lag that is a vertical downward pursuit, the excursion of the upper eyelid lags the globe. Lagophthalmos is the incomplete closure of eyelid, which is due to the protrusion of the eyes.

TED also causes lower and upper lid retraction. Enlargement of the levator muscle by the action of immune cascade is one of the proposed mechanisms through which upper lid retraction occurs.

2. Orbital changes

The changes that can be observed in the orbit are as follows:

– EOM and hypertrophy of the orbital fat within the bony orbit. This raises the pressure within the orbit.

– Proptosis, the classic sign of TED.

– Venous congestion which leads to the swelling and redness of the eyelids. Additionally, it also causes caruncular edema.

– Venous and lymphatic stasis in the orbit. This leads to an elongated half-life of inflammatory cytokines which leads to a cycle of inflammation.

– Elevated episcleral venous pressure which leads to an increase in intraocular pressure and open-angle glaucoma.

– Fracture of the medial or inferior walls of the orbit, spontaneously, leading to auto-decompression.

3. Ocular surface changes

These are observed during the active phase. There may be eyelid-tear film-cornea that is a result of inflammatory damage to the mucous gland present in the conjunctiva.

There may also be inflammation of the lacrimal gland, which alters the protein profile of the tear film. This leads to the reduction in the rate of tear secretion.

Persistent lagophthalmos agitates the ocular surface elevating the rate of tear production, also the tear osmolarity.

There may also be:

– Dry eye symptoms

– Watering in 13-20% of the patients

– Superior limbic keratoconjunctivitis, which is the chronic inflammatory disease of the superior bulbar conjunctiva, upper cornea and limbus.

– Exposure-keratopathy and persistent dry eye.

– Corneal perforation, ulceration and endophthalmitis – the infection of the fluids or tissue inside the eyeball.

4. Optic nerve changes

The condition may lead to Dysthyroid optic neuropathy, a reversible damage to the optic nerve in TED patients. There may also be:

– Diminishing contrast sensitivity

– Color vision

– Diminished vision

– Constriction in visual field

These may be due to:

Optic nerve stretching
Compressive optic neuropathy is the most common cause.
Ischemic optic neuropathy is due to an increase in the resistance to the blood flow in orbital arteries. This leads to diminishing perfusion.
There is also the enlargement of the superior ophthalmic vein, which leads to a rise in the retro-bulbar pressure and impaired tissue oxygenation.

5. EOM changes

There is an inflammation of the EOM during the active phase of the condition.
There’s also the infiltration of EOM, which leads to the accumulation of hyaluronic acid and late-onset fibrosis. Most commonly, the inferior and medial rectus muscles are involved. This also involves the superior and lateral rectus and oblique muscles.
Loss of single binocular vision, restrictive strabismus.
Diplopia at presentation (6-18%). Diplopia in primary and inferior gaze is a serious complication.
During active disease, the condition may cause fluctuation of diplopia.

Diagnosis and treatment of TED

This condition is diagnosed during the active phase when the symptoms are visible. The persistent discomfort raises an alarm in the person experiencing it, which leads to a proper consultation.

It may be a general physician or your healthcare provider who can conduct a physical examination to provide you with a proper diagnosis.

The tests may include:

Physical eye exam where they examine your eyes, and eyelids
Computed Tomography or CT scan
Magnetic Resonace Imaging or MRI.
Ultrasound

Blood tests to check the level of thyroid and antibodies.

These tests help in concluding the cause of the symptoms and proceeding with the treatment.

Treatment of TED

The treatment options include the following:

Over-the-counter medicines to treat thyroid eye disease such as eye drops that relieve irritation, dryness, redness. Drops are OTC medication that generally does not require prescription and helps in keeping the eyes lubricated.

Additionally, patients may also benefit from selenium supplements if there is a low level of this mineral. Selenium for thyroid eye disease has been an effective option especially when there is a deficiency in the mineral’s level.

Prescription medicines such as anti-inflammatory drugs (prednisone), systemic steroids and rituximab. Alternatively, the doctor may suggest consumption of aloe vera juice to reduce inflammation.

Lifestyle changes that can help in improving your condition such as quitting smoking. This habit increases the risk of developing TED and decreases the treatment’s effectiveness. Using cool compress on eyes, wearing sunglasses, taping eyelids shut while sleeping, wearing glasses with prism or eye-patch to reduce double vision. Keeping a check on thyroid hormone levels, getting regular hormone tests.

Keeping your head elevated while sleeping can help reduce the swelling from thyroid eye disease.

The last resort that remains if the above options are unsuccessful includes surgical intervention. Thyroid eye disease surgery becomes relevant when symptoms or the overall condition are improved with other treatment options.

Radiation for treating TED. Thyroid eye disease radiology is a different field involving radiologists collaborating to diagnose and treat TED.

Surgical interventions for TED treatment:

Eye muscle surgery
Eyelid surgery
Orbital decompression surgery

These treatment options form the major mode of treating the symptoms that the patient experiences.

Conclusion

This was all on thyroid eye disease and other information such as its cause, symptoms that are usually visible, diagnosis and treatment.

The article takes an illustrative approach in describing the way this disease progresses.

It is the belief that it will help in visualizing the process, making it easier for readers to understand how the symptoms are coming up in their physiology.

Have any questions for us? Comment below and we’ll address them!

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