Thyroid Eye Disease (TED)

What is the most common cause of both bilateral and unilateral proptosis in an adult?

What is the major clinical risk factor for developing TED in patients with Graves disease?

Who is more likely to be affected by TED?

What can worsen TED in patients with hyperthyroidism?

What is the initial treatment option for acute compressive optic neuropathy?

Which treatment may be used in addition to steroids or when steroids are contraindicated or ineffective?

What is a potential adverse effect of the treatment for acute optic nerve compression?

What combined therapy may be more effective than steroids or radiotherapy alone?

What is a potential consequence of orbital decompression?

What is the most commonly indicated surgery for restrictive myopathy?

What may be used for mild lid retraction?

What is used for post-inflammatory complications in TED?

What percentage of TED patients develop long-term ocular problems?

What is a symptom of soft tissue involvement in TED?

What can lid retraction in TED result in?

What percentage of TED patients develop permanent ophthalmoplegia?

What is a clinical feature of TED?

What is a complication of TED that can cause severe visual impairment?

What is a part of the treatment for mild TED?

What is an investigation for TED patients to check for optic nerve compromise?

What is a consequence of proptosis in TED?

What is a stage that TED proceeds through?

What should be managed as part of TED treatment?

What is a feature of moderate to severe active TED disease treatment?

TED is not a common orbital disorder and rarely causes proptosis in adults.

Smoking is a major clinical risk factor for developing TED in patients with Graves disease.

Women are less likely to be affected by TED than men.

Thyroid ophthalmopathy involves an autoimmune reaction that leads to inflammation of extraocular muscles, orbital fat, and lacrimal glands.

Oral prednisolone is the first-line treatment for acute compressive optic neuropathy in TED.

Low-dose fractionated radiotherapy is used as the sole treatment for acute optic nerve compression.

Around 60% of patients with TED do not respond to treatment.

Orbital wall decompression may be considered if steroids are ineffective or contraindicated in TED.

Orbital radiotherapy is generally used as the sole treatment modality in TED.

Eyelid surgery should be performed before any necessary orbital and then strabismus procedures in TED.

Surgical decompression for proptosis in TED involves increasing the volume of the orbit by adding bony walls.

Botulinum toxin injection to the levator aponeurosis and Müller muscle is ineffective for mild lid retraction in TED.

Thyroid Eye Disease progresses through congestive and fibrotic stages, with 90% of patients developing long-term ocular problems.

Lid retraction occurs in about 50% of TED patients.

Proptosis in TED can lead to exposure keratopathy and corneal ulceration.

Between 30% and 50% of TED patients develop permanent ophthalmoplegia.

Optic neuropathy is not a serious complication of TED and does not cause severe visual impairment.

Investigations for TED include blood tests for thyroid disease and visual field testing for optic nerve compromise.

Mild TED treatment includes cessation of smoking, management of thyroid dysfunction, and use of lubricants, topical anti-inflammatory agents, and systemic steroids.

Moderate to severe active TED disease is not treated with systemic steroids.

Soft tissue involvement in TED presents with symptoms like red eyes, lacrimation, and signs such as epibulbar hyperemia and tear insufficiency.

Restrictive myopathy in TED is caused by subsequent degeneration of muscle fibers leading to fibrosis.

TED patients do not develop long-term ocular problems.

Thyroid Eye Disease does not proceed through congestive and fibrotic stages.