Orbital

Thyroid Eye Disease: Signs, Symptoms & Diagnosis

The clinical and radiological findings of thyroid eye disease — eye signs, orbital CT, disease-activity scoring (CAS), and severity grading.

Medically reviewed by Tamara R. Fountain, MDOculoplastic SurgeonLast updated June 2026

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Part of our complete guide to Thyroid Eye Disease (TED) — this page covers TED diagnosis and evaluation in depth.

Thyroid eye disease is recognized by a characteristic set of eye findings and graded by how active and how severe it is. This page covers the clinical signs, the orbital imaging, and the scoring systems used to guide treatment.

Thyroid eye disease showing lid retraction and proptosis

The hallmark findings of TED include proptosis, lid retraction, restricted eye movement, and periorbital swelling. The combination of these features gives the characteristic “staring” or “startled” appearance.

Clinical Findings

Proptosis (exophthalmos): Forward displacement of the globe due to expanded orbital volume. Hertel exophthalmometry readings > 21 mm, or ≥ 2 mm of asymmetry between the eyes, are considered significant (normal values vary by ethnicity). Thyroid eye disease is the most common cause of proptosis in adults, and is also the most common cause of bilateral proptosis
Eyelid retraction: Upper lid scleral show (limbus to upper lid margin >2 mm) and lower lid scleral show below the limbus. Both sympathetic over-stimulation and levator fibrosis contribute
Restrictive strabismus: Tight, fibrotic extraocular muscles restrict movement and cause diplopia, most commonly on upgaze (inferior rectus) and lateral gaze (medial rectus)
Periorbital edema and chemosis: Inflammatory swelling of eyelids, conjunctiva, and caruncle
Corneal exposure keratopathy: Incomplete eyelid closure and reduced blink rate from proptosis and lid retraction expose the cornea — causing dryness, pain, and risk of corneal ulceration
Compressive optic neuropathy (CON): The most vision-threatening complication — enlarged muscles at the orbital apex compress the optic nerve. Presents with decreased visual acuity, color desaturation, and relative afferent pupillary defect. Requires urgent treatment

Bilateral proptosis (exophthalmos) in thyroid eye disease

Conjunctival injection and chemosis in active thyroid eye disease

Optic disc edema from compressive optic neuropathy in thyroid eye disease

Thyroid eye disease appearance before and after treatment

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Disease Activity & Severity

TED has two distinct phases: an active (inflammatory) phase of variable duration (typically 6–24 months) followed by an inactive (fibrotic) phase. Timing of treatment is critical — most medical therapies work only during the active phase.

Clinical Activity Score (CAS)

The CAS assigns one point for each of the following signs of active inflammation:

Spontaneous orbital pain

Pain on eye movement

Eyelid erythema

Conjunctival injection

Chemosis

Swelling of the caruncle or plica

Eyelid edema

A CAS ≥ 3/7 indicates active disease. Active disease may respond to medical therapy such as corticosteroids and the IGF-1R inhibitor teprotumumab (Tepezza); teprotumumab requires monitoring for hearing impairment and hyperglycemia; it can harm a developing fetus, so it must not be used in pregnancy and effective contraception is required during treatment and for 6 months after the final dose; inactive disease does not — surgical rehabilitation is the appropriate approach for stable inactive TED.

Severity Classification

Mild TED

Minimal impact on quality of life
Lid retraction < 2 mm
Proptosis < 3 mm above normal
Mild corneal exposure
Transient or no diplopia
Managed conservatively; observation is appropriate

Moderate-to-Severe TED

Significant impact on daily life
Lid retraction ≥ 2 mm
Proptosis ≥ 3 mm above normal
Intermittent or constant diplopia
Corneal exposure requiring treatment
Active disease is usually treated with teprotumumab (Tepezza) or IV corticosteroids, individualized to the patient

Sight-threatening TED: Compressive optic neuropathy or severe corneal exposure requires urgent treatment — urgent high-dose IV corticosteroids and/or orbital decompression surgery regardless of disease phase. Any sudden decrease in vision, dimming of color, or severe eye pain warrants same-day emergency evaluation.

Conservative Management

Preservative-free lubricating eye drops (frequently) and gel or ointment at night

Selenium supplementation 200 μg/day for 6 months — shown to slow progression in mild active TED (evidence from selenium-deficient European populations)

Taping eyelids closed at night for lagophthalmos

Elevated head of bed to reduce morning periorbital edema

Prism glasses for diplopia

Smoking cessation — the single most impactful intervention a patient can make

Orbital & Muscle Anatomy

In TED, the extraocular muscles become infiltrated with inflammatory cells, expand due to glycosaminoglycan deposition, and eventually fibrosis. The inferior and medial rectus muscles are most consistently affected, producing the characteristic upward and outward gaze restrictions and diplopia.

Muscle	Primary Function	TED Involvement
Inferior rectus	Depression (downgaze)	Most commonly enlarged — causes hypotropia and limited upgaze; compresses optic nerve at apex
Medial rectus	Adduction	Second most affected — causes esotropia and limited abduction; diplopia on lateral gaze
Superior rectus / levator	Elevation / lid opening	Enlargement restricts downgaze; levator fibrosis and sympathetic Müller muscle stimulation cause lid retraction
Lateral rectus	Abduction	Less commonly enlarged
Superior oblique	Intorsion / depression	Rarely affected

For detailed orbital bone and muscle anatomy, see our Anatomy Overview page.