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.
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.
Eye Signs of Thyroid Eye Disease
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 >21 mm or >2 mm asymmetry is significant. Bilateral proptosis is the most common cause of proptosis in adults
- 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
ProptosisOrbital Changes
Interactive visualization showing orbital muscle changes and progressive proptosis associated with Thyroid Eye Disease.
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Radiological Findings
CT of the orbits characteristically demonstrates enlarged extraocular muscles (particularly inferior and medial rectus) with sparing of the tendinous insertions — a key feature distinguishing TED from orbital myositis, where the tendon is involved. The apex-to-equator ratio of enlargement predicts risk of optic neuropathy.
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 responds to immunosuppression (steroids, Tepezza); 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 requires Tepezza or IV steroids
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.
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
- 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.
Frequently Asked Questions
- What are the main signs of thyroid eye disease?
- Proptosis (bulging eyes), upper- and lower-lid retraction, restricted eye movement with double vision, redness and swelling, and — in severe cases — exposure of the cornea or compression of the optic nerve.
- What is the Clinical Activity Score (CAS)?
- A 7-point checklist of inflammatory signs (pain, redness, swelling) used to judge whether thyroid eye disease is in its active inflammatory phase, which guides whether medical therapy is appropriate.
- Why is an orbital CT scan done?
- CT shows the enlarged extraocular muscles characteristic of thyroid eye disease — typically with sparing of the tendon insertions — and helps assess crowding at the orbital apex that can threaten the optic nerve.
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