Thyroid Eye Disease

Thyroid Eye Disease (also called Graves’ orbitopathy or thyroid-associated ophthalmopathy) is an autoimmune condition where the body’s defense system mistakenly attacks the tissues around the eyes. The attack causes the eyelid tissues, eye muscles, and the soft fat behind the eyes to swell and stiffen. This swelling pushes the eyeballs forward, dries the eye surface, and can pull the eyes in different directions. People notice gritty, burning, or watery eyes, puffy lids, redness, light sensitivity, double vision, and sometimes bulging eyes. In severe cases, the swollen tissues press on the optic nerve, which can threaten sight. TED usually happens in people with Graves’ disease (an overactive thyroid), but it can occur with other thyroid problems or even when thyroid blood tests are normal. TED typically has an active (inflamed) phase that lasts months, followed by an inactive (stable) phase; treatment choices depend on which phase and how severe the disease is. Doctors commonly group TED as mild, moderate-to-severe, or sight-threatening to guide therapy. PMCBOPSS :

Thyroid Eye Disease (TED) is an autoimmune eye condition linked to thyroid problems, most often Graves’ disease. In TED, the body’s defense system mistakenly reacts against tissues around the eyes. The lining tissue in the eye socket, the eye muscles, and the fat behind the eyes become inflamed and swollen. This swelling pushes the eyes forward and makes the eyelids pull back. The eye muscles can become stiff, which limits movement and causes double vision. In severe cases, swollen tissue can press on the optic nerve and threaten sight. TED can happen when thyroid hormone is high, normal, or low, but it is most common in people who have or had Graves’ disease. Smoking strongly increases the risk and makes the disease worse. Early recognition and regular eye checks help protect vision.

Types of Thyroid Eye Disease

1) By disease activity

Active TED means the inflammation is “hot” and changing. The eyes feel irritated, red, watery, and painful, and symptoms may change from week to week. Inactive (or “burnt-out”) TED means the inflammation has settled. The tissues are no longer actively inflamed, but some changes, like protrusion or double vision, may remain. Doctors often use a simple score called the Clinical Activity Score (CAS) to judge activity. Higher scores mean more active disease and a greater chance that anti-inflammatory treatments will help.

2) By severity (commonly used in clinics)

• Mild: Symptoms are present but daily life is mostly normal. There is some grittiness, tearing, mild swelling, or a small change in appearance. Vision is not threatened.

• Moderate-to-severe: Symptoms disturb daily life. There may be clear protrusion of the eyes, eyelid retraction, exposure of the cornea, or double vision.

• Sight-threatening: There is corneal breakdown from exposure or pressure on the optic nerve at the back of the eye (dysthyroid optic neuropathy). This needs urgent care to save vision.

3) By thyroid status

• Hyperthyroid TED: TED with an overactive thyroid (often Graves’ disease).

• Euthyroid TED: TED even when blood thyroid levels are normal.

• Hypothyroid TED: TED with an underactive thyroid, often after treatment for Graves’ disease or in Hashimoto’s thyroiditis.

4) By tissue pattern

• Muscle-predominant: Eye muscles are more enlarged and stiff, causing pain with movement, limited up-gaze, and double vision.

• Fat-predominant: Fat behind the eye expands more, pushing the eyeball forward and changing appearance, sometimes with fewer movement limits.

5) By laterality and course

• Bilateral: Both eyes are involved (this is most common).

• Unilateral: One eye looks more affected or only one eye shows changes.

• Monophasic vs. relapsing: Many patients have a single active phase followed by a quiet phase. A smaller group have flares over time, especially if they keep smoking or thyroid levels swing.

Causes and Risk Factors

These “causes” are better understood as autoimmune drivers, triggers, and risk factors. TED starts because the immune system targets shared proteins in the thyroid and around the eyes, especially the TSH receptor and the IGF-1 receptor. The items below describe what raises the chance that this process starts or gets worse.

1. Autoimmunity to the TSH receptor (central mechanism). The body forms antibodies that stimulate the TSH receptor. These antibodies drive thyroid disease and also activate cells in the eye socket, causing swelling and tissue growth.

2. Graves’ disease. Most people with TED have current or past Graves’ hyperthyroidism. The same antibodies that trigger the thyroid often affect the orbit.

3. Hashimoto’s thyroiditis. TED can occur in people with an underactive autoimmune thyroid. It is less common than in Graves’ disease but still possible.

4. High levels of thyroid-stimulating immunoglobulins (TSI/TRAb). Higher antibody levels are linked with more active and severe eye disease.

5. Smoking (most powerful modifiable risk). Smoking makes TED more likely, more severe, and harder to treat. Secondhand smoke can also worsen TED.

6. Radioactive iodine therapy (RAI) without steroid protection. RAI for Graves’ disease can trigger or worsen active TED in some patients, especially smokers or those with high antibodies.

7. Rapid thyroid hormone swings. Big changes from hyperthyroid to hypothyroid, or long periods of poorly controlled thyroid levels, can fuel eye inflammation.

8. Genetic predisposition. Certain HLA types and immune regulation genes raise the risk of autoimmune thyroid disease and TED.

9. Female sex. Women have a higher risk of autoimmune thyroid disease and TED, likely due to immune and hormonal factors.

10. Middle age. TED can happen at any age, but it is more common between 30 and 60 years.

11. Family history of autoimmune disease. Relatives with thyroid autoimmunity, type 1 diabetes, celiac disease, or other autoimmune conditions point to a stronger immune tendency.

12. Stressful life events. Sudden stress does not “cause” TED by itself, but stress can disturb immune balance and thyroid control, which may precipitate flares.

13. Selenium deficiency (mild association). Low selenium status has been linked with more active mild TED in some regions with low dietary selenium.

14. Vitamin D insufficiency (possible association). Vitamin D helps regulate the immune system; low levels may associate with more autoimmunity.

15. Iodine excess or other thyroid disruptors. Very high iodine intake or certain supplements can destabilize thyroid function in susceptible people.

16. Immune-activating cancer therapies. Interferon-α, interleukin-2, alemtuzumab, and immune checkpoint inhibitors can trigger autoimmune thyroid disease, and rarely TED.

17. Diabetes mellitus and metabolic inflammation. Systemic inflammation and microvascular issues might worsen tissue vulnerability around the eye.

18. Obesity. More fat tissue and systemic inflammatory signals may heighten orbital fat expansion and eye pressure.

19. Environmental pollutants and irritants. Air pollution and irritant exposure can aggravate surface inflammation and dry eye symptoms in TED.

20. Poor sleep and untreated obstructive sleep apnea. Nocturnal low oxygen and fluid shifts can swell orbital tissues and worsen morning eye puffiness.

Common Symptoms

1. Grittiness and dryness. Eyes feel sandy and sore because the surface is exposed and the tear film is unstable.

2. Redness and constant watering. The surface of the eye is inflamed, so vessels are more visible and the eye reflexively tears.

3. Light sensitivity. The inflamed surface and exposed cornea make bright light uncomfortable.

4. Pressure or pain around or behind the eyes. Swollen tissues increase pressure inside the socket.

5. Eyelid retraction and “staring” look. The upper lids sit higher and the lower lids sit lower, making the white of the eye more visible.

6. Swollen eyelids and puffy tissue around the eyes. Inflammation and fluid make the lids heavy and puffy, often worse in the morning.

7. Protruding eyes (proptosis). The eyes look pushed forward because the tissue behind them has expanded.

8. Difficulty closing the eyes fully, especially during sleep. This leads to exposure and drying of the cornea.

9. Foreign body sensation and burning. The surface dries and roughens, creating the feeling of something in the eye.

10. Double vision (diplopia). Stiff, enlarged eye muscles cannot move smoothly together, so images do not align.

11. Trouble looking up, down, or sideways. Movement is limited by tight muscles and pain with motion.

12. Blurred vision. The cornea dries, the tear film breaks, or pressure in the orbit affects focus and clarity.

13. Color vision seems duller or washed out. This can signal optic nerve pressure and needs prompt attention.

14. Decreased side vision or “dim” vision. Any new dimness or field loss can also mean optic nerve compression and needs urgent care.

15. Headaches or ache when using the eyes. Eye strain and inflammation can cause aching around the brow and temples.

Red-flag symptoms that need urgent eye care: new dim or blurred vision, new double vision that is constant, loss of color brightness, pain with eye movement, or inability to close the eye with increasing surface damage.

Diagnostic Tests

Doctors diagnose TED by combining how you feel, how your eyes look and move, what your thyroid tests show, and what imaging and function tests reveal. Below are 20 common tests grouped into Physical Exam, Manual Tests, Lab/Pathology, Imaging, and Electrodiagnostic studies.

A) Physical Exam

1. External inspection of eyelids and conjunctiva. The doctor looks for eyelid retraction, swelling, redness, chemosis (conjunctival swelling), and caruncle puffiness. These signs suggest active inflammation on the surface and in the eyelids.

2. Assessment of proptosis by observation. From the side and above, the doctor checks how far forward the eyes sit and whether one eye is more forward than the other. Uneven protrusion can indicate more pressure on one side.

3. Pupil exam and color-vision check at bedside. The doctor checks for a relative afferent pupillary defect and compares color brightness between eyes (often using a simple red object). Reduced brightness or a pupillary defect can signal optic nerve compression.

4. Ocular motility and alignment check. The doctor watches how each eye moves in all directions and looks for misalignment. Limitation in up-gaze or in certain directions suggests muscle tightness typical of TED.

B) Manual Tests

5. Visual acuity testing (standard eye chart). This measures how clearly you can see letters at a set distance. A sudden drop can signal exposure damage, corneal problems, or optic nerve pressure.

6. Exophthalmometry (Hertel or equivalent). A simple measuring device sits on the bony rims around the eyes to record how far the eyes protrude. It gives a number that can be tracked over time.

7. Intraocular pressure (IOP) measurement. Pressure is measured in primary gaze and again in up-gaze. TED can raise IOP when you look up because tight muscles compress the eye, so comparing positions helps detect the effect.

8. Cover–uncover and prism cover tests. These tests measure how the eyes line up and how much prism is needed to join double images. The number helps plan treatment for double vision.

9. Forced-duction test (usually in the operating room or clinic under anesthesia). The surgeon gently moves the eye to feel if a muscle is mechanically tight. A positive forced-duction test supports muscle restriction rather than a nerve palsy.

C) Lab and Pathological Tests

10. TSH (thyroid-stimulating hormone). A low TSH typically indicates hyperthyroidism from Graves’ disease; a high TSH suggests hypothyroidism. Stable, normal TSH is a goal during TED care.

11. Free T4 and Total/Free T3. These show actual thyroid hormone levels. Abnormal levels point to poor control and a higher risk of flares.

12. TSH receptor antibodies (TRAb/TSI). Higher levels support the diagnosis of Graves’ disease and are linked with TED activity and severity.

13. Anti-TPO and anti-thyroglobulin antibodies. These support autoimmune thyroid disease, including Hashimoto’s thyroiditis, which can coexist with TED.

14. General health labs when needed (e.g., complete blood count, liver and kidney function). These are baseline tests to guide safe treatment, to check for inflammation, and to prepare for any medicine that needs monitoring.

D) Imaging Tests

15. Orbital CT scan. CT shows enlarged eye muscles with tendon sparing (a classic pattern in TED), crowding at the orbital apex, and the amount of fat expansion. It helps plan surgery and assess optic nerve risk.

16. Orbital MRI with fat-suppression and STIR sequences. MRI shows active inflammation (bright signal in muscles and soft tissue) and differentiates water-rich inflamed tissue from fibrotic tissue. It is very helpful when vision is at risk.

17. Ocular ultrasound (B-scan). Ultrasound can show muscle enlargement and distinguishes solid tissue from fluid. It is quick and does not use radiation.

18. Optical coherence tomography (OCT) of the optic nerve and macula. OCT measures retinal nerve fiber layer thickness and macular structure. Thinning or swelling patterns can help detect early optic nerve damage from compression or surface disease affecting the center of vision.

E) Electrodiagnostic Tests

19. Visual evoked potentials (VEP). This test measures the brain’s electrical response to visual patterns. Reduced amplitude or delayed signals suggest optic nerve involvement from orbital crowding.

20. Pattern electroretinography (pERG) or electro-oculography (EOG) when indicated. These tests evaluate the retina and macula–optic nerve function complex. Abnormal results can support concerns about visual pathway stress when standard tests are borderline.

Non-Pharmacological Treatments (therapies and other measures)

Each item includes a brief description, purpose, and mechanism in simple terms.

1. Stop smoking completely
   Description: Get help to quit and avoid secondhand smoke.
   Purpose: Smoking makes TED more active, more severe, and treatment less effective.
   Mechanism: Smoke increases eye-tissue inflammation and reduces oxygen, worsening swelling and scarring. BOPSS :

2. Keep thyroid levels normal (euthyroid)
   Description: Work with your doctor to keep TSH, T3, and T4 in the target range.
   Purpose: Stable thyroid levels calm eye inflammation and reduce flare-ups.
   Mechanism: Hormone swings fuel immune activity; stability reduces immune triggers. BOPSS :

3. Nighttime eye protection (lubricating ointment + eyelid taping)
   Description: Apply ointment before sleep; gently tape lids if they don’t close fully.
   Purpose: Prevents corneal drying and abrasions.
   Mechanism: Creates a moisture seal over the eye surface.

4. Frequent daytime artificial tears
   Description: Use preservative-free drops regularly.
   Purpose: Relieves burning, grittiness, and fluctuating vision.
   Mechanism: Replaces the tear film and dilutes inflammatory molecules.

5. Cool compresses
   Description: Clean, cool compress over closed lids 5–10 minutes.
   Purpose: Reduces puffiness and discomfort.
   Mechanism: Cold causes blood-vessel constriction and slows inflammatory chemicals.

6. Sleep with head elevated
   Description: Use two pillows or a wedge.
   Purpose: Less morning eyelid swelling.
   Mechanism: Gravity limits overnight fluid pooling around the eyes.

7. Wrap-around sunglasses outdoors
   Description: Wear UV-blocking, wind-shielding glasses.
   Purpose: Reduces light sensitivity and dryness.
   Mechanism: Shields cornea from wind, dust, UV, and bright light.

8. Humidifier and environmental control
   Description: Add humidity and avoid fans on your face.
   Purpose: Eases dry-eye symptoms.
   Mechanism: Moist air slows tear evaporation.

9. Blink training and screen hygiene
   Description: Follow the 20-20-20 rule; consciously blink fully.
   Purpose: Less screen-related dryness.
   Mechanism: Restores the oily tear layer with each full blink.

10. Prism glasses for double vision
    Description: Stick-on or built-in prisms by an optometrist/ophthalmologist.
    Purpose: Fuses double images to single vision.
    Mechanism: Bends light so both eyes’ images line up on the retina.

11. Occlusion (patch or fogging lens)
    Description: Cover one eye when diplopia is frequent and prisms fail.
    Purpose: Prevents nausea and falls from double vision.
    Mechanism: Eliminates conflicting images.

12. Sodium restriction for a few weeks during puffy phases
    Description: Reduce salty foods.
    Purpose: Less tissue fluid and lid swelling.
    Mechanism: Lower sodium reduces fluid retention in inflamed tissues.

13. Manage allergies and sinus disease
    Description: Treat rhinitis/sinusitis if present.
    Purpose: Lowers extra inflammation around the orbit.
    Mechanism: Fewer inflammatory mediators near the eyes.

14. Protective eye gel shields in windy/dry settings
    Description: Moisture chamber goggles when cycling or in air-conditioned rooms.
    Purpose: Prevents corneal exposure and pain.
    Mechanism: Traps humidity around the eyes.

15. Botulinum toxin to upper-lid retraction (selected cases)
    Description: Small doses into upper-lid muscles by a specialist.
    Purpose: Temporarily lowers a retracted lid to protect the cornea.
    Mechanism: Weakens overactive muscle pull until inflammation settles.

16. Taping lower lids upward for exposure keratopathy
    Description: Gentle upward tape or specialized strips.
    Purpose: Covers more of the cornea.
    Mechanism: Increases lid-cornea contact to retain tears.

17. Eye-safe makeup and gentle lid hygiene
    Description: Hypoallergenic products; warm compress and gentle scrubs.
    Purpose: Improves meibomian gland function and comfort.
    Mechanism: Better oil layer reduces evaporation.

18. Driving and work adaptations
    Description: Anti-glare filters, frequent breaks, larger monitors.
    Purpose: Keeps you safe and reduces eye strain.
    Mechanism: Limits triggers that worsen dryness and diplopia fatigue.

19. Psychological support and patient groups
    Description: Counseling or support communities.
    Purpose: Lowers stress and improves adherence to care.
    Mechanism: Less stress-related immune activation and better self-care.

20. Steroid prophylaxis if you need radioactive iodine (RAI) and are at risk
    Description: If RAI is chosen to treat hyperthyroidism, some people at risk for TED worsening receive a short course of oral prednisone.
    Purpose: Reduces the chance RAI will flare eye disease.
    Mechanism: Glucocorticoids blunt the immune response triggered by thyroid tissue destruction. PMCOxford Academic

Drug Treatments

For each medicine, you’ll see drug class, common dosing/timing (typical adult ranges; individualize with your doctor), purpose, mechanism, and key side effects.

1. Teprotumumab (IGF-1 receptor inhibitor)
   Class: Targeted biologic (monoclonal antibody).
   Dose/Time: 8 IV infusions over ~24 weeks: first 10 mg/kg, then 20 mg/kg every 3 weeks.
   Purpose: Reduces proptosis, inflammation, and diplopia in active, moderate-to-severe TED.
   Mechanism: Blocks IGF-1R signaling on orbital fibroblasts and B cells that drive tissue swelling and fibrosis.
   Side effects: Muscle cramps, hearing changes, hyperglycemia (monitor closely in diabetes), infusion reactions; rare IBD flares. New England Journal of MedicinePubMed

2. Intravenous methylprednisolone (IVMP) pulses
   Class: Systemic glucocorticoid.
   Dose/Time: A common regimen is 500 mg weekly for 6 weeks then 250 mg weekly for 6 weeks (cumulative 4.5 g); higher cumulative doses (up to 7.5 g) are used for severe active disease—specialist protocols and monitoring are essential.
   Purpose: Rapidly dampens inflammation in active TED.
   Mechanism: Broad anti-inflammatory and immunosuppressive effects reduce tissue swelling and cytokine release.
   Side effects: Mood changes, elevated blood sugar, blood-pressure rise, liver enzyme elevation (dose-limited), infection risk, bone loss, weight gain. endocrinologia.org.mx

3. Oral prednisone
   Class: Glucocorticoid.
   Dose/Time: Often used short-term for flares or as RAI prophylaxis in at-risk patients (e.g., ~0.3–0.5 mg/kg/day then taper).
   Purpose: Controls inflammation or prevents RAI-triggered worsening.
   Mechanism/Side effects: Same as IVMP; oral form has more systemic exposure day-to-day. PMC

4. Mycophenolate mofetil / mycophenolate sodium
   Class: Steroid-sparing immunomodulator.
   Dose/Time: Often 500–1,000 mg twice daily (mofetil) or 360–720 mg twice daily (sodium) for several months; frequently combined with IVMP in active, moderate-to-severe TED.
   Purpose: Improves signs and allows steroid dose reduction.
   Mechanism: Inhibits lymphocyte proliferation by blocking purine synthesis.
   Side effects: GI upset, infection risk, liver enzyme changes. endocrinologia.org.mx

5. Tocilizumab
   Class: IL-6 receptor inhibitor biologic.
   Dose/Time: IV every 4 weeks (e.g., 8 mg/kg) or subcutaneous per protocol in steroid-resistant active TED.
   Purpose: Helps when IV steroids fail or are contraindicated.
   Mechanism: Blocks IL-6-driven inflammation in orbital tissues.
   Side effects: Infection risk, elevated lipids, liver enzyme rise; screen for TB and hepatitis. PMC

6. Rituximab
   Class: Anti-CD20 B-cell depleting biologic.
   Dose/Time: Common autoimmune dosing (e.g., 1,000 mg IV ×2 two weeks apart) in selected refractory active TED; evidence is mixed.
   Purpose: Considered in specialized centers when other options fail.
   Mechanism: Reduces autoantibody-producing B cells.
   Side effects: Infusion reactions, infections; rare PML—requires expert oversight. PMC

7. Orbital radiotherapy (RT)
   Class: Local anti-inflammatory therapy (not a drug but often grouped with medical treatments).
   Dose/Time: Typical total 20 Gy in 10 fractions to the orbits; sometimes combined with steroids.
   Purpose: Improves motility restriction, reduces activity, and can aid steroid taper in active disease.
   Mechanism: Dampens lymphocytes and fibroblast activity within the orbit.
   Side effects: Usually mild (transient skin/eye irritation); long-term data are limited; avoid in pregnancy. PubMed

8. Lubricants (tears, gels, ointments)
   Class: Ocular surface therapy.
   Dose/Time: Drops as often as needed; gels/ointments at night.
   Purpose: Relieve dryness and protect the cornea.
   Mechanism: Replaces tear film and reduces friction.
   Side effects: Blurring after gels/ointments (temporary).

9. Selenium (nutraceutical used as therapy in mild active TED)
   Class: Antioxidant micronutrient.
   Dose/Time: 100 micrograms twice daily for 6 months in selenium-deficient regions and mild active TED.
   Purpose: Improves quality of life and slows progression in mild cases.
   Mechanism: Antioxidant and immune-modulating effects in orbital tissues.
   Side effects: Usually well tolerated; avoid excess (risk of selenosis). New England Journal of Medicine

10. Topical anti-inflammatories (short courses, selected cases)
    Class: Mild topical steroids or cyclosporine/lifitegrast eye drops.
    Dose/Time: As prescribed by an eye specialist.
    Purpose: Treat ocular surface inflammation and discomfort.
    Mechanism: Local immune dampening on the ocular surface.
    Side effects: With topical steroids, prolonged use can raise eye pressure; use specialist guidance.

Dietary “Molecular” Supplements

Always review supplements with your doctor—some interact with thyroid or TED therapies.

1. Selenium — 100 mcg twice daily for 6 months in mild active TED where deficiency is likely; function: antioxidant; mechanism: supports glutathione peroxidase and reduces orbital oxidative stress. Evidence supports benefit in mild disease. New England Journal of Medicine

2. Omega-3 fatty acids (fish oil or algae oil) — 1–2 g/day EPA+DHA; function: tear-film support; mechanism: pro-resolving mediators reduce surface inflammation.

3. Vitamin D — 1,000–2,000 IU/day (adjust to level); function: immune modulation; mechanism: supports T-regulatory balance.

4. Vitamin B12 (if low) — usual repletion per labs; function: nerve health; mechanism: supports myelin and ocular surface sensation.

5. Vitamin A (avoid excess) — only if deficient; function: epithelial health; mechanism: supports mucin and corneal epithelium.

6. L-carnitine/acetyl-L-carnitine — 500–1,000 mg/day; function: mitochondrial support, may ease fatigue; mechanism: fatty-acid transport; limited TED-specific data.

7. Curcumin (with piperine or formulated for absorption) — 500–1,000 mg/day; function: anti-inflammatory adjunct; mechanism: NF-κB modulation (adjunctive only).

8. Flaxseed/ground flax — 1–2 tbsp/day; function: plant omega-3; mechanism: tear-film support.

9. Magnesium (if low) — 200–400 mg/day; function: muscle comfort and sleep; mechanism: cofactor in neuromuscular calming.

10. Probiotics (multi-strain) — daily; function: gut-immune balance; mechanism: may reduce systemic inflammatory tone; data in TED are indirect.

Note: Only selenium has RCT evidence specific to mild TED; the rest are supportive for dryness or overall immune health rather than proven TED disease-modifiers. New England Journal of Medicine

Regenerative / Stem-Cell”–Type Therapies

Below are biologics or regenerative-style adjuncts sometimes discussed for TED. I clearly mark what is established versus experimental.

1. Teprotumumab — established targeted biologic
   Dose/Function/Mechanism: As above; blocks IGF-1R to reverse proptosis and activity in active, moderate-to-severe TED. This is the leading disease-modifying therapy with RCT evidence. New England Journal of Medicine

2. Tocilizumab — established for steroid-resistant active TED (specialist use)
   Dose/Function/Mechanism: As above; IL-6 pathway blockade can reduce activity when steroids fail. PMC

3. Rituximab — mixed evidence, specialist-only
   Function/Mechanism: B-cell depletion; consider only in refractory cases after expert discussion of risks and uncertain benefit. PMC

4. Autologous serum tears — regenerative ocular-surface adjunct
   Dose: Often 20% serum drops 4–6×/day prepared by specialized pharmacies.
   Function/Mechanism: Patient’s own growth factors and vitamins support corneal healing in exposure keratopathy.

5. Amniotic membrane therapy (cryopreserved graft or self-retaining insert)
   Dose/Use: In-office or surgical placement for persistent epithelial defects.
   Function/Mechanism: Provides anti-inflammatory cytokines and scaffolding that promotes corneal healing.

6. **Stem-cell–based therapies (mesenchymal/limbal) — experimental only
   Status: Not approved for TED disease modification; use only in clinical trials for severe surface disease where appropriate. No standard dose exists outside trials.
   Function/Mechanism: Aims to rebalance inflammation and promote tissue repair; safety and efficacy in TED are unproven.

Surgeries

Surgery is typically staged in the inactive phase and in this order: decompression → strabismus → eyelids. In emergencies (optic nerve compression or corneal threat), surgery is done urgently.

1. Orbital decompression
   Procedure: Removes small sections of bone ± orbital fat to create space behind the eye.
   Why: Brings the eye back (reduces bulging), relieves pain/pressure, and treats optic-nerve compression when present.

2. Strabismus (eye-muscle) surgery
   Procedure: Weakens or repositions tight, fibrosed eye muscles (often inferior or medial rectus).
   Why: Reduces or eliminates double vision in straight-ahead and reading gaze.

3. Upper-lid retraction repair
   Procedure: Recesses the overactive lid retractor muscles; may add spacer grafts.
   Why: Lowers a high upper lid to cover the cornea and improve appearance.

4. Lower-lid lengthening
   Procedure: Spacer graft or retractor release to raise a pulled-down lower lid.
   Why: Protects the cornea and improves symmetry.

5. Temporary or permanent tarsorrhaphy (lid-to-lid stitch)
   Procedure: Partially closes the eyelids.
   Why: Urgent corneal protection when exposure is severe and other measures fail.

(Practice-pattern and timing align with international consensus statements.) PMC

Practical Preventions

1. Quit smoking and avoid secondhand smoke. BOPSS :

2. Keep thyroid hormones in the target range with regular blood tests. BOPSS :

3. If you receive radioactive iodine and are at risk, ask about short-course prednisone prophylaxis. PMC

4. Treat dry eye early and consistently (tears by day, ointment by night).

5. Wear wrap-around sunglasses outdoors and use a humidifier indoors.

6. Sleep on an extra pillow to reduce morning puffiness.

7. Limit excess salt during puffy phases.

8. Manage allergies/sinus disease promptly.

9. Keep diabetes and blood pressure controlled (helps with medication safety, especially biologics and steroids).

10. Keep all eye and endocrine appointments; TED is a team sport between ophthalmology and endocrinology.

When to See a Doctor

• Same-day/urgent: Sudden drop in vision, washed-out color vision, eye pain with movement, new central blur or shadow, severe bulging with inability to close the eye, severe corneal pain or light sensitivity, rapidly worsening double vision, or new headaches behind the eye. These can signal optic-nerve compression or corneal danger. BOPSS :

• Soon (days to weeks): New persistent redness, swelling, tearing, gritty pain, or double vision; trouble reading or driving due to diplopia; worsening dryness despite lubricants; new lid retraction or increasing bulge.

Simple “What to Eat / What to Avoid”

• Eat more:

1. Selenium-rich foods (Brazil nuts—very small portions, 1–2 nuts a few times a week, fish, eggs) to maintain adequate selenium without overdosing. New England Journal of Medicine

2. Fatty fish or algae-based omega-3 sources (salmon, sardines, algae oil).

3. Plenty of water; hydration supports tears.

4. Colorful vegetables and fruits (antioxidants support tissue health).

5. Flaxseed, walnuts, and olive oil for healthy fats.

• Limit/avoid:

6. High-salt packaged foods during swelling phases (chips, instant soups).

7. Excess caffeine that worsens dryness for some people.

8. Smoking and alcohol excess (both worsen inflammation). BOPSS :

9. Very high iodine intake around RAI treatment decisions unless your thyroid team instructs otherwise (some seaweed products are extremely high in iodine).

10. Unverified “thyroid cure” supplements that may interfere with medications—always check with your doctor.

Frequently Asked Questions

1) Can TED occur if my thyroid blood tests are normal?
Yes. TED most often accompanies Graves’ disease, but it can appear with other thyroid issues or even with blood tests in the reference range. Eye and thyroid disease activity are related but not identical. BOPSS :

2) How long does the active phase last?
Typically several months (often up to a year or more), then the disease becomes inactive. Treatment intensity is highest during the active phase. BOPSS :

3) What is the Clinical Activity Score (CAS)?
It’s a simple checklist of inflammation signs (pain, redness, swelling). A higher CAS means more active inflammation and guides therapy choices. EUGOGO

4) When is teprotumumab considered?
In moderate-to-severe active TED where reducing bulging, inflammation, and diplopia is a priority, particularly when steroids aren’t enough or aren’t tolerated. It’s given by infusion every three weeks for eight doses. New England Journal of Medicine

5) Is selenium really helpful?
Yes—for mild active TED in regions where selenium intake is low. A 6-month course improved quality of life and slowed disease progression in a randomized trial. It isn’t a replacement for medical therapy in more severe disease. New England Journal of Medicine

6) Do steroids cure TED?
Steroids suppress inflammation and can rapidly improve symptoms, but they don’t reverse all structural changes. They are often used as time-limited courses with careful monitoring. endocrinologia.org.mx

7) What about orbital radiotherapy?
In the active phase, radiotherapy can help eye movement problems and reduce activity, often combined with steroids. Evidence suggests benefit, but long-term data are limited; it’s a specialist decision. PubMed

8) Will surgery fix my eyes?
Surgery is very effective for bulging, double vision, and lid position, but it’s usually timed for the inactive phase and may require more than one operation to address different problems.

9) Can TED cause vision loss?
Yes, if the swollen tissues compress the optic nerve or the cornea becomes severely exposed and ulcerates. Urgent treatment prevents permanent loss. BOPSS :

10) Does radioactive iodine worsen TED?
It can in some at-risk people. Your team may prescribe a short steroid course to reduce that risk. PMC

11) Are biologics safe?
Biologics like teprotumumab, tocilizumab, and rituximab require careful screening and monitoring. Benefits can be substantial, but risks (infections, metabolic effects, rare reactions) must be weighed individually. New England Journal of MedicinePMC

12) Will diet alone fix TED?
No. Diet supports overall health and dry-eye comfort but does not replace disease-modifying therapy when indicated. Selenium has specific evidence in mild active disease only. New England Journal of Medicine

13) Can TED come back after it becomes inactive?
Relapses are less common but can occur, especially with smoking or large thyroid-hormone swings. Keep regular follow-up and maintain thyroid stability. BOPSS :

14) Who should manage my care?
An oculoplastic/strabismus ophthalmologist and an endocrinologist working together. Complex cases may benefit from centers with TED expertise and access to infusion therapies and orbital surgery.

15) What’s the overall treatment plan?
Control thyroid function and risk factors → protect the eye surface → treat active inflammation with medicines like steroids, mycophenolate, biologics, or radiotherapy when appropriate → once stable, correct residual problems with staged surgery. This stepped plan is consistent with international guidelines. PMC

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: August 28, 2025.

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