Thyroid Eye Disease (TED) is an autoimmune condition causing inflammation in the muscle and fat tissues behind the eyes. It is most often associated with Graves’ disease, where the immune system attacks the thyroid gland, typically resulting in hyperthyroidism. The same antibodies targeting the thyroid can bind to receptors in the eye tissues, triggering a damaging inflammatory response. Treatment is divided into two phases: managing inflammation during the “active” phase and correcting lasting structural changes during the “inactive” or “stable” phase. The active phase, characterized by swelling, redness, and pain, can last up to two years. A multidisciplinary team, including an endocrinologist and an ophthalmologist, works to maintain stable thyroid hormone levels while addressing eye symptoms.
Supportive Care for Mild Symptoms
For individuals with mild TED symptoms, treatment begins with conservative, supportive care aimed at maximizing comfort and preventing irritation. A highly recommended lifestyle adjustment involves the complete cessation of smoking, as tobacco use significantly increases the risk of developing TED and is associated with more severe symptoms.
To manage morning eyelid puffiness, patients are advised to elevate the head of their bed during sleep. Sleeping with the head raised reduces fluid accumulation around the eyes overnight, lessening discomfort upon waking. Lubricating eye drops, gels, or ointments are standard care, providing artificial tears to soothe the dry, gritty sensation.
Non-preserved artificial tears are recommended for frequent daytime use. Thicker gels or ointments can be applied before sleep to protect the cornea, especially if the eyelids do not close completely. Patients with mild-to-moderate active disease may also benefit from a six-month course of selenium supplementation, a micronutrient that can help reduce TED symptoms. Regular monitoring by an eye specialist is maintained to detect any progression promptly.
Medical Interventions for Active Inflammation
When the disease is in its active phase and symptoms are moderate to severe, medical interventions are necessary to halt inflammation and prevent permanent damage. These treatments suppress the immune response attacking the orbital tissues.
Corticosteroids
Corticosteroids are a traditional first-line treatment for active, moderate-to-severe TED due to their potent anti-inflammatory effects. They are typically administered intravenously (IV) in high doses, such as methylprednisolone, to quickly suppress the immune system and reduce swelling and redness. While effective at managing orbital inflammation, corticosteroids have limitations, including a high rate of relapse and limited ability to reverse proptosis (eye bulging) or double vision.
Targeted Biologics
A more recent approach involves teprotumumab, a biologic medication specifically approved for active TED. Teprotumumab is a monoclonal antibody that targets the insulin-like growth factor-1 receptor (IGF-1R), which is upregulated in the orbital tissues of TED patients. By inhibiting this receptor, the drug blocks the signaling pathway that drives inflammation and tissue expansion. The treatment course consists of eight intravenous infusions given every three weeks over a six-month period. Clinical trials have demonstrated that teprotumumab significantly improves eye bulging, reduces inflammation, and can improve double vision.
Surgical Options for Correcting Structural Damage
Surgical intervention is generally reserved for the “inactive” or “stable” phase of TED, defined as a period where inflammation has been stable for at least six months. The goal of surgery is functional and cosmetic rehabilitation, addressing the permanent structural changes that occurred during the active phase. When multiple procedures are required, they are performed in a specific, sequential order to ensure the best outcome.
Orbital Decompression
The first procedure in the surgical sequence is typically orbital decompression, performed to reduce proptosis, or eye bulging. This surgery involves removing bone and/or fat from the eye socket to create more space for the orbital contents. Decompression also plays an important role in relieving pressure on the optic nerve, which can preserve vision in severe cases of optic neuropathy.
Eye Muscle Surgery
Following orbital decompression, if a patient still experiences double vision (diplopia), eye muscle surgery (strabismus surgery) is the next step. The inflammation of TED causes scarring and thickening of the eye muscles, restricting their movement and causing misalignment. The surgeon adjusts the length of the scarred muscles to correct alignment, which can restore single vision in the primary gaze.
Eyelid Surgery
The final stage of rehabilitation is eyelid surgery, which addresses issues like eyelid retraction, where the eyelids fail to cover the eye properly. This procedure repositions the eyelids to allow for full closure, protecting the cornea from drying out and improving appearance. Addressing the eyelids last ensures that the preceding orbital and muscle surgeries do not inadvertently alter the final position of the lids.