eMedicine Specialties > Ophthalmology > Orbit

Thyroid Ophthalmopathy: Treatment & Medication

Author: Edsel Ing, MD, FRCSC, Assistant Professor, Department of Ophthalmology & Vision Sciences, University of Toronto: Consulting Staff, Toronto East General Hospital
Contributor Information and Disclosures

Updated: Apr 30, 2008

Treatment

Medical Care

• Inform patients that TAO usually runs a self-limited but prolonged course over 1 or more years. Patients also should realize that no immediate cure is available.
• Most patients with TAO can be observed; the follow-up interval depends on disease activity.
  • Monitor for visual loss from corneal exposure and optic neuropathy and for strabismus development.
  • Visual field and color vision testing may help in early detection of visual loss.
• If a patient has dry eye symptoms, consider using artificial tears during the day, lubricating ointment at night, and punctal plugs.
• Sleeping with the head of the bed elevated may decrease morning lid edema.
• Encourage patients to stop smoking to decrease the risk of congestive orbitopathy.
• In patients with diplopia, prisms may be beneficial to those with small-angle and relatively comitant deviations.
  • Tape occlusion of one lens or segment of the glasses may be helpful. If this does not work, try an occluder or eye patch (with care not to compress the orbit).
  • The author does not recommend the use of eye exercises for patients with severe restrictive strabismus; doing so may elevate intraocular pressure.
  • Oral steroids usually are reserved for patients with severe inflammation or compressive optic neuropathy. Steroids may decrease the production of mucopolysaccharides by the fibroblasts. Pulse intravenous steroids (eg, methylprednisolone 1 g every other day for 3 cycles) can be considered.
  • Antitumor necrosis factor drugs, such as etanercept, infliximab, and daclizumab, have been used in patients with TAO, but more studies are required to determine their adverse effect profile as compared to steroids. Octreotide, pentoxifylline, nicotinamide, plasmapheresis, and intravenous immunoglobulin are not mainstream medical treatments of TAO.
    • Octreotide, a potent synthetic somatostatin analogue, has a beneficial effect in TAO, especially in patients with a positive Octreoscan-111. Lanreotide is a longer-acting somatostatin analogue, which is administered only once every 2 weeks; it may provide some benefit.
    • Pentoxifylline and nicotinamide may be useful. Both agents are believed to inhibit cytokine-induced glycosaminoglycan synthesis by the retroorbital fibroblasts.
    • The role of plasmapheresis and intravenous immunoglobulin (IV Ig) is not well delineated. One randomized trial of IV Ig (1 g Ig/kg body weight for 2 consecutive d q3wk) versus oral prednisolone (for 20 wk with initial dose of 100 mg/d) showed both treatments to be equally effective in patients with active TAO. Fewer adverse effects were observed in the IV Ig treatment group.
• Orbital radiation
  • This procedure sometimes is prescribed for moderate-to-severe inflammatory symptoms, diplopia, and visual loss in patients with TAO.
  • The radiation (1500-2000 cGy fractionated over 10 d) usually is administered via lateral fields with posterior angulation. Radiation is believed to damage orbital fibroblasts or perhaps lymphocytes.
  • Radiation requires several weeks to take effect, and it may transiently cause increased inflammation. Thus, most patients are maintained on steroids during the first few weeks of treatment.
  • Better response to radiation is observed in patients with active inflammation who are treated within 7 months of TAO onset.  Radiation may be more effective if combined with steroid treatment.  Studies that suggest that radiotherapy is ineffective in TAO must be scrutinized to ensure that the radiation was administered to appropriate candidates at the appropriate time. (Gorman's study used serum thyroid-stimulating immunoglobulin as a surrogate of active eye disease. Although the blood test is an indicator of immunologic activity, it may not reflect the clinical progression of TAO. Furthermore the patients in Gorman's study were enrolled at a median of 1.3 y after onset of eye symptoms, suggesting that many of the patients in the study would not have progressive eye symptoms or signs indicative of an ongoing orbital process.⁴ )
  • Cataract, radiation retinopathy, and radiation optic neuropathy are possible risks. They are not common if treatment is appropriately fractionated and the eyes are shielded. In Marquez's study, 12% of patients developed cataracts after irradiation with median follow-up of 11 years.⁵
  • Wakelkamp also believed that orbital irradiation for TAO is a safe treatment modality, except possibly for patients with diabetes mellitus.⁶ Radiation may be a relative contraindication for patients with diabetes mellitus because of the risk of worsening retinopathy.
  • Although improvement of motility disturbances can occur with radiotherapy, radiation is limited when used in isolation to treat diplopia.
• Optic nerve compression
  • Compressive optic neuropathy may present with blurry vision, visual loss, dyschromatopsia, or field loss. Patients may not have marked proptosis, but they usually show markedly decreased retropulsion (tight orbits).
  • If necessary, high-dose steroids and higher intravenous doses are given. If no response occurs after 24 hours, steroids probably will not work; at this point, the patient should have surgical decompression and maintain steroids.
  • Adjunctive cyclosporine, octreotide, and IV Ig are less common modalities of medical treatment.
  • If a good steroid response occurs, orbital radiation may be considered. In severe cases of TAO, combined steroids, radiation, and surgery may be required.

Surgical Care

Approximately 5% of patients may require surgical intervention. The patient should know that multiple-staged procedures may be required. In elective cases, listen carefully to what the patient desires; the patient's expectations may not be realistic. The timing of surgery is important. Unless compressive optic neuropathy or severe corneal exposure is present, surgery generally is delayed during the active inflammatory phase of TAO. Surgery usually is performed during the quiescent cicatricial phase of the disease. Taking preoperative photographs is advised. With strabismus surgery, document prism measurements or fields of single binocular vision. Recording baseline-automated perimetry also is useful. The sequence of surgery is important. If the patient has marked proptosis, strabismus, and lid deformity, perform surgery in the following order:

• Orbital decompression
  • Thoroughly explain the potential complications of orbital decompression (eg, blindness, hemorrhage, diplopia, periorbital numbness, globe malposition, sinusitis, lid malposition) to the patient before surgery.
  • Orbital decompression may be performed as the initial treatment of compressive optic neuropathy or used if medical treatment is ineffective. A combination of medical and surgical treatment may be required in compressive optic neuropathy.
  • Following bony orbital decompression, open the periorbita. Little reduction in proptosis occurs until the periorbita is slit.
  • To decompress the optic nerve, at least 2 orbital walls usually are decompressed (traditionally, the medial wall and floor of the orbit). Medial decompression for compressive neuropathy must be taken posteriorly all the way to the apex of the optic canal. Surgery can be approached from a transorbital or trans-sinus route. Transorbital routes include subciliary incisions, lid crease incisions, medial incisions (cutaneous, transcaruncular), and coronal incisions. Trans-sinus routes include transantral approaches and endoscopy.
  • Medial wall removal should not extend above the frontoethmoidal suture. This averts bleeding from the ethmoidal arteries and prevents cerebrospinal fluid (CSF) leaks.
  • When the orbital floor is removed, preservation of a strut of bone between the ethmoid and maxillary bones may reduce strabismus from inferomedial shift in the globe position.
  • Balanced decompression of the medial and lateral orbital walls frequently is described. Avoiding decompression of the orbital floor theoretically decreases the risk of postoperative diplopia and lid retraction.
  • Lateral wall decompression does little to relieve apical compression but helps to reproduce proptosis. Valgus repositioning of the orbital wall and orbital rim-onlay, porous-polyethylene grafts are adjunctive techniques to reduce proptosis.
  • Four-wall decompression (with decompression of the orbital roof) requires a neurosurgical approach.
  • Orbital fat decompression without bony removal has been described for TAO without apical compression. Candidates for orbital fat decompression should show predominant enlargement of the orbital fat compartment, rather than the rectus muscles on orbital imaging. Unlike cosmetic blepharoplasty, with orbital fat decompression, fat also is removed posterior to the equator of the globe. Inferiorly, the fat is removed through a transconjunctival approach, which may be facilitated with lateral canthotomy and cantholysis. Superiorly, fat removal is through a lid crease incision, usually confined to the nasal quadrant.
• Strabismus surgery
  • Successful, early strabismus surgery during active thyroid ophthalmopathy has been described, but strabismus surgery generally is delayed until TAO is inactive and the prism measurements have been stable for at least 6 months.
  • Patients should realize that the goal of surgery is to minimize diplopia in primary and reading positions. Expecting binocular single vision in all positions of gaze may not be realistic. Patients also should realize that multiple strabismus surgeries and prisms may be required.
  • Because of the restrictive myopathy of TAO, recessions, rather than resections, predominantly are performed. Whenever feasible, adjustable suture surgery is recommended. In patients intolerant of conscious suture adjustment, hang-back sutures can be adjusted using the corneal light reflexes. In select patients with TAO, strabismus surgery can be performed using topical anesthesia. To prevent ocular ischemic syndrome, do not operate simultaneously on more than 2 muscles per eye.
  • Surgery of the inferior rectus muscle deserves special mention. Inferior rectus muscle recession may decrease upper lid retraction, but it often results in lower lid retraction despite dissection of the lower lid retractors. Because the inferior rectus muscle has subsidiary actions (excyclotorsion and adduction), inferior rectus muscle recessions may lead to a component of intorsion and A-pattern strabismus.
  • If visualization during strabismus surgery is difficult, especially for the superior rectus muscle, a vertical lid split technique may be considered.
  • Botulinum toxin injections are used by some clinicians during the acute phase of TAO as a temporizing measure until orbital decompression can be completed.  Optic neuropathy following a botulinum toxin injection for strabismus in a patient with TAO has been reported.
• Lid-lengthening surgery
  • If restoration of the euthyroid state does not improve lid retraction, consider lid-lengthening surgery. This surgery decreases corneal exposure and can be used to camouflage mild-to-moderate proptosis.
  • Lateral tarsorrhaphies can decrease upper and lower lid retraction, but the author does not prefer this method.
  • Two to three millimeters of upper lid retraction can be ameliorated with a Müller muscle excision. Lateral levator tenotomy is often helpful to decrease the temporal flare. If further amounts of lid recession are required, levator recession can be considered.
  • Lower lid-lengthening usually requires a spacer material. Graft materials include human acellular dermis, tarsus, and conjunctiva from the upper lid, hard palate, and ear cartilage.
  • Horizontal tightening procedures (eg, lateral tarsal strip) increase scleral show in patients with proptosis.
  • In the horizontally tight eyelid, lateral canthal advancement is a useful adjunct to enhance the effect of retractor recession and reduction of temporal flare.
• Blepharoplasty
  • This is the last phase of restorative surgery in TAO. Lower lid blepharoplasty can be approached transconjunctivally if no excess lower lid skin is present.
  • Upper lid blepharoplasty is performed transcutaneously with conservative skin excision. Brow fat resection may be considered. Dacryopexy may be required if lacrimal gland prolapse occurs.

Consultations

• Patients with TAO benefit from consultation and follow-up care with an endocrinologist.
• Orbital decompression can be performed in conjunction with an otorhinolaryngologist, especially when endoscopic procedures are contemplated.
• Neurosurgical consultation is required when decompression of the orbital roof is performed.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisone (Deltasone, Orasone, Meticorten)

Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and suppresses lymphocytes and antibody production.

Methylprednisolone (Medrol, Solu-Medrol, Depo-Medrol)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

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