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Graves' Disease: Proptosis, Lid Retraction, Strabismus, Optic Nerve Compression

Graves' disease

Proptosis, lid retraction, strabismus, optic nerve compression
These are all ophthalmic manifestations of Graves' disease.

The soft tissues around the eyes are infiltrated by lymphocytes in Graves' Disease, an idiopathic autoimmune disorder. The orbital tissues probably share a common antigen with the thyroid gland and the dermis of the pre-tibial region.

Ophthalmic signs may be the first or only clinical evidence of the disease and require more treatment than its endocrine aspects.

The ophthalmic manifestations should be divided into two groups: hypermetabolic and infiltrative.

  • Hypermetabolic. By activating sympathetic pathways, excess thyroid hormone causes retraction of the upper eyelids, making the patient look perpetually excited—the "stare sign." When the patient is instructed to look downward, the upper eyelids remain elevated or begin moving downward only after a delay, a sign called "lid lag." More than a cosmetic blemish, lid retraction may cause discomfort as the cornea dries from inadequate protection.
  • Infiltrative. Lymphocytic infiltration of the orbital soft tissues, which bears no relationship to the level of thyroid hormone, can be the cause of serious ophthalmic damage.
As the inflamed conjunctiva becomes hyperemic (red) and boggy, the eyes tear and discharge mucus. The patient reports a feeling of tightness, irritation, and intermittent blurring of vision, much as one might experience with infectious conjunctivitis ("pink eye"). The lower eyelids become boggy, and palpation elicits a sense of rubbery induration that is only mildly tender.

When the extraocular muscles and orbital fat become inflamed, the eyes are displaced forward in the orbit (proptosis, exophthalmos), and the movements of the eyes may be limited. At first, the impaired eye movements are due to swollen, inefficient extraocular muscles. If the inflammation persists beyond a year, the muscles scar in a contracted, noncompliant state. Typically, some extraocular muscles are affected more than others, driving the eyes out of alignment in some fields of gaze, and causing the patient to experience double vision.

As the muscles swell, they may compress the optic nerve in the posterior orbit, where they are packed in a tight space. If the compression is not relieved, axoplasmic flow within the nerve comes to a halt, and vision fails. This compressive optic neuropathy is the most dreaded ophthalmic consequence of Graves' disease.

Another outcome of marked swelling of extraocular muscles and orbital fat is massive proptosis which interferes with the protective function of the eyelids and results in drying of the cornea. This "exposure keratopathy" is the second most feared ophthalmic manifestation of Graves' disease.

The combination of hypermetabolic and infiltrative ophthalmic signs gives away the diagnosis of Graves' disease.

But when the hypermetabolic component is absent and infiltrative signs are mild, the condition is often misdiagnosed as infectious or allergic conjunctivitis.

When one side is relatively spared, the physician may incorrectly diagnose an orbital tumor.

And when inflammation relatively spares the most visible tissues—the conjunctiva and eyelids—the physician may fail to consider Graves' disease as the explanation for diplopia or visual loss.

What to do?
The ophthalmic manifestations of Graves' disease may be pivotal in diagnosis, particularly when dysmetabolic signs are not prominent.

What about treatment of the eye signs?

Lid retraction and lag are sometimes reversed when the thyroid hormone levels are brought into the normal range.

Conjunctival inflammation may be treated with over-the-counter topical vasoconstrictors. If the conjunctiva or eyelids are particularly boggy, the patient may get some relief by sleeping with head propped up. In more severe cases, a mild diuretic may be indicated.

Treatment of the diplopia and impaired eye movements owing to extraocular muscle swelling is controversial. Some physicians use intermittent oral corticosteroids, which may be moderately effective. Others do not prescribe corticosteroids because their unproven efficacy must be balanced against the toxicity of chronic use. Diplopia can be palliated with prism spectacles and, once the active inflammation has subsided, with eye muscle surgery.

Corneal drying that results from lid retraction and proptosis is managed with artificial tears, and if severe, with surgical procedures aimed at narrowing the palpebral fissure height.

Optic nerve compression from enlarged muscles may be treated initially with high-dose corticosteroids, but definitive treatment consists of orbital x-irradiation or surgical removal of the medial and inferior orbital walls. If such treatment is delayed, blindness may be permanent.

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Originally created by Jonathan Trobe, M.D., University of Michigan Kellogg Eye Center
© 2009 The Regents of the University of Michigan

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