Endocrine ophthalmopathy

Thyrotoxicosis (Graves' disease) is an autoimmune disease that usually begins in the 3rd and 4th decades of life, with women predominating among those affected. Thyroid disease (endocrine ophthalmopathy) of the eye may occur without clinical and biochemical signs of thyroid dysfunction.

Systemic manifestations are more common, but their severity does not correlate with ocular symptoms. Graves' disease without signs of hyperthyroidism is called ocular or euthyroid Graves' disease. Ophthalmologists most often encounter this form of the disease.

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Endocrine Ophthalmopathy - What's Happening?

The pathogenesis of endocrine ophthalmopathy involves an organ-specific immune response in which a humoral agent (IgG antibody) causes the following changes.

Thickened extraocular muscles in thyroid eye disease on axial CT scan

1. An inflammatory process in the extraocular muscles. Characterized by polymorphic cellular infiltration in combination with increased secretion of glucose and glycates and osmotic accumulation of water. The muscles sometimes thicken to sizes 8 times larger than normal and can compress the optic nerve. Subsequent degenerative changes in the muscles ultimately lead to fibrous changes in them, limited mobility, and restrictive ophthalmopathy and diplopia.
2. Inflammatory cellular infiltration by lymphocytes, plasma cells, macrophages, and mast cells of the interstitial tissues, adipose tissue, and lacrimal glands with accumulation of glucosaminoglycans and fluid retention. This leads to an increase in orbital volume and a secondary increase in intraorbital pressure, which in itself may contribute to further accumulation of fluid in the orbit.

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Symptoms of endocrine ophthalmopathy

Endocrine ophthalmopathy may precede, coincide with, or follow thyroidism and does not correlate with the degree of thyroid dysfunction. The range of manifestations is very wide: from minor signs to complete loss of vision due to exposure keratopathy or optic neuropathy. There are 5 main clinical manifestations of endocrine ophthalmopathy:

1. soft tissue damage,
2. eyelid retraction,
3. exophthalmos,
4. optic neuropathy,
5. restrictive myopathy.

There are 2 stages of disease development.

1. The edema stage (inflammatory), the manifestations of which are redness of the eyes and painful sensations. It lasts for 3 years and only in 10% of cases leads to the development of persistent eye disorders.
2. A stage of fibrosis in which the eyeballs appear calm, but painless movement disorders persist.

Soft tissue damage

Clinical features

1. Symptoms: foreign body sensation, photophobia, lacrimation and a feeling of discomfort.
2. Signs
   • swelling of the eyelid and periorbital region due to edema and infiltration of tissues behind the tarso-orbital fascia, which may be accompanied by prolapse of fatty tissue into the eyelids;
   • hyperemia of the conjunctiva and episclera is a subtle sign of the severity of the inflammatory reaction. Local hyperemia may correspond to the zone of attachment of the tendon of the horizontal muscles to the sclera;
   • chemosis is a manifestation of conjunctival and semilunar fold edema. Mild chemosis appears as a small fold of excess conjunctiva that extends over the edge of the lower eyelid. With severe chemosis, the conjunctiva bulges between the eyelids;
   • superior limbal keratoconjunctivitis;
   • dry keratoconjunctivitis due to infiltration of the lacrimal glands.

Treatment of endocrine ophthalmopathy

1. Topical moisturizers for superior limbal keratoconjunctivitis, lid closure failure and dryness.
2. The head should be elevated during sleep with pillows to reduce periorbital edema.
3. Taping your eyelids together while you sleep may help relieve exposure keratopathy.