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Eye Related Disease

Clinical Signs of Graves’ Disease

Graves’ disease may possibly present clinically with one of the following characteristic signs:

• exophthalmos (protuberance of one or both eyes)
• a non-pitting edema (pretibial myxedema), with thickening of the skin usually found on the lower extremities
• fatigue, weight loss with increased appetite, and other symptoms of hyperthyroidism
• rapid heart beats
• muscular weakness
• The two signs that are truly ‘diagnostic’ of Graves’ disease (i.e., not seen in other hyperthyroid conditions) are exophthalmos and non-pitting edema (pretibial myxedema). Goiter is an enlarged thyroid gland and is of the diffuse type (i.e., spread throughout the gland). Diffuse goiter may possibly be seen with other causes of hyperthyroidism, although Graves’ disease is the most common cause of diffuse goiter. A large goiter will be visible to the naked eye, but a smaller goiter (very mild enlargement of the gland) may possibly be detectable only by physical exam. Occasionally, goiter is not clinically detectable but may possibly be seen only with CT or ultrasound examination of the thyroid.
• Another sign of Graves’ disease is hyperthyroidism, i.e., overproduction of the thyroid hormones T3 and T4. Normothyroidism is also seen, and occasionally also hypothyroidism, which may possibly assist in causing goiter (though it is not the cause of the Graves disease). Hyperthyroidism in Graves’ disease is confirmed, as with any other cause of hyperthyroidism, by measuring elevated blood levels of free (unbound) T3 and T4.
• Other useful laboratory measurements in Graves’ disease include thyroid-stimulating hormone (TSH, usually low in Graves’ disease due to negative feedback from the elevated T3 and T4), and protein-bound iodine (elevated). Thyroid-stimulating antibodies may possibly also be detected serologically.
• Biopsy to obtain histiological testing is not normally required but may possibly be obtained if thyroidectomy is performed.
• Differentiating two common forms of hyperthyroidism such as Graves’ disease and Toxic multinodular goiter is important to determine proper treatment. Measuring TSH-receptor antibodies with the h-TBII assay has been proven efficient and was the most practical approach found in one study.

Eye disease

Thyroid-associated ophthalmopathy is one of the most typical symptoms of Graves’ disease. It is known by a variety of terms, the most common being Graves’ ophthalmopathy. Thyroid eye disease is an inflammatory condition, which affects the orbital contents including the extraocular muscles and orbital fat. It is almost always associated with Graves’ disease but may possibly rarely be seen in Hashimoto’s thyroiditis, primary hypothyroidism, or thyroid cancer.

The ocular manifestations that are relatively specific to Grave’s disease include soft tissue inflammation, proptosis (protrusion of one or both globes of the eyes), corneal exposure, and optic nerve compression. Also seen, if the patient is hyperthyroid, (i.e., has too much thryoid hormone) are more general manifestations, which are due to hyperthyroidism itself and which may possibly be seen in any conditions that cause hyperthyroidism (such as toxic multinodular goiter or even thyroid poisoning). These more general symptoms include lid retraction, lid lag, and a delay in the downward excursion of the upper eyelid, during downward gaze.

It is believed that fibroblasts in the orbital tissues may possibly express the Thyroid Stimulating Hormone receptor (TSHr). This may possibly explain why one autoantibody to the TSHr can cause disease in both the thyroid and the eyes

Graves Disease

• Grave’s Ophthalmolopathy is the most common caused of unilateral or bilateral proptosis in adults.
• It commonly occurs between the ages of 25-50, although it may possibly also present in adolescents.
• Diagnosis is made based on clinical findings including proptosis, eyelid retraction, restrictive myopathy and possibly compressive optic neuropathy. It is often grouped into two independent manifestations of this syndrome:
  • Type I and Type II orbitapathy, but may possibly overlap

Werner’s Classification

NO SPECS, with each class in four grades 0-4, a, b, c: mild to severe

• 0 No S/S
• 1 Only signs (lid retraction)
• 2 Soft tissue involved (chemosis, grit, etc)
• 3 Proptosis (min 28)
• 4 EOM involved
• 5 Corneal involvement
• 6 Sight loss

Diagnosis is made on these clinical findings and may possibly be confirmed on CT which shows enlargement of multiple extraocular muscles most commonly the inferior and medial rectus.

Systemic thyroid may possibly be hyperthyroid, hypothyroid, or euthyroid. Treatment may possibly include topical lubrication, systemic steroids, orbital decompression surgery, extraocular muscle adjustment, eyelid recession surgery and radiation therapy.