Thyroid orbitopathy is known to have an effect on intraocular pressure (IOP). Infiltrative thyroid orbitopathy has been postulated to cause elevated IOP by two mechanisms. In one mechanism, enlarged extraocular muscles compromise orbital venous outflow, causing elevated episcleral venous pressure and a subsequent decrease in aqueous outflow facility. In the other mechanism, fibrotic extraocular muscles (primarily the inferior rectus) indent the globe in certain positions of gaze (primarily upgaze), thus raising IOP in that field of gaze.

A poster presentation at this year's annual meeting of the Association for Research in Vision and Ophthalmology in Fort Lauderdale, Florida, emphasized the correlation between thyroid orbitopathy and elevated IOP. Sundeep Dev, M.D., et al, from the Duke University Eye Center, reported on the change in IOP after orbital decompression surgery for thyroid orbitopathy. Of 19 eyes studied, a statistically significant mean decrease of 2.7 mmHg (19.7 to 16.9) occurred after decompression surgery. Furthermore, of the seven eyes with IOP greater than 21 mmHg preoperatively that were treated with topical anti-glaucoma medications, a mean decrease of 6.1 mmHg postoperatively was recorded. These eyes did not require any further antiglaucoma medications postoperatively.

In this study, all IOP measurements were made in the primary position of gaze, so that a correlation between a relative IOP elevation in upgaze pre- and post-orbital decompression surgery could not be made. However, the mechanism of elevated episcleral venous pressure as the cause of elevated IOP was suggested in one patient with high IOP who had a markedly dilated superior ophthalmic vein on orbital computed tomography scan preoperatively. On a postoperative CT scan, the superior ophthalmic vein returned to normal size and the IOP decreased.

At last year's ARVO meeting, Kimberly Peele, M.D., et al, of the Walter Reed Army Medical Center and the Allegheny General Hospital, presented a poster on the incidence of ocular hypertension in dysthyroid orbitopathy. In that study, 120 thyroid patients with IOP greater than 22 mmHg were identified and studied retrospectively. Of 94 patients with hyperthyroidism, 43 had IOP greater than 25 mmHg and 17 had IOP's greater than 30 mmHg. Sixteen patients with asymmetric proptosis had higher IOP in the more proptotic eye. Two patients had glaucomatous cupping and visual field loss requiring treatment - one with topical medications and one with surgery. Twelve patients were treated with topical medications for elevated IOP before their hyperthyroidism was diagnosed. However, once their hyperthyroidism was controlled, these twelve patients did not require antiglaucoma treatment. The study concluded that although elevated IOP occurs commonly with hyperthyroidism, glaucomatous damage associated is rare. Furthermore, the elevated IOP may resolve with treatment for the hyperthyroidism.

Dr. Peele also identified 18 patients who were hypothyroid and had elevated IOP. An association between hypothyroidism and elevated IOP has previously been noted, but it has received insufficient attention and remains notably underrecognized. In a comprehensive prospective study, (Kevin Smith, MD, et al. An association between hypothyroidism and primary open-angle glaucoma, Ophthalmology 100:1580-1584, 1993) the authors used a thyroid-stimulating hormone (TSH) immunoradiometeric assay as a screening test to determine if hypothyroidism was present in 64 patients with primary open-angle glaucoma (POAG). 64 control subjects were also tested for TSH levels. Of the POAG group, 23.4% were hypothyroid: 12.5% were known to be hypothyroid and 10.9% were diagnosed by the screening test during the study. Of the control subjects, 4.7% were hypothyroid, and this agreed with other studies which showed about a 5% incidence of elevated TSH in the general population.

The authors concluded that hypothyroidism is more common in patients with POAG, and a significant proportion of them are undiagnosed. They propose that in the hypothyroid state, decreased metabolism of glycosaminoglycans, specifically hyaluronic acid, leads to accumulation of hyaluronic acid in the trabecular meshwork, causing decreased outflow facility and increased IOP. They speculate that elevated IOP in hypothyroid patients may be lowered by returning the patient to the euthyroid state with thyroxin therapy. To support this hypothesis, the authors refer to a case report (Smith, K.D., et al, Reversal of poorly controlled glaucoma on diagnosis and treatment of hypothyroidism, Can J Ophthalmol, 27:347-7, 1992) where this occurred. Another case report (Ritch, R., and Podos, S.M., Hypothyroidism and glaucoma, Ophthalmology,101:623) had a similar result.

The papers mentioned above raise interesting questions regarding the treatment of elevated IOP associated with thyroid disease. When presented with a patient with elevated IOP, the examining ophthalmologist should inquire about the sometimes subtle symptoms of thyroid disease. The symptoms of hyperthyroidism are heat intolerance, fatigue, palpitations, dyspnea, insomnia, frequent loose stools, and weight loss. The symptoms of hypothyroidism are cold intolerance, hoarse voice, cold rough skin, constipation, apathy, slow speech, and fatigue. The ophthalmologist should look for ocular signs of thyroid disease like stare, lid lag, and frank proptosis in hyperthyroidism, and periorbital edema in hypothyroidism. Thyroid function tests should be ordered if a dysthyroid state is suspected.

If a dysthyroid state is found, elevated IOP may resolve with effective treatment of the thyroid disease. In cases of hyperthyroidism, elevated IOP can occur with infiltration of the extraocular muscles. This elevated IOP may occur before signs of ocular dysmotility or proptosis. If elevated IOP occurs only in a specific field of gaze due to fibrosis of a muscle, then IOP lowering treatment is probably not necessary. The occurrence of true glaucomatous optic nerve damage in hyperthyroid patients with elevated IOP is rare, and they can likely be effectively treated with conventional methods. However, for the rare patient with elevated IOP and glaucomatous optic nerve damage which persists in primary gaze and is unresponsive to medical and laser treatment, the ophthalmologist is confronted with a difficult management dilemma. The paper by Dr. Dev suggests that orbital decompression surgery prior to standard filtration surgery may be an effective treatment for a case such as this. However, the literature does not yet support this course of action, and since these patients are so infrequent, a prospective study would be difficult to perform. In cases of hypothyroidism, where metabolism of hyaluronic acid may be enhanced by thyroxin treatment, the euthyroid state should be reestablished before filtration surgery is performed.

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