|Thyroid Ophthalmopathy (Graves Disease)
Signs and Symptoms
Interestingly, ocular findings may occur independently from dysthyroid function. Euthyroid Graves disease is a condition where the characteristic ophthalmic manifestations of thyroid eye disease exist in the presence of a clinically and biomedically normal thyroid gland.
Most patients with ocular Graves disease manifest systemic hyperthyroidism. Up to 80 percent of patients with systemic hyperthyroidism develop some eye signs. Systemic signs of hyperthyroidism include weight loss despite increased appetite, nervousness, palpitations, tachycardia while at rest, systemic hypertension, and hyperreflexia. Conversely, lethargy, bradycardia and weight gain despite decreased appetite are signs of hypometabolism and potential hypothyroidism.
In 1969, the American Thyroid Association adopted the formal classification of Ocular Graves disease, represented by the pneumonic NOSPECS. The disease process passes through 6 stages: (0) No signs or symptoms present, (I) Only symptoms of ocular irritation (dryness, tearing, foreign body sensation), (II) Soft tissue involvement (periorbital edema), (III) Proptosis, (IV) Extraocular muscle involvement (ophthalmoplegia), (V) Corneal involvement (dense punctate epitheliopathy, infiltration and ulceration), (VI) Sight loss with or without visual field compromise secondary to compressive optic neuropathy. However, because the disease is recognized as variable, the formal classification was revised in 1974 to range from no manifestations to mild, moderate or severe manifestations.
The common, clinically diagnostic eye signs include: von Graefes sign (superior lid lag upon down gaze), Dalrymples sign (eyelid retraction), Stellwags sign (infrequent blinking), and Ballets sign (palsy of one or more extraocular muscles).
The histopathologic features of the malady include an infiltration of the thyroid gland, skin, extraocular muscles and orbital fat by lymphocytes, macrophages, plasma cells, mast cells and mucopolysaccharides. These changes are characteristic of, but not limited to, an immunologically mediated mechanism.
The systemic management of patients with ocular Graves disease lies in the domain of the endocrinologist. Agents that block the synthesis of thyroid hormone such as propylthiouracil (Tapazole) or decrease hypermetabolic symptoms such as propranolol (Inderal) have been proven effective. Systemic steroids, immunosuppressive agents like azathioprine, cyclosporin or cyclophosphamide in combination with orbital irradiation have shown promise in advanced cases. Today, surgical orbital decompression procedures are a last resort.
Since the primary concern proptosis and lid retraction presents is corneal exposure, ocular management is predominantly supportive. Typically, moistening the cornea with artificial tear drops and ointments is effective. Moisture shields that can be attached to the temples of spectacles help to preserve tears and retard tear evaporation. Punctal occlusion may be effective. Cases that involve moderate to severe keratopathy may require prophylactic topical antibiotics. Visual fields should be performed on patients with advanced stage disease, monitoring for the first sign of sight or field loss. Evaluation is usually every three to six months and is based upon severity.
Other reports in this section
Eyelids & Eyelashes | Conjunctiva & Sclera | Cornea
Uvea | Vitreous & Retina | Optic Nerve & Brain | Oculosystemic Disease
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