Graves Eye Disease
Are you experiencing symptoms of anxiety, irritability, fatigue and weight loss (despite of normal food intake)? Are your eyes bulging out more than they used to? You may have Graves Eye Disease.
What is Graves Eye Disease?
Graves Eye Disease is the most common cause of an overactive thyroid gland. This condition is autoimmune, meaning that it occurs when your immune system mistakenly attacks your thyroid gland and causes it to overproduce the hormone thyroxine.
The thyroid is a gland shaped like a butterfly located in front of the neck below the larynx, or voice box. This gland makes two thyroid hormones (triiodothyronine [T3] and thyroxine [T4]).
Thyroid hormones affect metabolism (the rate at which the body converts food into energy), brain development, breathing, heart and nervous system functions, body temperature, muscle strength, skin dryness, menstrual cycles, weight, and cholesterol levels.
The production of these hormones is regulated by another hormone called thyroid-stimulating hormone (TSH), which is made by the pituitary gland located in the brain. In Grave’s Disease your immune system makes antibodies called thyroid-stimulating immunoglobin (TSI) which attach to thyroid cells.
TSI mimics the action of TSH and stimulates the thyroid to make too much thyroid hormone resulting in symptoms such as: Heat intoleranceWeight lossPalpitationsSweatingIrritability
What is Graves Eye Disease (or Grave’s Ophthalmopathy)?
Most patients presenting with hyperthyroidism (or overactive thyroid) associated with Graves Eye Disease will have some evidence of
Thyroid Eye Disease.
Thyroid Eye Disease (TED), also known as Grave’s Ophthalmopathy (GO) is the most frequent manifestation of autoimmune hyperthyroidism outside of the thyroid gland.
Eye involvement can be observed in 25-50% of patients with Grave’s Disease, of whom 3-5% develop severe disease.
may present before the hyperthyroidism or even occur for the first time years after successful treatment of hyperthyroidism, GO has been described as a separate, organ-specific autoimmune condition which frequently coexists with Graves Eye Disease.
GO has its own natural history with a period of deterioration, followed by one of stability, and finally some improvement. Although separate conditions, GO will worsen if thyroid function is not controlled.
What are the signs and symptoms of GO?
GO is the most common cause of unilateral (i.e., affecting one eye) or bilateral (i.e., affecting both eyes) proptosis (the eyes appear to be popping out) in adults
GO is more common in women than in men and over 90% of GO patients have abnormal thyroid function testsSmoking is a risk factor for thyroid disease and greatly increases the occurrence of GO in patients with Grave’s DiseaseThere are four areas of the eye that can be affected by GO resulting in:Eyelid disordersEye surface disorders (such as Dry Eyes)Ocular Motility disordersOptic NeuropathySymptoms resulting from these areas of the eye being affected include:Red eye, foreign body sensation in the eye, tearingDecrease in visionDifficulty seeing color
Prominent or “bulging” eyesSigns resulting from these areas of the eye being affected include:Lid retractionIncomplete blinkReduced blinking
Limitation of eye movements, especially when looking upDecrease in vision and color visionPupil defectVisual Field defect
How is GO diagnosed?
If you experience sudden eye symptoms such as Diplopia, bulging eyeballs, or decrease in vision, consult your eye doctor immediately. The first step in diagnosing GO is getting a comprehensive eye examination.
Your eye doctor will pay close attention to the following:Functioning of your cranial nerves (since three of them control eye movement and the second one, or Optic Nerve can become inflamed), Vision, Color Vision, Pupil Function, Eye Movements, Exophthalmometry (measures how much each eyeball protrudes out; if one eye protrudes significantly more than the other or both protrude more than average, then GO may be suspected) LidsCorneaEye PressureRetinal CheckCheck baseline Visual Fields in early cases and then use this testing in advanced cases to rule out optic neuropathy
If the eye exam leaves your eye doctor suspicious of GO, he or she will recommend laboratory testing to rule out thyroid problems. Thyroid function testing will include measures of TSH, thyroxine (total and free T4), and triiodothyronine (T3), and thyroid stimulating immunoglobin (TSI). Also, orbital CT scan can help detect extraocular muscle enlargement.
How is GO treated/managed?
Any underlying thyroid disease should be managed by an endocrinologist. In terms of the eyes, surgery will be postponed until the eyes are stable for a period of nine to twelve months except in cases of Optic Neuropathy or extreme bulging of the eyes which could make symptoms of Dry Eyes severe.
Depending on the complications of the disease on the eyes, surgery proceeds in a stepwise fashion, moving from the back of the eye to the front of the eye:Orbital bone decompression: This procedure is used for compressive Optic Neuropathy and should be performed by an oculoplastic surgeon. Initial treatment involves use of oral steroids (prednisone 100 mg every day for up to 14 days).
The initial treatment of inflammation of the extraocular muscles of the eyes with the use of oral steroids (prednisone 80-100 mg every day for 1-2 weeks, then tapered over a month) is controversial. Fresnel prisms are used on eyeglasses to help with the Diplopia. Surgery is considered after a six-month stable interval and after orbital surgery is completed. Eyelid Reconstruction: For Dry Eyes caused by exposure, treatment involves lubricating drops up to every hour while awake and ointment every night. Lid taping or moisture glasses at night may help. Punctal occlusion is reserved for more severe dry eye symptoms. Finally, surgical eyelid recession (or lengthening) is considered after an adequate stable interval.
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