Management

Management

Eye symptoms

  • Hyperthyroidism almost always causes general eye symptoms like dryness and irritation, regardless of what the cause of the hyperthyroid state is. However, these need to be distuingished from Graves’ ophthalmopathy, which can only occur in patients who have Graves’ disease. (It may possibly also, rarely, be seen in Hashimoto’s thyroiditis, primary hypothyroidism, and thyroid cancer).
  • About 20-25% of patients with Graves’ disease will suffer from clinically obvious Graves’ ophthalmopathy, and not just from the eye signs of hyperthyroidism. Only 3 to 5% will develop severe ophthalmopathy.[15] However, when subjected to closer inspection (e.g. by magnetic resonance imaging of the orbits) many more patients have evidence of ophthalmopathy (primarily enlargement of retroocular muscles). It is estimated that for every 100,000 persons, 16 women and 3 men have Graves’ ophthalmopathy every year.
  • Although it is true that in most patients ophthalmopathy, goiter, and symptoms of thyrotoxicosis appear more or less coincidentally, it is also true that in certain cases eye signs may possibly appear long before thyrotoxicosis is evident, or become worse when the thyrotoxicosis is subsiding or has been controlled by treatment.[3] In approximately 20% of ophthalmopathy patients, ophthalmopathy appears before the onset of hyperthyroidism, in about 40% concurrently, and in about 20% in the six months after diagnosis. In the remainder, the eye disease first becomes apparent after treatment of the hyperthyroidism, more often in patients treated with radioiodine.
  • It can often be difficult to distinguish between eye symptoms due to hyperthyroidism and those due to Graves’ antibodies, not in the least because the two often occur coincidently. What can make things particularly difficult, is that many patients with hyperthyroidism have lid retraction, which leads to stare and lid lag (due to contraction of the levator palpebrae muscles of the eyelids). This stare may possibly then give the appearance of protruding eyeballs (proptosis), when none in fact exists. This subsides when the hyperthyroidism is treated.

Graves’ ophthalmopathy is characterized by inflammation of the extraocular muscles, orbital fat and connective tissue. It results in the following symptoms, which can be extremely distressing to the patient:

  • Most frequent are symptoms due to conjunctival or corneal irritation: burning, photophobia, tearing, pain, and a gritty or sandy sensation.
  • Protruding eyeballs (known as proptosis and exophthalmos).
  • Diplopia (double vision) is common.
  • Limitation of eye movement (due to impairment of eye muscle function).
  • Periorbital and conjunctival edema (accumulation of fluid beneath the skin around the eyes).
  • Infiltrative dermopathy (pretibial myxedema).
  • In severe cases, the optic nerve may possibly be compressed and acuity of vision impaired.
  • Occasionally loss of vision.

Due to hyperthyroidism

In the absence of Graves’ ophthalmopathy, patients may possibly demonstrate other ophthalmic signs due to hyperthyroidism:

  • Dry eyes (due to loss of corneal moisture).
  • A sense of irritation, discomfort, or pain in the eyes.
  • A tingling sensation behind the eyes or the feeling of grit or sand in the eyes.
  • Excessive tearing that is often made worse by exposure to cold air, wind, or bright lights.
  • Swelling or redness of the eyes.
  • Stare
  • Lid lag (Von Graefe’s sign)
  • Sensitivity to light.
  • Blurring of vision.
  • Widened palpebral fissures.
  • Infrequent blinking.
  • The appearance of lid retraction.

Strabismus

  • Double vision usually occurs because the eyes are out of alignment.
  • Misalignment often is caused by one or more eye muscles that are too short or “tight” because of scar tissue from Graves’ ophthalmopathy.
  • This scar tissue results from changes in the eye because of inflammation.

Prisms

  • Prisms may possibly be temporary (pasted on) or permanently ground into your lenses. However, prisms do not work for all people with double vision. Sometimes eye muscle surgery is a more effective treatment.

Eye Muscle Surgery

  • The goal of eye muscle surgery is to achieve single vision when looking straight ahead and when reading. During eye muscle surgery the muscle is cut from its attachment to the eyeball and reattached further back. Usually eye muscle surgery does not require an

Lower Eyelid Retraction

  • Graves’ ophthalmopathy generally causes the eyelids to open more widely. The front surface of the eyeball becomes exposed beyond the eyelids and causes discomfort and excessive tearing; exposure keratopathy.
  • Eyelid surgery is the most common surgery performed on Graves ophthalmopathy patients.
  • Lid-lengthening surgeries can be done on upper and lower eyelid to correct the patient’s appearance and the ocular surface exposure symptoms.
  • Marginal myotomy of levator palpebrae muscle can reduce the palpebral fissure height by 2-3 mm.
  • When there is a more severe upper lid retraction or exposure keratitis, marginal myotomy of levator palpebrae associated with lateral tarsal canthoplasty is recommended.
  • This procedure can lower the upper eyelid by as much as 8 mm. Other approaches include mullerectomy (resection of the Muller muscle), eyelid spacer grafts and recession of the lower eyelid retractors. Blepharoplasty can also be done to debulk the excess fat in the lower eyelid.
  • Surgically repositioning the eyelids can reduce the irritation. If orbital decompression, eye muscle and eyelid surgery are required, the eyelid procedure is generally performed as the final procedure in the series.

Upper Eyelid Retraction

  • The upper eyelid retraction might be worsened if the eye is unable to elevate normally (strabismus), and extra nerve impulses are sent simultaneously to the muscle which elevates the lid and to the muscle struggling to elevate the eye itself; once the restriction is treated (e.g. strabismus surgery), the degree of retraction often decreases.

Orbital decompression involves removing some bone from the eye socket to open up one or more sinuses and so make space for the swollen tissue and allowing the eye to move back into normal position.

The CT above shows the orbit on the left following orbital decompression. Note how the muscle bows inward, into the area of the sinus – now that this orbital wall has been surgically removed.

  • Optic Neuropathy. Even though some patients undergo spontaneous remission of symptoms within a year, many need treatment. The first step is the regulation of thyroid hormones levels by an endocrinologist.
  • Topical lubrication of the ocular surface is used to avoid corneal damage caused by exposure. Tarsorrhaphy is an alternative option when the complications of ocular exposure can’t be avoided solely with the drops.
  • Corticosteroids are efficient in reducing orbital inflammation, but the benefits cease after discontinuation. Corticosteroids treatment is also limited because of their many side effects. Radiotherapy is an alternative option to reduce acute orbital inflammation. Unfortunately, there is still controversy surrounding its efficacy. A simple way of reducing inflammation is smoking cessation, as pro-inflammatory substances are found in cigarettes.
  • Surgery could be done to decompress the orbit, to improve the proptosis and to address the strabismus causing diplopia . Surgery is performed once the patient’s disease has been stable for at least six months. In severe cases, however, the surgery becomes urgent to prevent blindness from optic nerve compression.
  • Eyelid surgery is the most common surgery performed on Graves ophthalmopathy patients. Lid-lengthening surgeries can be done on upper and lower eyelid to correct the patient’s appearance and the ocular surface exposure symptoms. Marginal myotomy of levator palpebrae muscle can reduce the palpebral fissure height by 2-3 mm. When there is a more severe upper lid retraction or exposure keratitis, marginal myotomy of levator palpebrae associated with lateral tarsal canthoplasty is recommended. This procedure can lower the upper eyelid by as much as 8 mm. Other approaches include mullerectomy (resection of the Muller muscle), eyelid spacer grafts and recession of the lower eyelid retractors. Blepharoplasty can also be done to debulk the excess fat in the lower eyelid.
  • If the optic nerve is compromised, and vision is threatened as a result of Graves’ disease, the term optic neuropathy could be applied.

Orbital Decompression Surgery

  • In orbital decompression surgery the bone between the orbit (eye socket) and the sinuses (air spaces next to the orbit) is removed.
  • A successful procedure improves vision and provides room for the eye to slip back into the orbit’s protection.
  • There are possible complications of the surgery, however.
  • You could experience lip numbness for several months after the operation.
  • Double vision could persist or it could develop anew after surgery

Orbital Decompression

Orbital Anatomy

  • Orbital volume and dimensions: = 30 cc, 35(Height) x 45(Width) x 45 mm(medial wall depth), globe 25 x 25 mm
  • Bones: (F)rontal, (M)axillary,(Z)ygomatic, (L)acrimal, (E)thmoid, (P)alatine, (S)phenoid
  • makes room to put the eyes back in the socket and correct the proptosis (bulging).
  • the bone between the orbit and the Sinuses (Sinus is the air spaces next to the orbit) is removed.
  • goal is to improve vision and provides room for your eye to slip back into the orbit’s protection.
  • complications
    • lid numbness
    • double vision
    • CSF leak (of cerebrospinal fluid that surrounds and protects the brain)