Thyroid-associated ophthalmopathy

 

Thyroid-associated ophthalmopathy

Definition

Thyroid-associated orbitopathy (TAO), frequently termed Graves ophthalmopathy, is part of an autoimmune process that can affect the orbital and periorbital tissue, the thyroid gland, and, rarely, the pretibial skin or digits (thyroid acropachy). Although the use of the term thyroid ophthalmopathy is pervasive, the disease process is actually an orbitopathy in which the orbital and periocular soft tissues are primarily affected with secondary effects on the eye.

Source : Emedicine 

Organ

Edema appears at the orbital tissues, which affects the muscles and causes muscle contractions causing a reduction in the mobility of the eye.

 

Symptoms

Patients may complain of the following ocular symptoms:

  • Dry eyes
  • Puffy eyelids
  • Angry-looking eyes
  • Bulging eyes
  • Diplopia
  • Visual loss
  • Field loss
  • Dyschromatopsia
  • Photopsia on upgaze
  • Ocular pressure or pain

Source : Emedicine 

 

Frequency

Thyroid eye disease, or Graves’ ophthalmopathy, is a potentially vision-threatening autoimmune disease that manifests most commonly in hyperthyroid patients (77 percent), and less frequently in euthyroid (20 percent) and hypothyroid (3 percent) patients.1 TED can precede or succeed the thyroid disease, usually within 18 months of each other in the majority of the patients.2 Although great variability in severity and duration of the disease can be observed, TED is ultimately a self-limiting disease that lasts about one year in non-smokers and three years in smokers. 

Source : Review of Opthalmology

 

Causes

  • Current smoking increases the risk of developing TED (relative risk of 7 for heavy smokers) although ex-smokers are not at increased risk. Risk increases with the number of cigarettes smoked and reduces on quitting. Smoking also increases the risk of ophthalmopathy after radio-iodine, although this can be reduced by corticosteroids.[10] Smoking also delays and reduces the efficacy of the other methods of treatment such as steroids and radiotherapy.
  • Female sex (due to the higher prevalence of thyroid disease in women).
  • Middle age.
  • There are some associated genes including HLA-DR3, HLA-B8 and the genes for CTLA4 and the TSH receptor.
  • Autoimmune thyroid disease.
  • Uncontrolled thyroid dysfunction. Thyroid dysfunction is associated with more severe TED, and tight control of thyroid function appears to reduce the severity of TED.
  • Radio-iodine therapy is associated with progressive Graves' ophthalmopathy. Thus, it can only be used in the inactive phase of the eye disease.

Source : Patient

 

Evolution

Although in many instances the disease is self-limiting, spontaneously improving within 2-5 years 3 often discomfort, cosmetic issues, the risk of corneal ulceration and optic nerve compression requires treatment. 

Source : Radiopaedia 

 

Diagnosis

The diagnosis of TAO is clinical and is based on the triad of characteristic eye findings, thyroid dysfunction, and imaging studies. In majority of cases, ophthalmopathy occurs in association with hyperthyroidism. 

Source : NCBI

 

Treatment

The hyperthyroidism and the eye disease should be treated independently. Most of the mild to moderate TAO cases shows improvement with treatment of the underlying hyperthyroidism.

The decision to treat TAO depends on the severity and the activity of the disease. The principal goals of therapy for TAO include pain relief, protection of vision and cosmetic improvement.

The major therapeutic options include corticosteroids, radiotherapy and surgical intervention. TAO is categorized as severe and non-severe for treatment purposes. Severe disease can be either active or inactive. Features of severe ophthalmopathy are marked proptosis, diplopia in primary gaze or reading, exposure keratopathy, corneal ulceration or perforation and compressive optic neuropathy.

Treatment options for severe, active cases include either medical decompression (steroids or radiotherapy) or surgical decompression. Majority of them prefer high doses of steroids first and surgical decompression if it fails. For severe, inactive disease, surgical decompression is the only option. Lid retraction in TAO is caused by sympathetic stimulation of the Muller’s muscle. Guanethidine or â-blocker eye drops has been tried for the treatment of lid retraction with varying degree of success. In patients with severe ophthalmopathy, if the disease is active the treatment is medical decompression by either steroids or radiotherapy and if the TAO is inactive orbital decompression and rehabilitative surgery is the choice.

Source : NCBI

 

 

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