thyroid eye disease autoimmune disorder characterised by infiltrative orbitopathy

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  • THYROID EYE DISEASE Autoimmune disorder characterised by infiltrative orbitopathy
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  • Graves' disease Graves' disease is the most common thyroid abnormality associated with thyroid orbitopathy, but other disorders of the thyroid can have similar ocular manifestations. These include Hashimoto's thyroiditis, thyroid carcinoma, primary hyperthyroidism, and neck irradiation. Approximately 40% of patients with Graves' disease have or will develop thyroid orbitopathy.
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  • THYROID EYE DISEASE Associated with normal to abnormal thyroid function which may coexist, precede or follow the orbitopathy. Related to but not the same as Graves Ophthalmopathy (GO) The natural history was described by Rundle and Wilson in 1945
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  • Thyroid status- Of those patients with thyroid orbitopathy, approximately 80% are clinically hyperthyroid and 20% are clinically euthyroid.4 Most patients with euthyroid Graves' orbitopathy, however, have some detectable laboratory evidence of subclinical hyperthyroidism. Both hyperthyroid and euthyroid patients can develop clinical signs and symptoms of thyroid orbitopathy. In general, patients with euthyroid Graves' disease tend to have less severe orbitopathy
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  • THYROID EYE DISEASE The goal is to identify and treat patients who are at particular risk of sight threatening complications. The disease has a finite period of activity until it becomes burnt out.The yellow region shows the early phase where there is the best response to treatment. Type 1 younger age group, whiter eyes with proptosis. Inflammation is mostly in orbital fat not muscles. Type 11 older patient with red eyes, severe sight threatening disease, tobacco addiction is frequent.
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  • General Considerations Severe exophthalmos and compressive optic neuropathy are slightly more common in older men. There appears to be an increased prevalence of thyroid disease in smokers, for whom the relative risk of developing Graves' orbitopathy is twice as high as it is for nonsmokers. The reason for this difference is not known, but one possibility is that the decreased immunosuppression in smokers may allow greater expression of autoimmune processes.
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  • PATHOGENESIS Type II reaction:- autoimmune antibodies target somatic tissues such as extraocular muscles causing an antigen-antibody reaction. A large number of lymphokines are implicated in the inflammatory process. Inflammation results in production of mucopolysaccharides by fibroblasts leading to swelling followed by collagen production resulting in restriction. There is a high concentration of macrophages in the inferior rectus muscle as well as CD4+ memory T cells and CD8 T cells. This may account for the clinical observation of maximal disease activity in this muscle.
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  • ETIOLOGY In 1956, Adams and Purves isolated a factor in the serum of patients with Graves' hyperthyroidism that caused stimulation of the animal thyroid gland. This factor was very similar to TSH but had a longer half-life. It was therefore called long-acting thyroid stimulator (LATS). In 1964, Kriss and colleagues showed that LATS had the structure of an IgG immunoglobulin and its action could be neutralized by thyroid tissue, indicating that it was an antibody. Further experiments showed that the antibody was directed against the receptor for TSH on the follicular cell of the thyroid gland.
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  • Thyrotropin receptor antibodies (TRAb). antibodies were originally classified into those with stimulatory properties called thyroid-stimulating immunoglobulin or antibody (TSI, TSAb) and those with inhibitory properties called TSH-binding inhibiting immunoglobulin or antibody (TBII, TBIA). Both of these groups are now referred to as thyrotropin receptor antibodies (TRAb).
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  • PHYSIOLOGY Hypothalamus TRH pituitary TSH thyroid T3 and T4 85% of T4 converted to T3 in tissues. T3 has 5 times the activity of T4.
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  • Pathology The predominant orbital pathology is inflammation of the orbital soft tissues and extraocular muscles. This immune-mediated inflammation consists mostly of lymphocytes and plasma cells, with a scattering of mast cells. These inflammatory changes differ from the more exuberant lymphocytic infiltration of the orbital fat and muscles, including their tendinous insertions seen in orbital pseudotumor
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  • Pathology The earliest change in extraocular muscles appears to be inflammation of the endomysial connective tissues, which stimulates endomysial fibroblasts to produce first hyaluronic acid and then collagen. In the acute stage there is inflammation, edema, and deposition of glycosaminoglycans. Eventually there is tethering of orbital tissues due to fibroblast proliferation.
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  • CLINICAL (orbitopathy in general is worst in the older age groups.) LID RETRACTION1. sympathetic overactivity2. infiltration of levator / SR complex3. hypotropia (retraction disappears on downgaze) SIGNS:- Dalrymples (lid retraction), von Graefe (lid lag), Kochers (staring appearance) INFILTRATION 1. soft tissue involvement :- chemosis, conjunctival injection over the recti insertions, puffy lids Superior limbic keratoconjunctivitis (SLK) due to redundant conjunctiva 2. muscle involvement :- diplopia due to restriction. Order of involvement IR, MR, SR (LR) Braleys sign = increased IOP on upgaze (>4mmHg) 3. proptosis :- TED is the commonest cause of unilateral or bilateral proptosis
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  • Sight Threatening Complications optic nerve compression :- 25mg/ day. Best effect in acute disease.Do not irradiate patients with diabetes mellitus as they are more susceptible to radiation retinopathy.2000rads/ 10days, effect starts at 4 weeks, maximal 4 months.">
  • Radiotherapy RETROBULBAR RADIOTHERAPY:- Trial of prednisone versus radiotherapy showed no difference in clinical improvement (about 50%).The patients all tolerated retrobulbar radiotherapy better than steroids Consider if steroid maintenance > 25mg/ day. Best effect in acute disease.Do not irradiate patients with diabetes mellitus as they are more susceptible to radiation retinopathy.2000rads/ 10days, effect starts at 4 weeks, maximal 4 months.
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  • Compressive Optic Neuropathy Compressive optic neuropathy can cause permanent visual loss. The treatment possibilities include high doses of corticosteroids, irradiation, and orbital decompression. Some patients require only one of these modalities, while other patients need combined therapies.
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  • Compressive Optic Neuropathy As in the treatment of acute congestive thyroid orbitopathy, radiation therapy is becoming increasingly popular. A retrospective series of 84 patients with compressive optic neuropathy treated with either corticosteroids or radiation therapy supports mounting evidence that radiation therapy may be safer and more effective than corticosteroids. Radiation therapy, however, must be administered in fractionated doses, which delays its beneficial effect. For this reason, if visual dysfunction progresses while the patient is on corticosteroids, surgical decompression is usually recommended if the patient is a surgical candidate.
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  • Orbital decompression Orbital decompression is indicated for compressive optic neuropathy when there has been failure of or contraindication for corticosteroids or radiation therapy or if corticosteroid dependence has developed with intolerable side effects. Other indications include excessive proptosis with exposure keratitis and corneal ulceration, pain relief, and cosmesis for disfiguring exophthalmos. Orbital decompression may also be indicated as a preliminary procedure to extraocular muscle surgery on a patient with sufficient proptosis to suggest that decompression might ultimately be required.
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  • Orbital decompression A variety of approaches may be used, each with its own advantages and associated complications. The transorbital (via fornix or eyelid) approach to inferior and medial wall decompression is the most common approach used by ophthalmologists. The addition of a lateral wall advancement has the advantage of both further increasing the orbital volume and simultaneously improving upper eyelid retraction; this is the technique we prefer.
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  • ORBITAL DECOMPRESSION Subciliary approach.Inferior & medial wall (6mm proptosis).Remove bone to posterior wall maxillary sinus (5mm more posterior on medial wall), Avoid IO neurovascular bundle, and the anterior and posterior ethmoidal arteries.Incise periosteum in A-P direction posteriorly and circumferentially anteriorly. Complications: visual loss, A pattern ET
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  • Motility Disorders A major source of morbidity in thyroid orbitopathy, and the most frequent problem associated with orbital decompression surgery, has been strabismus. In patients with relatively minimal degrees of ocular misalignment, diplopia can be avoided with a compensatory head posture, Fresnel plastic press-on prisms, or temporary occlusion. Unfortunately there is significant image degradation as larger prisms are used, limiting their efficacy. If there is marked asymmetry in ocular deviation in different fields of gaze, prisms are also less effective. In some cases during the inflammatory period, use of intramuscular botulinum tox


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