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REAL THYROID OPHTHALMOPATHY.pptx
- 1. Thyroid Ophthalmopathy Bipin Koirala Master’sof Optometry & Vision Science Himalaya Eye Institute
- 2.
- 3. Definition Thyroid eye disease(TED) is an autoimmune disease caused by the activation of orbital fibroblasts by autoantibodies directed against thyroid receptors. TED is a rare disease, which had an incidence rate of approximately 19 in 100,000 people per year .
- 4. Introduction These changes havealso been called as : Endocrine Exophthalmos Malignant Exophthalmos Dysthyroid Ophthalmopathy Ocular Graves’ Disease (OGD) Thyroid Eye Disease (TED)
- 5. Introduction Incidence of ThyroidEye Disease depending on thyroid disorder Hyperthyroidism-90% Primary hypothyroidism-1% Hashimoto thyroiditis-3% Euthyroid -6%
- 6. Thyroid gland Location: Anteriorneck beneath the larynx Endocrine gland and highly vascular and supplied by autonomic nervous system. Has over a million follicles that secrete thyroglobulin, a precursor of the thyroid hormones, On activation the thyroglobulin is re-absorbed, converted into the thyroid hormones triiodothyronine (T3) and thyroxine (T4),
- 7. Thyroid Negative feed back mechanism Theproduction of thyroid hormones is regulated by both the hypothalamus and the pituitary gland.
- 8. Hyper Thyroid Hyperthyroidism isa condition that results from an over- secretion of thyroid hormones. It is usually caused by an autoimmune disease known as Graves’ disease, Common causes : Thyroiditis Toxic adenomas, Toxic nodular/ multinodular goiters Thyroxine overdoses Excess iodine dietary intake.
- 9. Hypo Thyroid Hypothyroidism isdue to an underactive thyroid gland and results in a deficiency of thyroid hormones. Thyroid hormones are essential for normal development between birth and puberty and a deficiency causes irreversible mental retardation. Hypothyroidism can be caused by Hashimoto’s thyroidism,
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- 12. Pathophysiology TED being anautoimmune disease with orbital fibroblast as the primary target inflammatory attack and the EOM are secondarily involved Also the target antigen is shared b/w thyroid follicular cells and orbital fibroblast The activated T cells acts on fibroblast – adipocyte lineage with in orbit and will stimulate adipogenesis, fibroblast proliferation and GAG synthesis as a result of which EOM are enlarged due to infiltration and odema
- 13. Pathophysiology There is anincrease in the volume of the orbital contents, particularly the muscles, which can swell to eight times their normal size. There may be a secondary elevation of intraorbital pressure, and the optic nerve may be compressed. Later muscle fibres eventually leads to fibrosis, which exerts a tethering effect on the involved muscle, resulting in restrictive myopathy and diplopia
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- 15. Common Risk Factors Female(4-6 times) and middle aged Smoking (no of cigarettes per day) H/O auto immune thyroid disorder HLA-DR3 and HLA-B8 positive Genetic predispsition Life style
- 16. Symptoms : Ocular Dryeyes Ocular redness and irritation Reduced vision Bulged eye Diplopia Eyelid odema Pain and pressure around eye Field loss Dyschromatopsia
- 17. Clinical features (lidsigns) 1. Upper lid retraction (Dalrymple’s Sign) Seen in 90% cases Gives frightened and staring looks
- 18. Clinical features (lidsigns) G 2. Lid lag ( Von Graefe’s sign) Seen in 50 % cases Upper lid lags behind during down gaze.
- 19. Clinical features (lidsigns) 3. Fullness of lid (Enroth’s Sign) Puffy odematous swelling
- 20. Clinical features (lidsigns) 4. Difficulty in Lid Eversion (Gifford’s Sign) Due to odematous lid swelling
- 21. Clinical features (lidsigns) 4. Infrequent / Incomplete blinking (Stellwag’s Sign) 5. Presence of Glabellar furrow’s
- 22. Clinical Features (LidSigns) 1. Rosenbach's Sign: Fine tremors of the eyelids when closed. 2. Boston’s Sign: Jerky irregular movement of upper lid on downward gaze. 3. Kocher’s Sign: Increased lid retraction with visual fixation 4. Abadie Sign: Spasm of the levator palpebrae superioris muscle with retraction of the upper lid. 5. Riesman's sign: Bruit heard over the closed eye with a stethoscope.
- 23. Clinical features (Conjunctiva) Chemosisand Deep Injection of Conjunctiva (Goldzeiher’s Sign)
- 24. Clinical features (Pupil) Inequality of dilation of pupil Other Pupillary Signs: 1. Cowen’s Sign: Jerky pupillary constriction to light. 2. Lowy’s Sign: Mydriasis with instillation of lower concentration of adrenaline. 3. Knies’s sign: Unequal dilatation of pupil in dim light.
- 25. Clinical features (EOM) 1.Möbius Sign: Inability to converge. 2. Ballet Sign: Restriction of one or more extraocular muscles. (40 %) 3. Jendrassik's Sign: Limitation of abduction and rotation of eyeballs. 4. Suker’s Sign: Poor fixation on abduction.
- 26. Clinical features (EOM) Question1: What is the most commonly and initially affected EOM?? Answer: Inferior Rectus (Elevation defect is seen) Medial Rectus ( Defective abduction) @ IMSL
- 27. Clinical features (Facial) 1.Joffroy Sign: Absent creases in the forehead on superior gaze. 2. Jellinek's Sign: Hyperpigmentation of the superior eye folds. 3. Hertoge’s Sign: Loss of the lateral third of eyebrows 4. Sainton’s sign: Delayed forehead wrinkling on up gaze.
- 28. Which sign isshown in clinical photo? Answer: Joffroy Sign
- 29. Exophthalmos Common Sign Seen in60 % cases Bilateral (can be unequal) Self limiting Decreased orbital retropulsion
- 30. Exophthalmos Common Sign Seen in60 % cases Bilateral (can be unequal) Self limiting Decreased orbital retropulsion
- 31. Exposure Keratopathy andDiscomfort Gritty sensation/ lacrimation Photophobia Corneal exposure a/w Lagopthamos, Proptosis, Reduced blink
- 32. Optic Neuropathy Seen in60 % cases Mainly caused due to compression of Optic nerve by enlarged EOM orbital contents esp at Orbital apex A/w vision loss, RAPD, Defective color vision, slow progressing optic atrophy
- 33. Rare Associations Strabismus dueto muscle fibrosis Glaucoma Raised IOP in up gaze Increased Episcleral Venous pressure Increased Mucopolysaccharide deposit with in Aq. Outflow system
- 34. Differential Diagnosis Orbital orPreseptal cellulitis Carotid-cavernous fistula Idiopathic orbital inflammation (Pseudotumour) TED must be ruled out in all cases of B/L proptosis
- 35. Disease Course andPhases The pattern of the disease follow the Rundle’s curve which describe the plot of orbital disease severity against time 1.Initial phase- inflammatory phase duration may last from 6 – 18 months with orbital and periorbital signs i.e. proptosis and retraction. 2.Static phase- decrease in the inflammatory phase and minimal improvement. 3.Quiescent phase- gradual improvement with improved motility and retraction of the muscles
- 36. Disease Course (Rundle’sCurve)
- 37. Classification (NOSPECS) byATA ATA has classified Graves’ ophthalmopathy, irrespective of the hormonal status into following classes
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- 40. Investigations Laboratory test Thyroid hormonelevels (T3, T4, TSH) Anti thyroid antibodies.
- 41. Investigations (IMAGING) USG (BSCAN) To visualize the orbital structures and determining recti muscle enlargement. low cost, lack of ionizing radiation and relatively short examination time CT/MRI Detects proptosis, muscle thickness, thickening of optic nerve and anterior prolapse of the orbital septum (due to excessive orbital fat and/or muscle swelling), erosion of wall of orbit,
- 42. Investigations (IMAGING) USG (BSCAN) CT/MRI
- 43. What is CocaCola bottle sign??
- 44. Investigations (positional Tonometry) Tonometryin primary gaze and upgaze is performed An increase in intra-ocular pressure in upgaze helps in diagnosis of subclinical cases.
- 45. Basic Investigations 1. Correctedvisual acuity and Refraction 2. Color vision testing 3. Examination for an afferent pupillary defect 4. Extraocular muscle motility examination 5. Measurement of the lid fissure height in primary gaze
- 46. Basic Investigations 1. Measurementof upper and lower scleral show, 2. Exophthalmometry to detect proptosis 3. Slit-lamp biomicroscopy to assess the tear film and fluorescein pattern 4. Fundus examination to detect optic disc swelling or pallor.
- 47. Treatment Treatment can beclassified into that of 1. Mild disease (most patients), 2. Moderate to severe active disease, 3. Post inflammatory complications. 4. The first measure taken in all cases should be the cessation of smoking. 5. Thyroid dysfunction should also be managed adequately
- 48. Treatment (Mild disease) 1.Topical artificial tear drops in the day time and ointment at bed time are useful for relief of ocular surface drying 2. Head elevation with three pillows during sleep to reduce periorbital oedema. 3. Eyelid taping during sleep may alleviate mild exposure keratopathy. 4. Oral NSAIDs may be used for periocular pain.
- 49. Treatment (Optometry pointof view) 1. For diplopia, Fresnel prisms or occlusion therapy may be considered. 2. Prism for restricted ocular motility 3. Base in prism for reduced convergence 4. Others are lifestyle modifications e.g. sodium restriction to reduce water retention and tissue edema
- 50. Treatment (Moderate toSevere disease) 1. Guanethidine 5% eyedrops may decrease the lid retraction caused by overaction of Muller’s muscle. 2. Systemic steroids may be indicated in acutely inflamed orbit with rapidly progressive chemosis and proptosis with or without optic neuropathy 3. Radiotherapy (2000 rads given over 10 days period). It may help in reducing orbital oedema in patients where steroids are contraindicated
- 51. Treatment (Moderate toSevere disease) 5. Lateral tarsorrhaphy Performed in patients with exposure keratopathy (with mild to moderate proptosis) not responding to topical artificial tears 6. Extraocular muscle surgery. It should be carried out for left-out diplopia in primary gaze, after the congestive phase of disease is over and the angle of deviation is constant for the last 6 months.
- 52. Treatment (Post complications) 7.Orbital wall decompression It involves the orbital floor, medial wall, and lateral wall. In rare cases the roof of the orbit may also be decompressed surgically.
- 53. PATIENT’S DETAIL • Name:SHANTI SHARMA • Age: 33 years Sex: Female • Occupation: House wife • Mode Of Presentation : Regular eye checkup 56
- 54. HISTORY CHIEF COMPLAINT(S): • Grittiness,watering and burning Sensation • Symoptomatic during windy days 57
- 55. HISTORY OF PRESENTILLNESS • No h/o of eyeball pain • No h/o of photophobia • No h/o of diplopia or polyopia and shadowing of objects (ghost image) • No h/o of itching of eye(s) 58
- 56. PAST- OCULAR HISTORY •H/O using glasses since 1 year with Rx OD: -0.50 Dsph with 6/6̊ OS: - 0.50 Dsph with 6/6̊ • No other h/o of past ocular diseases and surgery • Using tear substitute for past 1 yr 59
- 57. PAST- SYSTEMIC HISTORY •No h/o of Diabetes Mellitus / Hypertension • H/0 hypothyroidism + • No h/o of surgical intervention for any disease • No h/o of any other systemic illness in past • h/o of use of systemic medication for hypothyroidism for 6 months • Tab. Thyronorm 25 mcg - OD 60
- 58. PERSONAL HISTORY • Nonvegetarian by diet • Does not consume alcohol and smoke • House wife by proffesion 61
- 59. FAMILY HISTORY • Noany systemic and ocular diseases in other family members • No family members being syndromic or with inherited abnormalities 60 65 33 25 62
- 60. General Physical Examination •Average built, well nourished • Weight – 54kg Height – 1.5m BMI - (21.10kg/m2) Vitals • Blood Pressure = 120/80 mmHg (Left arm, sitting position) • Pulse = 82 beats per min, regular. • Respiration rate= 18/min, regular • Temperature: 98.6⁰F General Examination • No pallor, icterus, clubbing, cyanosis, lymphadenopathy or edema. 63
- 61. OCULAR EXAMINATION On theday of presentation: RE VISUAL ACUITY LE 6/9 p UNAIDED 6/9 p 6/6 AIDED 6/6 6/6 PH 6/6 64
- 62. OCULAR EXAMINATION Normal HeadPosture Normal Normal Forehead & Eyebrows Normal EOM + + + + + + + + + + + + 65
- 63. OCULAR EXAMINATION Puffy L.lids/Normal Clear/Poor tear film Eyelids / Lashes Cornea/Tear flim Puffy L. lids/ Normal Clear/ Poor tear film RIGHT EYE LEFT EYE 66
- 64.
- 65. Normal (No congestion, chemosis, papillary reactionor follicles) Conjunctiva Normal (No congestion, chemosis, papillary reaction or follicles) Normal Episclera & Sclera Normal RIGHT EYE LEFT EYE 68
- 66. Normal in colorand pattern Round/Regular/Reactive (~3.0mm) (Direct & consensual) Iris Pupil Normal in color and pattern Round/Regular/Reactive (~3.0mm) (Direct & consensual) RIGHT EYE LEFT EYE 69
- 67. Normal Depth Quiet ANTERIOR CHAMBER Normal Depth Quiet ClearLens Clear Clear Vitreous Clear RIGHT EYE LEFT EYE 70
- 68. Round, Pink with sharpmargin Optic Disc Round, Pink with sharp margin 0.2:1 Cup: Disc Ratio 0.2:1 Healthy with GFR Macula Healthy A:V=2:3 Vessels A:V=2:3 RIGHT EYE LEFT EYE 71
- 69. EXAMINATIONS 10mm wet in5 minutes Schirmer tear test I 10mm wet in 5 minutes 5 sec spot noted Invasive TBUT 5 sec spot noted Normal (> 2/3 rd cornea hidden) Bells phenomenon Normal (> 2/3 rd cornea hidden) 18 Hertels (97) 18 No lid lag/ no lagophthalmos Lid lag/ lagopthalmos No lid lag/ no lagophthalmos RIGHT EYE LEFT EYE
- 71. TFT EXAMINATIONS 4.6 pmol/LT3 4.8 pmol/L 17.4 pmol/L T4 17 pmol/L 8 mU/L TSH 4.0 mU/L BEFORE (6 MONTHS AGO) AFTER (PRESENT)
- 72. Provisional Diagnosis • Nothyroid ophthalmopathy at present • Dry eyes Treatment/ Suggestions • Gtt. Optive – OU- 1dp – 4hrly- 4 weeks • FOLLOW UP 6 months with TFT monitor
- 73. References • Kanski’s clinicalophthalmology • AK khurana ophthalmology • Eye wiki AAO article • Any queries???
Editor's Notes
- #19 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #20 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #21 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #22 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #23 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #24 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #25 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #26 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #27 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #28 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #29 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #30 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #31 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #32 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #33 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #34 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #35 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #36 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #37 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.
- #38 The most common cause of unilateral or bilateral upper eyelid retraction is Graves’ ophthalmopathy, or thyroid eye disease. Early in Graves’ disease, eyelid malposition may result from increased sympathetic activity. With time, the levator palpebrae superioris and Müller’s muscle become hypertrophic, fibrotic, and adherent to orbital tissues. Patients with thyroid eye disease often have associated globe proptosis and lid lag along with eyelid retraction. Lower lid retraction is usually not seen in patients with Graves’ ophthalmopathy without concomitant retraction of the upper lids. Upper eyelid retraction in thyroid eye disease often has temporal flare, when retraction is more pronounced at the lateral aspect of the eyelid.