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Case Presentation 12/19 Presenting: clerk 陳豪宏 Instructor: 張丞賢老師 Patient Profile Name: 謝X莉 Age: 46 years old Gender: female Chart number: 24097375 Date of admission: 2011/12/12 Chief complaint Right eye pain for 1 week. Present Illness 1 This 46 years old female suffered from insidious right eye pain for 1 week. The accompanying symptoms are red eye, tearing (od). She had hyperthyroidism s/p subtotal thyroidectomy on 2011-8-18. Thyroid orbitopathy with compressive optic neuropathy was diagnosed this September. She was admitted to our hospital and received steroid pulse therapy on September 5th this year. Present Illness 2 After discharge on September 9th. She came for OPD follow-up on September 14th. Diplopia was still complained. OCT showed loss of nerve fibrous layer. She was admitted for operation on September 20th, during which orbital decompression (ou) of temporal sides and muscle recession of inferior rectus were done. On December 12th, she was admitted for steroid pulse therapy and orbital decompression of nasal sides. Present Illness Summary First Decompression Thyroidectomy (Temporal Sides) 08/18 09/19~09/23 First Steroid Therapy 09/05~09/09 Second decompression 12/12~ now(op:12/16) Past History 1. 2. 3. 4. 5. 6. 1. 2. 3. hyperthyroidism, s/p operation hypertension(+) asthma(+) heart disease(-) DM(-) depressive disorder under medical treatment Operation history: L-spine s/p operation 1.5 year ago hyperthyroidism s/p subtotal thyroidectomy on 2011-8-18 at 謝外科 Orbital Decompression on 09/20 Admission history: As listed in the Present Illness Personal History 1. 2. 3. 4. 5. 6. 7. Cigarette Smoking : +, 1/2 pack per day Alcohol : denied Occupation history : denied Contact history : denied Travel history : denied Family History: denied family systemic disease Allergy History: denied Nutritional and Mental status Nutritional Status: Weight: 81.6kg; Height: 151.5cm; BMI: 35.55 Mental Status: Consciousness: alert. Mentality: normal. Current Medicine 2011-9-13 PSY OPD Dr.葉怡君 EFEXOR速悅XR(Venlafaxine) 1#AM 1#HS */PC*28 Estazolam #(Eurodin)管四 #2 QD/HS* 28 Inderal 10mg (Propranolol) #1 BID/PC* 28 Xanax 0.25mg (Alprazolam)管四#1 BID/PC* 28 Zyprexa 5mg (Olanzapine)**** #1 QD/HS* 28 Physical Examination 1 Vital sign: BP: 131 / 105 mmHg, PR: 80 bpm, RR: 18 cpm, BT: 37 ℃ <Ophthalmic examination> 2011/12/12 OD OS Eyeball Conjunctiva Cornea AC Iris Pupil Light reflex Lens 25>-----------105------------<24 injection injection clear clear moderate, clear moderate-shallow, clear np np 4mm 4mm +/+ +/+ clear clear Physical Examination 2 Fundus C/D=0.4 EOM 20 | 35 ---|---45 | 30 C/D=0.7 disc: temporal pale 20 | 45---|---30 | 10 Tonopen: straight: R: 21,22 L: 22,23 Upward: R: 27,28 L: 27,29 Downward: R: 22 L:22 Vod: 0.1x 1/5 Vos: ND/10cm Orbital CT Hypertrophy of extraocular muscles (all of ou) Abnormal Lab finding 12/12: Hb: 12.0 MCV: 79.8 Hct: 35.3 Plt: 502k Diagnosis Thyroid orbitopathy with compressive optic neuropathy Plan: Pulse therapy of Solumedrol 500mg q12h IV Arrange Auto-P, VEP, OCT of disc. Orbital decompression under general anesthesia. Progress 12/13 S: eye pain(-) Red eye ↓ O: EOM: 20 40 45 20 35 10 35 (od) 10 (os) Cornea: clear Conjunctival congestion: ↓ Chemosis: ↓ AC: deep, clear A+P: arrange VEP, OCT of disk today. Prepare endoscopic decompression Progress 12/14 S: eye pain(-) O: EOM: 20 35 20 45 35 (od) 35 35 10 (os) Cornea: clear Conjunctiva: mild congested Chemosis: ↓ AC: deep, clear VEP: delayed potency and amplitude (ou) A+P: Keep pulse therapy day 2 Progress 12/15 S: Still blurred vision (ou) O: EOM: 20 35 45 20 40 35 35 (od) 20 (os) Cornea: clear Conjunctiva: Congestion ↓ ↓ Chemosis: (-) few SPK in the left lower eye IOP: 24.7 (os), 20.5 (od). A+P: Arrange endoscopic orbital decompression (ou) tomorrow Operation on 12/16 1. 2. 3. 4. 5. 6. Endoscopic orbital decompression done in this morning. (8.00 am) Procedures taken: Preparation for anesthesia Endoscope usage: Use periosteal elevator to destruct cribriform pyparacea temporally and posteriorly. Destruct the ethmoid bone. Rigid orbital soft tissue with fibrotic membran was noted. Incision of the fibrotic membrane and let the orbital fat protrude out from orbital medial wall. Hemostasis adequately. The operation was done successfully and the patient returned to the ward for recovery. Progress 12/16 S: no obvious pain of wound post-op. Still blurred vision O: Endoscopic wound of the surgery. Condition fine. A+P: Discussion A Brief Introduction of Thyroid Orbitopathy Thyroid Eye Disease Thyroid eye disease has many names: Thyroid-associated orbitopathy (TAO) Thyroid orbitopathy Grave's orbitopathy Among others All these terms mean the same thing: inflammation of the tissues around and behind the eye producing varying amounts of swelling and scarring. Introduction It is an autoimmune disease. There are at least various theories to explain its cause and development. Thyroid eye disease usually occurs in people with a history of thyroid problems. However, thyroid eye disease can occur decades before, or decades after, the development of thyroid gland disease. Pathogenesis The volume of 1. 2. GAG secretion by fibroblasts is increased by activated T-cell cytokines such as tumor necrosis factor (TNF) alpha and interferon gamma. The extraocular retroorbital connective and adipose tissue are increased, due to inflammation and the accumulation of hydrophilic glycosaminoglycans (GAG), principally hyaluronic acid, in these tissues. It implies that T-cell activation is an important part of this immunopathology. The accumulation of GAG causes a change in osmotic pressure, which in turn leads to a fluid accumulation and an increase in pressure within the orbit. These changes displace the eyeball forward and can also interfere with the function of the extraocular muscles and the venous drainage of the orbits. Pathogenesis (Summary) Autoimmune caused Inflammation T cell: TNF-a and interferon r Fibroblasts: GAG Osmotic pressure Fluid accumulation and IOP Eyeball forward Venous drainage malfunction EOM dysfunction ↑ ↑ ↑ ↑ Risk Factors 1. 2. 3. Treatment: Ra-I therapy may be more likely to lead to the development or worsening of TO than medication or subtotal thyroidectomy. Sex: TO: female > male According to studies, smoking definitely makes thyroid eye disease worse. 4. increase in the connective tissue volume of the orbit, but not the extraocular muscle volumes. Thyrotropin receptor autoantibodies Higher titer -> Higher prevalence and longer course of TO. Epidemiology Approximately 20 to 25 percent of patients with Graves' hyperthyroidism have clinically obvious TO. Along with the eye signs of thyroid hormone excess (lid retraction and stare), at the time of diagnosis of the hyperthyroidism. However, many more patients with Graves' hyperthyroidism have evidence of TO in imaging studies. Clinical Presentations proptosis and periorbital edema Clinical Presentations 2 1. 2. 3. 4. 5. 6. The patient may be distressed by the appearance of his or her eyes. Possible major symptoms: sense of irritation excessive tearing that is often made worse by exposure to cold air, wind, or bright lights eye or retroorbital discomfort or pain blurred vision Diplopia and occasionally loss of vision. Proptosis The degree of proptosis (exophthalmos) is dependent on the depth of the orbit and the degree of enlargement of the retroocular muscles and retroorbital fibrous and fatty tissue. The proptosis may be usually symmetric, but is often asymmetric, and may be accompanied by a sensation of pressure behind the eyeballs. The proptosis may be masked by periorbital edema, which is a common accompaniment. Apparent proptosis Many patients with hyperthyroidism have lid retraction secondary to thyroid hormone excess. It leads to stare and lid lag, resulting from contraction of the levator palpebrae muscles of the eyelids. The stare may give the appearance of proptosis, when none in fact exists ("apparent proptosis"). These signs alone do not indicate the presence of ophthalmopathy, and subside when the hyperthyroidism is treated. Physical Examinations 1 Inspection of the conjunctivae and periorbital tissue, looking for chemosis and periorbital edema. Determination of the extent to which the upper and lower lids can be closed. Because failure of apposition promotes drying and ulceration of the cornea. Assessment of EOM. inability to achieve or maintain convergence. Limitation of upward gaze. It leads to a characteristic head-back position in order to see ahead. double vision. Physical Examinations 2 exophthalmometer. measurement of the distance between the lateral angle of the bony orbit and an imaginary line tangent to the most anterior part of the cornea. The upper limit of normal is 20~22 mm. as high as 30 mm in patients with severe proptosis. Visual acuity and color vision should be assessed by simple reading tests and color charts, and visual fields should be evaluated by confrontation. Assessment of Severity NO SPECS by American Thyroid Association Class 0 — No symptoms or signs Class I — Only signs, no symptoms (eg, lid retraction, stare, lid lag) Class II — Soft tissue involvement Class III — Proptosis Class IV — Extraocular muscle involvement Class V — Corneal involvement Class VI — Sight loss (optic nerve involvement) Differential Diagnosis 1. 2. 3. 4. 5. 6. 7. eye signs of thyroid hormone excess Bilateral eye signs simulating TO: severe obesity Cushing's syndrome orbital myositis histiocytosis myasthenia gravis very rarely: orbital tumors statin-induced EOM myopathy. Differential Diagnosis 2 For possible unilateral TO, space-occupying lesions of the orbit must be ruled out first. When necessary, the diagnosis can be confirmed by ultrasonography and CT. It is important not to inject iodinated contrast material in patients with Graves' disease especially if radioiodine therapy is contemplated. If diagnos is not in doubt, only tests necessary are: serum TSH Free T4 TSHR antibodies. Treatment 1. 2. 3. treat according to the severity. Most patients have mild disease and do not have progression during follow-up. The treatment of TO includes reversal of hyperthyroidism relief of symptoms reduction of inflammation in the periorbital tissues. Effects of anti-hyperthyroidism therapies Subtotal thyroidectomy and antithyroid drugs do not appear to have a negative influence on the course of orbitopathy. However, there is increasing evidence that radioiodine therapy can cause the development or worsening of Graves' orbitopathy more often than antithyroid drug therapy or surgery. Symptomatic treatment Eye shades Artificial tears (saline eye drops) Raising the head of the bed when sleep. Photophobia and sensitivity to wind or cold air can be relieved by use of dark glasses. Glucocorticoids (oral or IV), are the primary treatment for severe Grave‘s orbitopathy. Radiation and surgical decompression can also be used in selected patients. Therapies for severe TO Oral Prednisone: Intravenous glucocorticoid pulse therapy: effective treatment for TO. More side effects. It has been seen to induce liver failure. Fewer side effects and better clinical outcome in Radiotherapy: benefits controversial Orbital decompression surgery 1. 2. Three major indications: If glucocorticoid therapy or orbital irradiation fails to halt progression of TO If loss of vision is threatened either by 1. 2. 3. ulceration or infection of the cornea changes in the retina or optic nerve For cosmetic correction of severe proptosis surgery should be avoided for as long as possible until the disease stabilizes under corticosteroid suppression Orbital decompression surgery The orbit may be decompressed by removing the lateral wall, the roof, or the medial wall and the floor. Uptodate suggests the last procedure, also known as transantral decompression. the surgeon removes the floor and medial wall of the orbit to allow decompression. It does not leave a scar on the face, and avoids craniotomy. Result of decompression surgery An excellent result can usually be achieved, with substantial reduction in proptosis and edema. However, diplopia usually does not improve and may worsen, so that eye muscle surgery is almost always needed later. Timing of Surgery: Clinical outcome appears to be better if decompression surgery is performed after rather than before glucocorticoid therapy. Other operations 1. Fat decompression surgery: 2. 3. Removal of the retroorbital adipose tissue Bilateral lateral tarsorrhaphy may be performed to minimize or prevent corneal damage. Surgical recession of Muller's muscle and the levator will correct upper lid retraction. However, decompression surgery is preferable for both of these problems because it is more effective both functionally and cosmetically. Reference Uptodate articles: 1. 2. Pathogenesis and clinical features of Graves' ophthalmopathy (orbitopathy) Treatment of Graves' orbitopathy (ophthalmopathy) The End Thank you.