Severe Graves' Ophthalmopathy After Retrobulbar Anesthesia for Cataract Extraction in a Patient With Mild Stable Thyroid Eye Disease

Daniel Chun-Hang Wai, Su-Chin Ho, Lay-Leng Seah, Kee-Siew Fong, Daphne Hsu-Chin Khoo


Thyroid. 2003;13(8) 

In This Article

Patient History

S.K.H., a 66-year-old Chinese male, was seen at the Singapore National Eye Center (SNEC) in May 1996 with a history of decreased visual activity (VA) in the left eye of 2 months' duration. It was noticed that he had mild proptosis of 21 mm in the right eye and 22 mm in the left. VA was 20/30 on the right; it could not be tested on the left because of the presence of a dense cataract. Computed tomography (CT) orbit scan showed bilateral proptosis, slightly more pronounced on the left, with normal extraocular muscles (Fig. 1). In 1984, he had had a right cataract extraction and intraocular lens implantation under retrobulbar anesthesia. Two microliters of an anesthetic solution consisting of 40 mL of 2% lignocaine and wylase and 20 µg of adrenaline was injected behind the orbit through the space below the orbit. There were no complications.

Computed tomography (CT) scan performed 2 months prior to retrobulbar block and cataract surgery showing mild bilateral proptosis but normal extraocular muscle volume. This patient had had mild Graves' ophthalmopathy for 24 years.

Left cataract extraction and intraocular lens implantation took place in July 1996, also under retrobulbar anesthesia. An anesthetic solution consisting of 40 mL of 2% lignocaine and wylase and 20 µg of adrenaline was used. Two milliliters was injected behind the orbit through the space below the orbit. Postoperatively, vision in the left eye improved to 20/30. However, the patient complained of diplopia 3 weeks later, which worsened progressively. By 6 months, he had progressive proptosis of 22 mm and 24 mm in the right and left eyes, respectively, with lagophthalmos, 2 mm on the right and 4 mm on the left. There was severe chemosis with keratopathy. In the right eye there was complete ophthalmoplegia, and in the left severe limitation of eye movement especially on vertical gaze. VA was 20/30 in the right and 20/40 in the left eyes, respectively. Color vision tested with Ishihara charts was normal. A blood test showed subclinical thyrotoxicosis: total thyroxine (TT4), 138 nmol/L (59-155); thyrotropin (TSH), 0.003 U/L (0.32-5.00). CT scan (not shown) done at this point showed bilateral enlargement of the extraocular eye muscles consistent with thyroid eye disease but no compression of the optic nerves. Two months later the patient had developed elevated triiodothyronine (T3) levels: total triiodothyronin (TT3), 4.7 nmol/L (1.2-3.4), free thyroxine (FT4), 25.2 pmol/L; TSH, not detected (0.52-5.04). The antibodies were all positive thyrotropin receptor antibodies (TRAb) 45.2 U/L (0-10), thyroidstimulating immunoglobulins (TSI) greater than 4000% (0-179.0) thyroglobulin antibodies (TgAb) 52.3 U/mL (0-0.3), thyroid peroxidase antibodies (TPOAb) greater than 100U/mL (0-0.3). At this point, he recalled a history of thyrotoxicosis in 1972 that resolved after taking some Chinese medicine. Prednisolone, 45 mg, and carbimazole 30 mg/d were prescribed. After 4 weeks of therapy, T3 levels normalized but there was no improvement in the eyes.

Because of the development of exposure keratopathy, the patient had bilateral threewall orbital decompression in May 1997. He continued prednisolone postoperatively and an attempt was made to taper the steroids. Four weeks postoperatively, proptosis was reduced to 19 mm bilaterally and chemosis in the right eye had resolved. However, each time the steroid dose was decreased the VA worsened, so the patient continued on steroid treatment. In September a decision was made to send him for 131I; he received 14 mCi on September 1, 1997. The following day, the patient complained of sudden decrease in VA and found himself unable to read the newspaper. On testing, VA in both eyes had decreased to 20/200. Over the next week, color vision fell from 13/15 to 5/15 in the right eye and from 14/15 to 8/15 in the left and VA deteriorated further to 20/400. A repeat CT orbit showed bilateral moderate proptosis, and symmetrical enlargement of the bellies of all extraocular muscles with crowding of the oribtal apices (Fig. 2). Oral steroid dosage was increased to 120 mg/d with improvements seen in VA but not in muscle motility. At that time the patient was referred to a neurologist for exclusion of myasthenia gravis. An electromyogram was performed and results were normal. His TRAb level in October 1997 was normal at 7.5 U/L. Throughout this period attempts had been made to taper steroids but the patient required high doses to maintain his VA. In June 1997 he developed pulmonary tuberculosis followed thereafter by a chronic bleeding gastric ulcer in November 1997. The decision was then made to stop highdose steroids and to begin orbital radiotherapy. He received 20 Gy divided in 10 fractions over a 2-week period. By the fifth dose (1 week), he reported improvement in vision, and 3 weeks after beginning radiotherapy, improvements in motility were evident. Using Hirchberg's corneal reflux method, the vertical range of movements improved to 5-10 degrees and lateral movement to 5-15 degrees. On completion of therapy, the patient showed gradual but progressive improvement of vision as well as eye movements over the next 8 months. However, he still had diplopia on looking at all directions and was therefore given a Fresnel prism in July 1998 and subsequently underwent right inferior rectus recession in March 2000. Throughout this period the patient's thyroid function tests were monitored every 3 months. In October 1999, he was found to be hypothyroid and was started on levothyroxine (LT4) replacement therapy. When last reviewed in November 2001 the range of movement of the extraocular muscles had improved and the patient demonstrated binocular single vision in the primary position. He is currently euthyroid, taking LT4 125 µg every day. TSI levels tested annually have remained greater than 4000% (normal range, 0%-179%) over the last 5 years.

Computed tomography (CT) scan performed 5 months after decompression surgery and 3 weeks after radioiodine therapy showing increased volume of medial and lateral recti. Apical crowding was seen with clinical evidence of optic nerve compression.


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