Sir,

Common features of active thyroid orbitopathy include eyelid and conjunctival oedema and redness, eyelid retraction, proptosis, and strabismus. Optic neuropathy may occur in 5% of cases.1 We report on a patient who developed optic neuropathy together with blepharoptosis. Both features resolved following orbital decompression in the active stage.

Case report

A 59-year-old man was referred with a history of sudden onset of blepharoptosis of the right upper eyelid, mild retraction of the left upper eyelid, and bilateral ocular redness with eyelid oedema since 8 months (Figure 1a and b). The levator function of the right eye was 3 mm and there was complete blepharoptosis. Elevation was bilaterally restricted, with duction values of 25 degrees. Fundoscopy showed tortuosity of the veins and papillary oedema in the right eye. The visual acuity was 6/9 OD and 6/6 OS, respectively. Exophthalmometry readings were 19 mm bilaterally.

Figure 1
figure 1

(a) Right eye blepharoptosis before orbital decompression. Preoperative levator function was 3 and 14 mm of the right and left upper eyelids, respectively. (b) Left eye upper eyelid retraction and congestive Graves’ orbitopathy before orbital decompression. (c) Resolution of the right eye blepharoptosis after orbital decompression. Note the bilateral upper eyelid retraction, masked by upper lid dermatochalasis. Postoperative levator function was 13 and 14 mm of the right and left upper eyelid, respectively.

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Laboratory investigations revealed autoimmune hyperthyroidism. Orbital CT scan examination showed bilateral thickening of rectus muscles (Figure 2a). We ruled out myasthenia gravis and intracranial lesions. Despite treatment with oral and intravenous steroids his orbitopathy progressed. Consequently, he underwent bilateral transconjunctival inferomedial orbital decompression. Postoperatively, the blepharoptosis and signs of bilateral optic nerve compression resolved over a period of 5 months (Figure 2b). Subsequently, bilateral upper eyelid retraction was noted (Figure 1c).

Figure 2
figure 2

(a) Bilateral proptosis with enlarged extraocular muscles prior to orbital decompression. Apical compression of the optic nerve (axial CT scan). Preoperative exophthalmometry values were 19-19-93. (b) Bilateral herniation of the orbital tissues into the ethmoid sinus after transconjunctival inferomedial orbital decompression (axial CT scan). Postoperative exophthalmometry values were 16-16-90.

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Comment

We hypothesize that the blepharoptosis was caused by a first degree injury due to compression and ischaemia of the branch of the oculomotor nerve supplying the Levator in the orbit. In first-degree oculomotor nerve injuries, which frequently result from microvascular obstruction, the continuity of the axons is maintained.2 Hence, full function returns once the flow is restored. The aetiology of the oculomotor nerve compression could be similar to that of optic nerve compression induced by apical crowding in a particularly tight orbit.3, 4 Hence, blepharoptosis in a patient with thyroid orbitopathy may indicate apical compression.