Endocrine Abstracts

Case History: A 70-year-old man of Chinese origin presents with a two-month history of worsening visual acuity and double vision. He denied systemic symptoms apart from marginal weight loss. Other medical history includes stable asthma, treated with inhalers. He has a niece and nephew with thyroid disease. He is an ex-smoker, retired accountant, and drinks occasional alcohol. On examination, he was normotensive with a body mass index of 22 kg/m² however was found to have new-onset atrial fibrillation. There was no upper limb tremor nor thyroid goitre present. There was eyelid swelling, gaze-evoked orbital pain, constant bilateral vertical diplopia, limited elevation of both eyes, and restricted adduction particularly severe in the right eye. A follow-up review described right-sided esotropia and deteriorating visual acuity (6/12) compared to the left (6/6). There was no conjunctival redness or chemosis and pupil reactions were normal.

Investigations: Thyroid-stimulating hormone (TSH) was undetectable <0.02 mU/l (0.27- 4.2), free thyroxine 22.5 pmol/l (10.8- 25.5) and free triiodothyronine 6.3 pmol/l (3.1-6.8). TSH receptor antibodies were positive 4.6 IU/l. Magnetic resonance imaging described marked swelling and oedema with signal alteration of orbital rectal muscles affecting the inferior and medial recti and homogenous enhancement of all the orbital rectus muscles with inflammatory stranding of the intraconal fat. Intraocular pressures were raised in each eye: 32 and 28 mmHg (12-22). An ultrasound reported both lobes of the thyroid to be normal in size. A benign solitary right 4mm hyperechoic nodule was noted. The great vessels were normal. There was no lymphadenopathy.

Outcome: The patient was started on Carbimazole 5mg once a day, Selenium 100 mg twice a day, lubricating eye drops, and high dose steroid therapy. He received 5 doses of intravenous methylprednisolone 500mg and then was switched to oral prednisolone 70mg titrating down by 5mg weekly. He has been anticoagulated and initiated on bisphosphonate therapy.

Conclusion with points for discussion: This gentleman presents with severe active grave”s ophthalmopathy (GO) without overt thyrotoxicosis or a diffuse goitre. The raised intraocular pressures are likely due to congestion of the intraocular muscles. The unilateral severity of ocular signs prompted diagnostic confirmation with orbital imaging. It is possible his presentation with GO proceeded impending thyrotoxicosis. Early multidisciplinary team involvement was vital due to the high clinical activity score which has improved since steroid therapy. It was important to also address other complications including cardiovascular risks and reduced bone mineral density.