A 62-year-old man presented with a painless decrease in visual acuity (VA) in the left eye (LA) of 2 days' duration. He had been seen 2 months previously for red eye, diagnosed with conjunctivitis, and treated with a fixed combination of dexamethasone and tobramycin. At that time VA was 1 and IOP 14mmHg in both eyes. Personal history was diabetes mellitus, hypertension, obesity, hepatic steatosis, hyperthyroidism, ischaemic heart disease and renal transplantation for chronic renal failure secondary to chronic pyelonephritis. His systemic medical treatment included prednisone 5mg/24h (Prednisone Alonga®, Sanofi Aventis), tacrolimus (Prograf®, MSD) and mycophenolate mofetil (Cellcept®, Roche).
Initial examination was VA of 1 in the right eye (RA) and 0.1 in the LA, normal biomicroscopy in the RA, in the LA there was intense conjunctival injection and central predominantly tarnished cornea with mild oedema and negative fluorescein staining, without Tyndall, synechiae, keratic precipitates or secretion. IOP was 18mmHg in OD and 46mmHg in OI. The fundus was difficult to visualise due to corneal oedema, but the papilla and macula were normal, with an applied retina and no peripheral lesions. On gonioscopy the angle was open, with no synechiae or neovessels. During the examination, the patient's somnolence and some respiratory difficulty were striking. He was also short, moderately obese and had a short neck.
The initial diagnosis was ocular hypertension in OI, and treatment was started with the fixed combination of brimonidine 0.2% and timolol maleate 0.5% (Combigan®, Allergan). He was referred to the glaucoma clinic and the pulmonology department, which subsequently diagnosed severe apnoea-hypopnoea syndrome.
One week later, VA was still 0.1 and conjunctival hyperemia, mild corneal oedema, mild superficial punctate keratitis, with IOP of 40mmHg persisted. Pachymetry was 512µm in OD and 574µm in OI (increase justified by corneal oedema). A differential diagnosis with a carotid-cavernous fistula or an orbital apex syndrome was suggested, and a computerised axial tomography (CAT) scan was requested. Treatment was changed to brinzolamide (Azopt®, Alcon Cusi), tafluprost (Saflutan®, MSD) and diclofenac sodium (Diclofenac-lepori®, Angelini Farmaceutica). Two days later, IOP was still at 30mmHg, so acetazolamide (Edemox®, Chiesi-Spain) and prednisone 60 mg (Prednisone Alonga®, Sanofi Aventis) were added orally.

Hyperemia progressively decreased, and corticosteroids were gradually reduced, but IOP remained above 26mmHg. CT ruled out any orbital and/or cranial disease. At 5 weeks, a peripheral ulcer of pseudodendritic appearance with positive fluorescein staining and infiltration of the edges appeared; corneal scraping was performed for culture and detection of C-reactive protein of herpes virus and treatment was started with topical (Zovirax®, Glaxo Smith Kline) and oral (Virex®, Biogen) acyclovir. Microbiological analysis confirmed positivity for HVS. With this treatment, the corneal lesion healed leaving a small peripheral leukoma, IOP normalised and visual acuity reached 0.8.