A case of ‘double hypopyon’ secondary to Pseudomonas aeruginosa keratitis in a patient with longstanding rubeotic glaucoma

Abstract

Editor, A 74-year-old man presented to eye casualty with a 2-day history of pain and redness in his left eye with associated mucopurulent discharge. He had a long history of problems in the left eye. The eye had no perception of light as a result of rubeotic glaucoma secondary to primary open-angle glaucoma and subsequent ischaemic hemi-retinal vein occlusion. He had longstanding bullous keratopathy of the left cornea due to chronic endothelial cell decompensation and raised intraocular pressure (IOP), but, until this episode, the eye had been comfortable on a regimen of prednisolone 1% drops four times daily and atropine 1% twice daily. The right eye was pseudophakic, with a posterior chamber intraocular lens and functioning trabeculectomy. The best corrected visual acuities were 6/9 Snellen in the right eye and no light perception in the left eye. The right eye was quiet with controlled IOP. The left eye had marked perilimbal injection with generalized corneal epithelial and stromal oedema. There was a central, roughly circular, shallow corneal ulcer with an approximate average diameter of 4.0 mm. There were inflammatory infiltrates at the periphery of the ulcer with no satel- lite lesions, and superficial stromal infiltrates in the ulcer base. Corneal sensation was absent. There was a hypopyon of 1 mm height and marked rubeosis iridis with extensive posterior synechiae and a dense cataract. Intraocular pressure in the left eye was 50 mmHg when measured with the Tonopen XLTM. Corneal scrapings were sent to microbiology for gram staining, culture and antibiotic sensitivity and the subject was treated empirically with a subconjunctival injection of 75 mg cefuroxime and 0.3 ml mydricaine no. 2 (Moorfields Eye Hospital Pharmacy, London, UK), equivalent to 3.6 mg procaine hydrochloride, 0.6 mg atropine sulphate, and 130 µg adrenaline acid tartrate in a vehicle of water for injection, sodium chloride 0.1% and sodium metabisulphate 0.1%. He was commenced on hourly topical ciprofloxacin 0.3% drops between 06.00 hours and 12.00 hours, atropine 1% drops twice daily, latanoprost 0.005% drops once daily and chloramphenicol 1% ointment at night, all to the left eye only. Topical steroid drops were discontinued. Topical beta-blockers and alpha-agonists were contraindicated due to coexisting respiratory and cardiovascular disease. Forty-eight hours later, the clinical picture had worsened and the eye had the unusual appearance of a ‘double hypopyon’, with pus levels visible in both the anterior chamber and within a cavitating corneal abscess that had developed in the mid to deep stromal layers (Fig. 1). Microbiology results were now available. Gram staining showed no polymorphs or organisms, but culture produced a light growth of Pseudomonas aeruginosa sensitive to ciprofloxacin, but resistant to cefuroxime and chloramphenicol. Two days after presentation, the eye had the unusual appearance of a double hypopyon, with pus levels visible in both the anterior chamber and within a cavitating corneal abscess that had developed in the mid to deep stromal layers. In view of longstanding blindness of the left eye, and ongoing pain, the eye was eviscerated, and the patient has progressed satisfactorily since surgery. Corneal bullae (Musch et al. 1983; Luchs et al. 1997) and topical corticosteroid therapy (Musch et al. 1983; Murray 1991) are known risk factors for the development of bacterial keratitis; however, the authors can find no previously reported cases of double hypopyon. We hypothesize that, in this patient, bacterial keratitis occurred following the rupture of a corneal bulla in an anaesthetic cornea and was compounded by the longterm use of topical prednisolone 1%. High IOP may have contributed to formation of both the bullae and the corneal abscess by further decreasing the corneal endothelial cell pumping function, leading to increased thickening of the cornea, thereby prohibiting access of the bacteria into the anterior chamber, causing a focus of infection to occur in the mid to deep stromal layers. Consequently, deeper stromal infiltration occurred with the formation of an abscess cavity within the corneal stroma. Pus settling within this cavity caused a second pus level and the appearance of a double hypopyon. Whilst it would have been desirable to avoid the use of a topical prostaglandin analogue in this setting, topical beta-blockers and alpha-agonists were contraindicated. Topical carbonic anhydrase inhibitors would have been an alternative choice of treatment; however, systemic carbonic anhydrase inhibitors were avoided due to the patient's frail state, and the low likelihood of effectiveness due to the longstanding nature of the corneal endothelial decompensation. Anterior chamber tap might also have been considered, but would have been likely to have provided only brief pressure lowering effects and would have presented an endophthalmitis risk. As this was a non-seeing eye, it seems likely that enucleation was unavoidable in this difficult situation.