Expulsive suprachoroidal haemorrhage is a rare event, usually complicating intraocular surgery, with often devastating results. There are few reports of spontaneous expulsive haemorrhage in the literature. We present a case of spontaneous expulsive choroidal haemorrhage and highlight potential aetiololgies.

Case report

A 74-year-old lady presented as an emergency with a history of severe pain of sudden onset and bleeding from her left eye while sitting at home. She described enough blood to fill two large tissues trickling onto her cheek. Her medical history included systemic hypertension, chronic renal failure, gout, and hypothyroidism.

On examination, she had no light perception in the affected eye and 6/6 in the fellow eye. There was extensive prolapse of tissue through a large corneal defect onto the left cheek with blood-clot admixed (Figure 1). The right eye was normal apart from a shallow anterior chamber and a peripheral surgical iridectomy.

Figure 1
figure 1

Acutely prolapsed oveal contents from left eye.

Twenty years earlier, she had a broad surgical iridectomy after admission for left acute-angle closure glaucoma, plus contralateral prophylactic peripheral iridectomy. The patient was lost to follow-up for 17 years, when she re-presented with failing painless vision in her left eye over several weeks. On this occasion she had perception of light only, corneal oedema, a shallow anterior chamber, a large cataractous lens, a raised intraocular pressure (IOP) of 44 mmHg, a closed drainage angle, a left afferent papillary defect, and a grossly cupped optic disc. Her other eye saw 6/6 with a pressure of 13 mmHg and a healthy optic disc. After intense medical treatment failed to control her IOP, ocular comfort was maintained with a drop regime of dexamethasone 0.1% b.d. and timolol 0.25% b.d. Unfortunately she was again lost to follow-up shortly with persistently raised IOP but a comfortable eye and a clear cornea, until her spontaneous expulsive choroidal haemorrhage.

An evisceration with a 16 mm acrylic ball implant was performed. Histology confirmed the extent of corneal perforation with stromal infiltration by neutrophils but no identifiable organisms. The iris was degenerate with necrotic uveal tissue and blood clot. There was no evidence of malignancy or vasculopathy.


There are few reports of spontaneous corneal perforation with expulsive haemorrhage in the literature.1 Our patient had multiple predisposing factors for this dramatic event, including advancing age, arteriosclerosis, systemic hypertension, persistently raised IOP, and chronic use of topical steroid. De Laage2 reported a case of giant corneal perforation secondary to chronic misuse of local steroid to the eyelids. We feel that this was the most likely trigger factor in our patient, resulting in a sudden reduction in the IOP and massive suprachoroidal haemorrhage in the presence of multiple other predisposing factors. Although the cornea was noted to be clear at her last assessment, 2 years elapsed before she presented with spontaneous expulsive suprachoroidal haemorrhage, and bullous keratopathy may have ensued in that time in an eye known to have a chronically raised IOP. It is unlikely, however, that bacterial keratitis would have complicated pre-existing bullous keratopathy as non identifiable organisms were noted on histological examination. Of note, there was no evidence of keratopathy in the fellow eye that could predispose to perforation,3 and a vasculitis screen was unremarkable. It is possible that the corneal perforation followed the suprachoroidal haemorrhage and further rise in IOP, but less likely.

This case highlights the potential risks of long-term topical steroid use, especially in the context of prior eye disease, which may have compromised the integrity of the cornea.