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Editor,—Spontaneous intracorneal haemorrhage leading to corneal discoloration is an uncommon occurrence. The few such reported cases of spontaneous intracorneal haemorrhage have been due to contact lens related deep stromal neovascularisation, erosion of a vessel due to corneal ulceration, and rupture of reopened ghost vessels in a patient with interstitial keratitis and systemic hypertension. Corneal blood staining clinically represents a reddish-brown, or greenish-yellow discoloration of the cornea resulting from blunt trauma and subsequent hyphaema with raised intraocular pressures or less commonly by intrastromal haemorrhage in the presence of corneal vascularisation.1 The term “corneal blood staining” has been used to refer only to the latter in this case report—a case of spontaneous intracorneal haemorrhage related to acne rosacea associated corneal vascularisation.
A 72 year old man was seen at the eye casualty unit with a 3 week history of reduced vision and ocular discomfort in his left eye. There was no history of trauma.
His ocular history included chronic posterior blepharitis and peripheral corneal ulcers (upper cornea) in the left eye related to acne rosacea. This patient had also had an uneventful cataract surgery in the same eye some 3 years previously and had not been seen in the eye department since. Relevant medical history includes treatment for paroxysmal atrial fibrillation with sotalol. The patient had been taking warfarin until 2 months before the original presentation. The clinical findings were left eye visual acuity −6/60 (Sn) improving to 6/12p with a pinhole; circumciliary congestion and an area of reddish-brown discoloration (6.0–6.5 mm) inferotemporally on the cornea, clinically resembling corneal blood staining. The intraocular pressure was within normal limits and no other ocular abnormality was detected. The other eye had a visual acuity of 6/6p with pinhole and appeared to be normal. On review, 2 months after initial presentation, he was noted to have shrinkage of the area of discoloration revealing underlying prominent superficial and deep stromal corneal vessels adjacent to the area of discoloration, and some lipid deposition close to the deeply vascularised limbus. On further follow up 5 months later, the patient had retained the same visual acuity of 6/60 (Sn) improving to 6/12p with pinhole. Though the ciliary congestion persisted, the patient was not in any discomfort. The area of discoloration had a greenish-yellow tinge now and measured 5.7–4.2 mm.
Deep intracorneal haemorrhage is most often seen after intraocular surgery, after direct, blunt ocular trauma, and in a vascularised cornea. The contribution of systemic factors such as diabetes or hypertension is unclear.2 Acne rosacea is known to cause peripheral vascularisation especially involving the inferonasal and inferotemporal quadrant. These vessels are known to progress in the absence of acute symptoms.3 In our patient, the corneal blood staining was a result of direct bleeding into the corneal stroma from the deep stromal vessels. The deep stromal vascularisation appears to have developed insidiously as in similar cases reported subsequent to contact lens wear.2 3 Corneal blood staining either from persisting hyphaema or deep intracorneal haemorrhage represents deposition of haemoglobin and its breakdown products within the cornea.4 A histopathological analysis of blood stained corneas, most of which were associated with raised intraocular pressures, indicated a gradient of haemoglobin degradation from the posterior to the anterior corneal stroma, extracellular haemoglobin particles being concentrated more posteriorly while haemosiderin laden keratocytes predominated anteriorly.1 Animal model experiments in rabbits utilising total persistent hyphaema with sustained increased intraocular pressures have also revealed similar results.5 Endothelial degeneration accompanies corneal blood staining and keratocytes appear to be actively involved in haemoglobin degradation.5 Porphyrin induced photosensitivity producing cytotoxic oxygen species within the blood stained cornea have also been considered as contributing to endothelial and keratocyte degeneration.6 Clearing of blood staining is thought to be a result of the phagocytic action of the keratocytes and from a diffusion of haemoglobin into the conjunctival circulation and the anterior chamber.7 The pattern of peripheral, posterior, and anterior stromal clearing observed seems consistent with diffusion of haemoglobin breakdown products out of the cornea as the primary mechanism of clearing.4 In the absence of a hyphaema, therapeutic efforts are directed towards prevention of corneal blood staining—for example, treating the corneal ulcer vigorously, correction of entropion or treatment of systemic hypertension.2 7 The presence of deep stromal vascularisation secondary to any cause must be watched carefully and managed as a potentially vision threatening complication especially in contact lens wearers. Once intracorneal bleeding has occurred, Giessleret al advise waiting for a spontaneous clearing, although it may take 2 or 3 years or more.7 In the absence of severe associated pathology, corneal blood staining has been noted to clear without permanent corneal opacity changes.4 Penetrating keratoplasty may be considered.
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