Vetnews | Desember 2025 42 « BACK TO CONTENTS Regulars I Ophthalmology Column The clinical appearance of a corneal sequestrum is unmistakable. The lesion usually develops unilaterally. Bilateral lesions can arise simultaneously or sequentially but tend to occur most often in Persians or other brachycephalic breeds. An oval to circular pigmented lesion commonly develops in the central or paracentral cornea, its colour progressing from translucent amber to darker bronze, then to an impervious jet black with chronicity. The location may vary depending on the inciting cause. The margins of the discolouration are typically ill-defined in the early stages but become more distinct over time. A subtle bronze tint often extends peripherally into the stroma surrounding a discrete sequestrum. The size of the sequestrum varies, with diameters ranging from 1 to 10 mm. The depth of the lesion also varies and can extend from the superficial stroma to Descemet’s membrane. As the sequestrum progresses and opacifies, lesion depth becomes increasingly difficult to determine without the benefit of advanced imaging modalities such as ultra-high-resolution ultrasound. This makes it difficult to speculate how effective a keratectomy surgery may be. The lesion may also appear raised above the surrounding cornea as corneal epithelium can migrate beneath the sequestrum, separating it from the deeper stroma. There are certainly reports of where the sequestrum may slough off in this manner, but this would be rare. Because the sequestrum lesion is uncomfortable, other clinical signs can include blepharospasm, ocular discharge, and conjunctival hyperaemia. The corneal epithelium is usually absent over and immediately surrounding the sequestrum, but uptake of fluorescein may be limited by the stromal necrosis, which may form a moat depression around the sequestrum or may be difficult to visualise over the sequestrum itself. Although corneal ulceration is common, corneal perforation is rare. Corneal vascularisation varies from mild to severe. Histology: Histologic features include a loss of keratocytes with stromal hyalinization and an amber-pink colouration on hematoxylin and eosin‐stained sections. The corneal lesion commonly involves the anterior stroma, but full‐thickness lesions, including Descemet’s membrane, occur. The sequestrum itself is characterised by coagulation necrosis and lacks keratocytes, inflammatory cells, and blood vessels. Its lamellar structure is still discernible, but indistinct. Often bordering the stromal necrosis is a foreign body–like reaction, with lymphocytes and plasma cells in early lesions, macrophages, neutrophils, and giant cells in more chronic cases and considerable karyorrhexis and karyolysis at the junction of diseased and normal tissue. Vascularisation or granulation tissue commonly encompasses or undermines the sequestrum. With chronicity, stromal vascularisation and inflammatory infiltrates encompass the sequestrum. As the stromal collagen degeneration progresses, it is distinguished clinically by discolouration of the affected corneal stroma, its colour progressing from subtle amber and bronze to jet black over time. The nature of the stromal discolouration remains a mystery. Melanin was proposed based on spectroscopic identification of chromophores with similar light absorption and microscopic detection of melaninlike particles, but a subsequent electron microscopic study failed to identify melanin granules. Another theory implicated tear-derived porphyrins in the stromal discolouration, based on their role in murine chromodacryorrhea, but no porphyrins were found in normal feline lacrimal glands, corneas, or corneal sequestra to support that hypothesis. Traces of iron, copper, and other metals have been found in the necrotic tissue. Feline tear composition remains an area of interest as a source of the discolouration, suggested by the brown colour of affected cats’ ocular discharge and the staining of contact lenses, conjunctival grafts, and small intestinal submucosal grafts that occurs during treatment. Treatment options: When examining a corneal sequestrum case, it is essential to perform a thorough ocular examination, paying particular attention to the adnexa conformation and any mechanical causes of irritation. In such instances, a partial permanent tarsorrhaphy or correction of medial entropion [medial blepharoplasty] may minimise corneal damage in brachycephalic patients. Because a superficial sequestrum may eventually slough as the corneal epithelium undermines the necrotic tissue, some clinicians advocate a conservative medical approach that combines a topical prophylactic antibiotic, a topical hyaluronanbased lubricant, and a topical or oral antiviral if herpesvirus is suspected. This conservative approach may be adequate, but the concern is if the lesion progresses to a very deep sequestrum that involves concurrent malacia [melting] and near perforation. If the sequestrum is starting to slough already, then it may be possible to try and debride the loose tissue with scissors or a diamond burr following topical anaesthesia, repeating the process in subsequent visits until the removal is complete. Definitive removal of the sequestrum is indicated in persistent or deep lesions, especially as corneal inflammation progresses and pain increases. These options include a lamella keratectomy to remove the sequestrum as best as possible and retain as much healthy cornea as possible. The accepted concept is that covering the keratectomy site with something like a bandage contact lens, third eyelid flap, temporary tarsorrhaphy, cyanoacrylate adhesive, conjunctival pedicle graft, corneal-conjunctival transposition, small intestinal submucosal graft, amniotic membrane transplant, and bovine pericardial graft can all potentially assist with reducing recurrence. There are, however, variable success rates with these techniques. Conjunctiva, corneal-conjunctival transposition and amniotic membrane seem to be the most successful. Raised sequestrum starting to slough with undermining epithelium and granulation tissue
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