The corneal sequestrum (FCS) is a disease of the cat characterized clinically by the presence of signs such as blepharospasm, epiphora and eventually photophobia, accompanied by the presence of an irregular, dark brown or black spot of variable size, localized most of the times in the center of the cornea. It was first described by Verwer in 1965 under the name of corneal sequestrum. Superficial vascularization is an important feature of this condition and frequently an epithelial defect can be observed surrounding the plaque. Although no sex or age related prevalence of FCS has been observed, a breed predisposition has been noted. Persian appears to be the most commonly affected, followed by Himalayan, Siamese and DSH.
The etiology of the disease is not well understood. Since the condition was first reported, different theories were suggested. Cultures made in some clinical cases isolated Streptococcus, Staphylococcus, Moraxella and Aerobacter, but in all cases these bacteria were found to be an opportunistic. Fungi were also isolated from some other cases. It has also been proposed that the use of chemical caustics such as silver nitrate or iodine tincture can produce a FCS. However, no published accounts of FCS mention the use of silver nitrate, and only two have mentioned the use of iodine tincture. The prolonged use of epinephrine in man produces plaques similar to the ones produced by FCS, but the veterinary literature does not mention the use of this drug. It has been proposed that a high catecholamine content in the feline tears could play a role in the development of the disease.
Traumatic factors are directly related to the formation of a corneal ulcer over which a sequestrum is posteriorly established. As a result, various ulcer-causing conditions are associated with FCS but only as predisposing agents. Knetch emphasized the importance of the development of blepharospasm which, through corneal compression, devitalizes the bottom of the ulcer, thereby contributing to the development of necrosis of substancia propria. Other authors suggest that FCS could be a corneal dystrophy since by using electronic microscopy on affected corneas they could observe that the corneal epithelium was very modified with vacuolated basal cells; these vacuolae had a myelinic material inside and they looked similar to ones seen in lysosomal alterations secondary to defects in degradation of glycosaminoglycans observed in mucopolysaccharidosis in man.
Latest researches suggest that Feline Herpes Virus Type 1 (FHV 1) could play a role in the etiology of the disease. Some reports, using PCR to identify viral ADN, indicated that 5 (18%) of 28 specimens and 86 (55,1%) of 156 specimens respectively, were positive for FHV-1. However, in one of these reports, corneas from normal cats were also analyzed and 6 (46%) of 13 were also positives for FHV-1.
The condition may affect both eyes but more often affects only one. It is observed a well-developed superficial vascularization that surrounds and delimitates the sequestrum. A fluorescein-positive region of variable size can be observed around the plaque. The nucleus is localized in the center and looks like a dry, crusty tissue that is fluorescein negative but frequently retains rose bengal.
The plaque presents two different types of lesions:
A black, dry plaque with well-defined limits and a granular surface that rises above the level of the cornea; and
A dark brown plaque with ill-defined limits that protrudes only slightly.
The sequestrum is composed of desiccated and degenerated stroma. Histopathologically, it is characterized by the presence of necrosis of the stromal lamellae, and the black or brown color is due to desiccation rather than the presence of melanin or hemosiderin. This coagulative stromal necrosis varies in depth, causing a disconnection of the lamellae which favors spontaneous loosening.
No fibroblasts or inflammatory cells are associated with the necrotic areas. An inflammatory zone characterized by intense vascularization and the presence of giant cells, macrophages, lymphocytes and plasma cells, surround the stromal necrosis and is repeated toward the base of the plaque. Karyolysis and karyorrhexis can be observed at the junction of the sequestrum and the inflamed stroma.
If the patient is not treated, the plaque can loose spontaneously but generally recurs. Experience with topical treatments has not yielded good results. Lamellar keratectomy appears to be the only way to control the process. Depending on the depth of keratectomy, different techniques can be used added to surgical excision, in order to provide more support to the slimmed cornea. Lamellar corneoscleral transposition or its modification, corneoconjunctival transposition can be used for these cases. Lastly, lamellar keratoplasty was reported using frozen feline and canine corneas and biological membranes such as porcine small intestine submucosa.
References
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