Feline corneal sequestrum

Feline corneal sequestrum are a relatively common eye disease of cats which begins as a corneal ulcer and gradually worsens despite aggressive therapy[1].

Corneal sequestrum refers to the development of an opaque, dark brown to black plaque on the cornea which is a dead piece of corneal tissue. Sequestra are usually oval to round, they can be quite small to quite large, and they can extend deeply into the corneal tissue[2]. Some sequestra have the appearance of a shiny piece of black patent leather on the surface of the eye. Others have a browner, more bronzed appearance. Corneal sequestration can occur in cats of all ages and breeds. The breed with the highest frequency of occurrence is the Persian breed. Other at-risk breeds include Siamese, Burmese, and Himalayan cats. An association with FHV is suggested due to the response seen in a recent trial using antiviral medication such as famciclovir (Famvir) at 62.5 mg/cat daily for 3-4 weeks[3]. However it must be bourne in mind that the presence of corneal disease could cause trigeminal nerve stimulation, thus causing reactivation of latent virus from the trigeminal ganglion – thus the presence of FHV-1 virus in such corneas does not prove that they were the cause of the initial ulcer or the subsequent sequestrum.


The exact cause of feline sequestra is unknown. However, the development of a sequestrum is often associated with corneal trauma, dry eye (keratoconjunctivitis sicca), abnormal eyelid conformation, and viral infections (FHV, FCV)[4]. Genetics and conformation may also be involved since there is a definite breed predisposition. A thorough ophthalmic examination is essential to uncover any underlying problems. The process in the feline cornea may be a response to a variety of problems. Early reports suggested that corneal trauma from corneal ulcers, entropion, trichiasis, or exposure to caustic chemicals, could precipitate the corneal stromal necrosis. In addition, referred-genetics, tear-film composition, a primary corneal stromal metabolic or neurologic disturbance, or an infective agent may singly or in combination play a role. Feline sequestrum may occur whenever there is an irritation or chronic damage of the corneal stroma[5].

Corneal sequestration has been described in all breeds of cats but it is more common in the Persian breed followed by the Siamese, Burmese, Himalayan, and domestic short hair breeds. The predilection for certain breeds has promoted the speculation regarding a hereditary basis, and the condition has also been suggested to be a type of dystrophy. Nasisse (1998b) suggested that it is probably a nonspecific response to insult, seen more commonly in brachycephalic cats with exposure keratitis, and also occurs secondary to herpetic keratitis[6].

Stiles et al (1997) described the use of nested polymerase chain reaction (PCR) to detect feline herpesvirus 1 (FHV-1) DNA in ocular specimens from cats with sequestrum and from clinically normal cats. PCR was positive in 5 of 28 (18%) corneal specimens from cats with sequestrum and 6 of 13 (46%) clinically normal cats. The distribution of positive results was considered not significant. They suggested that FHV-1 might be less of a cause of the disease in commonly affected breeds like Himalayan and Persian, than other factors, such as corneal metabolic defects and lagophthalmos[7].

Nasisse et al (1998) by using PCR, obtained different results. They detected FHV-1 in 5.9% (1/17) of corneas from clinically normal cats and in 55.1% (86/156) from specimens from cats with corneal sequestra. Their data strongly implied the involvement of FHV-1 in the pathogenesis of the disease. However were similar to the suggestion made by Stiles et al (1997) concerning breed predisposition. Prevalence of FHV-1 DNA was significantly lower in Persian and Himalayan, compared with domestic shorthair and longhair breeds. At the same year Nasisse (1998a) considered that sequestration is a non-specific response to the substantial stromal damage done by FHV-1 under these conditions, and not the only cause of corneal sequestration[8][9][10]

Clincial signs

Sequestra can be painful. Affected cats may exhibit blepharospasm, lacrimation, enophtalmos, elevation of the nictitating membrane, and decreased activity and appetite that reflect the painful nature of the disease.

The signs of ocular pain may be subtle and include squinting, tearing, and elevation of the third eyelid. The lesion is usually in the central or paracentral cornea, circular or oval in shape, and it contains invariably pigments. Degeneration of collagen and accumulation of a brown pigment characterize it. The sequestrum most often affects the anterior third of the corneal stroma but can extend to descemet’s membrane in some cases. With chronicity, the sequestration becomes denser, and the edges may begin to separate from the adjacent corneal stroma. In addition, corneal neovascularization and perilesional edema occur[11].

Sequestra can remain for months to years and can cause secondary conjunctivitis and/or infection[12]. Additionally, the dead corneal tissue can act as a foreign body, causing the immune system to attack the sequestrum. During this attack, neighbouring healthy corneal tissue is damaged, and the eye can rupture. A sequestra can extrude (slough) from the eye’s surface and cause eye rupture. If this occurs, the eye unfortunately might need surgical removal (enucleation)[13].


  • Early stages of corneal sequestra can be treated conservatively with topical antibiotics/anti-inflammatory drops, in conjunction with a third eyelid flap.
  • Antiviral therapy using Famciclovir (Famvir) at 62.5 mg/cat oid/bid for 3-4 weeks or Acyclovir has shown a good response in some cases. Both drugs are well tolerated by most cats[14].
  • Keratectomy

A keratectomy (partial lamellar) of the cornea and a corneal graft can be performed. Unfortunately, a large population of these affected cats need the eye removed and if both eyes are affected, euthanasia is a common end result[15]. A superficial keratectomy involves separating the diseased surface layers from the normal underlying cornea. A corneal disc knife is used to glide between the individual corneal layers so that a clean margin is attained. Failure to attain a clean margin results in sequestrum recurrence. After the keratectomy is performed either a third eyelid flap or a temporary tarrsorrhaphy are placed to protect the cornea whilst it is healing.

  • Conjunctival Pedicle Flap

A conjunctival pedicle flap is used for patients with deep sequestrums or patients that are predisposed to recurrence. These patients include those under the age of 8 years and Persians. Firstly a keratectomy is used to remove the diseased cornea. Then a thin tongue of conjunctiva is dissected off the sclera and sutured directly onto the cornea using 8-0 or 9-0 suture material. As with a superficial keratectomy a temporary tarrsorraphy is placed.

  • Clear Corneal-Conjunctival Transposition

For certain cases a clear corneal-conjunctival transposition can be used to treat deep cases and those prone to recurrence. Firstly a keratectomy is performed to remove the diseased cornea. Then a section of adjacent normal cornea is undermined to the limbus and into the conjunctiva. This entire section is then transposed over and onto the keratectomy site. The transposed tissue is then sutured down onto the cornea and a temporary tarrsorrhaphy is placed.


  1.  Morgan, R.V (1994) Feline corneal sequestration: a retrospective study of 42 cases (1987-1991). J Am Anim Hosp Assoc, v.30, p.24-69
  2.  Whitley, R.D. et al (1993) Diagnosing and treating disorders of the feline conjunctival and cornea. Vet Med88(12): 1138-1149
  3.  Malik R et al (2009) Treatment of feline herpesvirus-1 associated disease in cats with famciclovir and related drugs. JFMS 11:40-48
  4.  Kirschner, S.E. (1992) Diseases of the cornea and sclera. ln: MORGAN, R.V. Handbook of small animal practice. 2.ed. Philadelphia.: Saunders. p.1063-1076
  5.  Glaze, M.B. & Gelatt, N.K. (1998) Feline ophthalmology. ln: GELATT, N.K.. Philadelphia.: Lippincott Williams & Wilkins, 1998. p.997-1052
  6.  Ejima, H. et al (1993) Detection of iron a blackish lesion is a case of feline corneal sequestration. Vet. Med Sci. 55(6):1051-1052
  7.  Stiles J.M.C. et al (1997) Use of nested polymerase chain reaction to identify feline herpesvirus in ocular tissue from clinically normal cats and cats with corneal sequestra or conjunctivitis. Am J Vet Res 58(4): 338-342
  8.  Nasisse, M.P (1998a). Ocular viral diseases of animals. Magrane basic course in ophthalmology. Madison : University of Wisconsin. p.5
  9.  Nasisse, M.P (1998) Disease of the conjunctiva and cornea. In: The North American Veterinary Conference, 1998, Orlando. Proceedings… Orlando : Eastern States Veterinary Association, 1998b. 12:533-534
  10.  Nasisse, M.P et al (1998). Detection of feline herpesvirus 1 DNA in corneas of cats with eosinophilic keratitis or corneal sequestration. Am J Vet Res 59(7): 856-8
  11.  Slatter, D. Fundamentals of veterinary ophthamology. 2.ed. Philadelphia : Saunders, 1990. Cap.11: Cornea and sclera: p.157-303
  12.  Wilkie, D.A (1994) Diseases and surgery of the eye. ln: Sherding, R.G. The cat diseases and clinical management. 2.ed. New York: : Churchill Livigstone
  13.  Devidson, H.J. et al (1992) Determination of protein concentrations and their molecular weight in tears fro, cats with normal corneas and cats with corneal sequestrum. Am J Vet Res 53(10):1756-1759
  14.  Murphy, C.J (1992) Disorders of the cornea and sclera. ln: Bonagura, J.D, Kirk, R.W. Kirk’s current veterinary therapy: small animal practice – XI. Philadelphia : Saunders, 1992. p.1101-1111
  15.  Pentlarge, V.W (1996) Corneal sequestration in cats. In: GLAZE, M.B. Ophthalmology in small animal practice. Trenton : Veterinary Learning Systems. p. 219-225

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