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Keratoconjunctivitis sicca

Deficiency of the aqueous part of the tear film that dries and inflames the cornea and conjunctiva. Usually immune-mediated; without treatment it leads to corneal pigmentation, ulcers and loss of vision.

Disease · InflammatoryDog

Draft, not yet reviewed by a veterinarian. Content may contain errors. It is published so the community can review it.

What it is

Keratoconjunctivitis sicca (KCS, "dry eye") is inflammation of the cornea and conjunctiva caused by insufficient production of the aqueous tear film. Without tears, the corneal epithelium dries, goblet cells produce more mucus, and the cornea responds with vascularisation, pigmentation and ulceration. The most common cause in the dog is an immune-mediated adenitis that progressively destroys the lacrimal gland and the gland of the third eyelid. Other causes include:

  • Drugs, notably sulfonamides (such as trimethoprim-sulfonamide combinations).
  • Neurogenic loss of the parasympathetic supply to the lacrimal gland, often with a dry nostril on the same side.
  • Removal of the gland of the third eyelid, canine distemper, trauma, radiation therapy and congenital gland hypoplasia.

Who it affects

Immune-mediated KCS is most common in middle-aged dogs of predisposed breeds: West Highland white terrier, English cocker spaniel, English bulldog, shih tzu, Lhasa apso, pug, Pekingese, Cavalier King Charles spaniel and Yorkshire terrier.

Anatomy involved

The tear film has three layers: an outer lipid layer from the tarsal glands of the eyelids, a middle aqueous layer produced by the lacrimal gland (dorsolateral to the eyeball, under the orbital ligament) and the gland of the third eyelid, and an inner mucin layer from the conjunctival goblet cells. Parasympathetic fibres reaching the lacrimal gland travel with the facial nerve to the pterygopalatine ganglion; the same pathway supplies the lateral nasal gland, which explains the dry nostril in neurogenic KCS. The cornea has no blood vessels and depends on the tear film for oxygen and nutrients.

Clinical signs

Thick mucoid to mucopurulent discharge that sticks to the lids, conjunctival hyperaemia, a dull, lustreless cornea, blepharospasm and, in chronic cases, corneal vascularisation, pigmentary keratitis and ulcers. The disease is often bilateral and may be mistaken for bacterial conjunctivitis.

Diagnosis

  • Schirmer tear test I (without topical anaesthetic): values of 15 mm/min or more are normal; values below about 10 mm/min with compatible signs confirm the diagnosis, and intermediate values are suspicious.
  • Fluorescein to detect corneal ulcers.
  • Review of drug history, and examination of the nostrils and facial nerve function.

Treatment

The basis of treatment is topical immunomodulators that stimulate tear production, ciclosporin or tacrolimus, applied for life. They are combined with tear substitutes, mucolytics and treatment of secondary infection. Drug-induced KCS may resolve after the drug is withdrawn. When the glands are destroyed and medical treatment fails, parotid duct transposition redirects saliva onto the eye; saliva differs from tears and may leave mineral deposits on the cornea. Early treatment preserves vision.

References

  1. Gelatt KN (ed). Veterinary Ophthalmology, 6th ed. Wiley-Blackwell (2021)
  2. Maggs DJ, Miller PE, Ofri R. Slatter's Fundamentals of Veterinary Ophthalmology, 6th ed. Elsevier (2018)
Study material. Not a substitute for diagnosis or veterinary consultation.Edit on GitHub