Lacrimal apparatus, dog
Lacrimal apparatus, dog. Illustration by Dr. Gheorghe Constantinescu.
The tear production and drainage system is vital for health of the outer eye. Tear glands within the orbit (lacrimal and in some species Harder gland) as well as the superficial tear gland of the nictitating membrane (third eyelid) produce the collective preocular or precorneal tear film. This film consists of three layers: outer lipid (from the Meibomian glands), middle aqueous layer (from lacrimal and third eyelid glands), and deep layer (mucus) from the goblet cells within the conjunctiva.
The tear drainage system consists of two lacrimal puncta (except in the rabbit and pig, which have only one punctum), two canaliculi, the lacrimal sac (within the bony lacrimal fossa), and the long and often tortuous lacrimal duct (to empty tears within the forward nasal cavity).
Hypertrophy, inflammation, and prolapse of the gland of the nictitating membrane (cherry eye) is common in young dogs and certain breeds (eg, American Cocker Spaniel, Beagle, Lhasa Apso, Pekingese, English Bulldog). In the acute stage, the red glandular mass swells and protrudes over the leading margin of the nictitans, and there is a mucopurulent discharge. Although the swelling may recede for short periods, the gland eventually often remains prolapsed. Because it is a major tear gland, it should be preserved if possible; the gland should be replaced and anchored with sutures to the orbital rim, periorbital fascia, or nictitans cartilage, or covered with adjacent mucosa (envelope or pocket techniques). Partial excision should be avoided. Complete excision may predispose to keratoconjunctivitis sicca (see below) in 30%–40% of dogs in later life. Surgical or medical resolution of cherry eye still predisposes ~20% of these dogs to future keratoconjunctivitis sicca. Therefore, these dogs should be monitored for several years after undergoing surgery.
Dacryocystitis (inflammation of the lacrimal sac) usually is caused by obstruction of the nasolacrimal sac and proximal nasolacrimal duct by inflammatory debris, foreign bodies, or masses pressing on the duct. It results in epiphora, secondary conjunctivitis refractory to treatment, and occasionally a draining fistula in the medial lower eyelid. Irrigation of the nasolacrimal duct reveals an obstruction of the duct, reflux of mucopurulent discharge from the lacrimal puncta, or both. Radiographs of the skull after injection of contrast material into the duct (dacryocystorhinography) may be necessary to establish the site, cause, and prognosis of chronic obstructions. Therapy consists of maintaining patency of the duct and instilling topical antibiotic solutions. Tubing (polyethylene or silicone) or 2-0 monofilament nylon suture temporarily catheterized in the duct may be necessary to maintain patency during healing. When the nasolacrimal apparatus has been irreversibly damaged, a new drainage pathway can be constructed surgically (conjunctivorhinostomy or conjunctivoralostomy) to empty tears into the nasal cavity, sinus, or mouth.
Imperforate lacrimal puncta are an infrequent cause of epiphora in young dogs. In foals, atresia of the nasal (distal) end of the nasolacrimal duct is a common cause of early epiphora and chronic conjunctivitis. In calves, multiple openings of the nasolacrimal duct may empty tears onto the lower eyelid and medial canthus, causing chronic dermatitis. Therapy in dogs and foals consists of surgically opening the blocked orifice and maintaining patency by catheterization for several weeks during healing.
Keratoconjunctivitis sicca (KCS) is due to an aqueous tear deficiency and usually results in persistent, mucopurulent conjunctivitis and corneal ulceration and scarring. KCS occurs in dogs, cats, and horses. In dogs, it is often associated with an autoimmune dacryoadenitis of both the lacrimal and nictitans glands and is the most frequent cause of secondary conjunctivitis. Distemper, systemic sulfonamide and NSAID therapy, heredity, and trauma are less frequent causes of KCS in dogs. KCS occurs infrequently in cats and has been associated with chronic feline herpesvirus 1 infections. In horses, KCS may follow head trauma.
Topical therapy consists of artificial tear solutions, ointments, and, if there is no corneal ulceration, antibiotic-corticosteroid combinations. Lacrimogenics such as topical cyclosporin A (0.2%–2%, bid), tacrolimus (0.02%, bid), or pimecrolimus (1%) may increase tear production; cyclosporine increases tear formation in ~80% of dogs with Schirmer tear test values ≥ 2 mm wetting/min. Ophthalmic pilocarpine mixed in food may be useful for neurogenic KCS (dogs 20–30 lb [10–15 kg] should be started on 2–4 drops of 2% pilocarpine, bid). Mucolytic agents (eg, 10% acetylcysteine) lyse excess mucus and restore the spreading ability of other topical agents. In chronic KCS refractory to medical therapy, parotid duct transplantation is indicated. In general, canine KCS requires longterm (often for life) topical lacrimogenic therapy.