Chapter 139 Diseases of the Lacrimal System
The overall function of tears is to protect and nourish cornea, sweep debris into nasolacrimal canaliculi, and lubricate the eyelids. They also have a refractive function. An understanding of the anatomy and innervation of the lacrimal system, as well as the formation, composition, and function of the precorneal tear film, is important to the understanding of the physiology, pathogenesis, diagnosis, and treatment of its diseases.
ANATOMY AND PHYSIOLOGY OF THE LACRIMAL SYSTEM
• The secretory components of the lacrimal system include the main and accessory lacrimal glands, the gland of the nictitans (third eyelid), the meibomian glands, and the conjunctival goblet cells.
• The main lacrimal gland is a tubuloacinar gland located dorsolateral to the globe between the globe and the orbital ligament and the zygomatic process of the frontal bone. It produces between 50% and 70% of the aqueous tear layer.
• The gland of the nictitans is also a tubuloacinar gland and is located ventromedially at the base of the T-shaped cartilage that supports the nictitans. It produces between 30% and 50% of the aqueous tear layer.
• The meibomian (tarsal) glands are modified sebaceous glands located in the distal aspect of the tarsus that open onto the edge of both eyelids in a row of small openings. They number approximately 20 to 40 per eyelid and produce the lipid component of the preocular tear film. The innervation of the meibomian glands is parasympathetic in origin.
• The conjunctival goblet cells are heterogeneously dispersed in the dog; i.e., the highest numbers are located along the lower nasal and middle fornices and the lower tarsal portion of the palpebral conjunctiva. Their function is to produce the mucus component of the tear film.
• The accessory eyelid glands are the glands of Moll and Zeis. The glands of Moll are modified sweat glands, and the glands of Zeis are prominent sebaceous glands. Their function is unknown.
• The excretory components include the superior and inferior lacrimal puncta and their canaliculi, nasolacrimal sac, and ducts.
• The superior and inferior lacrimal puncta allow the exit of the tear film from the lacrimal lake to the canaliculi then to the nasolacrimal duct.
Precorneal Tear Film
• The precorneal tear film has three layers: the lipid layer, the aqueous layer, and the mucus layer.
• The lipid layer is the outer layer that is produced by meibomian glands and functions to prevent evaporation of aqueous layer.
• The aqueous layer is the middle layer that is produced by the main lacrimal gland and gland of the nictitating membrane. It flushes foreign material from the conjunctival sac; lubricates for the passage of the eyelids over the cornea; provides a medium for transferring oxygen, inflammatory cells, immunoglobulins, lysozyme, and lactoferrin to the cornea; and gives a smooth surface to the cornea for optimal optical efficiency.
• The mucus layer is the innermost layer that is produced by goblet cells on the conjunctiva. It functions as a surfactant and stabilizer of the aqueous layer and spreads tears across the cornea, adhering to the microvilli of the corneal and conjunctival epithelium by charged polyanions enhancing the even spread of the tear film over the corneal surface. The mucin also filters trapped and foreign particles, forming mucus strands that are moved to the medial canthus for clearance from the eye.
Innervation of the Lacrimal System
• The trigeminal nerve plays an important role in the neurogenic control of lacrimation. The ophthalmic division of the trigeminal nerve, as well as the zygomatic nerve, a branch of the maxillary division of the trigeminal nerve, provides afferent sensory information from the lacrimal gland, periocular structures, and globe. The cornea is directly innervated by free nerve endings of the trigeminal nerve that penetrate the limbus and enter the anterior corneal stroma. Stimulation of these nerve endings results in reflex tear formation.
DISEASES OF THE LACRIMAL SYSTEM
Diseases of the lacrimal system can be divided into those that cause a decrease in any component of the preocular tear film or those that cause epiphora. Keratoconjunctivitis sicca is primarily caused by an immunemediated disease against the lacrimal glands, resulting in a decrease in the aqueous component of the precorneal tear film. The other, less common causes will also be discussed. Diseases that cause epiphora, or excessive tearing, are usually secondary to a problem with tear drainage or irritation from periocular hairs contacting the corneal surface. These and their appropriate therapies will also be discussed.
Keratoconjunctivitis Sicca
• Keratoconjunctivitis sicca (KCS) can be due to qualitative and quantitative deficiencies of precorneal tear film.
• Congenital alacrima or congenital hypoplasia of the lacrimal acini occurs in miniature breeds (pug and Yorkshire terrier), is uncommon, and is characterized by complete lack of precorneal tear film production, resulting in severe dryness.
• Drug-related causes of KCS include systemic sulfonamide therapy, phenazopyridine, topical and general anesthesia, antihistamines, and etodolac.
• Other causes of KCS include supervoltage and megavoltage radiation therapy, excision of the gland of the nictitans, and neurologic abnormalities.
Keratoconjunctivitis Sicca Due to Quantitative Tear Deficiencies
Clinical Signs
• Acute cases with severe dryness present with acute pain, blepharospasm, and axial corneal ulceration. Ocular discharge in these cases is often mucopurulent to suppurative, and corneal ulceration may progress to perforation if not treated quickly and aggressively.
• The more common presentation is one of chronic conjunctival hyperemia with intermittent mucoid discharge.
• With time, the ocular discharge will become mucopurulent due to imbalance of the bacterial flora, allowing abnormal microorganisms such as beta-hemolytic Streptococcus, coagulase-positive Staphylococcus, gram-negative coliforms, and Pseudomonas to grow while normal flora (Staphylococcus species) decrease.
• The goblet cells also become hypertrophied and overproduce mucus, adding to the abnormal discharge.
• The cornea becomes lackluster in appearance and irregular, and it can develop edema, pigmentation, vascularization, areas of fibrosis, and possibly ulceration.
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