Tear Film Disorders in Dogs

Chapter 245


Tear Film Disorders in Dogs



Canine patients frequently are brought to the veterinary practitioner with chronic keratitis or conjunctivitis as a result of a tear film disorder. Keratoconjunctivitis sicca (KCS) is characterized by ocular discomfort, ocular discharge, redness, and corneal opacities that may lead to blindness. KCS results primarily from deficiency of aqueous tears, the fluid comprising approximately 95% of the total tear volume, and therefore sometimes is referred to as a quantitative tear deficiency. Deficiencies of the other primary tear components (mucin and lipid) have been referred to as qualitative tear deficiencies. This chapter focuses on quantitative tear film deficiencies in dogs.



Anatomy and Physiology


The precorneal tear film (PTF) is crucial for the maintenance of ocular surface health and clear vision. Its functions include serving as the primary oxygen source for the avascular cornea, lubricating between the eyelids and ocular surface, providing protective antimicrobial proteins, and removing debris and exfoliated cells. The PTF classically is described as a superimposition of three layers consisting of lipid, aqueous, and mucin components, including the innermost layer of glycocalyx extending from the superficial layer of the ocular surface epithelia.


The lipid layer is secreted by the meibomian glands and provides a thin, oily component to the PTF that retards evaporation and promotes a stable, even spread of tears over the cornea. Meibomian glands are highly developed in the dog; 20 to 40 glands per eyelid typically are present in the dog’s tarsal plate and form linear aggregates of secretory acini. The aqueous component of the PTF provides the avascular cornea with glucose, electrolytes, oxygen, and water. In dogs, aqueous tears are secreted by orbital and third eyelid lacrimal glands and consist of water, inorganic salts, proteins, glucose, urea, and surface-active polymers composed primarily of glycoproteins. Mucus, the third component to the PTF, is produced primarily by conjunctival goblet cells and is composed of mucin, immunoglobulins, urea, glycoproteins, salts, glucose, leukocytes, cellular debris, and enzymes. The mucous layer helps to provide a smooth refractive surface over the cornea, lubricates the cornea and conjunctiva, anchors the aqueous tear film to the corneal epithelium thus decreasing shear forces, inhibits bacterial adherence, and prevents desiccation. The health and function of the PTF depends not only on the production of normal secretory components but also on eyelid integrity, normal ocular motility, and an intact blink mechanism.


Deficiency of aqueous tears (i.e., quantitative tear deficiency) may result in inflammation, metaplasia, and necrosis of surface cells by several mechanisms. Tear deficiency results in hypertonicity and dehydration of the conjunctiva and cornea, hypoxia of corneal epithelium and subepithelial corneal stroma, increased susceptibility to ocular infections, frictional irritation by the eyelids and third eyelid, and accumulation of potentially toxic tissue metabolites such as lactic acid, desquamated cells, denatured mucus, and other microscopic debris. Qualitative tear film deficiencies are characterized by more rapid tear film breakup due to an abnormality in either the lipid or mucin component of the PTF and subsequent tear film instability.



Causes


A decrease in lacrimal secretions may result from a single disease process or a combination of conditions affecting the orbital and third eyelid glands. Immune-mediated KCS appears to constitute the largest group of clinical cases in dogs. Infectious causes of lacrimal adenitis include canine distemper and bacterial blepharoconjunctivitis caused by chronic staphylococcal infection. Congenital acinar hypoplasia is a breed-related cause (e.g., in Yorkshire and Bedlington terriers). Drug-induced KCS may occur in dogs treated with either systemic sulfonamides or repeated topical administration of atropine. Preanesthetic and anesthetic agents are known to reduce tear secretion, and anesthetic events lasting longer than 2 hours have a more prolonged effect on Schirmer’s tear test values than those lasting less than 2 hours. Removal of the third eyelid gland remains an important iatrogenic cause of dry eye in dogs. Decreased aqueous tear production may develop in association with systemic metabolic diseases such as hypothyroidism, diabetes mellitus, and Cushing’s disease. Other causes include uncorrected third eyelid gland prolapse, traumatic and inflammatory orbital diseases, loss of parasympathetic innervation to the lacrimal glands (cranial nerve VII), and loss of sensory innervation to the ocular surface (cranial nerve V).



Clinical Signs


Clinical signs are nonspecific in the early stages of KCS (i.e., red, inflamed eyes with intermittent mucoid or mucopurulent discharge); therefore the disease often is misdiagnosed as an ocular allergy or primary bacterial conjunctivitis. As the KCS becomes subacute or chronic, the ocular surface develops a lackluster appearance, the conjunctiva appears more hyperemic, and tenacious mucopurulent ocular discharge is observed. As the disease progresses, keratitis develops, characterized by corneal vascularization, pigmentation, and fibrosis, with or without ulceration. Blepharitis with periocular dermatitis often appears simultaneously with accumulation of exudates along the eyelids. Ocular discomfort intensifies, and affected eyes are often partially squinted or completely closed.



Diagnosis


Tear film abnormalities are diagnosed based on the presence of typical clinical signs, positive results on ocular staining with vital stains, and a finding of quantitative or qualitative tear deficiency. Rose bengal stain detects devitalized cells and subtle epithelial defects on either conjunctival or corneal surfaces. Fluorescein stain is used primarily to detect concurrent corneal ulceration but also may be used to evaluate tear breakup, or the ability of the corneal surface to retain a homogeneous tear covering. Schirmer’s tear test (STT) remains the standard for quantifying aqueous tear production. In any dog with a red, irritated eye, ocular discharge, or corneal disease of undetermined cause STTs should be performed.


STTs may be done either without topical anesthetic (STT I) or with topical anesthetic (SST II). Testing without anesthetic measures the ability of the eye to produce reflex tears in addition to basal secretions and is performed most commonly. STT I readings in dogs generally are interpreted as follows: 15 mm/min or more is considered normal production; 11 to 14 mm/min indicates early or subclinical KCS; 6 to 10 mm/min is classified as moderate or mild KCS; and 5 mm/min or less indicates severe KCS. Repetition of STT measurements is advised in dogs that are stressed by examination or receive medical therapy for ulcerative corneal disease because sympathetic stimulation caused by stress or current topical treatments (specifically atropine administration) may reduce tear secretions. Evaluation of patients with KCS also should include examination for possible associated systemic disease conditions (e.g., hypothyroidism), assessment of eyelid function and blink reflexes, and culture and cytologic analysis in selected cases. Secondary bacterial conjunctivitis is common in canine KCS cases and resistant microorganisms may develop if previous treatment has included a number of different antibiotic preparations.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Tear Film Disorders in Dogs

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