{"id":1013,"date":"2014-07-01T00:33:42","date_gmt":"2014-07-01T00:33:42","guid":{"rendered":"http:\/\/phosdev.com\/todaysveterinarypractice\/?p=1013"},"modified":"2022-02-16T15:55:14","modified_gmt":"2022-02-16T15:55:14","slug":"diagnosis-treatment-of-keratoconjunctivitis-sicca-in-dogs","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/ophthalmology\/diagnosis-treatment-of-keratoconjunctivitis-sicca-in-dogs\/","title":{"rendered":"Diagnosis & Treatment of Keratoconjunctivitis Sicca in Dogs"},"content":{"rendered":"

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Lori J. Best, DVM; Diane V.H. Hendrix, DVM, Diplomate ACVO; and Daniel A. Ward, DVM, PhD, Diplomate ACVO<\/em><\/p>\n

Keratoconjunctivitis sicca (KCS), is a relatively common condition in dogs, although the diagnosis is often overlooked. This article provides guidance on the pathophysiology, causes, diagnosis, and medical and surgical treatment for this condition.<\/p>\n

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K<\/span>eratoconjunctivitis sicca (KCS) is a relatively common condition in dogs. Although KCS can be diagnosed readily with a thorough ophthalmic examination, the diagnosis is often overlooked.<\/span><\/p>\n

KCS is an inflammatory condition of the cornea and conjunctiva, secondary to a deficiency of the precorneal tear film (PTF). KCS is categorized by tear film deficiency:<\/span><\/p>\n

\u2022 <\/span>Quantitative KCS<\/span> is a decrease in the <\/span>aqueous component<\/span> of the tear film as measured with the Schirmer tear test (STT); it is recognized more commonly in veterinary medicine.<\/span><\/p>\n

\u2022 <\/span>Qualitative KCS<\/span> is a decrease in the <\/span>lipid or mucin components<\/span> of the tear film and diagnosed by documenting decreased tear film breakup time (TBUT).<\/span><\/p>\n\n\n\n
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The Lacrimal System & Tear Film<\/span><\/strong><\/h3>\n

Normal PTF is estimated to be anywhere from 3 to 45 microns thick in humans and, in most species, is composed of aqueous, lipid, and mucin layers, which were once thought to be present in a laminar arrangement (Table 1<\/strong>).1,2<\/sup> More recent evidence suggests that PTF may resemble a muco-aqueous pool covered in a very thin lipid layer rather than a trilaminar structure.3<\/sup><\/p>\n\n\n\n\n\n\n\n
Table 1. Structure of Precorneal Tear Film<\/td>\n<\/tr>\n
<\/td>\nAREA OF PRODUCTION<\/td>\nFUNCTION<\/td>\nTYPE OF DEFICIENCY<\/td>\nDIAGNOSTIC TEST<\/td>\n<\/tr>\n
LIPID<\/td>\nMeibomian glands<\/td>\n\u2022 Limits evaporation
\n\u2022 Binds tear film to cornea
\n\u2022 Provides surface tension to prevent tear film overflow<\/td>\n		Qualitative<\/td>\nDecrease in TBUT<\/td>\n<\/tr>\n
AQUEOUS<\/td>\nOrbital and nictitans lacrimal glands<\/td>\n\u2022 Provides corneal nutrition, surface lubrication, and smooth surface for optical clarity
\n\u2022 Removes waste material and bacteria<\/td>\n		Quantitative<\/td>\nDecrease in STT value<\/td>\n<\/tr>\n
MUCIN<\/td>\nConjunctival goblet cells<\/td>\n\u2022 Enhances spread of tear film<\/td>\nQualitative<\/td>\nDecrease in TBUT<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Lacrimal secretion is stimulated via sensory input from the cornea, periocular structures, and globe. The ophthalmic and maxillary divisions of the trigeminal nerve serve as the afferent part of the reflex arc; then motor input travels to the lacrimal glands via the parasympathetic division of the facial nerve as the efferent arc. Tears are then secreted following contraction of lacrimal acinar myoepithelium.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

PATHOPHYSIOLOGY<\/span><\/strong><\/h2>\n

Tear film deficiencies lead to:<\/span><\/p>\n

\u2022 <\/span>Chronic inflammation of the ocular surface secondary to increased surface friction<\/span><\/p>\n

\u2022 <\/span>Secondary infection<\/span><\/p>\n

\u2022 <\/span>Dehydration and malnutrition of the corneal and conjunctival epithelium.<\/span><\/p>\n

This latter combination makes ulcerations more prone to infection, possibly resulting in keratomalacia and perforation.<\/span><\/p>\n

Chronic surface irritation results in:<\/span><\/p>\n

\u2022 <\/span>Conjunctival hyperemia<\/span><\/p>\n

\u2022 <\/span>Squamous metaplasia of the surface epithelium<\/span><\/p>\n

\u2022 <\/span>Hyperkeratinization of the surface epithelium<\/span><\/p>\n

\u2022 <\/span>Thickening of the corneal epithelium.<\/span><\/p>\n

Inflammatory cells and blood vessels enter the anterior corneal stroma, depositing pigment, lipids, and calcium. The vascularization and deposits stabilize the cornea and make it less susceptible to ulceration; however, their presence can result in vision loss.<\/span><\/p>\n

QUANTITATIVE KCS<\/span><\/strong><\/h2>\n

<\/h3>\n

Causes<\/span><\/strong><\/h3>\n

Causes of quantitative KCS\u2014organized by type of cause\u2014are listed in <\/span>Table 2<\/span><\/strong>. The most common cause is immune-mediated lacrimal adenitis. Transient decreases in tear production can be iatrogenically caused by:<\/span><\/p>\n

\u2022 <\/span>General anesthesia: Significantly decreases tear production for up to 24 H4<\/span><\/p>\n

\u2022 <\/span>Xylazine, medetomidine, and butorphanol: Significantly decrease tear production temporarily5,6<\/sup><\/span><\/p>\n

\u2022 <\/span>Topical or systemic atropine: Causes secondary decrease in tear production that is not clinically significant in most dogs.<\/span><\/p>\n

Therefore, artificial tear ointments are important adjuncts to sedation and anesthesia regimens, and should be continued until dogs are fully responsive and consistently blinking appropriately.<\/span><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
Table 2. Causes of Quantitative KCS<\/td>\n<\/tr>\n
CAUSE<\/span><\/td>\nPATHOGENESIS<\/td>\nPREDISPOSITION<\/td>\nDURATION<\/td>\nPROGNOSISa<\/td>\n<\/tr>\n
Disease (Ophthalmic)<\/td>\n<\/tr>\n
Chronic severe conjunctivitis<\/span><\/td>\nSwelling of excretory ductules of lacrimal gland<\/td>\nNone<\/td>\nVariable: Permanent if scarring present<\/td>\nGood<\/td>\n<\/tr>\n
Immune-mediated lacrimal adenitis (primary KCS)<\/span><\/td>\nImmune-mediated destruction of lacrimal tissue with secondary atrophy7<\/sup><\/td>\nMost common cause of canine KCSb<\/td>\nLifelong<\/td>\nGood<\/td>\n<\/tr>\n
Disease (Other)<\/td>\n<\/tr>\n
Canine distemper virus8<\/sup><\/td>\nLacrimal adenitis<\/td>\nUnvaccinated animals<\/td>\nVariable: Many spontaneously recover<\/td>\nGood to fair: If systemic disease survived, many recover<\/td>\n<\/tr>\n
Idiopathic neurogenic9<\/sup><\/td>\nIdiopathic: Present with ipsilateral dry nose<\/td>\nMiddle-aged female dogs<\/td>\nVariable<\/td>\nGood to fair: Some spontaneously resolve<\/td>\n<\/tr>\n
Leishmaniasis10<\/sup><\/td>\nLacrimal adenitis, especially surrounding lacrimal gland ducts, where amastigotes accumulate<\/td>\nAnimals in Mediterranean region or with travel history<\/td>\nVariable<\/td>\nFair<\/td>\n<\/tr>\n
Hereditary<\/td>\n<\/tr>\n
Congenital alacrima<\/td>\nDevelopmental absence of lacrimal tissue<\/td>\nYorkshire terrier overrepresented11<\/sup><\/td>\nPermanent; present at birth<\/td>\nPoor: Often requires surgery<\/td>\n<\/tr>\n
Medication<\/td>\n<\/tr>\n
Etodolac12<\/sup><\/td>\nNitrogen-containing pyrimidine\/pyridine rings have direct toxic effect on lacrimal acinar cells<\/td>\nNone<\/td>\nVariable<\/td>\nFair: If etodolac administration < 6 months, more likely to recover<\/td>\n<\/tr>\n
Sulfa-derivative medications13<\/sup> & related compounds14<\/sup><\/td>\nNitrogen-containing pyrimidine\/pyridine rings have direct toxic effect on lacrimal acinar cells<\/td>\nTypical onset within 30 days of medication initiation5<\/sup><\/td>\nVariable: May resolve in 45\u201360 days or sometimes lifelong<\/td>\nFair: Discontinue medication immediately after decrease in STT<\/td>\n<\/tr>\n
Treatment\/Trauma<\/td>\n<\/tr>\n
Iatrogenic: Removal of third eyelid gland<\/td>\nMay decrease tear production and TBUT15<\/sup><\/td>\nNone: History of removal of gland<\/td>\nVariable<\/td>\nFair<\/td>\n<\/tr>\n
Local radiation therapy16<\/sup><\/td>\nAcute adverse effect of radiation exposure<\/td>\nNone<\/td>\nVariable: Dose dependent and patient sensitivity<\/td>\nFair<\/td>\n<\/tr>\n
Trauma to lacrimal gland or nerves9<\/sup><\/td>\nDecreased production\/ distribution of PTF due to decreased blinking and\/or increased evaporation secondary to lagophthalmia17<\/sup><\/td>\nNone<\/td>\nVariable<\/td>\nFair to poor<\/td>\n<\/tr>\n
a. Based on initiation of medical management
\nb. Many breeds are predisposed to primary KCS, including, but not limited to, the American cocker spaniel, cavalier King Charles spaniel, West Highland white terrier, and brachycephalic breeds (eg, English bulldog)18<\/sup><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

<\/h3>\n

Clinical Signs<\/span><\/strong><\/h3>\n

Clinical signs associated with quantitative KCS are listed in <\/span>Table 3<\/span><\/strong>.<\/span><\/p>\n

Diagnosis<\/span><\/strong><\/h3>\n

KCS is diagnosed after consideration of:<\/span><\/p>\n

\u2022 <\/span>History: <\/span>Ask historical questions that explore previous drug administration, vaccinations, and surgical procedures.<\/span><\/p>\n

\u2022 <\/span>Ophthalmic Examination: <\/span>Perform a complete ophthalmic examination in all dogs presenting with new clinical signs (<\/span>Table 3<\/span><\/strong>) or disease progression.<\/span><\/p>\n

\u2022 <\/span>STT: <\/span>This test is the cornerstone of quantitative KCS diagnosis; interpret results in light of clinical signs. A Schirmer tear test 1 (STT1)\u2014performed without application of surface anesthetic agents\u2014assesses reflex tear production. Normal production in dogs is > 15 mm\/min.<\/span><\/p>\n\n\n\n
\n\n\n\n\n\n
Table 3. Clinical Signs of Quantitative KCS<\/td>\n<\/tr>\n
\u2022 Thick, adherent mucopurulent discharge (Figure 1<\/strong>)
\n\u2022 Conjunctivitis
\n\u2022 Blepharospasm
\n\u2022 Dry, lusterless corneal appearance
\n\u2022 Ulcerative keratitis, ranging from superficial ulcers to perforations (Figure 2<\/strong>)
\n\u2022 Corneal pigmentation (Figures 3 and 4<\/strong>), neovascularization, and\/or keratinization<\/td>\n<\/tr>\n
Of the breeds predisposed to KCS, many have distichia, physiologic exophthalmia with lagophthalmos, and medial canthal entropion\u2014all conditions that can cause conjunctivitis and keratitis.<\/em><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

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Figure 1.<\/strong> Two-year-old castrated male chihuahua. Note corneal neovascularization and pigmentation, thick and adherent mucopurulent discharge, and keratinization of corneal epithelium; STT was 0 mm\/min.<\/em>
\n Figure 2.<\/strong> Four-year-old castrated male mixed breed dog. Note descemetocele, corneal edema, and mucopurulent ocular discharge; STT was 0 mm\/min.<\/em>
\n Figure 3.<\/strong> Three-year-old spayed female Shih Tzu. Note corneal neovascularization and mild keratinization; STT was < 5 mm\/min.<\/em>
\n Figure 4.<\/strong> Three-year-old spayed female Olde English Bulldogge. Note conjunctival hyperemia, corneal neovascularization, pigmentation, keratinization, and thick mucopurulent discharge.<\/em><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

QUALITATIVE KCS<\/span><\/strong><\/h2>\n

Causes<\/span><\/strong><\/h3>\n

The causes of qualitative tear film deficiency are not completely understood.<\/span><\/p>\n

\u2022 <\/span>Chronic blepharitis with meibomianitis can lead to decreased production of the lipid layer. Infectious causes of blepharitis include <\/span>Staphylococcus<\/span>, <\/span>Candida<\/span>, and<\/span>Malassezia<\/span> species.19<\/sup><\/span><\/p>\n

\u2022 <\/span>Decreased goblet cell density and subsequent mucin layer deficiency are most likely caused by chronic conjunctival inflammation secondary to infectious disease or immune-mediated disease.20<\/sup><\/span><\/p>\n

Clinical Signs<\/span><\/strong><\/h3>\n

Clinical signs of qualitative tear film deficiency are more subtle than those seen with quantitative disease, and include:<\/span><\/p>\n

\u2022 <\/span>Blepharospasm<\/span><\/p>\n

\u2022 <\/span>Mild corneal neovascularization<\/span><\/p>\n

\u2022 <\/span>Mucus discharge.<\/span><\/p>\n

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Diagnosis<\/span><\/strong><\/h3>\n

If qualitative KCS is suspected based on history and clinical signs:<\/span><\/p>\n