PEER REVIEWED

Diagnosis & Treatment of

Keratoconjunctivitis Sicca
in Dogs
Lori J. Best, DVM; Diane V.H. Hendrix, DVM, Diplomate ACVO; and
Daniel A. Ward, DVM, PhD, Diplomate ACVO
University of Tennessee

K
eratoconjunctivitis sicca (KCS) is a relatively conjunctival epithelium.
common condition in dogs. Although KCS This latter combination makes ulcerations more
can be diagnosed readily with a thorough prone to infection, possibly resulting in keratomala-
ophthalmic examination, the diagnosis is cia and perforation.
often overlooked.
KCS is an inflammatory
condition of the cornea and
THE LACRIMAL SySTEM & TEAR FILM
conjunctiva, secondary to a normal PTf is estimated to be anywhere from 3 to 45 microns thick in humans and,
deficiency of the precorneal in most species, is composed of aqueous, lipid, and mucin layers, which were once
tear film (PTF). KCS is cat- thought to be present in a laminar arrangement (Table 1).1,2 more recent evidence
egorized by tear film defi- suggests that PTf may resemble a muco-aqueous pool covered in a very thin lipid
ciency: layer rather than a trilaminar structure.3
• Quantitative KCS is a
decrease in the aqueous Table 1. structure of Precorneal Tear film
component of the tear AREA OF TyPE OF DIAGNOSTIC
film as measured with the FUNCTION
PRODUCTION DEFICIENCy TEST
Schirmer tear test (STT);
LIPID meibomian • limits evaporation Qualitative Decrease in
it is recognized more glands TbuT
• binds tear film to
commonly in veterinary
cornea
medicine.
• Provides surface
• Qualitative KCS is a tension to prevent
decrease in the lipid or tear film overflow
mucin components of
AQUEOUS orbital and • Provides corneal Quantitative Decrease in
the tear film and diag-
nictitans nutrition, surface sTT value
nosed by document-
lacrimal lubrication, and
ing decreased tear film glands smooth surface for
breakup time (TBUT). optical clarity
• removes waste
PATHOPHySIOLOGy material and bacteria
Tear film deficiencies lead
MUCIN conjunctival • enhances spread of Qualitative Decrease in
to:
goblet cells tear film TbuT
• Chronic inflammation of
the ocular surface sec- lacrimal secretion is stimulated via sensory input from the cornea, periocular
ondary to increased sur- structures, and globe. The ophthalmic and maxillary divisions of the trigeminal nerve
face friction serve as the afferent part of the reflex arc; then motor input travels to the lacrimal
• Secondary infection glands via the parasympathetic division of the facial nerve as the efferent arc. Tears
• Dehydration and malnu- are then secreted following contraction of lacrimal acinar myoepithelium.
trition of the corneal and

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 Diagnosis & Treatment of Keratoconjunctivitis Sicca in Dogs |

Chronic surface irritation results in: QUANTITATIVE KCS

• Conjunctival hyperemia
• Squamous metaplasia of the surface epithelium
• Hyperkeratinization of the surface epithelium
• Thickening of the corneal epithelium.
Inflammatory cells and blood vessels enter the
anterior corneal stroma, depositing pigment, lip-
ids, and calcium. The vascularization and deposits
stabilize the cornea and make it less susceptible to
ulceration; however, their presence can result in
vision loss.
Causes
Causes of quantitative KCS—organized by type of cause—are
listed in Table 2. The most common cause is immune-mediated
lacrimal adenitis. Transient decreases in tear production can be
iatrogenically caused by:
• General anesthesia: Significantly decreases tear production for
up to 24 H4
• Xylazine, medetomidine, and butorphanol: Significantly decrease
tear production temporarily5,6
• Topical or systemic atropine: Causes secondary decrease in tear
production that is not clinically significant in most dogs.

Table 2. Causes of Quantitative KCS

CAUSE PATHOGENESIS PREDISPOSITION DURATION PROGNOSISa
Disease (Ophthalmic)
Chronic severe Swelling of excretory ductules None Variable: Good
conjunctivitis of lacrimal gland Permanent if
scarring present
Immune-mediated Immune-mediated destruction Most common Lifelong Good
lacrimal adenitis of lacrimal tissue with cause of canine
(primary KCS) secondary atrophy 7 KCSb
Disease (Other)
Canine distemper Lacrimal adenitis Unvaccinated Variable: Many Good to fair: If
virus8 animals spontaneously systemic disease
recover survived, many
recover
Idiopathic Idiopathic: Present with Middle-aged female Variable Good to fair: Some
neurogenic9 ipsilateral dry nose dogs spontaneously
resolve
Leishmaniasis10 Lacrimal adenitis, especially Animals in Variable Fair
surrounding lacrimal gland Mediterranean
ducts, where amastigotes region or with travel
accumulate history
Hereditary
Congenital alacrima Developmental absence of Yorkshire terrier Permanent; Poor: Often
lacrimal tissue overrepresented11 present at birth requires surgery
Medication
Etodolac12 Nitrogen-containing None Variable Fair: If etodolac
pyrimidine/pyridine rings have administration < 6
direct toxic effect on lacrimal months, more likely
acinar cells to recover
Sulfa-derivative Nitrogen-containing Typical onset Variable: May Fair: Discontinue
medications13 & pyrimidine/pyridine rings have within 30 days of resolve in medication
related compounds14 direct toxic effect on lacrimal medication initiation5 45–60 days or immediately after
acinar cells sometimes lifelong decrease in STT
Treatment/Trauma
Iatrogenic: Removal May decrease tear production None: History of Variable Fair
of third eyelid gland and TBUT15 removal of gland
Local radiation Acute adverse effect of None Variable: Dose Fair
therapy16 radiation exposure dependent and
patient sensitivity
Trauma to lacrimal Decreased production/ None Variable Fair to poor
gland or nerves9 distribution of PTF due to
decreased blinking and/
or increased evaporation
secondary to lagophthalmia17
a. Based on initiation of medical management
b. 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

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| Diagnosis & TreaTmenT of KeraToconjuncTiViTis sicca in Dogs

Therefore, artificial tear ointments are important adjuncts
to sedation and anesthesia regimens, and should be contin-
ued until dogs are fully responsive and consistently blinking
appropriately.
Clinical Signs
Clinical signs associated with quantitative KCS are listed in
Table 3.
Diagnosis
KCS is diagnosed after consideration of:
• History: Ask historical questions that explore previous drug
administration, vaccinations, and surgical procedures.
• Ophthalmic Examination: Perform a complete ophthal-
mic examination in all dogs presenting with new clinical
signs (Table 3) or disease progression.
• STT: This test is the cornerstone of quantitative KCS diag-
nosis; interpret results in light of clinical signs. A Schirmer
tear test 1 (STT1)—performed without application of sur-
face anesthetic agents—assesses reflex tear production.
Normal production in dogs is > 15 mm/min.
QUALITATIVE KCS
Causes
The causes of qualitative tear film deficiency are not com-
pletely understood.
• Chronic blepharitis with meibomianitis can lead to
decreased production of the lipid layer. Infectious causes
of blepharitis include Staphylococcus, Candida, and
Malassezia species.19
• 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
Clinical Signs
Clinical signs of qualitative tear film deficiency are
more subtle than those seen with quantitative disease,
and include:
• Blepharospasm
• Mild corneal neovascularization
• Mucus discharge.
Diagnosis
If qualitative KCS is suspected based on history and
clinical signs:
• STT: Perform a STT to rule out quantitative aqueous
deficiency; STT results are normal in patients with
qualitative KCS.
• TBUT: Perform a TBUT to assess for deficiency in the
PTF’s mucin component.
1. Apply 1 drop of fluorescein stain to the eye, hold-
ing the eyelids open.
2. Under cobalt-blue illumination, examine the cornea.
Note how many seconds it takes for dark spots to
appear as the PTF “breaks up” the fluorescein layer.

1 3 Table 3. clinical signs of

Quantitative Kcs
• Thick, adherent
mucopurulent discharge
(Figure 1)
• conjunctivitis
• blepharospasm
• Dry, lusterless corneal
appearance
2 4 • ulcerative keratitis, ranging
from superficial ulcers to
perforations (Figure 2)
• corneal pigmentation
(Figures 3 and 4),
neovascularization, and/or
keratinization
Of the breeds predisposed to KCS,
many have distichia, physiologic exoph-
Figure 1. Two-year-old castrated male chihuahua. Note corneal thalmia with lagophthalmos, and medi-
neovascularization and pigmentation, thick and adherent mucopurulent al canthal entropion—all conditions that
can cause conjunctivitis and keratitis.
discharge, and keratinization of corneal epithelium; STT was 0 mm/min.
Figure 2. Four-year-old castrated male mixed breed dog. Note
descemetocele, corneal edema, and mucopurulent ocular discharge; STT was 0 mm/min.
Figure 3. Three-year-old spayed female Shih Tzu. Note corneal neovascularization and mild keratinization; STT was < 5
mm/min.
Figure 4. Three-year-old spayed female Olde English Bulldogge. Note conjunctival hyperemia, corneal neovascularization,
pigmentation, keratinization, and thick mucopurulent discharge.

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 Diagnosis & Treatment of Keratoconjunctivitis Sicca in Dogs |

Figure 5. Diagnostic algorithm for dogs presented with clinical signs of keratitis.

3. A normal TBUT is ≥ 20 seconds. Animals with quanti- inhibits proliferation of T-helper and cytotoxic T cells in the
tative deficiencies often have a TBUT of < 5 seconds, lacrimal gland and allows normal lacrimation.21
which indicates an unstable PTF.20 Cyclosporine also acts as an anti-inflammatory, decreases
• Conjunctival Biopsy: In cases of suspected mucin defi- pigmentation, normalizes goblet cell mucin secretion,22 and
ciency, obtain a conjunctival biopsy specimen to quanti- directly stimulates lacrimation, but the latter mechanism is
tate conjunctival goblet cell density. still poorly understood.23
• Eyelid Margin Examination: With a focus light and Efficacy. Topical preparations are very effective for tear
magnifying source, carefully examine the eyelid margin stimulation and reducing inflammation, with 81.8% of dogs
to identify deficiencies of the lipid component, which showing improvement (Figure 7, page 20).24,25 Dogs with a
often occur secondary to blepharitis (Figure 6) or mei- STT < 2 mm/min respond with increased tear secretion in
bomianitis. approximately 50% of cases, while dogs with a STT ≥ 2 mm/
min have an approximately 80% chance of responding.18
MEDICAL MANAGEMENT OF KCS Formulation. CsA is available as Optimmune 0.2% oph-
Primary medical therapy of both quantitative and qualita- thalmic ointment (merck-animal-health-usa.com). Com-
tive KCS consists of tear stimulants and tear replacements. pounded formulations are available in 1% and 2% corn or
Topical antibiotics and anti-inflammatory drugs are also
commonly used.
Dogs with KCS may have increased sensitivity to pain
associated with topical medications, because abnormal PTF
cannot provide a reflex dilution effect. This may be espe-
cially problematic with frequent application of tear replace-
ment medications that contain preservatives; some artificial
tear products are available without preservatives, but the
lack of preservatives requires single-use ampules, which
most owners find inconvenient.
In most patients with KCS, topical therapy is required
indefinitely. Clients should be educated about the chronic-
ity of KCS and the necessity of lifelong therapy.

Tear Stimulation
1. Cyclosporine A (CsA) Figure 6. Four-year-old castrated male Chihuahua with
Mechanism of action. Cyclosporine is an immunomodu- acute blepharitis.
lator that blocks normal production of interleukin-2, which

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| Diagnosis & TreaTmenT of KeraToconjuncTiViTis sicca in Dogs

Efficacy. May be used to stimulate tear

production in cases of neurogenic (quan-
A B titative) KCS. These cases are diagnosed
when ipsilateral dry nose is present in
conjunction with a low result on STT.
Formulation. 1% or 2% solutions
Therapeutic recommendations. Sprin-
kle 1 to 2 drops of 2% pilocarpine per
10 kg on top of food Q 12 H. System-
ic administration of pilocarpine is pre-
ferred because it can be irritating when
applied topically.28
Figure 7. Seven-year-old spayed female miniature pinscher. Note corneal Note that pilocarpine has a narrow
vascularization and pigmentation; STT was 7 mm/min (A). Same patient 3 therapeutic window, and while some cli-
months after topical CsA therapy; note resolution of corneal vascularization nicians advocate increasing the number
and thinning of pigment (B). of drops applied to food by 1 drop each
day until systemic adverse effects are
olive oil solutions; they may be more effective, but may also observed—such as vomiting, diarrhea, ptyalism, anorexia,
be more irritating to the eye. and bradycardia—we prefer to avoid these effects by only
Therapeutic recommendations. Apply ¼-inch strand of increasing the total dose by 1 or 2 drops before consider-
topical CsA Q 12 H, with a recheck STT in 1 month. For ing pilocarpine ineffective. Client education about adverse
optimal results, perform the STT approximately 3 to 4 H effects is important.
after application of CsA. Treatment failure can be diag-
nosed only after 12 weeks of consistent topical application. Tear Replacement
If treatment fails, attempt treatment Q 8 H or initiate treat- Tear replacement therapy provides lubrication until tear
ment with tacrolimus. stimulants are effective. Lifelong tear replacement therapy
With long-term use, CsA decreases corneal pigmentation may be needed in dogs that never respond to CsA or tacro-
and vascularization, even in patients that do not experience limus. These medications are available as solutions, gels,
increased tear production; therefore, its use is often con- and ointments, and have a wide variety of constituents.
tinued in these patients.18,24
1. Artificial tear solutions commonly contain 0.1% to
2. Tacrolimus 1.4% polyvinyl alcohol. Artificial tear solutions are useful
Mechanism of action. Tacrolimus has a similar, but more for removing debris and mucus from the ocular surface;
potent, mechanism of action compared with that of CsA. however, they are not feasible as monotherapy in most
Efficacy. Patients that are unresponsive to CsA may dogs with KCS due to the need for frequent application in
respond to tacrolimus.26,27 order to achieve adequate lubrication.
Formulation. Tacrolimus is generally compounded to a
0.03% ophthalmic aqueous suspension; however, formula- 2. Cellulose-based solutions/gels and viscoelastic prod-
tions may vary. ucts are more viscous and have slower evaporation times
Therapeutic recommendations. Apply 1 drop of topical than artificial tear solutions. They require application Q 4 to
tacrolimus Q 12 H, with a recheck STT in 1 month. Continue 6 H. Examples of cellulose-based solution and viscoelastic
treatment for several months before considering treatment products are hydroxypropyl and hyaluronate, respectively.
failure. In addition to increasing tear production, tacrolim-
us may decrease clinical signs, such as pigmentation asso- 3. Artificial tear formulations containing petrolatum,
ciated with chronic KCS, even if tear production does not mineral oil, or lanolin are the most viscous products
increase, but no long-term studies exist. and provide long-term lubrication, but can result in debris
Tacrolimus use for treating KCS in dogs is off-label; there- accumulation. They are best suited for patients with:
fore, the U.S. Food and Drug Administration approved • Lipid layer deficiencies
therapy—CsA 0.2% ophthalmic ointment (Optimmune)— • Lagophthalmos (administered prior to sleep)
should be used as first-line treatment, with tacrolimus • Owners who will be absent for long periods.
reserved for cases unresponsive to CsA.
Antibiotics
3. Pilocarpine A severe, mucopurulent discharge suggests a secondary
Mechanism of action. Parasympathomimetic drug (stimu- bacterial infection. Generally, use a broad-spectrum oph-
lates or mimics the parasympathetic nervous sytem). Upreg- thalmic antibiotic, such as triple antibiotic ointment (neo-
ulation of parasympathetic receptors secondary to denerva- mycin/bacitracin/polymyxin B) Q 6 to 8 H for approxi-
tion results in increased sensitivity of the lacrimal system mately 2 weeks. If empirical treatment fails to resolve the
to pilocarpine when compared with the rest of the body.9 discharge, perform culture and sensitivity.

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 Diagnosis & Treatment of Keratoconjunctivitis Sicca in Dogs |
Ulcer Therapy
While superficial, uncomplicated ulcers can be
treated with triple antibiotic ointment, CsA, and
lubricants, ulcers secondary to KCS are usually
complicated and require more intensive therapy.
1. Perform culture and cytology on stromal ulcers
and ulcers with a cellular infiltrate.
2. Apply topical antibiotics Q 2 H to infected
ulcers until the cornea stabilizes. Appropriate
antibiotics include:
• Ciprofloxacin 0.03% ophthalmic solution, or
other ophthalmic fluoroquinolones, used alone
or
• Tobramycin 0.03% ophthalmic solution and
cefazolin (33 mg/mL in artificial tear solution).
3. Use topical atropine to dilate the pupil and
decrease ciliary spasm, even though it is associ-
ated with decreased tear production. If the patient
remains uncomfortable while on atropine therapy,
the addition of oral NSAIDs may be considered.
4. Consider conjunctival graft placement in
addition to KCS therapy and frequent antibiotic
therapy for deep ulcers.
Anti-Inflammatory Agents
Anti-inflammatory therapy may be useful if conjunctival
inflammation is severe, possibly occluding lacrimal excre-
tory ducts. Corticosteroids can be used on a short-term
basis (1–4 weeks); discontinue if patient is nonresponsive.
Only consider using them, though, in animals with no
uptake of fluorescein dye.
Apply topical prednisolone acetate 1% or dexamethasone
0.1% topically Q 6 to 8 H. Use caution when using topical
corticosteroids because dogs with KCS can develop ulcer-
ative keratitis, infection, and keratomalacia.
Mucolytics
If a patient with KCS has copious mucopurulent discharge,
acetylcysteine 5% is often administered; however, its use is
not common due to its expense and toxicity to the epithe-
lium. In addition, the mucous layer provides some protec-
tion to the cornea. Frequent flushing with sterile eyewash,
instead, simply removes mucus without side effects.
SURGICAL MANAGEMENT OF KCS
After 3 to 6 months of medical therapy with no response,
surgical treatment for KCS can be considered. Surgery is
not always successful and, even when it is, patients often
need ongoing topical therapy.29
Treatment of Choice
Parotid duct transposition—in which the parotid duct and
papilla are dissected free of the oral mucosa, mobilized,
and transposed to the inferior cul-de-sac—is the surgical
treatment of choice. Open and closed methods have been
described.
tvpjournal.com
Challenges
This surgery is often performed by a board-certified oph-
thalmologist due to the difficulty of the procedure in some
dogs and often complicated aftercare. Potential complica-
tions include severance of the duct, occlusion of the duct
secondary to scar formation, development of white miner-
al crystalline corneal deposits, facial dermatitis, periocular
pyoderma, and excessive saliva production.
PROGNOSIS & MONITORING
Prognosis depends on the underlying etiology of KCS and
the patient’s response to treatment (Table 2). If KCS does
not respond to medical therapy, the prognosis is worse for
vision retention. In addition, most patients will require life-
long therapy with topical immunosuppressive medications.
Recently, chronic keratitis treated long-term with tacroli-
mus or CsA has been tenuously associated with increased
risk for corneal squamous cell carcinoma.30 However,
because the study was retrospective, clinical data are lack-
ing, and KCS alone may have resulted in a predisposition to
this condition. While this study is interesting, KCS should
be treated as described in this article.
Dogs with a diagnosis of KCS should be evaluated every
6 to 12 months to assess effect of treatment and progres-
sion of disease. n
CsA = cyclosporine A; KCS = keratoconjunctivitis sicca;
PTF = precorneal tear film; STT = Schirmer tear test; STT1
= Schirmer tear test 1; TBUT = tear film breakup time
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Lori J. Best, DVM, is a first-year oph-
thalmology resident at University of Ten-
nessee College of Veterinary Medicine.
She received her DVM from Colorado
State University and completed her small
animal rotating internship at University of
Tennessee.
Diane V.H. Hendrix, DVM, Diplomate
ACVO, is a professor of ophthalmology at
University of Tennessee College of Vet-
erinary Medicine. She received the Zoetis
Distinguished Veterinary Teaching Award
in 2013. Dr. Hendrix received her DVM
from University of Tennessee and com-
pleted her residency in comparative ophthalmology at Uni-
versity of Florida.
Dan A. Ward, DVM, PhD, Diplomate
ACVO, is a professor of ophthalmology at
University of Tennessee College of Vet-
erinary Medicine. He received the Pfizer
Distinguished Professor Award in 2012.
Dr. Ward received his DVM from Uni-
versity of Tennessee and completed his
ophthalmology residency, PhD in phar-
macology, and postdoctoral work in clinical pharmacology
at University of Georgia.
22 Today’s Veterinary Practice July/August 2014
VETROPOLYCIN®
(bacitracin-neomycin-polymyxin)
Veterinary Ophthalmic Ointment
NADA # 065-016. Approved by FDA.
WARNING: Do not use this product as a pre-surgical
ocular lubricant. Adverse reactions of ocular irritation
and corneal ulceration have been reported in association
with such use.
VETROPOLYCIN® HC
(bacitracin-neomycin-polymyxin-
hydrocortisone acetate 1%)
Veterinary Ophthalmic Ointment
NADA # 065-015. Approved by FDA.
CONTRAINDICATIONS: Ophthalmic preparations
containing corticosteroids are contraindicated in the
treatment of those deep, ulcerative lesions of the cornea
where the inner layer (endothelium) is involved, in fungal
infections and in the presence of viral infections.
WARNINGS: All topical ophthalmic preparations
containing corticosteroids with or without an
antimicrobial agent, are contraindicated in the initial
treatment of corneal ulcers. They should not be used
until the infection is under control and corneal
regeneration is well under way. Clinical and experimental
data have demonstrated that corticosteroids
administered orally or by injection to animals may
induce the first stage of parturition if used during the last
trimester of pregnancy and may precipitate premature
parturition followed by dystocia, fetal death, retained
placenta, and metritis. Additionally, corticosteroids
administered to dogs, rabbits, and rodents during
pregnancy have resulted in cleft palate in offspring.
Corticosteroids administered to dogs during pregnancy
have also resulted in other congenital anomalies,
including deformed forelegs, phocomelia, and anasarca.
THE INfORmATION bELOW APPLIES TO bOTH
VETROPOLYCIN AND VETROPOLYCIN HC.
STERILE - ANTIbACTERIAL
CAUTION: Federal law restricts this drug to use by or on
the order of a licensed veterinarian.
PRECAUTIONS: Sensitivity to these ophthalmic
ointments is rare, however, if a reaction occurs,
discontinue use of the preparation. The prolonged
use of antibiotic-containing preparations may result in
overgrowth of nonsusceptible organisms including fungi.
Appropriate measures should be taken if this occurs. If
infection does not respond to treatment in two or three
days, the diagnosis and therapy should be reevaluated.
Animals under treatment with VETROPOLYCIN HC
(bacitracin-neomycin- polymyxin with hydrocortisone
acetate 1 %) should be observed for usual signs of
corticosteroid overdose which include polydipsia,
polyuria and occasionally an increase in weight. Use
of corticosteroids, depending on dose, duration, and
specific steroid, may result in inhibition of
endogenous steroid production following drug
withdrawal. In patients presently receiving or recently
withdrawn from systemic corticosteroid treatments,
therapy with a rapidly acting corticosteroid should be
considered in unusually stressful situations. Care should
be taken not to contaminate the applicator tip during
administration of the preparation.
ADVERSE REACTIONS: Itching, burning or
inflammation may occur in animals sensitive to the
product. Discontinue use in such cases. SAP and
SGPT (ALT) enzyme elevations, polydypsia and
polyuria have occurred following parenteral or
systemic use of synthetic corticosteroids in
dogs. Vomiting and diarrhea (occasionally
bloody) have been observed in dogs.
Cushing’s syndrome in dogs has been
reported in association with prolonged or
repeated steroid therapy.
Manufactured for:
Dechra Veterinary Products
7015 College Boulevard,
Suite 525
Overland Park, KS 66211
866-933-2472
tvpjournal.com
 Dechra
ophthalmic

o i n t m e n t s

a r e ba c k

Now you can treat your canine and feline patients with
the trusted ophthalmic products, VETROPOLYCIN®
(bacitracin-neomycin-polymyxin) and VETROPOLYCIN® HC
(bacitracin-neomycin-polymyxin-hydrocortisone acetate 1%), that
are FDA-CVM approved for use in dogs and cats. The
choice is clear. Contact your Dechra Representative or
your Veterinary Distributor
for more information.

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from trained Veterinary Professionals. | 866-933-2472

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As with all drugs, side effects may occur. In field studies, the most common
side effects reported were ocular itching, burning, or inflammation in animals
sensitive to the product. Prolonged use may result in the overgrowth of non-
susceptible organisms including fungi. VETROPOLYCIN ONLY— Do not use
as a pre-surgical ocular lubricant. VETROPOLYCIN HC ONLY— This product
is not for use in animals with corneal ulcers, fungal infections, or viral
infections. Patients should be monitored for signs of corticosteroid overdose.
The safe use of this product has not been evaluated in pregnant animals. Refer
to the prescribing information for VETROPOLYCIN and VETROPOLYCIN HC for
complete details or visit www.dechra-us.com.

Dechra Veterinary Products, 7015 College Blvd., Suite 525, Overland Park, Kansas 66211, 866-933-2472 www.dechra-us.com