Updated information on ophthalmology

Transcription

Editorial
Updated information on ophthalmology
This special issue of the European Journal of Companion Animal Practice dedicated to veterinary ophthalmology can be
considered as sign of the development of the discipline in Europe. If we consider that 15% of companion animal patients
presented in general practice exhibit an ocular /adnexal disease, we must admit how essential ocular disease is, not only
for specialists, but also for the general practitioner. Therefore, access to updated scientific information is important in
order to give our patients the best treatment.
It is a fact that American veterinarians were the first to organize the specialty in modern history. However, we
should not forget that Europe has rich ophthalmology traditions through the past centuries, with pioneers who made
significant contributions to the discipline. From the ancient Greeks with treatises as Hippiatrica, the Romans and the
Italians, focus was mainly aimed at ophthalmology of large animals or at comparative ophthalmology (i.e. Leonardo
da Vinci). The critical period in the development of veterinary ophthalmology in Europe can be placed at the begining
of the 19th century. Considering this period, some of the more famous names should be mentioned: Bayer and Überreiter
from Austria, Nettleship and Gray from the United Kingdom, Jakob from Netherlands, Nicolas and Leblanc, authors
of textbooks in veterinary ophthalmology, from France, Berlin and Möller from Germany, Berrar from Hungary and
Magnusson from Sweden. Plus many others.
As previously mentioned, the first organization in the specialty was in the US. William G. Magrane was the instigator
of the foundation of the American Society of Veterinary Ophthalmology (ASVO) in 1957. The American College
of Veterinary Ophthalmologists (ACVO) was recognized in 1970. Ten years after came the idea of establishing an
international society (ISVO), which was formed during the world (WSAVA) congress in Barcelona, Spain.
In Europe, several countries already had their national ophthalmology societies. A step forwards was the founding
of the European society (ESVO), which was established in 1985. It is now a large and a very active association,
with activities mainly concentrated on organization of an annual meeting and the maintenance of a website with
information for veterinarians with an interest in ophthalmology. The next annual meeting will be held in Versailles
(near Paris) May 14-18th, 2008.
Following recommendations of the Advisory Board of the European Union for specialisation with a high standard
scientific selection, the ISVO decided to initiate the foundation of a European College of Veterinary Ophthalmologists
(ECVO). This College was officially registered in 1992. Today, the College has 58 diplomates. Currently, the ECVO
annual meetings are organized together with ESVO. Attendance by members of ECVO, ESVO, ISVO and national
specialty groups increases year after year. Thus, the last meeting in Genoa, Italy was very successful with a number of
delegates around 300.
Another role of ECVO is to organize education, training and qualification of panellist veterinarians to perform eye
certification. The goal is to harmonize certification for detection of inherited ocular diseases on a European basis. This
specific aspect is covered in one of the articles in this ophthalmology issue.
This brief introduction shows the increasing activity and significance of veterinary ophthalmology, and reflects the
need for a current stream of updated information. Thus, it is our hope that the present issue of EJCAP will be of interest
to the readers, being general practitioners with an interest in ophthalmology or more specialized ophthalmologists.
Maurice Roze
ISVO President
Ellen Bjerkås
ECVO and FECAVA past President
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OPHTHALMOLOGY
Avian ophthalmology
A. Bayón1, RM. Almela2, J. Talavera1
SUMMARY
Ophthalmology of birds has become an important part of avian medicine. The principal groups of birds that
veterinary ophthalmologists examine in their consultations include cage birds, sport, zoo and wildlife birds.
Knowledge on anatomical and physiological peculiarities of the eyes of these species will help in the interpretation
of the ocular investigation and in reaching appropriate diagnoses. Some of the most important differences that can
be outlined in bird eyes, compared to mammal eyes, include the small ocular size of some species and different
morphologies of the eyeball depending on the species. Likewise, the open orbit, voluntary contraction of the pupil
(striated sphincter muscle of the iris), ossicles in the sclera, avascular retina and the presence of the pecten protruding
into the vitreous chamber (vascular structure that nourishes the retina). Ophthalmic investigation includes a physical
ocular examination and complementary techniques, such as tonometry, ophthalmoscopy, electroretinography
and ultrasonography, among others, in order to identify the ocular lesions and to evaluate the severity. The
most frequent ocular diseases reported include malformations (palpebral agenesia, microphthalmia, cataracts),
primary or secondary inflammatory diseases of the eyelids and conjunctiva (poxvirus, chlamydia), trauma (ocular
haemorrhages, uveitis, cataracts, chorioretinitis), neoplasms and nutritional disorders (vitamin A deficiency).
ducks, geese, swans; Falconidae: falcons, sparrow-hawks,
eagles; Strigidae: eagle owl, barn owls) and those used in sport
(Columbiformes: pigeons).
This paper was commissioned by FECAVA for
publication in EJCAP.
INTRODUCTION
Prevalence of ocular diseases in birds, has been reported to be
7,6 %, and in the case of birds of prey, it is even higher, up to
14 - 26 % [2, 22]).
Over the last 20 years birds have become an important part of
veterinary ophthalmology consultations, not only because they
are frequently kept as pets, but also because there is an increasing
awareness of the environment and the conservation of nature
and its species. Good vision is especially important in birds due
to the direct influence on flight, feeding and breeding.
Basically, the morphology of the birds eyes, as well as their
physiology are similar to that of mammals, though certain
peculiarities exist that must be considered in order to carry out
a correct interpretation of the ocular examination. In addition, it
is important to consider that systemic diseases with ocular signs
are just as important in birds as in mammals.
The principal groups of birds include: domestic birds
(Psittaciformes: macaws, parrots, parakeets, cockatoos, nymphs;
Passeriformes: canary, mine), those living in zoological gardens
(Psittaciformes: parrots, parakeets) and wild birds (Anseriformes:
Generally, to allow a precise diagnosis, the same methods and
equipment for ocular examination that are used in mammals are
also used in birds, though with the limitations of the small ocular
size of some birds.
1) A. Bayón DVM PhD Dipl. CLOVE, RM, J. Talavera DVM PhD, Department of Animal Medicine and Surgery, Faculty of Veterinary Medicine, Murcia
University, 30100 Espinardo. Murcia. Spain. E-mail abayon@um.es.
2) Almela DVM, Veterinary Clinical Hospital, Murcia University, 30100 Espinardo. Murcia. Spain.
1
Avian ophthalmology - A. Bayón, RM. Almela, J. Talavera
Fig. 1 The skull of an owl illustrating the orbit with tubular shaped
exposed eye.
Fig. 2 Iridocorneal angle of an owl
This paper describes the anatomical and physiological
characteristics of the bird’s eyes, methods of ocular examination
and the most frequent ocular diseases.
segment though remaining concave . Globose shape is typical
for many diurnal birds, since they need high resolution for long
distances (diurnal birds of prey, insectivorous, ravens ...).
Tubular: in which the intermediate concave segment
elongates anteroposteriorly, forming a tube, before
joining the posterior segment at a sharp angle. The
cornea is at the front. This shape is typical of owls (Fig. 1).
Characteristics of birds visual function
The sensory organ of vision in birds is highly specialised for
adjustment to their living conditions, their visual acuity being 2
to 8 times higher than that of mammals. Their visual fields are
up to 360 º, the range of stereopsis is 0 º to 70 º, the maximum
spatial frequency (skill to distinguish a certain movement in
simple images) is over 160 images / second (10-15 in humans) and
a minimal detection of movements over 15 º/hour (movements
that are performed in a very slow way) [6, 21].
The extraocular muscles are rudimentary, thus ocular motility
is limited in comparison with mammals. There are 4 straight
muscles, 2 oblique ones, 1 pyramidalis muscle and 1 quadratus
muscle (they replace the retractor bulbi muscle in mammals,
which are innervated by cranial nerve VI and move the
nictitating membrane). Portions of Ist-VIth cranial nerves have
an intraorbital course, with the optic nerve being quite short.
The vascular plexus is in the ventrolateral zone of the orbit [15,
39, 18].
The perception of ultraviolet light is a common skill in the diurnal
birds due to the rods in the retina having a special sensitivity to
ultraviolet light. This ability plays a very important role in features
like bird communication, camouflage and orientation [6].
The infraorbital sinus and part of the cervicocephalic air sac
system are situated laterally, subcutaneous to the nasal area and
rostroventral to the eyes in several groups of birds (psitacidas,
storks ...). The sinus can be connected with pneumatised sections
of the skull bones that spread towards the upper parts of the
beak, jaw and orbit [15, 39].
Anatomy and ocular physiology
Orbit and globe
The globe is big compared to body size, with a posterior segment
disproportionately larger than the anterior segment (Fig. 1). The
back of the globe fits narrowly in the orbit, though many temporal
and dorsal zones are unprotected by bone. The diameter of the
equator of the globe exceeds the diameter of the anterior bony
orbital rim in many species. The orbits are separated only by a
thin bony structure or a septum of connective tissue [22].
Eyelids and ocular annexes
Birds have an upper and a lower eyelid plus a nictitating
membrane. The lower eyelid is more mobile than the upper one,
which allows it to cover a larger part of the eye during blinking.
It also has a fibroelastic tarsal plate. Near the palpebral margin
there are modified feathers for protection or for tactile function.
On hatching, eyelids are well developed and the palpebral
fissure is open in precocial birds (species in which the young
are relatively mature and mobile from the moment of hatching)
while the lids are sealed together and incompletely developed
in altricial birds (species hatched with lack of hair or down, and
which must be cared for by the adults). The time of opening
of eyelids in altricial birds is variable: in the case of cockatoos
it happens between 10-17 days after hatching and in macaws
17-26 days. The palpebral separation starts centrally, progressing
The shape of the eyes is supported by the 10 to 18 scleral ossicles
in the intermediate segment, as well as by the hyaline cartilage
present in the posterior segment of the sclera. There are three
basic shapes of the eyeball [15, 39]:
Flat: presenting with a short antero-posterior axis, flat or concave
ciliary region, convex cornea and hemispherical posterior
segment, this is typical of the majority of birds.
Globose: the ciliary region protrudes further from the posterior
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EJCAP - Vol. 17 - Issue 3 December 2007
medially and laterally. There are no meibomian glands at the
tarsal edge of the eyelids [15, 39].
and Cramptons muscles), which compress the annular cushion
[15, 39]). The ciliary processes are attached to the equatorial lens
capsule. Crampton’s muscle has connections with the peripheral
cornea, being able to produce changes in the corneal curvature
when it contracts. In several diving birds, the changing shape of
the lens produced by miosis is part of the accommodation. The
iris is generally brown, though other colours can also be present.
The stromal pigments of the iris are composed of carotenoids,
purines and pteridines; in some species the coloration of the iris
can change with age and sex. In red tail falcons there is a colour
shift from yellowish to grey when the birds reach 4 years of age;
in araraunas the iris changes from brown to grey when the birds
are one year old; in Amazons the iris changes from brown to
red or orange when they grow up; in cockatoos there is sexual
dimorphism, the females having a red coloured iris and males
dark brown or black, while in the young cockatoos the iris is
brown in both sexes.
The nictitating membrane is well developed and mobile; it is thin
and translucent and moves over the globe from a dorsonasal
position towards a ventrotemporal position, dragged by the
pyramidal muscle that originates from the back of the sclera
turning around the optic nerve and passing through a sling
formed by the quadratus muscle. The temporal top edge of the
nictitating membrane is firmly adherent to the underlying sclera
and is associated with the conjunctiva; while the pyramidalis
tendon is inserted along the lower nasal edge. The free edge
of the nictitating membrane has a marginal pigmented fold or
edging that facilitates the distribution of tears over the ocular
surface during blinking ]15, 39].
The iris muscles are mainly striated, with smooth muscles
appearing only in smaller proportion. This allows voluntary
contraction of the pupil. The striated circumferential muscle
seems to be the primary pupillary sphincter in all species. The
circular pupil responds rapidly to accommodation and voluntary
control, as seen for instance in stress during handling. There
is a direct pupillary reflex, but no consensual one, due to the
complete decussation of the optical nerve axons. A small degree
of anisocoria can be normal. The iridocorneal angle is well
developed (Fig. 2) [15, 25, 39].
Posterior segment
The vitreous body is large and transparent. The fundus is
normally grey or reddish in colour, with the choroidal vessels
not always visible. The optic disc is long and oval, but it is often
difficult to observe on ophthalmoscopy due to the pecten. The
pecten is a vascular prominence emerging from the retina and
protruding into the vitreous, of variable comb-like shape and
black in colour (Fig. 3). It is involved in the nutrition of the retina
and plays a role in intraocular acid – base balance, production
Fig. 3 Typical fundus oculi of a nocturnal raptor: the choroidal
vessels overlying the white sclera and the ventronasal periphery of
the pecten.
Fig. 4 Biomicroscopy examination in a duck.
The Harderian gland, situated near the base of the nictitating
membrane, is the main source of tears in birds. A wide canal, runs
from the gland and opens inside the conjunctival sac between
the eyeball and the nictitating membrane. The lymphoid tissue
associated with the conjunctiva, together with the Harderian
gland plays an important role in the humoral immunological
defence of the ocular surface. The lacrimal gland is positioned
inferotemporal to the globe (absent in penguins and owls). In
some birds, such as budgerigars, a nasal or salt gland lies in the
orbit dorsomedial to the globe. The duct of this gland penetrates
the frontal bone and enters the nasal cavity.
Anterior segment
Birds’ corneas are histologically similar to those of mammals.
The lens is soft and almost spherical in nocturnal birds, or
has a flattened anterior aspect in diurnal species, including
companion birds. An annular pad lies under the lens capsule in
the equatorial region, and can be separated from the centre of
the lens during cataract surgery. The power of the lens can be
increased by contraction of the mid-striate ciliary muscles (Brucke
3
of intraocular fluids and mechanically shakes the vitreous fluid
during ocular movements, facilitating the movement of fluids
inside the eye [4]).
The retina is avascular and without a tapetum. The type of
photoreceptors and the density vary among birds, but generally
rods and cones or double cones with oil droplets are present.
According to the specialisation of the retina to enhance the
resolution or sharpness, birds can be classified as:
Afoveate. These have an area centralis or visual line usually
present when there is absence of fovea), seen in the majority of
the domestic birds and some birds of land and water.
Monofoveate, having a central (majority of birds) or temporal
fovea (owls, swifts) with or without a visual line around the
fovea.
Bifoveate, with a principal central fovea and a temporal subsidiary,
with or without a visual line of enhancement of the sharpness
between the foveas (falcons, eagles, several passeriformes,
others that hunt during flight).
Fig. 5 Schirmer tear test in a little owl.
Colour vision is well developed and several species can detect
light in the ultraviolet range [22, 27].
Ophthalmological examination
The ophthalmologic examination in birds is similar to what is
performed in mammals with some peculiarities derived from the
anatomical and physiological differences. In general, the ocular
examination will follow a general examination of the animal.
First a complete clinical history must be gathered, as well as a
study of the habitat and nutrition. While the clinical history is
being taken, it is recommended that the animal should be kept
in its cage, in order to evaluate its visual acuity and state of
alertness as well as its general behaviour while being under the
control of the owner.
Fig. 6 Corneal ulcer stained with fluorescein in a jaco.
Ocular examination:
Inspection: Ideally, the ophthalmologic examination should be
carried out without the use of sedatives or anaesthesic agents,
since this can interfere with behaviour as well as with lacrimation
and reflexes.
The examination of the anterior segment and periocular
structures is carried out by means of a beam of light, otoscope
with a magnifying glass, direct ophthalmoscope (with a lens
of +25D or +40D) and a slit-lamp biomicroscope (Fig. 4). The
latter is necessary for examining the small eyes of some species
of birds since it allows magnification and visualisation of small
injuries. Likewise, expert help in handling birds is useful to hold
the animal whilst the clinician works the equipment [15].
Ocular reflexes: In birds the palpebral reflex is evaluated by
touching skin areas on the lateral and medial edge of the eyelid.
The nictitating membrane goes over the cornea quickly and
completely in normal birds; both eyelids will move easily, though
the lower one covers a larger area of the corneal surface than
the upper one. The globe does not retract and the eyelids may
not close completely in normal birds. The direct pupillary light
Fig 7. Corneal ulcer stained with fluorescein and examined with
cobalt blue light.
4
reflex may be evaluated by the use of a beam of bright light in a
dimly lit room [15, 18, 39].
Spontaneous pupil movements may happen due to situations
of excitement because of the voluntary control. Indirect or
consensual reflexes are not expected in birds due to the
complete decussation of the fibers of the optical nerve.
However, sometimes small responses can be provoked due to
the fact that the eyes are separated by a very thin septum. The
menace reaction is weak in birds with normal vision, thus it has
very little diagnostic importance. The conjunctional movements
of the eyes are minimal in the majority of the birds due to the
limited ocular motility [15].
The corneal reflex, though it is not routinely examined in birds,
is observed by means of blinking, movement of the nictitating
membrane and the negative response to external stimuli;
however, the eyeball does not retract due to the absence of the
retractor muscles of the globe.
Fig. 8 Tonometry with Tonopen® in a raptor.
Schirmer tear test: it is carried out mainly in birds of great size
(Fig. 5). In a study carried out in 255 birds of 42 species, Schirmer
tear test values have been obtained for Psittaciformes, being
3.2-7.5 mm/min without topical anaesthesia and 1.7-4.5 mm/
min with topical anaesthesia; in Falconiformes 4.1-14.4 mm/min
without anaesthesia and 2-4.2 mm/min with topical anaesthesia;
in Accipitriformes 10.7-11.5 mm/min without anaesthesia and
3.6-5.9 mm/min with topical anaesthesia [19, 39].
Staining: Topical fluorescein sodium, together with the cobalt
blue light reveals damage to the cornea (Fig. 6 and 7) or possible
obstructions in the lacrimal system. Staining with Rose Bengal
is carried out for the diagnosis of keratitis (it stains keratinized
epithelium) [39].
Cytology and cultures: These procedures may be necessary
when an infectious or parasitic problem is suspected (mites in the
periocular structures) and there is an ocular discharge. If ocular
mucus or mucopurulent secretion is observed, a sterile sample
for isolation of bacteria, mycoplasmas or virus is indicated. For
the isolation of Chlamydia it is preferable to gather samples
from the choanas, trachea or cloaca [15].
Fig. 9 Tonometry with Tonovet®.
The most frequent flora present in the conjunctival sac in
psittacines includes Gram positive bacteria (Staphylococcus
epidermidis Staphylococcus aureus, β-hemolytic Streptococcus,
Corynebacterium sp.); Gram negative bacteria are rare and only
reported to be isolated from 1 % of samples [40].
Corneal cytology is indicated in superficial erosions and progressive
ulceration associated with infiltrations of inflammatory cells. To
take a sample for cytology a topical anaesthetic is instilled (1 or
2 drops). After 60 seconds the sample can be obtained then the
smear stained with Giemsa or DiffQuick. One should be aware
that in birds topical anaesthetic can cause systemic toxicity and
even general anaesthesia.
Fig. 10 Intracameral injection of d-tubacurarine in a raptor in
order to induce mydriasis.
Tonometry: The equipment used to perform tonometry are
Tonopen® (applanation) (Fig. 8), Tonovet ® (rebound) (Fig. 9)
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Fig. 11 Indirect ophthalmoscopy.
Fig. 12 Electroretinography in a raptor, showing the placing of
electrodes.
Fig. 13 A Ultrasonography of a raptor’s eye showing normal
ocular structures. B. Color Doppler Ultrasonography showing
blood flow in the pecten (arrow). L, lens.
and Schiötz tonometer (indentation). In birds, the normal values
of intraocular pressure are as follows : In turkeys, 25 mm Hg
(applanation); in birds of prey, 11-16 mm Hg and in psittacines
20-25 mm Hg (applanation). In the study carried out by means of
Tonopen in 275 normal birds of 39 species the range of values is
between 9.2 and 16.3 mm Hg. The reproducibility of the values
is obtained with corneal diameters ≥9 mm, being limited in
corneal diameters <5 mm (20, 35). In large birds and by means
of the Schiötz tonometer, values of 15-17 mm Hg have been
obtained in falcons and 20 mm Hg in hens. Also the Tonovet has
been used in another study with 31 birds of prey, obtaining a
range of measures from 9 mmHg in small raptors and 40 mmHg
in large birds of prey [3].
mg/ml) (Fig. 10) (1, 22). A study in raptors proved the efficiency
of three curariform agents, obtaining the following results (25):
Vecuronium bromide topically (2 drops every 15 minutes): the
maximum reaction appears immediately after application, and
is effective for 4 hours .Alcuronium chloride causes mydriasis
of 3 hours’ duration, though in the study the majority of the
birds presented with palpebral paralysis and even paralysis of
the neck and hindlimbs in some birds. Pancuronium bromide
produces a very slight reaction.
Direct ophthalmoscopy is used most frequently, though it is
not the best in exotic birds, due often to the small size of the
eyes and also to the fact that the head of the clinician must
be close to the bird. When an injury is suspected, the indirect
ophthalmoscope can be used, since it allows exploration of a
very wide area of the fundus (with a reversed image) at a larger
distance from the clinician (Fig. 11). The lens required depends
on the size of the birds, from 20D-30D in large birds up to 90D
Direct and indirect ophthalmoscopy: The mydriasis necessary
for ophthalmoscopy in birds can be obtained by means of
general anesthesia with ketamine or by topical or intracameral
tubocurarine (d-tubocurarine chloride®, Sigma Chemical CO) (20
6
ophthalmology this noninvasive technique is used fundamentally
for ocular biometry and when the opacification of anterior
structures (cornea, anterior chamber, lens) prevent visualisation
of deeper structures (vitreous body and retina) (Fig 14). Likewise,
it offers information about diseases of the orbit (neoplasia,
foreign bodies). It can be carried out with general equipment or
special equipment for ophthalmology using linear transducers
of high frequency (7.5-11MHz). Colour Doppler ultrasonography
allows evaluation of vascularisation of the ocular structures.
Radiology is used in ophthalmology prior to other visual
techniques (ultrasonography, axial computerized tomography
and magnetic resonance) for the evaluation of the orbit and
cranium [15].
Axial Computerized Tomography provides detailed images
of the structures contained in the orbit (eyeball extraocular
muscles, optic nerve), as well as of the bones. It gives important
information for the diagnosis of orbital neoplasms, inflammatory
and traumatic diseases.
Fig. 14 Ultrasonography of a raptor with cataract, showing a
hyperechogenic lens (L).
Magnetic resonance: In small animals it is used fundamentally
in neuroophthalmology, due to the good resolution that it
provides for the evaluation of the soft tissues.
Ocular diseases
Congenital diseases
Palpebral malformations described (though infrequent) have
been partial agenesis of the top eyelid in birds of prey (peregrine
falcon) [16] and ankyloblepharon and cryptophthalmos (merging
of the eyelid margins) in nymphs [7].
The presence of microphthalmia can be the result of congenital
malformation or acquired phthisis bulbi. Bilateral microphthalmia
has been described in ducks, bilateral anophthalmia in
budgerigars and microphthalmia with presence of cataracts,
retinal dysplasia and retinal detachment in birds of prey [8,
15]. Phthisis bulbi has been observed frequently secondary to
uveitis, but is less evident than in mammals due to the presence
of the scleral ossicles. Therefore, the differentiation between
microphthalmia and phthisis depends on the clinical history and
the ocular examination [15, 39].
Fig. 15 Poxvirus in a canary.
in small species. The fundus of both eyes must be compared,
especially when some anomalies are present. The optic nerve
head is most often hidden under the pecten.
Corneal dermoids have been reported in a goose, in which
feathers grew out of the aberrant dermal tissue on the lateral
aspect of the globe. Unilateral corneo-conjunctival dermoid was
successfully removed from a blue-fronted Amazon parrot [39].
Fundus camera allows us to document posterior segment
diseases, including fluorescein angiography in large species. In
very small eyes the focal distance is not suitable.
Electroretinography is used for assessing retina function. It is
carried out on animals anesthetised by means of an intramuscular
combination of ketamine-medetomidine or by means of
inhalation anaesthesia, such as isofluorane. The authors carry
out the procedure by means of the same equipment as used in
mammals with a contact lens, monopolar Dawson Trick Litzkow
(DTL) fiber electrode (in very small eyes) and dermal electrodes.
The protocol is similar to the one established for dogs [28].
Ectropion and secondary exposure keratitis has been reported
in cockatiels.
Exophthalmos
Orbital diseases that cause exophthalmos are infrequent in
birds. If present, the anterior displacement of the globe can be
due to orbital trauma (fractures of the cranium); inflammation
(orbital post traumatic haemorrhage - very infrequent in
birds compared to mammals), inflammation of the Harderian
gland in psittacines, infections such as orbital abscesses that
BD and Doppler ultrasonography (Fig. 13A and B): in
7
Fig. 16 Periocular swelling associated with infraorbital sinusitis in
an African Grey Parrot.
Fig. 17 African Grey parrot with chlamydial conjunctivitis.
spread from the paranasal sinuses in Amazon and African
grey parrots, neoplasias such as lymphoreticular neoplasms,
adenocarcinoma and osteosarcoma in budgerigars, glioma of
the optical nerve, sarcomas, chromophobe pituitary adenoma
and medulloepithelioma in nymphs [1,11,30,32].
and protuberant lesions for Cnemidocoptes pilae in parakeets.
Vitamin A deficiency can cause conjunctival hyperkeratosis and
swelling of the eyelids similar to that caused by poxvirus [13,
39].
Treatment of poxvirus lesions should include topical antibiotic
ophthalmic ointments to reduce the incidence of secondary
infections with bacteria or fungus. Systemic antibiotics may also
be required in severely affected birds. Early lesions should be
flushed with dilute antiseptic solutions. Once scabs have formed
they should not be removed. It may be beneficial to soften the
scabs, however, with hot or cold compresses soaked in non
irritating baby shampoo. It has been reported that prophylactic
vitamin A supplementation of exposed birds decreases the
severity of infection [15, 39].
Treatment in cases of trauma and inflammatory diseases should
include systemic corticosteroid and anti-inflammatory drugs and
systemic and topical antibiotics (bacitracin-neomycin-polymyxin
B). If an orbital abscess is suspected systemic antibiotics should
be administered for 14 days. If this therapy fails to improve
the condition, an alternative antibiotic or reassessment of the
aetiology of the exophthalmos should be considered [15, 18].
If neoplasia is suspected or proved by biopsy or aspirate tests,
exenteration of the orbit is recommended, with enucleation and
removal of all orbital soft tissues. Before surgery, one should
assess the likelihood of metastasis or an association with primary
systemic disease or neoplasia elsewhere. Work-up should include
abdominal and thoracic radiography, haematology and serum
chemistry testing [15, 18].
Periocular swelling
Local or diffuse periocular swelling can progress from pathologies
that involve the eyelids, conjunctiva, infraorbital sinus or nasal
gland (in birds that have them).
Infraorbital sinusitis is frequent in psittacines, causing swelling
of the area medial and ventromedial to the eyeball (Fig. 16). It
is generally associated with diseases of the respiratory system.
The inflammation of the salt gland is seen as puffiness over the
globe and can be caused by ingestion of water with high levels
of sodium [15].
Palpebral and conjunctival neoplasms are not frequent. A
benign tumour of basophil cells has been reported in a parakeet,
histiocytic sarcoma in an owl, mastocytoma, cystadenoma in
jacos and subconjunctival hibernoma in a goose [39].
Eyelid disorders can be of traumatic or infectious origin, and
include lacerations, haemorrhages and abrasions. The most
frequently described causes of infectious eyelid diseases are
the following: blepharoconjunctivitis due to Staphylococcus
in Amazon parrots [34], fibrinopurulent blepharoconjunctivitis
secondary to Escherichia coli, Streptococcus spp. [9], Pasteurella
multocida [29], Actinobacillus spp. in waterfowl and Plasmodium
spp. in canaries, bilateral supraorbital abscesses due to
Pseudomonas spp in Amazon parrot [38] and poxvirus in dove,
Amazon parrot [12,24,31], canaries (Fig. 15) (14), mines, parrots
(31) and birds of prey, blepharitis due to parvovirus in geese
Conjunctivitis, keratoconjunctivitis and keratitis
Conjunctivitis can be classified clinically into three groups. The
first are those caused by strictly local factors, such as localised
conjunctival infection or foreign bodies. The second are those
in which conjunctivitis is a manifestation of periorbital or orbital
disease. These are mainly related to sinusitis. The third group
are those in which conjunctival hyperaemia is caused by a
septicaemia. Almost any organism causing systemic infection
can result in conjunctivitis. A careful examination of the bird
for upper respiratory disease is mandatory in determining the
causes of ocular discharge or conjunctival hyperaemia. Exposure
8
Conjunctivitis can also be secondary to poor hygienic sanitary
conditions due to the ammonia from faeces [15,39].
Treatment of conjunctivitis consists of administration of topical
antibiotics (bacitracin-polimyxin B, neomycin, tetracycline,
chloramphenicol) for 14 days. When respiratory signs exist in
addition an antibiotic should be administered parenterally. In
case of parasites, these can be removed with forceps under
topical anaesthesia. If this is impossible, the use of ivermectin
must be considered. Keratoconjunctivitis, a frequent ocular
disease in psittacines, can be caused by chlamydiosis, trauma
in the cage and deficiency of vitamin A. There have been
reported corneal crystalline deposits of unknown cause in 8.7
% of nymphs, parakeets and Amazons on necropsy. These
deposits have also been observed in Amazon parrots with
poxvirus. Bilateral deposits of cholesterol have been observed
in the corneal stroma in falcons (Fig. 18). Punctate keratitis
has been described in Amazons associated with sinusitis. The
lesions were bilateral, and the most common presenting signs
were blepharospasm and clear ocular discharge [15,39]. Keratitis
can be difficult to resolve, but, as a rule, topical antibiotics and
corneal bandaging techniques provide a sterile environment and
time for the corneal epithelium to heal. By extrapolation from
other species, anticollagenases should be used in deep ulcers,
especially in hotter climates, where corneal melting may be a
cause of rupture of the globe. Also, in the case of punctate
keratitis as well as antibiotic treatment the use of topical nonsteroid anti-inflammatories can be useful [15].
Fig. 18 Corneal degeneration in a Peregrine falcon.
to cigarette smoke, chemical fumes and other airborne
environmental toxins should always be considered in the
differential diagnostics of conjunctivitis, with or without signs of
upper respiratory disease [39].
Conjunctivitis in passerines can be caused by Newcastle virus,
paramyxovirus, poxvirus, cytomegalovirus, Streptococcus
spp, Erysipelothrix rhusiopathiae, Clostridium botulinum,
Mycobacterium avium serotype 2, Escherichia coli, Pseudomonas
aeruginosa, Bordetella avium, Chlamydophila psittaci (Fig.
17), Mycoplasma spp., Candida albicans, Aspergillus spp.,
herpesvirus, adenovirus,pneumovirus.
Uveitis
The principal causes of uveitis in birds include trauma, infections,
immunemediated inflammation and neoplasia [33,36]. A blunt
or sharp trauma can cause anterior and/or posterior uveitis,
frequently associated with haemorrhage (Fig. 19A and B). In
several studies carried out in birds of prey, hyphema was the
most frequent clinical finding, though also findings such as
hypopyon, fibrin clots, iridocyclodialysis (tearing of the iris) (Fig.
20), lens injuries and fractures of the scleral ossicles can be
The most frequent parasites are spirurids (Ceratospira, Oxyspirura)
in psittacines, mynahs; trematodes (Philophthalmus gralli),
nematodes (Thelazia in Senegal parrot; Setaria in passerines).
Figure 19. A. Hyphema in the anterior chamber in a raptor. B. The same eye seen with slit lamp.
9
Fig. 20 Iris rupture in a raptor.
Fig. 23 Anterior synechia, cataract and uveitis in an eagle.
Fig. 21 Tyndall effect in an owl with uveitis.
Fig. 24 Traumatic buphthalmos in an eagle.
Fig. 22 Intravitreal haemorrhage and white fibrin clots in a raptor.
Fig. 25 Traumatic cataract in a little owl.
10
present. Anterior uveitis can also develop secondary to corneal
ulcers as in mammals [2,22].
Ocular development anomalies such as microphakia,
development of lenses with abnormal material (lentoids as well
as dysplasia and detachment of retina) and hypoplasia of the
optic nerve have been described in birds of prey. Hereditary
cataracts have also been described in canaries (Fig. 28) with
an autosomal recessive model of transmission (Yorkshire and
Norwich canaries). Other aetiologies of cataracts include avian
encephalomyelitis, maternal vitamin E deficiency, trauma,
dinitrophenol (chicks) and chronic uveitis [15, 39].
Concerning infectious aetiologies of uveitis, the most important
are those secondary to viruses that affect birds, such as
encephalomyelitis, Marek’s disease and poxvirus. Septicaemia
due to any bacterial infection (Pasteurella multocida,
Salmonella, Mycoplasma gallisepticum) may cause uveitis.
Mycotic endophthalmitis has been associated with disseminated
aspergillosis and candidiasis in budgerigars. Toxoplasmosis has
caused chorioretinitis and blindness in canaries and raptors.
Clinical signs of the anterior uveitis in birds include photophobia,
blepharospasm, corneal oedema, Tyndall effect (Fig. 21), vitreous
opacity, hypotony or secondary glaucoma, miosis, dyscoria,
thickening of the iris or discoloration, rubeosis iridis and anterior
or posterior synechiae. In posterior uveitis, diffuse or focal retinal
oedema, haemorrhages near the pecten, retinal detachment
and vitreous opacity (Fig. 22) can be present. The visual function
can be diminished or abolished.
Lens opacities can be capsular, cortical and/or nuclear.
Hypermature cataracts can differ from the incipient ones by
their shrinking, capsular wrinkling and the presence of a deeper
anterior chamber. Luxation or subluxation of the lens (Fig. 29)
can accompany cataract primarily or as a secondary form.
Treatment of cataracts is, as in mammals, by means of
phacoemulsification, except for in very small eyes [17]. In birds
with very small eyes, complete blindness is not an exclusive
reason for the euthanasia since, for example, a canary blind from
bilateral cataracts can lead a normal life in its cage, providing
that the cage interior is not modified at all.
Sequelae of chronic uveitis include diffuse corneal oedema,
posterior synechiae causing pupillary occlusion and iris bombé,
anterior and posterior synechiae (Fig. 23), secondary glaucoma
(Fig. 24), cataracts (Fig. 25), retinal atrophy or detachment and
blindness (Fig. 26) [10].
Retinopathy and optic neuropathy
Retinal diseases include congenital anomalies, degeneration,
inflammation and detachment. Congenital retinal dysplasia has
been described in birds of prey (falcons fundamentally) [27].
Idiopathic degeneration has been reported in a budgerigar (37).
Trauma is the most frequent reason for injuries of the posterior
segment (Fig. 22) (26), especially in birds of prey, though it can
be associated with bacteraemia or viraemia. The chorioretinitis
lesions caused by Toxoplasmosis are easy to identify in birds of
prey (Fig. 30) [22].
Iatrogenic uveitis and reduction in intraocular pressure can be
mistaken clinically. The latter can appear during anaesthesia
in the same eye of decubitus in psittacines and birds of prey,
due to a larger pressure applied on the eye, provoking a forced
drainage of the aqueous humour [15].
Treatment of uveitis should include elimination of the cause,
control of inflammation, preservation of the pupil and prevention
and treatment of secondary glaucoma. Prescribe topical antibiotics
and topical and systemic anti-inflammatory agents (steroids and
non steroids) for symptomatic treatment of inflammation. It is
very important to watch out for systemic side effects (polyuria,
polydipsia, etc.). Mydriasis cannot be achieved by topical
therapy (e.g., atropine) in birds, and pupil preservation is best
accomplished by adequate control of inflammation [15,39].
Optic neuropathy can be associated with congenital anomalies
(hypoplasia of the optic nerve associated with cataract), trauma
(frequently provoking neuritis), neoplasia (chromophobe
adenoma of the pituitary gland causing compression of the optic
nerve, atrophy and blindness in parakeets and nymphs). The focal
or multifocal retinopathies and the optic neuropathies do not
interfere with vision, with only minor change in direct pupillary
light reflexes. Wide lesions in retina and optic nerve cause loss
of vision, variable degree of mydriasis and a deficiency in the
direct pupillary light reflex. Unilateral lesions cause anisocoria.
Cataracts frequently develop secondary to retinal degeneration.
The signs observed in the retina include depigmentation,
hyperpigmentation and loss of the choroidal vascular patterns
(Fig. 31). Intraretinal haemorrhages and haemorrhage around
the pecten can frequently be observed after ocular trauma, as
well as retinal oedema and detachment, which appears as grey
and slightly elevated areas. Acute traumatic retinopathy and/or
optic neuropathy are treated systemically with broad-spectrum
antibiotics and anti-inflammatory doses of corticosteroids
[2,15,22,39].
Glaucoma
Glaucoma can be secondary to uveitis and hyphema (Fig. 24).
It has been provoked, experimentally in birds maintained in
constant light or darkness. Primary glaucoma is not described in
birds due to the width of the iridocorneal angle. Buphthalmia is
not very severe in glaucoma, due to the inflexibility of the sclera
because of the ossicles. The safety and efficacy of the topical
and oral medications, routinely prescribed for mammals for
glaucoma, are unproven for birds. In severe cases, enucleation
of the eye or placement of a intrascleral prosthesis are the
treatments of choice in birds [15,39].
Cataracts
Cataracts in birds are those of congenital type and secondary to
nutritional deficiencies, trauma, age (senile cataracts) (Fig. 27)
and retinal degeneration [5,15,26, 39].
Blindness with normal pupil sizes and responses
Malformations, trauma, infections (bacterial, viral, parasitic and
fungal), intoxications (i.e. hexachlorophen causing reversible
blindness in parakeets) can cause central nervous system signs
11
[15]. Clinical signs include variable unilateral or bilateral blindness
with normal resting pupil sizes and pupillary light responses.
Other reported signs are disorientation, seizures and abnormal
behaviour. Therapy should be oriented to treat aetiology (i.e.
anti-inflammatory corticosteroid after trauma.)
REFERENCES
[1] ARNALL (L). - Anaesthesia and surgery in cage and aviary birds.
II. A regional outline of surgical conditions. Vet Rec, 1961;
73:173-178.
[2] BAYON (A), ALBERT (A), ALMELA (R.M.), TALAVERA (J), LÓPEZ
MURCIA (M.M.), SAGARMINAGA (J.L.). - Ocular disorders in
raptors in a 3-year-period (2002-2004). Proceedings ESVO-ECVO
Meeting, 2005; 117.
[3] BAYON (A), VECINO (E), ALBERT (A), ALMELA (R.M.), COZZI (A),
TALAVERA (J), FERNANDEZ DEL PALACIO (M.J.). - Evaluation
of intraocular pressure obtained by two tonometers and their
correlations with corneal thickness obtained by pachymetry in
raptors. Proceedings ESVO-ECVO Meeting, 2006; 154.
[4] BELLHORN (R.W). - Retinal Nutritive Systems in Vertebrates. Sem in
Avian and Exotic Pet Med, 1997, 6: 108-118.
[5] BELLHORN (R.W.) - Ophthalmologic disorders of exotic and
laboratory animals. Vet Clin North Am, 1973; 3:345-356.
[6] BENNETT (A.T.), CUTHILL (I.C.). - Ultraviolet vision in birds: What is
its function? Vis Res, 1994; 34:1471-1478.
[7] BUYUKMIHCI (N.C.), MURPHY (C.J.), PAUL-MURPHY (J), HACKER
(D.V.), LARATTA (L.J.), BROOKS (D.E.). - Eyelid malformation in
four cockatiels. J Am Vet Med Assoc, 1990;196:1490-1492.
[8] BUYUKMIHCI (N.C.), MURPHY (C.J.), SCHULZ (T). Developmental
ocular disease of raptors. J Wildl Dis, 1988, 24:207-213.
[9] CHEVILLE (N.F.), TAPPE (J), ACKERMANN (M), JENSEN (A). - Acute
fibrinopurulent blepharitis and conjunctivitis associated with
Staphylococcus hyicus, Escherichia coli, and Streptococcus sp. In
chickens and turkeys. Vet Pathol, 1988; 25:369-375.
[10] DAVIDSON (M.G.). - Ocular consequences of trauma in raptors.
In: MURPHY (C.J.), PAUL-MURPHY (J) (eds). Sem in Avian Exotic
Pet Medicine-Ophthalmology. Philadelphia, WB Saunders, 1997;
6:121-130.
[11] DUKES (T.W.), PETTIT (J.R.). Avian ocular neoplasia – a description
of spontaneously occurring cases. Can J Comp Med, 1983;
47:33-36.
[12] GRAHAM (D.D.), HALLIWELL (W.H.). - Viral diseases of birds of prey.
In: Fowler ME (ed). Zoo and Wild Animal Medicine. Philadelphia,
WB Saunders, 1981.
[13] JACOBSON (E.R.), MLADINICH (C.R.), CLUBB (S), SUNDBERG (J.P.),
LANCASTER (W.D.) - Papilloma-like virus infection in an African
gray parrot. J Am Vet Med Assoc, 1983; 183:1307-1308.
[14] JOHNSON (B.J.), CASTRO (A.E.) - Canary pox causing high mortality
in an aviary. J Am Vet Med Assoc, 1986;189:1345-1347.
[15] KERN (J). - Disorders of the Special Senses. In: ALTMAN (R.B.),
CLUBB (S.L.), DORRESTEIN (G.M.), QUESENBERRY (K). Avian
Medicine and Surgery. Philadelphia, W.B. Saunders Company,
1989; 563-589.
[16] KERN (T.J.), MURPHY (C.J.), HECK (W.R.). Partial upper eyelid
agenesis in a peregrine falcon. J Am Vet Med Assoc, 1985;1
87:1207.
[17] KERN (T.J.), MURPHY (C.J.), RIIS (R.C.). - Lens extraction by
phacoemulsification in two raptors. J Am Vet Med Assoc, 1984;
185:1403-1406.
[18] KERN (T.J.). - Exotic Animal Ophthalmology. In: GELATT (K.N.).
Veterinary Ophthalmology. Lippincott Williams & Wilkins,
Baltimore, 1999; 1273-1305.
Fig. 26 Traumatic haemorrage and retinal detachment in a raptor.
Fig. 27 Mature cataract in a duck.
Fig. 28 Typical cataract in a canary.
12
[19] KORBEL (R.), LEITENSTORFER (P.) - The modified Schirmer tear test
in birds-A method for checking lacrimal gland fuction. Tierärztl
Prax Ausg K Klientiere Heimtiere, 1998; 26:284-294.
[20] KORBEL (R.) - Tonometry in avian ophthalmology. J Assoc Av Vet,
1993; 7:44.
[21] KORBEL (R.T.) - Avian ophthalmology principles and application.
Proceedings WSAVA-FECAVA-AVEPA Congress, 2002; 214-217.
[22] KORBEL (R.T.) - Disorders of the Posterior eye segment in RaptorsExamination procedures and findings. In: LUMEIJ (J.T.), REMPLE
(J.D.), REDIG (P.T.), LIERZ (M.), 23. COOPER (J.E.). Raptor Biomedicine
III. Zoological Education Network. Florida. 2000;179-193.
[24] MACDONALD (S.E.), LOWENSTINE (L.J.), ARDANS (A.A.) - Avian
pox in blue-fronted Amazon parrots. J Am Vet Med Assoc, 1981;
179:1218.
[25]. MIKAELIAN (I.), PAILLET (I.), WILLIAMS (D.) - Comparative use of
various mydriatic drugs in kestrels (Falco tinnunculus). Am J Vet
Res, 1994; 55:270.
[26] MILLICHAMP (N.J.) - Exotic animal ophthalmology. In: Gelatt KN
(ed). Veterinary Ophthalmology ed.2. Philadelphia, Lea & Febiger,
1991.
[27] MURPHY (C.J.), KERN (T.J.), LOEW (E.), BUYUKMIHCI (N.C.),
BELLHORN (R.W.), DE LAHUNTA (A.), HECK (W..), GRAHAM (D.L.)
- Retinal dysplasia in a hybrid falcon. J Am Vet Med Assoc, 1985;
187:1208-1209.
[28] NARFSTRÖM (K.), EKESTEN (B.), ROSOLEN (S.G.), BERNHARD
(M.S.), PERCICOT (C.L.) OFRI (R.) - Guidelines for clinical
electroretinography in the dog. Doc Ophthalmol, 2002; 105:
83-92.
[29] OLSON (L.D.). Ophthalmia in turkeys infected with Pasteurella
multocida. Avian Dis, 1980; 25:423-430.
[30] PAUL-MURPHY (J.R.), LOWESTINE (L.), TURREL (J.M.), MURPHY
(C.J.) - Malignant lymphoreticular neoplasm in an African gray
parrot. J Am Vet Med Assoc, 1985; 187:1216-1217.
31. POONACHA (K.B.), WILSON (M.) - Avian pox in pen-raised bobwhite
quail. J Am Vet Med Assoc, 1981; 179:1264.
[32] RAMBOW (V.J.), MURPHY (J.C.), FOX (J.G.) - Malignant lymphoma
in a pigeon. J Am Vet Med Assoc, 1981; 179:1266-1268.
[33] SCHMIDT (R.E.), BECKER (L.L.), MC ELROY (J.M.) - Malignant
intraocular medulloepithelioma in two cockatiels. J Am Vet Med
Assoc, 1986; 189:1105-1106.
[34]. SHIMAKURA (S.), SAWA (H.), YAMASHITA (T.), HIRAI (K.) - An
outbreak of ocular disease caused by staphylococcal infection in
Amazon parrots (Amazona aestiva) imported into Japan. Jpn J Vet
Sci, 1981; 43:273-275.
[35]. STILES (J.), BUYUKMIHCI (N.C.), FARVER (T.B.) - Tonometry of
normal eyes in raptors. Am J Vet Res, 1994; 55:477-479.
[36] TSAI (S.S.), PARK (J.H.), HIRAI (K.), HAKURA (C.). Eye lesions in pet
birds. Pathology 1993;22:95-112.
[37] TUDOR (D.C.) - Retinal atrophy in a parakeet. Vet Med Small Anim
Clin, 1978; 73:1456.
[38] TULLY (T.N.), CARTER (T.D.) - Bilateral supraorbital abscesses
associated wih sinusitis in an orange-winged Amazon parrot
(Amazona amazonica) J assoc Avian Vet, 1993; 7:157-158.
[39] WILLIAMS (D.) - Ophthalmology. In: RITCHIE (B.W.), HARRISON
(G.J.), HARRISON (L.R.). (eds): Avian Medicine: Principles and
Application. Lake Worth, Fla: Wingers Publishing, 1994:673-694.
[40] ZENOBLE (R.D.), GRIFFITH (R.W.), CLUBB (S.L.) - Survey of
bacteriologic flora of conjunctiva and cornea in healthy psittacine
birds. Am J Vet Res, 1983; 44:1966-1967.
Fig. 29 Lens luxation associated with cataract in a raptor.
Fig. 30 Chorioretinitis secondary to toxoplasmosis in an owl.
Fig. 31 Retinal degeneration in an eclectus parrot.
13
OPHTHALMOLOGY
Current examination methods
of the canine eye
J. Beránek, P.J. Vít
SUMMARY
The scope of the present paper is to give an overview of the current examination methods of the eye to practitioners
who are involved in companion animal practice without being specialized in this field. The paper recommends a
basic instrumentarium for ophthalmology practice that have been found to be useful by the authors. Further, practical
approaches to ophthalmic examinations, as well as various examination methods used in the current ophthalmologic
practice are discussed. A description of individual steps during ocular examination and a flowchart recommending
the procedures are added in order to support systematic approach to case analysis.
h) Schirmer test strips are inevitable for diagnosing
keratoconjunctivitis sicca
i) Fluorescein test strips for diagnosing corneal defects
j) Rose bengal solution 0.5% or 1% for diagnosing
keratocojunctivitis sicca
k) Eye wash bottle to flush out discharge or stain from the eye
l) Tropicamide eye drops to dilate the pupil for lens and
fundoscopic examination
m) Topical anaesthetic
Due to its anatomical structure, the eye permits direct observation
of many pathologic processes as they develop. The vast majority
of ophthalmic conditions can be diagnosed with a few relatively
simple tools and techniques that almost every veterinarian
can learn and use in clinical practice. The following is a list of
equipment that we have found to be useful. It is meant as a
technical help to follow a standardized practical procedure.
As in any type of clinical examination, the detailed examination
of the eye should be preceded by taking the medical history,
such as client’s description of the clinical problem, previous
illnesses or injuries, therapies, and any conditions potentially
pertaining to the present problem. Numerous ophthalmic
conditions may be age-related or occur in specific breeds and
may be of hereditary origin. Knowledge of hereditary diseases
and their breed predisposition, as well as information on animal’s
pedigree are helpful. Client’s observations of the animal’s visual
ability during the day and in the dark, as well as its ability to see
moving and stationary objects may deliver useful hints to visual
function of the patient.
a) Focusing flash light or slit lamp provides oblique illumination
for examination the anterior segment of the eye (conjunctiva,
cornea, iris, anterior chamber, and lens)
b) Ophthalmic loupe, magnifying glass or binocular head
loupe
c) Schiötz tonometer or other tonometer is a necessity for
diagnosing uveitis and glaucoma
d) Set of lacrimal cannulae for examination a treatment of the
nasolacrimal system
e) Cilia forceps for treatment of distichiasis
f) Small blunt forceps for lifting the third eyelid and for
exploring the conjunctival sac for foreign bodies
g) Direct ophthalmoscope or biomicroscope for examination
of the posterior segment of the eye (aqueous humour,
fundus)
Ophthalmic examination is usually preceded by general
examination, because some systemic diseases may manifest
ocular signs. A preliminary visual inspection of the globe and
external ocular structures in day light or room light includes
bilateral judgment of the visual axis and positions of the
1) Small Animal Veterinary Clinic Pardubice, Czech Republic. E-mail med.prod@tiscali.cz
1
Current examination methods of the canine eye - J. Beránek, P.J. Vít
globes, symmetry of the external ocular structures, position
of the eyelids, size of the palpebral fissure, position of the
membrana nictitans, presence of nystagmus, unequal pupils,
blepharospasm, lagophthalmos, ocular or nasal discharge.
either eye is stimulated. The pupil of the consensual eye may
not constrict to the same extent as the pupil of the stimulated
eye. It should be taken into consideration that the pupillary light
reflexes are modified not only by changes in neural pathways,
but also by systemic or topical drugs or anxiety.
Adequate restraint is essential during the ophthalmic
examination. The majority of patients can be examined without
medication. Sedatives should be avoided whenever possible.
If sedation is necessary, potential drug effects on intraocular
pressure, miotic effects or protrusion of the nictitating
membrane should be taken into consideration. In our clinic, we
use medetomidine hydrochloride (Domitor) for sedation and
atipamezol hydrochloride (Antisedan) as an antidote. Ketamine
hydrochloride (11 mg/kg i.m.) can be used in intractable cats,
resulting in mydriasis and loss of blink reflex (prevention of
corneal dryness is necessary).
Staining techniques
Fluorescein staining is one of the most common staining
techniques, and indicated when there is evidence of corneal injury
or other discontinuity of the corneal surface or in any painful
eye with an unknown cause of pain. Corneal defects appear
green, particularly when cobalt filter or Wood’s lamp (ultraviolet
light) are used. Commercially available fluorescein strips are
sterile and will not alter subsequent examinations. Fluorescein
does not stain intact epithelium and does not penetrate through
the epithelial barrier. Once the barrier is damaged, fluorescein
penetrates into deeper corneal layers. The staining of the eye is
transient and usually disappears within 45 minutes.
Fluorescein is also used for assessment patency of the
nasolacrimal duct (see later in the text).
Eye examination using a light source
Closer eye examination should commence in a dimly lit room,
in order to obtain information about pupil size of each eye and
the transparency of individual ocular layers. The ocular adnexa,
conjunctiva and cornea should be examined with direct and
oblique illumination using focusing flash light or the direct
light beam of the ophthalmoscope. Head light has proved to
be practical, because it leaves both hands free and can be
focused where you are looking. A magnifying glass (1.5-4 fold
magnification) at a distance of 15-25 cm from the eye can also
be recommended.
Unlike fluorescein, rose bengal stains cells and their nuclei
by staining red devitalized corneal and conjunctival cells. It is
mainly used in for identification of corneal and conjunctival
lesions associated with keratitis sicca. Rose bengal is used as
1% aqueous solution or as paper strips. One drop of a topical
anesthetic should be instilled into the eye prior application of
rose bengal in order to prevent irritation.
Symmetry of adnexa, eye-lids (entropion, ectropion) and eye-lid
margins (trichiasis, distichiasis, chalazion), color and prominence
of conjunctival and scleral vessels are evaluated. The cornea
should be smooth, moist, transparent and free of vessels.
It is examined for opacities, inflammation, pigmentation,
degeneration, ulcerations, trauma or neoplasia. As cornea is
sensitive to touch, it is recommended to instill topical anesthetic
into the conjunctival sac before closer examination. When
anesthetic effect is present, small forceps can be used to pull the
third eyelid away from the corneal surface and examine its inner
surface for foreign bodies, hyperplastic tissue, inflammation,
follicle formation or changes on the lacrimal gland at its base.
If a corneal ulcer is present, it is important to know whether
the borders are regular or irregular, and whether the ulcer is
superficial or deep. It is useful to take scrapings from the ulcer’s
border and stain them with Giemsa for determination of cell
types. If the ulcer is deep, it is recommended to look for evidence
of anterior synechia, prolapsed iris, iridocyclitis, cataract, or
extrusion of the lens. The sclera is examined by assessing color,
plus presence of nodules, hemorrhages, lacerations, cysts,
tumors, injection of scleral vessels or edema. Generalized scleral
vessel injection indicates presence of deep located diseases,
such as uveitis or glaucoma.
Cytological, bacteriological and mycological
examinations
If conjunctival smears for cytology, bacteriology or mycology
are requested, topical anesthetics should not be used, because
they contain preservatives and may inhibit growth of bacteria
or damage mucosal cells. For microscopic examinations,
Giemsa staining is frequently used. Bacteriological culturing
is recommended especially in chronic conjunctivitis. A sterile
cotton swab moisted in sterile saline is used to transfer the
smear material onto a sterile agar plate. Dry swabs can be used
to mechanically debride an ulcer periphery, which is stained
by fluorescein. Severe corneal ulcers, conjunctivitis resistant to
treatment or eyes with chronic purulent discharge should be
cultured for bacteria and fungi. A sterile metal spatula can be
used for collecting samples for bacteriology or cytology.
Schirmer tear test
The test measures production of the aqueous portion of
the tear film (Fig. 1). It is extremely helpful in diagnosing
keratoconjunctivitis sicca. The Schirmer tear test I (STT I) should
be performed prior to using any medication or fluids. The test
strips are sterile and will not negatively influence subsequent
bacteriological or fungal examinations. This test is indicated in
all patients with mucoid or purulent ocular discharge and/or
chronic external ocular disorders. The test strip is placed behind
everted lower eye-lid; approximately one third of distance from
the medial canthus (use the correct side of the strip). The eyelids are kept closed by examiner for one minute. After one
minute, the strip is placed on the reading scale to obtain the STT
value in millimeters. Values greater than 10 mm are considered
The pupillary light reflex is examined in each eye with the
light source held 2 to 5 cm from the eye. The light beam is
directed along the optical axis, and the response time and
completeness of the reflex are noted for each eye. The response
of the nonstimulated eye is noted as the consensual reflex of the
stimulated eye. In healthy animals, both pupils respond when
2
The appearance of the fundus of the dog is quite variable.
The interpretation needs a certain level of experience and
may be difficult for an untrained veterinarian. In view of
numerous screening programs for hereditary eye diseases it
is recommended to let the examinations be done by specially
trained ophthalmologists in referral clinics.
Patency of the nasolacrimal duct
The lacrimal system is examined for excessive tearing or for
hypofunction of tear secretion and for any swelling, redness or
pain in the area of the medial canthus. When excessive tearing
occurs, it has to be determined if the tearing is induced by
partial or complete obstruction of the nasolacrimal system, by
increased lacrimal secretion due to chronic ocular irritation as
in distichiasis or trichiasis, or by a physiological increase in tear
production as may occur with uveitis. The first diagnostic step is
the test of patency of the nasolacrimal system. If dye is present,
it can be concluded that the lacrimal excretory system is patent
and epiphora is due to tear hyper secretion.
Fig. 1 Schirmer tear test of tear production.
to be physiological in dogs and cats, although some cats show
„normal“ values as low as 3 to 6 mm. Values between 5 and
10 mm are considered suspicious, and values below 5 mm are
diagnostic for keratoconjunctivitis sicca. The test values have
always to be interpreted in conjunction with the clinical signs.
A drop of fluorescein solution is placed into the conjunctival
sac. After two to five minutes, the nostrils are examined for
presence or absence of fluorescein dye. If no stain is present
in the nostrils, an obstruction of the excretory system can be
assumed and irrigation of the nasolacrimal system in indicated.
The irrigation is usually conducted under topical anesthesia. A
curved nasolacrimal cannula (23-gauge in dogs and 25-gauge in
cats) is routinely used. Flushing the nasolacrimal system is done
in a restrained patient; sedation or anesthesia may occasionally
be necessary, particularly in cats. The technique is as follows:
Place the cannula on a syringe (1-2 ml) which is filled with
water or saline solution. The cannula is gently inserted into the
upper lacrimal punctum. The tip of the cannula tip should be
directed medially and simultaneous movement of the syringe
towards the dorsal midline of the patient’s head should direct
the cannula into the lacrimal sac. As fluid comes out from the
lower punctum, pressure on the lower punctum will force the
fluid into the nasolacrimal duct. The fluid may come out of the
nostrils or the patient swallows the fluid. If resistance is noted
during irrigation, either the cannula is not in the lacrimal sac
or an obstruction of the nasolacrimal duct is present. Further
elucidation of the problem requests specific techniques, such as
contrast radiography or cannulation of the whole nasolacrimal
system.
Ophthalmoscopy
The most expeditious screening examination of the fundus can
be achieved by using hand lenses (10-40 D) and head light
(indirect ophthalmoscopy). For adequate visualization of the
fundus, the pupil has to be adequately dilated. The examination
needs to be done in a dark room. The lens is positioned 2.5 to
5 cm in front of the patient’s eye and the inspection is done at
an arm’s length, moving the lens toward or away from the eye,
until the entire lens is filled with the fundus image. The examiner
sees an inverted picture. An advantage of this approach is a
large field of view. The purchase costs, however, are quite high.
Any lesion seen by indirect ophthalmoscopy should be evaluated
by direct ophthalmoscopy.
Direct ophthalmoscopy is mainly used for examination of the
ocular fundus (fundus is that part of the inner eye which includes
the optic disc or papilla, the retinal vessels, tapetum lucidum
and nigrum), even though it can be also used for other eye
structures. For its relatively low purchase price, it is frequently
used in general practice.
Intraocular pressure (Tonometry)
Intraocular pressure (IOP) measurements are an inevitable part
of eye examination whenever suspicions of glaucoma exist.
It should be performed with the utmost care on eyes with
corneal injuries or deep corneal ulcers. The most commonly
used in general practice is the Schiötz tonometer. It is not
very accurate, but it is sufficient enough for estimations of
the IOP. After topical anesthesia, the corneal footplate of the
device is applied to the cornea in a perpendicular manner and
several readings are done, using 5 or 7.5 g weights. A table for
conversion (delivered with the device) helps to determine the
values in mm Hg. Ocular pressure values of 10 to 30 mm Hg are
considered to be physiological in dogs, values of 14 to 26 mm
Hg are considered to be physiological in cats. In the meantime,
The direct ophthalmoscope has a focus wheel with lenses
between + 40 dioptries (black) and – 25 dioptries (red). The
most expeditious way of examination is to set the focus wheel
at + 15 dioptries and using the large spot aperture. Working
at the arm’s length from the patient, lesions anywhere in the
cornea, anterior and posterior chambers, lens, or vitreous can be
visualized. In the next step, the focus wheel is set to 0 and the
examiner moves toward the patient until the fundus is clearly
seen. At a distance of 2.5 to 5 cm from the eye, the focus wheel
is used to obtain an optimal focus of the fundus. If a lesion is
elevated from the fundus, more positive dioptries are needed to
bring the lesion into focus and vice versa.
3
Fig. 2 Measuring
of IOP using
Tonovet.
Fig. 3 Ultrasonography
of the eye.
newer devices are available on the veterinary market, such as
TonoPen (Mentor Ltd.) or Tonovet (Tiolat Ltd.). They are easier to
operate (Fig. 2), deliver more accurate results, but they are more
expensive than the Schiötz tonometer. It should be kept in mind
that the intraocular pressure increases in severely restrained
patients (occlusion of the jugular veins) and that some drugs
can also influence intraocular pressure (decrease by sedatives,
increased by ketamine). Intraocular inflammatory processes,
such as anterior uveitis decrease intraocular pressure.
presence of pigments, adhesions, opacities, or position of the
lens (subluxation or luxation).
Electroretinography
Electroretinography (ERG) records electric potentials that arise
in the retina after light stimulation at different light intensities,
wave lengths, and exposure duration. The electroretinogram
represents the composite activity of millions of retinal cells,
extending from the pigment epithelium to the inner nuclear
layer. It is used for studies of the retinal function (not visual
function) and detection of early stages of the progressive retinal
degeneration (the PRAs), before retinal changes can be seen
by ophthalmoscopy. ERG is routinely used in genetic screening
programmes for hereditary eye diseases, before extraction
of hypermaturate lens cataracts, and in diagnosis of sudden
acquired retinal degeneration (SARD) and the PRAs. ERG
equipment is financially quite pretentious and interpretation of
the records requires high level of experience. Specialized clinics
use this method with increasing frequency. The European Society
of Veterinary Ophthalmology makes efforts to standardize the
ERG technique and to work out a global ERG protocol. Current
recommendations are described in another paper in this issue
of the EJCAP and can also be found in: Narfstrõm K, Ekesten
B, Rosolen SG, Spiess BM, Pericot CL, Ofri R - Committee for
a Harmonized ERG Protocol, European College of Veterinary
Ophthalmology. Guidelines for clinical electroretinography in
the dog. Documenta Ophthalmologica, 2002, 105, 83-92.
Gonioscopy
Gonioscopy enables direct observation of the iridocorneal angle
(pectinate ligament and drainage angle between iris and cornea)
in the anterior chamber, by use of gonioscopic lenses (Franklin,
Koeppe or Barkan). Besides detection of foreign bodies, tumors
or exudate in the iridocorneal angle, this examination is crucial
for reliable diagnose in patients with suspected glaucoma.
Routine examinations are conducted in dog breeds with
frequent incidences of glaucoma due to goniodysgenesis, such
as the basset hound.
The examination is conducted under topical anesthesia and firm
restraint. Sedation is required in some animals. The goniolens is
carefully positioned on the cornea, and the lens-cornea interspace
is filled with 1% methylcellulose (Franklin and Koeppe lens, saline
with the Barkan lens). The iridocorneal angle is examined with
respect to width, status of the pectinate ligament, inner and
outer pigment zones, and the outer trabecular meshwork. The
clinical classification of glaucomas (open angle, closed angle)
and the decision to use medical or surgical treatment are based
on gonioscopic findings.
Radiographic procedures (X-ray)
Orbital radiography enables identification of changes in
the orbit and paranasal cavities. It is an essential method in
traumatology.
Special Examination techniques
Dacryorhinocystography
Dacryorhinocystography is a radiographic examination of the
nasolacrimal duct using a contrast medium for localization of a
possible obstruction.
Slit lamp
The slit lamp provides oblique illumination for examination the
anterior segment of the eye, mainly of the cornea and lens. It
offers advantages in detecting minute corneal opacities and
exact localization of lens changes. Commonly used is a binocular
slit lamp biomicroscope with options of adjustable 5-40 times
magnification and a cobalt filter for highlighting changes in
the fluorescein test. Its relatively high purchase price may be a
limiting factor for general practice.
Computer Tomography and Magnetic Resonance Image
CT and MRI offer a wide scale of diagnostic possibilities
particularly in diseases of the orbit (Fig. 3).
Ultrasonography
Ultrasonograpgy (USG) utilizes beams of acoustic energy and their
echoes that localize and quantitate tissues of various densities
within the eye and orbit (Fig. 4, 5). The indications for diagnostic
The lens can also be examined by direct ophthalmoscopy
(slit beam aperture) in direct and oblique illumination for the
4
The sequence of examinations is quite essential, in order to
proceed in a systematic manner and because some diagnostic
procedures may adversely affect procedures that follow later.
The following examination procedure is recommended:
Tab. 1: Flowchart for ophthalmic examination.
Recommended procedure of the eye examination
Disease history
Visual inspection
Fig. 4 Ultrasonography of the eye after injury with large
hemathoma.
Discharge
No discharge
Sampling for bacteriology
Pupillary light reflex
Schirmer tear test
Normal
Low tear production High tear production
Tropicamide (if no ulcer)
Fig. 5 MRI technique for orbit examination. Histopatology
examination: lymphoma. Foto ©renk, Tomek, Klinika Jaggy, Brno.
Examination and slit lamp examination of the
anterior segment
USG include localization of retinal detachments, intraocular
and intraorbital tumors, and foreign bodies. This method is
particularly useful in eyes with an opaque cornea. Devices with
sector scanners of 7.5 or 10 mHz are recommended.
Fluorescein stain
Tonometry
Paracentesis
Paracenthesis of the anterior chamber may be indicated in
uveitis of potential mycotic aetiology. Paracenthesis of the
vitreous humor (hyalocenthesis) is indicated for the diagnosis of
severe inflammatory processes in the posterior segment. These
methods are used relatively rarely, even in referral clinics.
Gonioscopy (if necessary)
Vision tests
Corneal Computer Topography
Computer topography (keratoscopy) is used to exclude
astigmatism. This method examines corneal curvature by means
of concentric light beams (Placid rings). Final picture (distance
between rings) is analyzed by a computer. This technique has
been used in the development of contact lenses. Studies have
shown that the corneal curvature in middle and small dog breeds
is larger than in large dog breeds.
Lens examination
Ophthalmoscopy
Other diagnostic examinations
5
Suggested reading
Assessment of visual function in pets presents a difficult
problem. A common clinical test to assess vision is the „menace
reaction“ conducted by passing the hand in front of the animal’s
eyes to induce blink reflex or the „cotton ball test“ conducted
by dropping a piece of cotton in front of the dog’s eye; animal’s
response is evaluated. Occasionally, dogs and cats do not show
any response with these tests. The response of the pupil can
also be used as a sign of visual competence. Further method
of assessment of the visual system is the maze test. The light
intensity in the examining room can be varied, and alternate
patching of the eyes may be helpful. Frequently, valuable
information is obtained from the owner’s observations.
[1]
[2]
[3]
[4]
Information obtained by individual examination steps should be
recorded in patient’s health record, which can be passed on to
an ophthalmologist or as a part of the patient data sheet. A
specific form for ophthalmologic examinations can be obtained
from the European Society of Veterinary Ophthalmology.
6
GELATT (K.N.) - Ophthalmic examination and diagnostic
procedures, in: Textbook of veterinary ophthalmology, editor:
K.N. Gelatt, Lea & Febiger, Philadelphia, 1981, 195:231.
HACKER (D.) - Diagnostics, in: Small animal ophthalmology:
a problem oriented approach; editor: Robert L. Pfeiffer, W.B.
Saunders Company, Philadelphia, 1989, 11:23.
HARLING (D.E.) - A practitioner’s perspective, in: The Veterinary
Clinics of North America, Symposium on Ophthalmology, editor:
R.L. Pfeiffer, W.B. Saunders Company, 1980, 241:247.
Eye examination, in: Diseases of dogs and cats, editors: M.
Svoboda, D.F. Senior, J. Doubek, J. Klimes, Noviko AS, Brno, 2000,
553:556 (language: Czech).
OPTHALMOLOGY
Injuries in dogs’ eyes caused
by cat claws
E. Bjerkås
SUMMARY
Ocular injuries caused by cat claws are common and carry a guarded prognosis. Important prognostic factors include
the depth of the injury, time from injury to proper treatment, and eventual complications. If left untreated, such
injuries may lead to destruction of the eye and permanent blindness.
Examination and diagnosis
This paper is translated and reprinted from the
To establish an exact diagnosis, the eye and adnexa (area
around the eye) should be thoroughly examined. Sedation may
be necessary if the animal is upset or is unwilling to open the
eyelids. However, ventral rotation of the globe in sedation may
complicate the examination.
Norwegian Veterinary Journal 2006; 118: 593-596.
Introduction
Ocular injury after an unfriendly meeting with a cat is not
an uncommon entity. Injuries caused by cat claws are more
common in puppies than in older dogs. The cause may be that
the menace reaction if not fully developed until the puppy is
around three months old. Thus, the puppy will not react to
the cat paw by retracting or blinking [2,5]. The severity of the
injury may not be obvious initially, thus, it may be ignored by
the owner. But until proven otherwise, all injuries caused by cat
claws are to be considered penetrating. This implies that the
complication risk is high and that such injuries should be treated
as soon as possible.
The examination should include measurement of tear
production by Schirmer Tear Test. This may seem unnecessary,
but there are several dog breeds described with early developing
keratoconjunctivitis sicca. Lowered tear production will affect
wound healing and is therefore of prognostic significance.
The eye should be examined with the use of a focal light source
and magnification in a dimly lit room. Practical equipment includes
a head loupe and the otoscope light or a Finoff transilluminator.
Slit lamp-biomicroscopy is the optimal method, but the required
instrument is often not available in smaller clinics. One should
examine the eyelids, conjunctiva and especially the third eyelid
thoroughly, as injuries here are often overlooked. One should
also remember that the claw can be torn off during the blow
and remain hidden under one of the eyelids.
The injury can be divided into three categories.
1. The cat claw has hit its target but only the conjunctiva, upper,
lower and third eyelid(s) are injured
2. The cat claw has hit the cornea and caused corneal
perforation
3. The cat claw has perforated the cornea with concurrent
perforation of the iris and/or anterior lens capsule
The cornea should be examined from front, from above and
from the sides. One should not forget the part that is hidden
1) Prof Ellen Bjerkås, Norwegian School of Veterinary Science, Department of Companion Animal Clinical Sciences.
P.O.Box 8146 Dep., 0033 Oslo, Norway
1
Injuries in dogs’ eyes caused by cat claws - E. Bjerkås
Fig. 1 Fresh, perforating injury partly hidden beneath the third
eyelid. Topical atropine treatment has been initiated and the pupil
is dilating
Fig. 2 One day old perforating injury. The pupil has been dilated
by use of topical atropine. Corneal oedema complicates visibility of
the intraocular structures.
under the third eyelid (Fig. 1). Illuminating the cornea from the
side allows for a better visualisation of eventual injuries of the
anterior chamber. Examination from the side is also important
if some time has passed since the event and there is substantial
corneal oedema that complicates the examination (Fig. 2).
staining. However, important additional information is obtained
regarding whether the cornea has been perforated or not.
While shining the light on the cornea (preferably with ultraviolet
light as it shows the staining more clearly), the cornea is pushed
gently. If the cornea has been perforated, one might observe
a tiny stream of aqueous humour leaking from the wound
through the stain. This test is termed the “Seidel-test” and is a
useful method if corneal perforation is suspected.
Intraocular changes that may be present include
– Haemorrhage due to perforation of iris
– Prolapsed iris tissue through the corneal laceration
– Lens material in the anterior chamber due to rupture of the
lens capsule
Measuring intraocular pressure (IOP) is also important in the
evaluation of a case. There is a significant lowering of IOP if the
cornea has been perforated. If the perforation has been plugged
with fibrin and has stopped leaking, the IOP will still be lowered
in most cases due to a concurrent uveitis, due to the breakdown
of the blood-aqueous barrier. Classical signs in uveitis are miosis
(constricted pupil) and lowered IOP. Iris oedema is usually not
significant in an acute injury, but is more common in uveitis
caused by other factors.
Fresh haemorrhage can be observed directly if there is little
corneal oedema. Iris prolapse is diagnosed by shining the light
onto the eye from the side and observing the iris adhering to the
backside of the cornea. In case of protrusion, the (normally) dark
iris can be observed in the laceration (Fig.3).
Especially in puppies, it can be difficult to determine whether
the lens capsule is perforated or not. The lens is fairly soft in
the puppy, thus, lens material leaking out from a rupture can be
difficult to distinguish from the surrounding aqueous or from
material from the vitreous. In older dogs the lens proteins in
the cortex contain less water and the lens material leaking out
has the appearance of an opaque, mushroom-shaped opacity
in the anterior chamber. When the cornea is perforated, the
pupil constricts. The small pupil makes it difficult to observe a
rupture of the anterior lens capsule, as it may be hidden behind
the constricted iris. To obtain a full overview, the pupil should
be dilated, both as part of the examination and as initial medical
treatment.
Treatment
Conjunctival lacerations are usually not necessary to suture,
unless the injury is significant. If, however, the third eyelid
has been injured, suturing should be considered. The sutures
should not be placed so that they rub on the cornea. Lacerations
affecting the rim of the eyelid should be closed with an 8-suture.
Superficial corneal wounds may not require suturing, however,
such wounds are unfortunately uncommon after cat claw
attacks. Suturing should be considered if the wound is deep
and is affecting most of the stroma.
Perforating wounds
The principles for treatment of corneal perforations include
wound treatment, prophylaxis against infection, treatment of
uveitis, pain and eventual complications.
Staining of the injury with fluorescein-Na is routinely performed,
but should not be carried out until after a thorough initial
examination in which a full overview of the deeper structures is
obtained. Most often, a corneal injury can be observed without
2
Fig. 3 Perforating corneal wound at the limbus in an eight-week
old dog. The dark iris tissue protrudes through the defect.
Fig. 4 The same dog as in Fig. 3. The wound has been closed in two
layers by suturing the cornea and placing a conjunctival flap.
Pinpoint and small perforating ulcers may not require suturing,
as they are often sealed by a fibrin clot. However, if in doubt, it
may be better to put in a few sutures than to leave it as an open
wound. The suture is put through 2/3 of the corneal thickness
with thin suture material (7-0 or thinner) with a spatula needle.
Absorbable suture material does not require the stitches to be
removed later. The stitches should not be tied too tightly, but
sufficiently to prevent aqueous leakage between the stitches. If
the wound is large or with tissue loss making the wound difficult
to close, a conjunctival flap or other “bandaging”, for instance Vet
BioSISt™ is sutured to the wound edges after closure of as much
as possible of the cornea (Fig. 4). Enlargement is recommended
for corneal suturing. The optimal equipment is an operating
microscope, however magnifying glasses may be of valuable
help. Positioning of the eye during suturing is obtained either by
holding sutures, or by a small dosage of a muscle relaxant if good
monitoring of anaesthesia can be obtained (e.g. pancuronium
0.01-0.02 mg/kg) [5]. An attempt should be made to reposition
a protruding iris, and after suturing the eye can be reformed
with 0.2-0.3 ml of a viscoelastic material for intraocular surgery,
Balanced Salt Solution or Ringer acetate. Lateral cantothomy,
with enlargement of the eyelid opening may be indicated for
better access to the surgical field. After closure of the corneal
wound, the cantothomy is closed in two layers. The cantothomy
sutures should remain for two weeks.
treatment should be started during the consultation to monitor
the effect.
Choice of treatment to control pain and uveitis depends on
the severity of the corneal laceration. If there is only a small
ulcer, there are no complications and treatment is initiated early,
systemic treatment with a non-steroidal anti-inflammatory agent
(NSAID) may be sufficient. Topical NSAIDs may be considered,
but one should remember that wound healing may be delayed
[6,7]. If the wound has been sutured and/or there are significant
intraocular changes, steroids should be administered systemically
in immunosuppressive doses. Topical steroid treatment delays
wound healing, but may still be considered if the wound has
been sutured, to replace systemic steroids. For topical treatment
the ability of the preparation to penetrate the cornea should
be taken into consideration. Dexamethazone is more potent,
while prednisolone acetate has better corneal penetration [8].
Re-evaluation after start of treatment is important, either the
following day or within a few days to control effect of treatment.
Rechecks are also important to determine when steroid
treatment can be tapered. The degree of injury determines
whether additional pain treatment should be administered.
One should remember, however, that surgeries of the eye and
adnexa are painful procedures.
When all medical treatment has been stopped, the dog should
be re-examined after a week to ensure that there is no decrease
in intraocular pressure as sign of recurrence of the uveitis.
The normotensive eye is used as control. Anti-inflammatory
treatment should be continued until the intraocular pressure is
back to normal.
Broad-spectred antibacterial treatment is administered topically
and systemically. Ideally, the choice of antibiotic should be made
based on sampling result, however, this is not practically possible
as antibacterial treatment should be started immediately. If the
would is older and contaminated, a swab for Giemsa stain and
culturing should be taken.
In earlier days, suturing the third eyelid over the eye as a
“bandage” was frequently used. This does not, however, shorten
the wound healing time, but it prevents the veterinarian from
controlling the ocular changes and the effect of treatment.
Uveitis and pain treatment is initiated with topical atropine
0.5-1% every hour until the pupil is dilated. Later, atropine is
administered twice a day until the situation is stable. Atropine
3
Injuries in dogs’ eyes caused by cat claws - E. Bjerkås
References
[1] BUSSIERES (M.), KROHNE (S.G.), STILES (J.), TOWNSEND (W.M.)
- The use of porcine small intestinal submucosa for the repair
of full-thickness corneal defects in dogs, cats and horses. Vet
Ophthalmol 2004; 7: 352-59.
[2] GAROSI (L.) - The neurological examination. Platt SR, Olby NJ eds.
BSAVA Manual of canine and feline neurology. Gloucester, UK:
BSAVA, 2004: 1-23.
[3] GERDING (P.A.), ESSEX-SORLIE (D.), VASAUNE (S.), YACK (R.) - Use
of tissue plasminogen activator for intraocular fibrinolysis in dogs.
Am J Vet Res 1992; 53: 894-6.
[4] MATHIS (G.A.) - Clinical pharmacology and therapeutics. Gelatt KN,
ed. Veterinary Ophthalmology 3rd Ed. Philadelphia: Lippincott
Williams & Wilkins 1999: 291-354.
[5] SPIESS (B.M.), RÜHLI (M.B.), BOLLIGER (J.) - Augenverletzungen
durch Katzenkrallen beim Hund. Schweiz Arch Tierheilkd 1996;
138: 429-33.
[6] SUGAR (J.) CORNEAL PERFORATIONS. TASMAN (W.), JAEGER (E.A.)
- eds. Duane’s Clinical Ophthalmology on CD-Rom 2004 edition.
Philadelphia: Lippincott Williams & Wilkins 2004; Vol 6, Ch 32.
[7] TANI (E.), KATAKAMI (C.), NEGI (A). - Effects of various eye drops
on corneal wound healing after superficial keratectomy in rabbits.
Jpn J Ophthalmol 2002; 46: 488-95.
[8] VAN DER WOERDT (A.) - Lens Lens-induced uveitis. Vet Ophthalmol
2000; 3: 227-34.
[9] WEAVER (C.S.), TERRELL (K.M.) - Update: Do ophthalmic
nonsteroidal anti-inflammatory drugs reduce the pain associated
with simple corneal abrasion without delaying healing? Ann
Emerg Med 2003; 41: 134-40.
[10] WILKIE (D.A.), GEMENSKY-METZLER (A.J.) - Agents for intraocular
surgery. Vet Clin North Am - Small Anim Pract 2004; 34: 801-23.
Fig. 5 Two months after a penetrating injury with concurrent
laceration of the anterior lens capsule. There is synaechia between
the cornea, iris and lens. Cataract is present in the anterior cortex,
and the nucleus is clearly visible because of the loss of cortical
material.
Complications
The two most important complications after a cat claw injury
include penetration through the anterior lens capsule and
substantial intraocular haemorrhage. Small lens capsule ruptures
may seal off spontaneously and only result in moderate cataract
formation (Fig. 5). Regardless, however, lens capsule rupture
results in a severe, so-called phacoclastic uveitis [2,9], which
needs to be controlled by the use of steroids. It has been reported
that injuries less than _ mm long may be treated medically, while
larger injuries with extrusion of lens material into the anterior
chamber should be treated surgically [9]. The optimal method
in large lens capsule ruptures is phacoemulsification. The time
aspect is important, however, as rapidly developing corneal
oedema complicates surgery.
Large intraocular haemorrhage may be resorbed spontaneously.
If there is concurrent formation of fibrin, this can be dissolved
by use of tissue plasminogen activator (tPA) injected into the
anterior chamber 1-2 days after the injury occurred [5,10]. tPA
(Actilyse® Boehringer Eingelheim, diluted to 250 _g/ml, 0.1ml)
dissolves fibrin within a few hours, but should not be used if
there is still active haemorrhage present. The diluted preparation
can be stored at minus 80° C.
If treatment is delayed, or in cases of extensive injury,
uncontrollable uveitis may develop. Because of the clogging of
the iridocorneal angle with inflammatory debris, there is always
a risk of secondary glaucoma. In addition, lens injury or longstanding uveitis are both causes of secondary cataract [9].
4
OPTHALMOLOGY
Examination of the feline eye
and adnexa
S.M. Crispin1
SUMMARY
The feline eye is large and easy to examine and ophthalmic assessment is a rewarding procedure, provided that the
examiner is patient and the correct equipment is selected and properly used.
Various disposable items are also needed in order to perform
a range of diagnostic tests; the essential ones are topical
ophthalmic stains (e.g. fluorescein sodium), ocular irrigant
(e.g. sterile saline), local anaesthetic (e.g. proxymetacaine
hydrochloride), tropicamide 1%, Schirmer tear test papers,
cotton wool, sterile culture swabs, surgical blades, forceps, glass
slides, lacrimal cannulae, sterile syringes and needles.
This paper was commissioned for publication
in EJCAP
Introduction
It is often possible to reach an accurate ophthalmic diagnosis on
the basis of the history, observation and examination, provided
that the examiner is familiar with the normal function and
structure (Fig. 1) of the feline eye (globe) and adnexa (eyelids,
lacrimal apparatus, orbit and para-orbital areas), as well as the
selection and use of ophthalmic diagnostic equipment [5, 6, 18,
19, 20].
Use of Instruments
Focal Illumination
A Finhoff transilluminator or pen light provides a useful light
source for examination of the eye and adnexa (Fig. 2). In cats it
is possible to examine the drainage angle directly, if somewhat
incompletely, using focal illumination and this technique should
be included at this stage of the examination. If there is any
suggestion of abnormal intraocular pressure or abnormality of
the drainage angle, the intraocular pressure should be measured
as part of the assessment.
Equipment
The basic equipment required for examination consists of
a focal light source, ideally a Finhoff transilluminator, some
form of magnifying device, a condensing lens and a direct
ophthalmoscope. For those who take a particular interest in the
subject, additional equipment, notably a slit lamp biomicroscope,
binocular indirect ophthalmoscope and a device for measuring
intraocular pressure, will be required.
A
Magnification
Some form of magnification will be required as a diagnostic
aid and this is most readily achieved with a magnifying loupe
(ideally combined with a light source), an otoscope with
Figure 1. Gross specimens of the adult
feline globe (with acknowledgements
to J. R. B. Mould). The feline eye is
superbly adapted to vision under a
range of lighting conditions, including
dim light and near darkness. In (a)
note the almost spherical globe and
large cornea and lens, together with
the wide drainage angle and clearly
defined pectinate ligaments which
span the cleft between the iris (right)
and cornea (left). In (b) note the extent
of the tapetal fundus and the location
of the optic nerve head within the
tapetal fundus.
B
(1). Sheila Crispin, Cold Harbour Farm, Underbarrow, Kendal, Cumbria, LA8 8HD, UK
E-mail s.m.crispin@bris.ac.uk
1
Examination of the feline eye and adnexa – S.M. Crispin
Figure 3. An
otoscope with the
speculum removed
provides a simple
means of combining
magnification and
illumination. This
examination is best
performed in the dark.
Figure 2. A focal light source being used for examination of the eye
and adnexa. This examination should be performed in the dark and
the light shone from as many different angles as possible in order to
build up a full picture.
Figure 4. The Kowa hand held models are excellent for use in cats
and cordless models such as the SL 14 are available. The Kowa SL2
illustrated here.
Figure 5. A Nikon desk mounted slit lamp biomicroscope in
use. Most cats can be examined with this type of slit lamp and
photography is much easier than with hand held models.
speculum removed (Fig. 3), a direct ophthalmoscope, or a slit
lamp biomicroscope.
Figure 6. A cat with lysosomal storage disease
(mucopolysaccharidosis). In (a) subtle pancorneal clouding is
apparent and details of the iris are indistinct (compare with the
normal external eyes illustrated in Fig. 16, 21). Such changes are
very obvious with slit lamp examination (b).
Slit lamp biomicroscopy
The slit lamp biomicroscope consists of a light source (diffuse
illumination or a slit beam) and a binocular microscope which
can be moved in relation to the light source. Whilst primarily a
A
B
2
Figure 8. Monocular indirect
ophthalmoscopy using a
commercially manufactured
instrument. Examination should
be performed in the dark, ideally,
following mydriasis.
Figure 7. Monocular indirect ophthalmoscopy being performed with
a 28D condensing lens and penlight. Mydriasis is desirable, if not
essential, for all types of indirect ophthalmoscopy and the technique
must be performed in the dark. A virtual and inverted image should
fill the whole of the lens if the technique is carried out correctly.
Figure 10. A direct ophthalmoscope (Keeler).
Indirect Ophthalmoscopy
This technique can be performed most simply following pupil
dilation with one drop of tropicamide 1%. Monocular indirect
ophthalmoscopy can be performed with a condensing lens (for
example, 20D or PanRetinal 2.2) and a focal light source (Fig. 7).
The lens is held some 2-8 cm from the cat’s eye and the fingers
of the hand holding the lens should rest lightly on the animal’s
head. The focal light source is shone through the lens from a
distance of some 50-80 cm (the distance between the cat’s eye
and the observer’s eye).
Figure 9. Binocular indirect ophthalmoscopy using a spectacle
indirect ophthalmoscope. Examination should be performed in the
dark following mydriasis.
means of providing magnified detail of the adnexa and anterior
segment, the posterior segment can also be evaluated if a high
dioptre (for example +90D) condensing lens is interposed. In
cats it is possible to use either a hand held model that needs a
mains electricity supply (Fig. 4), or a hand held cordless model
(Fig. 5), or a table mounted slit lamp.
Monocular indirect ophthalmoscopy produces an image which
is virtual (that is, viewed indirectly), inverted and magnified,
with the magnification depending on the strength of the lens.
More refined and expensive monocular ophthalmoscopes (Fig.
8) which produce an erect image are also available.
Focal examination
Gross lesions involving, for example, the eyelids, cornea, anterior
chamber, iris, lens or anterior vitreous can be examined with
a diffuse beam of light (Fig. 6a). When the diffuse beam is
narrowed to a slit (Fig. 6b) an optical section of, for example,
the cornea or lens may be visualised when the beam is directed
obliquely (up to an angle of 45 degrees).
The advantages of indirect ophthalmoscopy include a wide field
of view and a reasonable image, even when the ocular media are
cloudy. Binocular instruments (Fig. 9) are also available, although
they are expensive; they provide the additional advantage of
depth perception (stereopsis).
Retro-illumination
Retro-illumination uses the reflection from the iris, lens or ocular
fundus to illuminate the cornea from behind. Minute corneal
changes can be detected with this method. The technique is
impressive when the fundus reflex is used as the reflecting
medium following dilation of the pupil (mydriasis).
Direct Ophthalmoscopy
The direct ophthalmoscope (Fig. 10) consists of an on/off switch
with incorporated rheostat, a light source, a beam selector (for
example, large diameter beam, small diameter beam, slit beam
and red-free light as an alternative to the normal white light
source) and a selection of magnifying (black = +) and reducing
(red = -) lenses housed in a lens magazine. The observer looks
directly along the beam of light to view the object of interest.
3
Figure 12. Lens opacities
appearing as dark
silhouettes when viewed
using distant direct
ophthalmoscopy.
Figure 11. Distant direct ophthalmoscopy. This technique should
be performed in the dark and a mydriatic should not be used until
the size and shape of the pupils have been compared.
performed with the ophthalmoscope placed as close as possible
to the observer’s eye and some 2 cm from the patient’s eye,
usually with a setting of 0. Modern halogen bulbs provide very
bright illumination, so the examiner should employ the rheostat
which is incorporated in the on/off switch, both to ensure that
the light intensity is kept at comfortable levels for the patient
and to make sure that subtle lesions are not missed because
the light is too bright. The instrument should be lined up in the
correct position, with the light shining through the pupil, before
the examiner looks through the viewing aperture (Fig. 13a).
Fingers of the hand holding the ophthalmoscope can be rested
lightly against the animal, so that any head movements can be
accommodated and the position of the cat in relation to the
ophthalmoscope is more readily appreciated (Fig. 13b). The use
of over bright light is probably the commonest reason for failure
to examine the fundus adequately. Cats generally resent close
bright light and, because there is voluntary control over third
eyelid movement, the field of view can be limited. In addition,
the pupil constricts rapidly to a vertical slit when a bright light is
shone in a normal eye when a mydriatic has not been used.
Distant direct ophthalmoscopy
Distant direct ophthalmoscopy can be used as a quick screening
method prior to more detailed examination (Fig. 11); it is an
essential aspect of ophthalmic examination and can provide
information about the direction of gaze, pupil size and shape, as
well as the presence of any opacities between the observer and
the ocular fundus. Any opacities in the path of the fundus reflex
appear as silhouettes (Fig. 12). The ophthalmoscope is usually
set at 0 and the tapetal or fundus reflex is viewed through the
pupil, with the observer at about arm’s length from the patient.
Distant direct ophthalmoscopy is the easiest way of comparing
both eyes simultaneously.
Close Direct Ophthalmoscopy
Close direct ophthalmoscopy provides an image which is real (that
is, viewed directly), erect and magnified. Fundus magnification
is greatest with direct ophthalmoscopy, followed by panoptic
ophthalmoscopy and then indirect ophthalmoscopy.
It is easiest for spectacle wearers to remove their spectacles and
set the ophthalmoscope according to the prescription issued for
the eye they will use for examination. This allows the instrument
to be placed much closer to the observer’s eye.
Close direct ophthalmoscopy is used for examination of the
ocular fundus following indirect ophthalmoscopy and distant
direct ophthalmoscopy. Close direct ophthalmoscopy should be
Figure 13. Close direct ophthalmoscopy. This technique should be performed in the dark and mydriasis is essential for comprehensive
examination. The ophthalmoscope is placed in the correct position with the light shining through the pupil before the examiner looks
through the viewing aperture (a). The examiner is now viewing the fundus and the ophthalmoscope is manipulated to ensure that logical
examination of each quadrant is performed. Note how the instrument is steadied against the cat’s head and the lack of any restraint (b).
A
B
4
Figure 14. Normal adult
cat. Note the symmetry of
the face, eyes and pupillary
aperture.
Figure 15. Horner’s Syndrome. In this cat the asymmetry is
obvious as the palpebral aperture is smaller on the right and there
is also some prominence of the third eyelid and constriction of the
right pupil relative to the normal pupil of the left eye.
Protocol for Examination of the Eye
and Adnexa
History
Once the age, breed, sex and vaccination status of the cat has
been recorded, information about the present problem and
any previous health problems should be obtained, as well as
details of any current or past treatment. Other relevant enquiries
include the management and lifestyle of this cat and any others
with which it may come into contact.
Examination
Examination is usually best undertaken in a quiet room which
can be darkened completely and ophthalmic examination follows
general and neurological examination. Aspects of neurological
examination that relate specifically to ocular disease include
visual placing reactions, relevant cranial nerve examination and
autonomic nervous system assessment and these are included in
the protocol that follows. Ophthalmic examination is performed
in two parts; the first part in daylight or artificial light and the
second part in the dark.
Figure 16. External eye of a normal adult cat. The eyelid margins
(upper and lower eyelid) are clearly defined and heavily pigmented;
the leading edge of the third eyelid is also pigmented There is an
undisrupted corneal reflex (the camera flash) and the cornea fills
almost the whole of the palpebral aperture in this animal with only
a small area of bulbar conjunctiva visible laterally (temporally).
Note that there is no clear distinction of the pupillary and ciliary
zones of the iris and that relative lack of surface iris pigment
allows portions of the major arterial circle to be viewed at the iris
periphery.
Initially the cat is observed from a distance in order to assess
the nature and severity of the ocular problem. If appropriate,
the cat should be allowed to move freely about the consulting
room, under different lighting intensities, as a very crude way of
assessing vision (see below), as well as mental status, posture
and gait. Normal cats are often reluctant to move around in
strange surroundings, so obstacle tests are of limited value.
Likewise, there may be difficulties in interpreting the following
response, which is the ability to follow a cotton wool ball
usually when dropped from a height under conditions of normal
lighting. In a compliant patient both central and peripheral vision
can be tested in this way, but unfortunately, many normal cats
are indifferent to the test. In darkness the following response
can be tested by playing a bright light on the surface of the
examination table and this is often more likely to elicit the
interest of a normal cat and can be used as a rudimentary test
of vision.
from in front of the patient and from above. The incomplete
bony orbital rim should also be inspected both visually and
manually.
The lacrimal apparatus is not evaluated in any detail at this
stage, although the presence and position of the upper and
lower lacrimal puncta should be confirmed and the possibility of
abnormalities of production, distribution and drainage may be
suspected according to the clinical presentation. The frequency
and adequacy of blinking should be noted as an empirical means
of assessing distribution of the tear film.
Under conditions of daylight or artificial light the general
appearance of the eyes and adnexa is observed and each side
compared to ensure that they are symmetrical (Fig. 14, 15). The
position of the globe in relation to the orbit should be assessed
The external eye should be assessed (Fig. 16), starting with
the margins, outer and inner surfaces of the upper and lower
5
corneal reflex indicates a tear film deficit, a superficial corneal
abnormality (Fig. 18), or both. It may also be appropriate to
check corneal sensitivity at this stage, particularly in those
situations in which corneal anaesthesia may be part of the
clinical presentation (for example, herpetic keratitis). This can
be done in an empirical fashion by touching the cornea lightly
with a fine wisp of cotton wool (afferent arm – cranial nerve
V), which should elicit a brisk blink (efferent arm facial nerve
– cranial nerve VII) and retraction of the globe (efferent arm
abducens – cranial nerve VI) in the normal cat.
A quick assessment of the remainder of the eye is made at this
point, to check the pupil size and shape and any gross deviation
from normality requiring more accurate assessment in the dark.
It is also appropriate to assess the relevant cranial nerves (CNs)
and autonomic nervous system in more detail at this juncture
[4, 21].
Figure 17. A cat with extensive symblepharon as complication of
neonatal feline herpes virus (FHV-1) infection. There is occlusion
of the upper and lower lacrimal puncta, the third eyelid is adherent
to the palpebral conjunctiva and the ventral conjunctival fornix
has effectively been obliterated.
Cranial nerve II (Optic)
Vision is tested by means of an obstacle test, the following
response, menace response, dazzle reflex and visual placing
response, The limitations of an obstacle test and interpretation
of the following response have been outlined above.
The menace response evokes a blink in reaction to a hand or
object moved slowly and steadily towards the eye. As well as
the afferent sensory pathway (CN II), a motor pathway via the
facial nerve (CN VII) is involved. It is important not to generate
air movement as this can stimulate the cornea (CN V).
The dazzle reflex (retinal light reflex) is a subcortical reflex
which initiates a bilateral partial eyelid closure (CN VII) when a
bright light is shone into the eye.
The visual placing response involves moving the cat towards
the edge of a table and checking for appropriate extension and
placing of the thoracic limbs on the table.
Figure 18. The corneal reflex is disrupted in this cat. The
pathognomonic superficial dendritic ulcers associated with herpetic
keratitis have been stained with fluorescein.
Cranial nerve III (Oculomotor)
The oculomotor nerve (CN III) nerve is responsible for pupillary
constriction (via parasympathetic innervation), innervation of
extra-ocular muscles (dorsal, medial and ventral rectus, and
the ventral oblique) and partial innervation of the upper eyelid
(levator palpebrae superioris). CN III is assessed by observation of
pupil size (symmetry, direct and indirect pupillary light response,
eye position and eye movements).
eyelids. There is close apposition of the upper and lower eyelids
to the globe, so examination of their inner surface is not always
easy. Nonetheless this is an important aspect of examination
in a species in which developmental defects of the eyelids and
symblepharon are not uncommon (Fig. 17). The presence and
position of the third eyelid should be observed and its outer
surface inspected once the eyelid has been protruded by pressure
on the globe through the upper eyelid. The inner surface of the
third eyelid is not examined routinely.
Deficits of CN III produce mydriasis, inability to constrict the pupil
in response to light, ventrolateral strabismus with no movement
of the globe except laterally, and ptosis.
The ocular surface, defined as the continuous epithelium which
begins at the lid margin, extends onto the back of the upper
and lower eyelids, and both surfaces of the third eyelid, into
the fornices and onto the globe, is examined next. Naked eye
examination should indicate whether the appearance of the
ocular surface is normal. A light source can be used to ensure
that the corneal reflex is normal (in this situation the corneal
‘reflex’ is the light from the light source reflected in miniature on
the corneal surface without disruption). Any disruption of the
Cranial nerves IV (Trochlear) and VI (Abducens)
These nerves supply motor function to extra-ocular muscles.
The trochlear (CN IV) innervates the dorsal oblique, and the
abducens (CN VI) innervates the lateral rectus and retractor oculi
muscles.
A deficit of the trochlear (CN IV) causes mild rotation of the globe
with the dorsal aspect turned laterally (dorso-lateral rotation),
6
the abnormal direction is easiest to discern by examination of
the accompanying pupil rotation.
nerve or vestibular apparatus) disease. Positional nystagmus may
also be detectable, with nystagmus occurring or changing as the
position of the head is altered. Unilateral vestibular disease will
also result in a head tilt and circling to the side of the lesion,
with ataxia, whereas in bilateral disease the head becomes
hyperflexed with the chin tucked onto the sternum.
A deficit of the abducens (CN VI) causes medial strabismus and
a lack of globe retraction in response to touching the cornea as
described earlier.
Cranial nerve V (Trigeminal)
The trigeminal nerve (CN V) is responsible for sensory input
from the entire face, and also provides motor function to the
muscles of mastication.
It is worth noting that nystagmus and convergent strabismus
are common abnormalities in imperfect albinos such as Siamese
and Himalayan cats in which pigment production is deficient.
Melanin, an essential regulator of axonal growth, is deficient in
the retinal pigment epithelium of these breeds and this leads to
misdirected axonal projections from the eye to the brain, so that
central visual pathways do not develop properly. The misrouting
of the central visual fibres results in reduced visual acuity
and absence of binocular vision. The convergent strabismus
(esotropia) which develops at about three months of age in some
cats is probably a consequence of abnormal visual perception
and attempts by the brain to create a complete visual field. The
mechanism underlying the nystagmus, which is present in most
cats, is less well understood, but may be due to contradictory
information perceived at the level of the mesencephalon.
A deficit of motor function results in an inability to close the
mouth and reduced tone, with or without atrophy, of the
masticatory muscles.
Sensory function can be assessed in the three main branches of
the nerve (ophthalmic, maxillary and mandibular), but only the
ophthalmic branch is discussed as it is the branch which conveys
afferent sensory stimulation from the eye. The ophthalmic
branch is tested by the palpebral (blink) reflex (elicited by
touching the medial canthus, tested in conjunction with CN VII
which provides the motor input for the blink) and the corneal
(blink) reflex (see above). Stimulation of afferent fibres of the
ophthalmic branch will also stimulate tear secretion. Sensory
deficits of the cornea result in an exposure keratopathy which
particularly affects the exposed area of cornea in the palpebral
aperture.
Light Reflex Pathway (Pupillary Light Response)
Pupil size is controlled by the iris sphincter muscle (under
cholinergic parasympathetic control) and the iris dilator muscle
(under adrenergic sympathetic control) and the balance between
the two systems is in a constant state of flux. The pathway for
the light reflex originates in the retina following stimulation of
receptors by bright light and the afferent pathway begins in the
ganglion cell layer. A proportion of the second order neurones
in the optic nerve that carry impulses derived from stimulation
of receptor cells are pupillomotor fibres, which leave the optic
tract to enter the midbrain where they synapse with third order
neurones in the pretectal nucleus, which in turn synapse within
the parasympathetic component of the oculomotor nucleus.
There is extensive cross-over of both second order neurones
at the optic chiasm, and third order neurones at the caudal
commissure (between the pretectal and oculomotor nuclei)
allowing a bilateral pupillary light response (PLR) to stimulation
with light. Efferent parasympathetic fibres from the oculomotor
nucleus are contained in the oculomotor nerve (CN III), they
enter through the orbital fissure to synapse at the ciliary ganglion
lateral to the optic nerve, with post-ganglionic fibres passing in
two short ciliary nerves (medial and lateral) to innervate the iris
musculature. Partial internal ophthalmoplegia with a hemidilated
pupil occurs if only one of the two ciliary nerves supplying the
iris constrictor muscle is paralysed; a ‘D-shaped’ or ‘reverse
D-shaped’ pupil is the consequence, depending on which of the
two nerves is affected
Cranial nerve VII (Facial)
The facial nerve (CN VII) provides motor innervation to the
muscles of facial expression and parasympathetic fibres supply
the lacrimal glands (see below). The facial nerve becomes closely
associated with the vestibulocochlear nerve once it has left the
brain stem and they enter the internal auditory meatus together;
a single lesion may involve both nerves.
Abnormality of CN VII causes facial paralysis. Unilateral deficits
may be observed as asymmetry of the ears, eyelids, lips and
nose. Specific tests include the palpebral blink reflex (see CN V)
and corneal blink reflex (see CN V), the menace response (see
CN II), and observation of normal ear and facial movements.
When the cat attempts to blink, the globe is retracted and the
third eyelid sweeps across the cornea, but there is no movement
of the upper and lower eyelids.
Cranial nerve VIII (Vestibulocochlear)
The cochlear portion of the eighth cranial nerve (CN VIII) is
responsible for hearing, and the vestibular portion is responsible
for equilibrium of posture and gait and co-ordination of eye
movements
Oculosympathetic Pathway
Sympathetic innervation to the iris originates in the hypothalamus.
Upper motor neurones synapse with lower motor neurones
at the T1-T3 level of the spinal cord, and their axons exit and
travel in the thoracic and vago-sympathetic trunk to synapse
in the cranial cervical ganglion close to the tympanic bulla.
Postganglionic fibres pass through the middle ear and join the
ophthalmic branch of the trigeminal (CN V) nerve to innervate
Cochlear deficits result in deafness, while vestibular deficits may
manifest as nystagmus. If spontaneous horizontal nystagmus
is present, the fast phase moves away from the side of the
lesion. Nystagmus can be horizontal, vertical or rotatory; if it
is vertical, it indicates that the disease is of central origin (i.e. a
disease affecting the vestibular nucleus). The other two forms of
nystagmus can occur with either central or peripheral (vestibular
7
Figure 19. In this cat with multiple ocular defects there is some
reduction in the size of the eye (microphthalmos) note the exposed
bulbar conjunctiva laterally and third eyelid prominence. The iris
is markedly hypoplastic with obvious full thickness defects ventrolaterally. The lens equator is visible in the gap as are a few poorly
developed ciliary processes. Persistence of the tunica vasculosa
lentis, mainly as pupillary membrane remnants, is visible as faint
opacties in the pupillary aperture
Figure 20. This cat was scratched by another cat some years earlier
and at the time it was assumed that only the upper eyelid was
damaged (note that the eyelid remains swollen). In fact the globe
had also been penetrated and the lens directly damaged by the claw.
In this photograph a posteriorly luxated lens, with a hypermature
cataract, is apparent, together with focal changes of iris colour
(greyish) and iris neovascularisation. Pigmented strands, marking
the site of previous posterior synechiae, are apparent in the dorsal
aspect of the pupillary aperture.
the iris dilator muscle and the smooth muscle of the periorbital
muscles and eyelid. Damage to the sympathetic supply to the
eye results in Horner’s syndrome, of which the obvious ocular
features are third eyelid prominence, a reduced palpebral
aperture and a miotic pupil (Fig. 15).
the stimulated eye (dynamic contraction anisocoria). If the light is
swung to stimulate the fellow eye then the pupil of this eye will,
in turn, become more miotic and if the light is swung from one
eye to the other, the miosis will alternate (alternating contraction
anisocoria). This is the basis of the swinging flashlight test which
can be used to detect the presence of a relative afferent pupillary
defect (Marcus Gunn phenomenon). With a prechiasmal lesion,
for example, when the light is swung to stimulate the fellow
eye, the miotic pupil of this eye suddenly dilates whilst receiving
direct illumination - a positive swinging flashlight test.
Assessment of pupillary response
Pupillary assessment under a range of lighting conditions is a
standard feature of neuro-ophthalmological examination. The
shape, size and position of the pupils under normal conditions
of illumination are examined first, then the examination is
repeated with the lights dimmed; a technique which helps
in the differentiation of sympathetic and parasympathetic
defects. In bright light miosis due to sympathetic dysfunction
may be difficult to detect, because of the dominance of the
parasympathetic system. In dim light, however, such a defect
is obvious as the anisocoria (inequality of pupil size) becomes
more marked with the smaller pupil being on the affected side.
Conversely, the mydriasis found in parasympathetic paralysis
(for example, traumatic damage to the ciliary ganglion), may be
obvious in bright light, but difficult to detect in dim light.
Anisocoria (inequality of pupil size) may be a consequence of
topically or systemically administered drugs (e.g. mydriatics,
miotics, ketamine), congenital or acquired abnormalities of
the eye, the light reflex pathway, oculosympathetic system
(e.g. Horner’s syndrome), midbrain or cerebellum. The
underlying cause is not always obvious, particularly in relation
to inflammatory disorders and detailed investigations may
be required [2, 4, 21]. It is important to detect which eye is
abnormal and this may require careful observation of direct
and consensual pupillary light reflexes and pupillary dilation
in response to low lighting conditions. It is also important to
realise that mild inequality of pupil size is quite common in cats
and is assumed to be due to differences in basal sympathetic or
parasympathetic tone to the two eyes. The origin of this type of
anisocoria may be ‘central’ in so far as it relates to asymmetries
of supranuclear inhibitory control of the parasympathetic nuclei
of the oculomotor nerves.
The direct (ipselateral) and consensual (indirect and contralateral)
response to bright light is assessed next and this test is best
performed in conditions of near darkness. Partial decussation of
the optic nerve fibres at the optic chiasm and caudal commissure
of the midbrain ensures that the normal pupil response to a
bright light directed into one eye will be more intense miosis in
8
A
B
Figure 21. Normal iris (a) and ocular fundus (b) in a black cat
(normal pigmentation). Note that the optic nerve head is round
and slightly sunken. The three pairs of primary retinal vessels
curve over the rim and the venules (wider and darker) can be
readily distinguished from the arterioles (slightly more tortuous).
The optic nerve head is located within the tapetal fundus which is
reflective and slightly granular, part of the non tapetal fundus is
visible ventral to the optic nerve head..
is usually readily determined, whereas the depth is not always
easy to assess unless a slit lamp biomicroscope is used.
It may be sensible to instil a mydriatic once neuro-ophthalmological examination is complete, as mydriasis is needed for
comprehensive examination of the lens, vitreous and fundus.
This is because, in comparison with the dog, the pupil of normal
cats responds briskly and more completely to bright light and
the pupil shape changes from round to a narrow vertical slit,
resulting in a very limited field of view. Tropicamide 1% is the
drug of choice and one drop should be applied to each eye
at the end of the neuro-ophthalmological examination; it takes
some 15 minutes to achieve sufficient mydriasis for examination,
although maximal dilation takes about two hours [22].
The anterior chamber should also be optically clear. A slit beam,
rather than a diffuse beam, is used to detect subtle opacities
within the aqueous, be they focal or diffuse in nature. The depth
of the anterior chamber is also most easily assessed by use of
a slit beam, or by shining a beam of light across the eye from
lateral to medial. The anterior chamber is deep and the pectinate
ligament of the iridocorneal angle can be observed directly.
The iris of most cats is lightly pigmented and the distinction
between the pupillary zone (usually darker) and ciliary zone
(usually lighter) at the collarette is not always present, so that
the iris is of uniform colour. Colour variations may be present
between irides and within different sectors of the same iris.
Variations of pigmentation produce a range of colours. In the
least pigmented, genuinely subalbinotic iris, which is almost pink
in colour, the iris is often so thin that it can be transilluminated.
Full thickness iris defects are indicative of congenital (Fig. 19) or
acquired abnormality. Similarly, any acquired loss of iris detail or
change of iris colour is indicative of abnormality (Fig. 20).
In the dark
Darkness minimises distracting reflections and is an essential part
of ophthalmic examination. A light source and magnification,
or a slit lamp biomicroscope, is required for the first phase of
this examination. Both direct and indirect ophthalmoscopy are
required for examination of the ocular fundus in the second
phase and the techniques are complimentary rather than
exclusive.
The anterior segment (the internal structures of the globe up
to and including the lens) is examined with a light source and
magnification, or a slit lamp biomicroscope.
The limbus and cornea are examined first. Most of the limbus
is invisible in the normal cat except, sometimes, laterally. The
limbal zone is usually clearly defined because of a rim of pigment
on the corneal side.
The adult pupil is round when dilated and narrows to a vertical
slit on constriction. It is important to observe the size and shape
of the pupil, both constricted and dilated, paying particular
attention to the pupillary margin, as deviations from normal may
indicate posterior synechiae or neurological abnormalities. It is
also important to ascertain that no opacities can be detected in
the pupillary aperture or beyond.
The cornea should be of the right shape, size and profile, of
lustrous appearance and optically clear. Any opacities, whether
focal or diffuse, are abnormal, as is any vascularisation or other
infiltration. The extent and position of any corneal abnormality
The whole lens can only be examined in detail when a mydriatic
has been used, paying particular attention to its shape, position
and clarity. The light source is used to demonstrate the anterior
and posterior lens surfaces by observing the catoptric images
9
A
B
Figure 22. Normal iris (a) and ocular fundus (b) in a subalbinotic
cat. In this animal there is no tapetum and both retinal and
choroidal vessels are obvious against the creamy white scleral
background. There is sparse pigmentation ventral to the optic
nerve head.
which are visualised on the anterior lens capsule (erect) and the
posterior lens capsule (inverted). It is easier to establish these
boundaries by noting the relative movement of the images in
relation to the light source (parallax).
four quadrants of the ocular fundus are checked in whichever
order the examiner finds most convenient; for example, dorsolateral, dorso-medial, ventro-medial and ventro-lateral. The
tapetal fundus is extensive and reflective, finer details will not
be appreciated and subtle abnormalities will be missed if the
intensity of illumination is too high. It is easiest to record any
abnormalities using a simple diagram comprising a circle divided
into quadrants. Variations, which may or may not be of clinical
significance, can only be appreciated if there is an understanding
of the normal range of appearances. Fortunately there are fewer
normal variations in cats than dogs.
The posterior segment (the internal structures of the globe
beyond the lens) is examined next using some or all of a light
source, slit lamp biomicroscope, indirect ophthalmoscope and
direct ophthalmoscope.
The anterior vitreous is most easily examined with a pen light or
slit lamp and should be free of obvious opacities.
Recording
The findings of ophthalmic examination should be recorded
by means of annotated diagrams which take only seconds to
produce. Photography, of course, is also helpful, particularly as
a means of charting changes of appearance. Accurate recording
should be continued if the cat is examined on more than one
occasion and the importance of repeat examinations as a means
of monitoring progress and separating true abnormalities from
artefacts, cannot be overemphasised (Fig. 23).
Indirect ophthalmoscopy and direct ophthalmoscopy are
used to examine the ocular fundus and, to some extent, the
posterior vitreous. Indirect ophthalmoscopy provides low power
examination of a wide area and is particularly useful when the
ocular media lack optical clarity. Direct ophthalmoscopy provides
a magnified view of a relatively small area. Both distant direct
ophthalmoscopy (see above) and close direct ophthalmoscopy
should be used as part of routine examination.
Diagnostic Texhniques [10, 14, 20]
With either type of ophthalmoscopy the optic nerve head (optic
disc or papilla), which is situated within the tapetal fundus, is
located first and its size, shape and colour should be noted (Fig.
21). In cats the optic nerve head (ONH) is usually unmyelinated
so that the ONH is round in shape and slightly recessed, the optic
nerve becoming myelinated posterior to the lamina cribrosa.
The retinal vasculature is next examined, paying particular
attention to the number and distribution of the retinal vessels
as they hook over the rim; the venules are generally wider
and darker than the arterioles. The terminal choroidal vessels
appear as dark dots because they are viewed end on. In poorly
pigmented, subalbinotic, eyes the tapetum may be absent
and larger choroidal vessels will be visible (Fig. 22). Finally, all
Sampling techniques
Swabs and scrapes may be helpful in establishing aetiology
and should be taken from the affected area. Topical local
anaesthesia is not necessary when sampling the conjunctiva and
eyelid margins, but is essential for corneal samples.
It is important to select the correct culture medium; for example,
viral and chlamydial transport medium (VCTM) is needed for the
isolation of Chlamydophila and viruses, standard bacteriology
culture media are inappropriate. If there is any uncertainty as
to the normal microbiology of the conjunctival sac [11, 12, 25],
10
A
B
Figure 23. Feline hypertensive disease. The most obvious features in this cat are variations of retinal vessel calibre, retinal oedema, focal
bullous retinal detachments (largely as a consequence of subretinal effusion). An extensive area of pre-retinal haemorrhage is apparent
dorsally, Mean systolic blood pressure was 280mmHg at the time of the photograph (a). Within a week of treatment, mean systolic blood
pressure has fallen to 210mmHg, the retina has re-attached and the haemorrhage is resorbing (b), Systemic hypertensive disease is a
common condition in the cat and the eye is a most sensitive target organ. The two photographs illustrate the importance of sequential
examination and accurate recording.
or which diagnostic test to perform, it is prudent to contact
a diagnostic laboratory before taking the samples. Ocular
(conjunctival or corneal) and oropharyngeal swabs will be
required as part of the diagnostic work up in most cats which
present with ocular surface disease (Fig. 24a, 24b). Dacron or
cotton wool swabs have been used traditionally for obtaining
superficial cells from sites such as the conjunctiva and cornea,
but other instruments such as the cytobrush may be superior in
terms of the yield, distribution and preservation of cells [1].
abnormalities of the eyelid margin or ocular surface. A clean dry
glass slide is pressed gently, but firmly, against the abnormal area
and the preparation is air-dried and fixed in methanol. As these
smears can be difficult to interpret, they are best submitted to
an experienced pathologist. A minimum of two slides should
be sent.
Biopsies may be taken from the eyelids and conjunctiva
following topical anaesthesia. One drop of local anaesthetic
(e.g. proxymetacaine hydrochloride) is applied to the eye and
shortly afterwards a cotton-wool tip soaked in local anaesthetic
is held against the area which is to be sampled for approximately
one minute. More extensive surgery is better performed under
general anaesthesia, with topical anaesthesia as a useful adjunct.
A biopsy needle (fine needle aspiration biopsy) or surgical excision
is used to obtain the sample, which is transferred immediately
into fixative. The amount of fixative should be at least ten times
Scrapes are obtained with, for example, a sterile Kimura spatula
or the blunt end of a sterile 15 gauge Bard Parker disposable
scalpel blade. A smear is made directly onto a clean, dry,
glass slide and the preparation is air-dried, fixed in methanol
and Gram-stained, or it may be submitted to a pathologist for
staining and interpretation.
Impression smears are useful as a means of sampling
Figure 24. A conjunctival swab being taken from the lower conjunctival sac (a) and from the oropharynx. (b)
A
B
11
Topical ophthalmic stains
Fluorescein sodium is an orange dye which changes to green
in alkaline conditions (eg in contact with the normal preocular
tear film). It is mainly used to detect corneal ulceration (Fig. 18,
25) and is rapidly absorbed by the exposed hydrophilic stroma;
fluorescein does not stain the lipid-rich anterior epithelium or
Descemet’s membrane. Fluorescein should be applied after
other tests (e.g. Schirmer tear test, scrapes and swabs for
culture and sensitivity) have been performed, as the dye can
interfere with certain diagnostic tests [7]. Impregnated strips or
single dose vials may be used and it is usual to place the strip
or solution in the lower conjunctival sac and allow the blink to
distribute the fluorescein. A small quantity of sterile saline can
be used as an ocular irrigant to provide sufficient moisture and
to flush excess stain from the ocular surface. Subtle staining can
be demonstrated with a blue light source.
Figure 25. Multiple superficial erosions stained with fluorescein
and viewed in blue light. The cat had a nasal squamous cell
carcinoma and the ulceration was thought to be a consequence of
reactivation of latent FHV-1.
Fluorescein can also be used as a means of identifying aqueous
leakage (Seidel test) following corneal damage (Fig. 26) or after
corneal repair and is sometimes helpful when checking the
patency of the naso-lacrimal drainage apparatus (Fig. 27).
the volume of the specimen. Neutral buffered formaldehyde can
be used for routine light microscopy and immunohistochemistry.
Glutaraldehyde (2.5% in 0.1M cacodylate buffer) should be used
for electron microscopy.
Rose bengal is a red dye used to demonstrate ocular surface
and tear film abnormalities. It is not employed as a routine stain
because it irritant to the eye and can interfere with the isolation
of pathogens from corneal and conjunctival scrapes.
Corneal biopsy is useful on rare occasions. General anaesthesia
is required and the biopsy must include the edge of the stromal
infiltrate using a microsurgical scalpel blade. The biopsy can
be pressed directly onto a microscope slide for impression
cytology.
Schirmer Tear Test
The Schirmer I tear test is the method most commonly employed
to test aqueous tear film production (Fig. 26). The test should
be performed on the conscious, non-sedated cat so as to avoid
falsely low readings; even so, the values are likely to be noticeably
lower than those obtained in dogs. Topical local anaesthetic
solution is not used for a Schirmer I tear test (STT I) so that it
is stimulated (reflex) tear production which is being assessed.
Mean values of approximately 12mm (+/- 5) per minute are
obtained in normal cats. Schirmer II testing (STT II) checks basal
Aqueous and vitreous paracentesis are of occasional value.
For example, neoplastic cells can be harvested from the iris and
anterior chamber and the technique can aid identification of
intraocular yeasts and fungi
Figure 26. Penetrating injury to the cornea before (a) and after (b) staining with fluorescein. Gentle pressure applied to the globe via the
upper eyelid following application of fluorescein (forced Seidel test) indicated, on slit lamp examination, that subtle aqueous leakage was
present. Note that the third eyelid has been damaged in a previous fight.
A
B
12
Figure 28. A Schirmer tear test strip being used to check tear
production.
Figure 27. In this Persian cat with chronic epiphora, fluorescein
has been applied to both eyes, in sequence, and no fluorescein has
emerged from the nostrils or been visualised in the oropharynx.
Investigations of chronic epiphora can be difficult in this breed
for a number of reasons, including the facial anatomy (flat face),
overlong palpebral aperture, close apposition of the eyelids to the
cornea, shallow lacrimal lake, a wick effect from hairs at the medial
canthus and lower medial eyelid entropion. Poor distribution
and drainage of the tear film resulting in epiphora are a common
consequence.
Initial examination consists of visual inspection of the lacrimal
puncta. Their presence, size and position should be checked,
low power magnification may be useful.
Patency of the lacrimal system can be tested using fluorescein
drops instilled into the lower conjunctival sac, which may appear
at the ipselateral nostril (or the back of the throat) within 1-10
minutes of application in approximately 50% of normal cats.
In the other 50% of normal cats fluorescein fails to appear. A
positive result is therefore significant, whereas a negative result
does not necessarily mean that the duct is blocked. Both sides
should be tested but with sufficient time between tests to
avoid misinterpretation. If samples are required for culture and
sensitivity as detailed below, checking patency with fluorescein
is usually omitted.
secretion and is performed after the application of topical local
anaesthetic; mean values of approximately 10mm (+/- 5) per
minute are obtained with this technique [6]. With both tests the
range of values is wide; in one series of 76 cats the range for
Schirmer II tear tests was 1mm to 33mm and the test results for
cats of less than 12 months of age were significantly lower than
those obtained for cats of more than 12 months [24]. In general,
values of less than 8mm per minute should be regarded with
suspicion, especially if there is an abnormal ocular appearance
or disparity in the STT values between the two eyes. Repeated
values of less than 5mm, together with other clinical signs, are
indicative of a lack of aqueous component production, clinically
manifest as keratoconjunctivitis sicca.
When samples are required for culture and sensitivity they can be
obtained by irrigation with sterile water following cannulation
or catheterisation of the upper punctum and canaliculus; a
range of nasolacrimal cannulae are available and 24-25 gauge
disposable are ideal for cats.. It is best to perform all investigative
and treatment techniques under general anaesthesia to reduce
the risk of damage to the drainage apparatus. The pharynx
should be packed with moist, soft, gauze bandage and the
patient positioned with a head down tilt in order to prevent
inadvertent inhalation of the irrigating fluids.
The test is performed using commercially available test strips
which are up to 60mm in length, with a notch some 5mm from
the tip. The strip is bent at the notched region whilst still within
the packing so as to avoid contaminating the tip with grease
from the fingers, the tip is placed just within the conjunctival sac
(Fig. 28). The strip is removed after 1 minute and the value, in
millimetres, is read immediately as measured from the notch.
To confirm that drainage is normal, or to re-establish drainage
in uncomplicated cases, a set protocol should be followed.
Digital pressure is applied over the region of the lacrimal sac to
occlude the entrance to the nasolacrimal duct and sterile water
or saline is injected via a 25 gauge lacrimal cannula in the upper
punctum and canaliculus. Silver lacrimal cannulae are the most
satisfactory as they are less traumatic than plastic cannulae and
can be re-used after sterilisation. The liquid is injected with only
moderate force and should appear at the lower punctum almost
immediately. Once liquid appears, the lower punctum and
canaliculus is occluded by digital pressure and fluid should then
pass along the nasolacrimal duct and appear at the ipselateral
nares a short time after injection. Samples can be collected for
Investigation of naso-lacrimal drainage
The upper and lower lacrimal puncta are small openings located
near the eyelid margins approximately 2mm from the medial
canthus. They can be examined directly if the medial margins
of the eyelids are everted slightly. The excretory portion of the
lacrimal system consists of the lacrimal puncta, canaliculi, a
rudimentary lacrimal sac and the nasolacrimal duct. The duct
passes through the lacrimal bone along the medial surface of
the maxilla to the nasal cavity.
13
culture (aerobic and anaerobic) as fluid drips from the nares.
If it is impossible to establish patency using irrigation a fine
catheter or monofilament nylon may be passed through the
drainage system via one of the puncta. The end of the catheter
or nylon must be smooth and rounded to avoid iatrogenic
damage.
of foreign bodies in the eye and orbit. It may also be used to
locate intraocular and orbital space occupying lesions, but will
not distinguish the tissue of origin and may not always allow
differentiation of inflammation and neoplasia.
Computed tomography (CT) will locate and define
abnormalities within the eye, orbit and cranium and has been
used to evaluate orbital neoplasia in cats [3].
Dacryocystorhinography is a technique whereby an iodinebased contrast agent may be used to delineate the nasolacrimal
drainage system. After plain radiographs (usually lateral and
open mouth views) have been taken, the upper or lower
punctum and canaliculus is cannulated and 2-3ml of contrast
agent is injected as further radiographs are taken.
Magnetic resonance imaging (MRI) is the best method of
imaging currently available and provides superb detail of the
eye, orbit and intracranial structures [17]. The excellent spatial
and soft tissue resolution allows space-occupying lesions to be
delineated accurately; so necessary in surgical planning [23].
Tonometry
Tonometry is the measurement of intraocular pressure. The
MacKay-Marg electronic applanation tonometer is the most
accurate indirect device for use in cats; portable tonometers,
such as the ProTon, Tono-Pen, Tono-Pen XL and Tonovet, are
all reasonably accurate [15]. Results between the different
tonometers are not directly comparable and repeat measurements
should always be made with the same instrument. Furthermore,
it is sensible to build up a library of values from normal cats,
whatever instrument is selected for use. SchiØtz indentation
tonometry can also be used, but repeatable accurate results are
more difficult to achieve and electronic applanation tonometers
are a better choice, despite their greater expense.
REFERENCES
[1]
[2]
[3]
[4]
The mean normal intraocular pressure of conscious unsedated
cats has been reported as 22.2mm Hg ±-5.2 when measured
with the Mackay-Marg tonometer and this correlated with mean
readings of 21.6mm Hg obtained with the SchiØtz tonometer
and converted into millimetres of mercury using the human
calibration table, the Tono-Pen gave statistically significant
lower mean readings of 20.2mm Hg [16]. Another study, using
the Tono-Pen XL, indicated an intraocular pressure of 18.1 ±
0.31 mmHg over a 24-hour period. [8].
[5]
[6]
[7]
Topical local anaesthetic (proxymetacaine hydrochloride) is
applied prior to measuring the intraocular pressure in the
conscious non-sedated cat. Sedation and general anaesthesia
should be avoided prior to tonometry as they will affect
intraocular pressure; furthermore, topical mydriatics produce a
transient increase in intraocular pressure [22]. There is also a daily
variation of intraocular pressure that appears to be independent
of sex, age, or ocular disease [8].
[8]
[9]
[10]
Diagnostic Imaging [13, 17]
Radiography can be useful when there are bony changes or
radio-opaque foreign bodies, but it is of limited value in aiding
diagnosis of soft tissue problems of the eye and orbit.
[11]
[12]
Ocular ultrasonography (both A-scan and B-scan) is a
valuable method for soft tissue imaging in most species [9, 17],
including cats, and is best performed with a high frequency
transducer of between 7.5 - 10 Mz. The technique can be used in
conscious cats and general anaesthesia is not usually necessary.
Ultrasonography is used in biometric studies, to help with the
assessment of cloudy and opaque eyes and for identification
[13]
[14]
14
BAUER (G.A.), SPEISS (B.M.), LUTZ (H.) - Exfoliative cytology
of conjunctiva and cornea in domestic animals: A comparison
of four collecting techniques. Veterinary and Comparative
Ophthalmology, 1996, 6, 181-186.
BERCOVITCH (M.), KROHNE (S.), LINDLEY (D.) - A Diagnostic
Approach to Anisocoria. The Compendium on Continuing
Education for the Practicing Veterinarian, 1995, 17, 661-673.
CALIA (C.M.), KIRSCHNER (S.E.), BAER (K.E.), STEFANACCI (J.D.)
- The use of computed tomography scan for the evaluation of
orbital disease in cats and dogs. Veterinary and Comparative
COLLINS (B.K.), O’BRIEN (D.P.) - Autonomic dysfunction of the
eye. Seminars in Veterinary Medicine and Surgery, 1990, 5, 2436.
CRISPIN (S.M.) - Feline Ophthalmology. In: Notes on Veterinary
Ophthalmology. Blackwell, 2005, 177-227.
CRISPIN (S.M.) - Examination of the eye and adnexa. In: Barnett
KC and Crispin SM Feline Ophthalmology: An Atlas and Text.
London: WB Saunders Company, 1998, 1-10.
DA SILVA CURIEL (J.M.A.), NASISSE (M.P.), HOOK (R.R.), WILSON
(H.W.), COLLINS (B.K.), MANDELL (C.P.) - Topical fluorescein dye:
Effects on immunofluorescent antibody test for feline herpes
keratoconjunctivitis. Progress in Veterinary and Comparative
DEL SOLE (M.J.), SANDE (P.H.), BERNADES (J.M.), ABA (M.A.),
ROSENSTEIN (R.E.) - Circadian rhythm of intraocular pressure in
cats. Veterinary Ophthalmology, 2007, 10, 155-161.
DIETRICH (U.M.) - Ophthalmic examination and diagnostics,
Part 3: Diagnostic ultrasonography. In: Gelatt KN (ed) Veterinary
Ophthalmology 4th Edition. Volume 1. Blackwell Publishing, 2007,
507-519.
EKESTEN (B.) - Ophthalmic examination and diagnostics, Part 4:
Electrodiagnostic evaluation of vision. In: Gelatt KN (ed) Veterinary
Ophthalmology 4th Edition.. Volume 1. Blackwell Publishing, 2007,
520-535.
GASKIN (J.M.) - Microbiology of the canine and feline eye.
Veterinary Clinics of North America: Small Animal Practice, 1980,
19, 303-316.
GERDING (P.A), KAKOMA (I.) - Microbiology of the canine and
feline eye. Veterinary Clinics of North America: Small Animal
Practice, 1990, 20, 615-625.
KALLBERG (M.E.) - Ophthalmic examination and diagnostics, Part
2: Ocular imaging. In: Gelatt KN (ed) Veterinary Ophthalmology
4th Edition. Volume 1. Blackwell Publishing, 2007, 484-506.
MAGGS (D.J.). - Laboratory investigation of ophthalmic disease.
In. Peterson-Jones SM, Crispin SM. BSAVA Manual of Small Animal
Ophthalmology 2nd Edition. BSAVA, 2002, 23-29.
[15] MILLER (P.E.), PICKETT (J.P.), MAJORS (L.J). - In vivo and in
vitro comparison of Mackay-Marg and TonoPen applanation
tonometers in the dog and cat. Transactions of the American
College of Veterinary Ophthalmologists, 1988, 19, 53-58.
[16] MILLER (P.E.), PICKETT (J.P.) - Comparison of human and canine
tonometry conversion tables in clinically normal cats. Journal of
the American Veterinary Medical Association, 1992, 201, 10171020.
[17] MUNRO (E.), RAMSEY (D.T.). - Ocular Imaging. In. Peterson-Jones
SM, Crispin SM. BSAVA Manual of Small Animal Ophthalmology
2nd Edition. BSAVA, 2002, 1-12.
[18] MOULD (J.R.B.) - The right ophthalmoscope for you? In Practice,
1993, 15, 2, 73-76.
[19] MOULD (J.R.B.) - Ophthalmic Examination. In. Peterson-Jones
SM, Crispin SM. BSAVA Manual of Small Animal Ophthalmology
2nd Edition, BSAVA, 2002, 1-12.
[20] OLLIVIER (F.J.), PLUMMER (C.E.), BARRIE (K.P.) - Ophthalmic
examination and diagnostics. Part 1: The eye examination
and diagnostic procedures. In: Gelatt KN (ed) Veterinary
Ophthalmology 4th Edition. Volume 1. Blackwell Publishing,
2007, 438-484..
[21] SPARKES (A.H.) - Neuro-ophthalmology. In: Barnett KC and Crispin
SM (eds) Feline Ophthalmology: An Atlas and Text. London: WB
Saunders Company, 1998, 169-183.
[22] STADTBAUMER (K.), FROMMLET (F.), NELL (B.) - Effects of
mydriatics on intraocular pressure and pupil size in the normal
feline eye. Veterinary Ophthalmology, 2006, 4, 233-237.
[23] RAMSEY (D.T.), GERDING (P.A.), LOSONSKY (J.M.), KURIASHKIN
(I.V.), CLARKSON (R.D.) - Comparative value of diagnostic
imaging techniques in a cat with exophthalmos. Veterinary and
Comparative Ophthalmology, 1994, 4, 198-202.
[24] WATERS (L.) - The Schirmer II tear test in cats. – Clinical Research
Abstracts, British Small Animal Veterinary Association Congress,
Birmingham, 1994.
[25] WHITLEY (R.D.) - Canine and feline primary ocular bacterial
infections. Veterinary Clinics of North America: Small Animal
Practice, 2000, 30, 1151-1167.
15
OPTHALMOLOGY
Indolent ulcers in the dog
G. Janssens1
SUMMARY
Corneal ulcers are probably the most common problem of the canine eye seen in general veterinary practice.
Most of these ulcers result from a variety of traumatic and irritating conditions and usually respond well to medical
therapy alone, provided they are not too deep. However, indolent ulcers are different: they are chronic superficial
ulcers that result from a structural defect of the cornea and as a result they heal poorly and are usually refractory to
medical therapy alone.
in middle aged to older dogs, without any sex predisposition
and can occur in any canine breed, although Boxers and Corgis
are predisposed. There is no known mode of inheritance.
publication in EJCAP
Clinical findings
The normal cornea is a clear transparent structure composed
of several layers: epithelium, subepithelial basement membrane,
stroma, Descemet’s membrane and endothelium. These layers
contribute to the cornea’s unique transparency by providing a
non-keratinized surface, maintaining control of its water content
and of its highly organised arrangement of collagen fibrils and
ensuring the absence of blood vessels and pigment. Structural
adhesion of the epithelial layer to the underlying anterior
stroma is provided by hemidesmosomes and anchoring fibrils
that are firmly attached between the basal epithelial cells and
the subepithelial basement membrane. The epithelium has a
remarkable capacity of regeneration and usually heals within
approximately seven days.
Dogs with indolent ulcers often present with photophobia,
blepharospasm and epiphora. The pain may be moderate, but
it is minimal compared with other typical superficial ulcers and
it usually decreases with the chronic nature of the erosion. A
delayed vascular response may be seen with chronic lesions and
this is characterised by an ingrowth of superficial blood vessels
from the limbus.
Indolent ulcers can be diagnosed by the appearance of a loose
or redundant epithelial margin surrounding the ulcer and by
eliminating other causes of superficial corneal ulcers.
Fig. 1 The non-attached
lip of epithelium in a
refractory ulcer may
lie flat or may be folded
back on itself.
Indolent ulcers are also known as chronic epithelial erosion,
refractory superficial ulcer, Boxer ulcer, recurrent erosion,
refractory epithelial erosion and epithelial basement membrane
dystrophy. Because these ulcers are often breed-related,
develop spontaneously and may eventually affect both eyes,
they may be considered to represent a primary corneal epithelial
or superficial stromal dystrophy. Although the exact mechanism
of this dystrophy has not been fully resolved, it is generally
believed to be caused by a failure of attachment between the
basal epithelium to the underlying membrane, which is either
absent or abnormal.
Although indolent ulcers may occur in any species, including cats
and horses, it is more commonly seen in dogs. It is usually seen
1) Algemene Dierenkliniek Randstad, Frans Beirenslaan 155, 2150 Borsbeek, Belgium.
1
Indolent ulcers in the dog - G. Janssens
Fig. 2 Dry sterile cotton-tipped applicator.
Fig. 3 Diagram of the pattern used to perform grid keratotomy
(within blue circle).
A fluorescein stain can assist in the diagnosis as the dye will
not only stain the ulcerated area (exposed anterior stroma) but
it will also migrate under the loose flaps of the epithelium and
stain the surrounding anterior stroma. Consequently, the area of
staining is much larger than the size of the actual ulcer. Another
test for an indolent ulcer is to rub the margins of a superficial
ulcer gently with a dry sterile cotton-tipped applicator: if the
loose epithelium can be stripped off the test is positive.
bullae may rupture or lift the epithelium off the stroma. If all
those causes are ruled out, then persistent corneal erosion is
considered to be primary.
Histopathology
During the healing of the epithelial erosion, cell migration and
mitosis occur, but abnormal basement membrane material and
possibly hyalinized collagen prevent the epithelium from attaching
to the underlying stroma. Degeneration of basal epithelial cells,
paucity of hemidesmosomes and subepithelial fibrogranular
material is seen on histology. The basement membrane is
thickened and irregular in appearance. There is separation of
basal epithelial cells from their basement membrane.
In the case of corneal ulcers one should ALWAYS perform a
Schirmer Tear Test (STT). It is important to rule out secondary
causes of delayed healing, such as chronic irritation associated
with cilia (distichiasis, trichiasis, ectopic cilia) or entropion, facial
paralysis, lagophthalmos and infection. Abnormalities of the
preocular tear film, such as keratoconjunctivitis sicca and mucin
deficiency, may also contribute to ulcer formation. With severe
or chronic stromal edema, subepithelial bullae may form. These
Fig. 5 Eyelid speculum placed for better visualisation of the cornea.
The use of the speculum here is for demonstration purposes only
and is not routinely performed in practice.
Fig. 4 Fluorescein stain migrates under a loose flap of epithelium.
2
Fig. 6 Debridement with a dry, sterile, cotton-tipped applicator.
Fig. 7 Removed epithelium.
Treatment
outwards to the true edge of the erosion (the region where the
epithelium is properly attached to the underlying stroma). This
procedure enlarges the original ulcer.
It is important to inform the owners of the progression, expected
healing time and possible recurrence of the indolent ulcer in
the same eye and even the possibility that the second eye will
develop the same problem.
There are several steps that will facilitate healing by removing
epithelium and encouraging epithelial attachment.
Debridement and keratotomy
In most dogs, the mechanical debridement of the loose
redundant epithelium can be performed with a dry, sterile,
cotton-tipped applicator, after application of topical anaesthesia
0.4 % oxybuprocainhydrochloride (Minims, Chauvin, Brussels,
Belgium) three times with one minute intervals. With a circular
motion, the debridement starts at the apparent edge of the
erosion (the rim of the loosened epithelium) and then continues
A linear or grid keratotomy is then performed with a 25-27 gauge
needle on a 2 ml syringe or by just holding the needle hub. It
is recommended that this procedure be performed with good
magnification. Small parallel linear incisions are made in a gridlike fashion through the epithelium and basement membrane
to expose the underlying corneal stroma. To do this, the needle
should penetrate no further than 0.2-0.3 mm deep and the
linear incisions are placed 1-2 mm apart and must extend about
3mm into the normal epithelium surrounding the ulcer. Parallel
lines are made in a horizontal plane and then perpendicular to
this in a vertical plane. Epithelial cell migration will occur in these
lines and will enhance adherence to the corneal stroma. The
great advantage of this procedure is that it can be performed
Fig. 8 Completely debrided ulcer.
Fig. 9 Parallel lines extend 3mm into normal epithelium.
3
Indolent ulcers in the dog - G. Janssens
file is damaged
file is damaged
Fig. 10 This is not good positioning of the needle. It needs to be
more perpendicular to the corneal surface. It is important not to
push hard on the cornea.
Fig. 11 Two series of lines perpendicular to each other.
in most patients under topical anaesthesia. Only nervous dogs
require tranquilization or even general anaesthesia. Healing is
expected to occur in 80 to 85% of affected eyes within 10 to
14 days.
Superficial keratectomy
This technique is the most invasive and expensive of the surgical
procedures for treating indolent ulcers, although it is the most
successful. To perform a superficial keratectomy, the patient
must be anaesthetised and microsurgical instruments and
magnification (preferably an operating microscope) must be used.
First, the cornea is debrided as described above. Thereafter, an
incision is made into the superficial stroma around the debrided
area. One third of corneal thickness is removed from this area. A
third eyelid flap can be used to protect the cornea after surgery
(although not for the purpose of healing).
Punctate keratotomy is another similar technique. Here, small
superficial punctures are made instead of parallel lines. The
main disadvantage with this technique is the greater risk of
deeper damage to the cornea if the dog suddenly moves. Its
success rate is slightly lower than that with the linear keratotomy,
perhaps as a result of the reduced stromal surface area exposed
with punctate wounds as compared with linear.
In one study performed by Stanley et al (1998), a comparison
was made between the healing times of three different methods
of treatment: debridement with a sterile dry cotton swab, grid
keratotomy and superficial keratectomy with a third eyelid flap.
The latter gave the shortest healing time (seven days) and gave
100% success of healing after one procedure.
Post-operative therapy following these two procedures usually
consists of a broad spectrum antibiotic drop or ointment. These
medications are used for at least 10 days and a recheck is made
every 7-14 days.
Most of the superficial ulcers heal without corneal vascularisation,
although in some patients blood vessels may become visible at
the limbus and continue to migrate across the cornea towards
the lesion at a rate of 0.5-1mm per day. Sometimes there is an
extensive invasion of blood vessels in the cornea, forming a raised
red corneal plaque. These vessels eventually disappear after
several weeks, usually leaving minimal scar tissue afterwards.
Fig. 12 Example of extensive vascularisation after healing.
file is damaged
Some authors use topical corticosteroids to decrease the growth
of those vessels in the cornea once the indolent ulcer has healed.
However, we never use them after healing of an indolent ulcer.
In cases of indolent ulcers that have been treated previously
with topical corticosteroids, we prefer to perform only a
debridement initially and then at the recheck two weeks later,
we repeat the debridement and combine it with grid keratotomy
if necessary. The reason for this cautious approach is that we
do not want to create more corneal lesions at the risk of them
not healing properly with the influence of the previously applied
corticosteroids.
4
Acknowledgements
Other treatment possibilities
Many other therapies have been described for the management
of indolent ulcers. These include chemical cauterization (liquefied
phenol, aqueous iodine solution), hydrophilic contact lenses
and collagen shields, third eyelid flaps, temporary tarsorrhaphy,
tissue adhesives, topical fibronectin, epithelial growth factor,
aprotonin and polysulphated glycosaminoglycans.
The author is grateful to Edith Hampson for assisting with
language translations.
References and further reading
[1] BENTLEY (E.), MURPHYC (J.) - Topical therapeutic agents that
modulate corneal wound healing. In: The Veterinary Clinics of
North America, Small Animal Practice; 2004. p. 623-638.
[2] PETERSEN-JONES (S.), CRISPIN (S.) - Epithelial basement membrane
dystrophy. In: BSAVA, editor. BSAVA Manual of Small Animal
Ophthalmology. Gloucester: BSAVA; 2002. p. 136-138.
[3] STANLEY (R.G.), HARDMANN (C.), JOHNSON (B.W.) - Results of
grid keratotomy, superficial keratectomy and debridement for the
management of persistent corneal erosions in 92 dogs. Veterinary
Ophthalmology. 1998; 1: 233-238.
[4] WHITLEY (R.D.), GILGER (B.C.), - Diseases of the canine cornea and
sclera. In: Veterinary Ophthalmology, 3rd edn. Ed.K.N.Gelatt: 1999.
p. 635-646. Lippincott, Williams and Wilkens, Philadelphia.
[5] WILKIE (D.A.), WHITTAKER (C.) - Surgery of the cornea. In: The
Veterinary Clinics of North America, Small Animal Practice; 1997
Vol 27; no 5. p 1067-1077
Note from the author
In the author’s opinion, most cases of indolent ulcer heal well
with combined debridement and grid keratotomy. We perform
a superficial keratectomy in those cases that present with a
thick loose epithelial margin around the ulcer. This is because
the thickened epithelium is difficult to remove completely
with the debridement technique. Superficial keratectomy is
also performed in those cases that fail to heal following two
treatments of the combined debridement and grid keratotomy.
5
OPTHALMOLOGY
Ocular manifestations of some
canine infectious and parasitic
diseases commonly encountered in
the Mediterranean
A. Komnenou1, A.F. Koutinas1
SUMMARY
Many transmissible diseases, endemic in the Mediterranean area have been spread to countries where they have
never been diagnosed before, because of the increasing international trade and travel activities. The purpose of this
review is to describe the ocular manifestations of these infectious and parasitic diseases, which are also common in
Greece, along with some insights into their etiopathogenesis, differential diagnosis and treatment. While ehrlichiosis
(Ehrlichia canis), leishmaniosis (Leishmania infantum) and dirofilariosis (Dirofilaria immitis) mainly cause intraocular
disease, most often exemplified by immunological uveal tract damage, onchocercosis (Onchocerca spp) and thelaziosis
(Thelazia calipaeda) affect the adnexa and periocular tissues in the majority of cases. Apart from the specific treatment,
which may be either conservative or surgical, applied for the disease, topical glucocorticoisteroids, antibiotics and/or
mydriatics-cycloplegics accelerate the healing process and may prevent post-treatment complications.
Bacterial diseases
Canine Monocytic Ehrlichiosis (CME)
Canine monocytic ehrlichiosis (CME) is an important infectious
disease in the dog with worldwide distribution, including the
Mediterranean countries (Harrus et al 1997, Skotarczak 2003). It
is mainly caused by the gram negative and obligatory intracellular
bacterium Ehrlichia canis, affecting mainly the haematopoetic
cells and resulting in severe leucopenia and thrombocytopenia
(Harrus et al 1997, Scotarczak 2003, Neer and Harrus 2006).
This is a tick borne disease transmitted by the brown dog tick
(Rhipicephalus sanguineus), with the domestic dog, red fox and
golden jackal serving as a reservoir of infection in the nature
(Neer 1998).
publication in EJCAP
Introduction
Ocular signs have frequently been associated with systemic
diseases but their variability and non-pathognomonic nature
makes cause-and-effect association difficult to confirm. In
the Mediterranean region many canine systemic diseases are
endemic. However, recently they have spread to other countries
as well, since the international trade and mass movement of
people and animals is ever increasing. The most frequently
seen ocular manifestations in the everyday practice have been
associated with canine monocytic ehrlichiosis, leishmaniosis,
dirofilariosis, onchocercosis and thelaziosis, which will discussed
below.
Canine monocytic ehrlichiosis has a quite variable clinical
picture, depending on host immune reaction, clinical phase and
other yet undetermined factors (Harrus et al 1997 b). Typically,
1) A. Komnenou DVM, PhD and A. F. Koutinas DVM, PhD, DECVD, Clinic of Companion Animals, School of Veterinary Medicine, Aristotle University
of Thesaloniki, St. Voutyra 11, 546-27, Thessloniki, Greece. Phone + 30 2310-994443 or + 30 6945-53180. E-mail: natakomn@vet.auth.gr
1
Ocular manifestations of some canine infectious and parasitic diseases ... - A. Komnenou, A.F. Koutinas
its evolution includes three clinical phases, although there is an
overlapping that makes their distinction difficult, especially in
the endemic areas (Wadle and Litman 1988). The most severe is
the chronic phase in which the dog may develop severe bleeding
and/or anemia and profound bone marrow suppression of which
it eventually dies due to secondary bacterial infections (Martin
1999, Stiles 2000, Neer and Harrus 2006).
Ocular signs may be seen in all phases of CME and usually
accompany the other clinical manifestations of the disease, but
they can also be the only presenting complaint, though rarely
(Swanson and Dubielzig 1986, Gould et al 2000, Panciera et
al 2001, Leiva et al 2003, Komnenou et al 2007). Pathogenesis
of CME-associated ocular lesions has not been thoroughly
investigated and is still rather unclear. However, immunemediated mechanisms (vasculitis) and/or bleeding tendency
due to thrombocytopenia, thrombocytopathy and occasionally
monoclonal gammopathy, have all been incriminated for the
intraocular inflammation (Hoskins et al 1983, Swanson and
Dubiezig 1986, Harrus et al 1998, Moore and Nasisse 1999,
Panciera et al 2001, Harrus 2001).
Fig. 1 Melting scleral lesion, associated with canine monocytic
ehrlichiosis (E. canis) and resulting from an inflamed uveal tract
under the bulbar conjunctiva (OS).
Necrotic scleritis (fig. 1) is a rare but severe condition, also
associated with CME, which may lead to subconjunctival
uveal prolapse (Martin 1999, Stiles 2000, Komnenou et al
2007). Its pathogenesis remains unclear whereas the outcome
is apparently unpredictable, because of the erratic response
to treatment (Komnenou et al 2007). Blepharitis has been
witnessed in many cases and may be due to self-inflicted trauma
secondary to uveitis and/or conjunctivitis-induced discomfort
(Komnenou et al 2007). Cataract formation is most likely the
result of uveitis-induced release of inflammatory mediators,
which diffuse across the lens capsule, eventually causing
epithelial metaplasia, posterior migration, fiber degeneration
and liquefaction and necrosis of the lens (Davidson and Nelms
1999). Posterior lens luxation may appear secondary to uveitisinduced zonolysis or glaucoma, which is held responsible for the
progressive stretching and rupture of lens zonules (Davidson
and Nelms 1999, Komnenou et al 2007). Panophthalmitis, a
rare occurrence, is usually the result of a long-standing and
poorly-controlled uveitis. Sudden or progressive loss of vision
is a relatively common sequela to CME-induced anterior or
posterior segment disease, coinciding with chronicity (Harrus et
al 1998). The unusual orbital cellulitis (Fig. 2) and keratoconus
may be due to chronic and unresolved keratouveitis (Komnenou
et al 2007).
Uveitis is the most common ocular manifestation of CME (Leiva
et al 2005, Komnenou et al 2007) although in some other clinical
reports its prevalence is considered lower (Kuehn and Gaunt
1985). Experimental studies have demonstrated that all dogs with
active E. canis infection developed histopathologically-confirmed
anterior and/or posterior uveitis (Swanson and Dubielzig 1986,
Panciera et al 2001). It is generally accepted that bilateral anterior
uveitis is the most common presenting ocular condition (Kuehn
and Gaunt 1985, Panciera et al 2001, Stiles 2000, Mylonakis et
al 2004, Massa et al 2002, Komnenou et al 2007), compared
to panuveitis, which is usually followed by retinal detachment
(Leiva et al 2005). Anterior uveitis is generally characterized by
blepharospasm, photophobia, excessive lacrimation, conjuctival
congestion, corneal edema, deep corneal vascularization,
iridal hemorrhages, hyphema, keratic precipitates, miosis,
hypotony, aqueous flare, ciliary flash, multifocal nodules within
the iris stroma and iris hyperpigmentation (Kuehn and Gaunt
1985, Swanson and Dubielzig 1986, Harrus 1997, 1998, Frank
and Breitschwerdt 1999, Panciera et al 2001, Mylonakis et al
2004, Matin 1999, Stiles 2000, Gould 2000, Leiva et al 2005,
Komnenou et al 2007). The less common posterior uveitis is
usually expressed by retinal vascular engorgement and tortuosity,
chorioretinitis, serous or hemorrhagic retinal detachment, retinal
atrophy, choroidal, retinal or vitreal hemorrhages, chorioretinal
scarring and optic neuritis (Hoskins et al 1983, Leiva et al 2005,
Komnenou et al 2007).
Doxycycline hyclate, administered orally at the dose of 5 mg/
kg, every 12 h, for 4 – 6 weeks, is considered the gold standard
in the treatment of the natural disease (Breitschwerdt et al
1998, Mylonakis et al 2004). Other therapeutical options are
tetracycline (22 mg/kg, every 8 h, for 4 weeks), minocycline (10
mg/kg, per os, every 12 h, for 4 weeks) and imidocarb; the latter
is an antiprotozoal medication that is used at the dose of 5 mg/
kg, twice, 2 weeks apart, and is usually successful in treating
those dogs resistant to doxycycline E. canis infections (Sainz et
al 2000, Mylonakis et al 2004, Neer and Harrus 2006). Ocular
signs are usually ameliorated by anti-inflammatory therapy. For
that cause, glucocorticoids, both topical and systemic, have
been used with beneficial results in controlling uveitis (anterior
Secondary glaucoma, a sequela to chronic anterior uveitis, may
appear in some cases (Martin 1999). Ocular discharge, secondary
to conjunctivitis and conjunctival hemorrhages has also been
noted (Kuehn and Gaunt 1985, Woody and Hoskins 1991,
Frank and Breitschwerdt 1999, Hendrix 1999, Komnenou et al
1997). Deep corneal ulceration, an infrequent finding in CME
(Komnenou et al 2007), may be due to tear film abnormalities
(KCS) eventually resulting in secondary bacterial keratitis (Kern
1994, Frank et al 1999, Peterson-Jones et al 2001); however, this
issue merits further investigation.
2
Fig. 2 Frontal view of orbital cellulitis and panophthalmitis (O.S),
secondary to intraocular haemorrhage, in a mongrel dog with
canine monocytic ehrlichiosis (E.canis).
Fig. 3 A mongrel dog with anterior uveitis (OD) and panuveitis
(O.S), due to canine leishmaniosis. Also note the presence of severe
blepharitis and copious mucopurulent ocular discharge.
and posterior). Mydriatics – cycloplegics administered topically
should also be applied, 3 – 4 times daily.
usually appearing together with anterior uveitis, is less commonly
diagnosed (Fig.3). If present, multifocal chorioretinitis with
small hyperreflective foci, retinal detachment and hemorrhage
in the tapeteal fundus are usual findings (Molleda et al 1993,
Garcia Alonso et al 1996, Pena et al 2000). Uveitis may have an
immunologic (Roze 1986, Ferrer 1992, Molleda 1993) or allergic
basis similar to postkala-azar leishmaniosis of humans (el Hasan
et al 1998), because of the more often development in dogs
undergoing antileishmanial treatment (Slappendel and Ferrer
1998). Uveitis is difficult to control and, regardless of treatment,
may result in secondary glaucoma and panophthalmitis with
permanent loss of vision (Roze 1986, Ciaramella et al 1997).
Protozoan diseases
leishmaniosis
Canine leishmaniosis (CanL) is quite common and endemic in
Southern Europe (Greece, Spain, Portugal, France, Italy) where it
is caused by Leishmania infantum, a diphasic protozoan parasite,
transmitted by Phlebotomus sand flies (Deruere et al 1999,
Ciaramella et al 1997, Fisa et al 1999, Koutinas et al 1999, Baneth
2006). The natural reservoir of L. infantum is the domestic dog,
but many other mammalian species may be infected incidentally
(Baneth 2006). In Greece and in other Mediterranean countries
seroepidemiological studies have shown that infection rate
among the canine population varies from 1.6% – 40% (Betini
and Grattoni 1986, Argyriadis and Litke 1991, Martinez-Cruez et
al 1993), although more recent PCR-based studies increase the
prevalence of L. infantum infection to 70% – 80% (Leontides
et al 2002). The infection, either symptomatic or asymptomatic,
usually appears in immunosuppressed or genetically susceptible
dogs after being repeatedly bitten by infected sand flies over a
long period of time (Koutinas 2007).
Keratoconjuctivitis sicca (KCS) may also be associated with
CanL with a prevalence ranging from 2.6% to 26.8% among
the affected dogs. When it appears as a sole manifestation
of the disease, the corresponding figures is 3.7% - 16%
(Molleda et al 1993, Ciaramella et al 1997, Koutinas et al 1997,
Pena et al 2000). Clinically, KCS is usually characterized by
chemosis, hyperemia, purulent discharge, corneal edema and
uveovascularization (Fig.4). The exact pathogenic mechanism
has not yet been elucidated, but it is assumed to be the result
of the direct destruction of lacrimal and Meibomian glands due
to pyogranulomatous inflammation or obstruction of secretory
ducts due to the inflammation of the adjacent structures
(Naranjo et al 2005). It has also been postulated that KCS is
the result of tear hyposecretion following hypoesthesia of the
damaged cornea (Roze 1986, Xu etal 1996, Mathers 2000).
Cataract, granulomatous scleritis and orbital cellulitis have also
been reported as sporadic cases (Molleda et al 1993, Ciaramella
et al 1997, Pena et al 2000).
Ocular disease is quite common in CanL (16% - 80%), appearing
as anterior uveitis, conjunctivitis, keratoconjuctivitis sicca and
blepharitis or a combination thereof (Roze 1986, Molleda et
al 1993, Ciaramella et al 1997, Koutinas et al 1999, Pena et al
2000). CanL – induced ocular lesions are bilateral or unilateral
and may be the only or the main clinical manifestation in 3.7%
- 16% of the affected dogs (Molleda et al 1993, Ciaramella et al
1997, Koutinas et al 1999, Pena et al 2000).
Diagnosis of CanL is quite difficult if it is attempted solely on
clinical grounds and is usually confirmed by lymph node, bone
marrow, spleen and/or cutaneous cytology and histopathology,
along with measurement of blood serum specific antibody titers
by indirect immunofluorescence assay (IFA) and/or enzyme linked
immunoabsorbent assay (ELISA). In equivocal cases, polymerase
Anterior uveitis is most likely the most common ocular
manifestation of CanL (Garcia Alonso et al 1996, Pena et al 2000)
and regardless of its chronicity, is characterized by uveal and
corneal edema, miosis, fibrin formation in the anterior chamber
and multiple nodules within the iris stroma. Posterior uveitis,
3
Fig. 4 A canine leishmaniosis case with chronic
keratoconjunctivitis sicca (KCS) and blepharitis–periocular
dermatitis (OS). Note the globe retraction and corneal
neovascularization and hyperpigmentation with central leukoma.
Fig. 5 Part of a 3-worm cordon-like assembly protruding from
the congested bulbar conjunctiva (OD) in a dog with ocular
onchocercosis (Onchocerca spp).
chain reaction (PCR) testing in bone marrow, conjunctival or skin
samples may also be attempted (Solano –Galego et al 2001).
nematode species have affected the eye and surrounding tissues
in the dog (table 1).
The most effective antileishmanial treatment combines
N-methylglucamine antimoniate (100 mg/kg, subcutaneously,
every 24 h for 30 days) and allopurinol (10 mg/kg, per os, every
12 h for 6 to 12 months or for the rest of the life) and usually
results in clinical cure (Noli and Auxillia 2005). Antileishmanial
treatment should always be combined with topical
glucocorticosteroids or non-steroidal anti-inflammatory agents
and topical mydriatics – cycloplegics to control anterior uveitis.
Posterior uveitis necessitates systemic use of glucocorticosteroids.
Superimposition of bacterial infection in adnexa or ocular tissue
makes the use of appropriate antimicrobials, topical or systemic,
mandatory.
Dirofilaria immitis
Canine dirofilariosis (heartworm disease) is also enzootic in some
countries of the Mediterranean basin, such as Italy, Spain and
Greece (Genchi et al 1995, Guerrero et al 1995, Polizopoulou
et al 2000). Its causative agent Dirofilaria immitis, is the most
frequently reported intraocular nematode in the dog (Metcalf
et al 1982, Miller et al 1987, Martin 1999). Eyes are included
in the aberrant tissue localization of the parasite in the dog
(Rawlings 1995). Intraocular dirofilariosis has also been reported
in horses and humans (Moore et al 1983, Stringfellow et al
2002, Safranova et al 2004).
Heartworm disease is vectored by several mosquito species.
Fourth – stage larvae, after migration, may enter the eye
from the subconjuctival space where they are transformed to
immature adults or fifth-stage larvae, eventually to be localized
in the anterior chamber and/or the vitreous body (Weiner et
Parasitic disease
intra- and periocular parasitic infection is an uncommon
occurrence in the dog (Carastro et al 1992). Nevertheless, several
Table 1. Nematode species that may cause ocular and periocular damage in the dog.
Nematode species
Toxocara canis
Life stage involved
migrating larvae
Ocular localization
choroid, retina and optic
nerve
anterior chamber or vitreous
body
conjunctival sac
References
(Guin et al 1984, Johnson et
al 1989)
(Carastro et al 1992)
Dirofilaria immitis
immature adults
Thelazia californiensis and
Thelazia callipaeda
Onchocerca spp
adults
adults
palpebral conjunctiva, third
palpebra and sclera
Angiostrongylous vasorum
adults larvae
Trichinella spiralis
larvae
anterior chamber and
periocular tissues
eyelid
(Eberhard et al 2000, Szell
et al 2001a, Komnenou et al
2002, 2003, Zafros et al 2005,
Hermoshila et al 2005).
(King et al 1994,
Perry et al 1991)
(Restucci et al 1991)
4
(Morishige et al 1992)
before surgery, to paralyze the parasite and hence to prevent
its posterior movement, stimulated by surgical lights. Topical
anti-inflammatory agents along with mydriatics – cycloplegics
are highly recommended to control uveitis. Permanent corneal
opacity is the most common sequela, particularly in the chronic
cases (Carastro et al 1992). Prognosis for vision depends on the
chronicity of clinical signs and the successful elimination of the
parasite.
Onchocercosis
Onchocercosis may represent an important ocular disease
of dogs residing in Southern Europe. Onchocerca spp has a
worldwide distribution and infests various ungulate species
belonging to Equidae, Crevidae, Camelidae, Suidae and Bovidae
families as well as humans (Anderson 2000). In Europe, a new
Onchocerca species has been isolated from dogs with ocular
disease, which is similar to that of horses and humans, but there
is still confusion regarding its exact speciation. Onchocerca lupi
is considered to be responsible for the canine cases in Europe
(Rodonawa 1967, Sreter et al 2002a) but this option has recently
been disputed (Eberhard et al 2000, Komnenou et al 2002).
According to several authors, it is the same species that also
is responsible for the sporadic zoonotic infestations occurring
in Europe, where ocular involvement has been witnessed in 3
human cases (Burr et al 1998, Pampiglione et al 2001, Sreter
et al 2002b).
Fig. 6 A typical parasitic nodule (granuloma) over the sclera and
under the congested bulbar conjunctiva (OD) in a dog with ocular
onchocercosis (Onchocerca spp)
al 1981). This scenario is perhaps the more realistic, since the
dimensions of fifth – stage larvae prohibit the penetration of
uveal vasculature to reach the eye.
Affected dogs are usually admitted because of ocular
discharge, blepharitis, mild corneal opacity, photophobia and/
or visualization of the worm in the anterior chamber (Carastro
et al 1992). The resultant anterior uveitis, also considered to
be the most common ocular manifestation, is characterized by
epiphora, photophobia, blepharospasm, conjuctival hyperemia,
corneal edema, anisocoria and varying degrees of aqueous flare
(Carastro et al 1992). Its pathogenesis is most likely associated
with the release of toxic metabolites, direct mechanical injury
from the worm or immunologic reactions (Weiner et al 1981).
During ocular examination and because of focal illumination
(pen light) Dirofilaria worms may show an increased motility that
may deteriorate the discomfort of the affected dog (Carastro et
al 1992). In rare instances, the parasite may migrate into the
vitreous body.
Recently, sporadic cases of canine ocular onchocercosis have
been reported in the USA (Eberhard et al 2000, Zafros 2005),
Hungary (Szell et al 2001a, b, Sreter et al 2002a) and Germany
(Hermosilla et al 2005). In Greece, however, it is considered
a common disease (Komnenou et al 2002, 2003). Black flies
(Simulium spp) and gnats (Culicoides spp) serve as intermediate
hosts (Rommel et al 2000) while the prelatent and latency period
may last from months to years.
The most common presenting clinical signs include conjunctival
congestion, periorbital swelling and mild to severe ocular
discomfort (Komnenou et al 2002, 2003). According to our
experience all dogs can be affected, regardless of age, although
it is believed that adult dogs are more susceptible (Eberhard
et al 2000, Szell et al 2001a, Egyed et al 2002a). There is no
breed predisposition, but German shepherds seem to be
overrepresented. (Carastro et al 1992, Komnenou et al 2002,
2003). Two clinical forms of the disease, the acute and the chronic,
have so far been described. Severe conjunctivitis, conjunctival
congestion, chemosis, protrusion of the nictitating membrane,
mild to severe periorbital swelling, exophthalmos, blepharitis,
photophobia, excessive lacrimation, serous to mucopurulent
ocular discharge, diffuse corneal edema, corneal ulceration,
anterior and/or posterior uveitis, accompanied by variable ocular
discomfort, have all been noticed in various combinations in
the acute disease. In some cases free parts of male and female
worms are visible on the surface and/or under the conjunctiva
(fig 5), as well as within the ocular and periocular tissues after
their exposure (Eberhard et al 2000, Szell et al 2001a, Egyed et
al 2002a, Komnenou et al 2002, 2003, Zafros et al 2005).
Diagnosis will be based on direct observation of the parasite,
usually found in the anterior chamber, although corneal
edema, glaucoma and/or mechanical trauma may obstruct its
visualization. Diagnosis is further confirmed by immunological
(antigen-based ELISA) and parasitological (Knott’s modified)
tests (Rawlings 1995). Since occult dirofilariosis is common
among dogs with the intraocular disease, thoracic radiographs
should always be obtained (Carastro et al 1992).
Surgical removal of adult worms from the anterior chamber,
through a limbal incision, or less successfully by aspiration,
is the treatment of choice for the anterior uveitis. Systemic
chemotherapy,
with
diethylcarbamazine
(DEC)
and
photocoagulation with argon laser (in humans) have also been
proposed, but the antigens released by the massive death of
parasites may cause severe inflammatory reaction (Forman et
al 1984). Topical application of cholinesterase inhibitors, such
as 0.125% phospholine iodide, should be used immediately
In chronic cases, the worms typically reside within subconjuctival
5
nodules or cyst-like formations from where they invade the
retrobulbar space and penetrate the orbital fascia, eyelids,
conjunctiva, sclera and nictitating membrane, causing
exophthalmos and occasionally protrusion of the adnexa.
Infested dogs usually do not show evidence of ocular discomfort
when the nodules are palpated (Sreter et al 2002, Komnenou et
al 2002, Zafros et al 2005). The lesions may result in excessive
lacrimation, photophobia, ocular discharge, corneal edema,
anterior uveitis and perhaps secondary glaucoma (Eberhard et
al 2000, Szell et al 2001a, Egyed et al 2002a, Komnenou 2003,
Zafros et al 2005). In rare instances, the worms may invade
the anterior chamber accidentally. At surgery, the nodules are
visualized over the periocular area with the thread-like, whitish
fragments of the parasites often protruding from within (fig 6).
The opening of cyst-like formations may reveal the apparently
intact slender and long parasite,(Sreter et al 2002, Komnenou
et al 2002). Mechanical removal of filariae from the anterior
chamber is carried out through limbal incision. Histopathology of
parasitic nodules reveals a severe granulomatous inflammation
along with the mature parasite buried within.
Thelaziosis
Thelasia spp, commonly named eyeworm, is a spirurid
nematode that may cause ocular disease of variable severity
in several mammalian species. Canine thelaziosis is caused by
Thelazia callipaeda and Thelazia californiensis. The first species,
which occasionally infests other mammals such as cats, foxes
and rabbits, has been reported to occur in Russia, Far East
and Europe (Italy) (Ontrato et al 2003, Hermoshilla et al 2004,
Chermette et al 2004). Thelazia californiensis is confined to
western territories of the USA, affecting dogs, sheep, deer,
coyotes and bears (Anderson 2000). Both Thelazia species can
infest humans as well, causing conjunctivitis, pain and excessive
lacrimation (Otranto et al 2003). The intermediate host life cycle
and epidemiology of Thelazia callipaeda are poorly known,
although it has been suggested that more than one vector
(diptera species) or just one vector with worldwide distribution
(Musca domestica) is involved in the transmission of the disease
(Shi et al 1988).
The most common and characteristic clinical condition of canine
ocular thelaziosis is a persistent mucopurulent to purulent
conjunctivitis, which is resistant to conventional treatment. It
may be accompanied by other ocular manifestations, such as
blepharospasm, excessive lacrimation, corneal opacities and
ulceration. After a careful examination, milk-white parasites can
be visualized in the conjunctival fornix, under the nictitating
membrane, and within the conjunctival and lacrimal sacs
(Hermoshilla et al 2004, Lia et al 2004).
Diagnosis is based mainly on ocular examination and periocular
tissue biopsies. In acute cases, white thread-like worms or
their fragments may be visualized under the conjunctiva. In
chronic cases, the diagnosis is confirmed with histopathology
of periocular and/or inguinal skin biopsies, as Onchocerca
microfilariae cannot be detected in the blood. Interestingly, a
hypersensitivity reaction to microfilariae, inhabitating the skin
(Szell et all 2001a, b, Egyed et al 2002 a), may result in pruritic
cutaneous lesions similar to those seen in people, horses and
cattle (Markell et al 1992, Rommel et al 2000). Differential
diagnosis should include orbital cellulitis, retrobulbar abscesses,
nodular episcleritis and periorbital neoplasia (Szell et al 2001a,
Egyed et al 2002a, Komnenou et al 2002).
Surgical excision of as many of the periocular nodules
and cysts as possible could be considered as a treatment option.
Postoperatively, oral prednisolone (0,5 mg/kg, every 12 hours,
for 9 – 12 days), doxycycline hyclate (5 mg/kg, every 12 hours,
for 4 weeks) and topical antibiotics (every 8 hours for 9 days) are
strongly recommended: doxycycline is given for the potential
of Wolbachia endosymbiosis (Bandi et al 2001). To achieve the
complete elimination of the parasite, melarsomine (Immiticide®,
Merial) at the dose of 2.5 mg/kg, intramuscularly, every 24 hours,
for 2 days, followed by ivermectin (Valaneq®, MSD ) at 50 µg/
kg, once, and one month after the adulticide administration,
should be applied one week after the surgery. However, the
antihelmintic treatment, applied alone, may result in similar cure
rates. A periorbital pruritic edema is frequently noticed 2 – 3
days after the administration of melarsomine (Komnenou et al
2002, 2003). Anecdotally, milbemycin (Interceptor®, Novartis)
administered at the dose of 0.5 – 0.99 mg/kg, once per month,
for 6 months, or ivermectin (Heartguard-30®, Norden) at 5 – 6
µg/kg, once per month, for 6 months (from April to October,
coinciding with black fly and gnat peak activity) may provide
adequate prevention.
Diagnosis of thelaziosis is confirmed by the presence of the
parasites within the conjunctival and lacrimal sac on clinical
inspection of the eyes. At an earlier stage, the collection and
microscopic examination of conjunctival and lacrimal secretions
may be quite helpful in demonstrating the microfilariae (Otranto
et al 2004).
There is limited information regarding the treatment of
thelaziosis. Mechanical removal of parasites after instillation of
local anaesthetics (Bhaibulaya et al 1970) or the local instillation
of organophosphates, have been recommended. However, the
subcutaneous injection of ivermectin at the dose of 0,2 mg/kg
(Rossi and Peruccio 1989), combined with ophthalmic topicals
with antibiotics has been less disturbing and more effective.
Ocular instillation (1 – 2 drops) of 1% moxidectin in aqueous
solution has also been proven highly successful in the treatment
of canine thelaziosis, compared to the mechanical removal (Lia
and others 2004). Recently, a single dose of imidacloprid (10%)
and moxidectin (2.5%) combination in spot on formulation
(Advocate®, Bayer) has been shown to be a highly efficacious
(within 5 – 6 days) and easy-to-apply therapeutical modality
(Bianciardi and Otranto 2005)
6
References
Therapy XI. Philadelphia: WB. Saunders, 1992, pp 262-270.
[20] FERER (L.), AISA (M.J.), ROURA (X.), PORTUS (M.) (1995) - Serological
diagnosis and treatment of canine leishmaniasis. Vet Rec, 1995,
136:514-516.
[21] FISA (R.), GALLEGO (M.), CASILLEJO (S.), AISA (M.J.), SERRA (T.),
RIERA (C.), CARRIO (J.), GALLEGO (J.), PORTUS (M.) - Epidemiology
of Canine Leishmaniosis in Catalonia (Spain) the example of the
Priorat focus. Vet. Parasit 1999, 83(2):87-97.
[22] FORMAN (A.R.), CRUESS (A.F.), BENSEN (W.E.) - Ophthalmomyasis
treated by argon laser photocoagulation. Ophthalmology, 1984,
4: 163-165.
[23] GARCIA-ALONCO (M.), BLANCO (A.), REINA (D.), SERANO (F.J.),
ALONSO (C.), NIETO (C.G.) - Immunopathology of uveitis in the
canine leishmaniasis. Parasite Immunol, 1996, 8 (12): 617-623.
[24] GENCHI (C.), SOLARI-BASANO (F.), BANDI (C.), DI SACCO (B.),
VENCO (L.), VEZZONI (A.), CANCRINI (G.) - Factors influencing
the spread of heartworms in Italy. Interaction between Dirofilaria
immitis and Dirofilaria repens. Eds m. d. Soll, D.H. Knight.
Proceedings of the Heartworm Symposium 1995. American
Heartworm Society, 1995, pp 65-71.
[25] GUERRERO (J.), RODENAS (A.), GUTTIEREZ GALINDO (J.), FLORIT
(F.) - The extension of the prevalence of Dirofilaria immitis in
Cataluna, Spain. Eds M.D. Soll, D.H.Knight. Proceedings of the
Heartworm Symposium. American Heartworm Society, 1995,
pp73-77.
[26] GOULD (D.J.), MURPHY (K.), RUDORF (H.) - Canine Monocytic
Ehrlihciosis presenting as acute blindness 36 months after
importation into UK. J Small Anim Pract, 2000, 41:263-265.
[27] GWIN (R.M.), MERIDETH (R.), MARTIN (C.L.), KASWAN (R.L.) Ophthalmomyasis interna posterior in two cats and a dog. J Am
Anim Hosp Assoc 1984, 20: 481-486.
[28] HARRUS (S.), BARK (H.), WANER (T.) - Canine monocytic ehrlichiosis:
An update. Comp Cont Educ Vet Pract, 1997a, 19: 431-444.
[29] HARRUS (S.), KASS (P.H.), KLEMENT (E.), WANER (T.) - Canine
monocytic ehrlichiosis: a retrospective study of 100 cases, and
an epidemiological investigation of prognostic indicators of the
disease. Vet Rec, 1997b, 141: 360-363.
[30] HARRUS (S.), OFRI (R.), AIZENBERG (I.), WANER (T.) - Acute
blindness associated with monoclonal gammopathy induced by
Ehrlichia canis infection. Vet Microb, 1998, 78: 155-160
[31] HARRUS (S.), DAY (M.J.), WANER (T.), BARK (H.) - Presence of
immune-complexes, and absence of antinuclear antibodies, in
sera of dogs naturally and experimentally infected with Ehrlichia
canis. Vet Microb, 2001, 83: 343-349.
[32] HENDRIX (D.V.H) - Diseases and Surgery of the Canine Conjunctiva.
In: Veterinary Ophthalmology, 3rd edition (ed. Gelatt KN).
Lippincott Williams & Wilkins: Philadelphia, 1999, pp 619-634.
[33] HERMOSHILLA (C.), HERRMANN (B.), BAUER (C.) - First case of
Thelazia callipaeda infection in a dog in Germany. Vet Rec, 2004,
154:568-569
[34] HERMOSILLA (C.), HETZEL (U.), BAUSCH (M.), GRUBL (J.), BAUER.
(C.) - First autochthonus case of canine ocular onchocescosis in
Germany. Vet Rec, 2005, 156: 450-452.
[35] HOSKINS (J.D.), BARTA (O.), ROTHSCMITT (L.) - Serum hyperviscosity
syndrome associated with Ehcrlichia canis infection in a dog. J Am
Med Assoc, 1983, 183:1011-1012.
[36] JOHNSON (B.W.), KIRKPATRICK (C.E.), WHITELEY (H.E.) Et al
- Retinitis and intraocular larva migration in a group of Border
Collies. J Am Anim Hosp Assoc, 1989, 25:623-629.
[37] KERN (T.J.) - Diseases of the cornea and sclera. In: Saunders Manual
of Small Animal Practice (eds. Birchard SJ, Sherding RG). W.B.
Saunders: Philadelphia, 1994, pp 1197-1212.
[38] KING (M.C.A.), GROSE (R.M. R.), STARTUP (G.) - Angiostrongylus
vasorum in the anterior chamber of a dog’s eye. J Sm Anim Pract
1994, 35: 326-328.
[1] ANDERSON (R.C.) - Order Spirurida-suborder Spirurina. In Nematode
Parasites of Vertebrates: Their Development and Transmission (ed.
Anderson RC) CABI Publishing, New York 2000, 383-590.
[2] ARGYRIADIS (D), LITKE (O.) - Epizootiological study of dog
leishmaniasis in the central and eastern Macedonia and in
Thessaly. Bull Hell Vet Med Assoc, 1991, 42:30-4.
[3] BANETH (G.)- Leishmaniasis. In: Infectious Diseases of the Dog and
Cat, 3rd ed. GE Greene (eds), Saunders company, Philadelphia,
2005, pp 685 – 695.
[4] BHAIBULAYA (M.), PRASERTSILPA (S.), VAJRASTHIRA (S.) - Thelazia
callipaeda Railliet and Henry, 1910, in man and dog in Thailand.
Am. J Trop Med Hyg, 1970, 19: 476-479.
[5] BIANCIARDO (P.), OTRANTO (D.) - Treatment of thelaziosis caused
by Thelazia callipedae (Spiturida, Thelaziidae) using a topical
formulation of imidacloprid 10% and moxidectin 2.5%.Vet
Parasitol Apr 20, 2005, 129(1-2): 89-93.
[6] BREITSCHWERDT (E.B.), HEGARTY (B.C.), HANCOCK (S.L.) Doxycycline hyclate treatment of experimental canine ehrlichiosis
followed by challenge inoculation with two Ehrlihia canis strains.
Antimicrob Agents Chemoth, 1998, 42:362-368.
[7] BURR (W.E.), BROWN (M.F.), EBERHARD (M.L.) - Zoonotic Onchocerca
(Nematoda: Filarioidea) in the cornea of a Colorado resident.
Ophthalmology 1998, 105: 1194-1197.
[8] CARASTRO (S.M.), DUGAN (S.J.), PAUL (A.J.) - Intraocular dirofilariasis
in dogs .Comp Cont Ed Pract Vet, 1992, 14:209-212.
[9] CHERMETTE (R.), GUILLOT (J.), BUSSIERAS (J.) - Canine ocular
thelaziosis in Europe. Vet Rec, 2004, 154(8):248.
[10] CIARAMELLA (P.), OLIVA (G.), DE LUNA (R.), GRADONI (L.),
AMBROSIO (R.), CORTESE (L.), SCALONE (A.), PERSECHINO
(A.) - A retrospective study of canine leismaniasis in 150 dogs
naturally infected by Leihmania infantum. Vet. Rec, 1997,
141(21):539-543.
[11] DAVIDSON (M.G.), NELMS (S.R.) - Diseases of the Lens and
Cataract Formation. In: Veterinary Ophthalmology 3rd edition (ed.
Gelatt KN). Lippincott Williams & Wilkins: Philadelphia, 1999, pp
797-825.
[12] DEREURE (J.), PRATOLONG (F.), DETET (J.P.) - Geographical
distribution and the identification of parasites causing canine
leishmaniasis in the Mediterranean Basin, Canine Leishmaniasis :
an update. Proceedings of the International Canine Leishmaniasis
Forum. Barcelona 1999, pp. 18-25.
[13] EGYED (Z.), SRETER (T.), SZELL (Z.), BEESZTERI (B.), ORAVEZC
(O.), MARIALIGETI (K.), VARGA (I.) - Morphologic and genetic
characterization of Onchocerca lupi infection in dogs. Vet
Parasitol, 2001, 102(4):309-319.
[14] EGYED (T.), SZELL (Z.), NYIRO (G.), DOBOS-KOVACS (M.),
MARIALIGETI (K.), VARGA (I.) - Electron microscopic and molecular
identification of Wolbachia endosymbionts from Onchocerca lupi:
implications for therapy. Vet Parasit,, 2002a, 106(1): 75-82.
[15] EGYED (T.), SRETER (T.), SZELL (Z.), NYIRO (G.), MARIALIGETI (K.),
VARGA (I.) - Molecular phylogenetic analysis of Onchocerca
lupi and its Wolbachia endosymbiont. Vet Parasit, 2002b,
108:155-163
[16] EL HASAN (A.M.), KHALIL (E.A.), EL SHEIKH (E.A.), ZIIJLSTRA (E.E.),
OSMAN (A.), IBRAHIM (M.E.) - Post Kala-azar ocular leishmaniasis.
1998. Transac Roy Soc Trop Med Hyg, 1998, 92:177-179. .
[17] EBERHARD (M.L.), ORTEGA (Y.), DIAL (S.), SCHILLER (C.A.), SEARS
(A.W.), GREINER (E.) - Ocular Onchocerca infections in two dogs
in western United States. Vet Parasit, 2000, 90:333-338.
[18] FRANK (J.R.), BREITSCHWERDT (E.B.) - A retrospective study of
ehrlichiosis in 62 dogs from North Carolina and Virginia. J Vet
Intern Med, 1999, 13: 194-201.
[19] FERER (L.) - Leishmaniasis. In (ed. Bonagura K). Current Veterinary
7
[39] KOMNENOU (A.), EBERHARD (M.), KALDRMIDOU (E.), TSALIE
(E.), DESIRIS (A.) - Subconjunctival filariasis due to Onchocerca
spp in dogs: report of 23 cases in Greece. Vet Ophthal, 2002, 5,
119-126.
[40] KOMNENEOU (A.), EGYED (Z.), SRETER (T.), EBERHARD (M.L.) Canine Ocular onchocercosis in Greece: report of further 20 cases
and molecular characterization of the parasite and its Wolbachia
endosymbiont. Vet Parasit, 2003, 118:151-155.
[41] KOMNENOU (A.), MYLONAKIS (M. E), KOUTI (V.)., TENDOMA (L.) ,
LEONTIDES (L.), SKOUNTZOU (E.), DESSIRIS (A.), KOUTINAS (A.F.)
AND OFRI (R.) - Ocular manifestations of natural canine monocytic
ehrlichiosis (Ehrlichia canis): a retrospective study of 90 cases. Vet
Ophth, 2007, 10:137-142.
[42] KONTOS (V.J.) - A contribution o the study of canine leishmaniasis.
A clinical, serological and experimentally investigation. PhD Thesis,
Aristotelian University if Thesaloniki, Thesaloniki, Greece, 1986.
[43] KOUTINAS (A.F.), POLIZOPOULOU (Z.S.), SARIDOMICHELAKIS
(M.N.), ARGYRIADIS (D.) FYTIANOU (A.), PLEVRAKI (K.G.) Clinical Considerations of Canine Visceral Leishmaniasis in Greece:
A retrospective Study of 158 Cases (1989-1996). J Am Anim Hosp
Assoc, 1999, 35:376-383.
[44] KOUTINAS (A.) - Clinical Manifestations of Canine Leishmaniasis :an
update. Proc 25th ACVIM 621 Seattle WA PP, 2007, pp 611-623.
[45] KUEHN (N.F.), GAUNT (S.D.) - Clinical and hematological findings in
canine ehrlichiosis. J Am Vet Med Assoc, 1985, 86: 355-358.
[46] LEIVA (M.), PENA (T.), NARANJO (C.) - Ocular canine ehrlichiosis:
a 3-year course (abstract). 34th Annual Meeting of the American
College of Veterinary Ophthalmologists, Coeur D’ Aleue, ID, USA,
2003, pp 43-44.
[47] LEIVA (M.), NARANJO (C.), PENA (M.TR) - Ocular signs of
canine monocytic ehrlichiosis: a retrospective study in dogs
from Barcelona, Spain. Veterinary Ophthalmology, 2005, 8(6):
387-393.
[48] LEONTIDES (L.S.), SARIDOMICHELAKIS (M.N.), BILLINIS (C.),
KONTOS (V.), KOUTINAS (A.F.), GALATOS (A.,) MYLONAKIS
(M.A.), (2002) - A cross sectional study of Leishmania spp
infection in clinically healthy dogs with polymerase chain reaction
and serology in Greece. Vet Parasitol, 2002, 109:19-27.
[49] LIA (R.), TRAVERSA (D.), AGOSTINI (A), OTRANTO (D.) - Filed
efficacy of moxidectin 1per cent against Thelazia callipaeda in
naturally infected dogs. Vet Rec 2004, 154: 143-145.
[50] MARKEL (E.K.), VOGE (M.), JOHN (D.T.) - Medical Parasitology,
Philadelphia, W.B.Saunders, 1992, pp 315-322.
[51] MARTIN (C.L.) - Ocular Manifestations of Systemic disease. In:
Veterinary Ophthalmology, 3rd edn (Gelatt KN ed) Lippincott
Williams & Wilkins, 1999, pp 1401-1504.
[52] MARTINEZ-CRUZ (M.S.), MARTINEZ-MORENO (A.), MARTINEZMORENO (F.J.), HERNANTEZ RODRIGUEZ (S). - Epidemiologica de
leishmaniasis canina e la provincia de Cordova. Rev Iber Parasitol
1993, 51 :49-59.
[53] MILLER (W.), COOPER (R.B.) - Identifying and treating intraocular
Dirofilaria immitis in dogs. Vet Med 1987, 381-385.
[54] MASSA (K.L.), GILGER (B.C.), MILLER (T.L.) Et al - Causes of uveitis
in dogs :102 cases (1989-2000).Vet Ophthal 2002, 5:93-98.
[55] MATHERS (W.D.) - Why the eye becomes dry: a cornea and lacrimal
gland feedback model. CLAO J, 2000, 26(3): 159-165.
[56] METCALF (J.F.), JORDAN (K.M.) - Surgical removal of Dirofilaria
immitis from the eye of a dog. Vet Med, 1982, 1606-1608.
[57] MOLLEDA (J.M.), NOVALES (M.), GINEL (P.J.) ET AL-Clinical and
histopathological study of the eye in canine leishmaniasis. Isr J Vet
Med, 1993, 48:173-178.
[58] MOORE (P.C.), NASISSE (P.M.) - Clinical Microbiology. In: Veterinary
Ophthalmology 3rd edition (ed. Gelatt KN). Lippincott Williams &
Wilkins: Philadelphia, 1999, 275-276.
[59] MOORE (C.A.), SARAZAN (R.D.), WHITELY (R.D.), JACKSON (W.F.)
- Equine Ocular parasites: A review. Equine Vet J (Suppl) 1983, 2:
76-85,
[60] MORISHIGE (K.), SAITO (T.), MAEDA (S.), TANGY (U.) - Infection
rate of Thelazia callipedae in dogs and cats in Bingo District and
Okoyama City. Jap J Parasit, 1992, 41:431-433.
[61] MYLONAKIS (M.E.), KOUTINAS (A.), BREITSCHWERDT (E.D.),
HEGARTY (B.C.), BILLINIS (C.), LEONTIDES (L.), KONTOS (V.) Chronic canine ehrlichiosis (Ehrlichia canis): A retrospective study
of 19 natural cases. J Am Anim Hosp Assoc, 2004, 40: 174-184.
[62] NARANJO (C.), FONDEVILA (D.), LEIVA (M.) ROURA (X.), PENA
(T.) - Characterization of lacrimal gland lesions and possible
pathogenic mechanisms of Keratoconjunctivitis sicca in dogs with
leishmaniosis. Vet Parasitology 2005, 133:37-47.
[63] NEER (M.), HARRUS (S.) - Ehrlihiosis, Neoricketsiosis, Anaplasmosis
and Wolbachia Infection. In Greene: Infectious Diseases of Dog
and Cat . 3rd ed, Chap 28 , 2006, pp 203-232.
[64] NEER (T.M.) - Canine monocytic and granulocytic ehrlihiosis. In:
Infectious Diseases of the Dog and Cat. 2nd ed (Greene CE, ed)
W.B. Saunders, Philadelphia, 1998, 139-154.
[65] NOLI (C.) , AUXILIA (S.T.) - Treatment of canine Old World visceral
leishmaniasis: a systematic review. Vet Dermatology 2005, 16:
213 – 232
[66] ONTRATO (D.), FERROLIO (E.), LIA (R.P.), TRAVERSA (D.), ROSSI
(L.) - Current status and epidemiological observation of Thelazia
callipaeda (Spirurida, Thelaziidae) in dogs, cats and foxes in Italy:
a “concidence” or a parasitic disease of the Old Continent? Vet
Parasitol 2003, 16: 315-325.
[67] OTRANTO (D.), LIA (R.P.), BUONO (V.), TRAVERSA (D.),
GIANGASPERO (A.) - Biology of Thelazia callipedae (spirurida,
Thelaziidae) eyeworms in naturally infected definite hosts.
Parasitology 2004, 129, 5:627-33
[68] PAMPIGLONE (S.), VAKALIS (N.), LYSIMACHOU (A.), KOUPPARI
(G.), ORIHEL (T.C.) - Subconjunctival zoonotic Onchocerca in an
Albanian man. Ann Trop Med Parasitol 2001, 95: 827-832.
[69] PANCIERA (R.J.), EWING (S.A.), CONFER (A.W.) - Ocular
histopathology of ehrlichial infections in the dog. Vet Pathol 2001,
8: 43-46.
[70] PENA (M.T.), ROURA (X.), DAVIDSON (M.G.) - Ocular and Periocular
manifestations of leishmaniasis in dogs: 105 cases (1993-1998).
Vet Ophthal, 2000, 3 (1):35-41.
[71] PETERSON-JONES (S.M.), STANLEY (R.G.), SMITH (R.I.E.), SMITH
(J.S.) - Ocular Discharge. In: Small Animal Ophthalmology. A
Problem Oriented Approach 3rd edition (eds. Peiffer RL, PetersonJones SM), Saunders: Philadelphia, 2001, 219-253
[72] PERRY (A.W.), HERTLING (R.), KENNEDY (M.J.) - Angiostrongylosis
with disseminated larval infection associated with signs of
ocular and nervous disease in an imported dog. Can Vet J 1991,
135:326-328
[73] POLIZOPOULOU (Z.S.), KOUTINAS (A.F.), SARIDOMICHELAKIS
(M.N.), PATSIKAS (M.N.), LEONTIDIS (L.S.), ROUBIES (N.A.),
DESIRIS (A.K.) - Clinical and Laboratory observations in 91 dogs
infected with Dirofilaria immitis in northern Greece. Vet Rec ,
2000, 146: 466-469.
[74] RAWLINGS (C.A.), CALVERT (C.A.) - Heartworm Disease. In:
Textbook of Veterinary Internal Medicine, 4th edn (3ds S.J.
Ettinger and E.C. Feldman) W.B. Saunders, Philadelphia ,1995, pp
1046-1068.
[75] RESTUCCI (B.), DE VICO (G.) MELINO (P.) - Raro caso di melanoma
parpepraro associato a trichinellosi in un can. Acta Med Vet 1991,
37:107-102.
[76] RODONAWA (T.E.) - A new species of nematode., Onchocerca lupi
n. sp. From Canis lupus cubanensis. Soobshcheniya Akademmii
Nauk Gruzinskoy SSR 45, 1967, pp 715-719.
[77] ROZE (M.) - Manifestations Oculaires de la Leishmaniose. Canine
Recueil de Medicine Veterinaire. 1986, 19-26.
8
[88] SRETER (T.), SZELL (Z.), EGYED (Z.), VARGA (I.) (2002a) - Ocular
onchocercosis in dogs: a review. Vet Rec, 2002a, 151:176-180.
[89] SRETER (T.), SZELL (Z.), EGYED (Z.), VARGA (I.) - Subconjunctival
zoonotic onchocercosis in man: aberrant infection with
Onchocerca lupi? Ann Trop Med Parasito , 2002b, 96: 497-502
[90] STILES (J.) - Canine rickettsial infections. Vet Clin North Am: Sm
Anim Pract, 2000, 30: 1135-1149.
[91] STRINGFELLOW (G. J.), FRANZCO (I.C.F.), FRANZCO, (M.T.C),
WALKER (J.) - Orbital dirofilariasis. Clinical and Experimental
Ophthalmology 2002, 30:378-380.
[92] SWANSON (J.F.), DUBIELZIG (R.R.) - Clinical and histopathologic
characteristics of acute canine ocular ehrlichiosis. Transact Amer
Coll Vet Ophth, 1986, 17: 219-232.
[93] SZELL (Z.), ERDELYI (I.), SRETER (T.), ALBERT (M.), VARGA (I.) - Canine
ocular onchocercosis in Hungary. Vet Parasit 2001a, 97:243-249.
[94] SZELL (Z.), SRETER (T.), ERDELYI (I.), VARGA (I.) (2001b) - Ocular
onchocercosis in dogs: aberrant infection in an accidental host or
lupi onchocercosis? Vet Parasit 2001b, 101:115-125.
[95] WOODY (B.J.), HOSKINS (J.D.) - Ehrlichial diseases of dogs. Vet Clin
North Am: Small Anim Pract; 1991, 21: 75-98.
[96] WADLE (J.R.), LITTMAN (MP) - A Retrospective Study of 27 cases
of natural occurring canine ehrlichiosis. J Am Anim Hosp Assoc,
1988, 24: 615-620.
[97] WEINER (D.J.), AGUIRRE (G.), DUBIELZIG (R.) - Ectopic-site filarid
infection with immunologic follow-up of the host. Heartworm
Symp 1981, 51-54.
[98] XU (KP.), YAGI (Y.), TSUBOTA (K.), (1996)- Decrease in corneal
sensitivity and change in tear unction in dry eye. Cornea 15(3):
235-239.
[99] ZAFROS (M.) DUBIELZIG (R.D.), EBERHARD (M.), SCHMIDT (K. S.)
(2005) - Canine Ocular Onchocercosis in the United States: two
new cases and review of the literature. Vet Ophthal 8, 1: 51-57
[78] ROMMEL (M.), ECHERT (J.), KUTZER (R.), KORTING (W.), SCHNIEDER
(T.) - Veterinamediziniche Parasitologie. Berlin , Parey, 2000, pp
289-290, 420-414.
[79] ROSSI (L.), PERUCCIO (C.) - Thelaziosis oculare nel Cane :aspetti
clinici e terapeutici. Veterianaria 1989, 2:47-50 (in Italian, with
abstract in English).
[80] SAFRANOVA (E.), VOROBEV (A.A.), LATYSVENSKAIA (N.I.),
ERMILOV (V.V.), CHULKOVA (G.B.) - Dirofilariasis in the Volgograd
region-anew disease in the region. Med Parazitol (Mosk) 2004,
(2):51-4.
[81] SAINZ (A.), TESOURO (M.A.), AMOUSADEGUI (I.), RODRIGUEZ
(F.), MAZZUCCHELLI (F.) - Prospective comparative study of 3
treatment protocols using doxycycline or imidocarb dipropionate
in dogs with natural occurring ehrlichiosis. J Vet Intern Med,
2000, 14:134-139.
[82] SALES (A.J.), PITOU (S.), BERNUS (D.), HAAS (P.) - Leishmaniasis in a
horse. In : Advances in Veterinaray Dermatology, Vol3, Butterworth
Heinemann, Kwochka KW., Willemse T., von Tscharner G., Oxford,
1998, pp 458-459.
[83] SHI (Y.E.), HAN (J.J.), YANG (W.Y.), WEI (D.X.) - Thelazia callipaeda
(Nematoda : Spirurida):transmission by flies from dogs to children
in Hubei, China. Trans. R Soc Trop Med Hyg 1988, 82:627.
[84] SKOTARCZAK (B.) - Canine Ehrlihiosis. Ann Agric Environ Med,
2003, 10: 137-141.
[85] SLAPPENDEL (R.J.), GREENE (C.E.) - Leishmaniasis. In: Greene, ed
Infectious diseases of the dog and cat. Philadelphia: WB Saunders,
1990, 769-77.
[86] SLAPPENDEL (R.J.), FERER (L.) - Leishmaniasis, In Green C (ed).
Infectious Diseases of the dog and Cat (ed) Philadelphia, WB Co,
1998, p450.
[87] SOLANO - GALEGO (L.), MORE (P.), ARBOIX (M.), FERRER (L.) Prevalence of Leishamania infantum infection in the dogs living in
the area of canine leishmaniasis using PCR on several tissues and
serology. J. Clin. Microbiol, 2001, 39(2) : 560-563.
9
OPHTHALMOLOGY
Medical Therapy of Glaucoma
R. Ofri(1)
SUMMARY
Glaucoma is a painful disease that causes progressive loss of vision and frequently leads to blindness. Medical
treatment of glaucoma remains a therapeutic challenge because of the numerous causes of the disease and the
complexity of its pathogenesis. A large, almost bewildering, choice of available drugs, many of which have possible
ocular or systemic side-effects as well as specific contraindications, further complicates the clinician’s task.
This paper begins with a brief overview of our current understanding of the pathogenesis of glaucoma. It continues
with a review of methods of classifying glaucoma, and their implications for treatment of the disease. Goals of
treatment, principles of treatment, and the various classes of available drugs are described. The paper concludes with
a discussion of recent advances in the understanding of the pathogenesis of glaucomatous loss of vision, and their
therapeutic implications in the development of neuroprotective treatments for glaucoma.
reviewed at the end of this paper (see secondary degeneration
and neuroprotective treatments).
However, even though glaucoma is no longer defined as an
elevation in IOP, it is still accepted that increased IOP is the
primary risk factor in the pathogenesis of the disease. Indeed,
even though normotensive glaucoma is a well-recognized entity
in humans [3] and non-human primates [4], and may also exist
in dogs [Brooks DE, personal communications], most forms of
the disease in animals are characterized by ocular hypertension.
Therefore, current and approved medical therapies are those
that aim to lower IOP in glaucoma patients. Treatment modalities
aiming to prevent the neurodegenerative disease of the RGC are
still in experimental stages. These modalities, collectively known
as neuroprotection, are also reviewed at the end of this paper.
Current insights into the pathogenesis of glaucoma and
its treatment
Aqueous humor is a transparent fluid that fills the anterior and
posterior chambers, plus the pupil of the eye. It is produced in the
ciliary processes, and exits the eye through two major pathways;
the iridocorneal (conventional) outflow, and the uveoscleral
(unconventional) outflow. Equilibrium between production
and drainage of aqueous humor enables the body to maintain
constant intraocular pressure (IOP). For many years glaucoma
was defined as an elevation in IOP that is detrimental to normal
ocular function and to vision. With improved understanding of
the neurodegenerative processes affecting the retinal ganglion
cells (RGCs) during the course of the disease, the definition of
glaucoma has been modified to a group of diseases characterized
by decreased RGC sensitivity and function, progressing to RGC
death and loss of optic nerve axons, thus resulting in incremental
reduction in visual function progressing to blindness [1]. It is very
interesting to note that this revised definition of glaucoma does
not mention elevation in IOP. This is because glaucoma-induced
damage has been demonstrated to continue even after IOP has
been lowered successfully [2], and because some forms of the
disease (especially in primates) may be observed in normotensive
patients [3, 4]. Recent advances in our understanding of
the pathogenesis of these neurodegenerative processes are
Classification of Glaucoma: Implications for Treatment
Theoretically, an elevation in IOP could be the result of either
increased aqueous production or decreased aqueous drainage.
In practice, however, the elevation is caused by obstructions in
aqueous outflow pathways and not by increased production.
Depending on the nature of the obstruction, the disease may
be classified as primary, secondary or congenital. All three
forms of the disease have been documented in dogs and in
cats [5, 6]. Primary glaucoma is defined as an elevation in IOP
that is not caused by any concurrent ocular disease. Rather,
the disturbances to outflow (which are usually hereditary) are
caused by progressive narrowing of the iridocorneal angle or
by biochemical changes in the trabecular meshwork, leading
1) Dr. Ron Ofri, DVM, PhD, Diplomate European College of Veterinary Ophthalmologists, Senior Lecturer in Veterinary Ophthalmology, Koret School of
Veterinary Medicine, Hebrew University of Jerusalem, PO Box 12, Rehovot 76100, Israel. E-mail: ofri@agri.huji.ac.il
1
Medical Therapy of Glaucoma - R. Ofri
to a reduction in the volume of aqueous that is being drained
out of the eye. In secondary glaucoma, the obstruction to
aqueous outflow is a complication caused by another, primary,
ocular disease. For example, uveitis may cause obstruction of
the iridocorneal angle with inflammatory cells and mediators.
Posterior and/or peripheral anterior synechia could further
impede aqueous flow from the eye in uveitis. Obstruction of
the angle by vitreous (due to anterior lens luxation), red blood
cells (due to hyphema), melanocytes or intraocular neoplasms
will also result in secondary glaucoma. Congenital glaucoma
is the result of maldevelopment of the iridocorneal angle and/
or trabecular meshwork, which may be associated with other
ocular or systemic developmental abnormalities. In dogs, it has
recently been shown that breed-related (presumably primary,
inherited) glaucoma affects nearly 0.9% of pure bred dogs
in North America, with some breeds (e.g., American Cocker
Spaniel and Basset Hounds) having a prevalence > 5% [7]. A
similar percentage of the general canine population is affected
by secondary glaucoma [8]. In cats, on the other hand, the great
majority of glaucoma cases are secondary to another disease
(most commonly uveitis), and only 2-5% of all feline glaucoma
cases have been classified as primary [9, 10].
glaucoma that presents as a unilateral disease, the clinician
must provide prophylactic treatment to the second, unaffected
eye. A recent multicenter, open label clinical trial studied the
effect of prophylactic treatment of the unaffected eye with
0.5% betaxololol ophthalmic solution (one drop every 12
hours) [13]. It was shown that such treatment delayed the
onset of clinical disease in the unaffected eye by nearly two
years (median duration till disease onset was 8 and 31 months
in the control and treated animals, respectively) [13]. Therefore,
clinicians presented with cases of unilateral glaucoma must
perform a comprehensive ophthalmic examination of both
eyes. If signs of a primary disease that induced glaucoma (e.g.,
uveitis, lens luxation) are found in the affected eye, it is safe
to assume that the eye is suffering from secondary glaucoma,
and treatment may be administered only to this eye. However,
if no signs of a primary cause of glaucoma are found in the
affected eye, the patient should be referred to a specialist who
can perform gonioscopy to examine the iridocorneal angles.
If such an examination reveals angle abnormalities it may be
concluded that the animal is suffering from primary glaucoma in
the affected eye, and that the unaffected eye is predisposed to
a glaucoma attack. Therefore prophylactic treatment should be
instituted in the unaffected eye [13]. However, as noted earlier,
some dog breeds (e.g., the beagle and the Norwegian elkhound)
suffer from primary, open angle glaucoma. In this case aqueous
outflow is impeded by biochemical changes in the trabecular
meshwork, and therefore the gonioscopic examination of the
iridocorneal angle may be unremarkable. Prophylactic treatment
is nonetheless also advisable in these patients.
Another method of classifying glaucoma is based on the state
of the iridocorneal angle [1, 5]. Thus, glaucoma may be classified
as open angle if the iridocorneal angle is normal and the
obstruction to outflow is at the level of the trabecular meshwork
or further “downstream”. Alternatively, the disease may be
classified as narrow angle or even angle closure, depending on
the distance between the cornea and the base of the iris. It
should be noted that the two methods of classifying the disease
are complementary, rather than exclusive. Thus, an animal
may be suffering from primary open angle glaucoma (as seen
in the beagle dog) [11] or primary narrow angle glaucoma (as
seen in the American cocker spaniel) [12]. Similarly, an existing
ocular disease could induce secondary open angle glaucoma or
secondary narrow angle glaucoma.
Goals of therapy
The two major consequences of the elevation in IOP are loss of
vision and pain, and the primary goals of therapy are therefore
preserving vision and relieving pain. As noted earlier, loss of
vision in glaucoma is usually progressive, due to progressive
death of RGCs. However, acute attacks of glaucoma may be
characterized by acute loss of vision (depending on the duration
and magnitude of the IOP spike) [12, 14]. Furthermore, many pet
owners may not notice the early visual deficits that characterize
the initial stages of chronic glaucoma and which result from mild
elevation of IOP. As a result, even cases of chronic glaucoma may
present only when the animal is blind. In a retrospective study of
93 glaucomatous cat eyes, 67 eyes were blind at presentation
[15].
The classification of glaucoma should not be regarded as an
“abstract curiosity”. Rather, it carries important prognostic and
therapeutic consequences. In secondary glaucoma, successful
treatment of the disease hinges on treatment of the primary cause
(e.g., resolution of the posterior synechia or surgical removal of
the luxated lens and vitreous). Furthermore, it is possible that once
the primary cause has been successfully treated the glaucoma will
resolve and long-term anti-glaucoma therapy will not be required.
On the other hand, primary glaucoma usually requires lifelong
treatment. Furthermore, due to the hereditary nature of primary
glaucoma, affected animals should not be bred, and neutering of
the animal should be discussed with the owner.
Owners of glaucomatous animals should be counselled that
currently there is no therapy to restore vision that has been lost
to the disease (an exception to this may be animals that present
within a few hours of an acute glaucoma attack; in such cases,
blindness may be due to RGC ischemia rather than RGC death,
and vision may be restored following emergency lowering of IOP,
though long-term prognosis remains very guarded) [15]. Current
medical therapy, as well as the neuroprotective treatments
discussed at the end of this paper, may help preserve existing
vision, but will not restore vision to blind eyes. Unfortunately,
this sad state of affairs is not limited to veterinary medicine. It is
estimated that over 60 million people will be afflicted with the
disease by the end of this decade, and 8.4 million of them will
be bilaterally blind [16].
Classification of glaucoma according to cause and state of
angle is of great importance when the clinician is presented
with a case of unilateral glaucoma. While secondary glaucoma
may be a unilateral disease, primary glaucoma is inevitably a
bilateral disease even though one eye may develop a clinical
disease months to years before the other eye [12]. Therefore,
in cases of unilateral, secondary glaucoma it is acceptable to
treat only the affected eye. However, in cases of primary
2
However, this does not mean that eyes blinded by glaucoma
should not be treated. On the contrary, these eyes must be
treated to alleviate the pain inflicted by the disease. The pain
caused by glaucoma is acute in acute glaucoma, and the patient
may present with apathy, lethargy, blepharospasm, epiphora
and other noticeable signs of pain [1, 5]. In chronic glaucoma
signs of pain are far more subtle, and may not be noticed by the
owners. Indeed, many owners of animals blinded by glaucoma
will argue against the need for treatment, because “the animal
is not showing any obvious signs of pain”. Such owners will
frequently admit their mistake and will remark on the noticeable
improvement in the animal’s behavior and disposition following
successful lowering of IOP or enucleation of the blind eye.
Therefore, it is the practitioner’s duty to convince the owners
of glaucomatous patients to treat their animals (medically or
surgically) even if the eye is blind.
and judgment in selecting anti glaucoma drugs and monitoring
their effects.
Hypotensive drugs
Emergency lowering of IOP
Administration of hyperosmotic agents causes an elevation in
plasma osmolarity. This inhibits the ultrafiltration of plasma
in the ciliary processes, resulting in reduced aqueous humor
production [24, 25]. Furthermore, fluid may be absorbed from
the vitreous body and anterior chamber, leading to additional
IOP reduction. The two hyperosmotic drugs most commonly
used are mannitol (1-2 g/kg; dose administered over 30 min
through a slow intravenous drip) [24] and glycerol (1-1.5 g/kg,
orally) [25]. The former should be used cautiously in patients
suffering from cardiac or renal disease, and the latter should
not be used in diabetic patients. Both drugs are less efficacious
in cases of uveitis. Drinking water should be withheld for 3-4
hours after administrating the drug.
Principles of medical therapy
Medical management of glaucoma is a very complex discipline.
This is evidenced by the large number of drugs (and drug types)
available, by the potential effectiveness and toxicity of these
drugs in different species, by the numerous causes of glaucoma,
and by the guarded long-term prognosis. In the previously cited
retrospective study of glaucomatous cats, treatment succeeded
in preserving vision in only 9 of the 26 eyes that were visual at
presentation [15].
Many clinicians report that topical latanoprost (see below)
achieves very fast reduction of IOP in dogs, though clinical
studies are lacking.
Reduction of Aqueous Humor Production
Carbonic anhydrase inhibitors
Carbonic anhydrase is a key enzyme in the production of aqueous
humor, and therefore its inhibition leads to IOP reduction.
Systemic carbonic anhydrase inhibitors include acetazolamide
(4-8 mg/kg, 2 to 3 times daily) [26] and methazolamide (5-10 mg/
kg, 2 to 3 times daily) [27]. While methazolamide is considered
less toxic than acetazolamide, both drugs can induce metabolic
acidosis and hypokalemia, especially in cats. Therefore, systemic
administration has largely been replaced by topical medications
that came out in the mid 1990’s. Commercial topical preparations
include 2% dorzolamide [28] and 1% brinzolamide [29], and the
drugs are administered 3 times daily. Both drugs are effective in
lowering canine IOP, but only the former has been shown to be
effective in cats [30].
There are several categories of anti-glaucoma drugs. With the
possible exception of the recently-introduced prostaglandin
analogues, it is unusual to achieve a satisfactory, long-term
decrease in IOP using just one category of drugs. Usually, a
combination of two or more drugs is required for successful
treatment of glaucoma, and some studies have shown cumulative
or synergistic effect of various drug combinations [17]. Picking a
beneficial combination in a given patient depends on the eye’s
status (e.g., state of the angle, primary cause of the disease), but
may also involve some trial-and-error. Furthermore, it should be
noted that some drugs may lose their effectiveness with time as
circumstances, such as the state of the angle, change.
Beta blockers
These drugs act to reduce aqueous production through blocking
β receptors and reducing blood flow in the ciliary processes. The
two commonly used drugs in this category are 0.5% betaxolol
[31] and 0.25-0.5% timolol [32]; both are topical preparations,
administered twice daily. Only the latter has been evaluated in
cats [33]. The drugs may cause significant bradycardia due to
systemic absorption; thus their administration in small animals
and cardiac patients mandates monitoring.
Broadly speaking, anti-glaucoma drugs (with the exception of
hyper-osmotic agents) may act to reduce production of aqueous
humor, and/or to increase its drainage from the eye through
the iridocorneal angle or the unconventional pathways. It is
noteworthy that there are significant interspecies differences in
both the effectiveness and the toxicity of drugs. For example,
latanoprost (a prostaglandin analogue) is an extremely effective
drug in both humans [18] and dogs [19], but is ineffective in
cats that lack the receptor for the compound [20]. Conversely,
apraclonidine, an α2 adrenergic agonist, appears to be safe in
dogs [21] but is systemically toxic in cats, as it induces vomiting
and significant bradycardia [22]. And finally, some drugs may
be contraindicated in patients suffering from other systemic
or ocular disease. For example, mannitol should not be used
in patients suffering from cardiac or renal insufficiency (as it
may cause pulmonary edema or reduced glomerular filtration,
respectively) [23], and latanoprost is contraindicated in cases of
anterior lens luxation as it may cause vitreous entrapment and
pupillary block. Therefore, the clinician is urged to use caution
Adrenergic agonists
These drugs actually achieve lowering of IOP through 2
mechanisms: first, vasoconstriction in the ciliary processes
leads to reduced blood flow, resulting in lower aqueous humor
production; and second, increased aqueous drainage from the
eye, probably through unconventional pathways. Drugs include
ophthalmic solutions of 0.5% dipiverfin, 1-2% epinephrine
and 0.5% apraclonidine. The first two are non-selective
(sympathomimetic) α- and β- agonists [34], while the latter is a
specific α2 adrenergic agonist [21]. Apraclonidine may also cause
3
Medical Therapy of Glaucoma - R. Ofri
systemic hypertension, and its use in cats is contra-indicated
[22]. Brimonidine, another commercially available α2 adrenergic
agonist, has not been shown to be effective in dogs [35].
promising experimental results. For example, memantine, a
glutamate antagonist, has been shown to be neuroprotective
in both rodent [43] and monkey [44] models of glaucoma.
Indeed, in both Europe and the USA memantine is already
undergoing advanced clinical testing in humans suffering from
neurological disorders that may have a similar pathogenesis to
glaucomatous neuropathy, such as Alzheimer’s disease [45].
Similarly, unoprostone, a potent vasorelaxant, was shown to
antagonize the vasoconstrictive effect of endothelin-1 and to
improve retinal blood flow in human glaucoma patients [46].
Obviously, such drugs are not expected to restore vision which
has been lost prior to initiation of treatment. For example, in the
retrospective study of feline glaucoma cited in the introduction
[15], neuroprotection will not help the 67 glaucomatous cats
that were blind at presentation. However, it may very well
help preserve vision in the 26 cats that still had some vision
at presentation, and revolutionize our therapeutic approach to
glaucoma.
Increase in Aqueous Humor Drainage
Parasympathomimetic (cholinergic) agents
Cholinergic drugs cause ciliary body contraction, leading to
opening of the iridocorneal angle and increased drainage of
the aqueous humor through the conventional outflow pathway.
Pilocarpine is a direct-acting cholinergic drug, available in
concentrations of 0.5-8%, and applied 3-4 times daily [36].
Demecarium bromide is an indirect cholinergic drug (i.e., its effect
is not achieved by directly stimulating the cholingergic receptor;
rather, it inhibits acetyl choline esterase, thereby increasing the
amount of endogenous acetyl choline at the synapse), available
in concentrations of 0.125-0.25% and applied once daily [37].
The drugs cause local ocular irritation and may exacerbate preexisting uveitis. Long-term use may result in cholinergic toxicity,
and concurrent use of demecarium bromide with other acetyl
choline inhibitors (e.g., organophsphates for ectoparasites) is
contraindicated.
Conclusions
Prostaglandin analogues
These drugs were introduced 10 years ago, and have become the
treatment of choice in canine glaucoma. IOP is lowered following
increased drainage of aqueous humor through the unconventional,
uveoscleral pathways. Available topical drugs include 0.005%
latanaprost [19], 0.003% bimatoprost [18], 0.004% travoprost
[38] and 0.12% unoprosone isopropyl [39], and they are given
1-2 times daily. The drugs are ineffective in cats, contraindicated
in cases of anterior lens luxation (as they cause miosis) and should
be used with caution in cases of uveitis.
Ocular hypotensive drugs may be used to effectively lower IOP in
glaucoma patients. A large range of drugs is currently available,
and the clinician should select the appropriate drug based on
the animals’ signalment, the cause and severity of the disease,
the patient’s visual status, and the ocular and systemic health.
Meanwhile, improved understanding of the pathogenesis of
vision loss has enabled the development of new and exciting
treatment modalities for glaucoma. It is hoped that further
unraveling of the molecular mechanisms responsible for ganglion
cell death in glaucoma will lead to effective neuroprotective
treatment that will preserve retinal function in patients.
Further Reading
Secondary degeneration and neuroprotective therapies
As noted at the beginning of this review, today there is increasing
realization that other factors besides IOP are responsible for the
progressive loss of RGCs that is the scourge of glaucoma. It is
suggested that RGCs damaged by an initial rise in IOP, or due to
local ischemia, release various substances into their immediate
surroundings. The localized high concentrations of these
substances create a hostile micro-environment. Adjacent axons,
which were not damaged during the initial insult, undergo
secondary degeneration as a result of exposure to this toxic
milieu. This creates a “domino effect” in which RGCs continue
to degenerate even after IOP has been successfully lowered,
resulting in further loss of vision [2]. While many mediators
of secondary degeneration have been identified, the two
compounds receiving most attention are glutamate, an excitatory
neurotransmitter that is toxic in elevated concentrations, and
endothelin-1, which causes vasoconstriction and local ischemia
in the retina. Indeed, elevated levels of both glutamate [40, 41]
and endothelin-1 [42] have been demonstrated in the eyes of
glaucomatous dogs.
MAGGS (D.J.) – Ocular pharmacology and therapeutics. In Slatter’s
Fundamentals of Veterinary Ophthalmology, Eds David J Maggs,
Paul E Miller, Ron Ofri. Elsevier, St Louis, Missouri (2007).
REGNIER (A.) – Clinical pharmacology and therapeutics, Part I. In
Veterinary Ophthalmology, 4th edition, Ed Kirk N Gelatt. Blackwell
Publishing, Ames, Iowa (2007).
WILLIS (A.M.) - Ocular hypotensive drugs. In Ocular Therapeutics, Ed
Cecil P Moore. Veterinary Clinics of North America: Small Animal
Practice 34 (2004).
References
[1] GELATT (K.N.), Dennis (B.E.) - The canine glaucomas. In Veterinary
Ophthalmology, 3rd edition, Ed Kirk N Gelatt. Lippincott Williams
& Wilkins, Philadelphia (1999)
[2] SCHWARTZ (M.) - Lessons for glaucoma from other neurodegenerative diseases: can one treatment suit them all? J
Glaucoma. 2005;14:321-3.
[3] TRICK (G.L.) - Visual dysfunction in normotensive glaucoma. Doc
Ophthalmol. 1993;85:125-33.
[4] KOMAROMY (A.M.) et al. - Diurnal intraocular pressure curves in
healthy rhesus macaques (Macaca mulatta) and rhesus macaques
with normotensive and hypertensive primary open-angle
glaucoma. J Glaucoma. 1998;7:128-31.
[5] GELATT (K.N.), BROOKS (D.E..), KALLBERG (M.E.) - The canine
glaucomas. In Veterinary Ophthalmology, 4th edition, Ed Kirk N
Gelatt. Blackwell Publishing, Ames, Iowa (2007).
.
An obvious implication of the process of secondary degeneration
is that treatment with compounds which inhibit the toxic factors
may slow or stop the cascade of secondary degeneration, and
protect the undamaged neighboring axons. This therapeutic
approach is known as neuroprotection, and is showing
4
[6] TOWNSEND (W.M.) - Feline Ophthalmology. In Veterinary
Ophthalmology, 4th edition, Ed Kirk N Gelatt. Blackwell Publishing,
Ames, Iowa (2007).
[7] GELATT (K.N.), MACKAY (E.O.) - Prevalence of the breed-related
glaucomas in pure-bred dogs in North America. Vet Ophthalmol.
2004;7:97-111.
[8] GELATT (K.N.), MACKAY (E.O) - Secondary glaucomas in the dog in
North America. Vet Ophthalmol. 2004;7:245-59.
[9] WILCOCK (B.), PEIFFER (R.L.), DAVIDSON (M.G.) – The cause of
glaucoma in cats. Vet Pathol. 1990;27:35-40.
[10] HAMPSON (E.C.), SMITH (R.I.), BERNAYS (M.E.) -. Primary
glaucoma in Burmese cats. Aust Vet J. 2002;80:672-80.
[11] GELATT (K.N.), GUM (G.G.) - Inheritance of primary glaucoma in
the beagle. Am J Vet Res. 1981;42:1691-3.
[12] MAGRANE (W.G.) - Canine glaucoma. II. Primary classification. J
Am Vet Med Assoc. 157;131:372-8.
[13] MILLER (P.E.) et al. - The efficacy of topical prophylactic antiglaucoma
therapy in primary closed angle glaucoma in dogs: a multicenter
clinical trial. J Am Anim Hosp Assoc. 2000;36:431-8.
[14] BROOKS (D.E.), SIMS (M.H.), GUM (G.G.), BLACKSTOCK (M.J.) Changes in oscillatory potentials of the canine electroretinogram
during acute sequential elevations in intraocular pressure. Prog
Vet Comp Ophthalmol. 1992;2:80-93.
[15] BLOCKER (T.), VAN DER WOERDT (A.) - The feline glaucomas: 82
cases (1995-1999). Vet Ophthalmol. 2001;4:81-5.
[16] QUIGLEY (H.A.), BROMAN (A.T.) - The number of people with
glaucoma worldwide in 2010 and 2020. Br J Ophthalmol.
2006;90:262-7.
[17] PLUMMER (C.E.), MACKAY (E.O.), GELATT (K.N.) - Comparison
of the effects of topical administration of a fixed combination of
dorzolamide-timolol to monotherapy with timolol or dorzolamide
on IOP, pupil size, and heart rate in glaucomatous dogs. Vet
Ophthalmol. 2006;9:245-9.
[18] CHEN (M.J.) et al. - Comparison of the effects of latanoprost
and travoprost on intraocular pressure in chronic angle-closure
glaucoma. J Ocul Pharmacol Ther. 2006;22:449-54.
[19] GELATT (K.N.), MACKAY (E.O) - Effect of different dose schedules
of latanoprost on intraocular pressure and pupil size in the
glaucomatous Beagle. Vet Ophthalmol. 2001;4:283-8.
[20] STUDER (M.E.), MARTIN (C.L.), STILES (J.) - Effects of 0.005%
latanoprost solution on intraocular pressure in healthy dogs and
cats. Am J Vet Res. 2000;61:1220-4.
[21] MILLER (P.E.), RHAESA (S.L.) - Effects of topical administration of
0.5% apraclonidine on intraocular pressure, pupil size, and heart
rate in clinically normal cats. Am J Vet Res. 1996;57:83-6.
[22] COLBY (E.D.), MCCARTHY (L.E.), BORISON (H.L.) - Emetic action
of xylazine on the chemoreceptor trigger zone for vomiting in
cats. J Vet Pharmacol Ther. 1981;4:93-96.
[23] MANENTI (A.), BOTTICELLI (A.), BUTTAZZI (A.), GIBERTINI (G.)
- Acute pulmonary edema after over-infusion of crystalloids
versus plasma: histological observations in the rat. Pathologica.
1992;84:331-4.
[24] DUGAN (S.J.), ROBERTS (S.M.), SEVERIN (G.A.), - Systemic
osmotherapy for ophthalmic disease in dogs and cats. J Am Vet
Med Assoc. 1989;194:115-8.
[25] LORIMER (D.W.), HAKANSON (N.E.), PION (P.D.), MERIDETH (R.E.)
- The effect of intravenous mannitol or oral glycerol on intraocular
pressure in dogs. Cornell Vet. 1989;79:249-58.
[26] CARRIER (M.), GUM (G.G.) - Effects of 4% pilocarpine gel on
normotensive and glaucomatous canine eyes. Am J Vet Res.
1989;50:239-44.
[27] SKOROBOHACH (B.J.), WARD (D.A.), HENDRIX (D.V.) - Effects of
oral administration of methazolamide on intraocular pressure and
aqueous humor flow rate in clinically normal dogs. Am J Vet Res.
2003;64:183-7.
[28] GELATT (K.N.), MACKAY (E.O) - Changes in intraocular pressure
associated with topical dorzolamide and oral methazolamide in
glaucomatous dogs. Vet Ophthalmol. 2001;4:61-7.
[29] WILLIS (A.M.), DIEHL (K.A.), ROBBIN (T.E.) - Advances in topical
glaucoma therapy. Vet Ophthalmol. 2002;5:9-17.
[30] RAINBOW ME, DZIEZYC J. Effects of twice daily application of
2% dorzolamide on intraocular pressure in normal cats. Vet
Ophthalmol. 2003;6:147-50.
[31] MIKI (H.), MIKI (K.) - The effects on the intraocular pressure and
visual field resulting from a switch in the treatment from timolol
to betaxolol. J Ocul Pharmacol Ther. 2004;20:509-17.
[32] WILKIE (D.A.), LATIMER (C.A.) - Effects of topical administration
of timolol maleate on intraocular pressure and pupil size in dogs.
Am J Vet Res. 1991;52:432-5.
[33] WILKIE (D.A.), LATIMER (C.A.) - Effects of topical administration of
timolol maleate on intraocular pressure and pupil size in cats. Am
J Vet Res. 1991;52:436-40.
[34] GWIN (R.M.), GELATT (K.N.), GUM (G.G.), PEIFFER (R.L. Jr.) - Effects
of topical 1-epinephrine and dipivalyl epinephrine on intraocular
pressure and pupil size in the normotensive and glaucomatous
Beagle. Am J Vet Res. 1978;39:83-6.
[35] GELATT (K.N.), MACKAY (E.O) - Effect of single and multiple doses
of 0.2% brimonidine tartrate in the glaucomatous Beagle. Vet
Ophthalmol. 2002;5:253-62.
[36] WILKIE (D.A.), LATIMER (C.A.) - Effects of topical administration
of 2.0% pilocarpine on intraocular pressure and pupil size in cats.
Am J Vet Res. 1991;52:441-4.
[37] GUM (G.G.), GELATT (K.N.), GELATT (J.K.), JONES (R.) - Effect
of topically applied demecarium bromide and echothiophate
iodide on intraocular pressure and pupil size in beagles with
normotensive eyes and beagles with inherited glaucoma. Am J
Vet Res. 1993;54:287-93.
[38] CARVALHO (A.B.), LAUS (J.L.), COSTA (V.P.), BARROS (P.S.),
SILVEIRA (P.R.) - Effects of travoprost 0.004% compared with
latanoprost 0.005% on the intraocular pressure of normal dogs.
Vet Ophthalmol. 2006;9:121-5.
[39] OFRI (R.), RAZ (D.), KASS (P.H.), LAMBROU (G.N.), PERCICOT (C.L.) The effect of 0.12% unoprostone isopropyl (rescula) on intraocular
pressure in normotensive dogs. J Vet Med Sci. 2000;62:1313-5.
[40] BROOKS (D.E.), GARCIA (G.A.), DREYER (E.B.), ZURAKOWSKI (D.),
FRANCO-BOURLAND (R.E.) - Vitreous body glutamate concentration
in dogs with glaucoma. Am J Vet Res.1997;58:864-7.
[41] MCILNAY (T.R.), GIONFRIDDO (J.R.), DUBIELZIG (R.R.), POWELL
(C.C.), MADL (J.E.) - Evaluation of glutamate loss from damaged
retinal cells of dogs with primary glaucoma. Am J Vet Res.
2004;65:776-86.
[42] KALLBERG (M.E.), BROOKS (D.E.), GARCIA-SANCHEZ (G.A.),
KOMAROMY (A.M.), SZABO (N.J.), TIAN (L.) - Endothelin 1
levels in the aqueous humor of dogs with glaucoma. J Glaucoma
2002;11:105-9.
[43] SCHUETTAUF (F.), QUINTO (K.), NASKAR (R.), ZURAKOWSKI (D.)
- Effects of anti-glaucoma medications on ganglion cell survival:
the DBA/2J mouse model. Vision Res. 2002;42:2333-7.
[44] HARE (W.A.), WOLDEMUSSIE (E.), LAI (R.K.), TON (H.), RUIZ (G.),
CHUN (T.), WHEELER (L.) - Efficacy and safety of memantine
treatment for reduction of changes associated with experimental
glaucoma in monkey, I: Functional measures. Invest Ophthalmol
Vis Sci. 2004;45:2625-39.
[45] LIPTON (S.A.) - Possible role for memantine in protecting retinal
ganglion cells from glaucomatous damage. Survey Ophthalmol.
2003;48 Suppl 1:S38-46.
[46] MELAMED (S.) - Neuroprotective properties of a synthetic
docosanoid, unoprostone isopropyl: clinical benefits in the
treatment of glaucoma. Drugs Exp Clin Res. 2002;28:63-73.
5
OPTHALMOLOGY
The ECVO hereditary
eye disease Scheme
FC. Stades1 , E. Bjerkås2
SUMMARY
The European College of Veterinary Ophthalmologists (ECVO) scheme in order to control presumed inherited
eye diseases (PIED) is presented. The Scheme is now in use in seven European countries. In addition, individual
ECVO Diplomates work in accordance with the scheme in other countries. The national eye panels consist of ECVODiplomates plus well trained and examined veterinarians with a special interest in ophthalmology. Requirements
for education of panellists, plus procedures for the qualifying exams are outlined. The Scheme is for all presumed
inherited diseases of the eye and its adnexa. The results of the general eye examination are given on the certificate,
with emphasis on specified congenital and acquired PIED’s. Appeals procedures in case of conflicting results are
described, as well as the procedures for export and import of results. The ECVO certificate is both in English and the
national language and is readable and understandable for the well informed owner. The characteristics of some other
eye-schemes are discussed. Further information can be found on the ECVO website: www.ecvo.org.
European specialists would in the first decades not be sufficient
to screen all dogs and cats presented by owners and breeders.
Thus, a broader Scheme, including well trained, non-specialists
in existing European eye panels and a uniform, computer
compatible certificate, understandable to the owner, had to be
developed.
Introduction
The European College of Veterinary Ophthalmologists (ECVO)
was founded in 1992. The Objectives and Statements of ECVO
include: ”to advance veterinary ophthalmology in Europe and
increase the competence of those who practice in this field by”…
“encouraging research and other contributions to knowledge
relating to the pathogenesis, diagnosis, therapy, prevention, and
the control of diseases directly or indirectly affecting the eye of
all animals, and promoting communication and dissemination
of this knowledge”.
The aim of this article is to describe the design of the ECVO
Scheme and the main aspects of use of the certificate issued
after examination of an animal.
The ECVO Scheme
The main purpose of the ECVO Scheme (further referred to
as the Scheme) is the examination of the eyes of animals with
emphasis on presumed inherited eye disease (PIED). However,
examination also includes a general assessment of the eye and
adnexa. A certificate of eye examination is issued, focusing on
inherited conditions (Fig. 1 a,b). It is recommended that the
examination of an animal should be carried out annually. If the
examination is inconclusive, it might be necessary for the animal
to be re-examined at an earlier stage, i.e. within 6 months.
From the beginning it was clear to the founders of the College
that, in order to establish control programmes for hereditary
eye diseases in dogs and cats, it was necessary to have a
well trained group of examiners for high quality screening
and uniform evaluation of the findings. The small number of
1) Frans C. Stades, DVM, PhD, Dipl ECVO, University of Utrecht, Faculty of Veterinary Medicine, Department of Clinical Sciences of Companion Animals, Ophthalmology Section, PO Box 80 154, NL-3508 TD Utrecht, the Netherlands
2) Ellen Bjerkås DVM, PhD, Dipl ECVO, Norwegian School of Veterinary Science, Department of Companion Animal Clinical Sciences, P.O.Box 8146
Dep, 0033 Oslo, Norway
1
The ECVO hereditary eye disease Scheme - FC. Stades, E. Bjerkås
Fig. 1 a, b Front and back of the Dutch version of the ECVO certificate.
2
3
Screening of whole litters at the age of 6-8 weeks can also be
performed under the Scheme, with a specific litter certificate
being issued.
also be examined during the combined, annual Nordic Panel
examination. The examination consists of a written section of
multiple choice and/or essay questions on hereditary ophthalmic
related diseases, an examination based on slides of hereditary
ophthalmic (related) diseases, and, after having passed the first
two parts of the examination, the candidate must pass a final
section of live case evaluation.
The Scheme is now used in Austria, Denmark, Finland, Germany,
the Netherlands, Norway and Switzerland. In addition, individual
ECVO Diplomates are using the ECVO certificate in Israel, Spain
and UK.
The Scheme has some restrictions and duties, such as:
• The Panellist is obliged to work under the regulations of the
Scheme
• When an eye examination has been completed within the
Scheme, a certificate must be issued. This means that any
preliminary examination which may preclude the notification
of the results is not accepted as being valid
• If an eye patient is examined by a Panellist and a hereditary eye
disease is recognised, the Panelist is strongly recommended
to issue an ECVO certificate
• Records must be kept, and in order to remain a Panellist a
minimum number of 100 examinations for the Scheme per
year is required
• In case of continuing misdiagnosis or misbehavior of a Panellist,
the Panellist is to be reexamined, or the ECVO is entitled to
stop his/her contract
When national eye panels are established, these should be
encouraged to work under the rules of the Scheme. In this
way, the scientific quality of examiners is ensured. Two types
of panellists are at present accepted by the ECVO to perform
eye examinations under the Scheme: 1. practicing Diplomates
of the ECVO, and 2. Eye Scheme Examiners (non-Diplomate
of the ECVO, further to be called ESE). The ESE are qualified
veterinarians, examined and accepted for a restricted period of
five years. However, the contract may be extended ad infinitum
by the ECVO. For those countries where a nationally recognised
Scheme has been in existence for more than five years, the
national panel and well trained ESE can be allowed to work
under the Scheme.
Before ESE-candidates can qualify to sit the examination for
the Scheme, the candidate must document having examined
under supervision a sufficient number of dogs and cats of
specific breeds and with defined diseases (Fig. 2). The breeds
and diseases/conditions are specified in an appendix of the
educational requirements. The candidate must have participated
in recognised continuing education courses, and relevant
literature, according to a defined list, has to be studied.
The eye examination and the certificate
Animals can be examined as individual animals, or through litter
screening and group examinations for societies or breed clubs,
e.g. at a dog show. For the examination the animal’s registration
documents identifying the dog must be available, as well as the
result of any previous certification, including gene testing. In
some countries the registration data can be confirmed online in
the national registry. If the documents are not available or the
identification of the animal cannot be confirmed online, then
examination can be undertaken but the certificate will not be
issued until the Panellist has proper information on the dog’s
identity. Prior to the examination, the owner or agent must
sign the certificate, verifying that the details given regarding
the animal are correct, and permitting that the results of the
examination are available for publication. These data are
included in the upper part of the certificate (Fig. 3). Certificates
for the Scheme can only be issued for pedigree dogs, which can
be identified by either tattoo or microchip. For cats this is not
yet compulsory.
The examination in order to qualify for the Scheme should be
coordinated and directed by at least one member of the Genetics
Committee of the ECVO and by one member of the Examination
Committee or the Board of the ECVO. The examinations are
generally organised nationally. Individuals can for the moment
Fig. 2 Training session for Finnish and Swedish future Eye
Scheme Examiners. The photo was taken some years ago and all the
veterinarians are now qualified as ESE.
All animals presented under the Scheme undergo a general
examination of the eye and adnexa, with the use of a mydriatic
for examination of deeper structures included in the procedure.
The minimum equipment to be used for the examination is a slit
lamp biomicroscope and a binocular indirect ophthalmoscope.
The use of other equipment is optional.
Gonioscopy is an optional, additional examination. If performed,
it has to be recorded on the certificate. It is recommended that
gonioscopy is done on one occasion in all breeds in which
primary glaucoma is known to occur. If any additional method
of examination, e.g. electroretinography (ERG), according to
a standardized protocol [1] is used, the certificate is only valid
4
Fig. 3 Details of the Dutch version of the upper part of the ECVO certificate.
Examination results
together with a specific document. Specified congenital and
acquired presumed hereditary eye diseases are listed on the
certificate, which is readable and understandable for the well
informed owner.
Results regarding PIED are marked in the lower section of the
certificate (Fig. 4). For rare, but important, disabling anomalies,
as well as important eye diseases not (yet) mentioned on the
certificate, a box for the category “other” can be ticked, and
the name of the anomaly written on the certificate. The results
for acquired eye diseases are valid for 1 year. The results for
congenital diseases are valid throughout the animal’s life, even
if the condition is masked and cannot be diagnosed at a later
stage.
Details of all ocular or periocular lesions and conditions found
at the time of examination, whether relating to hereditary eye
diseases or not, are drawn and/or written in the descriptive
comments section in the middle of the certificate (Fig. 4).
Less important eye diseases, not yet proven to be inherited
in the particular breed and not interfering with vision, can
be mentioned in this section as N.B. , under investigation.
Eye diseases affecting vision, such as severe retinal dysplasia,
cataract, lens luxation and retinal degenerations are always to
be considered as a PIED and should be marked as such.
The result of the examination for a PIED can be:
1 Unaffected: which signifies that there is no clinical evidence
of the PIED
Fig. 4 Details of the Dutch version of the lower part of the ECVO Certificate.
5
2 Undetermined: i.e. clinical features that could possibly fit the
PIED, but the changes are inconclusive
3 Suspicious: i.e. minor, but specific signs of the PIED. Further
development will confirm the diagnosis, and the owner is
recommended to present the dog for re-examination after
6-12 months
4 Affected: if there is clinical evidence of the PIED.
For several PIED’s specifying boxes are given, providing details on
the type of e.g. retinal dysplasia - RD - (focal, geographic, total)
or cataract (cortical, posterior polar etc). In the “Comments”
section, extra boxes are provided for ticking off mild, moderate
or severe manifestation of the anomaly, enabling the examiner
to indicate the degree/severity/significance of involvement.
to be able to establish the correct diagnosis.
Further details of the Scheme are issued by the Genetics
Committee of the ECVO, after hearing the national panel liaison
officers, and are confirmed by the Board of the ECVO.
Further details and information to the panellists is given in the
Procedure notes, which are updated at least every two years.
In September 2005 the biannual European meeting between
the kennel clubs, veterinary associations and ECVO was
arranged in Paris. The recommendations from this meeting
have been implemented in the Scheme and include guidelines
for additional procedures as well as procedures for examination
results of imported/exported dogs. A list of breeds advised to
be examined for persistent pupillary membrane (PPM) or by
gonioscopy for pectinate ligament abnormality (PLA) was drawn
up. If a dog is exported, all results of former examinations should
follow the dog together with the pedigree. The “exporting”
registry provides all results of former examinations on presumed
inherited eye diseases and the “importing” registry is obliged to
include them. If the animal is “affected” by a PIED, this diagnosis
will not be changed unless the dog has been re-examined by
the appeals authority of the new registry.
It is important to emphasise that the examiner is giving the
results of his or her examination and evaluation.
Once the examination has been completed, the results are
recorded on the certificate, including details of localisation and
type of any lesion present. Any information considered important
by the Panellist should be included in the “Comments” section.
The original certificate is submitted to the appropriate kennel
club or national Scheme authority, one copy to the appropriate
breed club (if allowed by national legislation), one copy is directly
issued to the owner and one copy is retained by the Panellist.
Recently, the German national panel (DOK) has started online
registration of the results, with a printout handed out to the
owner immediately after the examination. A direct check for
results of previous examinations is not yet possible at the time
of writing.
Gene testing for eye diseases does not replace clinical eye
examination. This aspect is considered of great importance, as
for example one breed may be affected by more than one form
within a group of diseases, e.g. the PRAs.
Procedure notes
The procedure notes include guidelines for filling out the
certificate. Schematic illustrations of ocular and extraocular
structures on the form facilitate drawings for more detailed
information (Fig. 4). In addition, the procedure notes informs
about the interpretation of the clinical findings and the use of
the ECVO certificate. To enable easier translation into other
languages it is recommended to include conclusive comments in
English. When appropriate, the name of the disease in the list of
‘Definitions’ in the procedure notes should be used.
Further information regarding the procedure notes can be found
on the ECVO website: www.ecvo.org.
The recommendations for breeding will be for the relevant body
to decide, i.e. national kennel clubs or breed clubs. The national
eye panel should assist in drawing up recommendations for
breeding.
Conflicting results of eye examinations
In the event that the results of two eye examinations of the same
animal conflict, the most adverse judgment is valid until the animal
is examined by the assembled national panel or by the Chief
panellist, whose decision will be final. However, for conditions
which may be changed artificially, (e.g. distichiasis, entropion) or
may be masked or resolve during aging (e.g. collie eye anomaly
(CEA) and retinal dysplasia) the results are definite. If possible,
it is also recommended that “suspicious” cases are re-examined
by the national panel or Chief Panellist after the prescribed
period (Fig. 5). The result of this examination will be final.
Discussion
In addition to the ECVO Scheme, national schemes for control of
PIED’s are in use in Europe as well as in other parts of the world.
In USA the Canine Eye Registry Foundation (CERF) registers
results of eye examinations, in Europe national schemes have
been established in many countries, including UK (The British
Veterinary Association-Kennel Club-International Sheepdog
Society [BVA] Scheme) and Sweden (The Swedish Society of
Veterinary Ophthalmology [SSVO] Scheme).
Appeals Procedure
Appeal cases should be examined at either a national panel
meeting (ideally at least 4 times/year), or by a Chief panellist
(usually an ECVO Diplomate), within a restricted period,
preferably within 60 days.
The main characteristics and differences of the three schemes
specifically mentioned are:
The CERF scheme allows only recognized specialists (Diplomates
of the American College of Veterinary Ophthalmologists [ACVO])
as examiners and uses a computer compatible certificate. The
dog should be microchipped or tattooed for the result to be
An exception is made for the congenital eye anomalies that may
be camouflaged at an older age. Dogs with these diagnoses
must be re-examined as soon as possible for the appeals body
6
registered. However, several non-compatible systems are in use
in the USA, and CERF currently does not require the examiner to
verify the permanent identification of the examined animal.
The SSVO scheme includes ESE and ECVO-recognised specialists.
The educational demands are shared by all four Nordic countries.
To be allowed to sit the examination, the number of animals
to be examined under direct supervision doubles that of the
ECVO Scheme. Certificates for the Swedish scheme can be
issued for pedigree dogs, but only when they can be identified
by either tattoo or microchip. The SSVO-scheme certifies only
for inherited non-adnexal eye diseases, but it does include a
general examination of the eye and its adnexa. The certificate is
in Swedish only and is readable and understandable for the well
informed Swedish-reading owner. If signs of a PIED are found,
this is specified in handwriting by the examiner. The examiner
also has to state if he or she considers this disease inherited or
not.
All abnormalities must be recorded, no matter the significance
to the examiner, e.g. all cataracts “larger than punctate” are
considered inherited. If an abnormality is detected that is
not considered to be inherited, it should be described in the
“Comments” section.
All data are collected by the CERF, which publishes the overall
results. The individual dogs’ identities are confidential. For a
fee to CERF the data are also linked to the dogs’ registration
numbers and forwarded to the American Kennel Club. The
results can also be used for advertising. Annual renewal is
required. If wished, the owner can inform the specific breed
club of the examination results.
In case of appeal, the dog is referred to a (Swedish) ECVO
Diplomate, whose decision is final. Offspring of several specified
breeds will not be registered by the Swedish Kennel Club, unless
both parents have been examined, and in cases of one or both
parents being affected with a specified PIED (mainly the PRAs
and lens luxation).
The BVA scheme includes ESE and recognised British and European
specialists. The certificate is readable and understandable for
the well informed owner, and a list of specified congenital and
of required PIED’s is given in the procedure notes. Certificates
for the Scheme can be issued for pedigree dogs, regardless of
whether they can be identified by tattoo/microchip or not. The
BVA-scheme certifies for inherited non-adnexal eye disease
only, but it does include a general examination of the eye and
its adnexa. Eleven different inherited eye conditions are only
certified in certain breeds (approximately 50), while in other
breeds (some 45), the same eye conditions are listed as “under
investigation”. In the remaining breeds the conditions are
identified, but not listed under the BVA-scheme.
In most other European countries the breed club issues breeding
rules or breeding advice.
The aim for the future is to reach a world-wide scheme with one
international certificate. However, there is still a long way to go
before this goal can be achieved.
Reference
[1] NARFSTRÖM (K.), EKESTEN (B.), Rosolen (S.G.), SPIESS (B.M.),
PERICOT (C.L.), OFRI (R.) - Committee for a Harmonized ERG
Protocol, European College of Veterinary Ophthalmology.
Guidelines for clinical electroretinography in the dog. Documenta
Ophthalmologica, 2002, 105, 83-92.
If in doubt, or in cases where it is likely that the clinical appearance
will change with time, a re-examination after 6 months is
recommended, or the dog is examined by second panellist.
If two panellists disagree on a diagnosis, or in case of appeal, the
dog is referred to the Chief panellist, whose decision is final.
7

Updated information on ophthalmology

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