Page 201 - WSAVA2018
P. 201

D. Maggs1
1Professor Ophthalmology, University of California Davis, USA. Introductory Philosophy
Hyperemia of the surface of the globe or so-called “red-eye” is not only one of the most common reasons for a client presenting their pet for veterinary care,
but potentially one of the most critical. As veterinary ophthalmologists, some of the most worrisome cases we see are those were ocular redness was misinterpreted as allergic conjunctivitis or “he must have got some
dust in his eye” and thereby serious and potentially blinding diseases such as uveitis, glaucoma, dry eye, or ulcerative keratitis were missed. The goal of this lecture is to heighten awareness of the differential diagnoses that may cause ocular hyperemia and to define
methods to differentiate these. We will look at eyes with conjunctivitis, keratitis, uveitis, glaucoma, and orbital disease.
Ocular Blood Vessels are a Diagnostician’s Best Friend
In many ways, ocular blood vessels are the diagnostician’s best friend since they “always” go to where the problem is. That is, if there is superficial irritation (irritation of the conjunctiva or superficial cornea) then superficial blood vessels will become hyperemic. However if inflammation involves deeper structures – uveitis, glaucoma, scleritis, or deep (stromal) keratitis - then deeper (episcleral) blood vessels become engorged. Thus, clinically differentiating superficial conjunctival vessels from deep episcleral vessels changes the diagnosis, diagnostic testing necessary, treatment, and prognosis.
Clinically Relevant Anatomy and Physiology
For the purposes of this session we will categorize blood vessels overlying the sclera into 2 distinct
and clinically useful classes: deep or episcleral and superficial or conjunctival blood vessels. In the normal animal, the blood vessels in the bulbar conjunctiva are so fine that the conjunctiva appears almost transparent permitting the white sclera to be seen through it.
The palpebral conjunctiva is normally a pale pink
but can become more obvious with hyperthermia or excitement, and should be approximately the same color as other mucus membranes. Bulbar conjunctival vessels extend right up to the limbus. Episcleral vessels – although larger – are usually not prominent when seen through subconjunctival tissues. The exception is some brachycephalic individuals, particularly dogs, in which one or two obvious episcleral blood vessels are sometimes seen in normal, uninflamed eyes. Episcleral
blood vessels supply the intraocular structures via the uveal tract and therefore “dive” through the sclera at the iris root – a millimeter or two behind the limbus. The importance of these anatomical facts will become more obvious when we discuss some of the means to differentiate deep from superficial blood vessels.
Mechanisms of Ocular Hyperemia
In addition to physiologic vasodilation due to hyperthermia, there are (at a mechanistic level) two common ways a blood vessel becomes hyperemic or “injected”.
· Vasodilatation due to release of inflammatory media-
· Hydrostatic engorgement due to decreased venous return.
Inflammation. The release of vasoactive mediators
at a specific site acts locally to cause (among other things) dilation of the blood vessels that supply that site. Therefore this mechanism for hyperemia dictates that
a reasonably “focused” vasodilatation should ensue. That is, if there is uveal inflammation, and release of vasoactive factors within the uvea, then the deep or episcleral blood vessels that supply the uveal tract should become injected. By contrast, conjunctival inflammation should incite only conjunctival vessel hyperemia. This strict rule breaks down somewhat with more significant or major inflammation. Insults such
as uveitis that are severe enough to induce episcleral congestion will sometimes also produce some “innocent bystander” hyperemia of the overlying and smaller conjunctival blood vessels; however the inverse is unlikely. Therefore, satisfying yourself that episcleral congestion is not present is the most critical decision whenever “red eye” is a presenting sign.
Hydrostatic congestion. Blood vessels terminating
(in the case of arterioles) or originating (in the case of venules) in the conjunctiva and uvea share a common pathway through the orbit to and from the major
vessels of the head and neck. Therefore orbital disease can cause enlargement (“injection”) of deep and/
or superficial ocular vessels via hydrostatic pressure (decreased venous return) and via local inflammatory effects on these vessels en route to and from the eye. Therefore all eyes with hyperemia should be examined for evidence of altered globe position (strabismus, enophthalmos, or exophthalmos) and - so long as there is no risk of globe rupture - should also be retropulsed.
Differentiation of deep episcleral and superficial conjunctival hyperemia
Conjunctival vessels are superficial, small (fine), branch frequently, move easily with gentle pressure from a cotton-tipped applicator or by lateral motion of the upper eyelid, extend to the limbus, and blanch within seconds after application of 1 drop of a topical vasoconstrictor
Your Singapore, the Tropical Garden City
  tors (i.e., “inflammation”)

   199   200   201   202   203