3 As clinicians for animal patients, we must gather most of our evidence by what we can observe, feel, smell, and hear. Laboratory and imaging methods then either support our working diagnosis or assist in the development of a list of differential diagnoses which it is hoped will allow us to isolate and ascertain the abnormality, develop strategies for treatment, and provide an accurate prognosis. In this introductory clinical chapter, some of the common clinical signs and observations are summarized, and their pathogenesis and significance presented. In the subsequent chapters additional information of some of these abnormal findings are expanded. Animals with ophthalmic diseases can show pain through a number of clinical signs. Blepharospasm is mediated by reflex involving branches of the trigeminal nerve within the cornea and conjunctiva (sensation), and the facial nerve (motor) which innervates the orbicularis oculi muscle, which is responsible for closure of the palpebral fissure. The source of the pain can be within the orbit, eyelids, conjunctiva, cornea, iris, and ciliary body. Pain receptors within the lens, vitreous, and retina‐choroid apparently do not exist. There is also an axonal reflex by which corneal pain is directly transmitted to the anterior uvea, resulting in the release of prostaglandins, histamine, and acetylcholine, a breakdown of the blood–aqueous barrier, iridocyclitis, and aqueous humor flare. This pathway is completely local and does not involve any sensory or motor neural pathway or the brain. Blepharospasm usually signals pain and possible inflammation, therefore the clinician should recognize the need to examine and determine the cause (Figure 3.1). Essential or primary blepharospasm appears rare in animals. Figure 3.1 (A) Pain/blepharospasm in a cat secondary to entropion. The eyelid outer margin and hair are directly contacting the conjunctival and corneal surfaces. (B) Pain/blepharospasm secondary to distichiasis and a corneal ulcer in a young Bichon Frise. (C) Blepharospasm in a horse with severe anterior uveitis and infected corneal ulcer and blepharitis. There is an abundance of mucoid ocular discharge. (D) Subtle pain in a horse may be demonstrated not by overt blepharospasm but instead by a downward deviation of the cilia (eyelashes). Conjunctival discharges are divided into: serous or catarrhal; mucus (mucoid); and mucopurulent. Often conjunctivitis in animals is secondary to eyelids, nasolacrimal and tear, and corneal diseases. The character of these conjunctival discharges can vary throughout the disease as well as their quantity. Following an insult, the conjunctival flora in secondary conjunctivitis proliferates resulting in mucopurulent exudates that can mask the original insult. As conjunctivitis becomes chronic, secondary thickening, pigmentation, and follicle formation develop (Figure 3.2). Figure 3.2 (A) Epiphora can be the result of overproduction of tears, usually a reflex manifestation of pain, or because there is an obstruction of outflow of tears through the nasolacrimal apparatus. This horse has severe anterior uveitis and pain. (B) Mucopurulent discharge usually indicates chronicity or severity. It is common in keratoconjunctivitis sicca as a compensatory mechanism for the lack of aqueous tears. The position of the globe within the orbit varies by species and, especially in the dog, by breed. Changes within the orbit tissues can also influence the position of the globe within the palpebral fissure. Loss of fatty tissues or fibrosis after trauma or orbital surgery can result in reduced orbital tissue (enophthalmia) and restricted globe mobility. In contrast, increase in the orbital mass associated with cellulitis, mucocele formation, and neoplasia can force the globe forward into the palpebral fissure (exophthalmia) and cause strabismus. The direction of the strabismus can often assist in the localization of the mass (Figure 3.3). Figure 3.3 (A) Exophthalmos is the anterior displacement of the globe. In this cat, a retrobulbar squamous cell carcinoma has pushed the globe forward. There is conjunctival hyperemia and chemosis and serosanguinous ocular discharge. (B) Same cat as in part A from a view looking down. If exophthalmos is subtle, the dorsal view can make the difference in globe position more appreciable. (C) When the globe is farther back into the orbit than usual, this is referred to as enophthalmos. This occurs as the result of pain, loss of orbital contents, or sympathetic denervation to the periocular structures. (D) Strabismus is the deviation of the globe from its normal directional axis. This dog has a dorsolateral strabismus of the right globe. (E) Dorsal strabismus in a Chihuahua following trauma. Globe size varies widely among the animal species, and for many of the domestic species direct and ultrasonic measurements are available. Globes smaller than normal are termed microphthalmia and those larger than normal are macrophthalmia (also termed megalophthalmia) (Figure 3.4). Corneal and globe measurements are closely related. The differences in globe size in dogs is also related to breed and has not been documented to date. Figure 3.4 (A) Microphthalmia is a congenitally small globe. (B) Phthisis bulbus is an acquired reduction in size of the globe, usually the result of chronic inflammation or chronically elevated intraocular pressure that damages the ciliary body over time and reduces its ability to produce aqueous humor in quantities sufficient to keep the globe turgid. (C) Buphthalmos is an enlargement of the globe resulting from elevation in intraocular pressure with glaucoma. The conjunctiva, consisting of the palpebral, fornix, and bulbar components, accommodates eyelid movements as well as movements of the globe. The conjunctiva is also important in tear dynamics and immunologic protection of the external ocular surfaces. Its superficial layer contains minute lymphoid follicles which provide the different immunologic components. As part of the conjunctival inflammatory response, local vasodilation of conjunctival vessels occurs. These conjunctival vessels have a small diameter and branching pattern, blanch quickly to topical 1–2% epinephrine, and are mobile and move when the conjunctival surface is manipulated (Figure 3.5). Figure 3.5 (A) Conjunctival hyperemia, especially of the ventral conjunctiva, in a dog, associated with conjunctivitis and ectropion. Note the enlarged lymphoid follicles which indicate some degree of chronicity. (B) Severe conjunctival hyperemia in a cat affecting the upper and lower palpebral conjunctiva and the conjunctiva of the nictitans. (C) Conjunctival hyperemia in an English Bulldog with keratoconjunctivitis sicca. (D) Chemosis is edema of the conjunctiva. It can be quite pronounced, especially in allergic conditions. (E) Conjunctival hyperemia in a horse secondary to an allergy. Ciliary flush or a diffuse hyperemia of both the bulbar conjunctiva and episcleral blood vessels is associated with inflammation of the iris and ciliary body (Figure 3.6). Ciliary flush should be distinguished clinically from conjunctival hyperemia because it signals intraocular involvement and inflammation. As the iridal and ciliary vasculature are supplied primarily by branches of the anterior ciliary arteries and veins that traverse the anterior sclera, it is not surprising that these same vessels are involved with the hyperemia and exudation that occurs with irritated anterior uveal vasculature. Figure 3.6 Iridocyclitis and associated ciliary flush secondary to corneal ulceration and uveitis in a dog. Chemical mediators for these vascular responses include histamine, serotonin, plasmin, kinins, complement, and the eicosanoids (prostaglandins and leukotrienes). Knowledge of the exact substances involved in these inflammatory responses facilitates the development of specific or targeted therapy. With acute and chronic ocular hypertension, the episcleral veins become enlarged. It is important to distinguish the deeper episcleral vessels from the more superficial conjunctival blood vessels (Figure 3.7). Episcleral blood vessels have a larger diameter, do not branch, are not mobile with conjunctival movements, and do not rapidly blanch to topical 1–2% epinephrine (they will vasoconstrict, however, in a few minutes rather than seconds for the conjunctival vessels). Figure 3.7 (A) Combination of episcleral venous congestion (associated with elevated intraocular pressure) and ciliary flush (associated with iridocyclitis) in a Shih Tzu with uveitis, secondary glaucoma, and a corneal ulcer. (B) Combination of episcleral venous congestion (associated with elevated intraocular pressure) and ciliary flush (associated with iridocyclitis) in a Beagle with lymphoma. (C) Episcleral injection in an American Cocker Spaniel with primary glaucoma and a subluxated lens. (D) Episcleral injection in a Bassett Hound with primary glaucoma and a subluxated lens. (E) Episcleral injection in a Golden Retriever with pigmentary uveitis and secondary glaucoma. Note the diffuse corneal edema and the fibrin clot in the pupil. There is posterior synechiae as well. To remain clear, the cornea must be slightly dehydrated (detumescence). This state is normally maintained by an energy dependent Na2+/K+ pump within the corneal endothelium. With damage to the endothelium, such as with surgery or iridocyclitis, this endothelial pump is impaired and edema develops within the corneal stroma. The edema interrupts the orderly arrangement of the corneal stromal fibers and glycosaminoglycans causing the cornea to appear cloudy or bluish in color. As this corneal opacity is made up of extracellular fluids for the most part, topical applications of hyperosmotic agents (such as 2–5% NaCl or glucose) can temporarily reduce this edema, and permit improved visualization of the inner ocular structures. When significant amounts of fluid accumulate in the cornea, it can coalesce into superficial microbullae, which often rupture and create superficial corneal ulcers (Figure 3.8).
Clinical Signs and Their Interpretations
Blepharospasm and Ophthalmic Pain
Ocular Discharge
Globe Position
Globe Size
Vascular Changes
Conjunctival Vascular Response
Ciliary Flush
Episcleral Vascular Response
Corneal Changes
Edema
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