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The evaluation and diagnosis of retinal conditions are challenging for many veterinary practitioners. These difficulties are due to numerous reasons, including the infrequent use of specialized equipment made for the examination of the ocular fundus, the learning curve that exists to get a reliably detailed view of the retina and choroid, and the recollection of specific knowledge needed to interpret the type of lesions present. For etiological characterization, fundus lesions can be divided into two categories: those that are caused by primary ocular disease and those that are an extension of systemic disease, or Ocular Manifestation of Systemic Disease (OMSD). By reviewing the relative structure and function of the retina and ocular fundus, as well as ocular examination techniques, veterinarians can understand the most common categories of retinal conditions presented by dogs.
The retina is the innermost layer of the ocular fundus (fundus meaning the deep end of the eye opposite the cornea and pupil), or posterior portion. The neuroretina consists of multiple layers that capture an image and transmit it to the brain through a series of neural connections beginning with the photoreceptor layer and ending with the ganglion cell layer that leads to the optic nerve and brain. The retina itself, upon direct examination, is largely invisible to the naked eye due to its thinness, visible only through the blood vessels that course through the retinal tissue and form the characteristic radiant pattern that emerges from the optic nerve and supplies blood to the retina in an arborizing pattern to the retinal periphery.
The retina is only fixed to the eye in two places: at the optic nerve and at the equator, or the periphery ocular fundus. The rest of the retinal surface area is physically held to the ocular fundus by apposition with the vitreous, pressing the retina up against the fundus to maintain its connection to the retinal pigmented epithelium (RPE layer), which is the deepest portion of the retina and the part of the ocular fundus that we primarily visualize. Behind the RPE, as seen through the pupil, is the choroid, with the scleral tissue further back. Normally, the sclera and much of the choroid are not visible unless specific eye conditions allow direct viewing of the choroid through the visual axis (e.g., subalbinotic or merle dogs). In many dogs, the RPE is lacking pigment in a specific central area, often triangular, known as the tapetum lucidum, or shining layer. The tapetal region is usually brightly colored and serves to enhance light vision in low-light conditions.
When light travels into the eye, it is initially perceived by the photoreceptors that lie deepest in the retina, furthest from the cornea and pupil, abutting the RPE layer. The neural transmission then travels from the photoreceptors rostrally through the neural retina to the ganglion cell and nerve fiber layer, which is the anterior-most layer that abuts the vitreous. The nerve fiber layer transmits the nerve impulse to the optic disk and optic nerve, which then carries the signal to the occipital cortex in the brain. Retinal physiology is a highly metabolic process that requires substantial energy and metabolism, with the extremely high retinal blood flow velocity to maintain retinal function. (The retina has the second-highest blood flow velocity in the body, just after the kidney). When the retinal function is disrupted, either physically or metabolically through disease, the visual neural pathway is broken, and partial or total vision loss can result.
The neuroretina is extremely fragile when subject to physical stress and will tear easily. The normal canine retina is about 180 to 200 microns thick at the center. The retina is as fragile as wet tissue paper, making it difficult to handle; therefore, only a few veterinary ophthalmology subspecialists with posterior segment surgery equipment can perform retinal reattachment surgery in dogs. Many veterinary ophthalmologists can stem the advance of retinal tears with laser retinopexy using a diode laser to weld the retina to the RPE and choroid.
Retinal disease is typically diagnosed with ophthalmoscopy. Indirect ophthalmoscopy is often preferred for a comprehensive view of the fundus, while direct ophthalmoscopy provides a detailed view of smaller sections of the retina. The retinal examination includes not only ophthalmoscopy, but also other aspects of the ocular examination that play a critical role, including pupillary light reflexes, color-specific testing to differentiate between rod and cone disease, maze testing, tonometry, and menace/dazzle reflex testing. When the visual axes are not clear or the nature of the retinal disease is not discernible by examination alone, other diagnostics may include ultrasonography or electroretinography. Ultrasound can be used to confirm the nature and extent of retinal detachments or intraocular masses when they are not directly visible due to other ocular changes, such as cataracts, globe position, corneal cloudiness, or eyelid swelling.
Vision breakdown related to retinal disease can be divided into two categories: 1) physical separation of the retina from the ocular fundus (a.k.a. detachment) and 2) primary or secondary conditions in the retina itself that disrupt the neural tissue function and vital visual pathways. These two causes are not mutually exclusive and may overlap at times.
Diseases in which there is a physical separation of the retina from RPE and choroid are categorized as retinal detachments. They can occur due to physical trauma to the eye and retina, as well as diseases that cause the retina to pull away from the ocular fundus through metabolic or biochemical changes, often as a manifestation of systemic disease. Traumatic or physical pulling of the retina from the ocular fundus can have various causes in dogs. The ones we see most frequently are related to head trauma, lens instability and subluxation (almost always anterior), and marked vitreous degeneration. Within this last vitreous degeneration category, there are some breeds where the retina spontaneously detaches peripherally from its border attachments, referred to as disinsertion. We see this almost exclusively in Shih Tzus. Mass effect of intraocular tumor, either primary or metastatic, may also cause the retina to detach if the tumor is pushing or pulling at the retina as it expands in size.
Retinal detachments can be subdivided into two categories relative to the state of intactness: rhegmatogenous and non-rhegmatogenous. Rhegmatogenous detachments are those that have tears or holes, leaving the retina incomplete. Often, these detachments have pulled away from their natural position and frequently lie in the inferior globe, like a drape or veil, over the optic disk. Non-rhegmatogenous detachments have no tears and can be further characterized into bullous detachments that billow anteriorly, giving a “morning glory” or “parachute” appearance. Bullous detachments can tear and become rhegmatogenous detachments in time.
Metabolic or biochemical changes in the eyes also may or may not lead to retinal detachment. These comprise both vascular and infiltrative conditions, including systemic hypertension, infiltrative cancer, infectious diseases (e.g., fungal retinopathies like aspergillus, histoplasmosis, blastomycosis, and cryptococcosis), toxoplasmosis, heartworm disease or other parasitic ophthalmomyiasis of insect larvae, and other vasculopathies related to hematologic disorders, such as coagulopathy or polycythemia. The most common conditions we see in dogs that are related to infiltrative disease are cancers, such as lymphoma or meningioma, steroid-responsive idiopathic bullous retinal detachments, fungal and toxoplasma infections, and autoimmune diseases, including uveodermatologic syndrome/Vogt-Koyanagi-Harada Syndrome (VKH), which is commonly seen in Akitas and other Northern breeds.
Retinal diseases that do not involve detachment are typically related to degenerative diseases or biochemical loss of retinal function. These conditions include the retinal degenerations familiar to us as a collection of diseases termed progressive retinal atrophy (PRA), or progressive rod-cone degeneration (PRCD). Most, but not all, retinal degenerations are bilateral and have a genetic component. They can be early or late onset in age, and the rate of progression can vary. Most rod-cone degenerations present as a loss of night vision first, followed by day vision, while cone-rod degenerations can occur with day vision lost first, followed by night vision. Sudden Acquired Retinal Degeneration Syndrome (SARDS) is a subset of these conditions that has a particular onset in midlife and is rapid in progression. It is sometimes associated with hyperadrenocorticism (Cushing’s), but the cause-and-effect relationship of this association is unclear. There is usually no treatment for SARDS or other retinal degenerations. These conditions are painless, but some dogs may develop cataracts, which can cause uveitis in certain cases. The Orthopedic Foundation for Animal’s Blue Book lists retinal degeneration across all OFA breeds. Additionally, a variety of genetic tests are available to confirm the diagnosis of several genetic variants of canine retinal degeneration.
Over time, retinal degenerations are characterized by retinal thinning that leads to increased tapetal reflectivity, attenuation of retinal blood vessels, and diminished pupillary light reflexes. Loss of pupil movement in red light indicates reduced rod function (night vision), while loss of movement in blue light reflects decreased cone function (day vision). In early stages of disease, or when the retina is not visible due to cataracts, an electroretinogram is often used to rule in retinal degeneration as a cause of vision loss. To further confirm a retinal degeneration diagnosis, which differs from retinal detachment, techniques such as ocular ultrasound or optical coherence tomography (OCT) are used to differentiate.
It is worth mentioning that there can be causes of blindness with a clear visual axis that are not related to retinal disease, mainly diseases of the optic nerve and visual cortex of the brain. Optic neuritis is a set of conditions where the optic nerve is inflamed, which blocks the transmission of vision signals to the brain and presents as blindness. Often, the retinal examination is unremarkable, and pupillary reflexes are variable but frequently remain intact with all light colors, suggesting the retina is intact and functioning. Meningitis (MUE, or GME), optic nerve inflammation from cancer, vascular disruption to the optic nerve, and trauma are frequent causes of optic nerve dysfunction. The optic nerve may look inflamed or swollen with ophthalmoscopy or OCT. Treatment with anti-inflammatories, advanced imaging of the brain, and cerebrospinal fluid analysis with full neurological evaluation are often recommended to fully evaluate and care for vision loss associated with optic nerve disease.
Diseases of the retina can be caused either by retinal detachment and tear, or by conditions where the retina remains in place but loses function due to other degenerative, infiltrative, or vascular diseases. Ophthalmoscopy and enhanced imaging, including electroretinography, ocular ultrasound, and other imaging (MRI, OCT), can assist in better characterizing retinal disease. Serology and, in some cases, ocular aspirates (or ocular histopathology) can rule in infectious diseases where more in-depth neurological evaluation and care can be done to diagnose and manage diseases of the optic nerve and visual cortex.
