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Retinal Disease Nick Cassotis, DVM, Dipl

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Retinal Disease Nick Cassotis, DVM, Dipl Thank you to our sponsor! Retinal disease Nick Cassotis, DVM, Dipl. ACVO Evaluation of the ocular fundus and establishing a diagnosis of retinal disease are complicated by good visualization of the posterior portion of the eye. The two methods for evaluation of the retina and optic nerve head are direct ophthalmoscopy and indirect ophthalmoscopy. Direct ophthalmoscopy creates a very magnified view of the optic nerve head and the immediate surrounding retina. This allows for excellent visualization of the optic nerve, however, is considered by most ophthalmologists to be a poor way of understanding the health and structure of the posterior ocular tissues. Indirect ophthalmoscopy is almost exclusively used by veterinary ophthalmologists for evaluation of the animal fundus. This examination skill requires very little instrumentation: either a 20 or 28 diopter lens and a light source. Pupillary dilation with tropicamide (not atropine) will facilitate easy visualization. As a beginner, you will benefit from pupillary dilation, holding the light source in your right hand close to your face, obtaining a tapetal reflection (aim from a low angle toward the tapetum) and hold the lens 3-5cm from the cornea in your outstretched left hand. You will benefit from a technician holding the patient’s eyelids open. Practice until this is a quick and easily performed technique. The lecture reviews techniques for indirect ophthalmoscopy and video indirect ophthalmoscopy in an effort to increase the use of this particular skillset in general practice. Indirect ophthalmoscopy improves visualization of the entire retina and optic nerve head. The technique will be compared to the more commonly performed and often blurry overmagnified direct ophthalmoscopy. Normal retinal structure and ophthalmoscopic appearance will be presented. Variations-of- normal are frequently encountered between breeds and coat colorations. For example, the presence of a tapetum, size of the tapetum, coloration of the tapetum can vary widely. Additionally, color dilute animals may not have retinal pigmentation allowing for clear visualization of the underlying choroidal vasculature. Dogs and cats have fairly standard vascular distribution for their retinas. These paired superior, medial, lateral, and at times inferior retinal venules and arterioles leave the optic nerve head and arborize as they extend peripherally. The optic nerve head size and degree of myelination can vary by species. Dogs have significant variation in optic nerve head myelination and range from minimal to exuberant. Cats have minimal intraocular myelination allowing for visualization of just the optic nerve head. Retinal disease states and their appearance emphasized in this lecture: Hypertensive retinopathy Retinal detachments Retinal Degenerations Acquired forms Heritable forms SARD Hypertensive retinopathy Most commonly encountered clinical sign of animals with hypertensive retinopathy is retinal hemorrhage. Said differently, animals presenting with retinal hemorrhage should be assessed for hypertension. However, it must be stated that the presence of intraocular hemorrhage is not pathognomonic for hypertension. In fact, intraocular hemorrhage (hyphema or retinal hemorrhage) even in combination with retinal detachment suggests ruling out hypertension, but other causes of vasculitis must remain on your rule out list. If clinical signs of vascular tortuosity and/or subretinal edema are noted, then hypertension is very likely. Retinal Detachments Rhegmatogenous (torn retina) Breed related predominance for example Shih Tzus and Bichons. Secondary to other congenital anomalies such as severe colobomas in Collie Eye Anomaly. Traumatic etiology Serous Infectious inflammatory causes Non-infectious inflammatory causes (immune mediated) Neoplastic Traction Traction band contracture creating retinal detachment. Acquired retinal degenerations and serous retinal detachments (chorioretinitis) Infectious inflammatory and non-infectious inflammatory disorders of the choroidal and retinal vasculature will result in multifocal retinal inflammation, hemorrhage, and if corrected degenerations with varied effects on vision. In these cases, perivascular edema, cellularity, and hemorrhage will be noted. These signs lead to the appearance of hyporeflectivity. This inability to perceive the choroidal tapetum indicates cellular or fluid accumulation beneath the retina. Retinal vascular prominence, tortuosity, or abrupt termination all indicate potential severe disease. Given the absence of primary vascular disorders in our animal species, the recommendation is for full systemic work up and an expansive rule out list of infectious and non-infectious causes to vasculitis. Neoplastic emboli or early sites of metastatic disease will commonly appear as solitary mass effects within the retina. Heritable progressive retinal degenerations Group of heritable / genetic disorders that result in progressive loss of photoreceptors due to accumulation of neurotoxic by products of phototransduction. The loss of an enzyme in the recycling of photopigment results in neurotoxin accumulation and a slow die off of rods and cones. Variable forms exist that are cone specific, rod specific, and pan retinal. Treatments are still experimental. Depending on the stage of degeneration funduscopic examination may reveal a normal retina, vascular attenuation, early hyperreflectivity, or pronounced retinal vascular absence and strong hyperreflectivity. Changes will be diffuse across the retina and symmetrical between eyes. Sudden Acquired Retinal Degeneration (SARD) This is a frustrating, quickly advancing, permanently blinding disease of dogs without a known etiology or proven treatment. Progression to blindness occurs over 1-2 months. Progressive pupillary dilation and vision loss are recognized. Light reflexes can be preserved in early cases which can cause confusion. Despite the dogs being blind, the retina appears normal in the early stages of the disease. This disconnect between severity of clinical signs and retinal appearance appropriately results in questioning if the lesion is retinal vs central in origin. Electroretinography is performed to differentiate between retinal and central vision loss in these patients. A flat (no response) ERG indicates SARD. In cases with normal ERG readings, the diagnosis of SARD is not accepted and referral for neurologic examination should be suggested. SARD patients often have cooccurring polyuria, polydipsia, and at times liver enzyme elevations (ALT and ALP). Cushing’s syndrome is not uncommonly discovered in SARD patients. Neoplasia -Primary neoplasms of the retina, choroid, or optic nerve head are rare. Astrocytoma, glioma, and choroidal melanomas have been described. -Secondary / metastatic neoplasms are most commonly encountered. The appearance of these tumors tends to be nodular accumulations of subretinal cellularity that mimics the appearance of inflammatory disorders in the early stages of disease. The exception being melanomas which are heavily pigmented solitary mass effects. Often times as a neoplastic mass effect expands, retinal detachment or hemorrhage will occur and obscure the clear visualization of the mass effect. In the aforementioned disease states, there are many overlapping clinical signs. For patients presenting with posterior segment hemorrhage, retinal detachment, or subretinal cellularity you should consider not only primary causes of ocular damage such as trauma or primary intraocular neoplasia, but also consider ocular manifestation of systemic disease. Systemic disease associations can be concluded by obtaining a blood pressure and submitting CBC, Chemistry, Coagulopathy, and infectious disease panels. Additionally, radiography of the chest and ultrasound of the abdomen are indicated. .
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