Aging dogs are predisposed to several ocular abnormalities ranging from benign changes to vision-threatening or painful diseases. Fortunately, most ocular diseases can be diagnosed through an examination alone or with the addition of a few simple diagnostic tests. This article discusses ocular diseases common in aging dogs and focuses on conditions that are more likely to become problematic for the patient. BOX 1 contains recommended supplemental reading for further information about the specific conditions and treatments.
What Is A “Senior” Dog?
According to the 2019 American Animal Hospital Association Canine Life Stage Guidelines, the mature adult stage of a dog’s life begins at the completion of physical and social maturation (most often 3 to 4 years old) and lasts until the final 25% of the individual’s estimated lifespan is reached, while the senior stage is defined as the last 25% of the individual’s estimated lifespan through end of life.1 For example, if the estimated expected lifespan of a Shih Tzu is 13 years, then it has entered its senior years by the age of 10. A Labrador retriever, which might have an estimated expected lifespan of 10 years, has entered its senior years by the age of 8.
It is recommended that a senior dog have at least semiannual examinations.1 Senior visit are expected to take more time than a young adult or mature adult visit and should be allotted as such on appointment and fee schedules. The goal is to perform a thorough examination and appropriate health screening to detect abnormalities early, enhance the quality of life, and promote longevity.2 A thorough eye evaluation is therefore recommended at each senior dog’s routine examination.
The Ocular Examination
Take a Complete History
A thorough and comprehensive history can gain insight into problems of which the owner may be unaware. Eye-related questions for apparently healthy senior dogs can include:
- Have you noticed any redness in the whites of the eyes, eye discharge, or rubbing at the eyes?
- Have you noticed any change in the color of the eyes?
- Have you noticed any changes in vision, including difficulty navigating stairs and curbs? Is there a difference in vision during full sunlight versus dim lighting or a dark room?
- Over what length of time have you noticed these changes?
- Have you tried any over-the-counter medications, and if so, what and for how long?
If there is an ocular presenting complaint, questions may be tailored to the individual problem.
Perform a Brief Ocular Examination
- Observe the pet on the floor, off-leash, prior to handling. Watch how the pet navigates the room in an unfamiliar environment.
- Look at the patient’s eyes at eye level (bring them up to you on an examination table or come down to them) and evaluate for symmetry in the ambient light. Test menace response and palpebral reflex.
- Turn off the lights in the room and use a focal light source (e.g., penlight, Finoff transilluminator) for pupillary light reflexes. If the menace response is absent, be sure to test the dazzle reflex (blink response to bright light). These combined light reflexes assess retinal and central nervous system function even if the patient has something obscuring their vision that would cause an absent menace response, such as a cataract.
- With a light source in hand, use 2× to 4× magnification (e.g., an Optivisor; Donegan Optical Company, doneganoptical.com) to briefly examine the eyelid margins and cornea.
- Stand an arm’s distance away from the patient’s head with a light source and look for a tapetal reflection (retro illumination).
- Perform an undilated fundic examination, ideally with indirect ophthalmoscopy using a Pan Retinal 2.2 or 28D (Volk, volk.com) handheld lens and the light source; these lenses give a less magnified and wider field of view, allowing visualization of more of the fundus at a time in an undilated patient.
- Based on the above results, any owner concerns, and the patient’s signalment, determine the need for further diagnostic tests and/or a dilated ophthalmic examination (using 1% tropicamide solution).
A gradual decrease in tear production is expected as dog’s age. Schirmer tear test (STT) values of ≤ 10 mm/min are diagnostic for dry eye, while values of 11 to 14 mm/min are considered a “gray zone” and should be taken into consideration with the breed, ocular examination, and clinical signs. Values of 15 to 25 mm/min are considered normal. In one study, the mean STT decreased by 0.4 mm every year in aging dogs.3
In addition, dogs with endocrinopathies (e.g., diabetes mellitus, hyperadrenocorticism, hypothyroidism) are at higher risk of reduced tear production.4 This is especially of consequence to dogs that have always been on the low end of normal. Accordingly, performing the STT in routine senior examinations is advisable for any dog, but maybe most important in small- to medium-breed dogs predisposed to dry eye, such as American cocker spaniels, English bulldogs, pugs, and Shih Tzus.5
Since tears are the main source of nutrition and immunity for the cornea, low tear production can have consequences for the ocular surface, including conjunctivitis, bacterial overgrowth, corneal ulcers, corneal vessels (keratitis), and corneal pigmentation.6 Thus, low tear production should be taken seriously if diagnosed, especially if any (sometimes even subtle) clinical signs are noted. In a study specifically screening STT in senior dogs, 10% (10/98) of patients had a low STT (< 15 mm/min); only 1 of these 10 dogs was clinical for decreased tear production.7
If a low STT value is obtained on routine screening in an asymptomatic patient, repeating the test a few weeks later is advised to confirm a diagnosis before starting potentially lifelong treatment. Pending the repeat test, a topical lubricant will benefit the patient and not skew future results. If a patient remains borderline in the absence of clinical signs, a decision can be made on whether to start a lacrimostimulant medication or to continue to monitor (with the use of just topical lubricant) based on the patient and client.
Intraocular pressure (IOP) also decreases with age in dogs.8,9 The normal IOP range varies slightly depending on the tonometer used but is generally considered to be 10 to 25 mm Hg in normal, young dogs. It is not unusual for senior dogs to have low IOPs (< 7 mm Hg); however, in the absence of signs of anterior uveitis, this finding does not have clinical consequences for the animal’s ocular health and no further monitoring or treatment is necessary.8,9
Evaluation of IOP in asymptomatic senior dogs during routine examinations is not necessary unless the examiner wants to monitor IOP in breeds at risk for glaucoma. The age of onset for primary closed-angle glaucoma is most often mature adult to senior (4 to 10 years old), but glaucoma occasionally occurs in young adults.10
Unlike low IOP, a high IOP (> 25 mm Hg) should be taken seriously, even in the absence of or with minimal clinical signs, as glaucoma can cause rapid vision loss.11 However, a falsely elevated IOP of approximately 25 to 30 mm Hg is not uncommon in a clinical setting. Traction on the eyelids (especially lateral traction) or pressure on both jugular veins (tight collar or manual restraint) can significantly increase IOP values.12 In the author’s experience, other common causes for a falsely elevated IOP are a stressed/moving/uncooperative patient, forward movement of the rebound tonometer (e.g., Tonovet, tonovet.com) each time the examiner pushes the button (i.e., failure to keep the hand steady), holding the probe of the rebound tonometer too far away from the cornea, and too much manual force when touching the footplate of an applanation tonometer (e.g., Tono-Pen Vet; Reichert, reichert.com) to the cornea. If a falsely elevated IOP is suspected, try addressing all the above variables and, if applicable, decreasing the patient’s stress and anxiety with gabapentin or trazodone, as these drugs have been shown to not clinically alter the IOP.13,14
Eyelid Tumors in Dogs
Dogs are more predisposed to eyelid neoplasms as they age, particularly sebaceous gland adenomas and melanomas. However, approximately 90% of eyelid masses in dogs behave benignly.15 The decision to remove an eyelid mass depends on several factors, including (1) the size of the mass and speed of growth of the mass; (2) the location of the mass on the eyelid; (3) impairment of the normal blink process; (4) local irritation, including ulceration of the dermis, bleeding, corneal vascularization, or corneal ulceration; and (5) any unusual characteristics that indicate the mass could be malignant (e.g., of conjunctival origin).16
If the patient is bothered by the mass, the mass is growing rapidly, or there are concerns for malignancy, it is best to remove it. Debulking and cryotherapy or pentagonal resection with primary closure are most often sufficient to treat these tumors in dogs.17 Regardless of the likelihood of benign behavior, histopathology is always recommended if tissue is removed.
Corneal Changes in Dogs
As dogs age, they become predisposed to several corneal pathologies, especially indolent ulcers, corneal degeneration, and corneal endothelial disease.
Indolent ulcers are superficial, noninfected corneal ulcers characterized by a loose epithelium refractory to healing. Most dogs that develop indolent ulcers are 7 to 10 years old.18 Indolent ulcers can be treated with routine ulcer management plus debridement of choice (e.g., diamond burr, grid keratotomy) with an approximately 70% to 90% success rate with the first debridement.18,19 Routine ulcer management should always include a broad-spectrum topical antibiotic (e.g., neomycin-bacitracin-polymyxin B), topical and/or oral analgesia (e.g., atropine and/or gabapentin), and an Elizabethan collar.
Crystalline corneal degeneration includes corneal calcium and/or lipid deposition concurrent with corneal inflammation.20 These deposits can be spontaneous or secondary to systemic or ocular diseases (e.g., kidney disease, hyperadrenocortism, hypertriglyceridemia, dry eye, glaucoma) that can change the mineral composition, osmolality, or pH of the tears or metabolism of the epithelial cells.20
The most common form of corneal degeneration and the most detrimental to older dogs is calcium deposition, also known as calcareous corneal degeneration.21 Calcium deposits cause secondary inflammation, vascularization, and disruption of the corneal epithelium, often leading to corneal ulcerations.20,21 The deposits range from sparse and lacy to dense white crystalline opacities, most often in the superficial axial cornea (FIGURE 1A).20-22 The average age of affected dogs is 13 to 14 years.20,22
Calcium deposits warrant investigation into possible underlying causes with a history from the owner, bloodwork, and a thorough eye examination (STT, IOP, and fluorescein stain) but do not necessarily require treatment if they are mild and nonprogressive (not getting larger or denser) and there are no concurrent corneal ulcers.
Progressive deposits can be treated with topical application of ethylenediaminetetraacetic acid (EDTA) 1% to 4% compounded in artificial tears 2 to 4 times per day; secondary corneal ulcers should be treated with routine ulcer management.21 Diamond burr debridement has been successfully used as a treatment modality in corneal ulcers associated with calcium deposits but should only be used for superficial ulcers (FIGURE 1B), not for ulcers associated with any stromal loss.20
Corneal ulcers can sometimes be deep if calcium has sloughed on its own from the corneal stroma, leaving a fragile eye (FIGURE 2A). These deep, noninfected corneal ulcers are best treated with keratoplasty (corneal or conjunctival grafting surgery) if possible, as they pose a high risk for corneal perforation (FIGURE 2B).
Topical steroids may exacerbate both corneal calcium and corneal lipid and should be avoided if corneal deposits are observed.20,22
Corneal Endothelial Dystrophy
Corneal endothelial dystrophy (CED) and senile corneal endothelial degeneration result in excessive corneal edema due to a primary loss of corneal endothelial cells, with affected dogs being a median age of 12 years.23 Some breeds (e.g., Boston terrier, Chihuahua) are predisposed to CED, and it is likely a heritable condition.23 The corneal edema appears as a blue-gray opacity and causes an increased thickness of the corneal stroma (mean of 1325 µm central corneal thickness versus 587 µm in normal dogs).23 The edema starts temporally and is often asymmetric between eyes (FIGURE 3A), but over several months the condition progresses to bilateral diffuse edema (FIGURE 3B). Vision is impaired when the edema affects the whole cornea, and conjunctival hyperemia is common, though the condition is nonpainful by itself. Since this diagnosis is one of exclusion, other causes of progressive or diffuse corneal edema need be ruled out, including anterior uveitis, endotheliitis, glaucoma, and corneal ulceration.
When the edema becomes severe enough, bullae or blisters form and pop, leading to corneal ulcers (FIGURE 4A). These secondary corneal ulcers can be refractory to healing, but they are most often superficial and noninfected. Thus, they are treated routinely, but with the addition of topical hypertonic saline (5% NaCl) to pull fluid out of the superficial cornea.23 Standard CED without corneal ulcers can also be managed with topical hypertonic saline ointment 3 to 6 times per day;23-25 anecdotally, this medication does not clear the cornea but reduces the chance of future bullae and corneal ulcers.
The predominant surgical intervention performed for advanced CED is a superficial keratectomy and conjunctival advanced hood flap (FIGURE 5).25 Another, less complicated alternative if a refractory corneal ulcer is present is a thermokeratoplasty (FIGURE 4B), which heats the corneal stroma, causing contraction that leaves less room for fluid to accumulate in the cornea; however, this approach causes moderate corneal scarring.26 The only definitive treatment for CED in humans is the replacement of the endothelial cells with an endothelial transplant (Descemet’s stripping endothelial keratoplasty); this procedure is currently in the early stages of development for dogs.27
Intracorneal stromal hemorrhage can be seen in senior dogs but is relatively uncommon. Stromal hemorrhage occurs when fragile corneal blood vessels leak blood into the stroma (FIGURE 6A). A recent study showed that the average age of patients diagnosed with this condition was 11.5 years, and 60% had systemic diseases, such as diabetes mellitus, hypothyroidism, hyperadrenocorticism, or hypertension, that could lead to fragile blood vessels.28
If stromal hemorrhage is diagnosed, the recommendations include a full eye examination to determine the underlying cause for the corneal vascularization, as well as screening for systemic hypertension in all cases and endocrinopathies if other clinical signs warrant such testing. The hemorrhaged blood takes several weeks to months to clear (FIGURE 6B). Topical steroids can be used to resolve corneal blood vessels; the blood itself does not need to be treated. However, underlying causes (e.g., dry eye, systemic hypertension, endocrinopathies) do warrant treatment if discovered.
Iris Atrophy in Dogs
Senile iris atrophy occurs in senior animals of all species but is most commonly noted in dogs. The atrophy occurs within the muscle and stroma and leads to an irregular pupillary margin, holes in the iris, and sluggishness or absence of pupillary reflexes (FIGURE 7).29 Especially in the early stages, it causes a mild anisocoria because 1 side is more advanced. Senile iris atrophy is common in poodles, miniature schnauzers, and Chihuahuas, but can occur in any breed.29 Patients may exhibit some mild photophobia in bright light due to the inability to constrict properly, but typically this is considered a benign problem with no treatment or cure.29 To rule out glaucoma, IOP should be measured when a dilated pupil with sluggish pupillary light reflex is observed, especially if other clinical signs exist.
Lens Changes in Dogs
Lenticular changes are common in aging dogs. Nuclear sclerosis, an increased density, and hardening of the lens nucleus associated with a progressively gray opacity in the center of the lens, is found in all dogs older than 7 years (FIGURE 8A).30 Nuclear sclerosis is visible to the naked eye as cloudiness of the lens; thus, owners often present their dog for suspected cataract formation. In mild to moderate stages, the condition does not appear to clinically impede vision and does not obscure the retina for examination. However, in advanced stages, once a dog is approximately 12 years old, the density can be great enough to cause nearsightedness or a myopic shift (difficulty seeing objects far away) and visual acuity reduction,31 as well as distort the practitioner’s examination of the retina.7 This change in vision is minimal enough that it does not warrant cataract surgery.
Senile cataracts develop most often in the periphery of the lens cortex and are slow to progress (over years). Senile cataracts are very common in dogs older than 10 years, and all dogs older than 13 years are expected to have some degree of cataractous changes.32 A dilated lenticular examination is important to differentiate nuclear sclerosis from cataracts, as well as to help stage and monitor cataracts in subsequent visits (FIGURE 8B).
Unfortunately, no validated medical options currently exist to decrease the progression of nuclear sclerosis or senile cataracts. Cataract surgery is an option if the patient’s vision is affected, the dog is deemed an appropriate candidate for anesthesia, and the eyes have adequate retinal function as determined by an electroretinogram (ERG).
Vitreous Changes in Dogs
Vitreal opacities called asteroid hyalosis (FIGURE 9) or synchysis scintillans are small, sparkly particles of calcium and phosphorus or lipid, respectively. These changes occur in aging dogs or secondary to a history of inflammation.33 The opacities (“floaters”) do not seem to influence vision in dogs. However, when advanced, their presence can make it more challenging to evaluate the fundus clearly. No diagnostic tests or treatment are needed when this finding is observed.
Retinal Changes in Dogs
Systemic hypertension leads to ocular lesions in at least 62% of dogs.34 The retina and choroid are most commonly affected owing to the numerous small capillaries within the choroid susceptible to vascular ischemia, a condition known as hypertensive chorioretinopathy.34 The most common manifestation of canine hypertensive chorioretinopathy is retinal hemorrhage (ranging from petechiae to larger regions; FIGURE 10), but other sequelae include serous retinal detachments, subretinal edema, and tortuous retinal vessels.34 Hyphema (blood in the anterior chamber), vitreal hemorrhages, and stromal hemorrhages are other, less common manifestations of ocular lesions secondary to systemic hypertension.28,34
Acute onset of blindness or change in color of the eye may be the presenting complaint, but incidental ocular lesions from systemic hypertension can also be found during a routine examination. Accordingly, systemic hypertension should be ruled out in dogs with any of the above-mentioned ocular lesions and clinical signs. Additionally, dilated indirect fundic examination is strongly encouraged for patients with known systemic hypertension or known systemic disorders that can lead to hypertension (e.g., renal disease, diabetes mellitus), or during routine examinations once the patient has reached senior age.2
Documentation of a systolic blood pressure greater than 160 mm Hg in a calm patient on 2 or more occasions is diagnostic for systemic hypertension; alternatively, the presence of target organ damage justifies diagnosis and initiation of treatment after a single measurement greater than 160 mm Hg.35 The risk of ocular lesions substantially increases when the systolic blood pressure exceeds 180 mm Hg.35 Looking for and treating an underlying cause are important for gaining control of elevated blood pressure, as most cases of canine systemic hypertension are secondary.35 While the prognosis for return of vision is unknown in a dog with blindness due to hypertensive chorioretinitis, about 50% of cats that were blind at presentation regained some vision following successful treatment of systemic hypertension.36 With treatment, the goal blood pressure is between 120 and 150 mm Hg, but any decrease in blood pressure decreases the risk of future target organ damage.35,37
Senile retinal degeneration is observed in dogs, but it is little studied.38 In retinal degeneration, the photoreceptors degenerate, leading first to impaired vision in dim lighting (i.e., nyctalopia) due to loss of rods, then reduction of daytime vision due to loss of cones as the disease progresses. Senile retinal degeneration is typically slow (over months to years) and should only clinically affect senior patients.
To assess the patient’s vision in light versus dark, perform a maze test. Turn the lights off in a darkened room (i.e., with no windows or with blinds covering windows) containing a few obstacles, such as cones, chairs, and/or trash cans. Place the dog on the floor with its nose in the corner, and watch it navigate the room (without making noise/calling its name). Then turn the light on and monitor for any change in confidence in navigating or other changes in behavior. On neuro-ophthalmic examination, pupils may be slightly mydriatic in ambient light and slow to constrict but also may be unaffected. On dilated fundic examination, a pale optic nerve, decreased retinal vessel size (attenuation), and subtle peripheral hyperreflectivity with furrowing are observed (FIGURE 11). While examination and age should provide a diagnosis, an ERG can determine the ultimate quantitative retinal function. In one study of miniature poodles and Yorkshire terriers, ERG values were 15% to 30% lower in a group of older dogs (10 to 14 years) compared with a group of younger dogs (3 to 5 years).39
Though the veterinary literature on medical treatments for retinal degeneration is sparse, dietary supplements, including lutein, zeaxanthin, β-carotene, and vitamins C and E, have been shown to have some protective effects against macular degeneration and cataracts in humans. A recent study showed that dietary supplementation with omega-3 fatty acids in normal puppies had positive benefits on visual acuity and that higher levels of serum DHA (docosahexaenoic acid) were correlated with higher ERG amplitudes.40 Another recent study showed daily antioxidant supplementation (lutein 20 mg, zeaxanthin 5 mg, β-carotene 20 mg, astaxanthin 5 mg, vitamin C 180 mg, and vitamin E 336 mg) for 6 months increased ERG amplitude values in normal mature adult dogs compared with a control group in which ERG values declined slightly in the same 6-month period.41
While no studies have yet been performed on the above combinations of carotenoid and antioxidant supplementation in dogs affected by retinal degeneration, one study suggested that short-term omega-3 fatty acid supplementation had no effect on the DHA levels within the retina or on ERG amplitudes in dogs affected with progressive rod-cone degeneration (a specific inherited form of retinal degeneration).42 Although it is not expected that damage to the retina could ever be completely halted or reversed with supplements, targeted supplements may provide some benefit for ocular health in senior dogs.
Recommendations and Owner Compliance
While most of the above diagnoses can be detected or suspected on ocular examination, several require a few additional diagnostic tests and several require lifelong treatment or monitoring. Clear, up-front recommendations about why certain diagnostic tests and treatments are recommended and why some treatments are lifelong will greatly improve owner compliance. When presented with clear recommendations, pet owners are 7 times more likely to follow through with recommendations.1 A shared decision also helps solidify these recommendations with the client. For example, after making recommendations, consider asking, “How does that plan sound to you?” or “What questions do you have about our recommendations?” This action of a shared decision results in increased owner satisfaction and compliance.1 If any ocular condition is not improving with treatment as expected or a second opinion is desired, referral to a board-certified veterinary ophthalmologist is advised.
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2. Epstein M, Kuehn NF, Landsberg G, et al. AAHA senior care guidelines for dogs and cats. JAAHA. 2005;41(2):81-91. doi: 10.5326/0410081
3. Hartley C, Williams DL, Adams VJ. Effect of age, gender, weight, and time of day on tear production in normal dogs. Vet Ophthalmol. 2006;9(1):53-57. doi: 10.1111/j.1463-5224.2005.00437.x
4. Williams DL, Pierce V, Mellor P, Heath MF. Reduced tear production in three canine endocrinopathies. J Small Anim Pract. 2007;48(5):252-256. doi: 10.1111/j.1748-5827.2007.00349.x
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6. Best LJ, Hendrix DVH, Ward DA. Diagnosis & treatment of keratoconjunctivitis sicca in dogs. Todays Vet Pract. 2014;4(4):16-22.
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11. Reinstein S. Acute glaucoma: a true emergency. Todays Vet Pract. 2018;8(2):38-46.
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13. Shukla AK, Pinard CL, Flynn BL, Bauman CA. Effects of orally administered gabapentin, tramadol, and meloxicam on ocular variables in healthy dogs. Am J Vet Res. 2020;81(12):973-984. doi: 10.2460/ajvr.81.12.973
14. Pelych L, MacLeese J, La Croix N. Effects of oral trazodone on canine tear production and intraocular pressure. Abstr 49th Annu Sci Meet Am Coll Vet Ophthalmol Minneap Minn Sept 26-29 2018. 2019;22(3):E25-E26. doi: 10.1111/vop.12631
15. Wang S, Dawson C, Wei L, Lin C. The investigation of histopathology and locations of excised eyelid masses in dogs. Vet Rec Open. 2019;6(1):e000344. doi: 10.1136/vetreco-2019-000344
16. Foote BC. Diagnosis and treatment of eyelid tumors. Todays Vet Pract. 2022;12(1):64-71.
17. Zibura AE, Henriksen M de L, Rendahl A, et al. Retrospective evaluation of canine palpebral masses treated with debulking and cryotherapy: 46 cases. Vet Ophthalmol. 2019;22(3):256-264. doi:10.1111/vop.12585
18. Dees DD, Fritz KJ, Wagner L, et al. Effect of bandage contact lens wear and postoperative medical therapies on corneal healing rate after diamond burr debridement in dogs. Vet Ophthalmol. 2017;20(5):382-389. doi: 10.1111/vop.12412
19. Wu D, Smith SM, Stine JM, et al. Treatment of spontaneous chronic corneal epithelial defects (SCCEDs) with diamond burr debridement vs combination diamond burr debridement and superficial grid keratotomy. Vet Ophthalmol. 2018;21(6):622-631. doi: 10.1111/vop.12556
20. Nevile JC, Hurn SD, Turner AG, Morton J. Diamond burr debridement of 34 canine corneas with presumed corneal calcareous degeneration. Vet Ophthalmol. 2016;19(4):305-312. doi: 10.1111/vop.12304
21. Anastassiadis Z, Read RA, Bayley KD. Topical ethylenediaminetetraacetic acid (EDTA) administration following corneal diamond burr keratotomy for calcareous corneal degeneration in canines. Vet Ophthalmol. 2022;5(3)225-231. doi: 10.1111/vop.12969
22. Sansom J, Blunden T. Calcareous degeneration of the canine cornea: calcareous degeneration. Vet Ophthalmol. 2010;13(4):238-243. doi: 10.1111/j.1463-5224.2010.00791.x
23. Leonard BC, Kermanian CS, Michalak SR, et al. A retrospective study of corneal endothelial dystrophy in dogs (1991–2014). Cornea. 2021;40(5):578-583. doi: 10.1097/ICO.0000000000002488
24. Samuel M, Thomasy SM, Calderon AS, et al. Effects of 5% sodium chloride ophthalmic ointment on thickness and morphology of the normal canine cornea. Vet Ophthalmol. 2019;22(3):229-237. doi: 10.1111/vop.12582
25. Horikawa T, Thomasy SM, Stanley AA, et al. Superficial keratectomy and conjunctival advancement hood flap (SKCAHF) for the management of bullous keratopathy: validation in dogs with spontaneous disease. Cornea. 2016;35(10):1295-1304. doi: 10.1097/ICO.0000000000000966
26. Michau TM, Gilger BC, Maggio F, Davidson MG. Use of thermokeratoplasty for treatment of ulcerative keratitis and bullous keratopathy secondary to corneal endothelial disease in dogs: 13 cases (1994-2001). JAVMA. 2003;222(5):607-612. doi: 10.2460/javma.2003.222.607
27. Boo G, Whittaker CJG, Caruso KA, et al. Early postoperative results of Descemet’s stripping endothelial keratoplasty in six dogs with corneal endothelial dystrophy. Vet Ophthalmol. 2019;22(6):879-890. doi: 10.1111/vop.12666
28. Violette NP, Ledbetter EC. Intracorneal stromal hemorrhage in dogs and its associations with ocular and systemic disease: 39 cases. Vet Ophthalmol. 2017;20(1):27-33. doi: 10.1111/vop.12340
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33. Ofri R. Diseases of the vitreous. In: Maggs DJ, Miller PE, Ofri R, eds. Slatter’s Fundamentals of Veterinary Ophthalmology. 6th ed. St. Louis, MO: Elsevier; 2018:342.
34. LeBlanc NL, Stepien RL, Bentley E. Ocular lesions associated with systemic hypertension in dogs: 65 cases (2005–2007). JAVMA. 2011;238(7):915-921. doi: 10.2460/javma.238.7.915
35. Acierno MJ, Brown S, Coleman AE, et al. ACVIM consensus statement: guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats. J Vet Intern Med. 2018;32(6):1803-1822. doi: 10.1111/jvim.15331
36. Young WM, Zheng C, Davidson MG, Westermeyer HD. Visual outcome in cats with hypertensive chorioretinopathy. Vet Ophthalmol. 2019;22(2):161-167. doi: 10.1111/vop.12575
37. Dixon-Jimenez A, Rapport G, Brown SA. Systemic hypertension in dogs & cats. Todays Vet Pract. 2011;1(2):20-26.
38. Bellows J, Colitz CMH, Daristotle L, et al. Defining healthy aging in older dogs and differentiating healthy aging from disease. JAVMA. 2015;246(1):77-89. doi: 10.2460/javma.246.1.77
39. Rosolen SG, LeGargasson JF, Dubus E, et al. The effect of aging on the retinal function in two selected breed of dogs. Invest Ophthalmol Vis Sci. 2010;51(13):5577.
40. Zicker SC, Jewell DE, Yamka RM, Milgram NW. Evaluation of cognitive learning, memory, psychomotor, immunologic, and retinal functions in healthy puppies fed foods fortified with docosahexaenoic acid–rich fish oil from 8 to 52 weeks of age. JAVMA. 2012;241(5):583-594. doi: 10.2460/javma.241.5.583
41. Wang W, Hernandez J, Moore C, et al. Antioxidant supplementation increases retinal responses and decreases refractive error changes in dogs. J Nutr Sci. 2016;5:e18. doi: 10.1017/jns.2016.5
42. Aguirre GD, Acland GM, Maude MB, Anderson RE. Diets enriched in docosahexaenoic acid fail to correct progressive rod-cone degeneration (prcd) phenotype. Invest Ophthalmol Vis Sci. 1997;38(11):2387-2407.