Common Causes of Sudden Blindness in Dogs:

Sudden Acquired Retinal Degeneration (SARD), Immune-Mediated Retinal Detachment Syndrome and Diabetes Mellitus Induced Mature Cataract are common causes of blindness in dogs.

Steve Dugan, DVM, MS, Diplomate of the ACVO

Sudden Acquired Retinal Degeneration (SARD)

Sudden acquired retinal degeneration (SARD) is characterized by a sudden (< 1 month), usually total, permanent blindness in an otherwise healthy dog.  SARD is nonpainful and idiopathic but possibly immune-mediated.  Dachshunds, Miniature Schnauzers and females are overrepresented.  Affected dogs present with dilated and nonresponsive or poorly responsive pupils, fail a maze test under well- and dimly-lighted conditions, and have an ophthalmoscopically normal fundus.  Middle aged to older dogs are affected and occasionally Cushing’s-like clinical signs (polyphagia, weight gain, polyuria, and polydipsia) develop in conjunction with SARD.  Laboratory abnormalities consistent with hyperadrenocorticism are common although definitive biochemical proof of the disease is often lacking in dogs with SARD.

The electroretinogram (ERG) represents a summation of electrical potentials originating from the rod and cone photoreceptors and is necessary for definitively ruling in or ruling out SARD.  The ERG is a nonpainful electrophysiologic test.  Tropicamide is instilled, the patient is dark adapted, topical proparacaine is instilled, a ground stick pin electrode is inserted within the skin of the forehead, a reference stick pin electrode is inserted adjacent to the lateral canthus, and a gold leaf electrode embedded within a contact lens is placed on the cornea after applying a methylcellulose gel.  A light is flashed at the eye and the electrical response is amplified and recorded on a computer.  An absent or extinguished ERG response supports the diagnosis of SARD.  If, on the other hand, the ERG yields normal electrical responses for both eyes, then the loss of vision is considered central; i.e., bilateral optic neuritis, an optic chiasmal lesion at the base of the brain, or an optic tract and/or visual occipital cortex based problem.  A neurologic consultation is then recommended and a CSF analysis and MRI of the skull may be pursued.

There is no validated medical or surgical treatment available for SARD.  As a result, owners are informed their dog with be handicapped thereafter but can still enjoy a high quality of life nonetheless.   In a recent peer-reviewed journal article involving 100 dogs with SARD, owners generally perceived that dogs with SARD have moderate to excellent quality of life and most owners (95%) discouraged euthanasia for dogs with SARD.

Immune-Mediated Retinal Detachment Syndrome

Immune-mediated retinal detachment syndrome typically affects middle-aged and older dogs, is nonpainful, of rapid onset, and eliminates most or all of the functional vision.  Affected dogs present with a bilateral, nonrhegmatogenous, serous, bullous retinal detachment which may involve all or most of the fundus.  Following the comprehensive ophthalmic examination, a physical examination is performed, a blood pressure is obtained, and a comprehensive blood profile is submitted.  If ancillary diagnostic tests rule out infectious disease or other systemic causes, corticosteroids and/or other nonsteroidal immunosuppressive medication are begun; e.g., mycophenolate mofetil (Cellcept) which can be combined with prednisone, is inexpensive, has minimal side effects, and is typically given at 10mg/kg PO BID; and, azathioprine (Imuran) which also can be combined with prednisone, is moderately expensive, can have significant hepatotoxicity and bone marrow suppression, and is typically begun at 2 mg/kg PO daily and tapered.  It may take 2 to 4 weeks for the retinas to reattach, most vision returns, the fundus ultimately illustrates minimal scarring, and the immunosuppressive therapy is very slowly tapered, and in most cases, eventually stopped altogether.

Diabetes Mellitus Induced Mature Cataract

The majority of dogs with diabetes mellitus will develop cataracts within 5-6 months from the time of diagnosis of the disease.  Diabetes induced cataracts can develop remarkably quickly and can cause a complete loss of vision in less than 48 hours.

As blood glucose levels increase, glucose also increases within the aqueous humor, glucose readily diffuses across the lens capsule, an aldose reductase pathway converts glucose to sorbitol, sorbitol accumulates within the lens as it cannot diffuse through lens cell membranes, the osmotic gradient increases, water enters the lens and irreversibly changes the lens structure via lens fiber swelling and rupture, vacuole formation, and clinically evident cataract.

Once the primary care DVM believes the diabetes is relatively well-controlled and the owner is determined to be interested in possibly pursuing cataract surgery, a comprehensive ophthalmic examination/consultation via an ophthalmologist is warranted.  After a careful history, the ocular examination consists of close evaluation of the PLR’s (interested in posterior synechiae), menace responses, IOP’s, and slit lamp biomicroscopy (especially interested in the anterior chamber depth, presence or absence of aqueous flare, presence or absence of keratic precipitates, and contour of the anterior lens capsule).  Rapidly developing, bilaterally symmetric cataract formation in dogs is commonly associated with lenticular intumescence and subsequent phacolytic (lens-induced) uveitis.  If lens-induced uveitis (LIU) is noted, then dependent upon the severity of the LIU, the patient may be started on prednisolone acetate 1% suspension, dexamethasone 0.1% solution, and/or flurbiprofen topically and carprofen or similar NSAID orally.

An electroretinogram (ERG), ocular ultrasonogram, and comprehensive blood profile to include cholesterol and triglycerides are scheduled if the patient’s eyes have not suffered from severe LIU, glaucoma etc.  As given above, the ERG is a nonpainful electrophysiologic test that quantitatively determines the health, or lack thereof, of the retinal photoreceptors.   The ocular ultrasonogram can usually be performed using a topical anesthetic and gentle restraint and determines if the retina is attached or detached and whether any vitreal debris/floaters have developed.  If the ocular ultrasonogram identifies a retinal detachment, it is unlikely cataract removal surgery will be recommended due to the pre-existing, vision eliminating complication.  If the cholesterol and triglycerides are too high, then the patient is returned to the primary care DVM with the aim of reducing the lipids preoperatively as their elevation can predispose the patient to lipemic aqueous syndrome (LAS) which can irreversibly damage an otherwise successful postoperative outcome.  The Miniature Schnauzer is especially predisposed to hyperlipidemia and secondary LAS.

If the patient’s diabetes is well-controlled and the eyes are determined to be healthy other than the cataracts, then phacoemulsification cataract surgery can be pursued.  Diabetic dogs constitute a large proportion of our cataract surgery patients.  The patient is anesthetized, maintained on sevoflurane, paralyzed using atracurim, placed on a ventilator, the lenses removed via phacoemulsification, and intraocular (artificial) lens implants are inserted.  Not all patients are acceptable candidates for artificial lens implants but in those aphakic (no lens) patients, functional vision can still be achieved postoperatively.

Cataract surgery is an elective procedure and requires a significant time commitment on the owner’s part.  The patient must wear a protective Elizabethian collar and remain quiet with no barking, no jumping, wrestling etc for at least three weeks postoperatively.  Assuming no unforeseen complications develop, the postoperative evaluations are performed at 24 to 48 hours, 1 week, 3 weeks, 3 months, and twice per year thereafter.

The success rate for cataract surgery is case dependent and can range from 60-90% for a postoperative visual and comfortable eye dependent upon the age of the patient, the breed, the presence or absence of concomitant major medical issues, the duration of the cataracts, the presence or absence of pre-existing adverse ocular manifestations caused by the cataracts, etc.  The most common postoperative vision eliminating complications include glaucoma and retinal detachment.   Postoperative capsular opacification (PCO) is an extremely prevalent longterm complication following canine cataract removal surgery and artificial lens implantation with a published incidence of 69-100%.  Fortunately, however, PCO only rarely causes a marked decline in postoperative vision.  The incidence of postoperative ocular hypertension (POH), postoperative glaucoma and blindness have recently been reported to be significantly higher in Labrador Retrievers (probabilities of postoperative blindness in Labradors were 5%, 9%, 15%, and 27% at weeks 4, 26, 52, and 104, respectively) versus non-Labradors.  In another very recent retrospective study, 148/179 (82.7%) postoperative cataract surgery patient eyes were functionally visual at the end of the study period.  Blindness occurred in 18/179 (10.0%) eyes and reduced vision in 13/179 (7.3%) eyes.  The most common postoperative complications in this study were: POH 22.9%, corneal lipid opacity 19.0%, uveitis 16.2%, intraocular hemorrhage 12.3% (intraocular hemorrhage, a common cause of an undesirable outcome, was 494.5 time more likely in Boston Terriers and 174.4 times more likely in Poodles), retinal detachment 8.4% (more common in Boston Terriers, Poodles, the Bichon Frise, and Shih Tzu), and glaucoma 6.7%.  The odds of blindness were significantly greater in the eyes of Boston Terriers; i.e., blindness was 290.4 times more likely in the eyes of Boston Terriers compared with the eyes of mixed breed dogs.

Despite the potential for minor as well as severe postoperative phacoemulsification problems, the odds of obtaining a successful outcome still far outweigh the odds for failure in most cases, and as such, the surgery is well worth the cost, time commitment, and inherent risks for many owners, and in those patients that experience a positive outcome, the owners are typically extremely pleased.

References:

1) Miller PE, Galbreath EJ, Kehren JC, et al. Photoreceptor cell death by apoptosis in dogs with sudden acquired retinal degeneration syndrome. AJVR 1998; 59: 149-152; 2) Stuckey JA, Pearce JW, Giuliano EA, et al., Long-term outcome of sudden acquired retinal degeneration syndrome in dogs. JAVMA 2013: 243: 1426-1431; 3) Andrew SE, Abrams KL, Brooks DE, et al., Clinical features of steroid responsive retinal detachments in twenty-two dogs. Vet Comp Ophthalmol 1997; 7: 82-87; 4) Klein HE, Krohne SG, Moore GE et al., Postoperative complications and visual outcomes of phacoemulsification in 103 dogs (179 eyes): 2006-2008. Vet Ophthalmol 2011; 14: 114-120; 5) Moeller EA, Blocker T, Esson D, et al., Postoperative glaucoma in the Labrador retriever; incidence, risk factors and visual outcome following routine phacoemulsification. Vet Ophthalmol 2011; 14: 385-394; 6) Bras ID, Colitz CMH, Saville WJA, et al., Posterior capsular opacification in diabetic and nondiabetic canine patients following cataract surgery. Vet Ophthalmol 2006; 9: 317-327; 7) Sigle KJ, Nasisse MP. Long-term complications after phacoemulsification for cataract removal in dogs; 172 cases (1995-2002). JAVMA 2006; 228: 74-79; 8) Schmidt GM, Vainisi SJ. Retrospective study of prophylactic random transscleral retinopexy in the Bichon Frise with cataract. Vet Ophthalmol 2004; 7: 307-310.