What are your clinical diagnoses, etiology of the unilateral blindness, and prognosis for return of vision in the right eye?

History and clinical signs

A 5-year-old, spayed female, chocolate Labrador retriever was referred to the ophthalmology service at the Western College of Veterinary Medicine (WCVM) with a 5-day history of redness of her right eye and bilateral third eyelid prolapse. The dog had a 3-day history of decreased appetite, lethargy, and diarrhea; was restless; and would whine intermittently during the night. The referring veterinarian had diagnosed bilateral glaucoma. Current medical management included bilateral topical therapies of timolol maleate (Timoptic 0.5%; Sabex, Boucherville, Quebec), q12h; pilocarpine (Miocarpine 1%; CibaVision Canada, Mississauga, Ontario), q24h; and dorzolamide hydrochloride (Trusopt 2%; Merck Frosst, Kirkland, Quebec), q8h; and oral metronidazole, q12h. On presentation at the WCVM, the dog had a cutaneous fentanyl patch on her left lateral thorax and had received ketoprofen, IM, q24h, for 2 d without resolution of the ocular pain. Additional therapy included oral methazolamide, which had been discontinued 2 d previously.

Physical examination confirmed that abnormalities were limited to the eyes. There was bilateral third eyelid prolapse. Pain was not evident when the mouth was opened, and erythema or swelling was not detected caudal to the last upper molar teeth. Retropulsion of both globes was unremarkable. The right eye exhibited moderate conjunctival and episcleral injection and mydriasis (Figure 1). The menace response was absent in the right eye. There were negative right direct and left consensual pupillary light reflexes. The palpebral and oculocephalic reflexes were intact in both eyes. Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) values were within the normal reference range. Fluorescein dye (Fluor-I-Strip AT; Ayerst Laboratories, St. Laurent, Quebec) staining was negative. Applanation tonometry (Tonopen XL; Biorad Ophthalmic Division, Santa Clara, California, USA) revealed intraocular pressures (IOPs) of 54 mmHg and 9 mmHg in the right and left eye, respectively. Slit lamp biomicroscopy (Kowa SL-14; Kowa, Tokyo, Japan) revealed mild diffuse corneal edema of the right eye. Gonioscopy of the left eye revealed goniodysgenesis. Indirect ophthalmoscopy (Heine Omega 200; Heine Instruments Canada, Kitchener, Ontario) revealed a focal flat, serous retinal detachment, dorsal to the optic disc, and optic disc cupping of the right eye (Figure 2). Abnormalities were not detected in the left fundus.

Figure 1. The right eye of a 5-year-old, Labrador retriever. Note the third eyelid prolapse, moderate conjunctival and episcleral injection, and mydriasis.

Figure 2. The fundus of the right eye of the 5-year-old, Labrador retriever. Note the dorsal, focal, grey, tapetal hyporeflective triangle involving the 12 o'clock retinal vessels, and the dark peripapillary region. These changes are consistent with a focal, flat, serous retinal detachment and optic disc cupping, respectively.

Discussion

Our clinical diagnoses were acute right primary glaucoma and left goniodysgenesis. The right ocular blindness was deemed secondary to the glaucomatous retinal and optic nerve damage. The bilateral third eyelid prolapse was due to bilateral globe retraction in response to general malaise from the ocular pain of acute primary glaucoma in the right eye. Despite the aforementioned antiglaucoma therapies, the IOP in the right eye remained elevated 5 d following the onset of ocular signs. The prognosis for vision return was considered guarded to poor. The affected eye did not have evidence of chronic glaucoma, including buphthalmia and secondary lens subluxation/luxation, or corneal vascularization. Emergency therapy for the primary glaucoma was initiated. The dog was treated with topical latanoprost (Xalatan 0.005%; Pharmacia and Upjohn, Mississauga, Ontario) at 1 drop on the right eye, q24h, in the evening (1). Topical timolol maleate and dorzolamide hydrochloride were continued at 1 drop on both eyes, q12h. The dog's IOP decreased to within the normal range within 1 h.

After 2 d of therapy, the IOP was 36 mmHg in the right eye, which remained blind. Surgical options for the blind, glaucomatous globe include enucleation or evisceration with placement of an intrascleral silicone prosthesis. Continued medical management, transscleral cyclophotocoagulation, anterior chamber shunting, and intravitreal gentamycin injection are considered less effective for the long-term control of both the glaucoma and subsequent pain in the blind globe. The owners requested an evisceration and prosthesis of the right eye.

Results from routine presurgical blood analyses were unremarkable. The following day, the dog was routinely sedated, induced with propofol (Rapinovet; Schering Canada, Pointe-Claire, Quebec), and intubated. General anesthesia was maintained via inhalational halothane (Halathane BP; MTC Pharmaceuticals, Cambridge, Ontario). The right globe was routinely prepared for surgery via lavage with dilute (1:25) povidone-iodine solution. The dog was positioned in dorsal recumbency, and the right eye was eviscerated. The premeasured silicone implant was placed. The scleral and conjunctival incisions were routinely closed using 7-0 polyglactin 910 (Vicryl; Ethicon, Medical Products, Peterborough, Ontario). The intraocular contents were placed in 10% neutral buffered formalin and submitted for histologic evaluation. The right eye was treated with topical ciprofloxacin (Ciloxan; Alcon Canada, Mississauga, Ontario), 1 drop, q6h, until reexamination in 3 wk. Timolol maleate and dorzolamide hydrochloride were continued at 1 drop of each medication on the left eye, q12h.

Light microscopic evaluation of the eviscerated contents confirmed retinal degeneration, secondary to primary glaucoma. There was no evidence of uveitis or neoplasia.

Glaucoma is a frequent cause of irreversible blindness in dogs; at least 12 000 new cases of glaucoma are being diagnosed by veterinary ophthalmologists in the United States every year (2). Glaucoma is characterized by an increase in IOP above that which is compatible with the normal health of the globe. Accepted normal range for IOP in the dog is 15 to 25 mmHg (3); glaucoma is diagnosed when canine IOP exceeds 30 mmHg. Glaucoma develops when the normal outflow path of aqueous humor from the posterior chamber, through the pupil and into the iridocorneal angle trabecular meshwork and into collecting veins, is obstructed (3,4). Glaucoma is a neurodegenerative disorder, as it results in retinal ganglion cell death (5). Glaucoma also compromises optic nerve blood supply and reduces axoplasmic flow, resulting in visual field loss and blindness (5).

Glaucoma can be classified into congenital, primary, and secondary types. Congenital glaucoma involves maldevelopment of the anterior segment and aqueous pathways of the eye (6). Secondary glaucoma arises as a sequela of a demonstrable intraocular disease, such as lens luxation, uveitis, hemorrhage, retinal detachment, intraocular neoplasm, intumescent cataract, or postoperatively following lensectomy (3,4,7). Assuming the intraocular disease is medically or surgically treatable, secondary glaucoma may be resolved. This case did not exhibit an inciting intraocular disease. The focal retinal detachment was assumed to develop secondary to the elevated IOP.

Primary glaucoma usually starts as a unilateral disease but eventually is bilateral (4). The etiologies for primary glaucoma are unknown, although anatomical defects in the iridocorneal filtration angle are present (4,8). Purebred dogs with increased incidence of primary glaucoma include the American cocker spaniel, basset hound, Samoyed, and bouvier des Flandres (7). To the authors' knowledge, primary glaucoma has not been previously reported in the Labrador retriever.

There are numerous medical therapies available to treat glaucoma. Latanoprost is a prostaglandin F_2α analogue, which acts to increase uveoscleral outflow of aqueous humor. This medication has been reported to significantly reduce IOP in healthy dogs without inducing adverse ocular effects (1). Latanoprost was useful in the short-term reduction of IOPs in the right eye of this case.

Surgical options of enucleation or evisceration and prosthesis provide long-term pain relief for eyes that are permanently blind due to persistent primary glaucoma. Surgical therapies, including transscleral lasering of the ciliary body (cyclophotocoagulation) and anterior chamber shunts, do not presently provide permanent long term control of primary glaucoma. Prophylactic antiglaucoma therapy for the, as yet, unaffected eye is advisable to help delay the onset of glaucoma in that eye (2).

The authors have demonstrated that anterior to frontal sinus shunting of aqueous humor in normal dogs is a safe and effective means of reducing IOPs (9). Anterior chamber to frontal sinus shunting appears to be a promising surgical technique in certain cases of canine primary glaucoma (10). The authors are presently advising anterior chamber to frontal sinus shunting in acute cases of primary glaucoma in which the eye retains vision (10). Histologic evaluation of the globe or intraocular contents, following enucleation or evisceration and prosthesis, respectively, is advisable in order to confirm the ocular diagnosis of primary glaucoma.