Unilateral phacoemulsification and intraocular lens implantation in a dachshund

Abstract

A 1.5-year-old, spayed, female dachshund was presented with a cataract and lens-induced uveitis in the left eye. The cataract progressed from immature to hypermature in 4 months. Phacoemulsification and intraocular lens implantation was performed and the dog remains visual in the left eye 1 year post-surgery.

A 1.5-year-old, spayed, female dachshund was referred to the Western College of Veterinary Medicine (WCVM) Small Animal Clinic for assessment of a cataract in the left eye (OS). The owner reported that the dog had had a red, painful eye and opaque lens for 1 wk. There was no history of any other medical or surgical problems. The vaccination status was current. The dog was fed dry hypoallergenic food (Hill’s z/d; Hill’s Pet Food, Topeka, Kansas, USA).

The dog was bright and alert and in good body condition; it weighed 4.9 kg. Results from a physical examination revealed that the body temperature and the heart and respiration rates were within normal reference ranges. Left conjunctival and scleral hyperemia and blepharospasm were present. The menace response and the palpebral, occulocephalic, and both the direct and consensual pupillary light reflexes were normal in both eyes (OU).

A Schirmer tear test (Schirmer Tear Test Strips; Alcon Canada, Mississauga, Ontario) was performed and the results were found to be within normal reference intervals, OU (>10 mm/1 min). Fluorescein staining (Fluorets; Bausch & Lomb Canada, Markham, Ontario) was negative in OU. Intraocular pressures were estimated with an applanation tonometer (Tonopen XL; Biorad Ophthalmic Division, Santa Clara, California, USA), after application of 0.5% proparacaine hydrochloride (Alcaine; Alcon Canada), and found to be 11 mmHg in the OD and 8 mmHg in the OS (normal: 15 to 25 mmHg). Pharmacological mydriasis was achieved with 0.5% tropicamide (Mydriacyl; Alcon Canada), and slit-lamp biomicroscopy (SL-14, Kowa Company, Japan) revealed an immature cataract and microphakia in the OS. A fundic examination was completed by indirect ophthalmoscopy (Heine Omega 200; Heine Instruments, Kitchener, Ontario) and the results were normal in the OD and inconclusive in the OS due to the lens opacity. The ophthalmic diagnoses were immature cataract and secondary lens-induced uveitis in the OS. Therapy was initiated with prednisolone acetate 1% (Sandoz Prednisolone; Sandoz Canada, Boucherville, Quebec), 1 drop, q12h, in the OS to control the mild-moderate lens-induced uveitis.

Transpalpebral ultrasonography was performed to evaluate the posterior segment with a 10 MHz transducer (Logiq 3; General Electric Medical Systems, Baie d’Urfé, Quebec) and sterile ultrasound gel. The OD was determined to be normal (Figure 1A). The OS contained an immature cataract and small areas of hyperechogenicity in the vitreous (Figure 1B). These hyperechoic areas were consistent in appearance with vitreous liquefaction, as the hyperechoic areas were moveable and did not extend posteriorly to the optic disc.

Figure 1.

A — Ultrasonographic appearance of the normal lens in the right eye upon initial presentation. B — Ultrasonographic appearance of the immature cataract in the left eye. Note the hyperechoic areas in the posterior chamber.

The dog was returned to the WCVM 2 mo later for further diagnostic testing. A complete ophthalmic examination was repeated at this time and all parameters were found to be within normal reference limits, except for the intraocular pressure in the OS, which remained low at 8 mmHg. Transpalpebral ultra-sonography was repeated and the hyperechoic areas in the vitreous in the OS were no longer apparent; the OD still appeared to be normal. An electroretinogram (Cadwell Sierra II; Cadwell Laboratories, Kenewick, Washington, USA) was performed with a corneal contact lens (ERG-jet; Universo SA, La Chaux-de-Fonds, Switzerland) and platinum subdermal needle electrodes (Cadwell Low Profile Needle Electrodes; Cadwell Laboratories) and found to be within normal reference ranges in OU.

Four months after the initial presentation, phacoemulsification and intraocular lens implantation were completed in the OS. The presurgical database was unremarkable, except for a mild decrease in globulins at 22 g/L (normal: 23 to 27 g/L) and hyposthenuria (urine specific gravity of 1.006). An electroretinogram was repeated and the results were within normal reference ranges in OU. The intraocular pressures were measured and found to be 11 mmHg in the OD and 15 mmHg in the OS. Slit-lamp biomicroscopy and photographs (Canon DS6031, Canon, Tokyo, Japan) (Figure 2) confirmed that the cataract was resorbing and becoming hypermature. The dog had been given prednisolone acetate 1%, topically, 1 drop, q12h, in the OS since presentation; on the day before surgery, the frequency was increased to q6h. In addition to prednisolone acetate 1%, diclofenac sodium 0.1% (Voltaren; Novartis Pharmaceuticals, Mississauga, Ontario), 1 drop, ofloxacin 0.3% antibiotic solution (PMS-Ofloxacin; Pharmascience, Montreal, Quebec), 1 drop, atropine (Alcon Canada), 1 drop, and tear replacement gel (Tear-Gel; Novartis Pharmaceuticals, Basel, Switzerland) were administered topically to the OS, q6h.

Figure 2.

Digital photograph of the hypermature cataract in the left eye on the day of phacoemulsification and intraocular lens implantation.

The dog was premedicated with hydromorphone (Hydromorphone; Sabex, Boucherville, Quebec), 0.1 mg/kg body weight (BW), IM, and acepromazine (Atravet; Ayerst Veterinary Laboratories, Guelph, Ontario), 0.05 mg/kg BW, IM; anesthesia was induced with propofol (Rapinovet; Scherling-Plough Animal Health, Division of Scherling Canada, Pointe Claire, Quebec), 4 mg/kg BW, IV, and maintained with 2% sevo-flurane (Sevorane; Abbott Laboratories, Saint-Laurent, Quebec). Muscle paralysis was induced with atracurium (Atracurium besylate 10 mg/mL; Sandoz Canada), 0.2 mg/kg BW, IV, to keep the globe centered and to prevent any ocular movement during surgery. The dog was placed in dorsal recumbency, and the OS was prepared aseptically with betadine solution and draped routinely.

Stay sutures were placed in the ventral bulbar conjunctiva, using 5-0 monofilament nylon (Monosof; United States Surgical, Norwalk, Connecticut, USA), and a step-shaped corneal incision was completed with a 300-μm restricted entry blade, 1 mm from the sclera. The corneal incision was enlarged, using a 2.5-mm keratome. The anterior chamber was inflated with a viscoadherent (Ocucoat viscoadherent; Bausch & Lomb Surgical). Lens capsulotomy was performed with a 20-g microsurgical knife; the capsular incision was enlarged with scissors, and the edges torn and removed with utrata forceps. Phacoemulsification was completed, using a small ultrasonic probe with an average power of 22% and a time of 2.25 min. The residual lens cortex was removed with a J-loop aspiration tool and the capsule was polished. The corneal incision was then further enlarged with a 3.2-mm keratome and a 41 diopter acrylic lens with 12 mm haptics (PFI 12-SE Intraocular Lens Dioptrix, L’Union, France) was implanted within the lens capsule. The corneal incision was closed with a 9-0 vicryl (Ethicon; Johnson and Johnson Medical Products, Markham, Ontario) in a continuous cruciate pattern and the viscoadherent was aspirated from the eye.

Recovery from anesthesia was uneventful. A recheck ophthalmic examination was performed the following morning and no postsurgical complications were seen. The intraocular pressures were 11 mmHg in the OD and 14 mmHg in the OS. The intraocular lens implant was centered and there was mild posterior capsular opacity and vitreous degeneration. The dog was discharged with instructions to the owner that an Elizabethan collar was to be worn for 4 wk and exercise limited to leash walks. The dog was to receive 1 drop each of prednisolone acetate 1% suspension, diclofenac sodium 0.1% solution, ofloxacin 0.3% antibiotic solution, and tear replacement gel topically in the OS, q6h, for 3 wk. The morning after surgery, 0.5% tropicamide was administered in the OS; subsequently, the dog was to receive 1 drop, q12h, for 3 wk.

The dog was reexamined 3 wk after surgery; the OS had focal sutures, a scar where the corneal incision had been made, and pseudophakia with mild capsular fibrosis. The medications were revised, so that the dog now received prednisolone acetate 1% suspension, diclofenac sodium 0.1% solution, ofloxacin 0.3% antibiotic solution, and tear replacement gel topically, 1 drop, q8h, in the OS for another 3 wk, after which the frequency was decreased to q12h. Three months postsurgery, the prednisolone acetate 1% solution was discontinued due to the detection of a pinpoint ulcer on the cornea in the OS when it was stained with fluorescein dye. Diclofenac sodium 0.1% eye drops, q12h, in the OS were continued. Five months later, the dose was decreased to q24h, as the dog continued to do well. Slit-lamp biomicroscopy revealed minimal posterior capsular fibrosis; a fundic examination was easily performed and the results were normal. No complications have been noted 1 y post surgery.

Discussion

There are numerous causes of cataracts in dogs, including genetic mutation, metabolic disease (diabetes), intraocular disease (uveitis, glaucoma, retinal degeneration, lens luxation), trauma, and nutritional and toxic influences. There are many ways in which to classify cataracts: cause, age of onset, location, and stage of maturation. There are 5 stages of cataract maturity. The 1st stage is an incipient cataract, which may then progress to become an immature, mature, hypermature, and, then, Morgagnian cataract (1). This dog’s cataract was classified as immature at the time of diagnosis, as tapetal reflection and details of the fundus were still slightly visible. At the time surgery was pursued, the cataract had progressed to hypermature and was resorbing. A hypermature cataract may show evidence of lens resorption, mineralization within the lens, or wrinkling of the anterior lens capsule (2). A cataract does not have to go through all these stages (1). A congenital cataract was likely, given the microphakia noted at the time of referral to the WCVM. The other etiologies that were considered included traumatic and developmental. There was no evidence of trauma, chronic uveitis, or metabolic disease. Inherited (developmental) cataracts are the most common; however, they are almost always bilateral (1).

Elective removal of a unilateral cataract is increasing in frequency, as the success rate of cataract surgery has improved dramatically and the short-term success rate is now about 95% (1). If the patient has secondary uveitis, surgery may be the best option, as it may be easier to manage the uveitis once the cataract has been removed (1). Lens-induced uveitis develops with cataracts due to the release of antigenic lens proteins through the lens capsule (3). The uveitis in this case resolved with the use of prednisolone acetate 1% solution, topically. It is important to reduce the uveitis presurgically in order to decrease postoperative complications, such as glaucoma, retinal detachments, and synechia. It is possible that without surgery, a young dog may completely resorb the lens and gain back some aphakic vision. However, chronic lens induced uveitis, intracapular fibrosis, secondary glaucoma, and retinal detachments often develop during resorption (4).

Electroretinography to evaluate retinal function and ultra-sonography to evaluate the posterior segment are important presurgical screening tools when a thorough examination is impeded by a lens opacity (2). In this case, ultrasonography revealed hyperechoic areas in the posterior segment and, due to the moveable nature of the opacities, they were proposed to represent vitreous degeneration. The diagnosis of vitreous degeneration was confirmed at surgery and no remnants of the hyaloid artery or primary vitreous were seen. Liquefaction of the vitreous is caused by a decrease in the hyaluronic gel and an increase in the free water content of the vitreous body (5); it occurs with vitreous degeneration. Liquefaction is seen on ultrasonographs as multiple echogenic lines within the vitreous that show marked aftermovement (6). A study looking at ultrasonographic abnormalities of canine eyes found that 23% of eyes with cataracts also have vitreous degeneration (2). Other possible causes for the hyperechoic areas in the posterior chamber include persistent hyaloid artery (PHA) and persistent hyperplastic primary vitreous (PHPV). Color-flow Doppler evaluation could have been performed to look for a perfused hyaloid artery with either a PHA or a PHPV (4,7). It was not performed in this case, because the hyperechoic areas in the vitreous did not extend to the optic nerve.

Anterior and posterior lens capsule opacities may be present before or develop after surgery. Lens epithelial cells metaplase and induce fibrous membranes that opacify and increase capsular wrinkling, may obstruct vision, and induce intraocular lens decentration. This appears to be more of a concern when cataract surgery is performed in a young dog. A primary posterior capsulectomy is an option in young dogs as a prophylactic measure, but it was not completed in this case (4). If a capsular opacity that obstructs vision develops, a posterior capsulectomy may be completed.

This dog remains visual in OU, and postsurgery, the dog was comfortable without any active uveitis and with being administered diclofenac sodium 0.1%, q24h.