Spontaneous Chronic Corneal Epithelial Defects (SCCEDs)

 By: Rachel Mathes, DVM, MS, DACVO


Spontaneous chronic corneal epithelial defects or so called “SCCED” lesions are superficial corneal ulcers that occur in middle-aged, usually large breed dogs, although they may be seen in any breed (1).  SCCED lesions, also known as non-healing ulcers, “indolent” ulcers and “Boxer” ulcers, have a typical clinical presentation and appear as large superficial corneal ulcers with marked epithelial lipping (1,2).The epithelial lip may be seen using focal illumination (e.g. Finhoff transilluminator) or may be highlighted with fluorescein staining with the stain noted to migrate under the epithelial lip. Once the loose epithelium is debrided, the ulcer is often much larger than what is seen prior to debridement. These ulcers may also be associated with dramatic secondary corneal vascularization and granulation tissue.


Although the exact cause of SCCEDs is not known, this defect is thought to be an abnormality in the adhesive mechanism of the corneal epithelium to the stroma (1,3). Upregulation of matrix metalloproteinase (MMP) 2 and 9 is not a characteristic of these lesions (4). An acellular, hyaline membrane is found on histopathology in the ulcer bed and is thought to be contributory in preventing normal epithelial adhesion during the healing process (1).  Although uncommonly these ulcers may become secondarily infected and prophylactic antibiotic therapy is warranted, bacterial infections are not causative in these cases. Aggressive antibiotic therapy or periodic switching of topical antibiotics will have no effect on these ulcers and may potentiate resistant bacterial infection.


Treatment for SCCEDs is aimed at creating very superficial stromal abrasion mechanically. Occasionally, debridement of the ulcer with a sterile cotton tipped swab will effect healing. More commonly, however, a more aggressive treatment such as a diamond burr keratectomy or grid keratotomy is required to initiate healing (3.5). Grid keratotomies cause more stromal damage and resultant astigmatism than diamond burr keratectomies (5). Recent studies have shown a very high success rate after diamond burr keratectomy with 70% healed at 1 week and 92.5% healed at 2 weeks (3). Topical chondroitin sulfate may also be beneficial in promoting epithelial adhesion and may decrease surface shearing forces (5). 

 Picture A  Picture B


                        Image  ( A )

                       Image  ( A )

                      Image ( B )

                     Image ( B )

Typical SCCED lesions are pictured. Not the prominent irregular, raised corneal granulation tissue and epithelial margin (arrow) with fluorescein stain migrating under the epithelial lip (A). A well demarcated focally extensive superficial ulcer is present with an epithelial margin after debridement (B).  


1. Bentley, et al. Spontaneous chronic corneal epithelial defects in dogs: a review. J Am Anim Hosp Assoc. 2005: 41; 158-65.

2. Ledbetter, et al. Efficacy of two chondroitin sulfate ophthalmic solutions in the therapy of spontaneous chronic corneal epithelial defects and ulcerative keratitis associated with bullous keratopathy in dogs. Vet Ophthalmol. 2006: 2; 77-87.

3. Gosling, et al. Management of spontaneous chronic corneal epithelial defects in dogs with diamond burr debridement and placement of a bandage contact lens. Vet Ophthalmol. 23 April 2012, online early view.

4. Carter, et al. Expression of matrix metalloproteinase 2 and 9 in experimentally wounded canine corneas and spontaneous chronic corneal epithelial defects. Cornea. 2007: 10; 1213-1219.

5. Da Silva, et al. Histologic evaluation of the immediate effects of diamond burr debridement in experimental superficial corneal wounds in dogs. Vet Ophthalmol. 2011: 4; 285-291.

Limbal Melanomas

By: Rachel Mathes, DVM, MS, Diplomate ACVO

Facts about Limbal Melanomas:

  • Benign, slow growing tumors in dogs and cats
  • Very responsive to a variety of therapies
  • Low rate of metastasis
  • Low rate of recurrence with treatment
  • Early referral recommended

Limbal melanomas are benign, slowly growing tumors of limbal melanocytic origin. These tumors typically occur along the dorsomedial to ventrolateral limbal arc of the globe at the corneal and scleral junction.1 A bimodal age distribution has been described with a peak occurrence at 3-4yrs of age and 7-10yrs of age in dogs (1,2). These tumors are thought to have an inherited basis as Golden Retrievers are four times more likely and Labradors are three times more likely to develop this compared to other breeds (1). Though benign, limbal melanomas may become globe-threatening with growth due to local invasion. Often, secondary keratitis with corneal lipid deposition will occur as a result of the tumor presence (2,3).  While these tumors are less common in cats, they may occur and have a similar clinical course as canine melanomas (3).  Feline and canine limbal melanomas are amenable to a variety of therapies including surgical debulking with a combined keratectomy and sclerectomy, cryotherapy, laser photocoagulation, radiation and surgery with homologous and autologous grafting (2,3,4). In one recent study, only 1 our of 30 tumors recurred after a combination therapy protocol (2). In addition, the incidence of side effects from surgery was low with less than 10% of complications being potentially globe threatening (2).  After laser photocoagulation, a low recurrence was reported with 1 out of 15 masses recurring at 3 months and 2 out of 15 recurring at one year. Twelve of the fifteen tumors did not recur (3). 

Long term control and vision are attainable and reasonable goals with appropriate therapy. Early referral is recommended to preserve vision and globe integrity.

A dorsomedial limbal melanoma in the left eye is pictured. The mass is heavily pigmented, raised, irregular and well-demarcated with an arc of white corneal lipid at the leading edge.

Inherited Eye Disease and OFA Certification

By Rachel Mathes, DVM, MS, DACVO

Inherited ocular disease in purebred dogs is an important cause of potentially preventable ocular conditions. These conditions range from irritating (e.g. distichia, lacrimal micropuncta) to vision-threatening (e.g. PRA, micropapilla, cataracts). This is a large group of ocular diseases that are typically characterized by autosomal recessive genetic transmission. They are often marked by a clinical onset later in life. These characteristics make prevention through selective breeding and early detection difficult. In addition, many of these genetic traits are so common in the purebred dog population that complete omission of carrier dogs in the breeding pool would significantly narrow the gene pool for particular breeds and would not be warranted or reasonable due to possible selection for other abnormal traits. Recently, a change was made to the ophthalmic certifying agency supported by the American College of Veterinary Ophthalmologists (ACVO). While the Canine Eye Registry Foundation (CERF) still exists, the ACVO has partnered with the Orthopedic Foundation for Animals (OFA) to provide a centralized database of eye examinations performed by board-certified veterinary ophthalmologists on dogs in the United States.

Breeders are encouraged to have any canine purebred breeding pair certified with the OFA Eye Database. Eye examinations are performed by a Diplomate of the American College of Veterinary Ophthalomologists and information from the eye examination is submitted to the OFA. The OFA recommends submission of the eye examination forms even if the dog is not “clear” of inherited ocular disease. Submission into the database is complimentary for any dog with a “failing” grade (ocular condition known to be inherited in which breeding is not recommended). A nominal fee applies to certify dogs deemed free of clinical inherited ocular disease or dogs in which a diagnosis is made in which a designation of “breeder option” has been given. An example of this would include Cavalier King Charles Spaniels examined and noted to have distichiasis. Because this trait is common in the breed and does not typically cause clinical ophthalmic pathology, the breeder has the option to breed the dog, even though it is affected with a known inherited ocular trait. While it cannot be determined if a “normal” dog is a carrier for a specific trait based on ophthalmic examination, information on affected and unaffected dogs is valuable for many reasons. Ongoing genetic research and data collection is vital for prevention of vision-threatening inherited ocular conditions, such as PRA (progressive retinal atrophy) (see Figure A and B). Portland Veterinary Specialists offers OFA Eye Canine Registry examinations for all purebred dogs.


                      Picture ( A )

                     Picture ( A )

                   Picture  ( B )

                   Picture  ( B )

Picture legend:

A normal indirect fundic photograph is depicted (A). Note the 15-20 prominent arterioles emerging from the optic disc with three main retinal venules (larger and more tortuous than the arterioles). The vessels extend to the fundic periphery. A patient with PRA is depicted (B). There is vascular attenuation manifested by loss of visible arterioles and lack of vascular extension to the fundic periphery. There is also generalized tapetal hyperreflectivity.


Dr. Rachel Mathes, DVM, MS, Diplomate ACVO

 Facts about Glaucoma

• Secondary glaucoma more common than primary glaucoma

• Females overrepresented 2:1 for primary glaucoma

• Primary glaucoma typically associated with iridocorneal angle closure and increased intraocular pressure during middle age (6-8 years old)

• Canine glaucoma tends to be aggressive

• Feline glaucoma is almost exclusively secondary

• Concurrent institution of prophylactic therapy for the contralateral eye should be instituted if an eye is enucleated for primary glaucoma

• Imperative to address IOP spikes immediately as they may quickly cause complete blindness

Glaucoma is a term used to describe a group of diseases that cause elevated, often severely, intraocular pressure. This condition is very painful and treatment is aimed not only at preservation of vision, but also for pain management. The pain of glaucoma may be referred pain (migrane headache) and patients may exhibit discomfort by decreased activity, increased sleeping or subtle changes in behavior.1 The signs of pain may not even be noted by the owner until the discomfort is treated, at which time the patient may be noted to return to normal activity or “act like themselves again.” Primary, or breed related, glaucoma in dogs is most commonly due to closure of the aqueous drainage angle or Primary Angle Closure Glaucoma (PACG).1 Females are approximately twice as likely to develop PACG compared to males.2 PACG has different features for different canine breeds, however, the end result is failure of normal aqueous outflow, causing significant intraocular pressure elevation. Acute primary glaucoma may often be treated medically or surgically if addressed immediately, even if there is vision loss at the time of increased intraocular pressure.1,3,4 Chronic primary glaucoma causes extensive intraocular damage and blindness. Therapy is aimed at preventing intraocular pressure spikes, decreasing intraocular pressure and maintaining functional vision.4-7 This therapeutic goal is rarely achieved long term with medication alone and surgical intervention is almost always necessary.5 To preserve functional vision, glaucoma surgery is usually recommended early in the disease course due to the aggressive nature of this disease. Typical surgeries performed include laser cyclophotocoagulation (ciliary body destruction) and anterior chamber valve placement.5 The combination of these surgeries resulted in good control of the intraocular pressure in 76% of cases.5 In cases of irreversibly blind globes, more permanent salvage procedures are recommended as glaucoma is painful (enucleation or an intrascleral prosthesis).

Secondary glaucoma results from other underlying ocular pathology. The most common causes are lens luxations (most often seen in Terrier breeds), uveitis and cataracts. Treatment is aimed at reducing the intraocular pressure and addressing the underlying cause of pressure elevation. Topical glaucoma therapy should be limited, in cases of secondary glaucoma, to medications that do not exacerbate pre-existing ocular disease. Topical carbonic anhydrase inhibitors (e.g. dorzolamide, brinzolamide) or topical beta blockers (e.g. timolol) are recommended for primary or secondary glaucoma. Prostaglandin analogs (e.g. latanoprost, travaprost), while often the first line of therapy for primary glaucoma, should be avoided for secondary glaucoma therapy as they may exacerbate pre-existing ocular disease.


          Image ( A )

         Image ( A )

                   Image ( B )

                   Image ( B )


A patient with acute glaucoma is depicted (A). Note the severe scleral injection and corneal edema. Acute glaucoma must be addressed immediately in order to preserve vision and treat patient discomfort. A patient with chronic glaucoma is depicted (B) Note the significant buphthalmos (globe enlargement), scleral injection and corneal edema. This eye is irreversibly blind, but is quite painful. Therapy is aimed at providing long term patient comfort. Prophylactic therapy should always be instituted in the contralateral eye if an eye is removed for intractable, primary glaucoma.


1. Reinstein S, et al. Canine glaucoma: pathophysiology and diagnosis. Compend Contin Educ Vet. 2009:10;450-2.

2. Tsai S, et al. Gender differences in iridocorneal angle morphology: a potential explanation for the female predisposition to primary angle closure glaucoma in dogs. Vet Ophthalmol. 2012:15S1;60-3.

3. Scott E, et al. Early histopathologic changes in the retina and optic nerve in canine primary angle-closure glaucoma. Vet Ophthalmol. 2013:16S1;79-86.

4. Dees D, et al. Efficacy of prophylactic antiglaucoma and anti-inflammatory medications in canine primary angle-closure glaucoma: a multicenter retrospective study (2004-2012). Vet Ophthalmol. 2013:5.

5. Sapienza J, et al. Combined transscleral diode laser cyclophotocoagulation and Ahmed gonioimplantation in dogs with primary glaucoma: 51 cases (1996-2004). Vet Ophthalmol. 2005:8:121-7.

6. Miller P, et al. The efficacy of topical prophylactic antiglaucoma therapy in primary closed angle glaucoma in dogs: a multicenter clinical trial. J Am Anim Hosp Assoc. 2000:36:431-8.

7. Willis A, et al. Advances in topical glaucoma therapy. Vet Ophthalmol. 2002:5;9-17.

Feline Herpesvirus: Ocular Manifestations

By: Rachel Mathes, DVM, MS, Diplomate ACVO

Feline herpesvirus-1 (FHV-1) is a common viral agent in cats, ubiquitous in the feline population.1It is estimated that 90-95% of cats harbor the virus, usually as a latent infection.  Most often this virus does not cause clinical disease in healthy cats; however, a certain percentage of cats develop recurrent or recrudescent disease.1,2Neonatal infections may cause serious ocular disease or blindness.  Most often, however, if an adult cat is affected, this disease causes ocular morbidity with varied severity.3Viremia appears to be important in the initial infection, but may be of less importance in recrudescent disease.4FHV-1 is directly epitheliotoxic to conjunctival and corneal epithelial cells.  Because of this, the most common ocular manifestations of FHV-1 disease are keratitis and conjunctivitis.5Feline herpesvirus is difficult to detect using serology, PCR and VI (virus isolation), therefore, the diagnosis is usually made based on clinical suspicion of disease.4Feline herpesvirus 1 cause changes to the preocular tear film with affected cats having an increased tear film break up time (increased drying on the ocular surface) and decreased goblet cell density.6Clinical signs may vary with herpetic disease, but blepharospasm (squinting), blepharedema (eyelid swelling), conjunctival hyperemia, chemosis (conjunctival edema), variable corneal ulceration, and corneal vascularization are commonly present (figure).1Secondary signs related to chronic irritation may also be noted and include corneal sequestrae, entropion, dry eye disease, corneal perforation and secondary bacterial infections. Treatment is aimed at supportive care including tear stimulants, tear replacers, reducing environmental and external stressors, and topical antibiotics if corneal ulcers are present.  Antiviral therapy is sometimes recommended in severe cases of FHV-1 infections.7Options for antiviral medications include topical and/or systemic therapy.8Oral lysine has not been shown to improve the clinical signs of herpetic disease.9In fact, lysine has caused worsening of clinical signs in some studies.10This disease may be frustrating to treat and treatment may extend weeks, months or years.  Because the virus is so common in feline populations, caution is advised in treating any cat exhibiting signs of keratitis or conjunctivitis with a topical or oral steroid as steroids have been shown to cause viral recrudescence. 

          Image  ( A )

          Image  ( A )

                          Image ( B )

                        Image ( B )

 The left (A) and right (B) eye of a patient with clinical signs of herpesvirus are depicted.  Eyelid swelling, conjunctival hyperemia and chemosis are present in both eyes.  This patient was also sneezing on examination, a sign consistent with active herpetic disease. Both eyes were painful, as manifested by the third eyelid elevation.  The right eye has extensive corneal vascularization and corneal ulceration present.  Cats presenting with active corneal and conjunctival disease should receive supportive therapy +/- antiviral medications.  Topical and oral steroids should always be avoided.



1. Gould D. Feline herpesvirus-1: ocular manifestations, diagnosis and treatment options.  J Feline Med Surg. 2011; 13: 333-46.

2. Zicola A, et al. Feline herpesvirus 1 and feline calicivirus infections in a heterogenous cat population of a rescue shelter. J Feline Med Surg. 2009;11;1023-7. 

3. Wieliczko A, et al. Feline herpesvirus 1 and Chlamydophila felis prevalence in cats with chronic conjunctivitis. Pol J Vet Sci. 2010;13:381-3.

4. Westermeyer H, et al. Assessment of viremia associated with experimental primary feline herpes

5. Hillstrom A, et al. Evaluation of cytologic findings in feline conjunctivitis. Vet Clin Pathol. 2012;41:283-90.

6. Lim C, et al. Effects of feline herpesvirus 1 on tear film breakup time, Schirmer tear test results and conjunctival goblet cell density in experimentally infected cats.  Am J Vet Res. 2009;70:394-403.

7. Fontenelle J, et al. Effect of topical ophthalmic application of cidofovir on experimentally induced primary ocular feline herpesvirus-1 infection in cats. Am J Vet Res. 2008;69:189-93.

8. Thomasy S, et al. Pharmacokinetics of famciclovir and penciclovir in tears following oral administration of famciclovir to cats: a pilot study. 2012;15:299-306.

9. Rees T, et al. Oral supplementation with L-lysine did not prevent upper respiratory infection in a shelter population of cats. J Feline Med Surg. 2008;10:510-3.

10. Drazenovich T, et al. Effects of dietary lysine supplementation on upper respiratory and ocular disease and detection of infectious organisms in cats within an animal shelter. Am J Vet Res. 2009:70:1391-400.

Cataracts and Cataract Surgery

By: Rachel Mathes, DVM, MS, Dipolmate ACVO

Facts about Cataracts

  • Inherited cataracts are the most common type in dogs
  • 50% of diabetic dogs get cataracts within 6 mos and 80% of diabetic dogs within 16 mos of diagnosis
  • Success rate of cataract surgery is 90-95%
  • Best surgical outcome is associated with immature cataracts prior to complete blindness

Cataracts, or opacities of the lens, occur commonly in dogs and are most often inherited. The second most leading cause of cataracts in dogs is canine diabetes mellitus. Feline cataracts are typically secondary to underlying systemic or ocular pathology and are much less common than canine cataracts. Cataracts may cause vision loss or progress to total blindness. In addition, cataracts may cause other ocular complications such as chronic uveitis, retinal detachments and glaucoma. Cataracts may be unpredictable and variable in their progression. The treatment for cataracts causing vision loss is small-incision cataract surgery performed by phacoemulsification and aspiration with placement of an artificial lens to achieve emmetropia (normal focusing power) (1,2). No medical therapy has been shown to treat cataracts.

Cataract surgery has dramatically improved in human and veterinary medicine in the last several decades with small-incisional (~3mm) surgery becoming the standard of care. Phacoemulsification or phacofragmentation of the lens with automated aspiration has replaced more archaic intracapsular lens extraction surgeries (1,3).  The success rate for cataract surgery is very high with overall estimates at 90-95% short term and 85-95% long term (1,4). Certain breeds such as Labradors, Cocker Spaniels and Boston Terriers have been identified as having a higher risk of complications after cataract surgery, however, the overall complication rate is still low (2,4). Complications after cataract surgery may include retinal detachments, glaucoma, uveitis, corneal ulceration and chronic intraocular inflammation with fibrovascular membrane formation. Hypermature cataracts have been associated with a higher postoperative incidence of glaucoma (4).  Immature cataracts have a lower incidence postoperatively of complications than mature and hypermature cataracts (1,3,4).  In addition, subjectively, the adjustment period to normal vision after surgery is shorter and smoother for patients that are not completely blind prior to cataract surgery.

The overall client satisfaction with cataract surgery is also very high, being around 85-90%. Dissatisfaction was associated with failure to have regularly scheduled rechecks performed with the cataract surgeon. Therefore, long term rechecks are emphasized for any client having cataract surgery performed in their pet. Cataract surgery has a high success rate and is a viable therapy for restoration of vision for patients with blinding cataracts.  

                           Image ( A )

                           Image ( A )

                            Image  ( B )

                            Image  ( B )

A patient with a blinding, mature cataract is depicted (A). Notice the iridal darkening from chronic uveitis and complete lens opacity. A patient one day after cataract surgery is shown (B). Note the translucent artificial lens and overall comfort. This patient’s vision was restored following cataract removal.


1. Miller TR, et al. Phacofragmentation and aspiration for cataract extraction in dogs: 56 cases (1980-1984). J Am Vet Med Assoc. 1987; 190: 1577-80.

2. Klein HE, et al. Postoperative comnplications and visual outcomes of phacoemulsification in 103 dogs (179 eyes): 2006-2008.

3. Sigle KJ, Nasisse MP. Long term complications after phacoemulsification for cataract removal in dogs: 172 eyes (1995-2002). J Am Vet Med Assoc. 2006; 228: 74-9.

4. Biros DJ, et al. Development of glaucoma after cataract surgery in dogs: 220 cases. J Am Vet Med Assoc. 2000; 216: 1780-6..

5. Appel SL, et al. Evaluation of client perceptions concerning outcome of cataract surgery in dogs. J Am Vet Med Assoc. 2006; 228: 870-5.