Scleritis is an uncommon and poorly understood disease process in dogs [
Clinical signs associated with canine scleritis include ocular hyperemia, ocular pain, and exophthalmos, as well as clinical signs associated with secondary anterior uveitis, posterior uveitis, conjunctivitis, or keratitis. Clinical signs are frequently unilateral upon initial admission but the disease will often progress to affect the other eye [
Histologically, canine scleritis is characterized by a diffuse granulomatous cell infiltrate composed predominantly of tissue macrophages, lymphocytes and plasma cells. In severe cases, the inflammatory cells may completely efface normal scleral tissue [
The purpose of this report is to highlight the clinical and histopathological features of a case of presumed immune-mediated non-necrotizing granulomatous scleritis in a dog. This is a unique presentation of the disease because of the associated scleral rupture, and has not been previously reported to the authors’ knowledge.
A 10-year-old male castrated Chihuahua was presented to the University of Tennessee College of Veterinary Medicine ophthalmology service for evaluation of blepharospasm, mucoid ocular discharge, and progressive swelling of the superior conjunctiva of the right eye (OD) (Figure
Appearance of right eye on initial presentation. Notice fluctuant swelling of the conjunctiva. There is also mild corneal edema and neovascularization.
There were no abnormalities on general physical examination aside from a mild fever of 39.4°C. On ophthalmic examination, pupillary light reflexes and menace responses were normal in both eyes (OU). Schirmer tear tests and intraocular pressures were within normal limits OU and both eyes were negative for fluorescein stain uptake. The left eye (OS) was normal on slit lamp biomicroscopy and indirect ophthalmoscopy. The following abnormalities were observed in the OD: moderate blepharospasm, mucoid ocular discharge, pain on palpation of the periorbital tissues, conjunctival swelling and chemosis, mild corneal edema and neovascularization adjacent to the superotemporal limbus, and mild aqueous flare. The lens, vitreous and fundus were within normal limits OD. Based on the ocular exam findings, an ocular ultrasound was recommended.
Ultrasonographic images were obtained using a 15 MHz linear array probe. An area of hypoechogencity, possibly representing fluid accumulation or a cyst, was identified adjacent to the ventral limbus OD. Potential differential diagnoses for this structure were staphyloma, occult scleral rupture, or conjunctival foreign body with surrounding seroma formation. Based on these findings, periocular exploratory surgery was recommended. The owner declined surgical intervention and opted to continue therapy with BNP-Dex.
The patient was presented 2 weeks later for a recheck examination. At that time a fever of 40.4°C was present and the OD was markedly more uncomfortable compared to the initial visit. The left eye was normal. Severe periorbital swelling and pain were identified OD (Figure
Appearance of right eye 2 weeks after initial presentation. Notice severe periorbital swelling, conjunctival hyperemia, and corneal edema and neovascularization.
Based on the worsening clinical course, lack of response to treatment, and with differentials that included surgically treatable lesions, the owner consented to surgical exploration of the right periorbital region.
A complete blood cell count, serum biochemistry panel with electrolytes, and urinalysis were submitted prior to anesthesia. The complete blood cell count revealed a neutrophilia of
The patient was placed in sternal recumbency and the right eye was sterilely prepped and draped. A 1 cm lateral canthotomy was made with tenotomy scissors and a 6–0 silk stay suture was placed at the superior limbus. The superior bulbar conjunctiva was then incised approximately 2 mm posterior to the limbus with curved tenotomy scissors and the conjunctiva bluntly dissected with tenotomy scissors while the bulb was rotated inferiorly. Hemorrhagic chemosis, sclerosis, and pockets of fibrinonecrotic material were encountered throughout the conjunctiva. The peri-orbital musculature was also noted to be sclerotic. No cystic structures or foreign bodies were encountered superiorly, so exploration was continued nasally and inferonasally. Upon examination of the inferonasal aspect of the globe, a scleral rupture was found at the 4 o’clock position, approximately 3 mm posterior to the limbus (Figure
Intraoperative appearance. The conjunctiva has been dissected away and uveal tissue can be seen prolapsing through the region of scleral rupture (yellow arrow).
A histologic section of the enucleated globe was made via sagittal section through the entire eye. The tissue sample was stained with hematoxylin and eosin (H&E) and with Masson’s trichrome. There was a severe diffuse granulomatous scleritis present, more concentrated at the level of the limbus (Figures
Low power view of the globe. The lens is artifactually fragmented (arrow). There is a marked inflammatory response centered at the limbus. In addition, there is retinal detachment and accumulation of fluid in the subretinal space. The cornea is markedly thickened and there is early keratitis.
At the limbus, a markedly severe multinodular inflammatory infiltrate is present within and expanding from the limbus.
The inflammatory infiltrate is distinctive in that it is composed of recurring clusters of neutrophils surrounded by reactive foamy macrophages (pyogranulomas) which coalesce to create the limboscleral inflammation.
Sclera at the limbus. In this Masson trichrome stained section, there is marked separation of collagenous stroma (blue) by the eosinophilic cellular infiltrate. The collagen is not necrotic.
Periodic acid-Schiff (PAS) and GMS stains failed to reveal fungi or yeasts and Ziehl-Neelsen (Zn) and Fite’s failed to reveal mycobacteria or atypical mycobacteria. A 16sRNA test performed to further rule out infectious causes of scleritis was positive. The cloned PCR products were sequenced, but the sequences did not correlate with any specific microbial species. A conjunctival swab of the right eye was negative for aerobic, anaerobic, and fungal organisms. Urine was negative for blastomyces and histoplasma antigen, and serologies were negative for
The patient was discharged the day after surgery on amoxicillin/clavulanic acid oral suspension, carprofen, and omeprazole. The temperature had returned to normal at 39°C. At suture removal 10 days later, the surgical site had healed without complication. On subsequent recheck appointments, the patient’s left eye exhibited focal scleral thickening and anterior uveitis that was responsive to an immunosuppressive dose of prednisolone (2 mg/kg/day). The patient also developed ecchymoses on his ventral abdomen. The patient had a normal platelet count, no history of trauma, and normal clotting times when these lesions developed. For this reason, the patient was treated with pentoxifylline for presumptive immune-mediated vasculitis.
Canine idiopathic scleritis is an uncommon diagnosis and has been rarely reported [
A diagnosis of primary scleritis was made as opposed to scleritis secondary to uveal inflammation because the sclera was affected first clinically and was more affected by granulomatous inflammation than the uvea. Histopathologic findings similar to those reported here have been described in other cases of granulomatous scleritis [
Scleral thinning has been previously associated with necrotic scleritis and scleritis secondary to
Scleral rupture in this case was most likely secondary to scleral thinning and staphyloma formation. The sclera is composed of irregularly arranged collagen and elastic fibers. In scleritis, these fibers are dissected by granulomatous inflammation and in this case the connective tissue fibers were almost completely effaced multifocally. The lack of normal collagen structure creates a weakened focus of sclera where normal intraocular pressure can result in scleral thinning and protrusion of uveal tissue. With severe staphyloma formation, scleral rupture can occur.
Scleral rupture usually results in irreversible vision loss. Cases of scleral rupture secondary to scleritis in dogs have not been well described in the peer-reviewed literature. Surgical repair of these cases is difficult due to the inability of the abnormal sclera to hold suture. Further investigation is warranted to determine the most appropriate treatment and diagnostic recommendation in new cases of scleritis. At this time, it seems most prudent to perform diagnostic tests to rule out infectious causes of scleritis and then institute aggressive immunosuppressive therapy.
Right eye
Left eye
Both eyes.
Lori J. Best drafted the paper and participated in clinical decision making and case diagnostics. Shelley J. Newman provided interpretation of histopathology and revised paper for appropriate intellectual content. Daniel A. Ward participated in case management and diagnostics and revised paper for appropriate intellectual content. Diane V. H. Hendrix participated in case management, diagnostics, and paper revision.