Clinical Case Challenge: Ophthalmology (Dog)
A 4-year-old male, neutered, mix breed dog, Canon, presented to the Ophthalmology Service at Tufts Foster Hospital for Small Animals for a two-month history of ocular redness and discharge involving the left eye (OS). Canon was previously treated with topical neo/poly/dex ointment (q12h) for approximately one month, with minimal improvement.
Ophthalmic examination revealed menace response, dazzle reflex, and pupillary light reflexes (direct and indirect) were present, bilaterally (OU). Tear production and intraocular pressures were within normal reference ranges. Fluorescein staining was negative OU. Detailed anterior segment examination revealed moderate conjunctival hyperemia and scleral injection OS. Paraxial corneal deposition, consistent with lipid, was noted dorso-laterally, in conjunction with a perilimbal mass-like lesion (Fig 1).
Further examination demonstrated the peri-limbal mass emanated fromr a larger, multi-lobulated mass involving the neighboring sclera (Fig 2). Intraocular examination demonstrated no indication of active inflammation (i.e., flare). Posterior segment examination revealed multi-focal hyperpigmented foci subtending the retina within the superior half of the fundus, laterally (Fig 3).
An ocular ultrasound was performed to further characterize the mass and extent of involvement. The scleral mass was solid and of mixed echogenicity, extending posteriorly beyond the equator of the globe. No evidence of choroidal thickening and/or retinal detachment was noted.
Based on examination findings, what are your primary differentials? What further diagnostics would you consider, and what treatment options would you recommend?
Based on the clinical appearance and primary location of the mass (i.e. sclera), differentials including nodular granulomatous scleritis (NGE), non-necrotizing scleritis, necrotizing scleritis, parasitic granuloma (i.e., onchocerca), and neoplasia were considered. The primary ruleout was NGE.
Further diagnostics included a complete blood count and serum biochemistry profile and a scleral biopsy to determine the nature of the mass. Optical coherence tomography (OCT) was also performed to further characterize posterior segment changes. The CBC and biochemistry were unremarkable. Histopathology of the scleral mass demonstrated features consistent with chronic granulomatous inflammation. Predominant cell populations included lymphocytes, plasma cells, and histiocytes. Based on these findings, a diagnosis of NGE was made. Optical coherence tomography of the posterior segment demonstrated a normal retinal architecture with no evidence of retinal thinning and/or detachment. Pigmentary changes noted on ophthalmoscopy were believed to reflect hypertrophy/hyperpigmentation of the underlying retinal pigmented epithelium, due to scleral extension and subsequent choroidal inflammation.
Nodular granulomatous episcleritis is an immune-mediated disease process, of unknown etiology, exhibiting a breed predisposition (Collies, Cocker Spaniels, and Shetland sheepdog). Several reports have demonstrated lymphocytic cell populations to consist primarily of T-cells. Nodular granulomatous episcleritis is generally considered to be benign, often exhibiting good response to medical therapy. In relatively mild cases, topical therapy may suffice. However, often concurrent systemic administration of immunosuppressive therapy is warranted. Various regime have been employed and include the use of corticosteroids, azathioprine, or cyclosporine. Alternatively, intra-lesional or subconjunctional injections of corticosteroids may be utilized. Cryotherapy has also been recommended.
In the case presented herein, after discussion with the owners, a combination of topical (prednisolone acetate and cyclosporine) and systemic therapy (prednisone) was employed. Following the initiation of therapy, Canon demonstrated slow, but significant signs of improvement, with reduction of the scleral mass and conjunctival/scleral injection (Fig 4). As is common with many presumed immune mediated disease, duration of therapy is prolonged. A slow taper of medications is recommended and should be determined based on clinical signs and response to therapy.