Disseminated Idiopathic Lipid Keratopathy in a Normolipemic Cat PDF

DOI: 10.1111/vop.13038 | Revised: 25 October 2022 | Accepted: 29 October 2022 CASE REPORT Disseminated idiopathic lipid keratopathy in a normolipemic cat Andrés Botello-­Bárcenas1 | Rodrigo García-­Santisteban1 | 2 3 Abelardo Rodriguez-­Reyes | Dennis E. Brooks | Gustavo Adolfo García-­Sánchez1 1 Ve...

DOI: 10.1111/vop.13038 | Revised: 25 October 2022 | Accepted: 29 October 2022 CASE REPORT Disseminated idiopathic lipid keratopathy in a normolipemic cat Andrés Botello-­Bárcenas1 | Rodrigo García-­Santisteban1 | 2 3 Abelardo Rodriguez-­Reyes | Dennis E. Brooks | Gustavo Adolfo García-­Sánchez1 1 Veterinaria Oftalvet, Mexico City, Mexico 2 Asociación Para Evitar la Ceguera en México, Mexico City, Mexico 3 Brookseyes LLC, Alachua, Florida, USA Correspondence Rodrigo García-­Santisteban, Veterinaria Oftalvet, Avenida Coyoacán 1141, 04310 Mexico City, Mexico. Email: [email protected] Abstract Objective: To report a case of idiopathic lipid keratopathy in a normolipemic cat. Animal Studied: A 10-­year-­old neutered female European domestic cat. Results: A cat was evaluated for bilateral white corneal deposits. Slit-­lamp examination revealed multiple, well-­defined, round, stromal, cream-­colored deposits of different sizes associated with generalized superficial corneal vascularization. Blood lipids were normal, and no history of travel to tropical locations or ocular trauma was present. Topical betamethasone/gentamicin 0.1% suspension q 12 hours did not result in any improvement of clinical appearance after one week. Tomography following the initial therapy revealed dense, hyperreflective deposits with posterior shadowing in the anterior and mid stroma of both corneas. A four-­ week course of itraconazole 0.01% ophthalmic cream was prescribed q 12 hours with no improvement. Four months after the initial examination, a diagnostic superficial keratectomy and amniotic membrane implantation were performed. Histopathological analysis showed membrane bound vacuoles with infiltration of foamy macrophages suggesting a diagnosis of primary lipidosis. The post-­surgical period was unremarkable, and ten days later, the patient was re-­examined. Opacification from a corneal leukoma was observed in the excision site with mild fibrotic tissue. Two months post-­keratectomy, no further changes were detected in the cornea, and the patient was managed only with topical lubricant. Conclusions: To our knowledge, this is the first report of idiopathic corneal lipidosis in a cat and may be considered as a differential diagnosis of corneal disease in felines. KEYWORDS cat, cornea, feline, keratectomy, lipid keratopathy, ocular tomography 1 | I N T RO DU CT ION Lipid keratopathy (LDK) consists of lipid deposition in corneal tissue that usually occurs secondary to ocular or systemic disease such as trauma, thyroid disease, infection or hyperlipidemia.1–­4 Although primary idiopathic cases have been reported in some species, no such findings have been reported in cats.5–­9 LDK was reported for the first © 2022 American College of Veterinary Ophthalmologists. Veterinary Ophthalmology. 2023;26:71–77.  wileyonlinelibrary.com/journal/vop | 71 14635224, 2023, 1, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/vop.13038 by Royal Veterinary College, Wiley Online Library on [13/02/2023]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License Received: 24 February 2022 | BOTELLO-­BÁRCENAS et al.    time in felines secondary to a chronic corneal ulcer which developed progressive vascularization and lipid deposition in the form of a unilateral compact plaque.10 A similar case of corneal lipidosis in a cat was also reported as a side effect of lipid therapy for permethrin toxicosis.11 A normolipemic cat was reported to develop post-­traumatic conjunctival lipid granulomas which resolved after surgical excision.12 Diagnosis usually requires histopathological analysis to identify lipid vacuoles in corneal tissue, and treatment consists of controlling the underlying cause to deter further lipid deposition and prevent corneal opacification.1 The present report details the findings, treatment, and follow-­up of a cat presenting with primary bilateral LDK. The findings described here may account for a new variant of corneal lesions and differential diagnosis that, if confirmed with biopsy, could prevent unnecessary treatments such as antibiotics and steroids in similar patients. 2 2.1 | C A S E RE PORT | History/examination findings A 10-­year-­old neutered female European domestic cat with no significant past medical history presented with a chief complaint of multiple “white spots” on the surface of both eyes noticed 2 months before initial evaluation. Upon general physical examination, the cat appeared mildly malnourished but comfortable, with no apparent blepharospasm. Ophthalmic examination revealed multiple round, well defined cream-­colored lesions in the stroma of both corneas. (Figure 1). Mid-­stromal corneal vascularization adjacent to the lesions and a perivascular infiltrate were also noted. FIGURE 1 2.2 | Medical management and diagnostic testing The cat was given topical hyaluronic acid-­based lubricant (Humectan, Santgar Laboratories, Mexico) and a combination of topical betamethasone/gentamicin suspension (0.1% Betagen, Santgar Laboratories) q 12 h. The owner was also instructed to return in 1 week in order to perform corneal optical coherence tomography (OCT) scanning, as well as blood tests. Upon subsequent examination, corneal abnormalities remained unchanged. OCT scan (Primus 200, Carl Zeiss) was performed and revealed multiple dense, homogeneous deposits of hyperreflective material in the anterior and mid-­ stroma with underlying posterior shadowing (Figure 2). Urinalysis revealed scarce red blood cells associated to the method of urine collection (cystocentesis). A small amount of indeterminate lipids was also detected, although no casts were seen. Fasting basic metabolic panel revealed mild hyperglycemia (9.29 mmol/L, normal 3.8–­ 7.9) attributed to the release of epinephrine due to the stress caused by blood extraction, as well as mild elevation of alanine aminotransferase (ALT) (135 U/L, normal 22–­ 84), and elevated creatinine kinase (CK) (588 U/L, normal