Introduction

• Cause: two main categories: crystalline stromal dystrophy, hereditary and lipid keratopathy (increased circulating lipids or after surgery).
• Signs: opacification of cornea.
• Diagnosis: signs, laboratory investigation.
• Treatment: manage underlying cause, keratectomy may be required.

Pathogenesis

Etiology

• Previous corneal trauma.
• New blood vessels leak lipid into cornea.
• Elevated blood lipid levels (in some cases).

• Limbal melanoma.
• Episcleritis.
• Pannus.
• Leak from new blood vessels to deposit in cornea.
• Stromal dystrophy.
• Hereditary.

Predisposing factors

• Susceptible breeds.

Specific

• Corneal injury.
• Systemic blood lipid elevation, ie hypothyroidism.

Pathophysiology

• Crystalline stromal dystrophy: non-painful, non-vascularized lesions with characteristic granular or ground glass appearance affecting central/paracentral cornea as circular or oval lesion (inherited + bilateral without systemic changes).
• Lipid keratopathies: painful, vascularized lesions - usually secondary and may be associated with increased circulating lipids .
• Secondary lipid infiltration: non-painful, non-vascularized. Secondary to limbal melanoma, episcleritis, pannus, leak from new blood vessels to deposit in cornea.

• Lipid deposited in anterior stroma of central or paracentral cornea due to innate abnormality or localized error in corneal lipid metabolism.
• Lesions may be deeper and more extensive in Siberian Husky Siberian Husky.

• Crystalline lipid deposits penetrate corneal epithelium → irritation, vascularization and possibly ulceration Keratitis.
• May be associated with abnormal levels of circulating lipids.
• Usually occurs in conjunction with corneal degeneration.
• Calcium is also involved in this pathological process.

Timecourse

• Lifelong disease with slow progression in the dystrophies.
• Keratopathy can occur following acute injury.

Diagnosis

Treatment

Outcomes