Management of the complicated corneal ulcer

Corneal ulceration is defined as geographic loss of epithelium and stroma to a varying depth down to Descemet’s membrane. The complex pathophysiology driving corneal ulceration is broadly represented by uncontrolled local stromal hydrolysis mediated by hydrolases released primarily from sequestered leucocytes, these being present as part of the normal inflammatory response to often minor initial corneal insult. Opportunist pathogens, including fungi, facilitate and accelerate the lytic process via their leucoattractant properties. In ulceration, the innate hydrolase inhibitory mechanisms present in the cornea and ocular surface, and integral to the normal inflammation–counterinflammation homeostasis necessary to maintain ocular health, are overwhelmed, allowing exponentially accelerating stromal lysis and consequent leucocyte recruitment and progressing the ulcerative process. Ulceration can progress in the absence of infection, driven by the host innate immune response ...