Alkali Burns of the Eye

Ocular alkali lesions in dogs: acetylcysteine and blood serum effects

“…11 Ophthalmic events after alkali burns were systematically studied previously and corneal opacification and poor adhesion of epithelium to the adjacent stroma were described. 12 Similar signs were found in the present study, in which the epithelium could be easily removed when with a sterile swab after alkali contact. Ocular discharge was mucous or mucopurulent, mild to moderate and tended to disappear gradually.…”

“…15 The inefficiency of acetylcysteine in the treatment of corneal ulcers was reported. 12 In our study there were no differences between the corneas that received acetylcysteine and those that received other treatments. The inefficiency of blood serum in the treatment of alkali-induced corneal ulcers had been reported in rabbits.…”

“…14 Vessels have been reported after one week and localized mainly in the anterior third of the stroma. 12 In our study, vascularization occurred at the same site after 3 days. Ulcer evolution was similar to that reported in the literature also in terms of perforations, which were more common around the tenth day.…”

“…3 After 30 days of ulceration, one G1 dog presented small corneal epithelial vesicles, as previously reported by others in cases of stromal degeneration. 15 Some animals presented flat cells, as described before, 12 and others exhibited an epithelium of many layers and swelling of the basal layer. 10 Pigmentation occurred in a small number of animals 30 days after alkali contact.…”

Ocular alkali lesions in dogs: acetylcysteine and blood serum effects

“…11 Ophthalmic events after alkali burns were systematically studied previously and corneal opacification and poor adhesion of epithelium to the adjacent stroma were described. 12 Similar signs were found in the present study, in which the epithelium could be easily removed when with a sterile swab after alkali contact. Ocular discharge was mucous or mucopurulent, mild to moderate and tended to disappear gradually.…”

“…15 The inefficiency of acetylcysteine in the treatment of corneal ulcers was reported. 12 In our study there were no differences between the corneas that received acetylcysteine and those that received other treatments. The inefficiency of blood serum in the treatment of alkali-induced corneal ulcers had been reported in rabbits.…”

“…14 Vessels have been reported after one week and localized mainly in the anterior third of the stroma. 12 In our study, vascularization occurred at the same site after 3 days. Ulcer evolution was similar to that reported in the literature also in terms of perforations, which were more common around the tenth day.…”

“…3 After 30 days of ulceration, one G1 dog presented small corneal epithelial vesicles, as previously reported by others in cases of stromal degeneration. 15 Some animals presented flat cells, as described before, 12 and others exhibited an epithelium of many layers and swelling of the basal layer. 10 Pigmentation occurred in a small number of animals 30 days after alkali contact.…”

Downregulation of the Transglutaminase 2–NF-κB Inflammatory Axis by a Fusion Protein of Cementoin and Secretory Leukocyte Protease Inhibitor Reduces Corneal Angiogenesis

“…Corneal alkali burns remain a major cause of severe ocular surface damage, frequently leading to chronic inflammation, corneal neovascularization (CNV), stromal remodeling, and permanent visual impairment despite advances in acute clinical management [ 1 , 2 , 3 , 4 , 5 ]. The persistence of these adverse outcomes highlights the need for therapeutic strategies capable of modulating not only early inflammatory events but also the downstream molecular pathways that drive pathological angiogenesis and fibrotic remodeling [ 6 , 7 , 10 ].…”

Ocular alkali lesions in dogs: acetylcysteine and blood serum effects

“…11 Ophthalmic events after alkali burns were systematically studied previously and corneal opacification and poor adhesion of epithelium to the adjacent stroma were described. 12 Similar signs were found in the present study, in which the epithelium could be easily removed when with a sterile swab after alkali contact. Ocular discharge was mucous or mucopurulent, mild to moderate and tended to disappear gradually.…”

“…15 The inefficiency of acetylcysteine in the treatment of corneal ulcers was reported. 12 In our study there were no differences between the corneas that received acetylcysteine and those that received other treatments. The inefficiency of blood serum in the treatment of alkali-induced corneal ulcers had been reported in rabbits.…”

“…14 Vessels have been reported after one week and localized mainly in the anterior third of the stroma. 12 In our study, vascularization occurred at the same site after 3 days. Ulcer evolution was similar to that reported in the literature also in terms of perforations, which were more common around the tenth day.…”

“…3 After 30 days of ulceration, one G1 dog presented small corneal epithelial vesicles, as previously reported by others in cases of stromal degeneration. 15 Some animals presented flat cells, as described before, 12 and others exhibited an epithelium of many layers and swelling of the basal layer. 10 Pigmentation occurred in a small number of animals 30 days after alkali contact.…”

Downregulation of the Transglutaminase 2–NF-κB Inflammatory Axis by a Fusion Protein of Cementoin and Secretory Leukocyte Protease Inhibitor Reduces Corneal Angiogenesis

“…Corneal alkali burns remain a major cause of severe ocular surface damage, frequently leading to chronic inflammation, corneal neovascularization (CNV), stromal remodeling, and permanent visual impairment despite advances in acute clinical management [ 1 , 2 , 3 , 4 , 5 ]. The persistence of these adverse outcomes highlights the need for therapeutic strategies capable of modulating not only early inflammatory events but also the downstream molecular pathways that drive pathological angiogenesis and fibrotic remodeling [ 6 , 7 , 10 ].…”

Ocular alkali lesions in dogs: acetylcysteine and blood serum effects

“…11 Ophthalmic events after alkali burns were systematically studied previously and corneal opacification and poor adhesion of epithelium to the adjacent stroma were described. 12 Similar signs were found in the present study, in which the epithelium could be easily removed when with a sterile swab after alkali contact. Ocular discharge was mucous or mucopurulent, mild to moderate and tended to disappear gradually.…”

“…15 The inefficiency of acetylcysteine in the treatment of corneal ulcers was reported. 12 In our study there were no differences between the corneas that received acetylcysteine and those that received other treatments. The inefficiency of blood serum in the treatment of alkali-induced corneal ulcers had been reported in rabbits.…”

“…14 Vessels have been reported after one week and localized mainly in the anterior third of the stroma. 12 In our study, vascularization occurred at the same site after 3 days. Ulcer evolution was similar to that reported in the literature also in terms of perforations, which were more common around the tenth day.…”

“…3 After 30 days of ulceration, one G1 dog presented small corneal epithelial vesicles, as previously reported by others in cases of stromal degeneration. 15 Some animals presented flat cells, as described before, 12 and others exhibited an epithelium of many layers and swelling of the basal layer. 10 Pigmentation occurred in a small number of animals 30 days after alkali contact.…”

Downregulation of the Transglutaminase 2–NF-κB Inflammatory Axis by a Fusion Protein of Cementoin and Secretory Leukocyte Protease Inhibitor Reduces Corneal Angiogenesis

“…Corneal alkali burns remain a major cause of severe ocular surface damage, frequently leading to chronic inflammation, corneal neovascularization (CNV), stromal remodeling, and permanent visual impairment despite advances in acute clinical management [ 1 , 2 , 3 , 4 , 5 ]. The persistence of these adverse outcomes highlights the need for therapeutic strategies capable of modulating not only early inflammatory events but also the downstream molecular pathways that drive pathological angiogenesis and fibrotic remodeling [ 6 , 7 , 10 ].…”