Common drugs that can cause keratoconjunctival toxicity include: aminoglycosides, chloramphenicol, idoxuridine (IDU), adenosine, trichothecene, B. receptor blockers, epinephrine, surface anesthetics, the preservative benzalkonium chloride (BAC), and thimerosal. There are many types of ophthalmic antimicrobial drugs, which have been widely used in clinical practice. It is well known that the aminoglycosides among ocular antibacterial drugs have the most obvious damage to the corneoconjunctival epithelium, and their toxic effects are reduced in the order of gentamicin, neomycin and tobramycin. The mechanism of action may be related to the non-selective inhibition of protein synthesis of cells by this class of drugs. Fluoroquinolones have little damage to the corneoconjunctival epithelium at therapeutic doses, and of these drugs, of which ofloxacin and norfloxacin are the most toxic to the corneal epithelium. The inhibition of corneal stromal cell proliferation by long-term application of fluoroquinolones is more obvious than that of aminoglycosides, and its mechanism of action may be through interference with mitochondrial DNA synthesis and induction of corneal stromal cell apoptosis, thus delaying wound healing and causing corneal perforation in severe cases. Chloramphenicol can cause punctate exfoliation of corneal epithelium. Long-term application of antiglaucoma drugs such as trichothecene, B-agonist blockers and epinephrine may lead to a subclinical inflammatory conjunctival response, which is characterized by a decrease in conjunctival epithelial cupped cells and an increase in macrophages, lymphocytes and fibroblasts. Drug toxicity studies have shown that after 20 min of exposure to rabbit corneal epithelial cells with 2% maurobrine, the epithelial cells can be reduced by villi and the cell membrane can be wrinkled. 0.1% dipivoxil can cause abnormal proliferation of corneal epithelium. Continuous use of antiglaucoma drugs for more than 3 years can shorten the inferior vault conjunctiva and affect the efficacy of filtration surgery. Results of a multicenter study showed a significantly lower incidence of ocular surface toxicity with antiglaucoma medications that do not contain preservatives. The toxic effects of surface anesthetics on the ocular surface were mainly manifested by delayed healing of corneal epithelial and stromal wounds. The toxic effects are related to the type of anesthetic used, the concentration of the drug, and the duration of action. Single doses of surface anesthetics are usually not toxic to the ocular surface, while corneal stromal inflammation, corneal infiltration, edema, and Diaphragm folds can occur when anesthetics are abused. Some studies have shown that surface anesthetics exhibit toxicity when incubated with rabbit corneal epithelial cells for 30-60 minll and that human corneal cells show cytoskeletal damage when incubated with surface anesthetics for 15 min. Among all the toxic effects of eye drops, the toxicity of preservatives is easily overlooked. Currently, the more commonly used preservatives are BAC and thimerosal. The toxic effect of preservatives on the eye occurs rapidly, 0.007% BAC can make 50% of the cultured corneal epithelial cells lysed in less than 2 min. the common concentration of BAC is 0.004% a 0.010%. The damage of preservatives on the ocular surface is mainly through the following channels: (1) damage to the corneal epithelial villi, thus reducing the stability of the tear film. (2) The effect on the lipid layer is similar to that of a detergent, which accelerates tear evaporation. (3) Indirectly destabilize the tear film by reducing the density of conjunctival cupped cells. (4) Reduces the proliferation and viability of corneal cells, impairs the epithelial barrier, and delays wound healing. (5) Histological and cytological tests show inflammatory reaction of the conjunctiva, squamous metaplasia and subconjunctival fibrosis.The toxic effects of BAC are manifested as papillary conjunctivitis, punctate keratopathy, aggravation of dry eye symptoms, inhibition of cell movement, delay of wound healing, occurrence of allergic lid margin conjunctivitis, etc. At high concentration (0.1%), it can cause corneal neovascularization.