With the continuous development of pharmaceutical technology, there are more and more eye drops available in the clinic, and the widespread use of antibacterial drugs, antiglaucoma drugs and nonsteroidal anti-inflammatory dmgs (NSAIDs) provides a variety of options for clinical treatment, but certain Ocular surface toxic reactions to certain eye drops are also becoming more common. The inappropriate use or even abuse of drugs in clinical practice occurs because physicians do not fully understand the characteristics of the drugs or misdiagnose the disease. In particular, drug abuse not only increases the financial burden of patients, but also may lead to drug-induced toxic side effects, and related cases are not uncommon. Therefore, clinical ophthalmologists should not only focus on the efficacy of drugs, but also ignore their potential toxic side effects. When using a drug or a new drug for the first time, physicians should be familiar with both the therapeutic effects of the drug and its toxic side effects (including those of preservatives), so as to avoid ocular surface damage caused by drug toxicity. So, what are the manifestations of ocular surface toxicity of eye drops? Generally speaking, the conjunctiva and cornea are the first line of defense of the eye, which are the inevitable pathways for the application of various eye drops, and are also the sites of toxic damage of eye drops. The ocular surface toxicity of eye drops is often non-specific, mainly damaging the conjunctiva and cornea. 134 cases (13.09%) out of 1024 ophthalmology referrals were observed by Wilson to be drug toxicity reactions, of which the most common conjunctival reactions were toxic papillae, follicles and delayed allergic reactions, and conjunctival scarring could occur in severe cases. Conjunctival papillae are generally small and can occur in both the upper and lower lid conjunctiva; conjunctival follicles occur mainly in the lower lid or lower dome conjunctiva. Based on the proliferative reaction of the conjunctival papillae, pseudophakic aspergillosis and drug-induced ocular aspergillosis can occur; the former manifests as an inflammatory conjunctival reaction, persistent epithelial defects, and conjunctival scar formation, which stops progressing when toxic drugs are discontinued; the latter continues to develop after discontinuation of toxic drug use. Corneal toxicity is manifested by superficial punctate corneal epithelial lesions, which are heavier below the nose. With the prolongation of drug use and the intensification of toxicity, punctate staining can be diffuse or lamellar, and some patients can show pseudo-dendritic corneal ulcers, which are characterized by tiny dendrites that can appear in multiple places at the same time, without the typical dendritic end expansion characteristic of herpes simplex dendritic corneal ulcers, and corneal melting and perforation in severe cases. Some studies have reported these symptoms with NSAIDs, and although it is not certain that topical application of NSAIDs is the direct cause of corneal melting, ophthalmologists must be cautious when using these drugs in patients with dry eyes, cataracts, and post-keratoconus surgery and incomplete corneal epithelium.