Background: Patients with dacryocystitis should be treated for their infection by endoscopic dacryocystorhinostomy (EN-DCR) before any intraocular surgery. However, there is no unified standard for the specific time interval between the two surgeries. This study aimed to determine the appropriate interval for intraocular surgery in patients with previous EN-DCR for chronic dacryocystitis.

Methods: The medical files of all patients who underwent intraocular surgery after EN-DCR surgery in our hospital from 2016 to 2019 were reviewed. The EN-DCR data of patients undergoing intraocular surgery at different time intervals and the incidence of endophthalmitis after intraocular surgery were compared.

Results: A total of 116 patients (92 females and 24 males, mean age 64.06±7.78 years) underwent EN-DCR and intraocular surgery met the inclusion criteria. The interval between EN-DCR and intraocular surgery varied from 5–475 days. The number of patients undergoing cataract surgery after EN-DCR is the largest (75, 64.7%). All patients (100%) who had previously undergone EN-DCR did not develop endophthalmitis infection after intraocular surgery at a follow-up of 12 months.

Conclusions: For patients with dacryocystitis who have undergone EN-DCR surgery, there is no time limit when choosing the timing of intraocular surgery. For patients requiring intraocular surgery, operation can be arranged as soon as possible to solve their problems as long as the patients had patency on lacrimal passage irrigation and no secretions.

Background: To investigate the effect of sirolimus (SRL) eye drops on acute alkali-burn-induced corneal neovascularization (CNV) and explore its possible mechanism.

Methods: A total of 57 male Sprague-Dawley rats weighing 160–180 g were randomly divided into four groups including a normal control group (NC group, n=12), an untreated alkali-burned model control group (MC group, n=15), a blank eye drop treatment group (BT group, n=15), and an SRL eye drop treatment group (ST group, n=15). Corneal inflammation and CNV were observed and scored under a slit-lamp microscope 3, 7, and 14 days after alkali exposure. Three rats were randomly sacrificed in each group before modeling and 3, 7, 14 days after modeling, and the corneas of right eyes were harvested for Western blotting to compare the expression levels of VEGFR2 and caspase-3.

Results: Corneal inflammation scoring showed that the corneal edema and conjunctival congestion were severe in the MC, BT, and ST groups 1 day after alkali exposure but were alleviated at day 3. The corneal transparency was significantly higher in the ST group than in the MC and BT groups at days 7 (F=9.77, P<0.05) and 14 (F=5.81, P<0.05). At day 1, the corneal limbal vascular network was markedly filled. SNV was obvious at days 3, 7, and 14. The new blood vessels were shorter and sparser in the ST group than in the MC and BT groups, and the CNV scores showed significant differences among these groups (day 3: F=8.60, P<0.05; day 7: F=11.40, P<0.05; and day 14: F=41.59, P<0.01). Western blotting showed that the expressions of VEGFR2 and caspase-3 were low before modeling and showed no significant difference among the different groups (F=0.52, P>0.05; F=0.98, P>0.05). The corneal expression of VEGFR2 became significantly higher in the MC and BT groups than in the ST group 3, 7, and 14 days after alkali exposure, and there were significant differences in relative gray-scale values among these groups (day 3: F=32.16, P<0.01; day 7: F=85.96, P<0.01; day 14: F=57.68, P<0.01). The increase in the corneal expression of caspase-3 was significantly larger in the ST group than in the MC and BT groups at days 3, 7, and 14, and there were significant differences in relative gray-scale values among groups (day 3: F=32.16, P<0.01; day 7: F=53.02, P<0.01; day 14: F=38.67, P<0.01).

Conclusions: SRL eye drops can alleviate acute alkali-burn-induced corneal inflammation and inhibit alkali-burn-induced CNV in rat models. It can reduce VEGFR2 expression and increase caspase-3 expression in the corneal tissue, which may contribute to the inhibition of alkali-burn-induced CNV.