Preloaded Monoka (Lacrijet) and congenital nasolacrimal duct obstruction: Initial results.

STUDY OBJECTIVE: To study the performance of a pre-loaded Monoka stent in the management of congenital nasolacrimal duct obstruction (CNLDO). STUDY DESIGN: Non-randomized study of consecutive cases. MATERIALS AND METHODS: A preloaded classic Monoka silicone stent contained entirely inside its introducer (Lacrijet) was used to treat a consecutive series of subjects with CNLDO over an 11-month period (May 2019-March 2020). Only subjects with chronic symptomatic CNLDO were included. Subjects with intermittent tearing, canalicular pathology, trisomy 21, facial cleft, or history of lacrimal surgery were excluded. Intraoperative findings were recorded, including the degree and location of the nasolacrimal obstruction, successful metal to metal contact with the probe, any difficulties encountered by the Lacrijet device itself, procedure duration, tolerability of the fixation punctal plug, and finally, inspection of the stent after withdrawal of the inserter. Functional success was defined as disappearance of all symptoms of epiphora. RESULTS: A total of 45 preloaded Monoka Lacrijet stents (Lcj) were placed consecutively in 38 children. The mean age was 27.9 months (12-78 months). The mean procedural duration was 2.8minutes (range: 1-10min). The overall success with disappearance of all symptoms of epiphora was 88.8% (40/45). Surgery in cases of simple mucosal stenosis was successful in 92.2% (35/38) of cases, with a mean follow-up time of 7.9 months (range: 1 to 12 months). The duration of stent intubation was for this group was 32 days (range: 1-103). The surgical outcomes for the other 7 cases with more complex intraoperative findings are summarized in the publication. All withdrawn probes were intact. CONCLUSIONS: The Lacrijet stent system is a simple and reliable pushed intubation device for CNLDO in appropriately selected cases where bony stenosis of the canal is minimal.

Intralacrimal migration of Masterka® stents.

BACKGROUND: Tearing and conjunctivitis in children are commonly due to lacrimal drainage system obstruction. Congenital nasolacrimal obstruction is a common pathology treated by probing with or without silicone stent insertion, depending upon the age of the child. The silicone stent is self-retaining and placed for at least one month. Masterka® is a recent version of Monoka®, which may lead to the same surgical complications, such as intralacrimal migration. SUBJECTS AND METHODS: The medical records of two patients surgically treated with the Masterka® probe for nasolacrimal duct obstruction, who developed intralacrimal migration of the stent, were retrospectively reviewed and analyzed. A 41-month-old child and an 18-month-old child presented with disappearance of the silicone tube after 7 days and 2 years respectively. In the first case, the tube migrated completely within the lacrimal system and became externalized through the nose at 2 years, while in the second case, the Masterka® was retrieved through a canalicular approach. In both cases, infants had no further tearing. DISCUSSION: The frequency self-retaining stent disappearance is estimated at 15%. Among these cases, intralacrimal migration is only reported in 0.5% of cases. To prevent intralacrimal migration, the surgical technique must follow a certain number of rules. Management, based on residual epiphora, is discussed. CONCLUSION: Prevention of intralacrimal migration of self-retaining stents involves a rigorous analysis of the relationship between the meatus and the fixation head at the time of placement. After lacrimal intubation, scheduled monitoring is necessary to screen for stent disappearance. Management is based on clinical findings, anterior rhinoscopy and even exploratory canaliculotomy.

Lidocaine toxicity to rat retinal ganglion cells.

PURPOSE: To examine the effects of the local anesthetic, lidocaine, on rat retinal ganglion cells (RGC) in vitro and in a modified in vivo assay. METHODS: For in vitro experiments, RGC were dissociated from freshly harvested Long Evan's rat pup retinas. The RGC were incubated overnight with varying concentrations of lidocaine (0.5-12.0 mM). Surviving cells were assayed at 24 hours. In an in vivo assay, 7-day-old Long-Evans rat pups were anesthetized and 2 microl of lidocaine (final intraocular concentration: 0.03-15 mM) or vehicle was injected intravitreally. Intravitreal coinjection of nimodipine or MK801 (dizocilpine) were also performed in a subset of animals. A week after injection, rat pups were sacrificed and each retina removed, dissociated and plated separately. RGC survival was immediately assessed. Living RGC were identified on the basis of morphology and counted in a masked fashion. RESULTS: Lidocaine is toxic in a dose dependent fashion to RGC in vitro. Lower concentrations (0.5 mM and 1.0 mM) were non-toxic; 2.0, 6.0 and 12.0 mM lidocaine killed 25%, 88% and 99% of the RGC respectively. Intravitreal lidocaine was also toxic to RGC in a dose dependent fashion. Lidocaine concentrations of 3.0 mM, 7.5 mM and 15 mM killed 25%, 38% and 44% of the RGC. This effect was blocked by the simultaneous administration of either nimodipine or MK801. CONCLUSIONS: Lidocaine is toxic to RGC both in vitro and in vivo. This effect is blocked in vivo by the simultaneous administration of agents known to block glutamate mediated neuronal death, suggesting that excitotoxicity may be involved in this process.