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 All withdrawn probes were intact.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.

Insertion of a preloaded Monoka™ stent for congenital nasolacrimal obstruction: Intraoperative observations. A preliminary study.

STUDY OBJECTIVE: To study the intraoperative deployment of a pre-loaded probe for a "pushed" monocanalicular nasolacrimal intubation. STUDY DESIGN: Non-randomized study of consecutive cases. MATERIALS AND METHODS: Description: A classical Monoka™ silicone stent with the silicone tube attached at right angles to the punctal plug is contained entirely inside an introducer connected to a piston. Insertion: The procedure begins with intubation of the nasolacrimal duct with the metallic introducer. Traction on the piston retracts the metallic introducer inside the handpiece. This relative shortening progressively ejects the stent, starting with its free end at the bottom of the introducer. The operation was observed endoscopically under single-blind conditions. RESULTS: Twenty-eight preloaded Monoka™ stents were placed consecutively, in 28 congenital nasolacrimal duct intubations in 22 patients (28 sides). Endoscopic examination showed that the free part of the stent was progressively ejected from the introducer during retraction of the piston. Insertion of this pushed stent into the nasal cavity was effective in 23/28 cases (82.1%). A total of 28 preloaded stent insertions were attempted and 23 were correctly deployed. DIFFICULTIES ENCOUNTERED: At the end of nasolacrimal duct intubation, contact between the punctal plug and the lacrimal punctum was problematic in four cases (4/28=14.2%). At the beginning of stent placement, premature ejection of the punctal plug within the end of the introducer occurred in five cases (5/28=17.8%). These five stents failed to insert properly into the nasal cavity. At the end of insertion, retention of the punctal plug in the introducer occurred in two cases (2/28=7.1%). COMPLICATIONS: No cases of intraoperative or postoperative epistaxis were observed. CONCLUSIONS: Intraoperative nasal endoscopy validated the concept of the preloaded Monoka stent and its deployment. Reproducibility and improved reliability may require a change in stenting technique and a design modification.

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.

Pilocarpine toxicity in retinal ganglion cells.

PURPOSE: Muscarinic agents reduce intraocular pressure by enhancing aqueous outflow, probably by stimulating ciliary muscle contraction. However, pilocarpine is a well characterized neurotoxin and is widely used to generate animal seizure models. It was therefore investigated whether pilocarpine was also toxic to retinal ganglion cells. METHODS: Dissociated whole retinal preparations were prepared from postnatal day 16 to 19 rats. Retinal ganglion cells had been previously back-labeled with a fluorescent tracer. Retinal cells were incubated with pilocarpine, lithium, and inositol derivatives, and viability of the retrogradely labeled retinal ganglion cells was assayed after 24 hours. RESULTS: Pilocarpine was toxic to retinal ganglion cells in a dose-dependent fashion. This toxicity was potentiated by lithium and blocked by epi- and myo-inositol. CONCLUSIONS: Pilocarpine is toxic to retinal ganglion cells in a mixed culture assay. This toxicity appears to depend on the inositol pathway and is similar to its mode of action in other neurons. However, 0.4 mM pilocarpine (the lowest concentration that did not affect ganglion cell survival) is roughly 1000-fold higher than the vitreal concentration and 20-fold higher than the scleral concentration that can be obtained with topical administration of 2% pilocarpine in the rabbit eye.

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.