Time of ureteral ejection of sodium fluorescein in the cystoscopic assessment of ureteral patency in patients undergoing total laparoscopic hysterectomy

Objective: To evaluate the time of ureteral ejection of intravenous sodium fluorescein in the assessment of ureteral patency in patients undergoing total laparoscopic hysterectomy (TLH). Material and Methods: Fifty-four women undergoing TLH were studied in a public teaching hospital in Culiacan, Sinaloa, Mexico. They underwent cystoscopic evaluation of ureteral patency after intravenous administration of 100 mg of sodium fluorescein. The present study analyzed the time elapsed in minutes from the intravenous administration of fluorescein to the outflow of stained urine by one or both ureteral meatus, the degree of urine staining, and the impact of body mass index (BMI) (BMI; normal, overweight, and obesity) on ejection time. Results: The overall average time elapsed to visualize the ejection of fluorescein through at least one ureteral meatus was 7.5 minutes [95% confidence interval (CI): 6.3-8.7]. There were no significant differences in the time of ureteral ejection of fluorescein taking BMI into account (p=0.579), with a mean time for normal BMI of 8.1 minutes (95% CI: 5.1-11.2), for overweight of 7.0 minutes (95% CI: 5.5-8.5), and for obesity of 7.8 minutes (95% CI: 5.3-10.3). Conclusion: Intravenously administered 10% sodium fluorescein dye is rapidly eliminated and strongly stains urine, which makes it useful for identifying ureteral patency during cystoscopy after TLH. Fluorescein excretion is not affected by patient BMI.

Corrigendum: The Blood-Brain Barrier Breakdown During Acute Phase of the Pilocarpine Model of Epilepsy Is Dynamic and Time-Dependent.

[This corrects the article DOI: 10.3389/fneur.2019.00382.].

The Blood-Brain Barrier Breakdown During Acute Phase of the Pilocarpine Model of Epilepsy Is Dynamic and Time-Dependent.

The maintenance of blood-brain barrier (BBB) integrity is essential for providing a suitable environment for nervous tissue function. BBB disruption is involved in many central nervous system diseases, including epilepsy. Evidence demonstrates that BBB breakdown may induce epileptic seizures, and conversely, seizure-induced BBB disruption may cause further epileptic episodes. This study was conducted based on the premise that the impairment of brain tissue during the triggering event may determine the organization and functioning of the brain during epileptogenesis, and that BBB may have a key role in this process. Our purpose was to investigate in rats the relationship between pilocarpine-induced status epilepticus (SE), and BBB integrity by determining the time course of the BBB opening and its subsequent recovery during the acute phase of the pilocarpine model. BBB integrity was assessed by quantitative and morphological methods, using sodium fluorescein and Evans blue (EB) dyes as markers of the increased permeability to micromolecules and macromolecules, respectively. Different time-points of the pilocarpine model were analyzed: 30 min after pilocarpine injection and then 1, 5, and 24 h after the SE onset. Our results show that BBB breakdown is a dynamic phenomenon and time-dependent, i.e., it happens at specific time-points of the acute phase of pilocarpine model of epilepsy, recovering in part its integrity afterwards. Pilocarpine-induced changes on brain tissue initially increases the BBB permeability to micromolecules, and subsequently, around 5 h after SE, the BBB breakdown to macromolecules occurs. After BBB breakdown, EB dye is captured by damaged cells, especially neurons, astrocytes, and oligodendrocytes. Although the BBB permeability to macromolecules is restored 24 h after the start of SE, the leakage of micromolecules persists and the consequences of BBB degradation are widely disseminated in the brain. Our findings reveal the existence of a temporal window of BBB dysfunction in the acute phase of the pilocarpine model that is important for the development of therapeutic strategies that could prevent the epileptogenesis.

Skull Base Meningiomas and Cranial Nerves Contrast Using Sodium Fluorescein: A New Application of an Old Tool.

Objective The identification of cranial nerves is one of the most challenging goals in the dissection of skull base meningiomas. The authors present an application of sodium fluorescein (SF) in skull base meningiomas with the purpose of improving the identification of cranial nerves. Design A prospective study within-subjects design. Setting Hospital Ernesto Dornelles, Porto Alegre, Brazil. Participants Patients with skull base meningiomas. Main Outcomes Measures Cranial nerve identification. Results The group of nine meningiomas was composed of one cavernous sinus, three petroclival, one tuberculum sellae, two sphenoid wing, one olfactory groove, and one temporal floor meningioma. The SF enhancement in all tumors was strong, and the contrast with cranial nerves clearly evident. There were one definite olfactory nerve deficit, one transient abducens deficit, and one definite hemiparesis. All lesions were resected (Simpson grades 1 and 2). The analysis of the difference of the delta SF wavelength between the meningiomas and cranial nerve contrast was performed by the Wilcoxon signed rank test and showed p = 0.011. Conclusions The contrast between the enhanced meningiomas and cranial nerves was evident and assisted in the visualization and microsurgical dissection of these structures. The anatomical preservation of these structures was improved using the contrast.

Use of sodium fluorescein in skull base tumors.

OBJECTIVE: The authors present this study using sodium fluorescein (SF) to enhance skull base tumors by performing a quantitative digital analysis of tumor enhancement. The purpose of this study is to observe the grade of SF enhancement by the tumors. METHODS: A prospective experiment within-subjects study design was performed which included six patients with skull base lesions. Digital pictures were taken before and after the SF systemic injection, using the same light source of the microsurgical field. The pictures were analyzed by computer software which calculated the wavelength (WL) of the SF pre- and post-injection. RESULTS: THE GROUP OF TUMORS WAS AS FOLLOWS: one vestibular schwannoma, three meningiomas, one craniopharyngioma and one pituitary adenoma. The SF enhancement in all tumors was strongly positive. The digital analysis of the pictures, considering the SF WL pre- and post-injection, presented P = 0.028 (Wilcoxon T test). CONCLUSIONS: The enhancement of the tumors by SF was consistent and evident. The introductory results suggest the possibility of using SF as an adjuvant tool for the skull base surgery. Further studies should test the clinical application of the SF in skull base tumors.