Confirmation of success rate of landmark-based caudal blockade in children using ultrasound: A prospective analysis.

BACKGROUND: Caudal epidural anesthesia is a frequently performed regional anesthesia block in infants and young children. Traditional landmark-based blind needle insertion remains the norm with no immediate, objective method to determine the presence of local anesthetic in the epidural space. Increasingly, ultrasound-imaging is used in pediatric regional anesthesia with demonstrated improvements in block efficacy and efficiency. The value of ultrasound-imaging in confirming success rate of traditional caudal placement is not well defined. AIM: To assess the success rate of conventional landmark-based caudal technique using ultrasound-imaging. METHODS: Prospective observational study of 30 children ages 1 month to 7 years undergoing surgical procedures with consent for caudal blockade. Provider success rate of caudal blockade placed by landmark technique was measured using ultrasound-imaging of needle tip and local anesthetic flow in the epidural space. RESULTS: Ultrasound-imaging demonstrated 80% success to correct positioning of the needle tip and local anesthetic in the epidural space. Failure was associated with decreasing experience and presence of anatomic variances. All improperly positioned needles were subsequently successfully positioned using real-time ultrasound-imaging. Mean time for confirmatory ultrasound-imaging (SD; range) was 1 minute (0.3; 1-3). CONCLUSION: The use of ultrasound-imaging can be used to identify proper needle placement in the sacral epidural canal and facilitate subsequent corrected placement.

Different mechanisms preclude mutant CLDN14 proteins from forming tight junctions in vitro.

Mutations in claudin 14 (CLDN14) cause nonsyndromic DFNB29 deafness in humans. The analysis of a murine model indicated that this phenotype is associated with degeneration of hair cells, possibly due to cation overload. However, the mechanism linking these alterations to CLDN14 mutations is unknown. To investigate this mechanism, we compared the ability of wild-type and missense mutant CLDN14 to form tight junctions. Ectopic expression in L mouse fibroblasts (LM cells) of wild-type CLDN14 protein induced the formation of tight junctions, while both the c.254T>A (p.V85D) mutant, previously identified in a Pakistani family, and the c.301 G>A (p.G101R) mutant, identified in this study through the screen of 183 Spanish and Greek patients affected with sporadic nonsyndromic deafness, failed to form such junctions. However, the two mutant proteins differed in their ability to localize at the plasma membrane. We further identified hitherto undescribed exons of CLDN14 that are utilized in alternative spliced transcripts. We demonstrated that different mutations of CLDN14 impaired by different mechanisms the ability of the protein to form tight junctions. Our results indicate that the ability of CLDN14 to be recruited to these junctions is crucial for the hearing process.