Cochlear implantation under conscious sedation with local anesthesia; Safety, Efficacy, Costs, and Satisfaction.

OBJECTIVE: To evaluate the safety, efficiency, cost effectiveness, and satisfaction of patients undergoing cochlear implantation under conscious sedation versus general anesthesia. STUDY DESIGN: Retrospective case review of 20 patients who underwent cochlear implantation under conscious sedation which was compared to 20 age-matched patients where surgery was performed under general anesthesia. METHODS: Perioperative times, length of stay, anesthesia drug costs, postoperative complications, and patient satisfaction were compared between the two groups. RESULTS: Conscious sedation was associated with decreased drug costs, surgery time, and anesthesia time. Length of stay was significantly longer for patients undergoing general anesthesia. Patient satisfaction was superior with conscious sedation. Perioperative morbidity was not significantly different between the two groups. CONCLUSION: Conscious sedation for cochlear implantation is a safe, efficient, and cost-effective alternative to general anesthesia. The efficacy of conscious sedation for cochlear implant surgery may expand the treatment of profound hearing loss to the elderly who are deemed too sick for general anesthesia or are fearful of the cognitive or medical consequences of general anesthesia.

Tumor-specific microsatellite instability: do distinct mechanisms underlie the MSI-L and EMAST phenotypes?

Microsatellite DNA sequences display allele length alterations or microsatellite instability (MSI) in tumor tissues, and MSI is used diagnostically for tumor detection and classification. We discuss the known types of tumor-specific MSI patterns and the relevant mechanisms underlying each pattern. Mutation rates of individual microsatellites vary greatly, and the intrinsic DNA features of motif size, sequence, and length contribute to this variation. MSI is used for detecting mismatch repair (MMR)-deficient tumors, which display an MSI-high phenotype due to genome-wide microsatellite destabilization. Because several pathways maintain microsatellite stability, tumors that have undergone other events associated with moderate genome instability may display diagnostic MSI only at specific di- or tetranucleotide markers. We summarize evidence for such alternative MSI forms (A-MSI) in sporadic cancers, also referred to as MSI-low and EMAST. While the existence of A-MSI is not disputed, there is disagreement about the origin and pathologic significance of this phenomenon. Although ambiguities due to PCR methods may be a source, evidence exists for other mechanisms to explain tumor-specific A-MSI. Some portion of A-MSI tumors may result from random mutational events arising during neoplastic cell evolution. However, this mechanism fails to explain the specificity of A-MSI for di- and tetranucleotide instability. We present evidence supporting the alternative argument that some A-MSI tumors arise by a distinct genetic pathway, and give examples of DNA metabolic pathways that, when altered, may be responsible for instability at specific microsatellite motifs. Finally, we suggest that A-MSI in tumors could be molecular signatures of environmental influences and DNA damage. Importantly, A-MSI occurs in several pre-neoplastic inflammatory states, including inflammatory bowel diseases, consistent with a role of oxidative stress in A-MSI. Understanding the biochemical basis of A-MSI tumor phenotypes will advance the development of new diagnostic tools and positively impact the clinical management of individual cancers.