The Laryngoscope
-
A critical step in thyroidectomy involves definitive identification of the recurrent laryngeal nerve (RLN). Using the laryngeal mask airway, identification of the RLN can be facilitated by stimulation of the nerve while monitoring vocal cord movement with a fiberoptic laryngoscope. We present this technique as an effective and safe means to identify the RLN during thyroid surgery, with significant advantages over existing techniques in appropriately selected patients. ⋯ Laryngeal mask airway anesthesia with intraoperative fiberoptic laryngoscopy to identify the RLN is effective and safe in carefully selected patients. Advantages include decreased postoperative throat discomfort, absence of coughing during emergence from anesthesia, and elimination of the possibility of vocal cord mobility impairment secondary to RLN ischemia from the endotracheal tube balloon. In addition, this technique is applicable in operations besides thyroid surgery, in which definitive identification of the RLN is indicated.
-
Oxidative stress plays a substantial role in the genesis of noise-induced cochlear injury that causes permanent hearing loss. We present the results of three different approaches to enhance intrinsic cochlear defense mechanisms against oxidative stress. This article explores, through the following set of hypotheses, some of the postulated causes of noise-induced cochlear oxidative stress (NICOS) and how noise-induced cochlear damage may be reduced pharmacologically. 1) NICOS is in part related to defects in mitochondrial bioenergetics and biogenesis. Therefore, NICOS can be reduced by acetyl-L carnitine (ALCAR), an endogenous mitochondrial membrane compound that helps maintain mitochondrial bioenergetics and biogenesis in the face of oxidative stress. 2) A contributing factor in NICOS injury is glutamate excitotoxicity, which can be reduced by antagonizing the action of cochlear -methyl-D-aspartate (NMDA) receptors using carbamathione, which acts as a glutamate antagonist. 3) Noise-induced hearing loss (NIHL) may be characterized as a cochlear-reduced glutathione (GSH) deficiency state; therefore, strategies to enhance cochlear GSH levels may reduce noise-induced cochlear injury. The objective of this study was to document the reduction in noise-induced hearing and hair cell loss, following application of ALCAR, carbamathione, and a GSH repletion drug D-methionine (MET), to a model of noise-induced hearing loss. ⋯ These data lend further support to the growing body of evidence that oxidative stress, generated in part by glutamate excitotoxicity, impaired mitochondrial function and GSH depletion causes cochlear injury induced by noise. Enhancing the cellular oxidative stress defense pathways in the cochlea eliminates noise-induced cochlear injury. The data also suggest strategies for therapeutic intervention to reduce NIHL clinically.