The effect of lidocaine on apoptotic neurodegeneration in the developing mouse brain / 대한마취과학회지

BACKGROUND: General anesthetics induce neuronal apoptosis in the immature brain. Regional anesthesia using local anesthetics can be an alternative to general anesthesia. Therefore, this study investigated the possible effect of lidocaine on neuronal apoptosis. METHODS: Fifty-one 7-day-old C57BL6 mice were allocated into control (group C), lidocaine (group L), lidocaine plus midazolam (group LM) and isoflurane (group I) groups. Group C received normal saline administration. Groups L and LM were injected with lidocaine (4 mg/kg, subcutaneously) only and the same dose of lidocaine plus midazolam (9 mg/kg, subcutaneously). Group I was exposed to 0.75 vol% isoflurane for 6 h. After 6 h, apoptotic neurodegeneration was assessed using caspase-3 immunostaining and terminal deoxynucleotidyl transferase dUTP nick-end labelling (TUNEL) staining. RESULTS: For the entire brain section, neuronal cells exhibiting caspase-3 activation were observed more frequently in group I than in group C (P < 0.001). In the thalamus, apoptosis of group L was more frequent than that of group C (P < 0.001), but less freqent than that of groups LM and I (P = 0.0075 and P < 0.001, respectively). In the cortex, group I experienced more apoptosis than group L and C (all Ps < 0.001). On TUNEL staining, the difference in apoptosis between the lidocaine and control groups was marginal (P = 0.05). CONCLUSIONS: Lidocaine induced minimal apoptosis in the developing brain compared with isoflurane and lidocaine plus midazolam. However, we cannot fully exclude the possible adverse effect of subcutaneously administered lidocaine on the developing brain.

A Case of Wernicke's Encephalopathy in a Postoperative Patient with Parenteral Nutrition and Temporary Oral Feeding: A Case Report / 대한구급학회지

Wernicke's encephalopathy is an acute neurological disorder, caused by thiamine deficiency, which is clinically characterized by a triad of ophthalmoplegia, ataxia and disturbances of consciousness. Most frequently, the encephalopathy is a consequence of chronic alcoholism, but it may occur in other forms of malnutrition or malabsorption, such as in prolonged parenteral nutrition without the addition of thiamine, total gastrectomy, gastrojejunostomy, severe anorexia or hyperemesis gravidarum. Thiamine requirement increases during critical illness and in chronically depleted patients, and its supplementation may influence the outcome of the disease. We report a case of a 73-year-old man, who presented with recurred colon cancer, who was affected by Wernicke's encephalopathy while undergoing oral feeding and parenteral nutrition. This case suggests that we should be more aware of potential thiamine deficiency in critically ill patients, even those undergoing parenteral nutrition and temporary oral feeding.