Journal of anesthesia
-
Journal of anesthesia · Oct 2018
Randomized Controlled Trial Comparative StudyAnalgesic effects of methadone and magnesium following posterior spinal fusion for idiopathic scoliosis in adolescents: a randomized controlled trial.
To provide optimal conditions for neurophysiological monitoring and rapid awakening, remifentanil is commonly used during pediatric spinal surgery. However, remifentanil may induce hyperalgesia and increase postoperative opioid requirements. We evaluated the potential of methadone or magnesium to prevent remifentanil-induced hyperalgesia. ⋯ With the dosing regimens in the current study, the only benefit noted with methadone was a decrease in perioperative opioid requirements. However, given the potential for hyperalgesia with the intraoperative use of remifentanil, adjunctive use of methadone appears warranted.
-
Journal of anesthesia · Oct 2018
Predictors for sustained new-onset atrial fibrillation in critically ill patients: a retrospective observational study.
Although new-onset atrial fibrillation (AF) is frequently observed in the intensive care unit (ICU), the incidence and predictors for sustained new-onset AF have not been investigated, except for cardiac surgery patients. We have evaluated potential predictors for sustained new-onset AF in a mixed ICU. ⋯ These predictors might be useful in future interventional studies to identify patients who are likely to sustain new-onset AF.
-
Journal of anesthesia · Oct 2018
The tendinous septum of the semispinalis capitis muscle spatially separates the dorsal ramus between C3 and C4.
Local anesthetic injection into the medial head of the semispinalis capitis muscle can anesthetize the greater occipital nerve (GON) and third occipital nerve (TON) simultaneously (greater and third occipital nerve block: GTO block). Alternatively, inter-semispinal plane (ISP) block can anesthetize the dorsal rami of the cervical spinal nerves from C4 to T4. The GON, TON, and the dorsal rami of the inferior level cannot be blocked with a single injection. ⋯ Both dyes were clearly separated by the tendinous septum running obliquely inside the semispinalis capitis muscle (SCA). The tendinous septum of the SCA may have a relatively strong connection with the dorsal edge of the semispinalis cervicis muscle, and this structure may stem the injectate spread. Therefore, the GON and TON, running through the medial head of the SCA, and the dorsal rami of the inferior level are spatially separated by the tendinous septum, and cannot be blocked with a single injection.
-
Journal of anesthesia · Oct 2018
Remifentanil suppresses increase in interleukin-6 mRNA in the brain by inhibiting cyclic AMP synthesis.
Neuronal inflammation is caused by systemic inflammation and induces cognitive dysfunction. IL-6 plays a crucial role in therapies for neuronal inflammation and cognitive dysfunction. Remifentanil, an ultra-short-acting opioid, controls inflammatory reactions in the periphery, but not in the brain. Therefore, the anti-inflammatory effects of remifentanil in neuronal tissue and the involvement of cAMP in these effects were investigated in the present study. ⋯ Remifentanil suppressed increase in IL-6 mRNA levels in the brain in an inflammatory state, and this effect may be attributed to its direct action on neuronal cells through the inhibition of intracellular cAMP rather than corticosterone.
-
Journal of anesthesia · Oct 2018
Dexmedetomidine mitigates sevoflurane-induced cell cycle arrest in hippocampus.
Epidemiologic studies suggest the possibility of a modestly elevated risk of adverse neurodevelopmental outcomes in children exposed to anesthesia during early childhood. Sevoflurane is widely used in pediatric anesthetic practice because of its rapid induction and lower pungency. However, it is reported that sevoflurane leads to the long-term cognitive impairment. Some evidence revealed that the selective α2-adrenoreceptor agonist dexmedetomidine (DEX) exerts neuroprotective effects in various brain injury models of animals. But the role of DEX on sevoflurane-induced neuro-damage remains elusive. ⋯ Sevoflurane suppressed neuron cell proliferation via inhibiting the expression of BDNF and TrkB, and DEX relieved the neurotoxicity induced by sevoflurane via α2 adrenergic receptor. These findings provided new evidence that DEX exerted as a neuroprotective strategy in sevoflurane-induced neuro-damage, and provided new basis for the clinical application of DEX.