Seminars in anesthesia最新文献

Adrenergic receptors appear to play an important role in the modulation of pain. There is now abundant evidence that activation of adrenergic receptors can, in certain circumstances, generate impressive analgesic effects. However, under other circumstances, adrenergic receptors can contribute to chronic neuropathic pain and hyperalgesia. This review will focus on the beneficial effects of adrenergic pain modulation, and the circumstances when this modulation appears to magnify pain. This review will also address controversies surrounding how these two opposing processes occur via the same mediators.

Cyclic adenosine monophosphate (cAMP) is an important intracellular second messenger whose levels are tightly regulated within intracellular subdomains. Generation, detection, and degradation of cAMP is influenced by signaling complexes localized to specific regions of the cell by scaffolding proteins, such as muscle A kinase-anchoring protein (mAKAP). The distribution of cAMP within myocytes differs after β1 adrenergic receptor (β1AR) activation relative to β2AR activation as a result of differences in the interaction of these receptor subtypes with signaling complexes. β1AR stimulation generates a global increase in cAMP, whereas β2AR stimulation elicits a cAMP increase only within restricted areas of the cell. Phosphodiesterase 4D (PDE4D) plays an important role in this process.

Understanding the neuronal mechanism of general anesthesia both helps and benefits from research into the neurobiological basis of consciousness. Although several theories have been proposed, current evidence from sensory electrophysiology, event-related potentials, and functional brain imaging suggests that the failure of conscious perception at a critical depth of anesthesia may best be interpreted as “information received but not perceived” due to the disintegration of cortical information processing. Cortico-cortical and thalamocortical information transfer may depend on the synchronization or coherence of gamma oscillations that may be suppressed by general anesthetic agents; however, the exact mechanism of these effects is yet unclear. The extent of thalamic involvement in the cortico-cortical disintegration of information processes in anesthesia needs further investigation. It is likely that different anesthetic agents affect different neuronal pathways in their action to produce unconsciousness. A common effect of several volatile anesthetic agents may be the suppression of recurrent feedback signaling between cortical sensory and higher association regions. Elucidation of the neurofunctional systems involved in anesthetic-induced unconsciousness is among the important future challenges for anesthesia research.

Delirium is a neuropsychiatric syndrome of disordered consciousness and cognition whose hallmark is a gross deficit of attention. A frequent complication in critically ill medical and surgical patients in the general hospital, especially those in the intensive care unit, delirium should be considered a state of acute brain failure, alongside other types of organ failure. It is caused not by geographic assignment to the intensive care unit but by diverse medical and surgical conditions and their treatments. As such, its definitive treatment is reversal of these underlying medical and surgical problems, and minimization or outright discontinuation of offending therapies.

Unintended awareness with recall is estimated to occur during about 1 in every 750 general anesthetics. Patients experiencing intraoperative awareness may develop symptoms of post-traumatic stress disorder. To understand how awareness during general anesthesia occurs, its risk factors, strategies for prevention, and the potential role of various drugs used during anesthesia, I begin with a brief review of research on how and where anesthetics suppress different central nervous system functions. I critique the major clinical studies on intraoperative awareness, discussing a number of uncertainties arising from limitations in the scientific methods applicable in this setting. Controversies in this topic are due in part to inconsistent and inadequate data on the impact of awareness events on patients, and divergent views about the value of encephalographic monitoring. I also outline strategies for preventing intraoperative awareness and managing cases when they occur.

The current clinical practice of balanced anesthetic technique has obscured many of the observed physiologic parameters that once indicated the depth of anesthesia. Consequently, there is an increased need for assessing anesthetic effects on consciousness with processed electroencephalography (EEG). This article discusses the concept of anesthetic depth and the principles of EEG-based monitors, with a particular focus on bispectral analysis.

With the introduction of mechanical ventilation, patients suffering neurological catastrophes who previously would have perished are now often systemically supported, thereby bringing the concept of brain death into existence. Brain death is defined as the irreversible loss of the clinical function of the entire brain, including the brainstem, and may result from a number of causes. The correct diagnosis of brain death is essential from several standpoints: to ensure that unnecessary treatments and procedures are not performed, to provide a sense of finality for families concerned about prognosis, to preserve vital critical care resources, and to allow for the possibility of organ donation. The concept of brain death is accepted in most countries and cultures, but ethical arguments remain regarding certain concepts, such as the concept of isolated brainstem death or higher-brain death. This review will assist the clinician in understanding the concepts behind brain death, the proper technique for determination, and the areas of controversies that remain.

Fetal anatomic study demonstrates that, by 20 weeks gestation, the requisite cytoarchitecture believed to be necessary for consciousness (eg, the thalamus and associated subcortical structures) and its proper connections are in place and accompanied by a coordinating electroencephalogram (EEG) rhythm. Given the structural and functional integrity of these portions of the brain, it is reasonable to conclude that consciousness is at least possible from this point in fetal development. If a more stringent threshold for continuous EEG activity is required, then it would appear that by 30 weeks gestation, consciousness is possible. If we are to accept that consciousness is possible by 20 weeks (or, more conservatively, 30 weeks), then it also would appear possible that fetuses could experience something approximating “pain.” The mere possibility of consciousness and an experience of pain (however rudimentary) would appear to mandate the provision of appropriate anesthesia and analgesia to fetuses undergoing surgical intervention.

A significant number of neonates are born with conditions requiring surgery or develop such problems after birth. By reviewing the pathophysiology, clinical presentation, and treatment of neonatal cardiovascular compromise, this chapter highlights the problems specific to the cardiovascular system in neonates requiring surgery. Finally, the chapter describes the most common and challenging neonatal surgical disease entities with a primary emphasis on their pre-operative, surgical, and post-operative cardiovascular management.

The anomalies associated with Down syndrome present some interesting challenges for the anesthesiologist. Airway difficulties, a potentially unstable cervical spine, and a high incidence of congenital heart disease all require careful consideration. Impaired immune function predisposes to chronic infections and demands attention to asepsis during invasive procedures. Finally, there is the very considerable challenge of providing kind and considerate anesthesia care and effective postoperative pain management for a cognitively impaired child.