Der Anaesthesist
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Pre-emptive analgesia is based on the idea that analgesia initiated before a nociceptive event will be more effective than analgesia commenced afterwards, and that its effects will outlast the pharmacological duration of action of the analgesic used. The idea of pre-emptive analgesia is based upon experimental neurophysiological work demonstrating that afferent nociceptive impulses result in alterations of central nervous system function. These changes, most easily elicited by C-fibre afferents, particularly affect the spinal dorsal horn. ⋯ Clinical studies have so far only used short-term analgesia. To permit extrapolation from the experimental to the clinical situation, pre-emption in the surgical context must correspond adequately to the duration and extent of the nociception involved. Studies of pre-emptive analgesia in a clinically relevant form, i.e. where nociception and analgesia are correctly matched, are called for.
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Pharmacological praemedication. In patients receiving regional anaesthetics induction of deep sedation prior to the performance of the block should be avoided because during the installation of the nerve block it is an advantage to have a cooperative patient. Adequate anxiolytic effects are achieved by oral administration of chloracepate (0.3-0.5 mg/kg body weight). ⋯ Pulse oxymetric monitoring of the potentially endangered respiratory function is obligatory. The individual transition to general anaesthesia is not easy to determine. Therefore, it is essential that, whenever the need arises, intubation and mechanical ventilation intervention procedures be carried out immediately.
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The goal of therapy in patients with severe head injury is to avoid secondary brain damage. Analgesia and sedation are an essential part of the therapy, and several drugs are in current use. However, few controlled clinical trials have been performed so far, and none of these drugs has proved to be superior. ⋯ More clinical studies are warranted. Gamma-hydroxybutyrate (GHB) is a physiological substance, which has only sporadically been investigated for sedation in patients with head trauma. The few available studies show beneficial res
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Cerebral blood flow autoregulation, CO2 reactivity and the pressure-volume relationship may be impaired or abolished in patients with intracranial mass lesions, brain trauma, cerebral vasospasm or increased cerebral elastance. Sedatives, analgetics, and anesthetics may induce major changes in cerebral blood flow, cerebral metabolism and intracranial pressure (ICP). The inadequate use of these drugs may aggravate the preexisting intracranial pathology and may worsen outcome. ⋯ Ketamine may increase ICP specifically in subjects with spontaneous ventilation. With mechanical hyperventilation and constant systemic hemodynamics, ketamine fails to increase ICP in most of the patients. Alpha-2-adrenergic agonists produce no significant changes in ICP, although there may be a transient decrease in ICP with lower doses.
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AIMS AND PATHOPHYSIOLOGY: Intensive care patients are exposed to a number of noxious stimuli. They require individual analgesia and sedation to reduce and moderate the stress response to endogenous and exogenous stressors. In patients with SIRS (systemic inflammatory response syndrome), pathophysiological conditions with multiple organ dysfunction or failure demand special efforts and a specific regimen of analgosedation. The main goals are the absence of cardiocirculatory depression or, if at all possible, cardiocirculatory stabilization, absence of negative pulmonary, renal, hepatic and immunological side effects, preservation of a moderate stress response, and vertical and horizontal control appropriate to the clinical situation.