Der Anaesthesist
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Sepsis and SIRS are characterised by increased hepatosplanchnic blood flow and oxygen transport due to sepsis-associated hypermetabolism with enhanced oxygen uptake. Regional hypermetabolism may be linked with a mismatch of oxygen availability and demand potentially resulting in a pathological splanchnic oxygen uptake/supply dependency. ⋯ The response of splanchnic haemodynamics and oxygen kinetics, however, to therapeutic interventions does not necessarily parallel the different metabolic pathways. Therefore, understanding of both tissue perfusion and oxygenation as well as metabolism is pivotal for evaluating the effects of different therapeutic strategies in intensive care medicine.
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Clinical characteristics of neuropathic pain, i.e. pain after nervous system lesions, are burning spontaneous pain, shooting pain attacks and evoked pains. Partly interacting pathophysiological mechanisms at the peripheral and central nervous system may be responsible for initiation and maintenance of chronic neuropathic pain. (1) Peripheral nociceptive fibers can be abnormally sensitized. (2) Central nociceptive second order neurons in the spinal cord dorsal horn can also be sensitized, i.e. they are hyperexcitable and start responding to non-noxious stimuli. (3) Degeneration of nociceptive neurons may trigger anatomical sprouting of low-threshold mechanosensitive terminals to central nociceptive neurons and may subsequently induce synaptic reorganization in the dorsal horn. By this mechanism activity in mechanosensitive neurons may be perceived as painful. (4) Peripheral nerve injury may induce a pathological interaction of the nociceptive system and the efferent sympathetic system. ⋯ Therefore, a thorough analysis of sensory symptoms may reveal the underlying mechanisms that are mainly active in a particular patient. In the next step novel drugs will be developed that address specifically the relevant mechanism combination. Drug therapies that are available today include NSAIDS, opioids, tricyclic antidepressants, anticonvulsives (carbamazepine, gabapentin), GABA-agonists, Capsaicin and NMDA-antagonists.
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Residual neuromuscular block is a major risk factor behind critical events in the immediate postoperative period. Residual weakness due to muscle relaxants is seen in more than thirds of postoperative patients with ventilatory failure and hypoxia. Residual neuromuscular block should therefore be regarded as a serious adverse event in the same way as we regard ventilatory depression due to opioids and anaesthetic agents. This presentation aim to clarify our present knowledge and shortcomings in the field of residual neuromuscular blockade.