Der Anaesthesist
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Imaging techniques with high spatial and temporal resolution (PET,fMRI, MEG) provide detailed information about the brains' processing of pain. Structures detected by these techniques are not understood as pain centers but as nodal points of a dynamic network which is influenced by physiological and psychological input. Imaging techniques can be used for the investigation of different pain components. ⋯ Until now only little is known about cortical structures mediating the cognitive pain component. In chronic pain the cortical and subcortical processing of nociceptive input is presumably modified. Reorganization in the primary somatosensory cortex is presented as an example of neuronal plasticity induced by chronic pain.
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Clinical Trial
[Quantification of blood loss. How precise is visual estimation and what does its accuracy depend on?].
Estimation of blood loss is a difficult task. Apart from measuring the volume of the suctioned blood the anaesthetist has to make a visual estimate of blood shed on the floor, spread in the surgeons' gowns and gloves and hidden in drapes and sponges at nearly every operation. We were interested in how exact visual estimation of blood loss can be and what factors influence accuracy and precision of the visual estimate. ⋯ Obviously our capability to estimate lost blood volumes is more influenced by our belonging to a professional group than by our professional experience. Do we not learn by experience? Diluted blood is overestimated, whereas in some other typical scenes blood loss is grossly underestimated. Simulations such as this one may improve our estimation capabilities and thus result in better patient care in the OR.
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Case Reports
[Epileptoform EEG activity: occurrence under sevoflurane and not during propofol application].
In a 62-year-old female patient without a history of epileptic seizures EEG monitoring (EEG monitor: Narcotrend) was routinely performed during propofol/remifentanil and during sevoflurane/remifentanil/nitrous oxide anaesthesia. In the first course of anaesthesia after a bolus of propofol 1% a continuous EEG slowing was followed by a burst suppression pattern without occurrence of epileptiform activity throughout this sequence. During the second course of anaesthesia the sevoflurane concentration was increased from 2 to 8 % by volume. After 5 min epileptiform activity appeared in the EEG at an endtidal concentration of 5.9% by volume.