European journal of emergency medicine : official journal of the European Society for Emergency Medicine
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This study was initiated to identify the incidence, risk factors and outcome predictors of patients admitted to hospital in the Netherlands because of accidental hypothermia. Information about these patients was available for study through the National Health Care Data Bank. Between 1987 and 1990, 612 accidental hypothermic patients were admitted: 185 hypothermic patients also suffered from submersion (HYPSUBS), but this was not the case in the remaining 427 patients (HYPNOTSUBS). ⋯ Almost half of the HYPNOTSUBS non-survivors died after more than 2 days. Because body temperature will have returned to normal by then, this must be the result of late complications. Most HYPSUB non-survivors died during the first 2 days, probably as a direct result of the submersion injury.
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Hypothermia is a frequent event in trauma patients and appears to be related to post-traumatic organ dysfunction, although in elective surgery hypothermia is known to prevent ischaemia reperfusion injury. Retrospectively we have analysed data from 641 trauma patients treated in our institution between 1988 and 1993. On admission to hospital the core temperature (cT) was > 34 degrees] C in the majority (64%) of patients, followed by 23.6% with a cT < 34 degrees C and 12.4% with a cT < 32 degrees C. ⋯ It also showed that hypothermia is not an independent prognostic factor for post-traumatic mortality. The different effect of hypothermia in trauma compared with elective surgery may be due to a lack of energy-storing phosphates like adenosine triphosphate (ATP). Further current investigations will identify the role of ATP in trauma-related hypothermia.
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Multimodality evoked potentials (EPs), linear electroencephalograms and Glasgow Coma Scale (GCS) scores were recorded within 24 h of cardiac arrest in 62 patients who were comatose following cardiopulmonary resuscitation. The cardiac arrest had a cardiac cause in 35 patients and a non-cardiac cause in 27 patients. The Glasgow Outcome Scale (GOS) scores were established 6 months after resuscitation. ⋯ However, while all patients who regained consciousness had normal EPs, not all patients in whom EPs were recordable survived. The GCS score showed a higher sensitivity and correlation with GOS score than EPs, but it was associated with a high percentage of false positive results, and its specificity was only 67%. The combination of the GCS score with EPs may be a promising strategy to counterbalance the respective limits of these methods and to reduce the loss of information due to sedation and myorelaxation, which impede clinical examination but not EP results.
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This paper reports on a fatal intoxication by oral ingestion of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D). At admission, the victim was unconscious. His condition deteroriated rapidly with blood loss from his mouth and nose. ⋯ The identity of the toxic xenobiotic was revealed by gas chromatography-mass spectrometry. Analytical quantification of the herbicide was performed by acid extraction prior to gas chromatographic examination using electron capture detection. His blood level of 2,4-D was 192 mg l-1.
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Comparative Study Clinical Trial
A comparison of the prognostic value of neuron-specific enolase serum levels and somatosensory evoked potentials in 13 reanimated patients.
Thirteen patients resuscitated after circulatory arrest due to cardiopulmonary aetiologies were studied with regard to survival and outcome. Exclusion criteria were known central nervous system disorders or death secondary to cerebrovascular accident. The serum level of neuron-specific enolase (NSE), presumably a reliable marker of neuronal death, was measured by enzyme immunoassay in peripheral blood samples over the course of 4 days at 12 h intervals. ⋯ In conclusion, pathological SSEPs and increased NSE levels are of comparable prognostic value. They may well be complementary investigations. The neuron-bound enzyme NSE is a biochemical marker which varies with the extent of neuronal damage, while absence of the cortical potentials may indicate neurophysiological loss of function.