The capability of accident and emergency departments to safely decontaminate victims of chemical incidents

OBJECTIVES: To evaluate the capability of accident and emergency (A&E) departments in six health regions of England to safely decontaminate casualties exposed to hazardous chemicals. METHODS: In January 1999 a postal questionnaire was sent to the clinical director of all A&E departments in Trent, North and South Thames, South and West, North West and, Anglia and Oxford Health Regions. The questionnaire inquired about characteristics of the department, decontamination facilities and equipment, and staff training. Nonresponders were sent a second questionnaire and contacted by telephone if they failed to respond to the second mailing. RESULTS: 308 of 326 departments identified (94%) returned a questionnaire. There was no significant difference in response rate by region (p = 0.99). Analysis was restricted to 154 major departments seeing more than 20000 new attendances per year. Of these 154 departments, 109 (71%) had a written chemical incident plan but only 55 (36%) maintained a list of nearby industrial chemical sites. Fifty nine departments (38%) stated that members of staff had received training in the management of chemically contaminated casualties in the preceding year. Eighteen departments (12%) possessed the level of personal protective equipment (PPE) recommended for decontamination by the Ambulance Services Association. Ninety six departments (62%) had a designated decontamination room but only seven (7%) of them incorporated all the features generally considered necessary for safe decontamination. Forty one units (27%) had the capability to decontaminate casualties outside of the department either with warm water from a shower attachment or with a mobile decontamination unit. Thirty six departments (23%) had neither a decontamination room nor the ability to decontaminate casualties outside the department. Only 16 units (10%) had both adequate PPE and either a decontamination room or the capability to decontaminate outside the department. CONCLUSIONS: This study has identified deficiencies in the current NHS capability to respond to chemical incidents. To resolve this, nationally recognised standards for decontamination facilities, equipment and training should be formulated, agreed and implemented.     

Human neocortical excitability is decreased during anoxia via sodium channel modulation.

When the central nervous system in humans is deprived of oxygen, the effects are potentially disastrous. Electroencephalographic activity is lost and higher brain function ceases rapidly. Despite the importance of these effects, the mechanisms underlying the loss of cortical activity are poorly understood. Using intracellular recordings of human neocortical neurons in tissue slices, we show that, whereas anoxia produces a relatively small depolarization and modest alterations in passive properties, it causes a major decrease in excitability. Whole-cell voltage-clamp studies of acutely isolated human neocortical pyramidal neurons demonstrate that anoxia and metabolic inhibition produce a large negative shift in the steady-state inactivation [h infinity (V)] curve for the voltage-dependent sodium current (INa). Inclusion of ATP in the patch pipette decreased the shift of the h infinity (V) curve by two-thirds. Because increased inactivation of INa decreases cellular metabolic demand, we postulate that this promotes neuronal survival during periods of oxygen deprivation. These data show a novel mechanism by which anoxia links metabolism to membrane ionic conductances in human cortical neurons.     

“If an acute event occurs,what should we do?” Diverse ethical approaches to decision-making in the ICU

Medicine, Health Care and Philosophy - The aim of this paper is to analyze an Intensive Care Unit case that required ethics consultation at a University Hospital in Northern Italy. After the case...     

Treatment-like steady-state methadone in rats interferes with incubation of cocaine sensitization and associated alterations in gene expression

In a previous study, steady-state methadone treatment was found to prevent associative cocaine learning, as well as related decreases in mRNA expression of preprohypocretin/preproorexin (ppHcrt) in the lateral hypothalamus (LH) and dopamine D2 receptor (DR2) in the caudate-putamen (CP), and increases in mu-opioid receptor in the ventral striatum of rats. To investigate whether the same regimen of methadone exposure could prevent the incubation of cocaine sensitization and related alterations in gene expression, male Sprague–Dawley rats received 45 mg/kg/day steady-dose “binge” cocaine administration (IP) for 14 days followed by mini-pumps releasing 30 mg/kg/day methadone (SC). After 14 days of methadone, and a subsequent 10-day drug-free period, all rats were tested for sensitization (cocaine test dose: 15 mg/kg) and brain tissue was collected to quantify mRNA expression. Rats exposed to cocaine displayed cocaine-induced stereotypy at test, as well as enhanced ppHcrt mRNA in the LH and reduced DR2 mRNA in the CP. Importantly, these alterations were significantly reduced in rats treated with methadone following cocaine. These results suggest that steady-state methadone can interfere with the incubation of neuroadaptations underlying changes in behavioral responses to cocaine and cocaine-associated stimuli, and that these effects can be observed even after withdrawal from methadone.     

ERP measures indicate both attention and working memory encoding decrements in aging

We investigated age-related attention and encoding deficits, and their possible interaction, by analyzing visual event-related potentials from young and older adults during a modified Sternberg word recognition task. Young adults performed more accurately, albeit not significantly so. P1 latency was shorter in young adults and correlated negatively with task accuracy (with age partialed out). These data support proposals that P1 indexes attentional suppression, which is less efficient in older adults. N1 was larger in older adults but did not correlate with accuracy. Young adults had higher P2 amplitudes and P2 latency correlated with accuracy (age partialed), supporting the view that semantic operations during encoding are affected by aging. These data indicate that attention (P1) and encoding (P2) decrements may contribute to memory or related cognitive decrements in aging, and P1 and P2 latency measures from appropriate paradigms may be salient ERP markers of these decrements.     

The endothelial microparticle response to a high fat meal is not attenuated by prior exercise

Triglyceride-rich postprandial lipoproteins are known to activate endothelial cells in vitro, contributing to atherosclerosis. Endothelial microparticles (EMP) are membranous vesicles released into the circulation from vascular endothelial cells that permit cell activation to be monitored in vivo. The objective of the study was to examine changes in EMP following a high fat meal, consumed with and without prior exercise. Eight recreationally active young men underwent two oral fat tolerance tests following either 100 min exercise at 70% VO₂peak (EX trial) or no exercise (CON trial) on the previous evening. Postprandial triglycerides were reduced (1.97 ± 0.31 vs. 1.17 ± 0.13 mmol L⁻¹, p < 0.05) and HDL-cholesterol (HDL-C) increased (1.20 ± 0.07 vs. 1.30 ± 0.08 mmol L⁻¹, p < 0.05) in the EX compared to CON trial. EMP (CD31+/42b−) increased postprandially (p < 0.05). However, counts were not different between trials (postprandial CON and EX trial counts × 10³ μL⁻¹, 3.10 ± 0.14 vs. 3.26 ± 0.37). There were no changes in sICAM-1 or sVCAM-1 postprandially and no differences between trials. Interleukin-6 (IL-6) and leukocytes increased postprandially (p < 0.05). IL-6 values were not different between trials. Leukocytes were higher at 0 h in the EX trial with CON and EX trial values similar at 6 h. EMP, but not sICAM-1 or sVCAM-1, increase in response to a high fat meal. However, EMP are not attenuated by acute exercise, despite a considerable reduction in postprandial lipemia and an increase in HDL-C. M. Harrison and R. P. Murphy contributed equally to this work.