The effect of evacuation on the number of victims following hazardous chemical release.

OBJECTIVE: In response to chemical releases, evacuation is considered an important strategy to limit victim exposure. To our knowledge, no previous studies have provided evidence-based information on the effect of evacuation on limiting the number of victims following a hazardous chemical release (HCR). This study attempts to evaluate the impact of evacuation on the number of victims resulting from different types of HCR. METHODS: The Hazardous Substances Emergency Events Surveillance (HSEES) database was used to test the hypothesis that evacuation is associated with a reduced risk of victims resulting from a HCR. A series of logistic regression models were developed in which the presence or absence of a victim was the primary outcome, with the specific chemical agent as the predictor. Where possible, the dataset was adjusted for confounding factors. The analysis was then stratified by presence or absence of evacuation, and odds ratios were compared for specific hazardous chemicals across strata. RESULTS: Of the recorded HCR events in our sample, 7.77% (2, 930 total evacuations) resulted in evacuation. Compared to no evacuation order, evacuation was associated with a significantly lower number of victims, per HCR, when the chemical involved was acid, ammonia, or chlorine. CONCLUSIONS: Evacuation remains the mainstay for prehospital care to limit victims of a HCR. Our analysis suggests that some types of HCR events are associated with fewer victims when evacuation is ordered.

Inhibition of Rho-kinase attenuates hypoxia-induced angiogenesis in the pulmonary circulation.

Pulmonary hypertension (PH) is a common complication of chronic hypoxic lung diseases, which increase morbidity and mortality. Hypoxic PH has previously been attributed to structural changes in the pulmonary vasculature including narrowing of the vascular lumen and loss of vessels, which produce a fixed increase in resistance. Using quantitative stereology, we now show that chronic hypoxia caused PH and remodeling of the blood vessel walls in rats but that this remodeling did not lead to structural narrowing of the vascular lumen. Sustained inhibition of the RhoA/Rho-kinase pathway throughout the period of hypoxic exposure attenuated PH and prevented remodeling in intra-acinar vessels without enlarging the structurally determined lumen diameter. In chronically hypoxic lungs, acute Rho kinase inhibition markedly decreased PVR but did not alter the alveolar to arterial oxygen gap. In addition to increased vascular resistance, chronic hypoxia induced Rho kinase-dependent capillary angiogenesis. Thus, hypoxic PH was not caused by fixed structural changes in the vasculature but by sustained vasoconstriction, which was largely Rho kinase dependent. Importantly, this vasoconstriction had no role in ventilation-perfusion matching and optimization of gas exchange. Rho kinase also mediated hypoxia-induced capillary angiogenesis, a previously unrecognized but potentially important adaptive response.

Sedation and analgesia for critically ill pediatric burn patients: the current state of practice.

The objective of this study was to assess current practice patterns and attitudes toward pediatric sedation and analgesia in United States (US) burn centers for critically ill patients. Survey-based questionnaire was sent to 119 Directors at US burn centers that care for pediatric patients. Forty-one surveys (34%) were analyzed. 48.8% of responding centers mandate pediatric consultation for pediatric burn patients based on factors such as age and burn size. The most common sedation and analgesic agents used were midazolam, fentanyl, morphine, ketamine, and diphenhydramine. Written sedation policies exist at 63.4% of centers. 90.2% of centers employ scoring systems to guide agent titration. 60.9% of respondents practice sedation holidays "always" or "usually." 90.2% of centers perceive the medications they routinely use are "always" or "often" efficacious in pediatric sedation and analgesia. 53.7% of respondents reported the presence of withdrawal signs and symptoms in their patient population. The lack of consensus guidelines for sedation and analgesia delivery to pediatric intensive care unit patients results in practice variation. The majority of centers perceive their sedation and analgesia strategies to be efficacious despite the heavy reliance on propofol and midazolam, both of which have questionable safety profiles in critically ill children.

Chronic hypoxia causes angiogenesis in addition to remodelling in the adult rat pulmonary circulation.

Chronic hypoxia caused by migration of native sea-level dwellers to high altitude or chronic lung disease leads to the development of increased pulmonary vascular resistance and pulmonary hypertension. This altitude-induced hypertension offers no obvious benefit and may indeed be maladaptive. A major mechanism thought to contribute to the development of pulmonary hypertension is hypoxia-induced loss of small blood vessels, sometimes termed rarefaction or pruning. More recent evidence caused us to question this widely accepted concept including the potent angiogenic effect of chronic hypoxia in all other vascular beds and the demonstration that new vessels can form in the pulmonary circulation when stimulated by chronic infection and lung resection. We tested the hypothesis that chronic environmental hypoxia causes angiogenesis in the adult pulmonary circulation by using stereological techniques combined with confocal microscopy to examine the resultant changes in pulmonary vascular structure in rats. We found that chronic hypoxia resulted in increased total pulmonary vessel length, volume, endothelial surface area and number of endothelial cells in vivo. This is the first reported demonstration of hypoxia-induced angiogenesis in the mature pulmonary circulation, a structural adaptation that may have important beneficial consequences for gas exchange. These findings imply that we must revise the widely accepted paradigm that hypoxia-induced loss of small vessels is a key structural change contributing to the development of pulmonary hypertension in high altitude adaptation and chronic lung disease.