Presumed Systemic Inflammatory Response Syndrome in the Pediatric Emergency Department.

OBJECTIVE: The aim of this study was to examine the incidence and outcomes of patients presenting with systemic inflammatory response syndrome (SIRS) in the pediatric emergency department (PED). METHODS: This was a descriptive, retrospective cohort study of all patients from birth to 18 years presenting to the PED of a single center on 16 days distributed over 1 year. The presence of presumed SIRS (pSIRS, defined as noncore temperature measurement and cell count when clinically indicated) and sepsis was determined for all study patients. Patients were followed up for 1 week. RESULTS: The incidence of pSIRS was 15.3% (216/1416). Suspected or proven infection was present in 37.1% (n = 525) of the study population and 76.4% (n = 165) with pSIRS, with no cases of severe sepsis or septic shock. Sensitivity and specificity of pSIRS for predicting infection were 31.4% (95% confidence interval [CI], 27.5%-35.6%) and 94.3% (95% CI, 92.5%-95.7%), respectively. Although patients with pSIRS had a relative risk of 2.4 (95% CI, 1.6-3.5; P < 0.0001) for admission, 74% were discharged home with no subsequent PED visits. Of defined sepsis cases, 75% were discharged home without return. CONCLUSIONS: Presumed SIRS and sepsis are relatively common in the PED. Use of pSIRS to screen for sepsis risks missing infection, whereas using pSIRS in the current sepsis definition results in overinclusion of nonsevere illness.

Use of geographic information systems to determine new helipad locations and improve timely response while mitigating risk of helicopter emergency medical services operations.

INTRODUCTION: Traumatic injury is a leading cause of morbidity and mortality, but these can be minimized by timely transport to definite care. Helicopter emergency medical services (HEMS) provide timely transport and can influence survival. However, accident analyses indicate that landing at an unsecured landing zone (LZ), particularly at night, increases the risk of aviation accidents. To ensure safety, some HEMS operations land only at designated, secured LZs. OBJECTIVE: This study utilized geographic information systems (GISs) to compare locations of scene call requests and secure LZs. The goal was to determine the optimal placement of new helipads as a strategy to improve access while mitigating the risk of aviation accidents. METHODS: Call request data from a large air medical transport service were used to determine the geographic locations of all requests for scene responses in 2006. Request locations were compared with the locations of existing helipads, and straight-line distances between scene and helipad were determined using the GIS application. The application was then used to determine potential locations for new helipads. RESULTS: During the study period, 748 requests for scene calls and 269 helipads were available. There were 476 (52.4%) requests at least 10 kilometers from a helipad and 356 (36.6%) requests at least 15 kilometers from a helipad. One particular region, Southwestern Ontario, was identified as having the highest number of requests >15 kilometers from the closest helipad. CONCLUSION: GISs can be used to determine potential locations for new helipad construction using historical call request data. This evidence-based approach can improve HEMS access while mitigating operational risk.

Hsp70 inhibits heat-induced apoptosis upstream of mitochondria by preventing Bax translocation.

Hsp70 overexpression can protect cells from stress-induced apoptosis. Our previous observation that Hsp70 inhibits cytochrome c release in heat-stressed cells led us to examine events occurring upstream of mitochondrial disruption. In this study we examined the effects of heat shock on the proapoptotic Bcl-2 family member Bax because of its central role in regulating cytochrome c release in stressed cells. We found that heat shock caused a conformational change in Bax that leads to its translocation to mitochondria, stable membrane association, and oligomerization. All of these events were inhibited in cells that had elevated levels of Hsp70. Hsp70 did not physically interact with Bax in control or heat-shocked cells, indicating that Hsp70 acts to suppress signals leading to Bax activation. Hsp70 inhibited stress-induced JNK activation and inhibition of JNK with SP600125 or by expression of a dominant negative mutant of JNK-blocked Bax translocation as effectively as Hsp70 overexpression. Hsp70 did not protect cells expressing a mutant form of Bax that has constitutive membrane insertion capability or cells treated with a small molecule activator of apoptosome formation, indicating that it is unable to prevent cell death after mitochondrial disruption and caspase activation have occurred. These results indicate that Hsp70 blocks heat-induced apoptosis primarily by inhibiting Bax activation and thereby preventing the release of proapoptotic factors from mitochondria. Hsp70, therefore, inhibits events leading up to mitochondrial membrane permeabilization in heat-stressed cells and thereby controls the decision to die but does not interfere with cell death after this event has occurred.