Whole body imaging in the diagnosis of blunt trauma, ionizing radiation hazards and residual risk.

Ever since the introduction of radiographic imaging, its utility in identifying injuries has been well documented and was incorporated in the workup of injured patients during advanced trauma life support algorithms [American College of Surgeons, 8th ed. Chicago, 2008]. More recently, computerized tomography (CT) has been shown to be more sensitive than radiography in the diagnosis of injury. Due to the increased use of CT scanning, concerns were raised regarding the associated exposure to ionizing radiation [N Engl J Med 357:2277-2284, 2007]. During the last several years, a significant amount of research has been published on this topic, most of it being incorporated in the BEIR VII Phase 2 report, published by the National Research Council of the National Academies [National Academy of Sciences, Washington DC, 2006]. The current review will analyze the scientific basis for the concerns over the ionizing radiation associated with the use of CT scanning and will examine the accuracy of the typical advanced trauma life support work-up for diagnosis of injuries.

Hepatic ischemia/reperfusion injury in P-selectin and intercellular adhesion molecule-1 double-mutant mice.

Neutrophil adhesion and recruitment represents one of the early cellular events that occur during hepatic ischemia/reperfusion (IR) injury and plays a critical role in determining the extent of tissue damage. The adhesion molecules, such as selectins and intercellular adhesion molecules (ICAM), are important in mediating neutrophil-endothelial cell interactions and neutrophil emigration. The goal of this study was to evaluate the role of P-selectin and ICAM-1 in hepatic IR injury. Male wild-type and P-selectin/ICAM-1-deficient (P/I null) mice underwent 90 minutes of partial hepatic ischemia followed by reperfusion at various time points (0, 1.5, 3, and 6 hours). Reperfusion caused a time-dependent hepatocellular injury in both wild-type and P/I null mice as judged by plasma alanine aminotransferase (ALT) levels and liver histopathology examination. Although ALT levels were slightly lower in the P/I null mice compared with the wild-type mice the differences were not statistically significant. Neutrophil infiltration to the ischemic liver was observed in both mouse groups after 6 hours of reperfusion; however, the infiltration to the midzonal region of the ischemic liver was more pronounced in the wild-type group. This study suggests that hepatocellular injury induced after hepatic IR was independent of P-selectin and ICAM-1 in this model of acute inflammatory tissue injury.