Nathan L. Huber

Hypobaric hypoxia exacerbates the neuroinflammatory response to traumatic brain injury.

OBJECTIVE To determine the inflammatory effects of time-dependent exposure to the hypobaric environment of simulated aeromedical evacuation following traumatic brain injury (TBI). METHODS Mice were subjected to a blunt TBI or sham injury. Righting reflex response (RRR) time was assessed as an indicator of neurologic recovery. Three or 24 h (Early and Delayed groups, respectively) after TBI, mice were exposed to hypobaric flight conditions (Fly) or ground-level control (No Fly) for 5 h. Arterial blood gas samples were obtained from all groups during simulated flight. Serum and cortical brain samples were analyzed for inflammatory cytokines after flight. Neuron specific enolase (NSE) was measured as a serum biomarker of TBI severity. RESULTS TBI resulted in prolonged RRR time compared with sham injury. After TBI alone, serum levels of interleukin-6 (IL-6) and keratinocyte-derived chemokine (KC) were increased by 6 h post-injury. Simulated flight significantly reduced arterial oxygen saturation levels in the Fly group. Post-injury altitude exposure increased cerebral levels of IL-6 and macrophage inflammatory protein-1α (MIP-1α), as well as serum NSE in the Early but not Delayed Flight group compared to ground-level controls. CONCLUSIONS The hypobaric environment of aeromedical evacuation results in significant hypoxia. Early, but not delayed, exposure to a hypobaric environment following TBI increases the neuroinflammatory response to injury and the severity of secondary brain injury. Optimization of the post-injury time to fly using serum cytokine and biomarker levels may reduce the potential secondary cerebral injury induced by aeromedical evacuation.

Omission of routine chest x-ray after chest tube removal is safe in selected trauma patients

BACKGROUND Definitive practice guidelines regarding the utility of chest x-ray (CXR) following chest tube removal in trauma patients have not been established. The authors hypothesized that the selective use of CXR following chest tube removal is safe and cost effective. METHODS A retrospective review of chest tube insertions performed at a level I trauma center was conducted. RESULTS Patients who underwent chest tube removal without subsequent CXR had a lower mean Injury Severity Score and were less likely to have suffered penetrating thoracic injuries. These patients received fewer total CXRs and had shorter durations of chest tube therapy and shorter lengths of stay following tube removal. Subsequent reinterventions were performed more frequently in the CXR group. The annual decrease in hospital charges by foregoing a CXR was

Prior thermal injury accelerates endotoxin-induced inflammatory cytokine production and intestinal nuclear factor-κB activation in mice.

16,280. CONCLUSIONS The selective omission of CXR following chest tube removal in less severely injured, nonventilated patients does not adversely affect outcomes or increase reintervention rates. Avoiding unnecessary routine CXR after chest tube removal could provide a significant reduction in total hospital charges.

Remote thermal injury increases LPS-induced intestinal IL-6 production.

The objective of this study was to increase the understanding of the “second-hit” response in thermal injury. The authors hypothesized that prior thermal injury increases the endotoxin-induced inflammatory response of intestinal mucosa. Mice underwent sham or 25% TBSA scald injury. Seven days after injury, mice were injected with lipopolysaccharide. Blood, jejunum, and colon specimens were obtained at intervals. Serum, jejunal, and colon inflammatory cytokine levels were measured by enzyme-linked immunosorbent assay. Jejunal and colon nuclear factor (NF)-&kgr;B activation was measured by electrophoretic mobility shift assay. After remote thermal injury, lipopolysaccharide exposure led to an acute increase in serum interleukin (IL)-6, IL-10, and chemokine keratinocyte-derived chemokine (KC) levels. This correlated with lipopolysaccharide-induced increased IL-6 in colon and chemokine KC in the jejunum and colon in burned mice when compared with sham-injured mice. Lipopolysaccharide-induced NF-&kgr;B activation occurred more rapidly in jejunum and colon from burned mice compared with sham-injured mice. Prior thermal injury accelerates lipopolysaccharide-induced inflammatory cytokine production systemically in jejunum and colon. The “second hit” of lipopolysaccharide led to earlier intestinal NF-&kgr;B activation in burned mice compared with sham-injured mice. These results indicate that there is a heightened inflammatory response by jejunum and colon in response to a “second hit” of lipopolysaccharide after burn injury.