New Versus Old, The i-View Video Laryngoscope Versus the GlideScope: A Prospective, Randomized, Crossover Trial.

BACKGROUND: A novel video laryngoscope device, the i-view, may extend intubation capability to the lowest echelons of deployed military medicine. The i-view is a one-time use, disposable laryngoscope. We compared time to completion of endotracheal intubation (ETI) between the i-view and GlideScope among military emergency medicine providers in a simulation setting. METHODS: We conducted a prospective, randomized, crossover trial. We randomized participants to i-view or GlideScope first before they performed 2 ETI-1 with each device. The primary outcome was time to completion of ETI. Secondary outcomes included first-pass success, optimal glottic view, and end-user appraisal. We used a Laerdal Airway Management Trainer for all intubations. RESULTS: Thirty-three emergency medicine providers participated. ETI time was less with GlideScope than i-view (22.2 +/- 9.0 seconds versus 30.2 +/- 24.0 seconds; p=0.048). Optimal glottic views, using the Cormack-Lehan scale, also favored the GlideScope (2 [1,2] versus 2[2,2]; p=0.044). There was no difference in first-pass success rates (100% versus 100%). More participants preferred the GlideScope (24 versus 9; p=0.165); however, participants agreed that the i-view would be easier to use than the GlideScope in an austere environment (4[4,5]). CONCLUSIONS: We found the GlideScope outperformed the i-view with respect to procedural completion time. Participants preferred the GlideScope over i-view, but indicated the i-view would be easier to use than the GlideScope in an austere setting. Our findings suggest the i-view may be a suitable alternative to GlideScope for US military providers, especially for those in the prehospital setting.

Development of the Defense Registry for Emergency Airway Management (DREAM).

INTRODUCTION: Airway obstruction is the second leading cause of potentially preventable death on the battlefield. Endotracheal intubation is a critical skill needed by emergency military physicians to manage these patients. Our objective is to describe the development of the Defense Registry for Emergency Airway Management (DREAM) at Brooke Army Medical Center (BAMC), a level 1 trauma center over a 7-month period. METHODS: Emergency physicians (EP) performing endotracheal intubations in the BAMC emergency department (ED) completed standardized data collection forms with information about each event. Trained study team members extracted additional data from the medical records. We cross-referenced each intubation with patient tracking systems in the department and would fill in missing variables through interview with the intubating operator and/or medical records review. RESULTS: The study period comprised January through July 2020. During the study period emergency physicians (EP) performed a total of 74 intubations. Reasons for intubation were related to trauma for 47 patients (64%) and medical conditions for 26 patients (36%). The median age was 51 (interquartile range 30-72) and most were male 48 (65.7%). Difficult airway characteristics encountered included blood in the airway (26%), facial trauma (23%), and airway obstruction (1%). Most intubations utilized video laryngoscopy, and the most frequently used airway devices were Macintosh-shaped (45%) and hyperangulated-shaped (41%). Overall, firstpass success rate was 93% (69) with majority of intubations performed by second-year emergency residents (61%) followed by first-year residents (28%). CONCLUSIONS: Most DREAM intubations were related to traumatic injuries. The most frequently encountered difficult airway characteristics were blood in airway and facial trauma. Most intubations were conducted using video laryngoscopy with a high first-pass success rate similar to other published studies. Expansion of the registry to other military emergency departments would enable a data-driven solution for development of individual critical task lists.

AMD3465, a novel CXCR4 receptor antagonist, abrogates schistosomal antigen-elicited (type-2) pulmonary granuloma formation.

CXCR4 is a major receptor for CXCL12 and is known to participate in multiple physiological systems. The present study tested a second generation CXCR4 antagonist, AMD3465, for effects on highly defined models of Th1- and Th2-cell-mediated hypersensitivity-type pulmonary granuloma formation. Type-1 and type-2 granulomas were induced, respectively, by intravenous challenge of sensitized CBA/J mice with Mycobacteria bovis purified protein derivative- or Schistosoma mansoni egg antigen-coated beads. Before challenge, mice were implanted with osmotic pumps releasing AMD3465 at 5 microg/hour (6 mg/kg/day). Compared to vehicle, AMD3465 had minimal effect on type-1 inflammation or cytokine responses in draining lymph nodes, but the type-2 inflammation was significantly abrogated with reductions in lesion size and eosinophil content as well as abrogated interleukin (IL)-5, IL-10, and IL-13 cytokine production in draining lymph nodes. The biased effect of AMD3465 correlated with greater CXCR4 ligand expression in the type-2 model. Treatment during a primary response impaired lymph node IL-2 production after both Mycobacteria bovis purified protein derivative and Schistosoma mansoni egg antigen challenge indicating an unbiased effect during immune induction. In summary, CXCR4 blockade inhibited eosinophil recruitment during type-2 granuloma formation and interfered with primary and secondary T-cell activation events in lymphoid tissue, suggesting potential therapeutic application for chronic hypersensitivity diseases.

Impaired lung dendritic cell activation in CCR2 knockout mice.

Dendritic cell (DC) recruitment is a hallmark event in antigen (Ag)-challenged lungs. We previously reported models for analyzing DC migration and activation in the lung after Th1- or Th2-eliciting pathogen Ag-bead challenge. To determine the role of chemokines in DC mobilization, we applied this analysis to CCR1, CCR2, CCR5, and CCR6 chemokine receptor knockout mice. Both Mycobacteria bovis protein Ags and helminthic, Schistosoma mansoni egg Ags elicited multiple chemokines, including CCR1, CCR2, CCR5, and to a lesser extent CCR6 ligands. DCs from wild-type lungs expressed transcripts for chemokine receptors, CCR1, CCR2, CCR5, and CXCR4. In all knockout strains, CD11c+ cells were recruited to Ag-beads likely because of receptor redundancy. However, DCs in CCR2-/- mice had significantly decreased MHCII and CD40 expression. This was associated with abrogated cytokine production in draining lymph node cultures. Analysis of local innate inflammation revealed a 50% reduction in macrophage recruitment in CCR2-/- mice. Bone marrow chimeras of mixed CCR2+/+ green fluorescent protein transgenic and CCR2-/- green fluorescent protein-negative cells confirmed the DC maturation defect was only among the latter population. In conclusion, CCR2 knockout confers an intrinsic DC activation defect and CCR2 ligands likely promote the local activation/maturation of inflammatory DCs.

The innate pulmonary granuloma: characterization and demonstration of dendritic cell recruitment and function.

Granulomas are innate sequestration responses that can be modified by superimposed acquired immune mechanisms. The present study examined the innate stage of pulmonary granuloma responses to bead-immobilized Th1- and Th2-inducing pathogen antigens (Ags), Mycobacteria bovis purified protein derivative (PPD) and Schistosoma mansoni soluble egg Ags (SEA). Compared to a nonpathogen Ag, PPD and SEA bead elicited larger lesions with the former showing accelerated inflammation. Temporal analyses of cytokine and chemokine transcripts showed all Ag beads induced tumor necrosis factor-alpha mRNA but indicated biased interleukin (IL)-1, IL-6, and IL-12 expression with PPD challenge. All beads elicited comparable levels of CXCL9, CXL10, CCL2, CCL17, and CCL22 mRNA, but PPD beads caused biased CXCL2 CXCL5, CCL3, and CCL4 expression whereas both pathogen Ags induced CCL7. Immunohistochemical, electron microscopic, and flow cytometric analyses showed that Ag beads mobilized CD11c+ dendritic cells (DCs) of comparable maturation. Transfer of DCs from PPD Ag-challenged lungs conferred a Th1 anamnestic cytokine response in recipients. Surprisingly, transfer of DCs from the helminth SEA-challenged lungs did not confer the expected Th2 response, but instead rendered recipients incapable of Ag-elicited IL-4 production. These results provide in vivo evidence that lung DCs recruited under inflammatory conditions favor Th1 responses and alternative mechanisms are required for Th2 commitment.

Differential effects of ageing on cytokine and chemokine responses during type-1 (mycobacterial) and type-2 (schistosomal) pulmonary granulomatous inflammation in mice.

Cytokine and chemokine responses during anamnestic type-1 and type-2 lung granuloma formation were evaluated in mice at 6,12,18 and 24-months of age. Lesions were induced by embolizing Sepharose beads coupled to Mycobacterium bovis purified protein derivative or soluble Schistosoma mansoni egg antigens. Type-1 inflammation was reduced by 18 months, whereas type-2 granulomas not until 24 months of age. In type-1 draining lymph nodes cultures, interferon-gamma (IFNgamma) declined to a nadir by 18, and then partly recovered at 24 months. In contrast, IL-4 was not significantly impaired in type-2 cultures until 24 months. Type-1 and 2 node cultures also displayed decreased IL-13, but paradoxically enhanced IL-5 production at 24 months. Chemokine transcripts in granulomatous lungs displayed age-related alterations. In the type-1 response, CXCL9 (monokine-induced by IFNgamma) declined with age then partly recovered at 24 months parallelling lymph node IFNgamma levels. Transcripts for MIP-2/CXCL2, IP-10/CXCL10, MCP-1/CCL2, and MCP-5/CCL12 increased at 24 months. In the type-2 response MCP-1/CCL2, MCP-3/CCL7, MCP-5/CCL12 and TARC/CCL17 collapsed at 24 months paralleling local IL-4 transcript levels, yet some chemokine transcripts such as KC/CXCL1 and eotaxin/CCL11 were unaffected. These findings suggest that cytokine and chemokine responses degrade differentially with age shifting Th1/Th2 crossregulatory pressures and local expression of chemokines.