A Comparison of Paramedic First Pass Endotracheal Intubation Success Rate of the VividTrac VT-A 100, GlideScope Ranger, and Direct Laryngoscopy Under Simulated Prehospital Cervical Spinal Immobilization Conditions in a Cadaveric Model.

OBJECTIVE: The primary goal of this study was to compare paramedic first pass success rate between two different video laryngoscopes and direct laryngoscopy (DL) under simulated prehospital conditions in a cadaveric model. METHODS: This was a non-randomized, group-controlled trial in which five non-embalmed, non-frozen cadavers were intubated under prehospital spinal immobilization conditions using DL and with both the GlideScope Ranger (GL; Verathon Inc, Bothell, Washington USA) and the VividTrac VT-A100 (VT; Vivid Medical, Palo Alto, California USA). Participants had to intubate each cadaver with each of the three devices (DL, GL, or VT) in a randomly assigned order. Paramedics were given 31 seconds for an intubation attempt and a maximum of three attempts per device to successfully intubate each cadaver. Confirmation of successful endotracheal intubation (ETI) was confirmed by one of the six on-site physicians. RESULTS: Successful ETI within three attempts across all devices occurred 99.5% of the time overall and individually 98.5% of the time for VT, 100.0% of the time for GL, and 100.0% of the time for DL. First pass success overall was 64.4%. Individually, first pass success was 60.0% for VT, 68.8% for GL, and 64.5% for DL. A chi-square test revealed no statistically significant difference amongst the three devices for first pass success rates (P=.583). Average time to successful intubation was 42.2 seconds for VT, 38.0 seconds for GL, and 33.7 for seconds for DL. The average number of intubation attempts for each device were as follows: 1.48 for VT, 1.40 for GL, and 1.42 for DL. CONCLUSION: The was no statistically significant difference in first pass or overall successful ETI rates between DL and video laryngoscopy (VL) with either the GL or VT (adult). Hodnick R , Zitek T , Galster K , Johnson S , Bledsoe B , Ebbs D . A comparison of paramedic first pass endotracheal intubation success rate of the VividTrac VT-A 100, GlideScope Ranger, and direct laryngoscopy under simulated prehospital cervical spinal immobilization conditions in a cadaveric model. Prehosp Disaster Med. 2017;32(6):621-624.

Lightning Strike in Pregnancy With Fetal Injury.

Injuries from lightning strikes are an infrequent occurrence, and are only rarely noted to involve pregnant victims. Only 13 cases of lightning strike in pregnancy have been previously described in the medical literature, along with 7 additional cases discovered within news media reports. This case report presents a novel case of lightning-associated injury in a patient in the third trimester of pregnancy, resulting in fetal ischemic brain injury and long-term morbidity, and reviews the mechanics of lightning strikes along with common injury patterns of which emergency providers should be aware.

Postobstructive pulmonary edema in the setting of aspiration and air travel.

BACKGROUND: Postobstructive pulmonary edema (POPE)-also referred to as negative pressure pulmonary edema-occurs with deep inspiration against a closed glottis or obstructed airway. The result can be life threatening, however, most cases have a self-limited presentation and resolve with supportive care. OBJECTIVE: Our aim was to critically evaluate a previously unreported mechanism in the exacerbation of POPE. CASE REPORT: This is a report of a 50-year-old woman who experienced an acute episode of hypoxia and altered mental status aboard a transcontinental flight. Her presentation was suggestive of pulmonary embolus. However, a detailed history yielded an episode of preflight choking relieved by the Heimlich maneuver. After 2 days of supportive care she was discharged with a complete return to baseline. CONCLUSIONS: Subclinical cases of POPE can be exacerbated by the low atmospheric pressure experienced on commercial airlines. With early recognition and supportive treatment, the patient returned to baseline before her discharge 2 days later. Making the diagnoses of POPE is not always straightforward for the practitioner and necessitates a broad differential. Initial supportive care focusing on maximizing respiratory support is critical.

NOD2 deficiency results in increased susceptibility to peptidoglycan-induced uveitis in mice.

PURPOSE: The innate immune receptor NOD2 is a genetic cause of uveitis (Blau syndrome). Intriguingly, in the intestine where polymorphisms of NOD2 predispose to Crohn's disease, NOD2 reportedly suppresses inflammation triggered by the bacterial cell wall component, peptidoglycan (PGN). Whether NOD2 exerts a similar capacity in the regulation of ocular inflammation to PGN has not been explored. METHODS: NOD2, NOD1, or MyD88 knockout (KO) mice and their wild-type (WT) controls were administered an intravitreal injection of PGN (a metabolite of which is the NOD2 agonist, muramyl dipeptide), or synthetic TLR2/1 and TLR2/6 agonists, Pam3CSK4 and FSL-1. Ocular inflammation was assessed by intravital microscopy and histopathology. Cytokine production in eye tissue homogenates was measured by ELISA. RESULTS: PGN triggered uveitis in mice. This inflammation was abolished in the absence of the TLR signaling mediator MyD88. NOD2 exerted a negative regulatory role because PGN-triggered eye inflammation was exacerbated in NOD2 KO mice. Increased intravascular response coincided with enhanced leukocytes within the aqueous and vitreous humors. The enhanced susceptibility of NOD2 KO mice to PGN uveitis coincided with increased cytokine production of IL-12p40, IL-17, and IL-23 but not IL-12p70, TNFα, or IFNγ. NOD1 deficiency did not result in the same sensitivity to PGN. Ocular inflammation induced by synthetic TLR2 agonists required MyD88 but not NOD2 or NOD1. CONCLUSIONS: NOD2 may serve differential roles in the eye to promote inflammation while also tempering cell responses to PGN akin to what has been reported in colitis.

NOD1 expression in the eye and functional contribution to IL-1beta-dependent ocular inflammation in mice.

PURPOSE: NOD1 plays an important role in host defense and recognizes the minimal component of bacterial cell walls, meso-diaminopimelic acid (iE-DAP). Polymorphisms in NOD1 are associated with autoinflammatory diseases characterized by uveitis such as Crohn's disease and sarcoidosis. NOD1 is homologous to NOD2, which is responsible for an autosomal dominant form of uveitis. Nonetheless, the role of NOD1 in intraocular inflammation has not been explored. The induction of uveitis by iE-DAP in mice and the potential contribution of interleukin (IL)-1beta were investigated. METHODS: BALB/c mice or mice deficient in caspase-1 or IL-1R1 and their congenic controls were injected intravitreally with iE-DAP or saline. The time course, dose response, and contribution of IL-1beta to ocular inflammation were quantified by intravital video microscopy, histology, and immunohistochemistry. NOD1 and IL-1beta were measured in eye tissue by immunoblotting and ELISA. RESULTS: NOD1 protein is expressed in the eye and promotes ocular inflammation in a dose- and time-dependent fashion. The authors previously defined the role of IL-1beta in NOD2 uveitis and tested whether NOD1 and NOD2 used similar mechanisms. Treatment with iE-DAP significantly increased IL-1beta, which was caspase-1 dependent. However, in contrast to NOD2, caspase-1 and IL-1R1 were essential mediators of iE-DAP-induced uveitis, suggesting that NOD1 and NOD2 induce ocular inflammation by distinct mechanisms involving IL-1beta. CONCLUSIONS: These findings demonstrate that NOD1 is expressed within the eye and that its activation results in uveitis in an IL-1beta-dependent mechanism. Characterizing the differences between NOD1 and NOD2 responses may provide insight into the pathogenesis of uveitis.

Characterizing extravascular neutrophil migration in vivo in the iris.

Extravascular neutrophil migration is poorly characterized in vivo. To test the hypothesis that this migration is a non-random process, we used videomicroscopy to monitor neutrophils in irises of living mice with endotoxin-induced uveitis (EIU). Paths of individual cells were analyzed. Nearly all of these cells were moving in divergent directions, and mean displacement plots indicated that the predominant movement was random. The paths of some cells were fit to bivariate autoregressive integrated moving average models that revealed at least two modes of movement: random search and linear trend. Cell speed was significantly reduced by the actin inhibitor, cytochalasin D. The pattern of migration for neutrophils is in marked contrast to what we previously described for antigen-presenting cells in the iris, but somewhat resembles recent descriptions for T cells within a lymph node. Characterization of extravascular migration of neutrophils has important implications for understanding infection and immunity.