Mass casualty events: what to do as the dust settles?

Care during mass casualty events (MCE) has improved during the last 15 years. Military and civilian collaboration has led to partnerships which augment the response to MCE. Much has been written about strategies to deliver care during an MCE, but there is little about how to transition back to normal operations after an event. A panel discussion entitled The Day(s) After: Lessons Learned from Trauma Team Management in the Aftermath of an Unexpected Mass Casualty Event at the 76th Annual American Association for the Surgery of Trauma meeting on September 13, 2017 brought together a cadre of military and civilian surgeons with experience in MCEs. The events described were the First Battle of Mogadishu (1993), the Second Battle of Fallujah (2004), the Bagram Detention Center Rocket Attack (2014), the Boston Marathon Bombing (2013), the Asiana Flight 214 Plane Crash (2013), the Baltimore Riots (2015), and the Orlando Pulse Night Club Shooting (2016). This article focuses on the lessons learned from military and civilian surgeons in the days after MCEs

Mass casualty events: what to do as the dust settles?

Care during mass casualty events (MCE) has improved during the last 15 years. Military and civilian collaboration has led to partnerships which augment the response to MCE. Much has been written about strategies to deliver care during an MCE, but there is little about how to transition back to normal operations after an event. A panel discussion entitled The Day(s) After: Lessons Learned from Trauma Team Management in the Aftermath of an Unexpected Mass Casualty Event at the 76th Annual American Association for the Surgery of Trauma meeting on September 13, 2017 brought together a cadre of military and civilian surgeons with experience in MCEs. The events described were the First Battle of Mogadishu (1993), the Second Battle of Fallujah (2004), the Bagram Detention Center Rocket Attack (2014), the Boston Marathon Bombing (2013), the Asiana Flight 214 Plane Crash (2013), the Baltimore Riots (2015), and the Orlando Pulse Night Club Shooting (2016). This article focuses on the lessons learned from military and civilian surgeons in the days after MCEs

Major venous injury and large volume crystalloid resuscitation: a limb threatening combination

INTRODUCTION: Major venous injury (MVI) affecting the lower extremity can result in subsequent amputation. The contribution of intraoperative resuscitation efforts on the need for amputation is not well defined. We hypothesized that intraoperative large volume crystalloid resuscitation (LVCR) increases the risk of amputation after MVI, while massive transfusion (MT) does not. METHODS: We performed a retrospective review of patients with infrarenal MVI from 2005 to 2015 at seven urban level I trauma centers. The outcome of interest was the need for secondary amputation. RESULTS: 478 patients were included. 31 (6.5%) patients with MVI required amputation. LVCR(p \u3c 0.001), combined arterial/venous injury (p = 0.001), and associated fracture (p = 0.001) were significant risk factors for amputation. MT did not significantly increase amputation risk (p = 0.44). Multivariable logistic regression model demonstrated that patients receiving ≥5L LVCR(aOR (95% CI): 9.7 (2.9, 33.0); p \u3c 0.001), with combined arterial/venous injury (aOR (95% CI):3.6 (1.5, 8.5); p = 0.004), and with an associated fracture (aOR (95% CI):3.2 (1.5, 7.1); p = 0.004) were more likely to require amputation. CONCLUSION: Patients with MVI who receive LVCR, have combined arterial/venous injuries and have associated fractures are more likely to require amputation. MT was not associated with delayed amputation

Systemic activation of dendritic cells by toll-like receptor ligands or malaria infection impairs cross-presentation and antiviral immunity

The mechanisms responsible for the immunosuppression associated with sepsis or some chronic blood infections remain poorly understood. Here we show that infection with a malaria parasite (Plasmodium berghei) or simple systemic exposure to bacterial or viral Toll-like receptor ligands inhibited cross-priming. Reduced cross-priming was a consequence of downregulation of cross-presentation by activated dendritic cells due to systemic activation that did not otherwise globally inhibit T cell proliferation. Although activated dendritic cells retained their capacity to present viral antigens via the endogenous major histocompatibility complex class I processing pathway, antiviral responses were greatly impaired in mice exposed to Toll-like receptor ligands. This is consistent with a key function for cross-presentation in antiviral immunity and helps explain the immunosuppressive effects of systemic infection. Moreover, inhibition of cross-presentation was overcome by injection of dendritic cells bearing antigen, which provides a new strategy for generating immunity during immunosuppressive blood infections.<br /