Scientific Session - f ACS

Scientific Session

44th ANNUAL RESIDENT TRAUMA PAPERS COMPETITION

Presented during the

99th ANNUAL MEETING

Committee on Trauma American College of Surgeons

Thursday, March 11, 2021

Virtual Meeting

Chicago, IL

Copyright © 2021 American College of Surgeons

633 N. Saint Clair St. Chicago, IL 60611-3295

facs.org

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Scientific Session

44th ANNUAL RESIDENT TRAUMA PAPERS COMPETITION

Presented during the

99th ANNUAL MEETING Committee on Trauma

American College of Surgeons

MODERATORS Patrick M. Reilly, MD, FACS Scott D’Amours, MD, FACS Eileen M. Bulger, MD, FACS Sharon M. Henry, MD, FACS

Thursday, March 11, 2021

Virtual Meeting

Chicago, IL

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Acknowledgements The American College of Surgeons gratefully acknowledges the generous support from the following individuals and organizations for the 44th Annual Resident Trauma Papers Competition: David P. Blake, MD, FACS* Kimberly A. Davis, MD, FACS Warren C. Dorlac, MD, FACS Kimberly M. Hendershot, MD, FACS Kimberly T. Joseph, MD, FACS* Tareq Kheirbek, MD, FACS Stefan W. Leichtle, MD, FACS* Keith R. Miller, MD, FACS* Patricia A. O'Neill, MD, FACS* Lisa A. Patterson, MD, FACS* Wayne E. VanderKolk, MD, FACS George E. Vates, MD, FACS The ACS Iowa Committee on Trauma The ACS Missouri Committee on Trauma Region 7 Committees on Trauma (Advances in Trauma) Benevity Two anonymous donations One anonymous donation* *Donations made during online meeting registration

Acknowledgement is for donations received between March 2020 and February 24, 2021.

Thank you for your interest in supporting the American College of Surgeons Committee on Trauma (ACS COT) programs with a financial commitment. Online: Donate securely online at facs.org/acsfoundation. Click “Donate Now.” You may also contact the ACS Foundation staff at 312-202-5338 or [email protected] with any questions or requests for donation information.

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Resident Trauma Papers Competition Program

1. Program Objectives

• Discuss new research in patient care for trauma injuries• Evaluate new methods for treatment of trauma patients

2. Disclosure Information

In accordance with the ACCME Accreditation Criteria, the American College of Surgeons must ensure that anyone in a position to control the content of the educational activity (planners and speakers/authors/discussants/moderators) has disclosed all financial relationships with any commercial interest (termed by the ACCME as “ineligible companies,” defined on page iv) held in the last 24 months (see page iv for definitions). Please note that first authors were required to collect and submit disclosure information on behalf all other authors/contributors, if applicable.

CONTINUING MEDICAL EDUCATION CREDIT INFORMATION

Accreditation The American College of Surgeons is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.

AMA PRA Category 1 Credits™ The American College of Surgeons designates this live activity for a maximum of 4.25 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Of the AMA PRA Category 1 Credits™ listed above, a maximum of 4.25 hours meets the requirements for Trauma.*

*The content of this activity may meet certain mandates of regulatory bodies. Please note that ACS has not and does not verify the contentfor such mandates with any regulatory body. Individual physicians are responsible for verifying the content satisfies such requirements.

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Program Requirements, Continued

Ineligible Company The ACCME defines an “ineligible company” as any entity producing, marketing, re-selling, or distributing health care goods or services used on or consumed by patients. Providers of clinical services directly to patients are NOT included in this definition.

Financial Relationships Relationships in which the individual benefits by receiving a salary, royalty, intellectual property rights, consulting fee, honoraria, ownership interest (e.g., stocks, stock options, or other ownership interest, excluding diversified mutual funds), or other financial benefit. Financial benefits are usually associated with roles such as employment, management position, independent contractor (including contracted research), consulting, speaking and teaching, membership on advisory committees or review panels, board membership, and other activities from which remuneration is received or expected. ACCME considers relationships of the person involved in the Continuing Medical Education (CME) activity to include financial relationships of a spouse or partner.

Conflict of Interest Circumstances create a conflict of interest when an individual has an opportunity to affect CME content about products or services of an “ineligible company” with which he/she has a financial relationship.

The ACCME also requires that ACS manage any reported conflict and eliminate the potential for bias during the educational activity. Any conflicts noted below have been managed to our satisfaction. The disclosure information is intended to identify any commercial relationships and allow learners to form their own judgments. However, if you perceive a bias during the educational activity, please report it on the evaluation.

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SPEAKERS / AUTHORS NOTHING TO DISCLOSE

DISCLOSURE

COMPANY ROLE RECEIVED

Peter Abraham, MD X Samantha Albacete, MD X Shadi Bsat, MD X Amanda Chelednik, MD X Rachel Y. Chen, MD X Julia R. Coleman, MD, MPH X Alexandra Dixon, MD, MPH X Jessica K. Friedman, MD X Hae Sung Kang, MD X Robert Keskey, MD X Elaa Mahdi, MD, MPH X Max Marsden, MBBS, BSc X Zachary A. Matthay, MD X Luis Saldarriaga, MD X Kyle Stigall, MD X Elizabeth W. Tindal, MD, MPH X Eric Walser, MD X

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DISCUSSANTS NOTHING TO DISCLOSE

DISCLOSURE COMPANY ROLE RECEIVED

Kathryn Beauchamp, MD, FACS X Stephanie Bonne, MD, FACS X Eileen M. Bulger, MD, FACS Atox Bio Ltd Consultant for

FDA review of a drug for patients with Necrotizing Soft Tissue infection, not relevant to COT work

Honorarium

Ashley B. Christmas, MD, FACS X Mark Cipolle, MD, FACS X Mitch Cohen, MD, FACS X Marie Crandall, MD, FACS X Warren Dorlac, MD, FACS Decisio Health

and Zibrio Small investor in both; no active role in the companies

Kimberly Hendershot, MD, FACS Decker Publications

Editor of medical student textbook Surgery Clerkship (none received to date)

Royalties

Sharon M. Henry, MD, FACS X Joakim J. Jorgensen, MD, FACS X Denise Klinkner, MD, FACS X Matthew Martin, MD, FACS Z-Medica Inc Advisory

Board Honorarium

Travis M. Polk, MD, FACS X Heena P. Santry, MD, FACS X Sonlee West, MD, FACS X

PLANNING COMMITTEE / EDITORIAL COMMITTEE

NOTHING TO DISCLOSE

DISCLOSURE

COMPANY ROLE RECEIVED

Scott D’Amours, MD, FACS X Julie A. Dunn, MD, FACS X Any Fenwick, MD, FACS X Brian Harbrecht, MD, FACS X Areti Tillou, MD, FACS X Alison Wilson, MD, FACS X Carrie Sims, MD, FACS X Patrick M. Reilly, MD, FACS X

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Committee on Trauma Resident Trauma Papers Competition Past Winners

1978 1st Place John A. Weigelt Runner Up Mary H. McGrath

1979 1st Place Joseph V. Boykin Runners Up Christopher C. Baker

Frank D. Manart

1980 1st Place Robert Tranbaugh Runner Up Gary M. Gartsman

1981 1st Place Kenneth Kollmeyer Runner Up Kenneth A. Kudsk

1982 1st Place Raj K. Narayan Runners Up George S. Fortner

Hani Shennib

1983 1st Place Mark DeGroot Runners Up Gregory Luna

1984 1st Place Ronald B. O’Gorman Runners Up Louis Ostrow

Frederick A. Moore

1985 1st Place Lawrence Reed Runner Up Frank Shannon

1986 1st Place Richard S. Downey Runners Up Richard Kiplovic Wiley W. Souba

1987 Basic Laboratory Science 1st Place Nicholas B. Vedder 2nd Place B. Timothy Baxter Clinical Research 1st Place Eric DeMaria 2nd Place John D.S. Reid

1988 Basic Laboratory Science 1st Place Gary Fantini 2nd Place David H. Livingston Clinical Research 1st Place Christoph Kaufmann 2nd Place Tomasso Bochicchio

1989 Basic Laboratory Science 1st Place David K. Magnuson 2nd Place Matthew L. Cooper Clinical Research 1st Place Bradley Reeves 2nd Place Danielle Desloges

1990 Basic Laboratory Science 1st Place William J. Mileski 2nd Place Gary A. Gelfand 2nd Place Jon C. Walsh (2nd Place Tie) Clinical Research 1st Place Miguel Lopez Viego

1991 Basic Laboratory Science 1st Place Roy W. Hong 2nd Place Benjamin O. Anderson Clinical Research 1st Place Karl Illig 2nd Place Carson Agee

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Committee on Trauma Resident Trauma Papers Competition Past Winners, Continued

1992 Basic Laboratory Science 1st Place Michael O’Reilly 2nd Place David Bensard Clinical Research 1st Place William S. Hoff 2nd Place Juan Manuel Sarmiento-Martinez

1993 Basic Laboratory Science 1st Place Thomas T. Sato 2nd Place Paul A. Taheri 2nd Place Alastair C.J. Windsor (2nd Place Tie) Clinical Research 1st Place Patricia Yugueros I.

1994 Basic Laboratory Science 1st Place James T. Wilson 2nd Place Robert F. Noel, Jr. Clinical Research 1st Place Stefan J. Konasiewicz 2nd Place Paul J. Gagne

1995 Basic Laboratory Science 1st Place Donald W. Pate 2nd Place Carol J. Cornejo Clinical Research 1st Place Russell R. Lonser 2nd Place John J. Keleman

1996 Basic Laboratory Science 1st Place Kenneth E. Drazan 2nd Place Carlton C. Barnett, Jr. Clinical Research 1st Place Peter D. Wearden 2nd Place Nicholas Namias

1997 Basic Laboratory Science 1st Place Randy J. Irwin 2nd Place Molly M. Buzdon Clinical Research 1st Place Preston R. Miller 2nd Place Katharina Pellegrin

1998 Basic Laboratory Science 1st Place Geoffrey Manley 2nd Place Gregory J. McKenna Clinical Research 1st Place E. Lynne Henderson 2nd Place Juan P. Carbonell

1999 Basic Laboratory Science 1st Place Andrew Kramer 2nd Place D. Kirk Lawlor Clinical Research 1st Place Garret Zallen 2nd Place Avery B. Nathens

2000 Basic Laboratory Science 1st Place Philip P. Narini 2nd Place George D. Oreopoulos Clinical Research 1st Place Joseph T. Rabban 2nd Place Avery B. Nathens

2001 Basic Laboratory Science 1st Place Deepa Soni 2nd Place Daron C. Hitt Clinical Research 1st Place John-Paul Veri 2nd Place Moishe Lieberman

2002 Basic Laboratory Science 1st Place Jonas Gopez 2nd Place Steven Casha Clinical Research 1st Place Ram Nirula 2nd Place Seong K. Lee

2003 Basic Laboratory Science 1st Place Eve C. Tsai 2nd Place Katherine Barsness Clinical Research 1st Place Steven Fox 2nd Place David J. Schultz

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2004 Basic Laboratory Science 1st Place Rachel G. Khadaroo 2nd Place Manuel B. Torres Clinical Research 1st Place Matthew Rosengart 2nd Place Carlos V. R. Brown

2005 Basic Laboratory Science 1st Place John M. Hwang 2nd Place Aaron M. Cheng Clinical Research 1st Place Felicia Ivascu 2nd Place Stephanie P. Acierno

2006 Basic Laboratory Science 1st Place Ananthakrishnan 2nd Place Jessica Deree Clinical Research 1st Place Alexander L. Eastman 2nd Place David O. Francis

2007 Basic Laboratory Science 1st Place Alexander Q. Ereso 2nd Place Sagar S. Damle Clinical Research 1st Place Alexandra Mihailovic 2nd Place Heather F. Pidcoke

2008 Basic Laboratory Science 1st Place Jason M. Seery 2nd Place Elizabeth A. Sailhamer Clinical Research 1st Place Joseph F. Golob, Jr. 2nd Place Sherene Shalhub

2009 Basic Laboratory Science 1st Place Elizabeth A. Sailhamer 2nd Place Reed B. Kuehn Clinical Research 1st Place Alexios A. Adamides 2nd Place Joseph DuBose

2010 Basic Laboratory Science 1st Place Angela L. F. Gibson [Reg 5] 2nd Place Arash Farahvar [Reg 2] Clinical Research 1st Place Barbara Haas, [Reg 12] 2nd Place Thomas M. Schmelzer [Reg 4]

2011 Basic Laboratory Science 1st Place Laura E. White [Reg 6] 2nd Place Marlene Mathews [Reg 2] Clinical Research 1st Place Levi D. Procter [Reg 4] 2nd Place Matthew D. Neal [Reg 5]

2012 Basic Laboratory Science 1st Place Laura E. White [Reg 6] 2nd Place Alex Cuenca [Reg 4] Clinical Research 1st Place Kristin Cook [Reg 2] 2nd Place Jennifer Roberts [Reg 5]

2013 Basic Laboratory Science 1st Place Abubaker A. Ali [Reg 5] 2nd Place Isaiah R. Turnbull [Reg 7] Kristin L. Long [Reg 4] (Tie) Clinical Research 1st Place Eiman Zargaran [Reg 11] 2nd Place David A. Hampton [Reg 10]

2014 Basic Laboratory Science 1st Place Michaela C. Kollisch-Singule [Reg 2] 2nd Place Matthew W. Ralls [Reg 5] Clinical Research 1st Place Hunter B. Moore [Reg 8] 2nd Place Vanessa J. Fawcett [Reg 10]

2015 Basic Laboratory Science 1st Place Simone M. Langness [Reg 9] 2nd Place Michaela C. Kollisch-Singule [Reg 2] Clinical Research 1st Place Deepika Nehra [Reg 10] 2nd Place Cherisse Berry [Reg 3]

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2016

Basic Laboratory Science 1st Place Rachel M. Russo [Reg 13] 2nd Place Sarah Ogle [Reg 9] Clinical Research 1st Place James P. Byrne [Reg 12] 2nd Place Lynn Hutchings [Reg 15]

2017

Basic Laboratory Science 1st Place Teresa C. Rice [Reg 5] 2nd Place Theresa Chan [Reg 9] Clinical Research 1st Place Stephanie A. Mason [Reg 12] 2nd Place Sabrina Balakrishnan, MBBS [Reg 16]

2018

Basic Laboratory Science 1st Place Michael Valliere [Reg 7] 2nd Place Theresa Chan [Reg 9] Clinical Research 1st Place Luke R. Johnson [Reg 13] 2nd Place Jarred R. Gallaher [Reg 4]

2019

Basic Laboratory Science 1st Place Elliott Williams [Reg 9] 2nd Place Patricia Martinez-Quinones [Reg 4] Clinical Research 1st Place Hope Villiard [Reg 7] 2nd Place Parin Boonthum [Reg 16]

2020

Basic Laboratory Science 1st Place Julia R. Coleman [Reg 8] 2nd Place Amanda M. Chipman [Reg 3] Clinical Research 1st Place Alexandra Dixon [Reg 10] 2nd Place Jetan H. Badhiwala [Reg 12]

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2021 Regional Winners Region 1 Elizabeth W. Tindal, MD, MPH Brown University/Rhode Island Hospital, Providence, RI “Live Fast, Die Young: An Evaluation of End-of-Life Care in Young Trauma Patients” Region 2 Elaa Mahdi, MD, MPH University of Rochester, Rochester, NY “Sustaining the Gains: Further Reductions in Unnecessary Computed Tomography Scans in Pediatric Trauma Patients” Region 3 Hae Sung Kang, MD Virginia Commonwealth University (VCU) Health, Richmond, VA “Fluid Resuscitation in Hemorrhagic Shock: Is It Time to Focus on Fluid Therapy That Increases Microcirculation?” Region 4 Peter Abraham, MD The University of Alabama at Birmingham, Birmingham, AL “Understanding the Geography of Trauma: Combining Spatial Analysis and Funnel Plots to Create Comprehensive Spatial Injury Profiles” Region 5 Robert Keskey, MD University of Chicago, Chicago, IL “Injury Severity Score Is an Ineffective Metric for Distinguishing Critical Injury across All Age Groups” Region 6 Jessica Friedman, MD Tulane University School of Medicine, New Orleans, LA “Mitochondrial Reactive Oxygen Species Cause Endothelial Glycocalyx Shedding in a Rat Model of Zone 3 REBOA” Region 7 Amanda Chelednik, MD University of Missouri, Columbia, MO “Artificial Intelligence Model Predicts Mortality in Rural Trauma Patients Utilizing Pre- Hospital Parameters” Region 8 Julia R. Coleman, MD, MPH University of Colorado-Denver, Denver, CO “A Mechanistic Exploration of Sex Dimorphisms in Coagulation: Calcium Signaling Drives Female-Specific Platelet Hyperactivity” Region 9 Zachary A. Matthay, MD University of California, San Francisco and Zuckerberg San Francisco General Hospital, San Francisco, CA “Leveraging the Catecholamine Response after Trauma: An Opportunity to Enhance Platelet-Dependent Hemostasis?”

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2021 Regional Winners Region 10 Alexandra Dixon, MD, MPH Oregon Health & Science University, Portland, OR “FFP Maintains Normal Coagulation While PCC Induces a Hypercoagulable State in a Porcine Model of Pulmonary Contusion and Hemorrhagic Shock” Region 11 Samantha Albacete, MD University of Alberta, Edmonton, AB “Alcohol Use and Trauma in Alberta after COVID-19 Lockdown: Over-Representation and Under-Treatment Are Opportunities for Improvement” Region 12 Eric Walser, MD Western University/London Health Sciences Center, London, ON “Standardization of Opioid Prescription after Trauma (STOP Trauma): A Prospective Intervention to Reduce Opioid Excessive Prescription” Region 13 Kyle Stigall, MD San Antonio Uniformed Services Health Education Consortium, San Antonio, TX “Performance of a Novel Temporary Arterial Shunt in a Military-Relevant Controlled Hemorrhage Swine Model” Region 14 Luis G. Saldarriaga, MD Universidad del Valle, Fundacion Valle del Lili, Cali, Colombia “Resuscitative Median Sternotomy Plus Endovascular Aortic Balloon Occlusion: New Surgical Approach for Penetrating Chest Trauma Management” Region 15 Max Marsden, MBBS, BSc Centre for Trauma Science, Blizard Institute, Queen Mary, University of London, Downe, Kent, United Kingdom “Trauma Laparotomy in the United Kingdom: A Prospective, Multi-Centre Observational Study” Region 16 Rachel Y. Chen, MBBS, MRCS Khoo Teck Puat Hospital, Singapore “CHOP (Critical Hemorrhage to Operating-Room Patient) Resuscitation Protocol Leads to Consistent and Superior Outcomes in a Tertiary Trauma Center: A Cumulative Summation (CUSUM) Analysis” Region 17 Shadi Bsat, MD American University of Beirut Medical Center, Beirut, Lebanon “Beirut Blast 2020: The Neurosurgical Experience from a Tertiary Referral Center in Lebanon”

Institution and location current at time of paper/abstract submission

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2021 Presentation Order Region 13 Kyle Stigall, MD San Antonio Uniformed Services Health Education Consortium, San Antonio, TX “Performance of a Novel Temporary Arterial Shunt in a Military-Relevant Controlled Hemorrhage Swine Model” Discussant: Warren C. Dorlac, MD, FACS Region 17 Shadi Bsat, MD American University of Beirut Medical Center, Beirut, Lebanon “Beirut Blast 2020: The Neurosurgical Experience from a Tertiary Referral Center in Lebanon” Discussant: Kathryn M. Beauchamp, MD, FACS Region 4 Peter Abraham, MD The University of Alabama at Birmingham, Birmingham, AL “Understanding the Geography of Trauma: Combining Spatial Analysis and Funnel Plots to Create Comprehensive Spatial Injury Profiles” Discussant: Sonlee D. West, MD, FACS Region 15 Max Marsden, MBBS, BSc Centre for Trauma Science, Blizard Institute, Queen Mary, University of London, Downe, Kent, United Kingdom “Trauma Laparotomy in the United Kingdom: A Prospective, Multi-Centre Observational Study” Discussant: Marie L. Crandall, MD, FACS Region 14 Luis G. Saldarriaga, MD Universidad del Valle, Fundacion Valle del Lili, Cali, Colombia “Resuscitative Median Sternotomy Plus Endovascular Aortic Balloon Occlusion: New Surgical Approach for Penetrating Chest Trauma Management” Discussant: Matthew Martin, MD, FACS Region 3 Hae Sung Kang, MD Virginia Commonwealth University (VCU) Health, Richmond, VA “Fluid Resuscitation in Hemorrhagic Shock: Is It Time to Focus on Fluid Therapy That Increases Microcirculation?” Discussant: Joakim J. Jorgensen, MD, FACS Region 7 Amanda Chelednik, MD University of Missouri, Columbia, MO “Artificial Intelligence Model Predicts Mortality in Rural Trauma Patients Utilizing Pre- Hospital Parameters” Discussant: Alison M. Wilson, MD, FACS

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2021 Presentation Order Region 8 Julia R. Coleman, MD, MPH University of Colorado-Denver, Denver, CO “A Mechanistic Exploration of Sex Dimorphisms in Coagulation: Calcium Signaling Drives Female-Specific Platelet Hyperactivity” Discussant: Heena P. Santry, MD, MS, FACS Region 2 Elaa Mahdi, MD, MPH University of Rochester, Rochester, NY “Sustaining the Gains: Further Reductions in Unnecessary Computed Tomography Scans in Pediatric Trauma Patients” Discussant: Denise B. Klinkner, MD, FACS Break There will be a 10-minute break before continuing with the Region 12 presentation Region 12 Eric Walser, MD Western University/London Health Sciences Center, London, ON “Standardization of Opioid Prescription after Trauma (STOP Trauma): A Prospective Intervention to Reduce Opioid Excessive Prescription” Discussant: Robert Shayn Martin, MD, FACS Region 10 Alexandra Dixon, MD, MPH Oregon Health & Science University, Portland, OR “FFP Maintains Normal Coagulation While PCC Induces a Hypercoagulable State in a Porcine Model of Pulmonary Contusion and Hemorrhagic Shock” Discussant: Mitchell J. Cohen, MD, FACS Region 11 Samantha Albacete, MD University of Alberta, Edmonton, AB “Alcohol Use and Trauma in Alberta after COVID-19 Lockdown: Over-Representation and Under-Treatment Are Opportunities for Improvement” Discussant: Ashley B. Christmas, MD, FACS Region 6 Jessica K. Friedman, MD Tulane University School of Medicine, New Orleans, LA “Mitochondrial Reactive Oxygen Species Cause Endothelial Glycocalyx Shedding in a Rat Model of Zone 3 REBOA” Discussant: Carrie A. Sims, MD, FACS

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2021 Presentation Order Region 1 Elizabeth W. Tindal, MD, MPH Brown University/Rhode Island Hospital, Providence, RI “Live Fast, Die Young: An Evaluation of End-of-Life Care in Young Trauma Patients” Discussant: Mark D. Cipolle, MD, FACS Region 5 Robert Keskey, MD University of Chicago, Chicago, IL “Injury Severity Score Is an Ineffective Metric for Distinguishing Critical Injury across All Age Groups” Discussant: Kimberly M. Hendershot, MD, FACS Region 9 Zachary A. Matthay, MD University of California, San Francisco and Zuckerberg San Francisco General Hospital, San Francisco, CA “Leveraging the Catecholamine Response after Trauma: An Opportunity to Enhance Platelet Dependent Hemostasis?” Discussant: Stephanie L. Bonne, MD, FACS Region 16 Rachel Y. Chen, MBBS, MRCS Khoo Teck Puat Hospital, Singapore “CHOP (Critical Hemorrhage to Operating-Room Patient) Resuscitation Protocol Leads to Consistent and Superior Outcomes in a Tertiary Trauma Center: A Cumulative Summation (CUSUM) Analysis” Discussant: Travis M. Polk, MD, FACS

Institution and location current at time of paper/abstract submission

Region 13 – Basic Science

Performance of a Novel Temporary Arterial Shunt in a Military-Relevant Controlled Hemorrhage Swine Model

Kyle Stigall, MD

INTRODUCTION Vascular injuries to the extremities have accounted for a significant portion of battlefield morbidity in recent conflicts. Delays in revascularization are associated with increased risks of ischemic necrosis, reperfusion injury, and amputation. Temporary vascular shunts (TVS) are frequently employed as a primary vascular damage control maneuver to establish temporary perfusion until definitive vascular reconstruction.

Thrombosis is a known complication of TVS and is associated with poor limb outcomes. Shunt patency depends on a variety of factors including shunt dwell time, injury location, and patient resuscitation status. These challenges illustrate the need for a shunt that is tolerant of low systemic blood pressure and longer dwell times.

Multiple commercially produced TVS are available, but none are designed specifically for use in vascular trauma applications. The ability to provide local anticoagulation and/or continuous monitoring of shunt patency would add significant value to a product for use in combat casualty care. The Trauma-Specific Vascular Injury Shunt (TS-VIS) is a novel TVS that seeks to address these needs. The shunt has an integrated side which allows for continuous monitoring of shunt pressure and delivery of therapeutic agents (Figure 1A). The aim of this study is to evaluate the TS-VIS against a commercially available TVS in a swine model of hemorrhagic shock and extremity vascular injury.

METHODS Fifteen female Yorkshire-landrace swine (70-90 kg) were allocated to one of three groups (n=5/group); based shunt treatment: commercially available Sundt shunt (SUNDT), TS-VIS with arterial pressure monitoring via the side port (TS-VIS), or TS-VIS with heparin infusion at 10u/kg/h through the side port (TS-VISHep). The animals underwent endotracheal intubation, placement of vascular access, and positioning of flow probes around bilateral femoral arteries. The following interventions were performed through a midline laparotomy: 1) splenectomy to prevent auto-transfusion, 2) ligation of the bilateral internal and circumflex iliac arteries to prevent antegrade collateral flow, and 3) isolation of the left external iliac artery (LEIA) for injury and shunt placement.

Following a ten-minute stabilization period, a 6 Fr introducer was inserted into the LEIA. Injury was simulated by occlusion of the vessel and a simultaneous controlled hemorrhage of 30% estimated blood volume. After a 30 minute “injury period,” the appropriate randomly assigned shunt was inserted into the LEIA through an arteriotomy (Figure 1B). The TS-VIS shunt side ports were connected to a standard fluid column arterial pressure monitor and the TS-VISHep sideports to a pump infusing unfractionated heparin at 10u/kg/h in normal saline at 50 mL/hr. Resuscitation with up to 3 units (500mL/unit) of shed blood volume occurred concurrently to maintain a MAP > 60.

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Systemic blood pressure, blood flow in both femoral arteries, and leg muscle oxygenation were continuously monitored for six hours or until shunt thrombosis. Thrombosis was defined as absence of a positive flow value from the left femoral flow probe for five minutes. Arterial blood samples were taken at baseline and at 30, 90, 150, 210, 270, 330, and 390 minutes after hemorrhage.

The primary outcome of the study was shunt patency time. Sample size was estimated at five animals per group to provide 80 percent power to detect a 60% difference in shunt patency between groups with a significance level of 0.05. Kaplan Meier and log ranks analysis were used for comparing overall shunt patency. Continuous variables were analyzed with one-way analysis of variance with Student-Neuman-Keuls post hoc testing.

RESULTS Fifteen animals weighing 78.4 ± 6.3 kg were used, five animals per experimental group. The three groups were homogeneous at baseline in terms of hemodynamics, thigh tissue oxygenation, and laboratory parameters.

Hemorrhage of 30.1% ± 0.7% of estimated blood volume resulted in significant hypotension with a MAP of 35.5 ± 7.3 mmHg across all groups at the time of shunt insertion, with no intergroup differences. Occlusion of the LEIA resulted in left femoral flow values of 0.4 ± 1.2 mL/min versus 90.9 ± 25.9 mL/min in the right femoral artery, with no significant intergroup differences. Animals were hypotensive at shunt placement (MAP 35.5±7.3 mmHg), and resuscitation raised MAP to >60 mmHg by 26.5±15.5 min (Figure 2). Shunt placement required an average of 4.5 ± 1.8 minutes with no difference between groups.

The TS-VIS and TS-VISHep groups outperformed the SUNDT group (P=0.04) (Figure 3). Two TS-VIS and one TS-VISHep thrombosed, all between 230 and 282 minutes. The remainder were patent for the entire six-hour observation period, with a median patency of 360 minutes for both TS-VIS groups. Only a single SUNDT maintained patency for six hours. Three thrombosed within 20 minutes and one thrombosed at 241 minutes. Median patency for the SUNDT group was 21 minutes (P=0.04 versus TS-VIS and TS-VIS Hep).

DISCUSSION Vascular injury accounts for approximately 17% of all battlefield injuries. Damage control surgery, TVS placement, and evacuation to higher levels of care are how many of these patients are treated. Limited resources and protracted evacuation periods extended TVS dwell times while increasing the risk for shunt thrombosis. The novel TS-VIS with its uniquely designed side port has the potential to mitigate this risk of thrombosis. The findings of this study reveal that the TS-VIS is effective at restoring distal blood flow in an injured extremity and has a superior patency rate when compared to a conventional vascular shunt.

Both the TS-VIS and TS-VISHep groups were found to be effective at restoring blood flow. There were no significant differences in the distal flow rate, in the markers of ischemia (pH, lactate, potassium), or in the heart rate. Similar placement times show that there was no increase difficulty in positioning the TS-VIS.

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There was a significant difference between the patency rate of the SUNDT group compared to the TS-VIS and TS-VISHep groups. The majority of SUNDT shunts thrombosed within the first 30 minutes of the protocol while both TS-VIS groups had median patency rates lasting up until study termination. As the SUNDT shunt and the TS-VIS have a similar length, inner lumen diameter, and are both made of silicone material, we believe the superior patency rates are related to the unique TS-VIS side port. Analysis of MAP and thrombosis time suggest shunt thrombosis is dependent on perfusion pressure within the shunt. The TS-VIS appears to be more tolerable of hypotension and variations in perfusion pressures.

Interestingly, there were no significant differences between the TS-VIS and TS-VISHep groups in regard to median patency time or patency rate. We believe this is due to the pressurization that the invasive arterial monitoring provides. Further studies are warranted to assess if localized heparin infusion would result in improved patency when assessed over an extended observation period greater than 6 hours.

CONCLUSION The TS-VIS with and without heparin infusion demonstrated sustained patency superior to that of the Sundt shunt under adverse hemodynamic conditions. Early patency appears dependent on blood pressure and this model of volume limited resuscitation provides a rigorous test for peripheral arterial shunts. No discernable benefit was observed by the addition of localized heparin therapy over constant arterial pressure monitoring by the TS-VIS side port within the first 6 hours of placement.

Figure 1. TS-VIS (A) TS-VIS alone (B) TS-VIS inserted into the left external iliac artery

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Figure 2. Blood pressure (blue arrow marks shunt placement/start of resuscitation)

Figure 3. Patency curve

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Region 17 – Clinical Research

Beirut Blast 2020: The Neurosurgical Experience from a Tertiary Referral Center in Lebanon

Shadi Bsat, MD

ABSTRACT August 4, 2020, is a date that will not only resign in the minds of the Lebanese, but in the mind of every single physician who reported to duty. On that day, a large amount of ammonium nitrate stored at the port of the city of Beirut, exploded, causing more than 200 deaths and 6,000 injuries.

In this paper, we will shed the light on this traumatic event that took place in the era of Covid-19, from a tertiary referral center in Lebanon. We will discuss what happened in the eyes of a neurosurgeon, from the ED experience, to the OR, and to the post op care. Also, we will present our results and review our setbacks at that day. This paper urges the medical personnel and the neurosurgeons in particular, to be aware of the potential for similar mass causality events and to make necessary preparations.

INTRODUCTION Many awful dates reside in the memory of the Lebanese population; dates that remind them of wars, of revolutions, of explosions, of massacres, of political and financial turmoil.. but August 4th, 2020 is a date that will not only resign in the minds of the Lebanese, but in the mind of every single physician who reported to duty on that day.

In this paper, we will shed the light on this traumatic event that took place in the era of Covid 19; an event that stands out among all others that took place in this country. We will discuss what happened in the eyes of a neurosurgeon, from the ED experience, to the OR, and to post-op care.

2020 BEIRUT EXPLOSION The explosion took place on Tuesday in the early evening; the code was immediately activated in the hospital in need of all hands on to help. AUBMC’s infrastructure was damaged, but luckily not destroyed like other hospitals in Beirut. Every physician from all different specialties reported immediately to the ER. The ER hosted residents from all surgical and non-surgical specialties, intensivists, attendings, nurses, clerks, administrative employees, and other workers. In a jiffy the ER was fully occupied with patients who rushed from the streets; patients with minimal injuries were sharing the same room; others were in the hallway, on chairs, on stretchers and some were laying on the ground.

Nothing mattered at that point but to keep everyone alive and help in the best way possible to alleviate everyone’s pain.

We were working under destroyed roofs, with minimal lighting due to malfunctioning electrical lines. We don’t have the luxury to access patient’s files, to open our computerized systems or log in patient data. We were working with minimal amount of PPEs available in a place were no precautions were taken to protect one another from spreading the COVID infection. No we did not have the luxury to wait for the routine COVID test to be out negative in order to operate on a patient and intubate

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Region 17 – Clinical Research him/her. Time was brain and whoever was in need of a craniectomy was rushed to get one. Was intubated despite the fear of spreading the infection in our systems. Chief complaints with type of injuries were written on each patient’s bed sheet. Surgical teams were divided according to their area of specialty to benefit the most out of every resident. As for neurosurgery, the whole team was present with all the attendings. We encountered a lot of injuries; many were superficial with scalp lacerations that were immediately dealt with; and others were fatal. Minor head injuries were taken up to the floors were medical students and nurses were taking care of them in the hallways. Patients who are in good status to be discharged home were immediately discharged to provide space for other casualties.We divided the team to have some residents in the OR and another in the ER. In collaboration with the surgical trauma team and the neurology team we were assessing every patient with a head trauma. Selection was based on how critical the patient’s status was depending on their neurological exam. We had 3 available CT scan rooms only! We were not able to screen everyone with a head trauma. Patients who were fully alert, and oriented with no deficits on exam did not undergo any imaging studies. Others with minor deficits were left aside for monitoring after noting their name and case presentation. Patients with severe head injuries, deficits on exam or altered level of consciousness were rushed to the CT scan room. Many non-surgical SAH and SDH were diagnosed and were monitored by the neurology team. Every patient’s name was written down for follow up. OR EXPERIENCE The scene was chaotic in the operating theater yet organized with proper division of tasks. After being assessed in the ED by the neurosurgery junior residents, surgical casualties were taken to the recovery room right away. Senior residents transported the patients to the operating room accompanied by an attending. Most of the cases were subdural and epidural hematomas. At one point, there were four operating rooms running at the same time. This is uncommon; given that we are usually prepared to run only two operating rooms simultaneously on a regular surgical day. The senior residents were playing the role of the primary surgeon, and the attendings were shifting from one room to another, making sure that the workflow is smooth. When it came to Nurses, they were very organized and helpful. Even those who were off work presented to offer help. The tasks were divided, and each nurse was waiting in his/her assigned room, preparing for the coming case. This did not just save time but lives as well, as it fastened the process. That night, we operated on 7 cases within almost 4 hours. Everything went smoothly except that we were short on sterile equipment in the cases that came last. We had to use general surgery kits and skip many steps that we usually perform in a regular craniotomy. However, It was acceptable since we were dealing with a simple craniotomy. We were working with only two drills, and we had to send each for sterilization directly after completing each craniotomy so that it can be ready for the case that followed. At that time, we were not sure about how many patients we are going to operate on, and we had to be ready for the worst scenario.

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POST-OP MANAGEMENT IN ICU AND ON FLOOR After finishing all surgeries, it was time to recap and reassess our neurosurgical patients. The general surgery trauma team was assigned to take care of all casualties admitted to the hospital. We prepared a unified list of patients in order not to miss any. Then, we performed a multidisciplinary round and passed by each case for a secondary survey. The same process was done in the intensive care unit, and a common round was done with the ICU team on all our patients. We were able to check on all our patients, re-examine, and order further workup when needed.

RESULTS A total of 25 patients were admitted under the care of neurosurgery team at the American University of Beirut Medical Center. 60% of the patients were males (n=15) and 40 percent were females (n=10). A total of 23 patients were adults with age range of (26-78) years and 2 were pediatric patients of 5 weeks and 9 months of age. Most of the patients had cranial pathologies (n=16), of which half were surgical candidates and the other half were admitted for observation. The rest of the patients (n=6) had spinal injuries, of which only 2 were surgical candidates, beside 3 patients who had both cranial and spinal pathologies who did not need any surgical intervention.

Of the 15 non-surgical patients, 8 had cranial injuries, 4 had spinal injuries and 3 had combined spinal and cranial injuries. Out of the 8 patients with cranial injuries, 7 had subarachnoid hemorrhage and one had subdural hematoma. Most nonsurgical patients with subarachnoid hemorrhage (n=5) were admitted to the ICU with an average length of stay of 4 days for monitoring and hourly neuro-checks. The patients with non-surgical spinal injuries had spine fractures such as C5 laminal fracture, mild L1 wedge fractures and T1 vertebral body fractures.

For the patient with cranial pathologies out of 16, 8 were surgical candidates mostly presenting with subdural or epidural hematomas with or without an underlying skull fracture. Five patients had a GCS of 3 on presentation and the 6th patient maintained a GCS of 13. 5 of these patients underwent decompressive craniectomy with control of the bleeding vessels especially cases with an epidural bleed. One of these patients had a depressed skull fracture of which was elevated with the trauma bone flap. Of these patients, one patient became brain dead in the recovery room about one hour postoperatively with bilateral fixed dilated pupils. Another patient was re-operated on after 1 hour in recovery room due to high drain output and hemodynamic instability, intra-operatively this patient had a severe injury to the superior sagittal sinus with uncontrolled bleeding, massive transfusion was initiated but the patient arrested multiple times during the surgery and did not pick up after aggressive resuscitation. The other patients were admitted to ICU postop for continuity of care. 2 out of 3 where discharged after an average of 2 weeks with good outcome, while the third patient is still debilitated, with a tracheostomy and feeding tube on the neurology/Neurosurgery service.

Two of the 16 cases with a depressed skull fracture and underlying epidural hematomas were evacuated through a craniotomy, admitted to regular floors and discharged on post-operative day 2 and 3. Another female patient had an acute subdural hematoma with a preserved GCS score, underwent a craniotomy was admitted also to the regular ward, discharged on day 4.

For patients with injuries to the spinal column, only two of them were surgical candidates. The first patient had a type 3 odontoid fracture with posterior dislocation, underwent C1-C3 screw fixation with pars and lateral mass screws, discharged home few days’ post procedure with rigid neck collar.

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The other patient presented on the day of the blast in severe hypovolemic shock due to hemothorax with multiple thoraco-abdominal injuries, underwent a thoracotomy with lobectomy for control of bleeding and had complicated ICU stay where he required renal replacement therapy. From our side he had bilateral traumatic pars fractures at L5 vertebrae with jumping facets and grade 2 spondylolisthesis. He underwent surgery after 1.5 months in-house with L4- S1 instrumentation laminectomy and reduction of spondylolisthesis down to grade 1. The plastic surgery team were on board with a V-Y plasty for closure of sacral defect. Patient was admitted to regular floor post operatively discharged after 1 week for aggressive rehab and physical therapy.

SETBACKS At our institution, we use a computerized health care system known by “Epic”, where all labs and imaging studies are ordered and processed through it. Using this system was not practical and applicable in such an event due to the big number of casualties that presented to the hospital and due to lack of personnel, be it doctors or nurses, who didn’t have a minute to enter any data on the systems. We thus were not able to find and recheck each patient’s labs and imaging studies. In many cases, we had to re-order studies that were already done just to make sure we were not missing any injury.

In such an event, this high-tech system was a setback. No patient data whatsoever was able to be entered. Not the name nor the patient’s medical number. The lab couldn’t have the time to both process the samples at hand and enter the results on the system. We couldn’t access blood types by a click on the system. We had patients who were bleeding due to other traumatic injuries and required transfusions.

This necessitates having a backup plan that should be activated in case of major events like this. Organized set of hardcopy files should be available once we face another similar disaster. It will save us some time, and will keep track of the lab and imaging studies performed on patients.

Patients under neurosurgery

care: n=25

surgical patients: n=10

cranial: n=8 spinal: n=2

non-surgical patients: n=15

cranial: n=8 spinal: n=4 spinal+cranial: n=3

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Not to forget to mention that despite all the challenges mentioned, there is one major challenge that outweighs all, which is working in the era of COVID-19. With limited PPEs, having to use used masks, and missing all screening COVID tools we previously applied, put all of us, in addition to any patient entering the hospital at risk. It takes one COVID positive patient, who needs urgent life-saving intubation to spread the virus in our ventilating system and infect others. The number of patients present in the ED outweighed its capacity. The rooms assigned for intubating/treating COVID suspected patients were all occupied with casualties. A whole body of doctors was standing naked in front of an infection that we all know might put an end to many of us, but we proceeded anyway. Assigning trauma rooms for suspected patients or for those in need of urgent intubation would have increased the risk of spreading the infection. DISCUSSION We were taught how to deliver bad news in medical school. It was a process we have to follow in order to succeed at delivering the news to the patient’s family. None of these rules stood out that day. Patient’s family rushed with us to the CT scan rooms. They were listening to our conversations amongst each other with all our jargon stating that surgery can’t salvage this woman’s brain because it has already herniated outside her skull, and no surgery can save this man’s brain from the diffuse subarachnoid hemorrhage. It was inevitable by all means. Inevitable for us to behave in the way we ought to do on a regular day. Inevitable for us to properly tell a 20 year old that her mom is brain dead. We had to rush from one patient to another in order to save as much people as we can. No time was given for us to practice medicine the way we want to. The way that implies explaining the full patients’ cases to their families, giving them the time to say goodbye when needed, to digest that the person they once knew is brain dead or drain injured where the chances are he/she will not wake up again. This was a traumatic experience for them and for us. No doctor had the time to check up on their own families. None of us was able to check the news to know what actually happened. We were working nonstop for hours, without giving our mind the time to comprehend the situation at hand. We kept wondering among ourselves if the people we know, our families and friends are still alive. Months have passed after the explosion, and discussions about August 4 didn’t settle. Many psychiatry teams and mental health programs were initiated at the hospital to help one another overcome the trauma we faced; but we believe this goes far beyond fixing. CONCLUSION Time was brain. All surgical patients successfully underwent surgery. A small number died before reaching the OR room; others survived their injuries, were taken to the floors and were discharged home. Those who required cranioplasty returned for surgery with smooth uncomplicated course after their first discharge. Psychiatry teams and neuropsychologists were on board and assessed each case.

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Region 17 – Clinical Research The explosion had its toll on us, be it on the team or on the hospital itself. However, it took resilience, organized teamwork and proper division of tasks to complete the task successfully and deliver our best to the patients. At the end, it is worth mentioning the effort it took each physician to put one’s worries aside in the light of such a trauma and to focus selflessly on delivering the best care possible to the patients. Our patients survived this blast; but did we really?

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Understanding the Geography of Trauma: Combining Spatial Analysis and Funnel Plots to Create

Comprehensive Spatial Injury Profiles

Peter J. Abraham, MD; Brandon M. Crowley, BS; Dylana Moore, BS; Shannon Stephens, EMTP; Michael Minor, BBA NRP; Russell L. Griffin, PhD; Zain Hashmi, MD; John B. Holcomb, MD;

Jeffrey D. Kerby, MD PhD; Jan O. Jansen, MBBS, PhD BACKGROUND Understanding geographic patterns of injury is essential to operating an effective trauma system and targeting injury prevention. The wide availability of data and mapping software has simplified the cartographic presentation of incident location data. However, the difference between case volume (absolute number of incidents), and incidence rate (number of cases per population) is not always well understood. Choropleth maps (maps shaded in relation to data) are helpful in showing spatial relationships, but are unable to provide estimates of spread, such as confidence intervals (CI). Funnel plots can overcome this issue and are a recommended graphical aid for comparisons in which an estimate of an underlying quantity is plotted against an interpretable measure of its precision, thereby quantifying degrees of confidence. The purpose of this project was to demonstrate the complementary roles of choropleth maps and funnel plots, and to inform the further development of the Alabama Trauma System. METHODS The State of Alabama (population 4.9 million) has a central Trauma Communications Center (TCC) which coordinates the Emergency Medical Service (EMS) transport for patients who meet the trauma system entry criteria. This is a retrospective analysis of TCC adult data from January 2014 through December 2016. We extracted demographic details and incident location, coded by county. QGIS, a freely available geographical information systems package (https://qgis.org/en/site/), was used to create choropleth maps of case volume. We then calculated the incidence rate (number of cases per population), using georeferenced census data, and again mapped the results using choropleth maps. Funnel plots were constructed to relate incidence rate to county population, with counties outside the 95% CI representing possible outliers and counties outside the 99% CI representing probable outliers. County incidence rates were compared to social vulnerability ranking based on the CDC Social Vulnerability Index (SVI), creating subgroups within the funnel plots. We also created histograms to evaluate the statistical distribution of the incidence rates to evaluate assumptions regarding normalcy. RESULTS We identified 23,290 trauma incidents during the study period, with an overall statewide incidence rate of 47 incidents per 10,000 persons. The highest number of trauma incidents occurred in Jefferson (n=5,487) and Mobile (n=2,980) counties, which are the most populous in the state. Figure 1 and 2 show the spatial distribution of case volume and incidence rates (cases/population), as choropleth maps, highlighting that case volume and incidence rates are not always congruent.

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Region 4 – Clinical Research For example, 3 of the 4 counties with the highest incidence rates had less than 200 total trauma incidents (Conecuh, n=190; Clay, n=143; Coosa n=111) during the three-year time period. Conecuh (157 per 10,000) and Walker (147 per 10,000) counties had the highest overall incidence rates, whereas Dale (1 per 10,000) and Madison (2 per 10,000) counties had the lowest trauma incidents per capita. For critical injuries, Walker (4.7 per 10,000) and Conecuh (4.1 per 10,000) counties again contained the highest incidence rates. Jefferson (19 per 10,000) and Escambia (18 per 10,000) counties had the highest penetrating injury incidence rates, whereas Conecuh (152 per 10,000) and Walker (135 per 10,000) counties had the highest blunt injury incidence rates.The funnel plot in figure 3 shows that only 7 counties had incident rates as expected for the population (within 95% CI), while 25 counties were probable high outliers (>99% CI), and 35 counties were probable low outliers (<99% CI) for overall trauma incidence rate per capita. There were no possible outliers (between the 95% and 99% confidence intervals). More than half of the lowest vulnerable counties (green markers) had higher injury rates (63% above mean, n=10) while the highest SVI counties (red markers) had the lowest injury rates (12% above mean, n=2). Figure 4 shows that the incidence rates are not normally distributed and instead follow a Poisson distribution. CONCLUSION This study demonstrates the utility of combining choropleth maps and funnel plot analyses to better describe the spatial injury profile in Alabama. The spatial distribution of trauma case volume follows that of the general population, with clusters around the metropolitan areas of Birmingham, Huntsville, and Mobile. This correlates with the location of the state’s Level I trauma centers, which is reassuring. The spatial distribution of incidence rates is different with the highest rates typically found in counties adjacent or proximal to the large metropolitan areas in the state. Conecuh and Walker counties have the highest trauma per capita rates, although case volume is low. While the shading on choropleth maps is illustrative, it does not provide a means of evaluating the significance of the differences between case volume and incident rates. The funnel plots aid the interpretation of these maps by clarifying the significance of these differences. In addition, lower SVI counties tended to have higher incidence rates compared to higher SVI counties. This approach and associated findings have implications for injury prevention. We acknowledge several limitations associated with this approach. Firstly, geographic analyses are subject to spatial autocorrelation. This means that neighboring areas tend to have similar characteristics, violating the assumption of independence. Furthermore, geographical data are rarely normally distributed. In summary, this study provides useful insight regarding the complementary roles of choropleth maps and funnel plots to describe geographic distribution of trauma in Alabama. Future work is required to address issues surrounding spatial autocorrelation and the non-parametric distribution of the incidence rates, which may be best approached using Bayesian methods. Comprehensive geospatial analyses may help guide a data-driven approach to trauma system optimization and injury prevention in Alabama and beyond.

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Figure 1. Choropleth county map of Alabama showing overall trauma incidence rates

Figure 2. Choropleth county map of Alabama showing incidence rates per population

Figure 3. Funnel plot showing overall incidence rates per 10,000 population

Figure 4. Histogram showing distribution of incidence rates

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Trauma Laparotomy in the United Kingdom: A Prospective, Multi-Centre Observational Study

Max Marsden, MBBS, BSc

BACKGROUND The advent of damage control surgery (DCS) in the late 1980s revolutionized trauma care for bleeding patients with abdominal injuries, resulting in improved clinical outcomes and a generation of new survivors. More recently, damage control resuscitation (DCR) strategies employ balanced resuscitation and empiric blood component therapy for rapid correction of trauma induced coagulopathy. In partnership with DCS, DCR has further reduced mortality and morbidity. Despite widespread use of both DCR and DCS across many trauma systems the mortality rate for hypotensive bleeding trauma patients who require emergency laparotomy remains at approximately 50%.1-3 In the United Kingdom (UK), the provision of major trauma care has undergone a series of radical changes since 2010. Implementation of regional major trauma networks have led to paradigm shifts in processes of care and improved overall survival.4 However, a lack of specific key performance indicators (KPI) in abdominally injured patients make it challenging to identify outcome improvements in these patients. The objectives of the study were first to describe the characteristics and outcomes of patients undergoing trauma laparotomy and laparoscopy within 24 hours of injury; second, processes of care and trauma specific KPIs; and finally, to identify opportunities for performance improvement in those patients who did not survive. METHODS A prospective multicenter observational study was conducted over six months from January 2019. Through the newly created trainee led National Trauma Research and Innovation Collaborative (NaTRIC) 34 hospitals across the UK submitted data to the study. The contributing sites included all 23 Major Trauma Centres in England. Research Ethics Committee approval was not required in line with the UK Health Research Authority guidance. Patient selection and data collection Both adults and children were eligible for inclusion if they had sustained a blunt or penetrating injury and had a laparotomy or laparoscopy within 24 hours of injury. Data were captured for a pre-defined 6-month period from 1st January 2019 until the 30th June 2019. Data were recorded on patient demographics, mechanism and characteristics of injuries, resuscitation, investigations and surgical management from pre-hospital care to hospital discharge. Patient data were recorded by investigators based at each participating centre and anonymised data were analysed centrally. Patients were excluded if more than 30% of their data was missing. No imputation for missing data was performed. Quality indicators and outcomes In the absence of specific standards for the management of patients undergoing emergency trauma laparotomy, we compared KPIs to existing standards from related emergent conditions. The standards were based on or taken from the national guidelines on Major Trauma, emergency laparotomy, and the NHS best practice tariff for trauma.

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Region 15 – Clinical Research KPIs included the proportion of patients with consultant (attending) led care and time intervals from injury to key events (arrival in hospital, arrival in the operating room (OR), knife-to-skin, imaging, and tranexamic acid (TXA) delivery). Subgroup analysis was performed for patients with major bleeding (defined as activation of the Major Haemorrhage Protocol (MHP) and receipt of at least one unit of red blood cells (RBC)).6 RESULTS Patient and management characteristics The study included 363 patients from 34 hospitals. The majority were young males with no co-morbidities who required surgery for control of bleeding (51%) or exploration of penetrating injuries (46%). More than half of the patients (211/363) had sustained penetrating trauma and there was substantial variation in penetrating injury rates between the study sites. On arrival to hospital a third (121/363) were shocked (lactate >4 mmol/L), 16% (58/363) were hypotensive (BP ≤90mmHg) and 42% (154/363) met the major bleeding (MB) definition. Laparoscopy was used in 16% of patients and varied widely across study sites. One third (19/57) of laparoscopic procedures were converted to laparotomy. Processes of care More than 90% of patients received consultant-led care in the emergency department (318/363) and OR (321/363). The MB subgroup had expedited timelines from ED arrival to knife-to-skin (MB: 119 (64-218) minutes vs No MB: 211 (135-425) minutes, p<0.001). MB non survivors had the shortest times in ED and lowest incidence of a reported delay in transfer to the OR (9%). Only one third of MB patients underwent surgery within two hours of ED arrival. Median operative times were longer in MB (MB: 120mins vs No MB: 105mins, p=0.005) with only 14% patients having surgery completed within one hour (Table 1).

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Region 15 – Clinical Research Table 1. Comparison of the processes of care between patient subgroups receiving abdominal surgery after injury All Non-MHP MHP Survivors MHP Non-

Survivors Number 363 209 122 32 Preoperative Care

TXA, n(%) 278 (77) 134 (64) 115 (94)** 29 (91)##

Preoperative delay, n(%) 65 (18) 44 (21) 18 (15) 3 (9)

CT, n(%) 310 (85) 198 (95) 95 (78)** 17 (53)## +

Consultant Team Leader, n(%) 318 (88) 173 (83) 115 (94)* 30 (94)

Intraoperative Care

Consultant Surgeon in OR, n(%) 321 (88) 175 (84) 114 (93)* 31 (97) Consultant Anaesthetist in OR, n(%) 278 (77) 137 (66) 111 (91)** 30 (94)

##

Key Timings

Time to TXA (IQR) 45 (29-71) 49 (29-90) 42 (28-63) 44 (29-57) Time from injury to ED, median (IQR) 66 (47-91) 60 (46-86) 70 (51-96) 74 (52-104)

Time from ED to KTS, median (IQR) 167 (109-358) 211 (135-425) 126 (76-221)** 65 (40-204)##

Time from OR arrival to KTS, median (IQR) 28 (16-43) 31 (20-47) 25 (16-38) 15 (5-24)

## ++

Operative time, median (IQR) 110 (75-160) 105 (73-139) 116 (80-190)* 135 (47-187) 1Includes conversions to open procedure (n=19) *p<0.05 **p<0.01, Non-MHP vs MHP Survivors; #p<0.05 ##p<0.01, Non-MHP vs MHP Non-Survivors; +p<0.05, ++p<0.01, MHP Survivors vs MHP Non-Survivors. CT, Computed Tomography; ED, Emergency department; FAST, Focused abdominal sonography in trauma; KTS, Knife-to-skin; MHP, Major haemorrhage protocol; OR = Operating room; TXA, Tranexamic acid. Survival outcomes The overall mortality rate was 9%. Two-thirds of deaths occurred within 24 hours of hospital arrival and 45% (15/33) died during the trauma laparotomy. The principal causes of mortality were uncontrolled bleeding (52%) and multiple organ failure (21%). Patients suffering blunt trauma had a greater risk of death compared to patients with penetrating injuries (16.6% vs 3.8%, risk ratio 4.3 [95% CI 2.0-9.4]). Major bleeding patients constituted a high-risk subgroup, accounting for 42% of the study cohort but 97% of deaths and 96% of blood components transfused. ISS was significantly higher in the non-survivors (36 vs 16, p<0.001) and those who died were more likely to have associated severe chest injuries (AIS ≥3: Non-Survivors 52% vs Survivors 36%, RR 1.8 [95% CI 0.9-3.5], p=0.12). CONCLUSION This study of more than 350 trauma laparotomies is the first to report national data from all MTCs following regionalization of care in the UK. We have described the patient demographics, mechanism of injuries, resuscitation practice, and surgical management. We observed high rates of senior clinician involvement but not complete in both bleeding and non-bleeding cohorts. Adherence to national guidelines was good in particular major hemorrhage protocol utilization and early TXA administration.

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Region 15 – Clinical Research The study identifies a 9% risk of death amongst patients undergoing abdominal surgery within 24 hours of injury. However, that risk is almost entirely confined to patients that are bleeding. More than a third of patients with hypotension on arrival in ED that get to the OR within 90 minutes still die from their injuries. Compared to mature trauma systems in the United States and cohort military studies, overall mortality compares favorably but remains unacceptably high. These findings support existing evidence that many patients who die from non-compressible torso hemorrhage continue to deteriorate despite modern surgical and trauma resuscitation practices. This group of bleeding patients represents a key focus of future research endeavors as their outcomes appear to be in contrast to the wider improvements in outcomes across the general trauma population.4 There is a requirement for validated key performance indicators for emergency trauma laparotomy in the UK and ROI, with national engagement amongst clinicians. Such measures may facilitate excellence in care, highlight and mitigate shortfalls, and identify avenues for novel therapeutic strategies for the patients in most need. REFERENCES 1. Clarke JR, et al. Time to laparotomy for intra-abdominal bleeding from trauma does affect survival

for delays up to 90 minutes. J Trauma. 2002;52:420-425. 2. Harvin JA, et al. Mortality after emergent trauma laparotomy: A multicenter, retrospective study. J

Trauma Acute Care Surg. 2017;83:464-468. 3. Marsden M, et al. Outcomes following trauma laparotomy for hypotensive trauma patients: A UK

military and civilian perspective. J Trauma Acute Care Surg. 2018;85:620-625. 4. Moran CG, et al. Changing the System - Major Trauma Patients and Their Outcomes in the NHS

(England) 2008-17. EClinicalMedicine. 2018;2-3:13-21. 5. Baksaas-Aasen K, et al. iTACTIC - implementing Treatment Algorithms for the Correction of

Trauma-Induced Coagulopathy: Study protocol for a multicentre, randomised controlled trial. Trials. 2017;18:486.

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Resuscitative Median Sternotomy Plus Endovascular Aortic Balloon Occlusion: New Surgical Approach for

Penetrating Chest Trauma Management

Luis G. Saldarriaga, MD; Michael Parra, MD, FACS; Yaset Caicedo, MD; Fernando Rodríguez, MD; Jose Julián Serna, MD; Alexander Salcedo, MD; Mauricio Millán, MD; Carlos Serna, MD;

Alberto García, MD; Carlos Ordoñez, MD, FACS BACKGROUND Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a minimally invasive procedure that obtains proximal vascular control of the aorta in hemodynamically unstable patients with life-threatening non-compressible torso hemorrhage (NCTH). REBOA has been considered as an absolute contraindication in patients suffering from thoracic trauma, but recent evidence has shown that it can be used safely in penetrating chest trauma without exacerbating ongoing surgical bleeding. One of the standard indications for an open resuscitative left antero-lateral thoracotomy in severely injured trauma patients is impending or full cardiac arrest upon presentation, but the use of REBOA in these cases challenges this conventional concept. We hypothesized that the combined use of a REBOA and a resuscitative median sternotomy can be used as a new surgical approach for penetrating chest trauma. Thus, we describe our experience with this newly developed therapeutic combination and contrasted it to that of patients who underwent open thoracotomy with aortic cross-clamping (TACC). MATERIAL AND METHODS Setting and data source A retrospective review of all adult patients suffering from thoracic trauma was performed at a level one regional trauma center in Cali, Colombia, from December 2014 to December, 2019. All patients with penetrating chest trauma that required an aortic occlusion using a REBOA and a resuscitative median sternotomy simultaneously were included. Our control group was 40 patients during the same time period that underwent TACC for the same indications. Patients and data Patient demographics, clinical course, procedural conditions, and clinical outcomes were collected from the institution's trauma registry. The study was approved by our institutional ethics and review board committee. All data was collected prospectively and the decision to place a REBOA resided on the treating trauma surgeon. The most common indication for REBOA placement was sustained hypotension (systolic blood pressure (SBP) <90 mmHg) that did not respond to initial resuscitation. All REBOA catheters were placed in Zone 1 by a separate surgical team while another surgical team performed the resuscitative median sternotomy simultaneously. Statistical analysis The continuous variables were described by median and interquartile range, the categorical variables by relative and absolute frequency. Fisher’s exact test and Chi-square test were used to compare categorical variables. The Mann-Whitney U test was used to compare continuous variables. Statistical analyses was performed using R-Language 3.5.6.

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Region 14 – Clinical Research RESULTS A total of 15 patients were managed by resuscitative median sternotomy and REBOA. The median age was 33 (IQR: 22-40) years, and 13 (88.7%) patients were males. Nine (60%) patients suffered gunshot wounds and 6 (40%) suffered stab wounds. The median injury severity score (ISS) was 25(25-30). Thoracic abbreviated injury score (AIS) > 3 was found in 13(86.6%) patients and 10 (66.7%) patients had thoracic vascular involvement. In-hospital cardiac arrest was seen in 6(40%) patients. Median systolic blood pressure (SBP) upon arrival was 70 mmHg (IQR: 59-88) with a median Glasgow Coma Score (GCS) of 14(IQR: 9-15). All REBOA's were placed in the operating room (OR) and the open surgical cutdown technique was most common used [12(80%)]. The REBOA was inflated in Zone I in all patients. The median SBP prior to REBOA placement was 60(50-77) mm Hg. The median duration of aortic occlusion was 41(IQR: 30-66) minutes. Damage control surgery principles were implemented in 10(66.7%) patients and the median intra-operative blood loss was 3000 mL (IQR:2575-3650). Intra-operative mortality was 13.3% and overall in-hospital mortality was 26.7% (Tables 1 and 2). Table 1. Baseline characteristics

Thoracotomy + Cross-Clamping Aorta

(n=40)

Resuscitative Median Sternotomy + REBOA

(n = 15) P

Age, median (IQR) 29(23-35) 33(22-40) 0.80 Male, n (%) 38(95) 13(86.7) 0.63

Trauma Mechanism Gunshot wound, n (%) 30(75) 9(60)

0.27 Stab wound, n (%) 10(25) 6(40)

Sign Vitals upon admission SBP, mm Hg, median (IQR) 25(0-76) 70(59-88) 0.003 Heart rate, bpm, median (IQR) 34(0-108) 109(93-126) 0.001 GCS, score, median (IQR) 8(3-13) 14(9-15) 0.01

Initial laboratory data pH, median (IQR) 6.98(6.68-7.19) 7.2(6.99-7.2) 0.15 Hemoglobin, mg/dl, median (IQR) 10.5(7.05-12.4) 10.3(8.25-14.4) 0.46 Lactate, mmol/L, median (IQR) 8.32(4.43-17) 5.52(4.07-10.1) 0.17

Injury Severity Head AIS > 3, n (%) 4(10) 2(13.3) 0.65 Thorax AIS > 3, n (%) 30(75) 13(86.6) 0.47 Abdomen AIS > 3, n (%) 13(32.5) 4(26.6) 0.75 ISS, median (IQR) 25(25-25) 25(25-30) 0.49 In-hospital cardiac arrest, n (%) 15(37.5) 6(40) 1 Intraoperative blood loss, ml, median (IQR) 3000(2000-4000) 3000(2575-3650) 0.69

Resuscitation Requirements Unit packed RBC, 6 h, median (IQR) 4(2-7) 5(4-8) 0.14 Unit packed fresh frozen plasma, 6 h, median (IQR) 3(2-5) 6(4-6) 0.02 Unit packed RBC, 24 h, median (IQR) 4(2-7) 6(5-10) 0.01 Unit packed fresh frozen plasma, 24 h, median (IQR) 3(2-6) 7(5-11) 0.001 Crystalloid, ml, median (IQR) 4000(2085-5848) 5858(4660-6844) 0.09 SBP: Systolic blood pressure, GCS: Glasgow Coma Scale, ISS: Injury Severity Score, CPR: Cardiopulmonary resuscitation. IQR: Interquartile range

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Region 14 – Clinical Research In contrast, a total of 40 patients underwent TACC. The injury severity and anatomic distribution of the wounds were similar to that of the REBOA + median sternotomy group. The median SBP upon arrival was 25(IQR: 0 – 76) mm Hg and the median Glasgow Coma Scale score was 8(IQR: 3-13). In-hospital cardiac arrest was present in 15(37.5%) patients. Biomarkers such as hemoglobin, lactate, and blood pH upon admission were not significantly different among groups. The intra-operative blood loss was similar among both groups (REBOA group: 3000 mL (IQR: 2575-2650) vs TACC group: 3000mL (IQR: 2000-4000), p=0.691). The median SBP in the operating room was 0(0-34) mm Hg which was lower to the REBOA group [60(50-77) mm Hg, p<0.001]. The median duration of aortic occlusion was 30(IQR: 20-45) minutes. Total blood transfused was similar between both groups during the first 6 hours of resuscitation. Intra-operative mortality was 57.5% and in-hospital mortality was 77.5%. (Table 1-2) Table 2. Anatomical distribution of the wounds and clinical outcomes

Thoracotomy + Cross-Clamping Aorta (n=40)

Resuscitative Median Sternotomy + REBOA (n = 15)

P

Vascular Lesion Vascular lesion, n (%) 21(52.5) 9(60) 0.61

Head or neck, n (%) 2(5) 3(20) 0.11 Common carotid artery 2/2 0

Internal jugular vein 0 3/3

Thorax, n (%) 14(35) 10(66.7)

0.06

Thoracic aorta 0 1/10

Left Subclavian artery 3/14 0

Pulmonary artery 8/14 2/10

Intercostal artery 6/14 4/10

Pulmonary vein 4/14 3/10

Innominate vein 0 2/10

Abdomen, n (%) 2(5) 2(13.3) 0.11

Pelvis, n (%) 3(7.5) 0 0.55

Organ lesion Lung AAST III-IV, n (%) 10(25) 3(20)

0.89 Lung AAST V, n (%) 6(15) 2(13.3)

Liver AAST III-IV, n (%) 2(5) 3(20) 0.14

Liver AAST V-VI, n (%) 3(7.5) 0

Spleen AAST III-IV, n (%) 0 1(6.7) 0.21

Spleen AAST V, n (%) 1(2.5) 0 Surgical Approach

Thoracic Damage Control, n (%) 12(30) 10(66.7) 0.02 Abdominal Damage Control, n (%) 7(17.5) 3(20) 1 SBP on operating room, median (IQR) 0(0-34) 60(50-77) <0.001 Duration of Aortic Occlusion, median (IQR) 30(20-45) 41(30-66) 0.04

Mortality Intraoperative mortality, n (%) 23(57.5) 2(13.3) 0.005 72-hour mortality, n (%) 31(77.5) 3(20) <0.001 In-hospital mortality, n (%) 31(77.5) 4(26.7) <0.001 ICU length of stay, median (IQR) 8(4-11) 10(6-16) 0.28 Hospital length of stay, median (IQR) 13(6-31) 17(11-24) 0.93 TRISS, median (IQR) 15.2(3.3-79.8) 72.2(50.2-89.8) 0.009 Predictive mortality (TRISS < 0.5) 24(60) 4(23.5) 0.01 SBP: Systolic Blood Pressure. ICU: Intensive Care Unit. TRISS: Trauma Injury Severity Score. IQR: Interquartile range

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Region 14 – Clinical Research CONCLUSION A resuscitative median sternotomy plus a REBOA is a new surgical approach for penetrating chest trauma management. This approach allows for a fast and early control of the source of thoracic vascular bleeding in patients with profound hemorrhagic shock. This newly devised concept should be ideally performed by two separate, highly skilled multidisciplinary surgical teams. The goal is that a team deploys the REBOA while the other performs the resuscitative median sternotomy. The combined use of a REBOA and a resuscitative median sternotomy is feasible and effective to achieve hemorrhage control and achieves improved overall survival when compared to similar patients managed with the traditional TACC.

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Fluid Resuscitation in Hemorrhagic Shock: Is It Time to Focus on Fluid Therapy That Increases Microcirculation?

Hae Sung Kang, MD; Jad Khoraki; Haoxuan Xu; Loren Liebrecht;

Ru Li; Martin Mangino INTRODUCTION The principles of resuscitation in hemorrhagic shock aim to restore oxygen delivery to mitochondria, which is impaired in shock. In trauma patients, resuscitation is commonly guided by blood pressure targets. Lactate, a biochemical surrogate of oxygen debt, is a better target but often is unreliable in directly measuring oxygen debt. Measuring the microcirculation (capillary flow) may be a superior resuscitative index to blood pressure as it could serve as a real time surrogate of end organ oxygenation. Furthermore, macrohemodynamics (MAP) can decouple from microcirculatory exchange in capillaries similar to what occurs in sepsis. Several studies have shown a similar decoupling in the setting of hemorrhagic shock while demonstrating the correlation between microcirculation and end organ damage. With the exception of lactate, this discordance also appears to be true between microcirculation and other indirect measurements of oxygen debt such as base deficit. The microcirculatory effects of conventional fluid therapy used in trauma, namely packed RBC and Lactated Ringer’s (LR), have been studied before. In particular, transfusion of blood product has shown to improve sublingual microcirculation in trauma patients with normal blood pressure. There are other novel therapies such as Polyethylene Glycol-20kDa (PEG-20k) and Vitamin C solutions that have been shown to improve microcirculation but have not been compared to the traditional therapy. In addition, the benefit of increased microcirculation in the early stages of resuscitation during hemorrhagic shock remains unknown. Our study shows the prognostic value of microcirculation in the resuscitation of porcine model of severe hemorrhagic shock and the benefits of restoring microcirculation in the early stages of resuscitation. METHODS Anesthetized Yorkshire pigs were shocked by arterial bleeding to a target lactate of 7.5-9 mM and resuscitated with a low volume (6.8 ml/kg, I.V.) of either LR solution, high dose vitamin C (200 mg/kg) in LR solution, fresh whole autologous blood (WB) or 10% PEG-20k in LR solution. Pigs were left further untreated and allowed to live up to 4 hours with monitoring of macrohemodynamics and microcirculation of the ileal mucosa and sublingual surface using real time orthogonal polarization spectral imaging (OPSI) or a histological method (ileum). The animals that survived to 240 minutes were euthanized. The OPSI videos were analyzed to determine the mean flow index (MFI) and proportion of perfused vessels (PPV) which signify capillary perfusion. MFI value rates flow ranging from 0 (absent) to 3 (normal) while PPV is calculated by 100 x (total number of vessels – [no flow + intermittent flow])/total number of vessels. H&E stain was utilized for the bowel and the RBCs in each sample was counted using an automated system to calculate the % of area of RBCs in the tissue section, which serves as a histological index of microcirculation.

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Region 3 – Basic Science RESULTS Pigs resuscitated with PEG-20k survived to 240 minutes with significantly higher MAP, microcirculatory perfusion, and lower lactate, compared to the other groups. (Figures 1, 2, and 3) WB produced the next best results followed by Vitamin C. LR solution had the worst results with pigs surviving less than 30 minutes and having the worst microcirculation. The ileal PPV showed significantly strong correlation with the sublingual PPV throughout the experiment. Multivariate linear regression analysis of MAP, lactate and PPV of ileum at 30 and 120 minutes with survival time as a dependent variable showed nonsignificant relationship between MAP and survival time and a significant relationship between lactate and survival time at 30 minutes but not at 120 minutes; PPV of ileum at 30 and 120 minutes after treatment were independently predictive of survival time (Table 2). DISCUSSION This is the first preclinical study to demonstrate the survival benefit of improved microcirculation during the earliest stage of resuscitation after hemorrhagic shock. Of the three measures (MAP representing macrocirculation, lactate representing metabolic oxygen deficit and PPV representing microcirculation), PPVs at 30 and 120 minutes post-resuscitation showed the strongest correlation to the survival time. As a result, the degree to which each treatment increased PPV corresponded with survival time though the survival time of the PEG-20k group was not significantly different from the blood group, which may be due to the survival time being capped at 240 min. The sublingual PPV, perhaps the most clinically relevant measurement of microcirculation, showed strong correlation to splanchnic PPV and was also internally validated by a histological assessment of microcirculation. Hemorrhagic shock manifested itself as decreased sublingual and ileal MFI and PPV. Lower intravascular volume results in decreased blood flow to the capillaries, ultimately leading to tissue hypoxia. Oxygen deprivation has many complications, including primary loss of cellular ATP followed by secondary release of inflammation mediators and impaired homeostasis of multiple intracellular conditions. Inactivation of sodium pump activity secondary to loss of ATP leads to intracellular and interstitial fluid accumulation, which in turn compresses the capillary space and produces a vicious cycle of decreased capillary perfusion and oxygen transfer with further ATP depletion. It is entirely possible that microcirculation dysfunction persists concurrent with a revitalized macrocirculation. This discordance was evident in this study at 30 minutes after resuscitation as MAP was not significantly different across the groups with the exception of the extremes and yet sublingual and ileal PPVs were significantly different in all of the groups. The decoupling resolved as the groups differentiated themselves; this suggests that PPV may herald a macro-hemodynamic outcome before it occurs. To reverse end organ damage, it is absolutely critical to break this vicious cycle of the dysfunctional microcirculation. Therefore, microcirculation plays a critical role in the outcome of resuscitation in hemorrhagic shock. In fact, in this model, the best predictor of survival time throughout the resuscitation was PPV. Given that PPV directly measures the total % of perfused capillaries of end organs, it is safe to assume that it is a closer approximation of the end organ perfusion (which dictates survival time) than lactate and MAP. This method to assess capillary perfusion was internally validated in this study by the corresponding histological assessment of microcirculation. If the subjects were allowed to survive beyond 4 hours, the survival time would have had an even greater correlation with PPV as many with higher PPV would have likely survived greater than 4 hours.

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Region 3 – Basic Science Since the end organ perfusion is one of the tenets of trauma resuscitation, we propose that capillary perfusion should be considered as one of the therapeutic indices of initial resuscitation. Clinically, given the evidence of close correlation of sublingual and intestinal microcirculation, it is feasible to measure patients’ sublingual microcirculation during resuscitation and titrate therapy based on its value. The selection of the resuscitative fluid should also be based on its ability to maximize microcirculation. Of the conventional resuscitative fluids, only WB was shown to have microcirculatory benefits. It is likely that RBCs and other macromolecular components of the blood allow efficient delivery of its components to the end organs. The two novel therapy groups (Vitamin C and PEG-20k) had previously been shown in other models to effectively increase microcirculation but not in a porcine hemorrhagic shock model. Vitamin C has been shown to have pleiotropic functions during septic shock (synthesis of vasopressors, antioxidant, downregulation of stress induced transcription factor and protection of glycocalyx). We suspect that it has similar physiologic functions during hemorrhagic shock as well. PEG-20K is as an oncotic and impermeant agent and has been shown to decrease total tissue water while drastically expanding the intravascular volume. Its superior performance in improving microcirculation and survival time compared to the WB group (demonstrated in our previous study) further illustrates the critical role of microcirculation in mortality benefit after hemorrhagic shock.

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Artificial Intelligence Model Predicts Mortality in Rural Trauma Patients Utilizing Pre-Hospital Parameters

Amanda Chelednik, MD

INTRODUCTION Trauma is the leading cause of death for persons age 0 to 45, and fourth leading cause of death overall for all ages.1 Although advances in pre-hospital care have been made, a significant outcome disparity exists between rural trauma patients and their urban counterparts.2,3 More than 40 million Americans live more than one hour from organized trauma care. National Transportation Safety Board statistics note that two thirds of fatal motor vehicle collisions occur in the rural setting.4 Traditional trauma outcome scoring models are heavily reliant on the abbreviated injury scores (AIS), with Trauma Injury Severity Score (TRISS) being the most commonly utilized. Reliance on AIS scoring limits accessibility to real time clinical decision making and TRISS performance is limited by the subjective nature of its components. Early identification of patients with increased risk of mortality will allow for appropriate prehospital triage, receiving hospital preparedness, and an accurate assessment of prognosis. We present a customized machine learning model to predict risk of mortality utilizing information available en route to and immediately after hospital arrival that is specifically tailored to our aging, rural population. METHODS Ten year single center Level I Trauma Registry Data (2010-2019) comprised the retrospective data set. Patients identified as transfers from an outside facility, with incomplete data sets, and those that died prior to admission to the trauma bay were excluded. The final patient cohort included those who were direct transports via ambulance or helicopter and had a complete data set. Mortality was defined as patient death prior to discharge. Gradient Boosting Machine (GBM), Random Forest (RF) and Support Vector Machine (SVM) machine learning techniques were trained, cross validated and compared. Model performance was assessed using accuracy, sensitivity, specificity, positive (PPV) and negative predictive values (NPV), and Area Under the Curve (AUC) discrimination. Model performance was then compared to TRISS. RESULTS 5,271 admissions comprised the data set for the machine learning model; of which, 327 (6.2%) expired. The median age was 41 years, 67% were male, 89% were Caucasian, and 90% of injuries were caused by blunt trauma with mean scene and ED Glasgow Coma Scale (GCS) of 13 and 13 respectively. Median, interquartile range (IQR) for transport time was 40.0 (23.0, 58.0) minutes. The median IQR length of stay was 3.6 (1.4, 7.6) days, and median IQR time till death for patients who died was 1.7 (0.26, 5.2) days. GBM method demonstrated the best performance: ROC-AUC 0.94, PR-AUC 0.57, accuracy 0.95, sensitivity 0.65, specificity 0.98, PPV 0.56, and a NPV of 0.98. TRISS performance metrics were: ROC-AUC 0.95, PR-AUC 0.63, accuracy 0.94, sensitivity 0.71, specificity 0.96, PPV 0.53, and a NPV of 0.98. Figure 1 depicts the ROC-AUC and PR-AUC.

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Region 7 – Clinical Research Variables included in our model were: scene and initial Emergency Department (ED) GCS components, systolic blood pressure, heart rate, age, scene pulse O2, gender, and transport time (Table 1).

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Region 7 – Clinical Research CONCLUSIONS Our best machine learning model (GBM) was non-inferior to a TRISS model in predicting mortality with the advantage of only requiring data readily available on hospital admission. A dynamic machine learning model can provide actionable intelligence by revising its risk prediction estimation with changes in patients’ clinical status en route, allowing for time critical resource allocation for patients in extremis. This early prediction of morality risk en route or on arrival can enhance triage performance and thus refine resource allocation on a local and regional level which can be critical for rural trauma systems with limited resources. Clinically, early prediction for mortality models span a wide array for practical applications beginning with pre hospital disposition, but not limited to level of care after triage. Future directions for this work include expansion of the model’s training data set with statewide morbidity and mortality data for all trauma patients that were never transported to our trauma system and a live field deployment study. REFERENCES

1. Mabry RL, Holcomb JB, Baker AM, Cloonan CC, Uhorchak JM, Perkins DE, Canfield AJ, Hagmann JH. United States army rangers in Somalia: An analysis of combat casualties on an urban battlefield. Journal of Trauma - Injury, Infection and Critical Care. 2000;49(3):515-529. https://doi.org/10.1097/00005373-200009000-00021

2. Harwell PA, Reyes J, Helmer SD, Haan JM. Outcomes of rural trauma patients who undergo damage control laparotomy. American Journal of Surgery. 2019;218(3):490-495. https://doi.org/10.1016/j.amjsurg.2019.01.005

3. Jarman MP, Castillo RC, Carlini AR, Kodadek LM, Haider AH. Rural risk: Geographic disparities in trauma mortality. Surgery (United States). 2016;160(6);1551-1559. https://doi.org/10.1016/j.surg.2016.06.020

4. Baker SP, Whitfield RA, O’neill B. Geographic Variations in Mortality from Motor Vehicle Crashes. New England Journal of Medicine. 1987. https://doi.org/10.1056/NEJM198705283162206

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A Mechanistic Exploration of Sex Dimorphisms in Coagulation: Calcium Signaling Drives Female-Specific Platelet Hyperactivity

Julia R. Coleman, MD, MPH; Anirban Banerjee, PhD; Kenneth Jones, PhD;

Marguerite Kelher, MS; Sanchayita Mitra; Ernest E. Moore, MD; Mitchell J. Cohen, MD; Jason M. Samuels, MD; Christopher C. Silliman, MD, PhD

INTRODUCTION Sex dimorphisms exist in coagulation, with females exhibiting a relative hypercoagulability as compared to their male counterparts. This female-specific hypercoagulability is characterized by shortened time to clot formation, increased rate of clot propagation, increased clot strength (an effect mainly of platelets), and higher fibrin contribution to clot strength (“functional” fibrinogen). In addition to increased clot strength platelets from females demonstrate higher activation with adenosine diphosphate (ADP) and arachidonic acid (AA) as compared to platelets from males. These sex dimorphisms in hemostatic capacity and platelet function have clinical significance, with female-specific hypercoagulability persisting after severe injury, and female sex conferring a survival benefit in the setting of trauma-induced coagulopathy (TIC) (decreased clot strength or platelet function) and shock. The exact mechanism driving survival benefit in females in the setting of TIC has yet to be elucidated; however, platelets are suspected to play a role. Platelets from both males and females are known to express estradiol receptors, and recent work highlights that there are sex-specific platelet activation and aggregation potentials related to ADP and platelet activating factor (PAF). Specifically, platelets from females have more robust ADP induced aggregation and activation, whereas platelets from males have more robust PAF-mediated aggregation and activation. These potentials can be manipulated by estradiol treatment such that after incubation in physiologically relevant concentrations of estradiol, platelets from males’ aggregation potential approximates that of females in an apparent “feminizing effect” of sex hormone treatment. It is unknown how estradiol may affect ADP and PAF signaling pathways, which act through distinct cascades. Specifically, PAF stimulates the P2Y1 receptor, which increases intracellular calcium, while ADP stimulates the P2Y12 receptor, which decreases intracellular cAMP. Interestingly, platelet estradiol receptor signaling converges on these same pathways. The objective of this study was to examine the downstream signaling pathways of ADP and PAF in platelets from males versus females. We sought to measure intracellular cAMP and perform RNA sequencing in platelets, with particular attention to those which relate to calcium signaling. We hypothesize that the sex-based differences in platelet activity are due to nongenomic effects of estradiol, as evidenced by sex dimorphisms in platelet RNA and cAMP signaling.

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Region 8 – Basic Science METHODS Apheresis platelets were collected from healthy volunteers. 1x108 platelets/ml were activated with either 20 µM of ADP (5 min) or 2 µM of PAF (10 min) and intracellular cAMP levels measured from the cell lysates by an ELISA. The cAMP levels were compared by sex using a Mann-Whitney test. Fresh platelets were also processed for RNA sequencing. Total RNA was isolated using Qiagen RNeasy miniprep kit. A total of 200-500 ng of total RNA was used to prepare the Illumina HiSeq libraries using the RNA Pico Kit (Takara Biosciences) and sequenced in a single pass 50bp (1x50bp) run on the Illumina HiSeq2000 platform. A custom computational pipeline consisting of the open-source gSNAP, Cufflinks, and R were used for alignment and discovery of differential gene expression. Each read generated by each sample was mapped to the human genome (hg19) by gSNAP, and transcript abundance (FPKM) derived by CUFFLINKS. From this, we determined significant gene expression using ANOVA in R. Once a gene list was formed, it was imported into the Ingenuity Pathway Analysis program to identify pathways molecules networks and upstream elements of interest. All analyses were conducted with R statistical software. Statistical significance was considered at p< 0.05. RESULTS Platelets from 53 healthy volunteers were assayed for intracellular cAMP, including 33 males and 20 females. There was no difference in age between the males (median age 64, interquartile range [IQR] 54-69) and females (median age 55, IQR 44-58) (p=0.17). There were no differences in cAMP levels by sex at baseline (38.5 [IQR 7.9-41.0] pmol/mL in females versus 24.5 [IQR 7.9-38.5] pmol/mL in males, p=0.19), or following ADP stimulation (36.0 [IQR 21.6-38.6] pmol/mL in females versus 20.4 [IQR 7.5-38.6] in males, p=0.32), or PAF stimulation (38.6 [15.2-38.8 IQR] pmol/L in females versus 15.2 [4.7-38.8 IQR] pmol/L in males, p=0.40). To look at the effect of age and menopause, we compared females by menopausal state (by age of 54, the average age of menopause) against similarly aged males. We did not identify an effect on platelet cAMP levels by age or menopausal state. Platelets from 17 separate healthy volunteers were assayed for RNA sequencing (6 females, 11 males). There was no difference in age between the males (median age 29, interquartile range [IQR] 24-59) and females (median age 51, IQR 36-61) (p=0.12). There were several significant differences between RNA profiles by sex (Table 2). Specifically, the following RNA-related genes were statistically higher in males: LIPE-AS1 (“LIPE Antisense RNA 1”; 2.27 fold change, p=0.01), RP11-732A19.8 (2.18 fold change, p=0.02), GNAS (1.85 fold change, p=0.04), AC009065.4 (1.78 fold change, p=0.03), and AC005795.1 (1.61 fold change, p=0.02). While some of these genes’ distinct function are poorly understood, it is known that RP11-732A19.8 is associated with micro-RNA involved in angiogenesis, GNAS encodes a stimulatory alpha subunit of a guanine nucleotide-binding protein associated with adenylate cyclase signaling (and infamously, when mutated is associated with McCune-Albright), and AC005795.1 is involved in mitochondrial respiratory chain complex I assembly and protein ubiquitination. The following RNA-related genes were statistically higher in females: BEST1 (1.38 fold change, p=0.01), FTH1 (1.39 fold change, p=0.03), CTD-2139B15.2 (“Long Intergenic Non-Protein Coding RNA 2111”; 1.38 fold change, p=0.007), MALAT1 (“Metastasis Associated Lung Adenocarcinoma Transcript 1”; 1.76 fold change, p=0.02), TREML1 (1.77 fold change, p=0.007), SAT1 (1.91 fold change, p=0.01), MAPRE2 2.51 fold change, p=0.006),

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Region 8 – Basic Science CENPO (“Centromere Protein O”; 2.62 fold change, p=0.01), DAZAP2 (“DAZ Associated Protein 2”; 2.84 fold change, p=0.01), RP11-275I14.4 (“ACBD3 Antisense RNA 1”; 8.57 fold change, p=0.02), CTB-36O1.3 (186 fold change, p=0.03), and HLA-S (“Major Histocompatibility Complex, Class 1 S”; 2611 fold change, p=0.03). FTH1 codes for ferritin heavy chain, MALAT1 regulates cell endothelial cell function and angiogenesis. SAT1 is an X-linked gene which encodes proteins required for polyamine metabolism and transport. CENPO encodes a component of the centromere complex, and DAZAP2 encodes a proline-rich protein required for transforming growth factor-beta signaling, ubiquitinase activity, cell signaling and transcription regulation, and RNA splicing (and when mutated, it associated with multiple myeloma). Interestingly, two of the genes which were found to have significantly higher levels of RNA in platelets from females were both related to calcium signaling: TREML1 (1.77 fold higher, p=0.007) and BEST1 (1.38 fold higher, p=0.03). CONCLUSION While sex dimorphisms in coagulation have been well-established, the exact mechanism underlying these dimorphisms has yet to be elucidated. Differences in clot strength on thrombelastography assays, sex-specific platelet reactivity with various stimulants, the presence of sex hormones on platelets, and manipulation of platelet behavior with estradiol all suggest that platelets may play a crucial role in sex dimorphisms in coagulation which influence clinical outcomes related to coagulopathy. While we did not identify significant differences in intracellular cAMP levels in activated platelets by sex, RNA sequencing highlighted unique sex dimorphisms in genes related to calcium signaling. In contrast to what one would expect based on the differences in platelet behavior after ADP and PAF stimulation, there were no statistically significant differences in intracellular cAMP levels. However, our RNA sequencing data suggested that calcium signaling, not cAMP, may be driving the sex dimorphisms in platelet function and intracellular signaling. Specifically, two of the genes which were found to have significantly higher levels of RNA in platelets from females were both related to calcium signaling: TREML1 and BEST1. Given the established increase in platelet aggregation, activation, binding to fibrinogen, and the increased fibrinogen contribution to clot strength in females relative to males, it is possible that TREML1 and BEST-1 are driving the mechanism of this sex dimorphism. These are the first results to our knowledge which suggest that TREML1 and BEST-1 as the mechanistic link behind sex dimorphisms in platelet function which may be affected by estradiol through nongenomic action.

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Sustaining the Gains: Further Reductions in Unnecessary Computed Tomography Scans in Pediatric Trauma Patients

Elaa Mahdi, MD, MPH

BACKGROUND The practice of “pan-scanning” pediatric blunt trauma patients from head to pelvis results in unnecessary computed tomography (CT) scans, exposure of children to excess harmful radiation, and increased health care costs. We previously retrospectively validated imaging algorithms and prospectively implemented them for all trauma activations and consultations. We aimed to reduce unnecessary CT scans in pediatric blunt trauma patients and maintain process improvement to continue improvements over time. METHODS This was quality improvement project conducted as a retrospective single center cohort study comparing the rates of CT scanning before and after implementation of imaging algorithms for the head, cervical spine, chest, and abdomen/pelvis. Imaging guidelines were utilized during all pediatric trauma activations and consultations starting July 2017. Only screening CT scans obtained shortly after arrival to the ED were included; CT scans specifically recommended by a subspecialty consulting service were excluded from the study. Patients with penetrating mechanism, suspicion of child physical abuse, and CT imaging prior to arrival were excluded. Children who arrived dead, died in the emergency department, or were taken directly to the operative room before CT imaging could be performed were also excluded. Chart review was performed to assess guideline adherence. Guideline adherence was maintained through repeated Plan-Do-Study-Act cycles including annual resident training, implementation of a web-based and mobile application-based tool, and most recently direct provider feedback for non-adherence to the guideline (Figure). RESULTS In the control period before guideline implementation (from July 2016 - June 2017), 42 patients had 107 CT scans, of which 48 (45%) were not indicated. After guideline implantation (July 2017 – September 2020), 278 patients had 446 CT scans, of which 126 (28%) were not indicated. Children in the pre-intervention period underwent an average of 2.54 (± 1.38) scans/patient, which was reduced to 1.60 (±1.29, p<0.0001) scans/patient post-intervention (Table). The rate of non-indicated scans was also reduced from 1.14 (±1.22) scans/patient to 0.47 (±0.78, p<0.0001) scan/patient post-intervention (Table). The median number of non-indicated scans per patient each month decreased from 1.25 to 0.45 CTs after guideline implementation. More recently, the median has decreased to 0.24 non-indicated CTs per patient (Figure). Charges from non-indicated scans decreased from $1,218.93/patient to $512.90/patient. The percentage of patients exposed to excess radiation from non-indicated scans decreased from 62% to 32%. Based on prior CT utilization, $196,276 were saved and 83 children were spared excessive radiation from CTs since guideline implementation. Reduction in non-indicated scans was statistically significant for CT chest (0.40±0.50 scans/patient to 0.13±0.34 scans/patient, p<0.0001, Table).

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Region 2 – Clinical Research There was a smaller improvement in rate of non-indicated head, cervical spine, and abdominal/pelvis scans, but not statistically significant. There were no clinically significant missed injuries identified with algorithm implementation. CONCLUSION Imaging algorithms for traumatically injured children coupled with robust quality improvement methodology can significantly reduce unnecessary CT scanning without compromising care. This practice reduces harmful radiation exposure in a sensitive patient population and can save health care systems money and resources. A mobile application-based tool and direct provider feedback have further improved guideline adherence.

Table: CT scans per patient comparing pre-intervention to post-intervention

Types of CT scans Pre-Intervention (07/2016-06/2017) Means (SD)

N¹=42

Post-Intervention (07/2017-09/2020) Mean (SD)

N¹=206

P-Value

Total CT scans per patient 2.55 (1.38) 1.60 (1.28) 0.0001 Total Non-Indicated² CT scans per patient 1.14 (1.22) 0.46 (0.77) 0.0001 Total Head CT scans per patient 0.62 (0.49) 0.68 (0.47) 0.4203 Total Non-Indicated Head CT scans per patient 0.17 (0.38) 0.09 (0.28) 0.1491 Total C-spine CT scans per patient 0.60 (0.50) 0.50 (0.50) 0.2673 Total Non-Indicated C-spine per patient 0.33 (0.48) 0.21 (0.41) 0.0936 Total Chest CT scans per patient 0.55 (0.50) 0.22 (0.42) 0.0001 Total Non-Indicated Chest CT scans per patient 0.40 (0.50) 0.13 (0.34) 0.0001 Total Abdominal/Pelvic CT scans per patient 0.79 (0.42) 0.43 (0.50) 0.0001 Total Non-Indicated Abdominal/Pelvic CT scans per patient 0.24 (0.43) 0.17 (0.37) 0.2780

¹Number of patients

²Non-Indicated-CT scans=Scans not recommended by the algorithm

CT = computed tomography; C-spine = Cervical spine

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Figure. Non-indicated CT’s per patient. The mean number of CT scans not-indicated by imaging guidelines per patient for each month (blue solid line) decreased after guideline implementation. The median number of scans (orange dashed line) also has decreased over time. The annotations show the interventions rolled out in consecutive Plan-Do-Study-Act cycles. Resident training occurred every July starting in 2017. In July 2018, a web-based application was launched to facilitate guideline usage. In July 2019, we emphasized cervical spine algorithm adherence and launched a mobile application. In January 2020 we initiated direct feedback to providers who obtained screening CT’s that were not indicated by the guidelines. CT = computed tomography.

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Standardization of Opioid Prescription after Trauma (STOP Trauma): A Prospective Intervention to Reduce

Opioid Excessive Prescription

Eric Walser, MD INTRODUCTION Opioid abuse is one of the major contemporary issues in health care, and trauma patients are at high risk for post-injury opioid use disorders. We undertook this study to determine if the introduction of a standardized pain management pathway was associated with (1) at least equivalent pain control and (2) a reduction in opioid prescription amongst patients admitted to a Canadian Level I trauma center. METHODS This was a prospective trial between January 2019 and February 2020, with introduction of a standardized pain management pathway in September 2019. Trauma patients admitted for > 24 hours and discharged home were eligible. Those with an ICU stay > 14 days, age > 85 years, or those using opioids at admission were excluded. The intervention included: (1) physician and nursing education; (2) emphasis on multimodal analgesia; (3) patient and family education. Recommendations were for rational prescribing based on inpatient opioid use, but discharge prescriptions were at clinician discretion. Patients completed a modified Brief Pain Inventory at their first trauma clinic visit (within 2 weeks of discharge). The primary outcome was patient-reported pain on a 10-point scale, compared using the two- sample t-test for non-inferiority (NI). Opioid prescriptions were converted to oral morphine equivalents (OME). Sample size for NI (p < 0.025) was determined a priori to be 44 patients in each group. Secondary outcomes were compared using chi-square test, Mann-Whitney U test, and independent samples t-test, where appropriate. RESULTS A total of 147 patients were included, 100 pre-intervention (Pre-I) and 47 post-intervention (Post-I). There were no significant differences between groups in terms of age (mean 49.8 (SD 18.4) Pre-I vs 48.8 (18.5) Post-I, p=0.76), gender (77% male Pre-I vs 68% Post-I, p=0.31), length of stay (median 3.5 days [IQR 2-5] Pre-I vs 3.0 [2-6] Post-I, p=0.77) or injury severity scores (mean 15.5 (SD 7.7) Pre-I vs 14.9 (8.5) Post-I, p=0.66). The mean pain scores were 4.7 (SD 2.3) in the Pre-I phase and 4.3 (SD 2.6) in the Post-I phase (mean difference -0.4, 97.5% CI -1.4 to 0.5, p<0.001 for NI, p=0.34 for superiority). There were no differences between groups in terms of qualitative measures of pain control both while admitted (76% good/ very good pain control Pre-I vs 68% Post-I, p=0.31) and post-discharge (59% Pre-I vs 53% Post-I, p=0.67). The amount of opioid prescribed at discharge was significantly less after intervention (median prescription 72 OME [IQR 0-144] Pre-I vs 0 OME [0-144] Post-I, p=0.013), corresponding to a 38% reduction in overall opioid prescription. There was a significant decrease in the number of patients receiving any opioid prescription at discharge (67% Pre-I vs 47% Post-I, p=0.019). There were no differences in the number of patients requiring an additional prescription after discharge (22% Pre-I vs 19% Post-I, p=0.67)

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Region 12 – Clinical Research CONCLUSION A standardized multimodal pain pathway with emphasis on patient and provider education was NI with respect to post-discharge pain and significantly reduced opioid prescription following trauma. We believe implementation of similar protocols will have a significant impact on the opioid crisis.

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FFP Maintains Normal Coagulation While PCC Induces a Hypercoagulable State in a Porcine Model

of Pulmonary Contusion and Hemorrhagic Shock

Alexandra Dixon, MD, MPH INTRODUCTION The tissue damage and hypoperfusion that occur following traumatic hemorrhage concurrently inhibit coagulation and promote fibrinolysis, resulting in acute traumatic coagulopathy (ATC).1 Early transfusion of plasma has been shown to improve morbidity and mortality following traumatic hemorrhagic shock.2-4 The transfusion of plasma improves hemodynamic stability, increases thrombin generation, reverses ATC, and suppresses dysfunctional inflammation. Prothrombin complex concentrates (PCCs) such as Kcentra are stored at room temperature, can be rapidly administered, and are lightweight.5 The use of Kcentra with FFP was associated with correction of coagulopathy, decreased requirement for red blood cell and FFP transfusion as well as lower mortality and decreased hospital length of stay when compared to transfusion with FFP alone.6,7 Given the extreme conditions and limited medical resources that Special Forces medics encounter when engaged in the prolonged field care of wounded warfighters, the low volume and easy portability of Kcentra make it desirable as an alternative to plasma-based resuscitation. We thus sought to evaluate the late effects of FFP and Kcentra on ATC. We hypothesized that Kcentra can provide the same hemostatic benefits of plasma in a combat relevant porcine model of pulmonary contusion and hemorrhagic shock. METHODS Our protocol was approved by our Institutional Animal Care and Use Committee along with the Department of Defense Animal Care and Use Review Office and has been previously published8. Following sedation, female Yorkshire crossbred swine (40-50kg) underwent endotracheal intubation. They were then maintained under general anesthesia with a combination of inhaled isoflurane and intravenous ketamine infusion. A captive bolt gun was used to create a pulmonary contusion (PC). A tube thoracostomy was placed to relieve any hemo/pneumothorax. To induce hemorrhagic shock (HS), a grade V liver injury was created using a modified clamp. The liver was then packed for hemostasis. Control animals were instrumented but uninjured. 80min after the PC, injured swine were randomized to receive 25 IU/kg of Kcentra (CSL Behring, USA), 1U FFP, or a 50mL lactated Ringer’s (LR) vehicle. All swine received a 500mL LR bolus. PC+HS swine received an additional 1mL of LR for every mL of blood loss. The intervention was given after hemostasis and initial resuscitation was completed to study its effects on coagulopathy over the course of the study. 48h after the injury, swine were euthanized. Monitoring of coagulation status was performed using thromboelastography (TEG; Haemonetics Corp., USA).

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Region 10 – Basic Science Data were analyzed by Pearson χ2, ANOVA, and Kruskal-Wallis tests as appropriate and significance assessed at p < 0.05. Post-hoc analyses were conducted with Tukey’s or Mann-Whitney U Tests with significance assessed at p < 0.0125. Analysis was conducted in IBM SPSS Statistics (IBM Corp., Armonk, NY, USA). RESULTS 27 swine received PC+HS. 9 injured swine were treated with KCentra, 9 were treated with FFP, and 9 were treated with LR vehicle. 9 animals were controls. There were no significant differences between the animals in regard to weight, urine output, total IV fluids received, volume of blood loss, chest tube output, or number of broken ribs (p>0.05). There were no significant differences in early death (p>0.05). When compared with control swine, the vehicle-treated injured animals had significantly shortened R time at 6, 36, and 42h, shortened K value at 30h, reduced α angle at 42h, and decreased LY30 at baseline and 12h (Figure 1).

Injured swine showed significant differences between FFP, Kcentra, and vehicle in K value and α angle at 3h, MA at 12, 18 and 30h, and LY30 at 12 and 18h (Fig 2). Post hoc analysis was significant for higher median α angle in Kcentra vs vehicle at 3h (79.7 deg (IQR 78.7, 80.7) vs 76.7 deg (IQR 72.9, 78.8), p=0.006) and higher median LY30 in Kcentra vs vehicle at 18h (1.7% (IQR 1.3, 3.2) vs 0.6% (IQR 0.4, 1.1), p=0.004). Additionally, a higher median MA was demonstrated in vehicle vs Kcentra at 12h (79.4 (IQR 78.0, 82.1) vs 75.0 (IQR 73.0, 77.1)) and 18h (82.9 (IQR 81.1, 84.2) vs 76.1 (IQR 73.8, 78.5), p<0.001).

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Region 10 – Basic Science DISCUSSION To prove that our porcine model of pulmonary contusion and hemorrhagic shock developed ACT, we compared TEGs from instrumented, uninjured controls with injured swine. Injured animals formed clot more rapidly than uninjured controls, as demonstrated by the shortened R and K times. Once they began to form clot, however, the injured swine had a slower rate of clot propagation, as demonstrated by the lower α angle. Finally, the injured swine had less clot lysis, as reflected by a lower LY30. It is known that swine are hypercoagulable at baseline and that this hypercoagulable state is augmented through the act of instrumentation9. Thus, instrumentation may have induced the coagulopathy seen in the control animals. Injured pigs treated with Kcentra had a more rapid initial clot propagation as demonstrated by a higher α angle at three hours than did pigs treated with vehicle. This difference was not seen after three hours. This observation fits with the rapid onset of action of Kcentra and supports the initiation of an early thrombin burst that it not demonstrated with the other treatments. While the swine treated with Kcentra did exhibit a more rapid clot propagation, they exhibited a lower clot strength later in the experiment than vehicle-treated swine with a higher degree of clot lysis. Through early restoration of factors and augmentation of the coagulation cascade, Kcentra may \lad to a delayed consumptive coagulopathy that is manifested by a decreased clot strength after 12h. After 18h, any differences in coagulopathy abated between injured swine treated with Kcentra and vehicle. Several limitations merit discussion. To begin, while we tried to limit any inter-subject variability by using only female Yorkshire crossbred swine weighing 40-50kg, we cannot control for subtle genetic variability between animals. Furthermore, while these are young pigs and should presumably be healthy, we cannot control for all infectious or traumatic exposures sustained prior to their transfer to our facility. Finally, our timeframe of 48 hours may not have been long enough to see a difference in survival. In conclusion, with this study, we demonstrate that our porcine model of pulmonary contusion and hemorrhagic shock does induce more coagulopathy than instrumented, but uninjured controls. Additionally, these data support the conclusion that Kcentra induces an early hypercoagulable state while FFP maintains normal coagulation. For this reason, Kcentra may be advantageous for the short-term management of wounded warfighters in austere conditions where the transportation of a bulky resuscitative adjunct such as plasma is prohibitive.

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Region 10 – Basic Science REFERENCES 1. Hess JR, Brohi K, Dutton RP, et al. The coagulopathy of trauma: a review of mechanisms. J

Trauma. 2008;65(4):748-754. 2. Holcomb JB, Wade CE, Michalek JE, et al. Increased plasma and platelet to red blood cell

ratios improves outcome in 466 massively transfused civilian trauma patients. Ann Surg. 2008;248(3):447-458.

3. Holcomb JB, del Junco DJ, Fox EE, et al. The prospective, observational, multicenter, major trauma transfusion (PROMMTT) study: comparative effectiveness of a time-varying treatment with competing risks. JAMA Surg. 2013;148(2):127-136.

4. Baraniuk S, Tilley BC, del Junco DJ, et al. Pragmatic Randomized Optimal Platelet and Plasma Ratios (PROPPR) Trial: design, rationale and implementation. Injury. 2014;45(9):1287-1295.

5. Rodgers GM. Prothrombin complex concentrates in emergency bleeding disorders. Am J Hematol. 2012;87(9):898-902.

6. Jehan F, Aziz H, O'Keeffe T, et al. The role of four-factor prothrombin complex concentrate in coagulopathy of trauma: A propensity matched analysis. J Trauma Acute Care Surg. 2018;85(1):18-24.

7. Zeeshan M, Hamidi M, Feinstein AJ, et al. Four-factor prothrombin complex concentrate is associated with improved survival in trauma-related hemorrhage: A nationwide propensity-matched analysis. J Trauma Acute Care Surg. 2019;87(2):274-281.

8. Smith S, McCully B, Bommiasamy A, et al. A combat relevant model for the creation of acute lung injury in swine. J Trauma Acute Care Surg. 2018;85(1S Suppl 2):S39-S43.

9. Mulier KE, Greenberg JG, Beilman GJ. Hypercoagulability in porcine hemorrhagic shock is present early after trauma and resuscitation. J Surg Res. 2012;174(1):e31-35.

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Alcohol Use and Trauma in Alberta after COVID-19 Lockdown: Over-Representation and Under-Treatment Are

Opportunities for Improvement

Samantha Albacete, MD BACKGROUND Alcohol is a major factor in traumatic injuries. Accreditation bodies recommend alcohol screening/intervention programs as trauma quality indicators. Previous research in Alberta reported increasing alcohol use prevalence in major trauma. The COVID-19 pandemic has also been linked to increased alcohol consumption. Our objective was to characterize injury characteristics and relationship to alcohol use during summer trauma season after COVID-19 lockdown, and compliance with alcohol misuse screening, at a level one trauma center in Edmonton, Alberta. METHODS Retrospective chart audit for trauma patients, 18-64 years old, admitted to the University of Alberta Hospital Trauma Service from June 1 to August 31, 2020. Variables included: demographics, injury characteristics, ethanol level on presentation, history of substance use, and screening/intervention. Tertiary surveys and psychiatry/addictions consultations were reviewed to assess screening/intervention compliance. Frequencies and basic descriptives were calculated. Logistic regression was performed to identify relationships between alcohol use and injury patterns. RESULTS One hundred seventy-six patients met inclusion criteria. Mean age was 40 (SD13.8) and 128 (72.7%) were male. Blunt injuries were most common (blunt 144, 81.8%; penetrating 27, 15.3%, burn 3, 1.7%), with average ISS 13 (1-45), and average length of stay 10.6 days (SD 14.6). Motor vehicle crashes (MVCs) predominated (66, 37.5%) followed by falls (33, 18.8%), sport-related injuries (30, 17.1%), and stabbings (17, 9.7%). 156 patients (88.6%) had an ethanol level (EtOH) drawn on presentation with 50 (32%) positive, and 33 of these (66%) legally intoxicated. Forty-five patients (25.6%) had a documented addiction history with alcohol use disorder, 29 of which presented with a positive EtOH. Of the 50 patients with elevated EtOH on presentation, the average age was 36 years (SD12.1) and mean EtOH level 36.9 mmol/L (SD23.3). MVCs were the most common mechanism (18, 36%). Screening for alcohol use disorder was performed in 39 (78%) of these 50 patients that presented with positive EtOH (unclear documentation in remainder). Addiction services were offered in 10/50 (20%). Positive EtOH was associated with younger age (36 vs 41 years, p=0.02). Logistic regression revealed that positive EtOH was significantly associated with stab mechanism of injury (OR 3.75, CI 1.1-11.6, p<0.05); intoxication further increased association with stab injury (OR 4.4, CI 1.4-15, p<0.01).

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Region 11 – Clinical Research CONCLUSIONS Prevalence of positive ethanol level in trauma patients is rising: 32% currently, compared to 24% from Alberta 2010 data. More than one quarter of MVC patients had positive EtOH, and intoxication increased odds of stab injury. Compliance with alcohol misuse screening was 78% with only 20% of patients offered intervention, despite 58% having alcohol use disorder. Interventions to reduce preventable injuries and alcohol misuse at the population and hospital level are needed.

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Mitochondrial Reactive Oxygen Species Cause Endothelial Glycocalyx Shedding in a Rat Model of Zone 3 REBOA

Jessica K. Friedman, MD; Sarah Abdullah, MBBS; Sharven Taghavi, MD, MPH, MS;

Chrissy Guidry, DO; Juan Duchesne, MD; Olan Jackson-Weaver, PhD INTRODUCTION Over the last two decades there has been a substantial decrease in mortality following extremity trauma, due in large part to the use of tourniquets.1 Unfortunately, similar gains have not been made in the mortality of patients with junctional and truncal hemorrhage.2 Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a promising technology for treatment of non-compressible hemorrhage in the prehospital and emergency department setting. However, its use is limited by distal ischemia and reperfusion injury.3 In addition to potentially irreversible ischemic injury, reperfusion following prolonged occlusion of the aorta causes profound oxidative stress and release of inflammatory mediators, which can lead to hemodynamic collapse.4 The endothelial glycocalyx is a protein and carbohydrate matrix secreted by endothelial cells, and forms an anti-coagulant, anti-inflammatory barrier on the luminal surface of endothelial cells. A major constituent of the glycocalyx is heparan sulfate, which is the physiologic counterpart to medicinal heparin.5 When the glycocalyx is damaged and shed, these molecules enter the circulation and causes coagulopathy.6 Endothelial glycocalyx shedding has been detected in experimental models of ischemia/reperfusion, but its role in REBOA has not been determined.7 Furthermore, very few therapeutic strategies for protection of the glycocalyx are known. Our lab previously demonstrated that mitochondrial reactive oxygen species (ROS) scavenger mitoTEMPOL decreases glycocalyx shedding in a rat model of hemorrhage. The first aim of this study was to determine the timeline of glycocalyx shedding in a rat model of REBOA. The second aim of this study was to determine if pre-treatment with mitoTEMPOL decreases glycocalyx shedding during reperfusion. METHODS Adult male Sprague Dawley rats weighing between 200 and 300 grams were anesthetized using inhaled isoflurane, and an internal jugular catheter was placed for blood sampling. A laparotomy was performed, and the abdominal aorta was isolated and clamped with an atraumatic vascular clamp below the renal arteries. The clamp was left in place for thirty minutes, followed by 15 minutes of unclamping. Heart rate and oxygen saturation were monitored throughout, and rats were euthanized by means of cutting the diaphragm at the completion of the experiment. Blood samples were taken at the following time points: prior to laparotomy, after 30 minutes of aortic occlusion, two minutes after reperfusion, and 15 minutes after reperfusion. All blood samples were collected in heparinized tubes. Blood was centrifuged at 500x gravity at 4 degrees Celsius and the glycocalyx protein syndecan-1 was quantified in the plasma samples using a specific ELISA, as a marker of glycocalyx shedding. A separate group of rats received identical clamping and blood sampling but were pre-treated with 5mg/kg IV mitoTEMPOL, a mitochondrial targeted superoxide dismutase mimetic, to scavenge mitochondrial reactive oxygen species prior to clamping of the aorta. N was equal to 5 in each group. Syndecan-1 levels were compared at all time points; a p value of < 0.05 was considered statistically significant.

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Region 6 – Basic Science RESULTS Plasma syndecan-1 levels were not elevated after 30 minutes of aortic occlusion. A significant increase in plasma syndecan-1 did occur two minutes after unclamping the aorta compared to baseline. This increase remained significant at 15 minutes after unclamping, though plasma syndecan-1 did not continue to rise. In rats pre-treated with the mitochondrial reactive oxygen species scavenger MitoTEMPOL, no increase in plasma syndecan-1 was detected at any time point (Figure 1). Figure 1. Plasma syndecan-1 levels as a marker of glycocalyx shedding.

*p<0.05 compared to baseline, #p<0.05 compared to 30 minutes occlusion, N = 5 per group DISCUSSION To our knowledge this is the first study which demonstrates a successful therapeutic strategy in the treatment of endothelial glycocalyx shedding caused by use of Zone 3 REBOA in an animal model. Additionally, our study shows that glycocalyx shedding occurs following distal reperfusion and not during occlusion of the aorta, indicating that glycocalyx damage occurs principally as a result of reperfusion injury rather than ischemic damage. These findings are in agreement with our previously presented cellular hypoxia/reoxygenation and rat hemorrhagic shock models. Reactive oxygen species are known to play a role in ischemia/reperfusion injury, but the predominant source of ROS has not been definitively demonstrated.8 We were able to prevent glycocalyx shedding with the use of a mitochondrial specific ROS scavenger, further supporting our previous findings that derangements in mitochondrial metabolism is the source of these toxic reactive oxygen species. Importantly, because we saw glycocalyx damage only after distal reperfusion rather than during occlusion, this study indicates that a REBOA could be placed in the pre-hospital arena and a therapeutic drug delivered prior to deflating the balloon to prevent reperfusion injury. Such an intervention has the potential to substantially increase the therapeutic benefit of REBOA.

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Region 6 – Basic Science Because we have previously shown that hemorrhage damages the glycocalyx, we chose not to hemorrhage our rats prior to occluding the aorta in this study to isolate any potential effects of REBOA. Based on the data presented here, future areas of research will include a combined hemorrhage/REBOA model and the comparison of different resuscitation strategies. REFERENCES 1. Kragh JF, Walters TJ, Baer DG, et al. Survival with emergency tourniquet use to stop bleeding

in major limb trauma. Ann Surg. 2009;249(1):1-7. 2. Holcomb JB. Transport time and pre-operating room hemostatic interventions are important:

improving outcomes after severe truncal injury. Crit Care Med. 2018;46(3):447-453. 3. Stewart IJ, Faulk TI, Sosnov JA, et al. Rhabdomyolysis among critically ill combat casualties:

associations with acute kidney injury and mortality. J Trauma Acute Care Surg. 2016;80(3):492-498.

4. Ribeiro M, Feng CY, Nguyen A, et al. The complications associated with Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA). World J Emerg Surg. 2018;13(20).

5. Sieve I, Munster-Kuhnel AK, Hilfiker-Kleiner D. Regulation and function of endothelial glycocalyx layer in vascular diseases. Vascul Pharmacol. 2018;100:26-33.

6. Ostrowski SR, Johansson PI. Endothelial glycocalyx degradation induces endogenous heparinization in patients with severe injury and early traumatic coagulopathy. J Trauma Acute Care Surg. 2012;73(1):60-66.

7. Annecke T, Fischer J, Hartmann H, et al. Shedding of the coronary endothelial glycocalyx: effects of hypoxia/reoxygenation vs ischaemia/reperfusion. Br J Anaesth. 2011;107(5):679-686.

8. Rubio-Gayosso I, Platts SH, Duling BR. Reactive oxygen species mediate modification of glycocalyx during ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2006;290(6):H2247-56.

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Live Fast, Die Young: An Evaluation of End-of-Life Care in Young Trauma Patients

Elizabeth W. Tindal, MD, MPH

INTRODUCTION Trauma remains the leading cause of injury, disability and death for those under the age of 45 in the United States. With an aging population, there has been a growing interest throughout medicine in advance care planning including proactive initiation of goals of care (GOC) discussions during acute hospitalizations. This has permeated the world of trauma surgery as well, leading to the 2017 publication of the American College of Surgeons Trauma Quality Improvement Program’s best practice guidelines for palliative care for high-risk patients of all ages. However, these guidelines are built on data from the study of older populations, calling into question whether this framework also applies to young trauma patients given their unique psychosocial needs. End-of-life (EOL) care within the young adult (YA) population, defined as those 16 to 40 years old, has previously been studied in oncology patients but never within the context of trauma. As prior research has shown, despite representing a relatively heterogeneous population, YA patients are often unified by a similar set of life stressors which accompany the transition from adolescence to mature adulthood and a less established support system composed of multiple “informal carers”. Additionally, following a significant change in health status, YA patients are more likely to struggle with existential questions surrounding their loss of self and loss of their future. Trauma only acts to exacerbate these issues for YA patients. Compounding this age group’s low rate of advance directive completion, prior research has shown that trauma patients are significantly less likely to be able to actively participate in these discussions as a result of their injuries. Leaving families and loved ones to make decisions on behalf of patients which have long-term emotional, financial and functional consequences. With this in mind, it is crucial that we have a better understanding of how the GOC decision making process differs for YA patients in order to provide the necessary support to patients and their loved ones. In this study, we hypothesized that GOC decision making in YA trauma patients would be complicated by age group-specific patient and social factors, resulting in a prolonged process. METHODS We performed a retrospective review of the trauma registry database as well as the electronic medical records from our level I trauma center. All adult (age ≥ 18) patients who were admitted following a traumatic event between April 2015 and October 2019 with an intensive care unit (ICU) length of stay (LOS) of at least one day were eligible for inclusion. Two study groups were created based on age, transition to comfort measures only (CMO), and in-hospital death. The Young-CMO group is composed of YA patients who were made CMO during their hospital course, while the Young-Died group represents YA patients who died without withdrawal of support (WOS).

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YA Patients

Young-CMO

Young-Died

n = 905 n = 39 n = 11

Age (years) 28.1 28.6 26.5**Male 79.4% 71.8% 81.8%Caucasian 65.9% 87.2%* 27.3%**

ISS 19.9 33.9* 33.8ED GCS 11.8 4.3* 6.1Head Injury 46.8% 79.5%* 54.5%Mechanism of Injury

Blunt 77.3% 79.5% 45.5%**Penetrating 15.9% 7.7%* 27.3%**

Thermal 4.5% 2.6% 0%

Hospital LOS (days) 14.9 10.9 13.8ICU LOS (days) 7.7 10* 7.4Vent use (days) 7.4 9 3.8Operation? 63.4%* 43.6% 45.5%Trach? 10.6% 15.4% 9.1%PEG? 8.9% 12.8% 0%

Married 33.3% 36.4%Children 23.1% 27.3%Employeed 70% 83.3%Self-inflicted Injury 0% 23.1% 30%

Pre-exisiting AD 0.1% 2.6% 0%Time to first family meeting (days) 2.7 0.3Patient involved 2.6% 9.1%Family involved 100% 90.9%Multiple decision-makers 79.5% 80%Family Disagreements 20.5% 16.7%Multiple family meetings 71.8% 85.7%Discussion of prognosis? 94.5% 100%Discussion of patient pref? 53.8% 33.3%Decision in-line with pt pref? 45% 0%

Table 1. Overview of young trauma population, outcomes and approach to end-of-life care

Goals of Care Process

Social History

Demographics

Trauma

Hospital Course

Region 1 – Clinical Research The registry provided data on baseline health status including comorbidities, nature and severity of traumatic injuries, hospital course, and ultimate disposition. Charts were manually reviewed to determine each patient’s GOC timeline with a focus on when discussions were initiated, who participated, relevant social history and the overall decision-making process. Data analysis was performed using SPSS software. Continuous variables were analyzed using independent two-sample t-tests, while categorical variables used chi-squared tests as appropriate. RESULTS A total of 4146 patients met inclusion criteria during the study period, including 905 (21.8%) YA patients. As shown in table 1, YA patients were an average of 28.1 years old, predominantly male (79.4%) and Caucasian (69.5%). They had high rates of substance use (48.1%) and mental health disorders (13.6%) but were otherwise healthy with minimal comorbidities including diabetes, cardiovascular or pulmonary disease. Blunt mechanisms, especially traffic accidents, were most common (77.3%), with nearly half of patients sustaining a head injury (46.9%). They had an average injury severity score (ISS) of 19.8 (standard deviation (SD) 11.4) and emergency department Glasgow coma scale (ED GCS) of 11.8 (SD 4.6). They spent an average of 14.9 days in the hospital with almost half of those in the ICU. Only two patients had advance directives in place prior to their admission. Among this cohort, 39 (4.3%) were made CMO and 11 (1.2%) died in the hospital without WOS. In comparison to the overall YA cohort, significantly more of those in the Young-CMO group were Caucasian (87.2 vs 64.9%, p< 0.05) but they were otherwise similar in terms of age (28.5 vs 28.1 years, p=0.8), gender (71.8 vs 79.8% male, p=0.2) and mechanism of injury (79.5 vs 77.3% blunt with 92.3 vs 78.6% traffic accidents, p=0.7 and p=0.08, respectively). There was a significantly higher rate of head injuries (79.5 vs 46.9%, p<0.05) with a lower ED GCS (4.3 vs 12.1, p<0.05) and higher ISS (33.9 vs 19.2, p<0.05). There was no difference in baseline health status including rates of substance use and psychiatric disorders. They had a shorter hospital LOS (10.9 days, p=0.2) but spent more of that time in the ICU (10 days, p<0.05). For those in the Young-Died group, there was no significant difference in demographics and baseline health status with the exception of the number of Caucasian patients (27.3 vs 87.2%, p<0.05) and the rate of blunt trauma (14 vs 86.1%, p<0.05) when compared to the Young-CMO group. Similarly, while there was no difference in ISS, Young-Died patients had a higher average ED GCS (6.1 vs 4.3, p<0.05).

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Region 1 – Clinical Research Though it was not statistically significant, there was a higher incidence of self-inflicted injuries (30 vs 23.1%, p=0.7) and, despite a longer hospital LOS (13.8 vs 10.9 days, p=0.4), they spent less time in the ICU (7.4 vs 10 days, p=0.45). The GOC experience for both groups were very similar. There was only one patient who was able to actively participate in these discussions, meaning that the vast majority (97.4%) of EOL decisions were made by family and loved ones. Approximately 80 percent of patients had multiple decision makers with parents most commonly involved, followed by siblings and significant others. These discussions were frequently complicated, with approximately one in five families encountering disagreements and more than 70 percent requiring multiple meetings before a decision was made. The time to first family meeting did differ between the groups with discussions initiated sooner in the Young-Died group (0.3 vs 2.7 days). While patient diagnoses and overall prognosis were discussed in almost all of these meetings, patient preference was only touched on in at most half of meetings. However, even when it was discussed, the initial family decision was contrary to this preference in the majority of cases. CONCLUSIONS Our results demonstrate that GOC decision making following trauma in YA patients is indeed complicated by numerous factors, resulting in a prolonged and challenging decision-making process which often fails to focus on patient preferences. Our study focused on YA patients who had been critically injured and whose long-term independence, functional status, and overall quality of life would unquestionably be impacted. The seriousness of these decisions and the fact that the burden falls on loved ones with little input from the patient themselves makes it essential that, as providers, we ensure that our approach to EOL care works as well as possible for our trauma patients across the age spectrum. By nature, this is a complicated process – influenced by patient, provider, and systemic factors – and an improved understanding of each of these variables will inevitably improve outcomes for all of those involved. Our findings demonstrate that there are multiple points of intervention which should be targeted to improve EOL care for the YA population. First and foremost, initiatives to encourage advance care planning and discussions about health care preferences should be targeted to primary care settings as well as educational and training institutions. While these types of systemic practices have traditionally targeted older patients, a renewed focus on younger populations would provide loved ones with information about patient wishes and reduce the stress related to making those decisions on their behalf. For the patient and family, the acute nature of the event and patient’s life-threatening injuries are frequently enough to aggravate existing tensions and difficulties within the family dynamic; this is only worsened by the GOC decision-making process. Additional support from social work to identify these issues as they develop and provide any resources that may be available plays an essential role in this process.

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Region 1 – Clinical Research For providers, since there were almost always multiple decision-makers and frequent disagreements amongst those involved, it is that much more important to establish from the beginning who will be the spokesperson for the family unit. Similarly, we found that the majority of these discussions failed to emphasize patient priorities or preferences and this is an area which could be addressed by providers as they are typically the ones guiding these discussions. This shift in focus could reduce the perceived burden placed on the decision makers since it reframes the discussion toward honoring the patient’s life and wishes. This study represents the first of its kind to evaluate the patient, family and provider experience during EOL care for this unique and vulnerable population. Though it is more qualitative in nature, it provides significant insight into the associated challenges and into potential areas for intervention to improve outcomes for all involved.

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Injury Severity Score Is an Ineffective Metric for Distinguishing Critical Injury across All Age Groups

Robert Keskey, MD; Mark Slidell, MD, MPH; Henry Biermann, BS; Justin Cirone, MD;

Tanya Zakrison, MD, MPH; Ken Wilson, MD; Jennifer Cone, MD, MHS; David Hampton, MD, MEng

BACKGROUND Trauma centers rely on injury scoring systems to attain accreditation, perform epidemiologic research, and benchmark their performance. Due to its ubiquity, ease of calculation, and utility in research, the Injury Severity Score (ISS) has remained the preeminent injury scoring system in trauma care.1 A patient’s ISS score is calculated as the sum of the squares of the highest Abbreviated Injury Scale (AIS) grade in each of the three most severely injured body areas.1 Although numerous statistical, administrative, and clinical limitations have been revealed, the ISS remains the “gold standard” of trauma severity grading.2-4 However, in light of updated AIS code sets and pediatric-specific scoring systems, newer studies have reexamined the utility of an ISS of 16 to define critically injured patients with increased risk of mortality.6-8 One study found that the ISS threshold of 15 over-estimated mortality risk for pediatric patients and argued a threshold of 25 more accurately defined severe injury in this group.9 Given the difference in physiologic response to injury between adults, adolescents, and young children, further research is warranted to identify appropriate ISS thresholds for severe injury by age. Additionally, it may be prudent to also separate these thresholds into blunt and penetrating trauma due to previously noted differences in ISS related mortality between blunt and penetrating trauma.10 Failure to employ age-continuous data-driven injury scoring systems to define severe injury may result in inaccurate performance benchmarking, misleading quality of care improvement goals, and wasted resource allocation.9 We theorized that pediatric and adult trauma centers employing the ISS scoring system inaccurately prognosticate patient outcomes due to flaws in ISS scoring which in turn negatively impacts quality improvement and benchmarking. Therefore, we hypothesized that a more effective and precise version of an ISS-based scoring system would incorporate additional elements such as patient age and mechanism of injury. METHODS Data were abstracted from the National Trauma Databank (NTDB) (2010–2016). Inclusion criteria were adult patients (≥18 years old) suffering blunt or penetrating trauma. Patients with incomplete or non-physiologic vital signs, and pediatric patients (< 18 years old) were excluded. Admission vital signs, Glasgow Coma Score (GCS), Injury Severity Score (ISS), mechanism of injury (blunt vs. penetrating), and hospital discharge disposition were analyzed. Cutpoint analysis using the Youden metric was performed to determine the optimal ISS survival cutpoint for each individual age by year in blunt and penetrating trauma. In order to determine ISS’s predictive ability for mortality across each individual age, linear discriminant analysis (LDA) was performed on blunt and penetrating trauma separately. Each age was partitioned into a training and validation cohort where 80% of the patients were used to develop a predictive model and the remaining 20% was used to validate the model. LDAs were performed using ISS, ISS > 16, ISS > 25, TRISS, and RTS.

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Region 5 – Clinical Research Receiver operator curves were developed and the area under the curve (AUC) were compared between each injury severity metric. Using the most significant variables on univariate analysis including AIS body region component score, GCS, presenting vital signs, and gender, a new injury severity metric, the trauma component score (TCS), was developed for each individual age. The AUC for each algorithm was plotted by age for comparison across every age. Locally weighted smoothing was used to clearly demonstrate age-related changes. All statistical analysis was performed in ‘R’. Significance was a p-value < 0.05. RESULTS There were 777,794 (Blunt: n=709,168, and Penetrating: n=68,626) trauma patients who met inclusion criteria. Blunt trauma patients were significantly older (53.6±21.3 y.o. vs 34.4±13.8 y.o.), were more likely to be female (87.4% vs. 59.2%), have a lower shock index (8.4% vs 18.2%), have a higher ISS score (11.1±8.5 vs 8.5±8.9), and a lower mortality (2.9% vs 3.4%) than penetrating trauma patients (p < 0.01). Consistent with prior studies, the optimal cutpoint predicting mortality for the entire cohort was an ISS of 16. However, when the optimal cutpoints were compared across each age and mechanism of injury there were significant differences (Figure 1A). For blunt trauma, the optimal cutpoint decreased as age increased. For blunt trauma patients greater than 70 y.o., the optimal ISS cutpoint was less than 16. In penetrating trauma, the optimal cutpoint was highly variable and was at or below an ISS of 16 for the majority of the cohort. The ability of ISS, TRISS, and RTS to predict mortality was assessed by LDA and AUC (Figure 1B,C). For blunt trauma, there was as significant reduction across all injury metrics to predict mortality as age increased. For penetrating trauma, there was less of a variation in the ability of injury metrics to predict mortality across all age years. In blunt trauma less than 35 y.o., an ISS of 25 had an improved AUC compared to ISS of 16. However, when the ISS was adjusted for individual age there was a significant improvement in predicting mortality compared to using dogmatic cutoffs in both blunt and penetrating trauma. When LDA modeling was conducted to create the TCS, the AUC improved across all age groups. For blunt trauma, there was as significant reduction across all injury metrics to predict mortality as age increased. For penetrating trauma, there was less of a variation in the ability of injury metrics to predict mortality across all age years. In blunt trauma less than 35 y.o., an ISS of 25 had an improved AUC compared to ISS of 16. However, when the ISS was adjusted for individual age there was a significant improvement in predicting mortality compared to using dogmatic cutoffs in both blunt and penetrating trauma. When LDA modeling was conducted to create the TCS, the AUC improved across all age groups.

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Region 5 – Clinical Research Figure 1. Comparison of the optimal ISS cutpoint (A) for predicting mortality by both age and mechanism

(Blunt = red line and Penetrating = green). Loess smoothing function applied with grey representing the standard deviation. LDA analysis determining the ability of injury metrics to predict mortality across each individual age year for both penetrating (B) and blunt (C) trauma. Area under the curve (AUC) was used to determine accuracy of the metric. TCS = Trauma Composite Score, RTS = Revised Trauma Score, TRISS = Trauma and Injury Severity Score CONCLUSION We have shown that using an arbitrary ISS cutoff is a poor predictor of mortality, particularly amongst older trauma patients and when used for penetrating trauma. As ISS is a commonly used metric for trauma outcomes research and quality improvement metrics, it is important that we begin to reconsider how injury severity is measured and utilized. Injury Severity Score has previously been shown to be an imperfect metric as it does not account for mechanism of injury, age, and presenting physiology. Both TRISS and RTS have attempted to account for these deficits with minimal improvement in predictive capabilities. Despite these known imperfections, ISS remains engrained in trauma registries.

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Region 5 – Clinical Research Our study results suggest that if ISS is utilized, a patients’ age should be a factor. As previously seen in pediatric trauma patients, an ISS of 16 is not associated with an increased ability to predict mortality and an ISS of 25 is more predictive in blunt trauma until the age of sixty. Additionally, given the increasing number of geriatric trauma patients, it is important to appreciate the significant decline in all injury severity metrics in older patients. For both quality improvement and research studies, we should regress from dogmatic injury severity cutoffs as a marker of mortality and adopt an age-based injury severity metric to better measure and predict outcomes. REFERENCES 1. Baker SP, O’Neill B, Haddon W Jr, Long WB. The injury severity score: A method for

describing patients with multiple injuries and evaluating emergency care. J Trauma. 1974;14:187-196.

2. Osler TM, Glance LG, Bedrick EJ. Injury Severity Scoring: Its Definition and Practical Application. In: Asensio JA, Trunkey DD, eds. Current Therapy of Trauma and Surgical Critical Care. 2nd ed. Philadelphia, PA: Elsevier; 2016.

3. Kilgo PD, Meredith JW, Hensberry R, Osler TM. A Note on the Disjointed Nature of the Injury Severity Score. J Trauma. 2004; 57(3):479-485.

4. Aharonson-Daniel L, Giveon A, Stein M, Israel Trauma Group (ITG), Peleg K. Different AIS Triplets: Different Mortality Predictions in Identical ISS and NISS. J Trauma. 2006 Sep;61(3):711-717.

5. Brown JB, Gestring ML, Leeper CM, Sperry JL, Peitzman AB, Billiar TR, Gaines BA. Characterizing injury severity in non-accidental trauma: Does injury severity score miss the mark? J Trauma Acute Care Surg. 2018 Oct;85(4):668-673.

6. Palmer CS, Gabbe BJ, Cameron PA. Defining major trauma using the 2008 Abbreviated Injury Scale. Injury. 2016 Jan;47(1):109-115.

7. Marcin JP, Pollack MM. Triage scoring systems, severity of illness measures, and mortality prediction models in pediatric trauma. Crit Care Med. 2002 Nov;30(11 suppl):S457-467.

8. Furnival RA, Schunk JE. ABCs of scoring systems for pediatric trauma. Pediatr Emerg Care. 1999 Jun;15(3):215-223.

9. Brown JB, Gestring ML, Leeper CM, Sperry JL, Peitzman AB, Billiar TR, Gaines BA. The value of the Injury Severity Score in pediatric trauma: Time for a new definition of severe injury? J Trauma Acute Care Surg. 2017 Jun;82(6):995-1001.

10. Rowell SE, Barbosa RR, Diggs BS, Schreiber MA; Trauma Outcomes Group, Holcomb JB, Wade CE, Brasel KJ, Vercruysse G, MacLeod J, Dutton RP, Hess JR, Duchesne JC, McSwain NE, Muskat P, Johannigamn J, Cryer HM, Tillou A, Cohen MJ, Pittet JF, Knudson P, De Moya MA, Schreiber MA, Tieu B, Brundage S, Napolitano LM, Brunsvold M, Sihler KC, Beilman G, Peitzman AB, Zenait MS, Sperry J, Alarcon L, Croce MA, Minei JP, Kozar R, Gonzalez EA, Stewart RM, Cohn SM, Mickalek JE, Bulger EM, Cotton BA, Nunez TC, Ivatury R, Meredith JW, Miller P, Pomper J, Marin B. Specific abbreviated injury scale values are responsible for the underestimation of mortality in penetrating trauma patients by the injury severity score. J Trauma. 2011 Aug;71(2 Suppl 3):S384-388. doi: 10.1097/TA.0b013e3182287c8d. PMID: 21814109.

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Leveraging the Catecholamine Response after Trauma: An Opportunity to Enhance Platelet-Dependent Hemostasis?

Zachary A. Matthay, MD; Alexander T. Fields; Brenda Nunez-Garcia;

Rachael A. Callcut; Carolyn M. Hendrickson; Lucy Z. Kornblith BACKGROUND In critically injured and hemorrhaging patients, extensive tissue injury and hypoperfusion can trigger alterations in coagulation and inflammation, known as trauma-induced coagulopathy (TIC).1,2 Impaired circulating platelet aggregation is a pronounced feature of TIC, but our knowledge of the underlying biology and clinical implications of this ex-vivo finding remains incomplete.3,4 Data supports a theory that impairments in platelet aggregation that are identified in ex-vivo assays of circulating platelets from trauma patients may be evidence of excessive in-vivo platelet activation that induces adhesion and aggregation at local injury sites, and resultant functional exhaustion in circulating platelets.5 Many surface receptor signaling pathways involved in platelet activation are known to be altered in TIC, including calcium mobilization, glycoprotein VI activation, and P-selectin translocation.6-9 However, the role of catecholamine signaling through platelet surface adrenoreceptors in TIC has not been well studied. This is of relevance, given the stress response to injury induces a surge of catecholamines, and in healthy donor blood epinephrine stimulates platelet aggregation.10,11 However, knowledge of the platelet response to epinephrine at concentrations observed in trauma, and under physiologic flow conditions is lacking. We hypothesized that (1) increased in-vivo plasma epinephrine concentrations in trauma patients are associated with impaired ex-vivo platelet aggregation from sampled circulating platelets, supporting the theory of functional exhaustion, but that (2) treating healthy donor platelets with epinephrine at concentrations observed in trauma enhances local environment platelet adhesion and aggregation under physiologic flow conditions in a microfluidic model. METHODS Patient selection and sample collection: Whole blood samples were collected from trauma patients on arrival to the emergency department as part of a longitudinal study evaluating coagulation and inflammation after trauma (2017-2020).4,12 Thirty-eight patients, not on antithrombotic agents, who had matched timepoint platelet aggregometry and viscoelastic assay results, and banked plasma were selected. These patients encompassed a range of injury severities (injury severity scores [ISS]) and extent of hypoperfusion (base excess). Platelet aggregometry (PA): PA was performed with the Multiplate® multiple electrode aggregometer according to the manufacturer’s protocol (Verum Diagnostica; Munich, Germany). Platelet aggregation was induced in recalcified, citrated blood at 37oC with adenosine diphosphate (ADP). Platelet aggregation was quantified as area under the aggregation curve (AUC) over 6 minutes. Rotational thromboelastometry (ROTEM): ROTEM was performed using citrated whole blood at 37oC with the ROTEM® delta machine (Pentapharm; Munich, Germany) and EXTEM reagent according to the manufacturer’s protocol. Clotting time (CT) in seconds (sec), clot formation time (CFT) (sec), alpha angle (degrees), maximum clot firmness (MCF) (mm), and maximum lysis (ML%) were recorded.

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Region 9 – Basic Science Plasma epinephrine measurements: Plasma samples were prepared from whole blood by centrifugation and immediately stored at -80°C. Epinephrine (EPI) was measured in duplicate with appropriate internal standards and controls by enzyme linked immunoassays using a commercially available kit (Abnova Corporation; Taiwan). The lower limit of detection (10pg/ml) is well below mean concentrations of EPI in plasma from healthy volunteers.13 Microfluidic model Platelet isolation: Whole blood from one healthy adult male was collected in 3.2% sodium citrate and centrifuged at 200xg for 20 minutes. The resulting platelet rich plasma was diluted 1:1 with HEPES-buffered Tyrode’s solution (HT) and prostaglandin-E1 was added to 1μM. Erythrocytes and leukocytes were pelleted at 800xg for 20 minutes. The supernatant was removed, and the platelet pellet was washed twice with HT buffer. Platelets were resuspended in HT with 3% bovine serum albumin, counted, and diluted with HT to 1x108 platelets/mL. Microfluidic perfusion: A commercially available device (Ibidi; Munich, Germany) containing 6 microfluidic channels (size: 0.1mm x 1mm x 17mm) was coated with collagen (100ug/ml) or no coating as control. At the inlet, this was connected with polyethylene tubing to a reservoir containing platelet rich plasma (1x10^8/L) and to a syringe pump at the outlet. After washing the system with blocking buffer, platelet rich plasma was flowed through the chamber at venous shear rates (100s-1) after recalcification (to [Ca2+] 3mM) and incubation with no agonist (control), medium dose EPI (10ng/ml), and high dose EPI (50ng/ml) for five minutes prior to perfusion through the device. Still images were recorded at 60x magnification using phase contrast microscopy at one minute intervals for five minutes, and the number of platelet adhesion events recorded for each of the treatment conditions by counting in 10 fields of view along each channel. Statistical analyses: Univariate analyses were performed to compare the relationships of patient characteristics, with EPI concentrations using the Mann-Whitney test and multivariable linear regression to test the association of EPI with platelet aggregation and viscoelastic measures, controlling for ISS and base excess. RESULTS In-vivo: The 38 trauma patients were characterized by a range of injury severity (median ISS 9, IQR 1-22) and degree of hypoperfusion (base excess 3.1mmol/L+5.5). Although platelet counts were normal (268+73x109/L), 52% had evidence of impaired ex-vivo platelet aggregation in response to ADP stimulation. On multivariable linear regression (controlling for injury severity and hypoperfusion), increasing EPI concentrations were associated with notable trends in impaired ex-vivo platelet aggregation, delayed clot initiation, decreased rate of clot formation, decreased clot strength, and significantly increased clot lysis (Table).

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Region 9 – Basic Science Table.

Ex-vivo: Healthy donor platelets subjected to venous flow conditions in collagen coated channels showed enhanced local environment platelet adhesion after ex-vivo incubation with EPI at 10ng/ml and 50ng/ml (1.5 and 3.0 fold, respectively) compared to untreated (Figure 1). Qualitatively, increasing EPI concentrations increased local environment platelet activation and aggregate formation under direct visualization by phase contrast microscopy (Figure 2).

Figure 1. Effect of Epinephrine on Local Environment Platelet Adhesion Events. Healthy donor platelets were treated with epinephrine (EPI) at 10ng/ml or 50ng/ml and perfused through a collagen coated microfluidic channel at a venous shear rate (100s-1). Untreated (control) platelets were perfused through a collagen coated channel and an uncoated channel as an additional control. Using direct visualization with phase-contrast microscopy at 60x magnification, the number of adhered platelets in 10 adjacent fields of view were counted after 10 minutes of perfusion and are represented above as box and whisker plots with (black dots=outside values).

Multivariable Regression Results

Coefficient for EPI

P-value

CI-low

CI-high

Platelet Aggregation (ADP stimulated, AUC) -1.11 0.06 -2.27 0.06

Clot formation time (seconds) 1.46 0.08 -0.17 3.10 Clot formation angle (degrees) -0.25 0.09 -0.55 0.04 Maximum clot firmness (mm) -0.35 0.06 -0.72 0.02 Maximum lysis (%) 0.94 0.02 0.15 1.73 Univariate Comparisons of EPI with Injury Severity and Outcomes Mean [EPI] pg/ml P-

value Injury Severity Score < 15 512

0.21 > 15 693 Multiple Organ Failure Yes 527

0.42 No 863 Vital Status at Discharge Alive 540

0.31 Expired 802 Table. Association of plasma epinephrine (EPI) concentrations with platelet aggregation, viscoelastic clotting measures, injury severity score, multiple organ failure, and mortality. ADP- adenosine diphosphate. AUC-area under the aggregation curve in units. CI-95% confidence interval. Coefficients represent the estimated change in the outcome for each 100pg/ml increase in the concentrations of EPI in multivariable linear regression models controlling for injury severity score and base excess, n=32. Viscoelastic measures from ROTEM extrinsic pathway channel results. Multiple Organ failure defined using Denver Criteria (14). Univariate comparisons made with non-parametric Mann-Whitney test.

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Figure 2. Effect of Epinephrine on Local Environment Platelet Activation and Aggregate Formation. Representative phase contrast microscopy images (60x) shown for healthy donor platelets perfused through microfluidic device (control) or after epinephrine (EPI) treatment (10ng/ml or 50ng/ml). (A) Uncoated channel, no agonist: minimal platelet adhesion, marked by arrows. (B) Collagen channel, no agonist: increased compared to A, but minimal spreading and no aggregate formation. (C) Collagen channel, 10ng/ml EPI: increased numbers of adhered platelets and formation of platelet aggregates (dotted circles). (D) Collagen channel, 50ng/ml EPI: largest density of adhered platelets compared to A-C, with aggregate formation (dotted circle), and platelet spreading (black arrows) indicating activation and shape change.

CONCLUSION In this study, we found that in trauma patients, increased in-vivo plasma epinephrine concentrations were associated with impaired ex-vivo circulating platelet aggregation and viscoelastic clotting measures, despite the known procoagulant actions of epinephrine. These findings provide additional support for functional exhaustion of sampled circulating platelets in trauma, which may not be phenotypically representative of platelet adhesion and aggregation behavior at local sites of injury in-vivo. This is further corroborated by our microfluidic model demonstrating enhanced healthy platelet adhesion and aggregation in local environments after treatment with epinephrine under venous flow conditions. Further defining the impact of catecholamines on platelet dependent hemostasis in injury is especially relevant given renewed interest in low dose vasopressin for treatment of shock in hemorrhaging trauma patients.15 Future work should address whether adrenergic agonists could instead be used as adjunctive hemodynamic support during resuscitation of critically injured patients, as this may confer the additional benefit of augmenting platelet dependent hemostasis.

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Region 9 – Basic Science REFERENCES 1. Kornblith LZ, Moore HB, Cohen MJ. Trauma-induced coagulopathy: The past, present, and

future. J Thromb Haemost. 2019;17(6):852-862. 2. Callcut RAM, Kornblith LZM, Conroy ASB, Robles AJM, Meizoso JPM, Namias NM, Meyer

DEM, Haymaker AB, Truitt MSM, Agrawal VP, et al. The why and how our trauma patients die: A prospective Multicenter Western Trauma Association study. Journal of Trauma and Acute Care Surgery. 2019;86(5):864-870.

3. Jacoby RC, Owings JT, Holmes J, Battistella FD, Gosselin RC, Paglieroni TG. Platelet activation and function after trauma. Journal of Trauma and Acute Care Surgery. 2001;51(4):639-647.

4. Kutcher ME, Redick BJ, McCreery RC, Crane IM, Greenberg MD, Cachola LM, Nelson MF, Cohen MJ. Characterization of platelet dysfunction after trauma. Journal of Trauma and Acute Care Surgery. 2012;73(1):13.

5. Pareti FI, Capitanio A, Mannucci L, Ponticelli C, Mannucci PM. Acquired dysfunction due to the circulation of "exhausted" platelets. Am J Med. 1980;69(2):235-240.

6. Matthay ZA, Fields AT, Nunez-Garcia B, Patel M, Cohen MJ, Callcut RA, Kornblith LZ. Dynamic Effects of Calcium on In Vivo and Ex Vivo Platelet Behavior After Trauma. J Trauma Acute Care Surg. 2020.

7. Verni CC, Davila A Jr., Balian S, Sims CA, Diamond SL. Platelet dysfunction during trauma involves diverse signaling pathways and an inhibitory activity in patient-derived plasma. J Trauma Acute Care Surg. 2019;86(2):250-259.

8. Lee MY, Verni CC, Herbig BA, Diamond SL. Soluble fibrin causes an acquired platelet glycoprotein VI signaling defect: implications for coagulopathy. J Thromb Haemost. 2017;15(12):2396-407.

9. Ramsey MT, Fabian TC, Shahan CP, Sharpe JP, Mabry SE, Weinberg JA, Croce MA, Jennings LK. A prospective study of platelet function in trauma patients. J Trauma Acute Care Surg. 2016;80(5):726-732; discussion 32-33.

10. Servia L, Jove M, Sol J, Pamplona R, Badia M, Montserrat N, Portero-Otin M, Trujillano J. A prospective pilot study using metabolomics discloses specific fatty acid, catecholamine and tryptophan metabolic pathways as possible predictors for a negative outcome after severe trauma. Scand J Trauma Resusc Emerg Med. 2019;27(1):56.

11. von Kanel R, Dimsdale JE. Effects of sympathetic activation by adrenergic infusions on hemostasis in vivo. Eur J Haematol. 2000;65(6):357-369.

12. Kornblith LZ, Kutcher ME, Redick BJ, Calfee CS, Vilardi RF, Cohen MJ. Fibrinogen and platelet contributions to clot formation: Implications for trauma resuscitation and thromboprophylaxis. J Trauma Acute Care Surg. 2014;76(2):255-256; discussion 62-63.

13. Meyer MA, Ostrowski SR, Overgaard A, Ganio MS, Secher NH, Crandall CG, Johansson PI. Hypercoagulability in response to elevated body temperature and central hypovolemia. J Surg Res. 2013;185(2):e93-100.

14. Sauaia A, Moore EE, Johnson JL, Ciesla DJ, Biffl WL, Banerjee A. Validation of postinjury multiple organ failure scores. Shock. 2009;31(5):438-447.

15. Sims CA, Holena D, Kim P, Pascual J, Smith B, Martin N, Seamon M, Shiroff A, Raza S, Kaplan L, et al. Effect of Low-Dose Supplementation of Arginine Vasopressin on Need for Blood Product Transfusions in Patients With Trauma and Hemorrhagic Shock: A Randomized Clinical Trial. JAMA Surg. 2019;154(11):994-1003.

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CHOP (Critical Hemorrhage to Operating-Room Patient) Resuscitation Protocol Leads to Consistent and Superior Outcomes in a Tertiary

Trauma Center: A Cumulative Summation (CUSUM) Analysis

Rachel Y. Chen, MD; J.T.T. Goo; L. Christie; D.J.K. Lee INTRODUCTION The standard protocol for exsanguinating trauma patients involves initial evaluation and resuscitation in the emergency department, which sets the stage for subsequent definitive care and disposition. This involves major coordination of resources, which may delay intervention especially as many present after office hours. Our center has employed a second-tier activation system (CHOP protocol) that immediately mobilizes all respective trauma specialists including interventional radiologists, and allows rapid access to the operating room. OBJECTIVE We hypothesized that exsanguinating patients managed by CHOP protocol have better overall outcomes and survival. METHODS We identified trauma patients fulfilling CHOP criteria from 2016 to 2019 and divided them into two groups: preCHOP (standard protocol) and CHOP. Data was extracted from a prospectively maintained trauma registry. Demographics, injury pattern and in-hospital data were analyzed. The key outcome studied was the impact of CHOP protocol on mortality. Success and failure were analyzed using CUSUM methodology. RESULTS Thirty-seven patients were managed by CHOP protocol since its introduction in March 2018 compared with 36 patients managed by standard protocol. Majority were blunt trauma (89.2% CHOP vs 91.7% preCHOP). The mean Injury Severity Score in the CHOP vs preCHOP group was 37 vs 39. We observed a significant improvement in time to intervention in CHOP patients (78min vs 113min), both during and after office hours. Mortality was significantly lower when compared to the predicted model (10.8 % vs 32%) and to the preCHOP group (10.8 vs 30.6%). The CHOP protocol produced a trend of successively desired outcomes leading to the CUSUM curve exhibiting z. This consistency was not seen in patients managed with standard protocol. CONCLUSION The CHOP protocol, a relatively novel system in the local context, was able to achieve sustained superior outcomes compared to standard protocol. It can be better enhanced through expansion of its activation process by paramedics in the pre-hospital setting.

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