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Massive transfusion with older packed red blood cells is associated with increased morbidity and mortality. As packed red blood cells age, they undergo biochemical and structural changes known as the storage lesion. We developed a novel solution to increase viscosity in stored packed red blood cells. We hypothesized that packed red blood cell storage in this solution would blunt storage lesion formation and mitigate the inflammatory response after resuscitation.Blood was obtained from 8- to 10-week-old C57BL/6 male donor mice or human volunteers and stored as packed red blood cell units for 14 days for mice or 42 days for humans in either standard AS-3 storage solution or EAS-1587, the novel packed red blood cell storage solution. Packed red blood cells were analyzed for microvesicles, cell-free hemoglobin, phosphatidylserine, band-3 protein, glucose utilization, and osmotic fragility. Additional mice underwent hemorrhage and resuscitation with packed red blood cells stored in either AS-3 or EAS-1587. Serum was analyzed for inflammatory markers.Murine packed red blood cells stored in EAS-1587 demonstrated reductions in microvesicle and cell-free hemoglobin accumulation as well as preserved band-3 expression, increase glucose utilization, reductions in phosphatidylserine expression, and susceptibility to osmotic stress. Serum from mice resuscitated with packed red blood cells stored in EAS-1587 demonstrated reduced proinflammatory cytokines. Human packed red blood cells demonstrated a reduction in microvesicle and cell-free hemoglobin as well as an increase in glucose utilization.Storage of packed red blood cells in a novel storage solution mitigated many aspects of the red blood cell storage lesion as well as the inflammatory response to resuscitation after hemorrhage. This modified storage solution may lead to improvement of packed red blood cell storage and reduce harm after massive transfusion.

Chest wall injuries are very common in blunt trauma and development of treatment protocols can significantly improve outcomes. Surgical stabilisation of rib fractures (SSRF) is an adjunct for the most severe chest injuries and can be used as a part of a comprehensive approach to chest injuries care. We hypothesized that implementation of a SSRF programme program would result in improved short-term outcomes.The characteristics of the initial group of SSRF patients (Early-SSRF) were used to identify matching factors. Patients prior to SSRF protocol underwent a propensity score match, followed by screening for operative indications and contraindications. After exclusions, a non-operative (Non-Op) cohort was defined (n=36) resulting in an approximately 1:1 match. An overall operative cohort, inclusive of Early-SSRF and all subsequent operative patients, was defined (All- SSRF). A before-and-after analysis using chi-squared, Students T-tests, and Mann-Whitney U-tests were used to assess significance at the level of 0.05.Early-SSRF (n=22) and All-SSRF (n=45) were compared to Non-Op (n=36). The selection process resulted in well matched groups, and equally well-balanced operative indications between the groups. The Early-SSRF group demonstrated shortened duration of mechanical ventilation and a decreased frequency of being discharged a long-term acute care hospital. The All-SSRF group again demonstrated markedly shorter duration of mechanical ventilation compared to Non-Op (median 6 days vs 16 days, p0.01), more decrease discharge to a long-term acute care hospital (9% vs. 36%, p=0.01), and reduced risk for tracheostomy (8.9% vs. 33.3% respectively, p0.01) CONCLUSION: The introduction of an operative rib fixation to a comprehensive chest wall injury protocol can produce improvements in clinical outcomes that decrease time on the ventilator and tracheostomy rates, and result in more patients being discharged to home. Creation and implementation of a chest wall injury protocol to include SSRF requires a multidisciplinary approach and thoughtful patient selection.

Background Blunt chest wall injury accounts for 15% of trauma admissions. Previous studies have shown that the number of rib fractures predicts inpatient opioid requirements, raising concerns for pharmacologic consequences including hypotension, delirium, and opioid dependence. We hypothesized that intercostal injection of liposomal bupivacaine would reduce analgesia needs and improve spirometry metrics in trauma patients with rib fractures. Methods A prospective, double-blinded, randomized placebo-control study was conducted at a Level 1 trauma center as an FDA investigational new drug study. Enrollment criteria included patients ≥18 years admitted to the ICU with blunt chest wall trauma who could not achieve >50% goal inspiratory capacity. Patients were randomized to liposomal bupivacaine or saline injections in up to 6 intercostal spaces. Primary outcome was to examine pain scores and breakthrough pain medications for 96-hour duration. The secondary endpoint was to evaluate the effects of analgesia on pulmonary physiology. Results 100 patients were enrolled, 50 per cohort, with similar demographics (ISS 17.9 bupivacaine 17.6 control) and comorbidities. Enrolled patients had a mean age of 60.5 years and 47% were female. Rib fracture number, distribution, and targets for injection were similar between groups. While both groups displayed a decrease in opioid use over time, there was no change in mean daily pain scores. The bupivacaine group achieved higher incentive spirometry volumes over days 1 and 2 (1095 mL, 1063 mL bupivacaine vs. 900 mL, 866 mL control). Hospital and ICU lengths of stay were similar and there were no differences in post-injection pneumonia, use of epidural catheters or adverse events bet ween groups. Conclusions While intercostal liposomal bupivacaine injection is a safe method for rib fracture-related analgesia, it was not effective in reducing pain scores, opioid requirements, or hospital length of stay. Bupivacaine injection transiently improved incentive spirometry volumes, but without a reduction in the development of pneumonia.Clinical Trial Registration: "Intercostal Liposomal Bupivacaine for the Management of Blunt Chest Wall Trauma" NCT02749968. Level of evidence Level 2 ; Therapeutic/Care Management.

Surgical residencies have implemented boot-camps for early acquisition of basic technical skills for interns. However, educators worry that retention is poor. We hypothesized that a structured boot-camp curriculum would improve skills.Interns underwent eight boot-camp sessions at the beginning of residency. Interns completed pre-, post-boot-camp, and end-of-year skills assessments, as well as post-boot camp and end-of-year porcine procedure labs. Proficiency was measured on a 5-point scale and by completion time.After boot-camp, interns improved all domains of knot-tying. Median time decreased for skin-closure (8.3 vs 9.9 min, p 0.01), peg transfer (57 vs 87 s, p 0.01), intracorporeal (178 vs 300 s, p 0.01), and extracorporeal knot-tying (140 vs 259 s, p 0.01). At the end-of-year assessment, interns exhibited retention of all skills and improved in knot-tying and central line skills. During the retention porcine lab, interns progressed basic but not complex skills.An eight-week boot-camp effectively improved technical skills among surgery interns. Interns retained all skills and improved upon techniques frequently practiced during intern year.

Context.— Delayed recognition of acute kidney injury (AKI) results in poor outcomes in military and civilian burn-trauma care. Poor predictive ability of urine output (UOP) and creatinine contribute to the delayed recognition of AKI. Objective.— To determine the impact of point-of-care (POC) AKI biomarker enhanced by machine learning (ML) algorithms in burn-injured and trauma patients. Design.— We conducted a 2-phased study to develop and validate a novel POC device for measuring neutrophil gelatinase-associated lipocalin (NGAL) and creatinine from blood samples. In phase I, 40 remnant plasma samples were used to evaluate the analytic performance of the POC device. Next, phase II enrolled 125 adults with either burns that were 20% or greater of total body surface area or nonburn trauma with suspicion of AKI for clinical validation. We applied an automated ML approach to develop models predicting AKI, using a combination of NGAL, creatinine, and/or UOP as features. Results.— Point-of-care NGAL (mean [SD] bias: 9.8 [38.5] ng/mL, P = .10) and creatinine results (mean [SD] bias: 0.28 [0.30] mg/dL, P = .18) were comparable to the reference method. NGAL was an independent predictor of AKI (odds ratio, 1.6; 95% CI, 0.08–5.20; P = .01). The optimal ML model achieved an accuracy, sensitivity, and specificity of 96%, 92.3%, and 97.7%, respectively, with NGAL, creatinine, and UOP as features. Area under the receiver operator curve was 0.96. Conclusions.— Point-of-care NGAL testing is feasible and produces results comparable to reference methods. Machine learning enhanced the predictive performance of AKI biomarkers including NGAL and was superior to the current techniques.

There is a paucity of data to predict early death or futility after trauma. The objective of this study was to characterize the laboratory values, blood product administration, and hospital disposition for patients with trauma who died within 72 h of admission.All deaths within 72 h of admission over a 5-y period at a level I trauma center were reviewed. Blood transfusion within the first 4 h of arrival and patient disposition from the emergency department to the operating room (OR), surgical intensive care unit, or the neuroscience intensive care unit (NSICU) were analyzed. Kaplan-Meier curves were generated to determine time to death.A total of 622 subjects were identified; 39.5% died in the emergency department, 10.6% went directly to the OR, 13.6% were admitted to the surgical intensive care unit, and 29.7% admitted to the NSICU. Of these subjects, 201 (32.2%) patients received blood within the first 4 h. By 24 h, early blood transfusion was associated with more rapid death for patients who were admitted to the NSICU (80% versus 60% mortality, P = 0.01) but not for patients taken directly to the OR (80% versus 70% mortality, P = 0.2). Admission coagulopathy by international normalized ratio (P 0.01), but not anemia (P = 0.64) or acidosis (P = 0.45), correlated with a shorter time to death. In contrast, laboratory values obtained at 4 h after admission did not correlate with time to death.Our data demonstrate that admission coagulation derangement and need for early blood product transfusion are the two factors most associated with early death after injury, particularly in those patients with traumatic brain injury. These data will help construct future models for futility of continued care in patients with trauma.

Packed red blood cell (pRBC) units administered during resuscitation from hemorrhagic shock are of varied storage ages. We have previously shown that RBC-derived microparticles' impact on thrombogenesis. However, the impact of storage age on pRBC coagulability is unknown. Therefore, we sought to investigate the effect of storage age on innate coagulability and aggregability of stored pRBCs.pRBCs prepared from male C57BL/6J mice were stored in Additive Solution-3 according to our standardized murine blood banking protocols for 14 days. Rotational thromboelastometry (ROTEM) was used to assess the innate coagulation status of fresh and 14-day old pRBCs. Viscoelastic coagulation parameters of clotting time (CT), clot formation time (CFT), alpha angle, and maximum clot firmness (MCF) were analyzed to determine coagulability. Plasma was added to the fresh pRBCs and 15-day old pRBCs to determine if the storage-associated coagulopathy was reversible with plasma. Statistical analyses were conducted with a Student's t-test.Fifteen-day old pRBCs demonstrated a significant reduction in MCF (10.3 vs. 24.4 mm, P-value0.001) and alpha angle (6.0 vs. 27.2 degrees, P-value0.001) as well as significant prolongation of CFT and CT (1126.5 vs. 571.4 s, P-value0.001) compared to fresh pRBCs. FFP addition to 15-day old and fresh pRBCs, demonstrated a significant reduction in MCF and persistent prolongation of CFT. This suggests that pRBCs lost coagulability as they aged and this deficit was not completely corrected by plasma administration.Storage duration may be an important factor in coagulation potential of pRBCs. Transfusion with older pRBCs may contribute to coagulopathy in massively transfused patients.

Noncompressible torso hemorrhage remains a leading cause of death. Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) placement may occur before transport; however, its efficacy has not been demonstrated at altitude. We hypothesized that changes in altitude would not result in blood pressure changes proximal to a deployed REBOA.A simulation model for 7Fr guidewireless REBOA was used at altitudes up to 22,000 feet. Female pigs then underwent hemorrhagic shock to a mean arterial pressure (MAP) of 40 mm Hg. After hemorrhage, a REBOA catheter was deployed in the REBOA group and positioned but not inflated in the no-REBOA group. Animals underwent simulated aeromedical evacuation at 8000 ft or were left at ground level. After altitude exposure, the balloon was deflated, and the animals were observed.Taking the REBOA catheter to 22,000 ft in the simulation model resulted in a lower systolic blood pressure but a preserved MAP. In the porcine model, REBOA increased both systolic blood pressure and MAP compared with no-REBOA (P 0.05) and was unaffected by altitude. No differences in postflight blood pressure, acidosis, or systemic inflammatory response were observed between ground and altitude REBOA groups.REBOA maintained MAP up to 22,000 feet in an inanimate model. In the porcine model, REBOA deployment improved MAP, and the balloon remained effective at altitude.

BACKGROUND: Recent military and civilian experience suggests that fresh whole blood may be the preferred for treatment of hemorrhagic shock, but its use is limited by its 21-day shelf life. The red blood cell storage lesion and coagulation status of packed red blood cells (pRBCs) salvaged from expired whole blood are unknown. We hypothesized that packed red blood cells can be salvaged from previously stored whole blood. METHODS: Cold stored, low-titer, O-positive, non-leukoreduced, whole blood units were obtained at 21 days of storage. Erythrocytes were separated by centrifugation, resuspended in AS-3, and stored for 21 additional days as salvaged pRBCs. The red blood cell storage lesion parameters of microvesicles, Band-3, free hemoglobin, annexin V, and erythrocyte osmotic fragility were measured and compared to pRBCs prepared at the time of donation and stored in AS-3 for 42 days (standard pRBCs). In additional experiments, murine pRBCs were prepared from expired whole blood units and compared to those stored under standard conditions. Mice underwent hemorrhage and resuscitation with standard and salvaged pRBC units and serum cytokines and free hemoglobin were determined. RESULTS: There were no significant differences in microvesicle formation or cell-free hemoglobin concentration between salvaged and standard pRBCs. There was decreased Band-3 and increased phosphatidylserine in the salvaged units as well as greater osmotic fragility. Salvaged pRBCs maintained consistent clot firmness. After hemorrhage and resuscitation in a murine model, salvaged pRBCs did not demonstrate increased serum cytokine levels. CONCLUSIONS: Salvaged pRBCs from previously stored whole blood accumulate the red blood cell storage lesion in a similar fashion to standard pRBCs and maintain consistent coagulability when reconstituted with plasma. Salvaged pRBCs are not associated with an increased inflammatory response when used for resuscitation in a murine model. Salvaged pRBCs may be a viable product for utilization in the treatment of traumatic hemorrhagic shock. LEVEL OF EVIDENCE: Level II (prospective laboratory study, therapeutic)

Introduction Traumatic brain injury (TBI) has become increasingly prevalent among the injuries sustained in the military. Many wounded warriors require emergency medical evacuation via helicopter and subsequently fixed wing transport. During aeromedical evacuation, both pilots and patients experience whole body vibration due to engine, rotor, and propeller rotation. The impact of posttraumatic vibration and hypoxia exposure characteristic of the aeromedical evacuation environment on TBI is currently unknown. Methods A swine TBI model of controlled cortical impact was utilized. The pigs first underwent TBI or sham injury and were subsequently exposed to vibration or no vibration and hypoxia or normoxia for 2 hours. They were monitored for an additional 4 hours following vibration/hypoxia and blood was drawn at hourly intervals for cytokine and serum biomarker analysis. Continuous physiologic and neurologic monitoring were utilized. Prior to the conclusion of the experiment, the animals underwent brain magnetic resonance imaging. At the end of the study, the brain was extracted for histologic analysis. Results Physiologic parameters except for peripheral capillary oxygen saturation (SpO2) were similar between all groups. The hypoxia groups demonstrated the expected decrease in SpO2 and pO2 during the hypoxic period, and this was sustained throughout the study period. The pH, pCO2 and electrolytes were similar among all groups. Neuron specific enolase was increased over time in the TBI group, however it was similar to the sham TBI group at all time points. There were no differences in IL-1β, IL-6, IL-8, TNFα, GFAP, HIF1α, syndecan-1, or S100β serum levels between groups. The mean ICP during cortical impact in the TBI group was 279.8 ± 56.2 mmHg. However, the postinjury ICP was not different between groups at any subsequent time point. Brain tissue oxygenation and perfusion were similar between all groups. Conclusion In this novel study evaluating the effect of vibration on short-term outcomes following TBI, we demonstrate that the moderate vibration and hypoxia simulating aeromedical evacuation do not impact short term outcomes following TBI.

Screening for blunt cardiac injury (BCI) includes obtaining a serum troponin level and an electrocardiogram for patients diagnosed with a sternal fracture. Our institution has transitioned to the use of a high sensitivity troponin I (hsTnI). The aim of this study was to determine whether hsTnI is comparable to troponin I (TnI) in identifying clinically significant BCI.Trauma patients presenting to a level I trauma center over a 24-mo period with the diagnosis of sternal fracture were screened for BCI. Any initial TnI more than 0.04 ng/mL or hsTnI more than 18 ng/L was considered positive for potential BCI. Clinically significant BCI was defined as a new-bundle branch block, ST wave change, echocardiogram change, or need for cardiac catheterization.Two hundred sixty five patients with a sternal fracture were identified, 161 underwent screening with TnI and 104 with hsTnI. For TnI, the sensitivity and specificity for detection of clinically significant BCI was 0.80 and 0.79, respectively. For hsTnI, the sensitivity and specificity for detection of clinically significant BCI was 0.71 and 0.69, respectively. A multivariate analysis demonstrated the odds ratio for significant BCI with a positive TnI was 14.4 (95% confidence interval, 3.9-55.8, P 0.0001) versus an odds ratio of 5.48 (95% confidence interval 1.9-15.7, P = 0.002) in the hsTnI group.The sensitivity of hsTnI is comparable to TnI for detection of significant BCI. Additional investigation is needed to determine the necessity and interval for repeat testing and the need for additional diagnostic testing.

The COVID-19 pandemic forced a sudden change from in-person to virtual interviews for the general surgery residency match. General surgery programs and applicants adopted multiple strategies to best mimic in-person recruitment. The purpose of this study was to evaluate applicant opinions of the virtual recruitment format.Postinterview survey responses for applicants interviewing at a single general surgery residency program in the 2020-2021 and 2021-2022 cycles were evaluated. All interviewed applicants were sent an anonymous survey assessing the virtual interview structure, their impression of the program, and their opinions on recruitment in the future.The response rate was 31.2% (n = 60). Most (88.4%) respondents reported a more favorable view of the program after a virtual interview. Factors that were most likely to create a favorable impression were residents (89.6%) and culture (81.0%). 50.8% of applicants favored virtual-only interviews. The majority of applicants (60.3%), however, preferred the virtual interview remain a component of the application process, 34.4% recommended that virtual interviews be used as an initial screen before in-person invites, while 19.0% suggested applicants should interview in-person or virtually without penalty. 62.1% favored capping the number of interviews offered by programs and accepted by applicants.The virtual interview format for general surgery residency allows applicants to effectively evaluate a residency program. Applicants are in favor of a combination of virtual and in-person interviews in the future. Innovation in the recruitment process, including limiting the number of applications and incorporating virtual events, is supported by applicants.

BACKGROUND: Several serum biomarkers have been studied to diagnose incidence and severity of traumatic brain injury (TBI), but a reliable biomarker in TBI has yet to be identified. Ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) has been proposed as a biomarker in clinical and preclinical studies, largely in the setting of isolated TBI or concussion. The aim of this study was to evaluate the performance of UCH-L1 as a serum biomarker in the setting of polytrauma and TBI. METHODS: Multiple variations of murine TBI and polytrauma models were used to evaluate serum biomarkers. The different models included TBI with and without hemorrhagic shock and resuscitation, isolated extremity vascular ligation, extremity ischemia/reperfusion, and blunt tail injury. Blood was drawn at intervals after injury, and serum levels of neuron-specific enolase, UCH-L1, creatine kinase, and syndecan-1 were evaluated by enzyme-linked immunosorbent assay. RESULTS: UCH-L1 levels were not significantly different between TBI, tail injury, and sham TBI. By contrast, neuron-specific enolase levels were increased in TBI mice compared with tail injury and sham TBI mice. UCH-L1 levels increased regardless of TBI status at 30 min and 4 h after hemorrhagic shock and resuscitation. In mice that underwent femoral artery cannulation followed by hemorrhagic shock/resuscitation, UCH-L1 levels were significantly elevated compared with shock sham mice at 4 h (3158 ± 2168 pg/mL, 4 h shock versus 0 ± 0 pg/mL, 4 h shock sham; P < 0.01) and at 24 h (3253 ± 2954 pg/mL, 24 h shock versus 324 ± 482 pg/mL, 24 h shock sham; P = 0.03). No differences were observed in UCH-L1 levels between the sham shock and the arterial ligation, vein ligation, or extremity ischemia/reperfusion groups at any time point. Similar to UCH-L1, creatine kinase was elevated only after shock compared with sham mice at 4, 24, and 72 h after injury. CONCLUSIONS: Our study demonstrates that UCH-L1 is not a specific marker for TBI but is elevated in models that induce central and peripheral nerve ischemia. Given the increase in UCH-L1 levels observed after hemorrhagic shock, we propose that UCH-L1 may be a useful adjunct in quantifying severity of shock or global ischemia rather than as a specific marker of TBI.

Background The risk assessment profile (RAP) score has been used to determine patients who would most benefit from lower extremity duplex ultrasound screening (LEDUS). We hypothesized that revising our LEDUS protocol to perform screening ultrasound examinations in patients with an RAP ≥8 within 48 h of admission would reduce the number of LEDUS performed without changing outcomes. Methods A retrospective review was conducted on trauma patients admitted from July 1, 2014, to June 30, 2015, and July 1, 2016, to June 30, 2017. In 2014-2015, patients with an RAP score ≥5 underwent weekly LEDUS examinations starting on hospital day 4. In 2016-2017, the protocol was changed to start screening patients with an RAP score ≥8 by hospital day 2. Both protocols screened with weekly ultrasounds after the first examination. Demographic data, injury characteristics, LEDUS examination findings, chemoprophylaxis type, and venous thromboembolism incidence were collected. Results A total of 602 patients underwent LEDUS examination in 2014-2015, whereas only 412 underwent LEDUS in 2016-2017. No significant difference was seen in the number of patients diagnosed with deep vein thrombosis (DVT) or pulmonary embolism. DVTs were most often identified on the first LEDUS examination in both cohorts. Of patients diagnosed with a DVT on an LEDUS examination, a significantly higher RAP score (12 versus 10), and a shorter time to first duplex (1 versus 3 d), and DVT diagnosis (2 versus 4 d) were observed in the 2016-2017 cohort. In patients diagnosed with a pulmonary embolism, no significant differences were demonstrated between cohorts. Conclusions Refinement of LEDUS protocols can decrease overutilization of hospital resources without compromising trauma patient outcomes.

Background Deep vein thrombosis (DVT) remains a significant cause of morbidity after injury. Lower extremity duplex ultrasound screening (LEDUS) is designed to identify early, asymptomatic DVTs in moderate and high risk patients. We sought to describe when thrombus is detected and identify which trauma patients benefit from LEDUS. Materials and methods A retrospective review was conducted on trauma patients who were moderate or high risk for venous thromboembolism based on risk assessment profile (RAP) scoring. Patients with RAP scores ≥5 underwent LEDUS on hospital Day 4 and then weekly. We defined moderate venous thromboembolism risk as an RAP score of 5-9 and high risk as an RAP score of ≥10. Demographics, injury characteristics, and chemoprophylaxis type and timing were analyzed. Results A total of 579 trauma patients underwent a total of 820 ultrasounds in 1 y. Eighty-eight acute DVTs were identified. There was only one progression of a below- to above-the-knee DVT. Patients with RAP scores ≥10 had significantly higher rates of DVTs compared with patients with lower RAP scores in addition to longer lengths of stay and time to DVT prophylaxis. Moderate- and high-risk patients had similar rates of pulmonary embolism. Two-thirds of all DVTs were diagnosed on the first screening examination. The rate of DVTs in patients with RAP scores 7-9 was 15.4% compared with 6.1% of those with RAP scores of 5-6. Conclusions LEDUS allows for early identification of asymptomatic DVTs. Moderate-risk patients with RAP scores of ≥7 should be considered for LEDUS, given higher rates of DVT.

Background Tranexamic acid (TXA) has been shown to reduce mortality in the treatment of traumatic hemorrhage. This effect seems most profound when given early after injury. We hypothesized that extending a protocol for TXA administration into the prehospital aeromedical setting would improve outcomes while maintaining a similar safety profile to TXA dosed in the emergency department (ED). Materials and methods We identified all trauma patients who received TXA during prehospital aeromedical transport or in the ED at our urban level I trauma center over an 18-mo period. These patients had been selected prospectively for TXA administration using a protocol that selected adult trauma patients with high-risk mechanism and concern for severe hemorrhage to receive TXA. Patient demographics, vital signs, lab values including thromboelastography, blood administration, mortality, and complications were reviewed retrospectively and analyzed. Results One hundred sixteen patients were identified (62 prehospital versus 54 ED). Prehospital TXA patients were more likely to have sustained blunt injury (76% prehospital versus 46% ED, P = 0.002). There were no differences between groups in injury severity score or initial vital signs. There were no differences in complication rates or mortality. Patients receiving TXA had higher rates of venous thromboembolic events (8.1% in prehospital and 18.5% in ED) than the overall trauma population (2.1%, P Conclusions Prehospital administration of TXA during aeromedical transport did not improve survival compared with ED administration. Treatment with TXA was associated with increased risk of venous thromboembolic events. Prehospital TXA protocols should be refined to identify patients with severe hemorrhagic shock or traumatic brain injury.

Whole blood is a powerful resuscitation strategy for trauma patients but has a shorter shelf life than other blood products. The red blood cell storage lesion in whole blood has not previously been investigated beyond the standard storage period. In the present study, we hypothesized that erythrocytes in stored whole blood exhibit similar aspects of the red blood cell storage lesion and that transfusion of extended storage whole blood would not result in a more severe inflammatory response after hemorrhage in a murine model. To test this hypothesis, we stored low-titer, O-positive, whole blood units, and packed red blood cells (pRBCs) for up to 42 days, then determined aspects of the red blood cell storage lesion. Compared with standard storage pRBCs, whole blood demonstrated decreased microvesicle and free hemoglobin at 21 days of storage and no differences in osmotic fragility. At 42 days of storage, rotational thromboelastometry demonstrated that clotting time was decreased, alpha angle was increased, and clot formation time and maximum clot firmness similar in whole blood as compared with pRBCs with the addition of fresh frozen plasma. In a murine model, extended storage whole blood demonstrated decreased microvesicle formation, phosphatidylserine, and cell-free hemoglobin. After hemorrhage and resuscitation, TNF-a, IL-6, and IL-10 were decreased in mice resuscitated with whole blood. Red blood cell survival was similar at 24 h after transfusion. Taken together, these data suggest that red blood cells within whole blood stored for an extended period of time demonstrate similar or reduced accumulation of the red blood cell storage lesion as compared with pRBCs. Further examination of extended-storage whole blood is warranted.

Thrombocytosis and leukocytosis are common after splenectomy. The potential effect of emergency surgery on these postoperative findings is unknown. We hypothesized that emergency splenectomy leads to a more profound and persistent hematologic change as compared to elective splenectomy.A retrospective review was conducted of patients who underwent elective or trauma splenectomy. Records were queried for platelet (PLT) and white blood cell (WBC) count prior to splenectomy, on postoperative days 1-5, and at day 14, 1 month, 3 months, 6 months, and 1 year. Complications, including thromboembolic events, infection, need for repeat operation, and readmission within 30 days of discharge, were recorded.463 patients were identified as being eligible for the study, with 173 patients in the elective cohort and 145 patients in each of the isolated trauma splenectomy and polytrauma cohorts. Both cohorts had peak thrombocytosis at week 2 postoperatively. However, polytrauma patients had a significantly higher peak platelet count (P0.01). The PLT:WBC ratio was lower in both trauma cohorts pre-operatively and postoperative day 1. Trauma splenectomy had a higher PLT:WBC ratio on days 2 and 3 whereas polytrauma had a lower ratio on days 4 and 5. Emergency cases had greater reoperation and infection rates, whereas elective cases were more likely to require readmission. Postoperative thromboembolic events were only higher in the polytrauma cohort.While trauma splenectomy resulted in more profound postoperative leukocytosis and thrombocytosis, there was no correlation with timing of infection or risk of thromboembolic events. These findings suggest that thrombocytosis and leukocytosis may be associated with thrombotic and infectious events but their presence alone does not indicate direct risks of concomitant infection or thrombosis.

Multimodal analgesia protocols have been implemented after elective surgery to reduce opioid use, however there is limited data on utility after polytrauma. Therefore, we investigated the impact of a multimodal analgesia protocol on inpatient and post-discharge outpatient opioid use after polytrauma.A retrospective review of patients admitted to a Level I trauma center between September 2017-February 2018 (prior to multimodal protocol; "pre-cohort") and October 2018-April 2019 (after multimodal protocol; "post-cohort") was performed. An outpatient controlled substance registry was utilized to capture morphine milligram equivalents (MME) and gabapentin dispensed in the 6 mo after injury.620 patients were included (295 pre-cohort, 325 post-cohort). Total inpatient MME decreased from 177.5 mg-130 mg (P= 0.01) between the cohorts. Daily inpatient MME decreased from 70.8 mg-44.7 mg (P0.01). Intravenous hydromorphone decreased from 2 mg in the pre-cohort to 1 mg in the post-cohort (P= 0.02). Inpatient oxycodone decreased from 45 mg-30 mg (P= 0.01). Concurrently, gabapentin increased from 0 mg-400 mg in the post-cohort (P0.01). Patients in the post-cohort were prescribed fewer MMEs than the pre-cohort at discharge (P0.05). However, the number of patients prescribed gabapentin increased from 6.1%-16% (P0.01).Implementation of an updated multimodal analgesia protocol decreased total MME, daily MME, hydromorphone, and oxycodone consumed while increasing gabapentin use. This suggests that while reducing opioid usage in-hospital is critical to reducing outpatient usage, multimodal pain protocols may lead to an increase in gabapentin prescriptions and utilization after discharge.

Intravenous (IV) minocycline is increasingly used to treat infections caused by multi-drug resistant (MDR)-Acinetobacter baumannii Despite being approved nearly 50 years ago, published information on its pharmacokinetic (PK) prolife is limited. This multi-center study examined the PK and probability of pharmacokinetic-pharmacodynamic (PK-PD) target attainment profile of IV minocycline in critically ill patients, with suspected or documented infection with Gram-negative bacteria. The PK study population included 55 patients who received a single 200 mg IV dose of minocycline. Plasma PK samples were collected pre-dose and 1, 4, 12, 24, 36, and 48 hours after initiation of minocycline. Total and unbound minocycline concentrations were determined at each timepoint. Probabilities of achieving the PK-PD targets associated with stasis and 1-log killing (fAUC:MIC of 12 and 18, respectively) were evaluated. A two-compartment population PK model with zero-order IV input and first-order elimination, which estimated a constant fraction unbound (fub) for minocycline, best characterized the total and unbound plasma minocycline concentration-time data. The only two covariates retained in the final PK model were body surface area [associated with central volume of distribution] and albumin (associated with fub). In the PK-PD target attainment analyses, minocycline 200 mg IV Q12H was predicted to result in a suboptimal PK-PD profile for patients with A. baumannii infections with MIC values ≥ 1 mg/L. These findings cast uncertainty on the appropriateness of the current minocycline FDA susceptibility breakpoints and suggest that clinicians should strongly consider only combination antibiotic therapy with IV minocycline for all patients with serious Acinetobacter sp infections.

Serum anti-factor Xa (anti-Xa) concentration may guide low molecular weight heparin chemoprophylaxis in trauma patients. Higher total body weight (TBW) is a risk factor for subprophylactic anti-Xa and venous thromboembolism (VTE). The purpose of this study was to evaluate TBW differences in patients with subprophylactic versus prophylactic trough anti-Xa.This retrospective study included adults admitted to the trauma service who received enoxaparin chemoprophylaxis, trough anti-Xa assessment, and screening duplex ultrasound. Initial enoxaparin dose was determined per trauma team weight-tiered protocol with subsequent 10 mg increase if anti-Xa was subprophylactic. Patients were stratified into subprophylactic (anti-Xa0.1 IU/ml) and prophylactic (anti-Xa ≥0.1 IU/mL) groups. The primary outcome was difference in TBW. Secondary outcomes were weight-adjusted enoxaparin dose (mg/kg), VTE, red blood cell (pRBC) transfusions.A total of 887 patients were included with 681 (76.8%) having subprophylactic anti-Xa. The subprophylactic group had significantly younger age, higher proportion male sex, higher Injury Severity Score (ISS), higher BMI, and longer length of hospital stay. The subprophylactic group had higher TBW (median [IQR], 87.8 [74-102] kg vs. 78.9 [68-91.8] kg; P0.001) which equated to a lower weight-adjusted dose (0.34 [0.3-0.41] mg/kg vs. 0.38 (0.33-0.44) mg/kg; P0.001). There were no differences in VTE (10.4% vs. 9.2%; P = 0.71) or pRBC administration (17.0% vs. 16.0%; P = 0.81).TBW is higher and weight-adjusted enoxaparin dose is lower in high-risk trauma patients with subprophylactic anti-Xa concentrations. These data suggest TBW should be considered when determining the optimal prophylactic enoxaparin dose in high-risk trauma patients.

Introduction Traumatic brain injury (TBI) induces acute hypocoagulability, subacute hypercoagulability, and persistently elevated risk for thromboembolic events. Splenectomy is associated with increased mortality in patients with moderate or severe TBI. We hypothesized that the adverse effects of splenectomy in TBI patients may be secondary to the exacerbation of pathologic coagulation and platelet activation changes. Methods An established murine weight-drop TBI model was utilized and a splenectomy was performed immediately following TBI. Sham as well as TBI and splenectomy alone mice were used as injury controls. Mice were sacrificed for blood draws at 1, 6, and 24 h, as well as 7 days post-TBI. Viscoelastic coagulation parameters were assessed by rotational thromboelastometry (ROTEM) and platelet activation was measured by expression of P-selectin via flow cytometry analysis of platelet rich plasma samples. Results At 6 h following injury, TBI/splenectomy demonstrated hypocoagulability with prolonged clot formation time (CFT) compared to TBI alone. By 24 h following injury, TBI/splenectomy and splenectomy mice were hypercoagulable with a shorter CFT, a higher alpha angle, and increased MCF, despite a lower percentage of platelet contribution to clot compared to TBI alone. However, only the TBI/splenectomy continued to display this hypercoagulable state at 7 days. While TBI/splenectomy had greater P-selectin expression at 1-h post-injury, TBI alone had significantly greater P-selectin expression at 24 h post-injury compared to TBI/splenectomy. Interestingly, P-selectin expression remained elevated only in TBI/splenectomy at 7 days post-injury. Conclusion Splenectomy following TBI exacerbates changes in the post-injury coagulation state. The combination of TBI and splenectomy induces an acute hypocoagulable state that could contribute to an increase in intracranial bleeding. Subacutely, the addition of splenectomy to TBI exacerbates post-injury hypercoagulability and induces persistent platelet activation. These polytrauma effects on coagulation may contribute to the increased mortality observed in patients with combined brain and splenic injuries.

Background Transfusion of blood products is the ideal resuscitative strategy after hemorrhage. Unfortunately, older packed red blood cells have been associated with increased morbidity and mortality after massive transfusion. These packed red blood cells accumulate biochemical and structural changes known as the red blood cell storage lesions. The effect of washing on the formation of red blood cell storage lesions is unknown. We hypothesized that washing packed red blood cells during storage would decrease the development of the red blood cell storage lesions. Methods Blood from 8- to 10-week-old male mice donors was stored as packed red blood cells for 14 days. A subset of packed red blood cells were washed with phosphate-buffered saline on storage day 7 and resuspended in AS-1 solution for an additional 7 days as washed packed red blood cells. Subsequently, the packed red blood cells were analyzed for microvesicle release, band-3 erythrocyte membrane integrity protein (Band-3), expression of phosphatidylserine, cell viability (calcein), accumulation of cell-free hemoglobin, and osmotic fragility. Results In the washed packed red blood cells group, there was less microvesicle accumulation, greater Band-3 expression, less phosphatidylserine expression, a decrease in cell-free hemoglobin accumulation, and a decrease in osmotic fragility, but no differences in red blood cells viability. Conclusion Washing packed red blood cells during storage decreases the accumulation of red blood cell storage lesions. This strategy may lessen the sequelae associated with transfusion of older packed red blood cells.

Background Applicants provide a photo with their application through the Electronic Residency Application Service, which may introduce appearance-based bias. We evaluated whether an unconscious appearance bias exists in surgical resident selection. Methods After the match, applicant data from the 2018 to 2019 and 2019 to 2020 application cycles were examined. Reviewers were not provided the applicant photo or self-identified race during the second cycle. Photos provided by candidates were then rated by 4 surgical subspecialty residents who had no prior exposure to applications or interview status. Photos were rated on perceived fitness level, visual appearance, and photo professionalism. An overall photo score was then calculated. Results In the study, 422 applications were reviewed and 164 received interview invitations during the 2018 to 2019 cycle. Alpha Omega Alpha membership (odds ratio, 2.31; 95% confidence interval, 1.18–4.51), overall photo score (odds ratio, 2.29, 95% confidence interval, 1.43–3.66), research (odds ratio, 5.61, 95% confidence interval, 2.84–11.20), age (odds ratio, 0.86, 95% confidence interval, 0.76–0.99), and step 2 (odds ratio, 1.06, 95% confidence interval, 1.03–1.09) were predictors for receiving an interview. For the 2019 to 2020 cycle, 398 applications were reviewed, and 75 applicants received an invitation. Step 2 (odds ratio, 1.07, 95% confidence interval, 1.02–1.12), research (odds ratio, 2.78, 95% confidence interval, 1.40–5.55), age (odds ratio, 0.82, 95% confidence interval, 0.71–0.95), and overall photo score (odds ratio, 2.27; 95% confidence interval, 1.14–4.52) remained predictors despite reviewers being blinded to the photo during this cycle. Conclusion Although objective metrics remain critical in determining interview invitations, overall perceived applicant appearance may influence the selection process. Although visual appearance was associated with receiving an interview, the Electronic Residency Application Service photo does not ultimately affect selection. This may suggest that appearance may influence other objective and subjective aspects of the application.

Traumatic brain injury (TBI) can lead to the development of chronic traumatic encephalopathy as a result of neuronal phosphorylated tau (p-tau) protein aggregation and neuroinflammation. Acid sphingomyelinase (Asm) may also contribute to post-TBI neurodegenerative disorders. We hypothesized that Asm inhibition would ameliorate p-tau aggregation, neuroinflammation, and behavioral changes after TBI in a murine model. TBI was generated using a weight-drop method. Asm inhibition in wild-type mice was achieved with a single injection of amitriptyline 1 h after TBI. Genetic Asm ablation was achieved using Asm-deficient mice (Asm(–/–)). Thirty days after TBI, mice underwent behavioral testing with the forced swim test for symptoms of depression or were euthanized for neurohistological analysis. Neuroinflammation was quantified using the microglial markers, ionized calcium-binding adaptor molecule 1 and transmembrane protein 119. Compared to sham mice, TBI mice demonstrated increased hippocampal p-tau. Mice that received amitriptyline after TBI demonstrated decreased p-tau compared to mice that received a saline control. Further, post-TBI Asm(–/–) mice demonstrated lower levels of p-tau compared to wild-type mice. Though a decrease in neuroinflammation was observed at 1 month post-TBI, no change was demonstrated with mice treated with amitriptyline. Similarly, TBI mice were more likely to show depression compared to mice that received amitriptyline after TBI. Utilizing a weight-drop method to induce moderate TBI, we have shown that genetic deficiency or pharmacological inhibition of Asm prevented hippocampal p-tau aggregation 1 month after injury as well as decreased symptoms of depression. These findings highlight an opportunity to potentially reduce the long-term consequences of TBI.

Background Andexanet alfa (andexanet) is the only FDA-approved medication for reversal of apixaban and rivaroxaban anticoagulation for life-threatening or uncontrolled bleeding. Infusion modifications may be required in surgical patients undergoing prolonged operative intervention but have not previously been described. Case Report A 78-year-old woman on rivaroxaban for atrial fibrillation was admitted to the trauma service for a mechanical fall, sustaining a T4 burst fracture with severe canal stenosis and spinal cord edema resulting in loss of strength and sensation in her legs. Clinically relevant rivaroxaban activity was verified with an elevated low molecular weight heparin anti-factor Xa assay, and laboratory confirmed coagulopathy was demonstrated by a prolonged prothrombin time, thromboelastography (TEG) R-time, and activated clotting time (ACT). The patient required urgent surgical intervention for spinal fixation. Given the expected prolonged duration of the procedure, standard dose andexanet was initiated with a prolonged infusion at half the standard rate during the operation. The procedure was successful and intraoperative TEGs demonstrated normalization of R-time and ACT throughout the procedure. The patient did not experience any complications postoperatively and successfully discharged to inpatient rehabilitation. Conclusion Modifications to the andexanet infusion may be required in surgical patients requiring rivaroxaban reversal for a prolonged procedure. Further data are needed to determine the optimal approach to infusion modification.

Traumatic brain injury (TBI) results in systemic changes in coagulation and inflammation that contribute to post-traumatic morbidity and mortality. The potential interaction of platelets and pro-inflammatory cytokines in the modulation of coagulation, microthrombosis, and venous thromboembolic events after moderate TBI has not been determined. Using a murine model, we hypothesized that the degree of platelet-induced coagulation varies depending on the platelet aggregation agonist platelet-induced coagulation changes in a time-dependent manner following TBI, and changes in platelet-induced coagulation are mirrored by changes in the levels of circulating pro-inflammatory cytokines. An established weight-drop model was used to induce TBI in anesthetized mice. Blood samples were collected at intervals after injury for measurements of platelet count, serum fibrinogen, pro-inflammatory cytokines, and determination of soluble P-selectin levels. Thromboelastometry was used to evaluate changes in hemostasis. Platelet function was determined using whole blood impedance aggregometry. Ten minutes following TBI, adenosine diphosphate-induced platelet aggregation decreased as measured by platelet aggregometry. Despite no changes in platelet counts and serum fibrinogen, platelet aggregation, pro-inflammatory cytokines, and soluble P-selectin were increased at 6 h after TBI. Rotation thromboelastometry demonstrated increased maximal clot firmness at 6 h. Platelet function and coagulability returned to baseline levels 24 h following head injury. Our data demonstrate that after TBI, acute platelet dysfunction occurs followed by rebound platelet hyperaggregation. Alterations in post-TBI platelet aggregation are reflected in whole blood thromboelastometry and are temporally associated with the systemic pro-inflammatory response.

BACKGROUND: Chronic traumatic encephalopathy is a consequence of repetitive mild traumatic brain injury (rmTBI). These injuries can result in psychiatric disorders that are treated with amitriptyline. Amitriptyline improves neuronal regeneration in major depression via inhibition of acid sphingomyelinase. We hypothesized that acid sphingomyelinase inhibition would preserve neuronal regeneration and decrease depressive symptoms following rmTBI in a murine model. METHODS: A murine model of rmTBI was established using a weight-drop method. Mice were subjected to mild TBI every other day for 7 days. Mice received amitriptyline injection 2 hours prior to each mild TBI. After the final mild TBI, mice underwent behavioral studies or biochemical analysis. Hippocampi were analyzed for markers of neurogenesis and phosphorylated tau aggregation. RESULTS: Mice that underwent rmTBI showed increased hippocampal phosphorylated tau aggregation one month following rmTBI as well as decreased neuronal regeneration by bromodeoxyuridine uptake and doublecortin immunohistochemistry. Mice with either genetic deficiency or pharmacologic inhibition of acid sphingomyelinase demonstrated improved neuronal regeneration and decreased phosphorylated tau aggregation compared to untreated rmTBI mice. Behavioral testing showed rmTBI mice spent significantly more time in the dark and waiting to initiate feeding compared to sham mice. These behaviors were partially prevented by the inhibition of acid sphingomyelinase. CONCLUSIONS: We established a murine model of rmTBI that leads to tauopathy, depression, and impaired hippocampal neurogenesis. Inhibition of acid sphingomyelinase prevented the harmful neurologic and behavioral effects of rmTBI. These findings highlight an important opportunity to improve recovery or prevent neuropsychiatric decline in patients at risk for chronic traumatic encephalopathy.

Coagulopathy and platelet dysfunction commonly develop after traumatic brain injury (TBI). Thromboelastography (TEG) and platelet function assays (PFAs) are often performed at the time of admission; however, their roles in assessing post-TBI coagulopathy have not been investigated. We hypothesized that compared to blunt TBI, penetrating TBI would (1) demonstrate greater coagulopathy by TEG, (2) be associated with abnormal PFA results, and (3) require more blood product transfusions. We performed a retrospective study of patients admitted to the neuroscience intensive care unit of a level 1 trauma center from 2013 to 2015 with head Abbreviated Injury Scale ≥3. Patients were compared by mechanism of injury (blunt vs. penetrating). Admission demographics, injury characteristics, and laboratory parameters were evaluated. VerifyNow® Aspirin and P2Y12 tests were used for platelet function analysis. Five hundred and thirty-four patients were included in the analysis. There were no differences between groups in platelet count or international normalized ratio; however, patients with penetrating TBI were more coagulopathic by TEG, with all of the TEG parameters being significantly different except for R time. Patients with penetrating head trauma were not more likely than their blunt counterparts to have abnormal PFA results, and PFA results did not correlate with any TEG parameter in either group. The penetrating cohort received more units of blood products in the first 4 and 24 h than the blunt cohort. Patients presenting with penetrating TBI demonstrated increased coagulopathy compared to those with blunt TBI as measured by TEG and need for transfusion. PFA results did not correlate with TEG findings in this population.

Background Posttraumatic coagulopathy and inflammation can exacerbate secondary cerebral damage after traumatic brain injury (TBI). Tranexamic acid (TXA) has been shown clinically to reduce mortality in hemorrhaging and head-injured trauma patients and has the potential to mitigate secondary brain injury with its reported antifibrinolytic and antiinflammatory properties. We hypothesized that TXA would improve posttraumatic coagulation and inflammation in a murine model of TBI alone and in a combined injury model of TBI and hemorrhage (TBI/H). Methods An established murine weight drop model was used to induce a moderate TBI. Mice were administered intraperitoneal injections of 10 mg/kg TXA or equivalent volume of saline 10 min after injury. An additional group of mice was subjected to TBI followed by hemorrhagic shock using a pressure-controlled model. TBI/H mice were given intraperitoneal injections of TXA or saline during resuscitation. Blood was collected at intervals after injury to assess coagulation by rotational thromboelastometry (ROTEM) and inflammation by Multiplex cytokine analysis. Soluble P-selectin, a biomarker of platelet activation, and serum neuron-specific enolase, a biomarker of cerebral injury, were measured at intervals. Brain homogenates were analyzed for inflammatory changes by Multiplex enzyme-linked immunosorbent assay, and splenic tissue was collected for splenic cell population assessment by flow cytometry. Results There were no coagulation, serum or cerebral cytokine, P-selectin, or neuron-specific enolase differences between mice treated with TXA or saline after TBI. After the addition of hemorrhagic shock and resuscitation to TBI, TXA administration still did not affect coagulation parameters, systemic or cerebral inflammation, or platelet activation, as compared with saline alone. At 24 hours after TBI, mice given TXA demonstrated lower splenic total cell counts central memory CD8, effector CD8, B cell, and increased naive CD4 cell populations. By contrast, TXA did not affect splenic leukocyte populations after combined TBI/H. Conclusions Despite clinical data suggesting a mortality benefit, TXA did not modulate coagulation, inflammation, or biomarker generation in either the TBI or TBI/H murine models. Administration of TXA after TBI altered splenic leukocyte populations, which may contribute to a change in posttraumatic immune status. Future studies should be done to investigate the role of TXA in the development of posttraumatic immunosuppression and risk of nosocomial infections.

Introduction Trauma patients may become hypoxic or iatrogenically hyperoxic in the early post-injury period. While both extremes of oxygenation may be harmful following injury, the mechanism has yet to be elucidated. We hypothesized that hypoxia or hyperoxia would induce changes in coagulation, creating a secondary insult exacerbating the primary injury. Materials and methods Mice underwent traumatic brain injury (TBI) or sham and were subsequently exposed to room air or brief hypoxia (15% FiO2) then sacrificed at intervals. Another cohort of uninjured mice underwent more prolonged hypoxia (10% FiO2) or hyperoxia (60% FiO2). Platelet function was evaluated by ADP- or ASPi-induced impedance aggregometry and viscoelastic coagulation parameters were assessed with rotational thromboelastometry. Results In uninjured mice, ADP-induced platelet aggregation was acutely increased after prolonged hypoxia, but this difference did not persist at 6 h. Hypoxic and hyperoxic TBI mice had increased ADP induced platelet aggregation at 1 h compared to the normoxia group. TBI mice demonstrated an early increased platelet aggregation after hypoxia or hyperoxia. Viscoelastic coagulation parameters were similar between hypoxic, hyperoxic and room air groups at 1 h and 6 h. However, ROTEM clotting time and clot formation time were prolonged and maximal clot firmness were lower in sham TBI/hypoxia mice at 24 h. Conclusion Post-TBI hypoxia and hyperoxia resulted in transiently increased platelet aggregation in response to ADP, without lasting effecting on platelet function or coagulation. Hypoxia also induced delayed hypocoagulability after platelet aggregation normalized. Brief changes in oxygenation may temporally affect coagulation and platelet aggregation, which could contribute to physiologic secondary injury after trauma.

OBJECTIVE As the competitiveness of applicants for general surgery residency grows, it is becoming challenging for programs to differentiate qualified candidates with a genuine interest in matching at their institution. The purpose of this study was to examine geographic trends in the general surgery match in order to elicit regional biases and optimize applicant interview selection strategies. DESIGN In this single-center retrospective study, geographical information regarding birth place, college, medical school, and final match institution for general surgery residency applicants was examined. SETTING This study was set at the University of Cincinnati College of Medicine. PARTICIPANTS All general surgery residency applicants interviewing at our institution between 2015–2017 were included. METHODS Academic variables and geographical information were collected for all applicants in the cohort. Statistical analyses were performed using chi-square and logistic regression techniques to determine any association between geography and match outcomes. RESULTS Of 198 applicants included in the analysis, approximately 25% matched at an institution located in the same state as their medical school. Total 75% of applicants matched at a residency program located less than 640 miles away from either their birth place, college, or medical school, while only 15% matched at an institution located over 1000 miles away and 4% matched over 2000 miles away. When examining applicant characteristics, there were no significant differences in gender, clerkship grade, United States Medical Licensing Exam scores, Alpha Omega Alpha Honor Society membership, or quality of recommendation letters between applicants who matched in the lowest and highest quartiles of distance to final residency program location. CONCLUSIONS A significant proportion of general surgery applicants matched at institutions located in a region near either their birth place, college, or medical school. Given the limited number of interviews able to be offered by institutions and the associated opportunity costs, general surgery programs should consider regional biases when evaluating residency applicants.

INTRODUCTION: The pathophysiology behind the subacute but persistent hypercoagulable state following traumatic brain injury (TBI) is poorly understood but contributes to morbidity induced by venous thromboembolism (VTE). Because platelets and their microvesicles have been hypothesized to play a role in posttraumatic hypercoagulability, administration of commonly utilized agents may ameliorate this coagulability. We hypothesized that utilization of aspirin, ketorolac, amitriptyline, unfractionated heparin, or enoxaparin would modulate the platelet aggregation response following TBI. METHODS: Concussive TBI was induced by weight drop. Mice were then randomized to receive aspirin, ketorolac, amitriptyline, heparin, enoxaparin, or saline control at 2 and 8 hours post-TBI. Mice were sacrificed at 6 or 24 hours after injury to determine coagulability by thromboelastometry (ROTEM), platelet function testing with impedance aggregometry, and microvesicle enumeration. Platelet sphingolipid metabolites were analyzed by mass spectrometry. RESULTS: ROTEM demonstrated increased platelet contribution to maximum clot firmness (%MCF-Platelet) at 6 hours following TBI in mice that received aspirin or amitriptyline, but this did not persist at 24 hours. By contrast, ADP- and arachidonic acid-induced platelet aggregation at 6 hours was significantly lower in mice receiving ketorolac, aspirin, and amitriptyline compared to mice receiving saline at 6 hours post-injury and only arachidonic acid initiated platelet aggregation was decreased by aspirin at 24 hours. There were no differences in microvesicle production at either timepoint. Platelet sphingosine-1-phosphate (S1P) levels were decreased at 6 hours in the group receiving amitriptyline and increased at 24 hours along with platelet ceramide levels at 24 hours in the amitriptyline group. CONCLUSION: Following TBI, amitriptyline decreased platelet aggregability and increased contribution to clot in a manner similar to aspirin. The amitriptyline effects on platelet function and sphingolipid metabolites may represent a possible role of acid sphingomyelinase in the hypercoagulability observed following injury. Additionally, inhibition of platelet reactivity may be an underappreciated benefit of low molecular weight heparins, such as enoxaparin.

Background Acute lung injury (ALI) is a frequent complication after severe trauma. Lung-protective ventilation strategies and damage control resuscitation have been proposed for the prevention of ALI; however, there are no clinical or laboratory parameters to predict who is at risk of developing ALI after trauma. In the present study, we explored pulmonary inflammatory markers as a potential predictor of ALI using a porcine model of hemorrhagic shock. Materials and methods Female swine were randomized to mechanical ventilation with low tidal volume (VT) (6 mL/kg) or high VT (12 mL/kg). After equilibration, animals underwent pressure-controlled hemorrhage (mean arterial pressure [MAP] 35 ± 5 mmHg) for 1 h, followed by resuscitation with fresh whole blood or Hextend. They were maintained at MAP of 50 ± 5 mmHg for 3 h in the postresuscitation phase. Bronchoalveolar lavage fluids were collected hourly and analyzed for inflammatory markers. Lung samples were taken, and porcine neutrophil antibody staining was used to evaluate the presence of neutrophils. ELISA evaluated serum porcine surfactant protein D levels. Sham animals were used as negative controls. Results Pigs that underwent hemorrhagic shock had higher heart rates, lower cardiac output, lower MAPs, and worse acidosis compared with sham at the early time points (P Conclusions Our study demonstrates the reproducibility of a porcine model of hemorrhagic shock that is consistent with physiologic changes in humans in hemorrhagic shock. Pulmonary neutrophil infiltration may serve as an early marker for ALI; however, the practicality of this finding has yet to be determined.

This Week in SCORE (TWIS) is a biennial, general surgery curriculum comprised of weekly online modules, readings, and multiple-choice quizzes. In this study, we examined the impact of required TWIS on American Board of Surgery In-Training Examination (ABSITE) scores and well-being among categorical general surgery residents.TWIS quiz completion became required in 2017. Residents attended weekly lectures, and ABSITE performance was incentivized with educational stipends. Surveys were distributed to assess study preferences, learning styles, burnout, and grit. Thirty-six categorical general surgery residents who took ABSITE in both 2017 and 2018 were evaluated in a paired-sample, retrospective analysis.After requiring TWIS, median ABSITE percentile increased by 12% (65%-77%, p = 0.001). Weekly TWIS completion (59% vs 89%, p0.001) and quiz results (62% vs 69%, p = 0.005) also improved. During this time, emotional exhaustion and depersonalization declined significantly, yet overall burnout scores did not change. Of 21 survey respondents, 66.7% (n = 14) increased weekly study time by a median of 2.5 hours. However, less than half used Surgical Council on Resident Education as their primary study tool. Only 23.8% (n = 5) reported that mandatory TWIS modified their study behavior, while 90.4% (n = 19) felt the culture of education had improved.After TWIS participation became required, ABSITE performances improved. Formalized curriculum with frequent assessment may foster accountability among residents, enhancing educational climate, well-being, and test performance.

The diagnosis and treatment of peripheral vascular casualties have evolved over the last decades, achieving high rates of limb salvage due to rapid diagnosis of vascular injury with staged, resource-guided surgical and postoperative management. This chapter will discuss the evolution of the care of vascular trauma as well as the modern treatment of extremity vascular injuries in the setting of far-forward military care, aeromedical evacuation, and delayed definitive revascularization. The use of early control of hemorrhage with tourniquets, rapid but balanced hemostatic resuscitation, use of temporary vascular shunts, and delay in definitive surgery until after transport is achieved to higher levels of care are the main paradigm shifts that predominate the care of peripheral vascular casualties.

BACKGROUND The relationship between the prehospital airway device used and later development of ventilator-associated pneumonia (VAP) is unknown. We sought to determine if the prehospital airway device choice is associated with an increased risk of VAP in risk-adjusted critically injured patients. METHODS We performed a retrospective analysis of all trauma patients requiring definitive airway placement before intensive care unit admission at a Level I trauma center from 2008 to 2012. Prehospital airway management strategies were classified as extraglottic device placement, endotracheal intubation, bag-valve mask ventilation (BVM), or lack of a prehospital airway with subsequent intubation at the trauma center. Patients were excluded if they were hospital transfers, were dead on arrival, died in the emergency department, or did not require at least 48 hours of mechanical ventilation. The primary end point was the development of VAP as determined by institutional guidelines for diagnosis. Logistic regression was used to determine risk factors for VAP. RESULTS A total of 317 patients met inclusion criteria. The median age was 37 years (interquartile range, 25-51 years), 75% were male, 78% sustained a blunt injury, and the median Injury Severity Score (ISS) was 29 (interquartile range, 21-34). Ninety-seven patients (30.6%) developed VAP. Prehospital airway strategies were as follows: 17 (5.4%) had extraglottic device placement, 28 (8.8%) had BVM, 84 (26.5%) had endotracheal intubation, and 188 (59.3%) had no prehospital airway placement and were intubated after arrival. The type of prehospital airway was not statistically significant in terms of VAP development (range, 26.1-42.9%; p = 0.15). The only statistically significant predictor of VAP was length of mechanical ventilation (univariate: odds ratio, 1.14; 95% confidence interval, 1.10-1.18; p ≤ 0.01; multivariate: odds ratio, 1.15; 95% confidence interval, 1.10-1.20; p ≤ 0.01). CONCLUSION Our data suggest that the prehospital airway device used was not associated with the development of VAP. LEVEL OF EVIDENCE Therapeutic study, level IV; epidemiologic study, level III.

BACKGROUND Resuscitation strategies for combined traumatic brain injury (TBI) with haemorrhage in austere environments are not fully established. Our aim was to establish the effects of various saline concentrations in a murine model of combined TBI and haemorrhage, and identify an effective resuscitative strategy for the far-forward environment. METHODS Male C57BL/6 mice underwent closed head injury and subjected to controlled haemorrhage to a systolic blood pressure of 25 mmHg via femoral artery cannulation for 60 min. Mice were resuscitated with a fixed volume bolus or variable volumes of fluid to achieve a systolic blood pressure goal of 80 mmHg with 0.9% saline, 3% saline, 0.1-mL bolus of 23.4% saline, or a 0.1-mL bolus of 23.4% saline followed by 0.9% saline (23.4+). RESULTS 23.4% saline and 23.4+ resulted in higher mortality at 6 h compared to 0.9% saline. Use of 3% saline required less volume to achieve targeted resuscitation, did not affect survival, and did not exacerbate post-traumatic inflammation. While 23.4+ resuscitation utilized lower volume, it resulted in hypernatremia, azotemia, and elevated systemic pro-inflammatory cytokines. All groups except 3% saline demonstrated progression of neuron damage, with cerebral oedema highest with 0.9% saline. CONCLUSIONS 3% saline demonstrated favourable balance of survival, blood pressure restoration, minimization of inflammation, and prevention of ongoing neurologic injury without contributing to significant physiologic derangements. 23.4% saline administration may not be appropriate in the setting of concomitant hypotension.

BACKGROUND: Penetrating injuries to the extremity proximal to the elbow or knee are anatomic criteria for full trauma team activation (FFTA) by the American College of Surgeon’s Committee on Trauma standards. This criterion lacks objective evidence-based support. Overtriage of trauma team activation may result in excessive costs and resource burden at trauma centers. We hypothesized that FFTA for penetrating injuries to the proximal extremities by anatomic criteria alone may lead to significant overtriage. METHODS: A 3-year retrospective review (2013–2015) was completed of all patients evaluated at an urban Level I trauma center with isolated penetrating extremity injuries. Data included the number of full and limited trauma team activations as well as criterion met, Injury Severity Score (ISS), injury, limb characteristics, and disposition. Overtriage was defined as FFTA for an ISS of 15 or less, with a goal rate less than 50%. RESULTS: We identified 6,335 total trauma team activations with 795 isolated penetrating extremity injuries. Of these injuries, 413 (51.9%) were injuries proximal to the joint. Within this subgroup, 71.2% of patients were discharged from the emergency department with a median ISS of 1 and no additional intervention. Only 5.3% of patients that did not meet additional FFTA criteria underwent immediate operative intervention. By comparison, 21% of FFTAs and 5.8% of limited trauma team activations underwent immediate operative intervention during the 3-year period. Of the 413 isolated penetrating proximal-extremity injuries, only one had an ISS of 15 or greater, resulting in a 99.7% overtriage rate. CONCLUSION: Penetrating injuries to the extremities are common in urban trauma centers. Full trauma team activation based on anatomic, rather than physiologic, criteria may lead to a significant overtriage rate. Further distinction in the level of trauma team activation may be made based on hard signs of neurovascular injury. LEVEL OF EVIDENCE: Epidemiological study, level III; Care Management, level IV.

Introduction Acute hemorrhage remains the leading cause of death in potentially survivable injuries. The use of topical hemostatic agents has increased over the last two decades with the evolution of damage control surgery. By 2008, the military widely adopted Combat Gauze as the hemostatic dressing of choice for compressible hemorrhage. The goal of this study was to compare the performance of a novel fibrin sealant patch to Combat Gauze in two clinically relevant models of hemorrhage. Materials and methods Yorkshire swine underwent unilateral femoral artery puncture or a grade V liver laceration with timed free bleeding then received either the fibrin patch or Combat Gauze packing with 3 minutes of standardized pressure. Animals were then resuscitated to maintain a mean arterial pressure of 60 mmHg for 4 hours. Hemostasis, blood loss, resuscitation volume, survival, vessel patency, and hematologic parameters were evaluated. Results Hemostasis was equivalent in both groups after hepatic and vascular injury. Survival was 80% in the fibrin patch vascular injury group and 100% in all other groups. Hematologic parameters were not significantly different between treatment groups. Femoral artery patency was 80% in both groups after vascular injury. With simulated ambulation after vessel injury, 60% of the Combat Gauze group and 80% of the fibrin patch group remained hemostatic (p > 0.05). In simulated re-exploration with packing removal, all animals rebled after hemostatic product removal. Conclusion There was no significant difference in hemostasis between a novel fibrin patch and Combat Gauze after extremity arterial or hepatic injury. This novel fibrin patch may have a clinical advantage over the Combat Gauze, as it can be left in the body, thereby limiting the potential need for reoperation.

Surgical education is essential to train the next generation of surgeons, scholars, and leaders. Surgical educators should create an education first culture, with cultivation of faculty development and recognition of education and teaching efforts. Mentorship programs are key to success of young surgeons and provide an opportunity to shape surgical careers. Education programs with advanced simulation curricula that emphasize innovation, paired with the goals of advancing the field of educational research, are necessary to promote forward progress. Teaching leadership in education is crucial to developing the key personnel to be the next champions for surgical education. Equipping surgical trainees and junior faculty with the tools necessary to nurture the future of surgical education needs to be a focus of every surgical training program.

Background Patients with mild to moderate traumatic brain injury (TBI) are often primarily managed by emergency medicine and trauma/acute care physicians. The Brain Injury Guidelines (BIG) were developed at an American College of Surgeons-accredited Level 1 trauma center to triage mild to moderate TBI patients and help identify patients who warrant neurosurgical consultation. The BIG have not been validated at a Level III trauma center. We hypothesized that BIG criteria can be safely adapted to an American College of Surgeons-accredited Level III trauma center to guide transfers to a higher echelon of care. Methods We reviewed the trauma registry at a Level III trauma center to identify TBI patients who presented with an Abbreviated Injury Severity-Head score greater than zero. Demographic data, injury details, and clinical outcomes were abstracted with primary outcome measures of worsening on second computed tomography of the head, neurosurgical intervention, transfer to a Level I trauma center, and in-hospital mortality. Patients were classified using the BIG criteria. After validating the BIG in our cohort, we reclassified patients using updated BIG criteria. Updated criteria included mechanism of injury, reclassification of anticoagulation or antiplatelet use, and replacement of the neurologic examination component with stratification by admission Glasgow Coma Scale (GCS) score. Results From July 2013 to June 2016, 332 TBI patients were identified: 115 BIG-1, 25 BIG-2, and 192 BIG-3. Patients requiring neurosurgical intervention (n = 30) or who died (n = 29) were BIG-3 with one exception. Patients with GCS score of less than 12 had worse outcomes than those with a GCS score of 12 or greater, regardless of BIG classification. Anticoagulant or antiplatelet use was not associated with worsened outcomes in patients not meeting other BIG-3 criteria. The updated BIG resulted in more patients in BIG-1 (n = 109) and BIG-2 (n = 100) without negatively affecting outcomes. Conclusion The BIG can be applied in the Level III trauma center setting. Updated BIG criteria can aid triage of mild to moderate TBI patients to a Level I trauma center and may reduce secondary overtriage. Level of evidence Care management, level IV.

Sphingolipids are a ubiquitous family of essential lipids with an increasingly understood role as biologically active mediators in numerous physiologic and pathologic processes. Two particular sphingolipid species, sphingosine-1-phosphate and ceramide, and their metabolites interact both directly and indirectly with endothelial cells to regulate vascular permeability. Sphingosine-1-phosphate generally augments endothelial integrity while ceramide tends to promote vascular leak, and a tight balance between the two is necessary to maintain normal physiologic function. The mechanisms by which sphingolipids regulate endothelial barrier function are complex and occur through multiple different pathways, and disruptions or imbalances in these pathways have been implicated in a number of specific disease processes. With improved understanding of sphingolipid biology, endothelial function, and the interactions between the two, several targets for therapeutic intervention have emerged and there is immense potential for further advancement in this field.

Background Posttraumatic hepatic artery pseudoaneurysm is a potentially devastating complication after complex liver injury. Increasing computed tomography (CT) use may lead to more frequent identification of posttraumatic hepatic complications. This study was designed to determine the rate of hepatic pseudoaneurysm after traumatic liver injury. Methods We conducted a retrospective review of patients at an urban level 1 trauma center over 5 y (2012-2016). Injury characteristics, patient management, and complications were extracted from trauma registry data and chart review. Results Six hundred thirty-four hepatic injuries (11 no grade/no CT, 159 grade I, 154 grade II, 165 grade III, 93 grade IV, and 52 grade V) were identified from our trauma registry. No patient with a grade I or II injury had a subsequent bleeding complication. Eighteen patients had a documented hepatic pseudoaneurysm: grade III n = 3 (1.8%), grade IV n = 6 (6.5%), grade V n = 9 (17.3%). The median time to pseudoaneurysm identification was 6.5 d. Seven pseudoaneurysms were found on asymptomatic surveillance CT-angiography on average 5 d after injury. Eleven patients were symptomatic at the time of CT-angiography performed at a median of 9 d after admission. Of the 11 symptomatic patients, four were in hemorrhagic shock, and two died from hepatic-related complications. Conclusions The incidence of hepatic artery pseudoaneurysm increases with higher grade liver injury. Aggressive surveillance for hepatic pseudoaneurysm with interval CT-angiography 5-7 d postinjury may be warranted, especially for grade IV and V injuries.

BackgroundApproximately 8% of traumatically injured patients require transfusion with packed red blood cells (pRBC) and only 1% to 2% require massive transfusion. Intraoperative massive transfusion was defined as requiring greater than 5 units (u) of pRBC in 4 hours. Despite the majority of patients not requiring transfusion, the appropriate amount and type of crystalloid administered during the era of damage control resuscitation have not been analyzed. We sought to determine the types of crystalloid used during trauma laparotomies and the potential effects on resuscitation.MethodsPatients who underwent laparotomy after abdominal trauma from January 2014 to December 2016 at the University of Cincinnati Medical Center were identified. Patients were grouped based on requiring 0u, 1u to 4u, and ≥5u pRBC during intraoperative resuscitation. Demographic, physiologic, pharmacologic, operative, and postoperative data were collected. Statistical analysis was performed with Kruskal-Wallis test and Pearson’s correlation coefficient.ResultsLactated Ringer’s (LR) solution was the most used crystalloid type received in the 0u and 1u to 4u pRBC cohorts, whereas normal saline (NS) was the most common in the ≥5u pRBC cohort. Most patients received two types of crystalloid intraoperatively. NS and LR were most frequently the first crystalloids administered, with Normosol infusion occurring later. The amount of crystalloid received correlated with operative length, but did not correlate with the estimated blood loss. Neither the type of crystalloid administered nor the anesthesia provider type was associated with changes in postoperative resuscitation parameters or electrolyte concentrations.DiscussionThere is a wide variation in the amount and types of crystalloids administered during exploratory laparotomy for trauma. Interestingly, the amount or type of crystalloid given did not affect resuscitation parameters regardless of blood product requirement.Level of evidenceLevel IV.

Bacterial growth in soft tissue and open fractures is a known risk factor for tissue loss and complications in contaminated musculoskeletal wounds. Current care for battlefield casualties with soft tissue and musculoskeletal wounds includes tactical and strategic aeromedical evacuation (AE). This exposes patients to a hypobaric, hypoxic environment. In this study, we sought to determine whether exposure to AE alters bacterial growth in contaminated complex musculoskeletal wounds and whether supplemental oxygen had any effect on wound infections during simulated AE.A caprine model of a contaminated complex musculoskeletal wound was used. Complex musculoskeletal wounds were created and inoculated with bioluminescent Pseudomonas aeruginosa. Goats were divided into three experimental groups: ground control, simulated AE, and simulated AE with supplemental oxygen. Simulated AE was induced in a hypobaric chamber pressurized to 8,800 feet for 7 hours. Bacterial luminescence was measured using a photon counting camera at three time points: preflight (20 hours postsurgery), postflight (7 hours from preflight and 27 hours postsurgery), and necropsy (24 hours from preflight and 44 hours postsurgery).There was a significant increase in bacterial growth in the AE group compared with the ground control group measured postflight and at necropsy. Simulated AE induced hypoxia with oxygen saturation less than 93%. Supplemental oxygen corrected the hypoxia and significantly reduced bacterial growth in wounds at necropsy.Hypoxia induced during simulated AE enhances bacterial growth in complex musculoskeletal wounds which can be prevented with the application of supplemental oxygen to the host.