Association Between Emergency Medical Service Agency Volume and Mortality in Trauma Patients.

OBJECTIVE: The aim of this study was to evaluate the association of annual trauma patient volume on outcomes for emergency medical services (EMS) agencies. BACKGROUND: Regionalization of trauma care saves lives. The underlying concept driving this is a volume-outcome relationship. EMS are the entry point to the trauma system, yet it is unknown if a volume-outcome relationship exists for EMS. METHODS: A retrospective analysis of prospective cohort including 8 trauma centers and 20 EMS air medical and metropolitan ground transport agencies. Patients 18 to 90 years old with injury severity scores ≥9 transported from the scene were included. Patient and agency-level risk-adjusted regression determined the association between EMS agency trauma patient volume and early mortality. RESULTS: A total of 33,511 were included with a median EMS agency volume of 374 patients annually (interquartile range: 90-580). Each 50-patient increase in EMS agency volume was associated with 5% decreased odds of 6-hour mortality (adjusted odds ratio=0.95; 95% CI: 0.92-0.99, P =0.03) and 3% decreased odds of 24-hour mortality (adjusted odds ratio=0.97; 95% CI: 0.95-0.99, P =0.04). Prespecified subgroup analysis showed EMS agency volume was associated with reduced odds of mortality for patients with prehospital shock, requiring prehospital airway placement, undergoing air medical transport, and those with traumatic brain injury. Agency-level analysis demonstrated that high-volume (>374 patients/year) EMS agencies had a significantly lower risk-standardized 6-hour mortality rate than low-volume (<374 patients/year) EMS agencies (1.9% vs 4.8%, P <0.01). CONCLUSIONS: A higher volume of trauma patients transported at the EMS agency level is associated with improved early mortality. Further investigation of this volume-outcome relationship is necessary to leverage quality improvement, benchmarking, and educational initiatives.

Omics Signatures of Tissue Injury and Hemorrhagic Shock in Swine.

OBJECTIVE: Advanced mass spectrometry methods were leveraged to analyze both proteomics and metabolomics signatures in plasma upon controlled tissue injury (TI) and hemorrhagic shock (HS)-isolated or combined-in a swine model, followed by correlation to viscoelastic measurements of coagulopathy via thrombelastography. BACKGROUND: TI and HS cause distinct molecular changes in plasma in both animal models and trauma patients. However, the contribution to coagulopathy of trauma, the leading cause of preventable mortality in this patient population remains unclear. The recent development of a swine model for isolated or combined TI+HS facilitated the current study. METHODS: Male swine (n=17) were randomized to either isolated or combined TI and HS. Coagulation status was analyzed by thrombelastography during the monitored time course. The plasma fractions of the blood draws (at baseline; end of shock; and at 30 minutes, 1, 2, and 4 hours after shock) were analyzed by mass spectrometry-based proteomics and metabolomics workflows. RESULTS: HS-isolated or combined with TI-caused the most severe omic alterations during the monitored time course. While isolated TI delayed the activation of coagulation cascades. Correlation to thrombelastography parameters of clot strength (maximum amplitude) and breakdown (LY30) revealed signatures of coagulopathy which were supported by analysis of gene ontology-enriched biological pathways. CONCLUSION: The current study provides a comprehensive characterization of proteomic and metabolomic alterations to combined or isolated TI and HS in a swine model and identifies early and late omics correlates to viscoelastic measurements in this system.

In Situ Pulmonary Thrombolysis and Perfusion Lung Angiography in Severe COVID-19 Respiratory Failure.

A proof-of-concept study using thrombolysis with catheter-directed tissue plasminogen activator (tPA) and pulmonary angiography imaging was performed to visualize perfusion deficits and reperfusion/therapeutic effects of tPA. DESIGN: A prospective, open-label, compassionate study. Descriptive statistics were presented for categorical variables and as means with sds for continuous variables. The Wilcoxon test was used to determine the differences between the two-related samples and a t test for continuous variables. Statistical significance was set at p value of less than 0.05. Agreement between observations was evaluated using the Kappa Cohen index and overall agreement using the Fleiss Kappa coefficient. SETTING: A single COVID-19 ICU of Mexico´s General Hospital Dr Eduardo Liceaga. SUBJECTS: Fifteen patients with severe Delta variant severe acute respiratory syndrome coronavirus 2 infection, 18-75 years old, requiring mechanical ventilation with a persistent Fio2 requirement of 70% or higher and Pao2/Fio2 ratio (or imputed ratio) less than 150 for more than 4 hours. The coagulation inclusion criteria were International Society on Thrombosis and Haemostasis score greater than 5, and presence of a d-dimer greater than 1,200, with viscoelastic testing using rotational thromboelastometry (Instrumentation Laboratories, Mexico City, Mexico) showing both hypercoagulability (EXTEM amplitude at 5 min > 65 FIBTEM > 30) and hypofibrinolysis (EXTEM maximum lysis < 8%). INTERVENTIONS: Catheter-directed tPA angiography and iFlow system analysis to assess pre-tPA baseline pulmonary perfusion and changes in response to thrombolysis. RESULTS: Nine patients had microvascular filling defects demonstrated by angiography, and good agreement was found with iFlow analysis (ƙ = 0.714). Statistically significant differences were identified in the area under the curve (AUC) region of interest/AUC reference tissue with and without filling defects in phase 2 DM -0.09206 (sd ± 0.16684) (p = 0.003). The Pao2/Fio2 values measured immediately and 48 hours after the procedure were significantly higher (p = 0.001 and p = 0.005, respectively). Statistically significant differences were found in d-dimer values (p = 0.007), Fio2 (p = 0.002), and oxygen saturation in arterial blood/Fio2 (p = 0.045), as well as in the number of patients who required prone positioning before, immediately after the procedure, and at 48 hours after the procedure (p = 0.002). CONCLUSIONS: Thrombolysis with catheter-directed tPA resulted in imaging evidence via pulmonary angiography and iFlow technology of improved lung perfusion in COVID-19 patients with severe respiratory failure.

Use of REBOA in the universe of magical realism: a real-world review / Uso de REBOA en el universo del realismo mágico: revisión de vida real

Abstract While reading the novella "Chronicle of a Death Foretold" by the Colombian Nobel Laureate Gabriel García-Marquez, we were surprised to realize that the injuries sustained by the main character could have been successfully treated had he received modern trauma care in which REBOA may have been considered. This is a discussion of Mr. Nasar's murder to explore whether he could have been saved by deploying REBOA as a surgical adjunct to bleeding control and resuscitation. In reading García-Marquez's novel we noted the events that unfolded at the time of Santiago Nasar's murder. To contextualize the claim that Mr. Nasar could have survived, had his injuries been treated with REBOA, we explored and illustrated what could have done differently and why. On the day of his death, Mr. Nasar sustained multiple penetrating stab wounds. Although he received multiple stab wounds to his torso, the book describes seven potentially fatal injuries, resulting in hollow viscus, solid viscus, and major vascular injuries. We provided a practical description of the clinical and surgical management algorithm we would have followed in Mr. Nasar's case. This algorithm included the REBOA deployment for hemorrhage control and resuscitation. The use of REBOA as part of the surgical procedures performed could have saved Mr. Nasar's life. Based on our current knowledge about REBOA in trauma surgery, we claim that its use, coupled with appropriate surgical care for hemorrhage control, could have saved Santiago Nasar's life, and thus prevent a death foretold.

Resumen Leyendo la novela "Crónica de una muerte anunciada" del Nobel de Literatura Gabriel García Márquez, nos sorprendió reconocer que las heridas provocadas al personaje principal se habrían podido tratar exitosamente en un centro de trauma moderno donde hubieran optado por REBOA. Hacemos referencia al asesinato del señor Nasar para explorar la posibilidad de que se hubiera podido salvar de haberse utilizado REBOA como adyuvante de la cirugía para reanimación y control de la hemorragia. En la lectura de la novela de García Márquez tomamos nota de los sucesos que tuvieron lugar en el momento del asesinato de Santiago Nasar. Para contextualizar la afirmación de que Nasar habría podido sobrevivir si le hubieran manejado sus heridas con REBOA, exploramos e ilustramos lo que habría podido hacerse de otra manera y porqué. El día en que murió, el señor Nasar sufrió múltiples heridas por arma blanca y si bien muchas de ellas fueron en el torso, el libro describe siete heridas mortales que comprometieron los órganos sólidos, además de lesiones vasculares mayores. Presentamos una descripción práctica del algoritmo para el manejo clínico y quirúrgico que habríamos seguido en el caso del señor Nasar. Este algoritmo incluye el uso de REBOA para el control de la hemorragia y la reanimación, el cual, como parte de los procedimientos quirúrgicos realizados, habría podido salvarle la vida a la víctima. Basados en nuestro conocimiento actual acerca del uso de REBOA en la cirugía de trauma, planteamos que, junto con la atención quirúrgica apropiada para controlar la hemorragia, este procedimiento habría podido salvarle la vida a Santiago Nasar y, por tanto, evitar una muerte anunciada.

The Association of Surgical Timing and Injury Severity With Systemic Complications in Severely Injured Patients With Pelvic Ring Injuries.

OBJECTIVES: To evaluate the relationship between timing of definitive fixation, injury severity, and the development of systemic complications in severely injured patients with pelvic ring injuries. DESIGN: Retrospective review. SETTINGS: Level 1 trauma center. PATIENTS: One hundred eighteen severely injured [Injury Severity Score (ISS) ≥ 16] adult patients with pelvic ring injuries undergoing definitive fixation, excluding patients treated with external fixation for hemodynamic instability. INTERVENTION: Early fixation (≤36 hours) in 37 patients and delayed fixation (>36 hours) in 81 patients. MAIN OUTCOME MEASUREMENTS: Systemic complications (acute respiratory distress syndrome, pulmonary embolism, deep venous thrombosis, sepsis, multi-organ failure, and death). RESULTS: The delayed fixation group had a higher ISS and had more patients with chest injuries. There was no detectable difference in the number of patients with systemic complications between early versus delayed fixation groups [8 (22%) vs. 29 (35%), P = 0.1]. The only difference detected in specific complications was a higher incidence of pneumonia with delayed fixation [16 (20%) vs. 0 (0%), P = 0.004] with 11 of the 16 cases being associated with chest injury. Univariate analysis showed an association between complication and time to fixation, ISS, Glasgow Coma Scale, pH, base excess, and injuries to the head, chest, and abdomen. On multivariate analysis, only ISS remained significantly associated with the development of complications [Odds ratio 2.6 per 10 point increase, 95% confidence interval (CI), 1.4-4.4]. CONCLUSIONS: These data suggest that the severity of injury is most highly associated with systemic complications after definitive fixation of pelvic ring injuries. LEVEL OF EVIDENCE: Therapeutic Level III. See Instructions for Authors for a complete description of levels of evidence.

Whole Blood Thrombin Generation in Severely Injured Patients Requiring Massive Transfusion.

BACKGROUND: Despite the prevalence of hypocoagulability after injury, the majority of trauma patients paradoxically present with elevated thrombin generation (TG). Although several studies have examined plasma TG post injury, this has not been assessed in whole blood. We hypothesize that whole blood TG is lower in hypocoagulopathy, and TG effectively predicts massive transfusion (MT). STUDY DESIGN: Blood was collected from trauma activation patients at an urban Level I trauma center. Whole blood TG was performed with a prototype point-of-care device. Whole blood TG values in healthy volunteers were compared with trauma patients, and TG values were examined in trauma patients with shock and MT requirement. RESULTS: Overall, 118 patients were included. Compared with healthy volunteers, trauma patients overall presented with more robust TG; however, those arriving in shock (n = 23) had a depressed TG, with significantly lower peak thrombin (88.3 vs 133.0 nM; p = 0.01) and slower maximum rate of TG (27.4 vs 48.3 nM/min; p = 0.04). Patients who required MT (n = 26) had significantly decreased TG, with a longer lag time (median 4.8 vs 3.9 minutes, p = 0.04), decreased peak thrombin (median 71.4 vs 124.2 nM; p = 0.0003), and lower maximum rate of TG (median 15.8 vs 39.4 nM/min; p = 0.01). Area under the receiver operating characteristics (AUROC) analysis revealed lag time (AUROC 0.6), peak thrombin (AUROC 0.7), and maximum rate of TG (AUROC 0.7) predict early MT. CONCLUSIONS: These data challenge the prevailing bias that all trauma patients present with elevated TG and highlight that deficient thrombin contributes to the hypocoagulopathic phenotype of trauma-induced coagulopathy. In addition, whole blood TG predicts MT, suggesting point-of-care whole blood TG can be a useful tool for diagnostic and therapeutic strategies in trauma.

Examining the Effect of Hypertonic Saline Administered for Reduction of Intracranial Hypertension on Coagulation.

BACKGROUND: Hypertonic saline (23.4%, HTS) bolus administration is common practice for refractory intracranial hypertension, but its effects on coagulation are unknown. We hypothesize that 23.4% HTS in whole blood results in progressive impairment of coagulation in vitro and in vivo in a murine model of traumatic brain injury (TBI). STUDY DESIGN: For the in vitro study, whole blood was collected from 10 healthy volunteers, and citrated native thrombelastography was performed with normal saline (0.9%, NS) and 23.4% HTS in serial dilutions (2.5%, 5%, and 10%). For the in vivo experiment, we assessed the effects of 23.4% HTS bolus vs NS on serial thrombelastography and tail-bleeding times in a TBI murine model (n = 10 rats with TBI and 10 controls). RESULTS: For the in vitro work, clinically relevant concentrations of HTS (2.5% dilution) shortened time to clot formation and increased clot strength (maximum amplitude) compared with control and NS. With higher HTS dosing (5% and 10% blood dilution), there was progressive prolongation of time to clot formation, decreased angle, and decreased maximum amplitude. In the in vivo study, there was no significant difference in thrombelastography measurements or tail-bleeding times after bolus administration of 23.4% HTS compared with NS at 2.5% blood volume. CONCLUSIONS: At clinically relevant dilutions of HTS, there is a paradoxical shortening of time to clot formation and increase in clot strength in vitro and no significant effects in a murine TBI model. However, with excess dilution, caution should be exercised when using serial HTS boluses in TBI patients at risk for trauma-induced coagulopathy.

Hemodynamically unstable pelvic fracture: A damage control surgical algorithm that fits your reality.

Pelvic fractures occur in up to 25% of all severely injured trauma patients and its mortality is markedly high despite advances in resuscitation and modernization of surgical techniques due to its inherent blood loss and associated extra-pelvic injuries. Pelvic ring volume increases significantly from fractures and/or ligament disruptions which precludes its inherent ability to self-tamponade resulting in accumulation of hemorrhage in the retroperitoneal space which inevitably leads to hemodynamic instability and the lethal diamond. Pelvic hemorrhage is mainly venous (80%) from the pre-sacral/pre-peritoneal plexus and the remaining 20% is of arterial origin (branches of the internal iliac artery). This reality can be altered via a sequential management approach that is tailored to the specific reality of the treating facility which involves a collaborative effort between orthopedic, trauma and intensive care surgeons. We propose two different management algorithms that specifically address the availability of qualified staff and existing infrastructure: one for the fully equipped trauma center and another for the very common limited resource center.

Las fracturas de pelvis ocurren en más del 25% de los pacientes con trauma severo y su mortalidad es alta, a pesar de los avances en la resucitación hemodinámica y las técnicas quirúrgicas. Esta mortalidad se explica por la hemorragia inherente y las lesiones extra pélvicas asociadas, las fracturas o las disrupciones ligamentarias de la pelvis aumentan el volumen del espacio pélvico, y conlleva a que la hemorragia pélvica se acumule en el espacio retroperitoneal. En poco tiempo, esto conduce a la inestabilidad hemodinámica y el rombo de la muerte. La hemorragia pélvica es un 80% venosa proveniente de los plexos pre-sacro / pre-peritoneal. El restante 20% es arterial por sangrado de las ramas de la arteria iliaca interna. Esta realidad podría ser cambiada a través de un manejo secuencial enfocado según la disposición de recursos del centro de atención y de un trabajo colaborativo entre ortopedistas, cirujanos de trauma e intensivistas. Este articulo propone dos algoritmos de manejo que están enfocados según la disponibilidad de un equipo calificado e infraestructura existente: uno para un centro de trauma totalmente equipado, y el otro para un centro con recursos limitados.

Preperitoneal Pelvic Packing Is Not Associated With an Increased Risk of Surgical Site Infections After Internal Anterior Pelvic Ring Fixation.

OBJECTIVE: To investigate the risk of postoperative surgical site infections after plate fixation of the anterior pelvic ring subsequent to preperitoneal pelvic packing (PPP). DESIGN: Retrospective observational cohort study. SETTING: Level I academic trauma center. PATIENTS: Adult trauma patients with unstable pelvic ring injuries requiring surgical fixation of the anterior pelvic ring. INTERVENTION: Pelvic plate fixation was performed as a staged procedure after external fixation and PPP/depacking (PPP group; n = 25) or as a single-stage primary internal fixation (control group; n = 87). MAIN OUTCOME MEASURE: Incidence of postoperative surgical site infections of the pelvic space. RESULTS: Anterior pelvic plate fixation was performed in 112 patients during a 5-year study period. The PPP group had higher injury severity scores and transfused packed red blood cells than the control group (injury severity score: 46 ± 12.2 vs. 29 ± 1.5; packed red blood cells: 13 ± 10 vs. 5 ± 2; P < 0.05). The mean time until pelvic depacking was 1.7 ± 0.6 days (range: 1-3 days) and 3.4 ± 3.7 days (range: 0-15 days) from depacking until pelvic fracture fixation. Two patients in the PPP group and 8 patients in the control group developed a postoperative infection requiring a surgical revision (8.0% vs. 9.2%; n.s.). Both PPP patients with a pelvic space infection had undergone anterior plate fixation for associated acetabular fractures. CONCLUSIONS: These data support the safety of the PPP protocol for bleeding pelvic ring injuries due to the lack of increased infection rates after fracture fixation. Caution should be applied when considering PPP in patients with associated acetabular fractures. LEVEL OF EVIDENCE: Therapeutic Level III. See Instructions for Authors for a complete description of levels of evidence.

Clot activators do not expedite the time to predict massive transfusion in trauma patients analyzed with tissue plasminogen activator thrombelastography.

BACKGROUND: Trauma patients with hypersensitivity to tissue plasminogen activator mediated fibrinolysis quantified by tissue plasminogen activator thromboelastography are at increased risk of massive transfusion. The tissue plasminogen activator thromboelastography assay has been tested in trauma patients using native thromboelastography with no exogenous activator. We hypothesize that adding an activator will expedite the time to results. METHODS: Healthy whole blood was assayed with and without exogenous plasmin, which acts to deplete inhibitors of fibrinolysis, mimicking trauma blood. Samples were assessed using native, kaolin, and rapid thromboelastography with and without tissue plasminogen activator. The tissue plasminogen activator thromboelastography indices of time to maximum amplitude and lysis at 30 minutes were contrasted between healthy blood with and without plasmin using the three different activators. The activators were then used with a tissue plasminogen activator thromboelastography in 100 trauma patients to assess performance in predicting massive transfusion. RESULTS: In healthy blood, regardless of activator, lysis at 30 minutes did not increase with plasmin alone, but did increase with tissue plasminogen activator (P = .012). Adding tissue plasminogen activator and plasmin increased lysis at 30 minutes (P = .036). Time to maximum amplitude was reduced with tissue plasminogen activator and plasmin compared with tissue plasminogen activator alone (P = .012). Activated thromboelastographies had increased lysis at 30 minutes (P = .002), but no difference in time to maximum amplitude compared with native thromboelastographies. In trauma patients, native tissue plasminogen activator thromboelastography had greater performance in predicting massive transfusion than activated tissue plasminogen activator thromboelastographies with no difference in time to maximum amplitude. CONCLUSION: Adding an activator to tissue plasminogen activator thromboelastography does not expedite time to maximum amplitude in healthy blood depleted of fibrinolysis inhibitors. Activated tissue plasminogen activator thromboelastographies are inferior to native tissue plasminogen activator thromboelastography for predicting massive transfusion and do not reduce the time to results.

Selective organ ischaemia/reperfusion identifies liver as the key driver of the post-injury plasma metabolome derangements.

BACKGROUND: Understanding the molecular mechanisms in perturbation of the metabolome following ischaemia and reperfusion is critical in developing novel therapeutic strategies to prevent the sequelae of post-injury shock. While the metabolic substrates fueling these alterations have been defined, the relative contribution of specific organs to the systemic metabolic reprogramming secondary to ischaemic or haemorrhagic hypoxia remains unclear. MATERIALS AND METHODS: A porcine model of selected organ ischaemia was employed to investigate the relative contribution of liver, kidney, spleen and small bowel ischaemia/reperfusion to the plasma metabolic phenotype, as gleaned through ultra-high performance liquid chromatography-mass spectrometry-based metabolomics. RESULTS: Liver ischaemia/reperfusion promotes glycaemia, with increases in circulating carboxylic acid anions and purine oxidation metabolites, suggesting that this organ is the dominant contributor to the accumulation of these metabolites in response to ischaemic hypoxia. Succinate, in particular, accumulates selectively in response to the hepatic ischemia, with levels 6.5 times spleen, 8.2 times small bowel, and 6 times renal levels. Similar trends, but lower fold-change increase in comparison to baseline values, were observed upon ischaemia/reperfusion of kidney, spleen and small bowel. DISCUSSION: These observations suggest that the liver may play a critical role in mediating the accumulation of the same metabolites in response to haemorrhagic hypoxia, especially with respect to succinate, a metabolite that has been increasingly implicated in the coagulopathy and pro-inflammatory sequelae of ischaemic and haemorrhagic shock.

Trauma Resuscitation Consideration: Sex Matters.

BACKGROUND: Sex dimorphisms in coagulation have been recognized, but whole blood assessment of these dimorphisms and their relationship to outcomes in trauma have not been investigated. This study characterizes the viscoelastic hemostatic profile of severely injured patients by sex, and examines how sex-specific coagulation differences affect clinical outcomes, specifically, massive transfusion (MT) and death. We hypothesized that severely injured females are more hypercoagulable and therefore, have lower rates of MT and mortality. STUDY DESIGN: Hemostatic profiles and clinical outcomes from all trauma activation patients from 2 level I trauma centers were examined, with sex as an experimental variable. As part of a prospective study, whole blood was collected and thrombelastography (TEG) was performed. Coagulation profiles were compared between sexes, and association with MT and mortality were examined. Poisson regression with robust standard errors was performed. RESULTS: Overall, 464 patients (23% female) were included. By TEG, females had a more hypercoagulable profile, with a higher angle (clot propagation) and maximum amplitude (MA, clot strength). Females were less likely to present with hyperfibrinolysis or prolonged activating clotting time than males. In the setting of depressed clot strength (abnormal MA), female sex conferred a survival benefit, and hyperfibrinolysis was associated with higher case-fatality rate in males. CONCLUSIONS: Severely injured females have a more hypercoagulable profile than males. This hypercoagulable status conferred a protective effect against mortality in the setting of diminished clot strength. The mechanism behind these dimorphisms needs to be elucidated and may have treatment implications for sex-specific trauma resuscitation.

Severe traumatic brain injury is associated with a unique coagulopathy phenotype.

BACKGROUND: Traumatic brain injury (TBI) patients present on a spectrum from hypocoagulability to hypercoagulability, depending on the injury complexity, severity, and time since injury. Prior studies have found a unique coagulopathy associated with TBI using conventional coagulation assays such as INR; however, few studies have assessed the association of TBI and coagulopathy using viscoelastic assays that comprehensively evaluate the coagulation in whole blood. This study aims to reevaluate the TBI-specific trauma-induced coagulopathy using arrival thrombelastography. Because brain tissue is high in key procoagulant molecules, we hypothesize that isolated TBI is associated with procoagulant and hypofibrinolytic profiles compared with injuries of the torso, extremities, and polytrauma, including TBI. METHODS: Data are from the prospective Trauma Activation Protocol study. Activated clotting time (ACT), angle, maximum amplitude (MA), 30-minute percent lysis after MA (LY30), and functional fibrinogen levels (FFLEV) were recorded. Patients were categorized into isolated severe TBI (I-TBI), severe TBI with torso and extremity injuries (TBI + TORSO/EXTREMITIES), and isolated torso and extremity injuries (I-TORSO/EXTREMITIES). Poisson regression was used to adjust for multiple confounders. RESULTS: Overall, 572 patients (48 I-TBI, 45 TBI + TORSO/EXTREMITIES, 479 I-TORSO/EXTREMITIES) were included in this analysis. The groups differed in INR, ACT, angle, MA, and FFLEV but not in 30-minute percent lysis. When compared with I-Torso/Extremities, after adjustment for confounders, severe I-TBI was independently associated with ACT less than 128 seconds (relative risk [RR], 1.5; 95% confidence interval [CI], 1.1-2.2), angle less than 65 degrees (RR, 2.2; 95% CI, 1.4-3.6), FFLEV less than 356 (RR, 1.7; 95% CI, 1.2-2.4) but not MA less than 55 mm, hyperfibrinolysis, fibrinolysis shutdown, or partial thromboplastin time (PTT) greater than 30. CONCLUSION: Severe I-TBI was independently associated with a distinct coagulopathy with delayed clot formation but did not appear to be associated with fibrinolysis abnormalities. Low fibrinogen and longer ACT values associated with I-TBI suggest that early coagulation factor replacement may be indicated in I-TBI patients over empiric antifibrinolytic therapy. Mechanisms triggering coagulopathy in TBI are unique and warrant further investigation. LEVEL OF EVIDENCE: Retrospective cohort study, prognostic, level III.

Empiric transfusion strategies during life-threatening hemorrhage.

BACKGROUND: Resuscitation guided by thrombelastography improves survival after injury. If bleeding is rapid, however, or if no thrombelastography data are available, the optimal strategy remains controversial. Our current practice gives fresh frozen plasma and red blood cells (1:2) empirically in patients with life-threatening hemorrhage, with subsequent administration based on rapid thrombelastography. We identified patients at risk of massive transfusion at 1 hour, examined their initial rapid thrombelastography, and used this value to provide empiric recommendations about transfusions. METHODS: Massive transfusion was defined as >4 units of red blood cells in the first hour. Patients managed by a trauma activation (2014-2017) had an admission rapid thrombelastography analyzed to determine what proportion met thresholds for administration of cryoprecipitate or platelets. RESULTS: Overall, 35 patients received >4 units of red blood cells in the first hour. Based on the admission rapid thrombelastography, 37% met criteria for both platelets and cryoprecipitate, 35% for either platelets or cryoprecipitate and 29% for neither. Kaplan-Meier analysis showed a significant delay in the administration of cryoprecipitate and platelets compared to fresh frozen plasma. CONCLUSION: Patients who require >4 units of red blood cells within the first hour should receive cryoprecipitate and platelets if thrombelastography results are not available. Point-of-care devices are needed for optimal care of trauma-induced-coagulopathy, but these data offer guidance in their absence.

Could resuscitative endovascular balloon occlusion of the aorta improve survival among severely injured patients with post-intubation hypotension?

Current literature shows the association of post-intubation hypotension and increased odds of mortality in critically ill non-trauma and trauma populations. However, there is a lack of research on potential interventions that can prevent or ameliorate the consequences of endotracheal intubation and thus improve the prognosis of trauma patients with post-intubation hypotension. This review paper hypothesizes that the deployment of REBOA among trauma patients with PIH, by its physiologic effects, will reduce the odds of mortality in this population. The objective of this paper is to review the current literature on REBOA and post-intubation hypotension, and, furthermore, to provide a rational hypothesis on the potential role of REBOA in severely injured patients with post-intubation hypotension.

Systemic hyperfibrinolysis after trauma: a pilot study of targeted proteomic analysis of superposed mechanisms in patient plasma.

BACKGROUND: Viscoelastic measurements of hemostasis indicate that 20% of seriously injured patients exhibit systemic hyperfibrinolysis, with increased early mortality. These patients have normal clot formation with rapid clot lysis. Targeted proteomics was applied to quantify plasma proteins from hyperfibrinolytic (HF) patients to elucidate potential pathophysiology. METHODS: Blood samples were collected in the field or at emergency department arrival and thrombelastography (TEG) was used to characterize in vitro clot formation under native and tissue plasminogen activator (tPA)-stimulated conditions. Ten samples were taken from injured patients exhibiting normal lysis time at 30 min (Ly30), "eufibrinolytic" (EF), 10 from HF patients, defined as tPA-stimulated TEG Ly30 >50%, and 10 from healthy controls. Trauma patient samples were analyzed by targeted proteomics and ELISA assays for specific coagulation proteins. RESULTS: HF patients exhibited increased plasminogen activation. Thirty-three proteins from the HF patients were significantly decreased compared with healthy controls and EF patients; 17 were coagulation proteins with anti-protease consumption (p < 0.005). The other 16 decreased proteins indicate activation of the alternate complement pathway, depletion of carrier proteins, and four glycoproteins. CXC7 was elevated in all injured patients versus healthy controls (p < 0.005), and 35 proteins were unchanged across all groups (p > 0.1 and fold change of concentrations of 0.75-1.3). CONCLUSION: HF patients had significant decreases in specific proteins and support mechanisms known in trauma-induced hyperfibrinolysis and also unexpected decreases in coagulation factors, factors II, X, and XIII, without changes in clot formation (SP, R times, or angle). Decreased clot stability in HF patients was corroborated with tPA-stimulated TEGs. LEVEL OF EVIDENCE: Prognostic, level III.