Nonoperative Management for Low-Grade Blunt Thoracic Aortic Injury.

BACKGROUND: Thoracic endovascular aortic repair (TEVAR) is the standard of care for the treatment of blunt thoracic aortic injury (BTAI) requiring intervention. Data suggest that low-grade BTAI (grade I [intimal tears] or grade II [intramural hematoma]) will resolve spontaneously if treated with nonoperative management (NOM) alone. There has been no comparison specifically between the use of NOM vs TEVAR for low-grade BTAI. We hypothesize that these low-grade injuries can be safely managed with NOM alone. STUDY DESIGN: Retrospective analysis of all patients with a low-grade BTAI in the Aortic Trauma Foundation Registry from 2016 to 2021 was performed. The study population was 1 primary outcome was mortality. Secondary outcomes included complications, ICU length of stay, and ventilator days. RESULTS: A total of 880 patients with BTAI were enrolled. Of the 269 patients with low-grade BTAI, 218 (81%) were treated with NOM alone (81% grade I, 19% grade II), whereas 51 (19%) underwent a TEVAR (20% grade I, 80% grade II). There was no difference in demographic or mechanism of injury in patients with low-grade BTAI who underwent NOM vs TEVAR. There was a difference in mortality between NOM alone and TEVAR (8% vs 18%, p = 0.009). Aortic-related mortality was 0.5% in the NOM group and 4% in the TEVAR group (p = 0.06). Hospital and ICU length of stay and ventilator days were not different between the 2 groups. CONCLUSIONS: NOM alone is safe and appropriate management for low-grade BTAI, with lower mortality and decreased rates of complication when compared with routine initial TEVAR.

Trends in prehospital cervical collar utilization in trauma patients: Closer, but not there yet.

OBJECTIVE: This study aims to assess the change in cervical spine (C-spine) immobilization frequency in trauma patients over time. We hypothesize that the frequency of unnecessary C-spine immobilization has decreased. METHODS: A retrospective chart review of adult trauma patients transported to our American College of Surgeons-verified Level I trauma center from January 1, 2014, to December 31, 2021, was performed. Emergency medical services documentation was manually reviewed to record prehospital physiology and the application of a prehospital cervical collar (c-collar). C-spine injuries were defined as cervical vertebral fractures and/or spinal cord injuries. Univariate and year-by-year trend analyses were used to assess changes in C-spine injury and immobilization frequency. RESULTS: Among 2906 patients meeting inclusion criteria, 12% sustained C-spine injuries, while 88% did not. Patients with C-spine injuries were more likely to experience blunt trauma (95% vs. 68%, p < 0.001), were older (46 years vs. 41 years, p < 0.001), and had higher Injury Severity Scores (31 vs. 18, p < 0.001). They also exhibited lower initial systolic blood pressures (108 mm Hg vs. 119 mm Hg, p < 0.001), lower heart rates (92 beats/min vs. 97 beats/min, p < 0.05), and lower Glasgow Coma Scale scores (9 vs. 11, p < 0.001). In blunt trauma, c-collars were applied to 83% of patients with C-spine injuries and 75% without; for penetrating trauma, c-collars were applied to 50% of patients with C-spine injuries and only 8% without. Among penetrating trauma patients with C-spine injury, all patients either arrived quadriplegic or did not require emergent neurosurgical intervention. The proportion of patients receiving a c-collar decreased in both blunt and penetrating traumas from 2014 to 2021 (blunt-82% in 2014 to 68% in 2021; penetrating-24% in 2014 to 6% in 2021). CONCLUSIONS: Unnecessary C-spine stabilization has decreased from 2014 to 2021. However, c-collars are still being applied to patients who do not need them, both in blunt and in penetrating trauma cases, while not being applied to patients who would benefit from them.

The more you have, the more you lose: Muscle mass changes in trauma patients with prolonged hospitalizations.

INTRODUCTION: Sarcopenia is a clinically relevant loss of muscle mass with implications of increased morbidity and mortality in adult trauma populations.  Our study aimed to evaluate loss of muscle mass change in adult trauma patients with prolonged hospital stays. METHODS: Retrospective analysis using institutional trauma registry to identify all adult trauma patients with hospital length of stay >14 days admitted to our Level 1 center between 2010 and 2017. All CT images were reviewed, and cross-sectional area (cm2) of the left psoas muscle was measured at the level of the third lumbar vertebral body to determine total psoas area (TPA) and Total Psoas Index (TPI) normalized for patient stature.  Sarcopenia was defined as a TPI on admission below gender specific thresholds of 5.45(cm2/m2) in men and 3.85(cm2/m2) in women.  TPA, TPI, and rates of change in TPI were then evaluated and compared between sarcopenic and non-sarcopenic adult trauma patients. RESULTS: There were 81 adult trauma patients who met inclusion criteria. The average change in TPA was -3.8 cm2 and TPI was -1.3 cm2. On admission, 23% (n = 19) of patients were sarcopenic while 77% (n = 62) were not. Non-sarcopenic patients had a significantly greater change in TPA (-4.9 vs. -0.31, p<0.0001), TPI (-1.7 vs. -0.13, p<0.0001), and rate of decrease in muscle mass (p = 0.0002). 37% of patients who were admitted with normal muscle mass developed sarcopenia during admission.  Older age was the only risk factor independently associated with developing sarcopenia (OR: 1.04, 95%CI 1.00-1.08, p = 0.045). CONCLUSION: Over a third of patients with normal muscle mass at admission subsequently developed sarcopenia with older age as the primary risk factor. Patients with normal muscle mass at admission had greater decreases in TPA and TPI, and accelerated rates of muscle mass loss compared to sarcopenic patients.

Chest and Pelvis X-Rays as a Screening Tool for Abdominal Injury in Geriatric Blunt Trauma Patients.

BACKGROUND: This study evaluates the utility of chest (CXR) and pelvis (PXR) X-ray, as adjuncts to the primary survey, in screening geriatric blunt trauma (GBT) patients for abdominal injury or need for laparotomy. METHODS: We performed a retrospective analysis of patients 65-89 years in the 2014 National Trauma Data Bank. X-ray injuries were identified by ICD9 codes and defined as any injury felt to be readily detectable by a non-radiologist. X-ray findings were dichotomized as "both negative" (no injury presumptively apparent on CXR or PXR) or "either positive" (any injury presumptively apparent on CXR or PXR). Rates of abdominal injuries and laparotomy were compared and used to calculate sensitivity and specificity. The primary outcomes were abdominal injury and laparotomy. The secondary outcomes included mortality, ventilator days, and hospital days. RESULTS: A total of 202 553 patients met criteria. Overall, 9% of patients with either positive X-rays had abdominal injury and 2% laparotomy vs. 1.1% and .3% with both negative (P < .001). The specificity for any positive X-ray was 79% for abdominal injury and 78% for laparotomy. The sensitivity was 69% for abdominal injury and laparotomy. The either positive group had fewer ventilator days (.3 vs. .8, P < .0001), longer length of stay (7 vs. 5, P < .0001), and higher mortality (6% vs. 4%, P < .0001) vs both negative. CONCLUSION: CXR and PXR can be used to assess for intra-abdominal injury and need for laparotomy. GBT patients with either positive X-rays should continue workup regardless of mechanism due to the high specificity of this tool for abdominal injury and need for laparotomy.

A national trauma data bank analysis of large animal-related injuries.

INTRODUCTION: Large animal-related injuries (LARI) are relatively uncommon, but, nevertheless, a public hazard. The objective of this study was to better understand LARI injury patterns and outcomes. MATERIALS AND METHODS: We performed a retrospective review of the 2016 National Trauma Data Bank and used ICD-10 codes to identify patients injured by a large animal. The primary outcome was severe injury pattern, while secondary outcomes included mortality, hospital length of stay, ICU admission, and mechanical ventilation usage. RESULTS: There were 6,662 LARI included in our analysis. Most LARI (66%) occurred while riding the animal, and the most common type of LARI was fall from horse (63%). The median ISS was 9 and the most severe injuries (AIS ≥ 3) were to the chest (19%), head (10%), and lower extremities (10%). The overall mortality was low at 0.8%. Compared to non-riders, riders sustained more severe injuries to the chest (21% vs. 16%, p<0.001) and spine (4% vs. 2%, p<0.001). Compared to motor vehicle collisions (MVC), riders sustained fewer severe injuries to the head (10% vs. 12%, p<0.001) and lower extremity (10% vs. 12%, p=0.01). Compared to auto-pedestrian accidents, non-riders sustained fewer severe injuries to the head (11% vs. 19%, p<0.001) and lower extremity (10% vs. 20%, p<0.001). CONCLUSION: Patients involved in a LARI are moderately injured with more complex injuries occurring in the chest, head, and lower extremities. Fall from horse was the most common LARI mechanism. Overall mortality was low. Compared to non-riders, riders were more likely to sustain severe injuries to the chest and spine. Severe injury patterns were similar when comparing riders to MVC and, given that most LARI are riding injuries, we recommend trauma teams approach LARI as they would an MVC.

Risk scoring models fail to predict pulmonary embolism in trauma patients.

BACKGROUND: We aimed to identify risk factors and risk scoring models to help identify post-traumatic pulmonary embolisms (PE). METHODS: We performed a retrospective review (2014-2019) of all adult trauma patients admitted to our Level I trauma center that received a CT pulmonary angiogram (CTPA) for a suspected PE. A systematic literature search found eleven risk scoring models, all of which were applied to these patients. Scores of patients with and without PE were compared. RESULTS: Of the 235 trauma patients that received CTPA, 31 (13%) showed a PE. No risk scoring model had both a sensitivity and specificity above 90%. The Wells Score had the highest area under the curve (0.65). After logistic regression, no risk scoring model variables were independently associated with PE. CONCLUSIONS: In trauma patients with clinically suspected PE, clinical variables and current risk scoring models do not adequately differentiate patients with and without PE.

A Prospective Study of Family Satisfaction Changes After Tracheostomy Placement in Trauma Patients.

BACKGROUND: Tracheostomy is a commonly performed procedure in surgical intensive care units. Although the indications and benefits of this procedure are well known, little has been studied in the adult surgical/trauma population about patient family satisfaction after tracheostomy placement. MATERIALS AND METHODS: We performed a prospective study at our academic level I trauma center from 2015-2016 in patients who underwent elective tracheostomy. Family members were asked to complete an eight-point questionnaire using a forced Likert scale of graded responses. Questionnaires were administered prior to tracheostomy and again at 24-and 72-hour post-tracheostomy placement. Responses were compared using univariate analysis. RESULTS: A total of 26 family members completed all 3 surveys. Family members believed loved ones appeared more comfortable, were more interactive, and were better progressing clinically. After 72 hours, family members felt less anxiety. There was no difference in perceptions of patient distress, ability to provide support, or their worry about scars, or comfort in visiting them. DISCUSSION: Family members believed tracheostomies provided greater patient comfort, increased interactive abilities, better progress in their care, and experienced less anxiety after placement. Family satisfaction may therefore be an additional benefit in support of earlier tracheostomy.

Incidence and Risk Factors for Acute Kidney Injury in Severely Injured Patients Using Current Kidney Disease: Improving Global Outcomes Definitions.

BACKGROUND: Acute kidney injury (AKI) is a significant cause of morbidity and mortality for critically injured trauma patients. The Kidney Disease: Improving Global Outcomes (KDIGO) practice guideline is the most up-to-date classification for AKI. The aims of this study were to determine the incidence and risk factors for AKI in critically injured trauma patients using the current KDIGO definitions. STUDY DESIGN: A prospective cohort study was performed at our academic, level 1 trauma center, from September 2017 to August 2018. All adult trauma patients admitted to the surgical ICU were included. The primary outcome was the development of AKI, as defined by KDIGO. Secondary outcomes included hospital and ICU length of stay, ventilator days, and mortality. RESULTS: There were 466 patients included and 314 (67%) developed AKI. Those who developed AKI were more often hypotensive on admission (7% vs 2%), had higher Injury Severity Scores (ISS) (19 vs 13), were more likely to have severe injuries to the chest (40% vs 24%) and extremities (20% vs 6%), received transfusion (41% vs 21%), sustained crush injuries (8% vs 1%), received radiocontrast (75% vs 47%), nephrotoxic medication (74% vs 60%), or vasopressors (15% vs 3%). After multivariate analysis, risk factors independently associated with AKI include age, Injury Severity Score (ISS), severe extremity injuries, radiocontrast, and vasopressors. Those who developed AKI had higher mortality (9% vs 2%). CONCLUSIONS: Using current KDIGO criteria, the incidence of AKI in critically injured trauma patients was higher than previously reported. Older patients, with more severe injuries to their extremities and chest and who have suffered crush injuries, appear to be the most a risk. AKI in the critically injured patient results in an almost 5-fold increase in mortality.

Keratinocytes produce IL-6 in response to desmoglein 1 cleavage by Staphylococcus aureus exfoliative toxin A.

Many skin infections are caused by Staphylococcus aureus, a bacterial pathogen that produces virulence factors associated with these conditions such as exfoliative toxins A and B (ETA, ETB) and the leukotoxin Panton-Valentine leukocidin (PVL). Herein, we examine the potential of skin-infecting S. aureus to produce virulence factors and their impact on the local immune response. Toxin gene profiles were generated from 188 S. aureus isolated as single infecting organisms from skin lesions and demonstrated a higher potential to express ETA, ETB, and PVL than community isolates (p < 0.001). Within the study isolate group, the prevalence of genes encoding PVL was higher among methicillin-resistant S. aureus (MRSA; n = 49), while genes encoding ETs were more prevalent in methicillin-susceptible S. aureus (MSSA; n = 139). When lesion-associated white blood cell (WBC) counts were dichotomized into high- or low-WBC-count-associated bacteria, the gene for ETA was found to be associated with a low WBC count among MSSA (p = 0.001). The ETA-induced mouse model of staphylococcal scalded skin syndrome was used to investigate the link between ETA and cytokine production. Elevated IL-6 levels in the serum and increased expression of IL-6 mRNA in the skin were detected in response to ETA exposure. These findings were recapitulated in vitro using primary human keratinocytes. Thus, S. aureus may influence the local immune response via ETA cleavage of desmoglein 1 and the induction of cutaneous IL-6 expression.

Cellular response to Trypanosoma cruzi infection induces secretion of defensin α-1, which damages the flagellum, neutralizes trypanosome motility, and inhibits infection.

Human defensins play a fundamental role in the initiation of innate immune responses to some microbial pathogens. Here we show that colonic epithelial model HCT116 cells respond to Trypanosoma cruzi infection by secreting defensin α-1, which reduces infection. We also report the early effects of defensin α-1 on invasive trypomastigotes that involve damage of the flagellar structure to inhibit parasite motility and reduce cellular infection. Short exposure of defensin α-1 to trypomastigotes shows that defensin α-1 binds to the flagellum, resulting in flagellar membrane and axoneme alterations, followed by breaking of the flagellar membrane connected to the trypanosome body, leading to detachment and release of the parasite flagellum. In addition, defensin α-1 induces a significant reduction in parasite motility in a peptide concentration-dependent manner, which is abrogated by anti-defensin α-1 IgG. Preincubation of trypomastigotes with a concentration of defensin α-1 that inhibits 50% trypanosome motility significantly reduced cellular infection by 80%. Thus, human defensin α-1 is an innate immune molecule that is secreted by HCT116 cells in response to T. cruzi infection, inhibits T. cruzi motility, and plays an important role in reducing cellular infection. This is the first report showing a novel cellular innate immune response to a human parasite by secretion of defensin α-1, which neutralizes the motility of a human parasite to reduce cellular infection. The mode of activity of human defensin α-1 against T. cruzi and its function may provide insights for the development of new antiparasitic strategies.

Thrombospondin-1 interacts with Trypanosoma cruzi surface calreticulin to enhance cellular infection.

Trypanosoma cruzi causes Chagas disease, which is a neglected tropical disease that produces severe pathology and mortality. The mechanisms by which the parasite invades cells are not well elucidated. We recently reported that T. cruzi up-regulates the expression of thrombospondin-1 (TSP-1) to enhance the process of cellular invasion. Here we characterize a novel TSP-1 interaction with T. cruzi that enhances cellular infection. We show that labeled TSP-1 interacts specifically with the surface of T. cruzi trypomastigotes. We used TSP-1 to pull down interacting parasite surface proteins that were identified by mass spectrometry. We also show that full length TSP-1 and the N-terminal domain of TSP-1 (NTSP) interact with T. cruzi surface calreticulin (TcCRT) and other surface proteins. Pre-exposure of recombinant NTSP or TSP-1 to T. cruzi significantly enhances cellular infection of wild type mouse embryo fibroblasts (MEF) compared to the C-terminal domain of TSP-1, E3T3C1. In addition, blocking TcCRT with antibodies significantly inhibits the enhancement of cellular infection mediated by the TcCRT-TSP-1 interaction. Taken together, our findings indicate that TSP-1 interacts with TcCRT on the surface of T. cruzi through the NTSP domain and that this interaction enhances cellular infection. Thus surface TcCRT is a virulent factor that enhances the pathogenesis of T. cruzi infection through TSP-1, which is up-regulated by the parasite.

Gene network analysis during early infection of human coronary artery smooth muscle cells by Trypanosoma cruzi and Its gp83 ligand.

Trypanosoma cruzi, the causative agent of Chagas' disease, infects heart and muscle cells leading to cardiac arrest, followed by death. The genetic architectures in the early T. cruzi infection process of human cells are unknown. To understand the genetic architectures of the early invasion process of T. cruzi, we conducted gene transcription microarray analysis, followed by gene network construction of the host cell response in primary human coronary artery smooth muscle (HCASM) cells infected with T. cruzi or exposed to T. cruzi gp83, a ligand used by the trypanosome to bind host cells. Using seven RT-PCR verified up-regulated genes (FOSB, ATF5, INPP1, CCND2, THBS1, LAMC1, and APLP2) as the seed for network construction, we built an interaction network of the early T. cruzi infection process containing 165 genes, connected by 598 biological interactions. This interactome network is centered on the BCL6 gene as a hub. Silencing the expression of two seed genes (THBS1 and LAMC1) by RNAi reduced T. cruzi infection. Overall, our results elucidate the significant and complex process involved in T. cruzi infection of HCASM cells at the transcriptome level. This is the first elucidation into the interactome network in human cells caused by T. cruzi and its gp83 ligand.

REGULATION of the EXTRACELLULAR MATRIX INTERACTOME by Trypanosoma cruzi.

It has been shown that the invasive trypomastigote forms of Trypanosoma cruzi use and modulate components of the extracellular matrix (ECM) during the initial process of infection. Infective trypomastigotes up-regulate the expression of laminin γ-1 (LAMC1) and thrombospondin (THBS1) to facilitate the recruitment of trypomastigotes to enhance cellular infection. Silencing the expression of LAMC1 and THBS1 by stable RNAi dramatically reduces trypanosome infection. T. cruzi gp83, a ligand that mediates the attachment of trypanosomes to cells to initiate infection, up-regulates LAMC1 expression to enhance cellular infection. Infective trypomastigotes interact with LAMC1 through galectin-3 (LGALS3), a human lectin, to enhance cellular infection. Silencing the expression of LGALS3 also reduces cellular infection. Some trypanosome surface molecules also interact with the ECM to facilitate infection. Despite the role of the ECM in T. cruzi infection, almost nothing is known about the ECM interactome networks operating in the process of T. cruzi infection. In this mini review, we critically analyze and discuss the regulation of the ECM by T. cruzi and its gp83 ligand, and present the first elucidation of the human ECM interactome network, regulated by T. cruzi and its gp83 ligand, to facilitate cellular infection. The elucidation of the human ECM interactome regulated by T. cruzi is critically important to the understanding of the molecular pathogenesis of T. cruzi infection and developing novel approaches of intervention in Chagas' disease.

Staphylococcus aureus virulence factors associated with infected skin lesions: influence on the local immune response.

OBJECTIVES: To evaluate Staphylococcus aureus isolates from infected skin lesions for their potential to produce immune system-modulating toxins and to correlate these with white blood cell (WBC) counts associated with these lesions. DESIGN: Specimens were obtained for bacterial culture and gram staining from 105 infected skin lesions, and the number of WBCs per low-power field (LPF) was determined. Chromosomal DNA was prepared from 84 bacterial isolates and subjected to real-time polymerase chain reaction analysis to determine the presence of genes encoding potential immunomodulating toxins. Bacterial populations were divided into 2 groups: those associated with low WBC counts (0-5 WBCs/LPF) and those with high WBC counts (> 5 WBCs/LPF). We applied chi(2) statistical analyses to compare the toxin gene profiles associated with WBC counts on initial swab for culture. PATIENTS: Samples were obtained from patients at a single geographic location. RESULTS: A higher than expected percentage of bacteria capable of producing the exfoliative toxins A and/or B (ETA and/or ETB) and Panton-Valentine leukocidin (PVL) was seen in all skin lesions infected with S aureus without regard to WBC count with initial cultures. Comparison of the toxins associated with the low WBC group vs the high WBC group showed that low WBC counts were associated with ETA and ETB, while high WBC counts were associated with PVL and toxic shock syndrome toxin. There were no differences in the clinical appearance of the lesions between groups. CONCLUSIONS: Staphylococcus aureus virulence factors ETA, ETB, and PVL are associated with WBC counts from infected skin lesions. The exact role they play in affecting the WBC counts remains to be determined.