Background

Since 1967, in California it has been illegal to openly carry a loaded firearm in public except when engaged in hunting or law enforcement. However, beginning January 1, 2012, public open carry of unloaded handguns also became illegal. Fatal and non-fatal (NF) firearm injuries were examined before and after adoption of the 2012 ban to quantify the effect of the new law on public health.

Methods

State-level data were obtained directly from California and nine other US state inpatient and emergency department (ED) discharge databases, and the Centers for Disease Control Web-Based Injury Statistics Query and Reporting System. Case numbers of firearm fatalities, NF hospitalizations, NF ED visits, and state-level population estimates were extracted. Each incident was classified as unintentional, self-inflicted, or assault. Crude incidence rates were calculated. The strength of gun laws was quantified using the Brady grade. There were no changes to open carry in these nine states during the study. Using a difference-in-difference technique, the rate trends 3 years preban and postban were compared.

Results

The 2012 open carry ban resulted in a significantly lower incident rate of both firearm-related fatalities and NF hospitalizations (p<0.001). The effect of the law remained significant when controlling for baseline state gun laws (p<0.001). Firearm incident rate drops in California were significant for male homicide (p=0.023), hospitalization for NF assault (p=0.021  male; p=0.025 female), and ED NF assault visits (p=0.04). No significant decreases were observed by sex for suicides or unintentional injury. Changing the law saved an estimated 337 lives (3.6% fewer deaths) and 1285 NF visits in California during the postban period.

Discussion

Open carry ban decreases fatalities and healthcare utilization even in a state with baseline strict gun laws. The most significant impact is from decreasing firearm-related fatal and NF assaults.

Level of evidence

III, epidemiology.

Background

Granular data on gun sales has been historically difficult to obtain. In 2016, California (CA) made monthly data from 1996 to 2015 publically available. Control charts are a method to analyze how a process changes over time in response to nonroutine events. We utilized this technique to study the impact of US mass shootings on CA gun sales.

Methods

Monthly gun sales were provided by the CA Department of Justice and monthly fatalities from the CDC Wonder Death Certificate Registry. Mass shooting events were obtained from after-action reports, news media, and court proceedings. Time-ordered data were analyzed with control charts with 95% confidence intervals (upper control limit, lower control limit) using QiMacros.

Results

Individual gun sales of 9,917,811 occurred in CA with a median monthly rate of 41,324 (range, 20,057-132,903). A median of 263 people lost their lives monthly from firearms (124 homicides, 128 suicides), totaling 53,975 fatalities from 1999 to 2015. Fifteen of 21 current deadliest mass shootings occurred during this study period with 40% from 2012 to 2015. Also, 36 school shootings occurred during the study (mean, 5 deaths; range, 0-33; 6 injuries; range, 0-23) with 31% in 2012 to 2015 at rate of 3 events/year versus 1.4 events/year in the 17 prior years (p < 0.05). Sales were generally consistent from 1996 to 2011 (except post-Columbine, Col). Starting in 2011, sales exceeded the 95% predicted upper control limit every single month. Before October 2011, there was no statistically significant sustained effect of mass shootings on sales (except Col); however, since a statistically significant proportional spike in sales occurred in the months immediately following every single deadliest mass shooting event. Every year since 2012, CA has strengthened gun laws in response to mass shootings yet sales have risen immediately preceding enactment of these laws each January.

Conclusion

Gun sales are more frequent since 2012, with an additional increase following both mass shootings and legislative changes enacted in response to these shootings.

Level of evidence

Epidemiology, level III.

Background

Payers have approached select complications as never events, yet there is rationale that achieving a zero incidence of these events is impractical. Prior 2005 National Trauma Data Bank (NTDB) analysis showed high rates (37%) of centers reporting no complications data making national estimates for determining standardized complication rates difficult to ascertain.

Methods

The 2008-2012 NTDB National Sample Program nationally weighted files were used to calculate yearly national estimates. Rates were compared in all centers and those reporting complications data. Hospital characteristics were compared using Student t test. In 2011, an other complication category was introduced; overall rates were calculated with and without this category. Yearly estimates were reported for patients receiving care within centers reporting complications data.

Results

From 2008-2012 NTDB, there were raw data on 3,657,884 patients. A total of 594,894 patients (16.3%) experienced one or more complications (82.7% one complication; 17.3% two or more complications). Excluding the other complication category, the overall weighted rate was 8.4% to 9.2%. Pneumonia was the most common complication (2.7-3.0%), occurring at twice the 2005 rate. The number of centers reporting no complications data dropped to 8.1% in 2011 (2008, 14.5%; 2009, 18.2%; 2010, 15.9%; 2012, 8.9%). By 2012, nearly all level I centers reported complications, whereas 46.4% of level IVs reported none (I 0.5%, II 2.7%, III 8.5%, p = 0.04). Data were reported the least frequently in nonteaching hospitals (15.8%, p = 0.007), those in the South (19.6%, p = 0.007), and those with less than 200 beds (23.6%, p = 0.005).

Conclusion

Overall rates of complications from 2008 to 2012 were nearly twofold higher than 2005 data. Reporting has increased, and NTDB may provide a valuable platform for establishing rational and achievable measures for specific complications.

Level of evidence

Prognostic and epidemiological, level IV.

Purpose

Troponin T levels are routinely checked in trauma patients after experiencing a ground-level fall to identify potential cardiac causes of syncope. An elevated initial troponin prompts serial testing until the level peaks. However, the high sensitivity of the test may lead to repeat testing that is of little clinical value. Here, we examine the role of serial troponins in predicting the need for further cardiac workup in trauma patients after sustaining a fall.

Methods

Retrospective review of all adult trauma activations for ground-level fall from January 1, 2021 to December 31, 2021 in patients who were hemodynamically and neurologically normal at presentation. Outcomes evaluated included need for cardiology consult, admission to cardiology service, outpatient cardiology follow-up, cardiology intervention and in-hospital mortality.

Results

There were 1555 trauma activations for ground-level fall in the study period. The cohort included 560 patients evaluated for a possible syncopal fall, hemodynamically stable, Glasgow Coma Scale score of 15, and with a troponin drawn at presentation. The initial median troponin was 20 ng/L (13-37). Second troponin values were drawn on 58% (median 33 ng/L (22-52)), with 42% of patients having an increase from first to second test. 29% of patients had a third troponin drawn (median 42 ng/L (26-67)). The initial troponin value was significantly associated with undergoing a subsequent echo (p=0.01), cardiology consult (p<0.01), admission for cardiac evaluation (p<0.01), cardiology follow-up (p<0.01), and in-hospital mortality (p=0.01); the initial troponin was not associated with cardiac intervention (p=0.91). An increase from the first to second troponin was not associated with any of outcomes of interest. Analysis was done with cut-off values of 30 ng/L, 50 ng/L, 70 ng/L, and 90 ng/L; a troponin T threshold of 19 ng/L was significant for cardiology consult (p=0.01) and cardiology follow-up (p=0.04). When the threshold was increased to 50 ng/L, it was also significant for admission for cardiac issue (p<0.01). When the threshold was increased to 90 ng/L, it was significant for the same three outcomes and in-hospital mortality (p=0.04).

Conclusion

The initial serum troponin has clinical value in identifying underlying cardiac disease in patients who present after ground-level fall; however, that serial testing is likely of little value. Further, using a cut-off of >50 ng/L as a threshold for further clinical evaluation would improve the utility of the test and likely reduce unnecessary hospital stays and costs for otherwise healthy patients.

Level of evidence

Level III.

BACKGROUND: On average, a person living in San Francisco can expect to live 83 years. This number conceals significant variation by sex, race, and place of residence. We examined deaths and area-based social factors by San Francisco neighborhood, hypothesizing that socially disadvantaged neighborhoods shoulder a disproportionate mortality burden across generations, especially deaths attributable to violence and chronic disease. These data will inform targeted interventions and guide further research into effective solutions for San Franciscos marginalized communities. STUDY DESIGN: The San Francisco Department of Public Health provided data for the 2010-2014 top 20 causes of premature death by San Francisco neighborhood. Population-level demographic data were obtained from the US American Community Survey 2015 5-year estimate (2011-2015). The primary outcome was the association between years of life loss (YLL) and adjusted years of life lost (AYLL) for the top 20 causes of death in San Francisco and select social factors by neighborhood via linear regression analysis and heatmaps. RESULTS: The top 20 causes accounted for N = 15,687 San Francisco resident deaths from 2010-2014. Eight neighborhoods (21.0%) accounted for 47.9% of city-wide YLLs, with 6 falling below the city-wide median household income and many having a higher percent population Black, and lower education and higher unemployment levels. For chronic diseases and homicides, AYLLs increased as a neighborhoods percent Black, below poverty level, unemployment, and below high school education increased. CONCLUSIONS: Our study highlights the mortality inequity burdening socially disadvantaged San Francisco neighborhoods, which align with areas subjected to historical discriminatory policies like redlining. These data emphasize the need to address past injustices and move toward equal access to wealth and health for all San Franciscans.

Objectives

Cell-free hemoglobin (CFH) is a potent mediator of endothelial dysfunction, organ injury, coagulopathy, and immunomodulation in hemolysis. These mechanisms have been demonstrated in patients with sepsis, hemoglobinopathies, and those receiving transfusions. However, less is known about the role of CFH in the pathophysiology of trauma, despite the release of equivalent levels of free hemoglobin.

Data sources

Ovid MEDLINE, Embase, Web of Science Core Collection, and BIOSIS Previews were searched up to January 21, 2023, using key terms related to free hemoglobin and trauma.

Data extraction

Two independent reviewers selected studies focused on hemolysis in trauma patients, hemoglobin breakdown products, hemoglobin-mediated injury in trauma, transfusion, sepsis, or therapeutics.

Data synthesis

Data from the selected studies and their references were synthesized into a narrative review.

Conclusions

Free hemoglobin likely plays a role in endothelial dysfunction, organ injury, coagulopathy, and immune dysfunction in polytrauma. This is a compelling area of investigation as multiple existing therapeutics effectively block these pathways.

Objective

The goal of predictive analytics monitoring is the early detection of patients at high risk of subacute potentially catastrophic illnesses. An excellent example of a targeted illness is respiratory failure leading to urgent unplanned intubation, where early detection might lead to interventions that improve patient outcomes. Previously, we identified signatures of this illness in the continuous cardiorespiratory monitoring data of intensive care unit (ICU) patients and devised algorithms to identify patients at rising risk. Here, we externally validated three logistic regression models to estimate the risk of emergency intubation developed in Medical and Surgical ICUs at the University of Virginia.

Approach

We calculated the model outputs for more than 8000 patients in the University of California-San Francisco ICUs, 240 of whom underwent emergency intubation as determined by individual chart review.

Main results

We found that the AUC of the models exceeded 0.75 in this external population, and that the risk rose appreciably over the 12 h before the event.

Significance

We conclude that there are generalizable physiological signatures of impending respiratory failure in the continuous cardiorespiratory monitoring data.

Background

Injury to the blood-brain barrier exposes endothelium rich in von Willebrand factor (vWF), which may play a role in altered platelet aggregation following traumatic brain injury (TBI). Ristocetin is an antimicrobial substance that induces vWF-mediated aggregation of platelets. We examined these mechanisms in injured patients by measuring the aggregation response of platelets to stimulating agonists (including ristocetin) via whole-blood multiple-electrode platelet aggregometry. We hypothesized that patients with TBI have an altered platelet aggregation response to ristocetin stimulation compared with patients without TBI.

Methods

Blood was collected from 233 trauma patients without thrombocytopenia. Platelet aggregation was assessed using multiple-electrode platelet aggregometry (Multiplate). Platelet aggregation response to stimulating agonists collagen, thrombin receptor-activating peptide 6, adenosine diphosphate, arachidonic acid, and ristocetin was measured. Factor activity was measured.

Results

Of the 233 patients, 23% had TBI. There were no differences in platelet aggregation responses to any agonists between TBI and non-TBI patients except ristocetin. Platelet aggregation response to ristocetin stimulation was significantly lower in TBI patients (p = 0.03). Patients with TBI also had higher factor VIII activity (215% vs. 156%, p = 0.01). In multivariate analysis, there was a significant independent association of impaired platelet aggregation response to ristocetin stimulation with TBI (odds ratio, 3.05; p = 0.04).

Conclusions

Given the importance of platelets in hemostasis, understanding the mechanisms of impaired platelet aggregation following injury is critical. The impaired platelet aggregation response to ristocetin stimulation and corresponding increase in factor VIII activity in TBI patients may be secondary to a TBI-induced effect on vWF quantity (due to injury-driven consumption of vWF) or vWF function with resultant increase in circulating factor VIII activity (due to impaired carrying capacity of vWF). Given there are multiple known therapies for vWF deficits including desmopressin, purified and recombinant vWF, and estrogens, these lines of investigation are particularly compelling in patients with TBI and hemorrhage.

Level of evidence

Prognostic study, level II.

Post-traumatic acute respiratory distress syndrome (ARDS) is associated with prolonged mechanical ventilation and longer hospitalizations. The relationship between post-traumatic ARDS severity and financial burden has not been previously studied. We hypothesized that increasing severity is associated with incrementally higher health care costs.Adults arriving as the highest level of trauma activation were enrolled in an ongoing prospective cohort study. Patients who survived ≥6 hours are included in the analysis. Blinded review of chest radiographs was performed by two independent physicians for any intubated patient with PaO2:FiO2 ratio (P/F) ≤300mgHg during the first 8 days of admission. The severity of ARDS was classified by the Berlin criteria. Hospital charge data was utilized to perform standard costing analysis.ARDS occurred in 13% (203/1586). The distribution of disease severity was 33% mild, 42% moderate, and 25% severe. Patients with ARDS were older (41 vs 35 years, p<0.01), had higher median ISS (30 vs 10, p<0.01), more chest injury (AIS≥3: 51% vs 21%, p<0.01), and blunt mechanisms (85% vs 53%, p<0.01). By ARDS severity, there was no significant difference in age, mechanism, or rate of traumatic brain injury. Increasing ARDS severity was associated with higher ISS and higher mortality rates. Standardized total hospital charges were four-fold higher for patients who developed ARDS compared to those who did not develop ARDS ($434K vs $96K, p<0.01). Furthermore, the daily hospital charges significantly increased across categories of worsening ARDS severity (mild $20,451; moderate $23,994; severe $33,316, p<0.01).The development of post-traumatic ARDS is associated with higher health care costs. Among trauma patients who develop ARDS, total hospital charges per day increase with worsening severity of disease. Prevention, early recognition, and treatment of ARDS after trauma are potentially important objectives for efforts to control health care costs in this population.IV STUDY TYPE: Economic and Value-based Evaluations.

Background

Impaired postinjury platelet aggregation is common, but the effect of transfusion on this remains unclear. Data suggest that following injury platelet transfusion may not correct impaired platelet aggregation, and impaired platelet aggregation may not predict the need for platelet transfusion. We sought to further investigate platelet aggregation responses to transfusions, using regression statistics to isolate the independent effects of transfusions given in discrete time intervals from injury on both immediate and longitudinal platelet aggregation. We hypothesized that platelet aggregation response to platelet transfusion increases over time from injury.

Methods

Serial (0-96 hours) blood samples were collected from 248 trauma patients. Platelet aggregation was assessed in vitro with impedance aggregometry stimulated by adenosine diphosphate, collagen, and thrombin receptor-activating peptide-6. Using regression, transfusion exposure was modeled against platelet aggregation at each subsequent timepoint and adjusted for confounders (Injury Severity Score, international normalized ratio (INR), base deficit, platelet count, and interval transfusions). The expected change in platelet aggregation at each timepoint under the intervention of transfusion exposure was calculated and compared with the observed platelet aggregation.

Results

The 248 patients analyzed were severely injured (Injury Severity Score, 21 ± 19), with normal platelet counts (mean, 268 × 10/L ± 90), and 62% were transfused in 24 hours. The independent effect of transfusions on subsequent platelet aggregation over time was modeled with observed platelet aggregation under hypothetical treatment of one unit transfusion of blood, plasma, or platelets. Platelet transfusions had increasing expected effects on subsequent platelet aggregation over time, with the maximal expected effect occurring late (4-5 days from injury).

Conclusion

Controversy exists on whether transfusions improve impaired postinjury platelet aggregation. Using regression modeling, we identified that expected transfusion effects on subsequent platelet aggregation are maximal with platelet transfusion given late after injury. This is critical for tailored resuscitation, identifying a potential early period of resistance to platelet transfusion that resolves by 96 hours.

Level of evidence

Therapeutic, level V.