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BACKGROUND: Emergency physicians commonly treat patients with atrial fibrillation (AF) or atrial flutter (AFL) with rapid ventricular response, and intravenous (IV) diltiazem is the most commonly used medication for rate control of such patients. We sought to compare rate control success and safety outcomes for emergency department (ED) patients with AF or AFL who, after a diltiazem bolus, received a diltiazem drip compared to those who did not receive a drip. METHODS: We performed a retrospective cohort study comparing outcomes of ED patients from a single hospital system with AF and AFL and a heart rate (HR) > 100 beats/min who received a diltiazem drip after an IV diltiazem bolus to those who received no drip. The primary outcome was a HR < 100 beats/min at the time of ED disposition. Secondary outcomes were hospital length of stay and safety (hypotension, electrical cardioversion, vasopressor use, and death). We compared groups using propensity score matching. RESULTS: Between January 1, 2020, and November 8, 2022, there were 746 AF or AFL patients eligible for analysis. Of those, 382 (51.2%) received a diltiazem drip and 364 (48.8%) did not. In the unadjusted analysis, the last recorded ED HR was <100 beats/min in 55.2% of patients in the drip group compared to 65.9% in the no-drip group (difference 10.7%, 95% confidence interval [CI] 3.7 to 17.7). After propensity matching, diltiazem drip use was associated with lower likelihood of rate control in the ED (OR 0.69, 95% CI 0.48-0.99) and 22.5 h (95% CI 12.2-36.8) longer hospital stay. CONCLUSIONS: For patients with AF or AFL, the use of a diltiazem drip after an IV diltiazem bolus was associated with less rate control in the ED.
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Aortoesophageal fistula is rare and typically presents itself to the emergency department as Chiari's Triad of mid-thoracic pain, sentinel arterial hemorrhage, and exsanguination after a symptom-free interval. However, fatal bleeding may be the first and last presentation of an aortoesophageal fistula. When a patient experiences massive hematemesis without witnesses, EMS may assume that bleed is of a traumatic mechanism. We present a case of a 59-year-old male with no previous medical history who was transported to a trauma center unconscious and with massive bleeding of unknown origin. Computed tomography revealed a thoracic aortic aneurysm and an aortoesophageal fistula. Bleeding was not controlled and the patient expired. Trauma bay personnel should follow an algorithm which includes a prompt tamponade of the bleed using a Sengstaken-Blakemore tube or esophageal balloon paralleled by massive transfusion and obtaining an early computed tomography scan to manage patients with massive gastroesophageal bleeding until appropriate surgical interventions can be initiated.
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Importance: Trauma centers must be readily equipped to handle a variety of life-threatening injuries and consequently may charge a fee for the activation of their trauma team. Regional and hospital-related variations in trauma activation fees across the US have not been formally assessed. Objective: To evaluate the variability of trauma activation fees from trauma centers across the US and examine whether certain hospital characteristics are associated with higher activation fees. Design, Setting, and Participants: This cross-sectional study used data from the American College of Surgeons website to identify all trauma centers in the US that were listed as verified from inception of the verification database through March 4, 2022 (N = 546). Five military hospitals were excluded, and trauma activation fees could not be found for 18 trauma centers; the remaining 523 hospitals were included in the analysis. Each hospital's publicly available chargemaster (a comprehensive list of a hospital's products, procedures, and services) was searched to obtain its trauma activation fees. Two levels of trauma activation fees were recorded: tier 1 (full activation) and tier 2 (partial activation). Hospital-specific data were obtained from the American Hospital Association website. All data were collected between January 2 and March 11, 2022. Linear regression analyses were performed to assess potential associations between hospital characteristics (type of control [for profit, government, church, or other nonprofit], hospital system [owner], number of staffed beds, and academic vs nonacademic status) and trauma activation fees. Main Outcomes and Measures: Median and mean trauma activation fees nationally and stratified by location, hospital system, and other hospital characteristics. Results: Of 523 trauma centers included in the analysis, most were located in the Midwest (180 centers) and West (129 centers). There were 176 adult level I trauma centers and 200 adult level II trauma centers; 69 centers had for-profit status, and 415 were academic. Overall, the median (IQR) tier 1 trauma activation fee was $9500 ($5601-$17 805), and the mean (SD) tier 1 trauma activation fee was $13 349 ($11 034); these fees ranged from $1000 to $61 734. Median (IQR) trauma activation fees were highest in the West ($18 099 [$10 741-$$27 607]), especially in California, where the median (IQR) activation fee was $24 057 ($15 979-$33 618). Trauma activation fees were also higher at for-profit hospitals, most of which were owned by the HCA Healthcare system, which had 43 trauma centers and a median (IQR) tier 1 trauma activation fee of $29 999 ($20 196-$37 589). Conclusions And Relevance: In this study, trauma activation fees varied widely among hospitals in the US. Regional variation in these fees was substantial, with hospitals in the West charging substantially more than those in other locations. In addition, for-profit hospitals charged more than other types of hospitals. These findings suggest that some patients with serious traumatic injuries will incur disproportionately high trauma activation fees depending on the trauma center to which they are brought. Therefore, standardization of trauma activation fees is warranted.
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Propriedade , Centros de Traumatologia , Adulto , Estados Unidos , Humanos , Estudos Transversais , Hospitais Privados , Honorários e PreçosRESUMO
Emerging evidence suggests that intratumoral interferon (IFN) signaling can trigger targetable vulnerabilities. A hallmark of pancreatic ductal adenocarcinoma (PDAC) is its extensively reprogrammed metabolic network, in which nicotinamide adenine dinucleotide (NAD) and its reduced form, NADH, are critical cofactors. Here, we show that IFN signaling, present in a subset of PDAC tumors, substantially lowers NAD(H) levels through up-regulating the expression of NAD-consuming enzymes PARP9, PARP10, and PARP14. Their individual contributions to this mechanism in PDAC have not been previously delineated. Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme in the NAD salvage pathway, a dominant source of NAD in cancer cells. We found that IFN-induced NAD consumption increased dependence upon NAMPT for its role in recycling NAM to salvage NAD pools, thus sensitizing PDAC cells to pharmacologic NAMPT inhibition. Their combination decreased PDAC cell proliferation and invasion in vitro and suppressed orthotopic tumor growth and liver metastases in vivo.