Intimate Partner Violence and Pregnancy: Nationwide Analysis of Injury Patterns and Risk Factors.

BACKGROUND: Intimate partner violence (IPV) is a significant cause of injury, and in pregnant patients (PIPV) poses a risk to both mother and fetus. Characteristics and outcomes for PIPV patients have not been well described. We hypothesize that PIPV patients have higher admission rates and mortality than non-IPV pregnant trauma (PT) patients and nonpregnant female IPV patients of childbearing age. We also hypothesize differences exist between PIPV and PT patient injury patterns, allowing for targeted IPV screening. STUDY DESIGN: The Nationwide Emergency Department Sample database was queried from 2010 to 2014 to identify IPV in adult women patients by injury code E967.3. Patients were compared in 2 ways, PIPV vs PT and PIPV vs nonpregnant female IPV patients. Demographics, injury mechanisms, and National Trauma Data Standard injury diagnoses were surveyed. Primary outcomes were hospital admissions and mortality. Logistic regression was used to estimate risk factors of the outcomes of hospitalization and IPV victimization in pregnant injured patients. RESULTS: There were 556 PIPV patients, 73,970 PT patients, and 56,543 nonpregnant female IPV patients. When comparing PIPV to PT, more PIPV patients had Medicaid coverage or were self-pay. Suffocation, head injuries, face/neck/scalp contusions, multiple contusions, and abrasions/friction burns were more prevalent in PIPV patients. Mortality and hospital admissions were scarce among all cohorts. Predictors of IPV victimization among injured pregnant patients include multiple injuries, head injuries, face/neck/scalp contusions, abrasions/friction burns, contusions of multiple sites, and those with Medicaid or self-pay coverage. CONCLUSIONS: Among injured pregnant patients, those with multiple injuries, head injuries, contusions of the face/neck/scalp, abrasions/friction burns, and multiple contusions should undergo IPV screening. Admissions and mortality are low; therefore, prevention measures should be implemented in the emergency department to reduce repeat victimization.

Who's being left behind? Uninsured emergency general surgery admissions after the ACA.

BACKGROUND: The Affordable Care Act (ACA) increased Medicaid coverage of Emergency General Surgery (EGS). We hypothesized that despite the ACA, racial and geographic disparities persisted for EGS admissions. METHODS: The Nationwide Inpatient Sample was queried from 2012 through Q3 of 2015 for Non-Medicare patient EGS admissions. Difference-in-Differences analyses (DID) compared payors, complications, mortality and costs in pre-ACA years (2012-2013) and post-ACA years (2014-2015Q3). RESULTS: EGS cases fell 9.1% from 1,711,940 to 1,555,033 NIS-weighted cases. Hispanics were still most likely to be uninsured but had improved coverage (OR 0.92, 95% CI: 0.88-0.96, p < 0.001). Risk of uninsured EGS admissions from the South region persisted (OR 1.52, 95% CI: 1.46-1.58, p < 0.001). Uninsured EGS patients had higher DID increased mortality than insured patients (0.31% higher, P = 0.003). Insured group DID costs increased more rapidly than in self-pay Patients (6.0% higher, P = 0.008) CONCLUSIONS: Post ACA, risk of uninsured EGS admissions remained highest in the South, in males, and Hispanics.

Blunt versus penetrating trauma: Is there a resource intensity discrepancy?

BACKGROUND: The rising cost of healthcare requires responsible allocation of resources. Not all trauma centers see the same types of patients. We hypothesized that patients with blunt injuries require more resources than patients with penetrating injuries. METHODS: This was a retrospective analysis of all highest-level activation trauma patients at our busy urban Level I Trauma Center over five years. Data included demographics, injuries, hospital charges, and resources used. A p value < 0.05 was significant. RESULTS: 4578 patients were included (2037 blunt and 2541 penetrating). Blunt patients were more severely injured, more often admitted, required more radiographic studies, had longer hospital, intensive care unit, and mechanical ventilation days, and therefore, higher hospital charges. CONCLUSIONS: Within one center, patients with blunt injuries required more resources than those with penetrating injuries. Understanding this pattern will allow trauma systems to better allocate limited resources based on each center's mechanism of injury distribution.

Advanced atherosclerosis is associated with increased medial degeneration in sporadic ascending aortic aneurysms.

OBJECTIVE: The pathogenesis of non-familial, sporadic ascending aortic aneurysms (SAAA) is poorly understood, and the relationship between ascending aortic atherosclerosis and medial degeneration is unclear. We evaluated the prevalence and severity of aortic atherosclerosis and its association with medial degeneration in SAAA. METHODS AND RESULTS: Atherosclerosis was characterized in ascending aortic tissues collected from 68 SAAA patients (mean age, 62.9 ± 12.0 years) and 15 controls (mean age, 56.6 ± 11.4 years [P = 0.07]) by using a modified American Heart Association classification system. Upon histologic examination, 97% of SAAA patients and 73% of controls showed atherosclerotic changes. Most SAAA samples had intermediate (types 2 and 3, 35%) or advanced atherosclerosis (types ≥ 4; 40%), whereas most control samples showed minimal atherosclerosis (none or type 1, 80%; P < 0.001 after adjusting for age). In a separate analysis, we examined the total incidence and grade distribution of medial degenerative changes among SAAA samples according to atherosclerosis grade. Advanced atherosclerosis was associated with higher grades of smooth muscle cell depletion (P < 0.001), elastic fiber depletion (P = 0.02), elastic fiber fragmentation (P < 0.001), and mucopolysaccharide accumulation (P = 0.04). Aortic diameter was larger in SAAA patients with advanced atherosclerosis than in patients with minimal (P = 0.04) or intermediate atherosclerosis (P = 0.04). Immunostaining showed marked CD3+ T-cell and CD68+ macrophage infiltration, MMP-2 and MMP-9 production, and cryopyrin expression in the medial layer adjacent to atherosclerotic plaque. CONCLUSIONS: SAAA tissues exhibited advanced atherosclerosis that was associated with severe medial degeneration and increased aortic diameter. Our findings suggest a role for atherosclerosis in the progression of sporadic ascending aortic aneurysms.

ADAMTS-1 and ADAMTS-4 levels are elevated in thoracic aortic aneurysms and dissections.

BACKGROUND: ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) is a recently identified family of extracellular metalloproteinases that has been shown to participate in tissue destruction. We hypothesized that ADAMTS-1 and ADAMTS-4 expression is increased in aortic tissues from patients with thoracic aortic aneurysms and dissections. METHODS: We examined ADAMTS-1 and ADAMTS-4 expression in human descending thoracic aortic aneurysms (n = 14), chronic descending thoracic aortic dissections (n = 16), and descending thoracic aortas from age-matched control organ donors (n = 12). In these tissues, we also evaluated the degradation of versican, a proteoglycan substrate of ADAMTS-1 and ADAMTS-4. In cultured macrophages, we examined whether ADAMTS-4 functions in macrophage infiltration by using a transwell assay. RESULTS: ADAMTS-1 and ADAMTS-4 protein and mRNA expression was significantly higher in thoracic aortic aneurysm and dissection tissues than in control aortic tissues. Double immunofluorescence staining showed the expression of ADAMTS-1 and ADAMTS-4 in smooth muscle cells and macrophages. Consistent with the upregulation of ADAMTS-1 and ADAMTS-4 in thoracic aortic aneurysm and dissection tissues, versican was degraded significantly more in these tissues than in control aortic tissues. In cultured macrophages, transforming growth factor-ß increased ADAMTS-4 protein levels and induced macrophage invasion, and the knockdown of ADAMTS-4 reduced cell invasion. CONCLUSIONS: Increased expression of ADAMTS proteins may promote thoracic aortic aneurysm progression by degrading versican and facilitating macrophage invasion.