Purpose Hepatic arterioportal fistula (HAPF) is an uncommon complication of hepatic trauma, which can manifest with abdominal pain and the sequelae of portal hypertension months to years after injury. The purpose of this study is to present cases of HAPF from our busy urban trauma center and make recommendations for management. Methods One hundred and twenty-seven patients with high-grade penetrating liver injuries (American Association for the Surgery of Trauma [AAST] - Grades IV-V) between January 2019 and October 2022 were retrospectively reviewed. Five patients were identified with an acute hepatic arterioportal fistula following abdominal trauma from our ACS-verified adult Level 1 trauma center. Institutional experience with overall surgical management is described and reviewed with the current literature. Results Four of our patients presented in hemorrhagic shock requiring emergent operative intervention. The first patient had postoperative angiography and coil embolization of the HAPF. Patients 2 through 4 underwent damage control laparotomy with temporary abdominal closure followed by postoperative transarterial embolization with gelatin sponge particles (Gelfoam) or combined Gelfoam/n-butyl cyanoacrylate. The final patient went directly for angiography and Gelfoam embolization after identification of the HAPF. All 5 patients had resolution of HAPF on follow-up imaging with continued post management for traumatic injuries. Conclusion Hepatic arterioportal fistula can present as a complication of hepatic injury and manifest with significant hemodynamic aberrations. Although surgical intervention was required to achieve hemorrhage control in almost all cases, management of HAPF in the setting of high-grade liver injuries was achieved successfully with modern endovascular techniques. A multidisciplinary approach to such injuries is necessary to optimize care in the acute setting following traumatic injury.

3621 Background: Colorectal cancer is the second leading cause of cancer deaths in the world to affect both men and women. Racial disparities have been known to affect the disease diagnosis and progression, and proliferative genomic studies have been undertaken to elucidate their relationship. In this study, we investigate the tumor mutation profile in colorectal adenocarcinoma (COAD) based on genetic ancestry using The Cancer Genetic Ancestry Atlas (TCGAA). Methods: 59 AA (African American) individuals in TCGAA COAD dataset were identified. To account for and eliminate the biases introduced by self-identification of races, we utilized TCGAA genomic analysis to accurately estimate the ancestral genomic composition of each individual. For each individual, percentages of European (EA), West African (WA), East Asian (EAA), and Native American (NA) ancestry were identified based on Local Ancestry in adMixed Populations (LAMP). Individuals were screened for dominant WA ancestry (≥50% based on LAMP) and assigned to three groups, ≥90%, 80-89%, and 50-79%. Differences in gene mutation frequency and overall survival were compared among the three subgroups of individuals with WA ancestry. Results: Based on genomic ancestry analysis, 58 individuals with dominant WA ancestry (Range 53%-100%) were identified. We classified them into three groups based on percentage of WA ancestry: ≥90% (n = 17), 80-89% (n = 26), and 50-79% (n = 15). APC was the most frequently mutated gene in all groups except ≥90% WA ancestry, which had the most mutation frequency in TP53. ≥90% WA ancestry showed the highest rate of mutation of 81.3% in TP53 compared to 70.8% (80-90% WA ancestry) and 40.0% (50-79% WA ancestry). Interestingly, ≥90% WA ancestry had the highest average rate of mutation (33%) for 7 tumor suppressor genes ( AMER1, APC, ARID1, FBXW7, TCF7L2, TGFBR2, and TP53), compared to 29% and 22% in 80-89% WA ancestry and 50-79% WA ancestry, respectively. In addition, ≥90% WA ancestry had a lower rate (19%) of mutation in 6 oncogenes ( BRAF, NRAS, KRAS, PIK3CA, SMAD4, and SOX9) compared to 24% in both 80-89% and 50-79% WA ancestry. Although not statistically significant, a higher percentage of WA ancestry in an individual was correlated with a downward trend in the overall survival rate (median survival 56.3 months in ≥90% WA ancestry vs 61.8 months in 80-89% WA ancestry). Conclusions: In this study, we analyzed different gene mutations correlated with African ancestry and their potential relationship to the etiology, progression, and prognosis of COAD. The mutation profile of these genes will allow us to investigate altered pathways associated with African ancestry and draw insight into colon cancer pathogenesis in various ancestry groups. Further studies are warranted to elucidate the role of genetic ancestry in tumorigenesis and disease progression and to identify potential therapeutic targets specific to groups disproportionately affected by cancer.

Background: Racial and ethnic healthcare disparities contribute to significant morbidity, mortality, and healthcare costs in cardiovascular disease. As one of the primary reasons for emergency department (ED) presentation, rapid assessment of patients with chest pain is necessary to guide further intervention and disposition. However, even with continued efforts to achieve health equity and eliminate disparities, Hispanics continue to face significant barriers to healthcare. Our goal was to assess the characteristics, and disposition, of Hispanic patients presenting to the ED with chest pain to identify potential targets for intervention to improve healthcare delivery. Methods: Data was obtained from the electronic medical record warehouse of a large, safety-net, academic hospital from January to December 2020. Patients who presented to the emergency department with a chief complaint of “chest pain” were identified and medical records were reviewed. Bivariate analyses were performed to identify the relationship between Hispanic ethnicity and ED disposition. Results: Hispanic patients who presented with chest pain represented only 4.78% (530 of 11095). Hispanics were of younger age (43.4 vs 48.5) and had lower BP (128.8/77.8 vs 134.5/81.5), but were 2.93 times more likely to be uninsured (2.44-3.51, 95% CI, p<0.05). Hispanic females were 1.58 more likely to present with chest pain (1.32-1.88, 95% CI, p<0.05). Although Hispanics were admitted more often (17.74 vs 16.79%), overall disposition from the ED (admit to inpatient, observation, discharge) was 1.39 times longer for this ethnic group (99.0 vs 71.0 min, p<0.05). Disposition for admitted Hispanics took 1.98 times longer, (86.0 vs 43.5 min, p<0.05). Discussion: Our study suggests that Hispanics with chest pain may experience delays in triage and disposition from the ED. Contributing factors may be due to higher prevalence of undocumented status, lack of insurance, language barriers, and a lack of Hispanic providers who promote healthcare equity. Our next steps are to begin a focused educational program for residents to demonstrate that physician driven interventions are an effective way to promote the elimination of racial and ethnic healthcare disparities.