Gastrojejunal Fistula Following Gastrostomy Tube.

Gastrostomy tubes are often placed in patients with poor voluntary intake, oropharyngeal dysphagia, or chronic illness to provide definitive nutritional access. Despite the widespread use of gastrostomy tubes, some patients can experience complications associated with this procedure including gastrocolic-cutaneous fistula and dislodgement of gastrostomy tube. This case discusses an instance of gastrojejunal fistula formation over one year after gastrostomy tube placement likely due to tube dislodgement. Imaging showed gastrostomy tube traversing the posterior wall of the stomach and creating a fistula into the jejunum, with the balloon inflated within the jejunum. Gastrostomy tube was removed and replaced, with gastrostomy tube study showing no extravasation of contrast. Patient is now doing well-tolerating tube feeds at goal.

Racial, Gender, and Neighborhood-Level Disparities in Pediatric Trauma Care.

BACKGROUND: Disparities in trauma outcomes and care are well established for adults, but the extent to which similar disparities are observed in pediatric trauma patients requires further investigation. The objective of this study was to evaluate the unique contributions of social determinants (race, gender, insurance status, community distress, rurality/urbanicity) on trauma outcomes after controlling for specific injury-related risk factors. STUDY DESIGN: All pediatric (age < 18) trauma patients admitted to a single level 1 trauma center with a statewide, largely rural, catchment area from January 2010 to December 2020 were retrospectively reviewed (n = 14,398). Primary outcomes were receipt of opioids in the emergency department, post-discharge rehabilitation referrals, and mortality. Multivariate logistic regressions evaluated demographic, socioeconomic, and injury characteristics. Multilevel logistic regressions evaluated area-level indicators, which were derived from abstracted home addresses. RESULTS: Analyses adjusting for demographic and injury characteristics revealed that Black children (n = 6255) had significantly lower odds (OR = 0.87) of being prescribed opioid medications in the emergency department compared to White children (n = 5883). Children living in more distressed and rural communities had greater odds of receiving opioid medications. Girls had significantly lower odds (OR = 0.61) of being referred for rehabilitation services than boys. Post hoc analyses revealed that Black girls had the lowest odds of receiving rehabilitation referrals compared to Black boys and White children. CONCLUSION: Results highlight the need to examine both main and interactive effects of social determinants on trauma care and outcomes. Findings reinforce and expand into the pediatric population the growing notion that traumatic injury care is not immune to disparities.

Acquired Factor XIII Deficiency in a 19-year-Old Male Following Ballistic Injury.

Factor XIII deficiency is a rare cause of post-operative bleeding. It poses a diagnostic challenge as standard coagulation tests including prothrombin time, international normalized ratio, and activated partial thromboplastin time are usually normal in factor XIII deficiency. We present the case of our patient, a 19-year-old male with acquired factor XIII deficiency diagnosed after ballistic injury with a post-operative course complicated by hemorrhage. This case demonstrates an uncommon cause of coagulopathy, acquired factor XIII deficiency, and the challenges it poses to post-operative management. The diagnosis of acquired factor XIII deficiency may be challenging, but a high clinical suspicion is imperative to avoid a missed diagnosis and delayed treatment.

Social determinants of trauma care: Associations of race, insurance status, and place on opioid prescriptions, postdischarge referrals, and mortality.

BACKGROUND: Racial disparities in trauma care have been reported for a range of outcomes, but the extent to which these remain after accounting for socioeconomic and environmental factors remains unclear. The objective of this study was to evaluate the unique contributions of race, health insurance, community distress, and rurality/urbanicity on trauma outcomes after carefully controlling for specific injury-related risk factors. METHODS: All adult (age, ≥18 years) trauma patients admitted to a single Level I trauma center with a statewide, largely rural, catchment area from January 2010 to December 2020 were retrospectively reviewed. Primary outcomes were mortality, rehabilitation referral, and receipt of opioids in the emergency department. Demographic, socioeconomic, and injury characteristics as well as indicators of community distress and rurality based on home address were abstracted from a trauma registry database. RESULTS: Analyses revealed that Black patients (n = 13,073) were younger, more likely to be male, more likely to suffer penetrating injuries, and more likely to suffer assault-based injuries compared with White patients (n = 10,946; all p < 0.001). In adjusted analysis, insured patients had a 28% lower risk of mortality (odds ratio, 0.72; p = 0.005) and were 92% more likely to be referred for postdischarge rehabilitation than uninsured patients (odds ratio, 1.92; p = 0.005). Neither race- nor place-based factors were associated with mortality. However, post hoc analyses revealed a significant race by age interaction, with Black patients exhibiting more pronounced increases in mortality risk with increasing age. CONCLUSION: The present findings help disentangle the social determinants of trauma disparities by adjusting for place and person characteristics. Uninsured patients were more likely to die and those who survived were less likely to receive referrals for rehabilitation services. The expected racial disparity in mortality risk favoring White patients emerged in middle age and was more pronounced for older patients. LEVEL OF EVIDENCE: Prognostic and epidemiological, Level III.

Application of the modified Nutrition Risk in Critically Ill score to nutritional risk stratification of trauma victims: A multicenter observational study.

BACKGROUND: The modified Nutrition Risk in Critically Ill (mNUTRIC) score was developed to identify patients most likely to benefit from nutritional therapies and to stratify or select study subjects for clinical trials. The score is not validated in trauma victims in whom adequate nutritional support is important and difficult to achieve. We sought to determine whether a higher mNUTRIC score was associated with worse outcomes and whether caloric and protein intake improved outcome more in patients classified as high risk relative to those classified as low risk. METHODS: We analyzed a prospectively collected database of patients from intensive care units globally. The primary outcome was 60-day hospital mortality, and the secondary outcome was time to discharge alive. We compared outcomes between high and low mNUTRIC score groups and also tested whether the association between outcome and nutrition intake was modified by the mNUTRIC score. RESULTS: A total of 771 trauma patients were included. Most (585; 76%) had a low-risk mNUTRIC (0-4) score, and 186 (24%) had a high-risk (5-9) mNUTRIC score. The overall 60-day mortality was 13%. Patients in the high mNUTRIC group had a higher risk of death than those in the low mNUTRIC group (adjusted odds ratio, 2.6; 95% confidence interval, 1.7-4.2). Overall, there was no relationship between caloric or protein intake and clinical outcomes. However, patients in the high mNUTRIC group fared better with increasing caloric and protein intake, whereas subjects in the low mNUTRIC score group did not (p values for interaction with the mNUTRIC score for time to discharge alive was p = 0.014 for calories and was p = 0.004 for protein). CONCLUSION: A high mNUTRIC score identifies trauma patients at higher risk for poor outcomes and those who may benefit from higher caloric and protein intake. LEVEL OF EVIDENCE: Epidemiological/Prognostic, level III.

Ventilator-associated events, not ventilator-associated pneumonia, is associated with higher mortality in trauma patients.

BACKGROUND: Ventilator-associated events (VAE), using objective diagnostic criteria, are the preferred quality indicator for patients requiring mechanical ventilation (MV) for greater than 48 hours. We aim to identify the occurrence of VAE in our trauma population, the impact on survival, and length of stay, as compared to the traditional definition of ventilator-associated pneumonia (VAP). METHODS: This retrospective review included adult trauma patients, who were Washington residents, admitted between 2012 and 2017, and required at least 3 days of MV. Exclusions included patients with Abbreviated Injury Scale head score greater than 4 and burn related mechanisms of injury. We matched trauma registry data with our institutional, physician-adjudicated, and culture-confirmed ventilator event database. We compared the clinical outcomes of ventilator-free days, intensive care unit length of stay, hospital length of stay, and likelihood of death between VAE and VAP. RESULTS: One thousand five hundred thirty-three trauma patients met criteria; 124 (8.1%) patients developed VAE, 114 (7.4%) patients developed VAP, and 63 (4.1%) patients met criteria for both VAE and VAP. After adjusted analyses, patients with VAE were more likely to die (hazard ratio [HR], 2.86; 95% confidence interval [CI], 1.44-5.68), than those with VAP, as well those patients with neither diagnosis (HR, 2.83; 95% CI, 1.83-4.38). Patients with VAP were no more likely to die (HR, 1.55; 95% CI, 0.91-2.68) than those with neither diagnosis. Patients with VAE had fewer ventilator-free days than those with VAP (HR, -2.71; 95% CI, -4.74 to -0.68). CONCLUSION: Critically injured trauma patients who develop VAE are three times more likely to die and utilize almost 3 days more MV than those that develop VAP. The objective criteria of VAE make it a promising indicator on which quality indicator efforts should be focused. Future studies should be aimed at identification of modifiable risk factors for VAE and their impact on outcome, as these patients are at high risk for death. LEVEL OF EVIDENCE: Retrospective cohort study, level III.

Thrombospondin-1-induced vascular smooth muscle cell migration and proliferation are functionally dependent on microRNA-21.

OBJECTIVES: Thrombospondin-1 (TSP-1) is a matricellular glycoprotein released from platelets at sites of arterial injury and is important in neointima development after balloon angioplasty. MicroRNAs are small noncoding RNAs that function by binding target gene mRNA and inhibiting protein translation. MicroRNA-21 (miR-21) is up-regulated after angioplasty, and inhibition of miR-21 leads to decreased intimal hyperplasia. In this study, we examined the effects of miR-21 inhibition on vascular smooth muscle cell (VSMC) processes. METHODS: VSMCs were exposed to TSP-1 and miR-21 inhibitor for 20 minutes. TSP-1-induced migration was assessed with a modified Boyden microchemotaxis chamber and proliferation with calcein-AM fluorescence. Phosphorylated extracellular signaling kinase (ERK) 1/2 expression was determined by Western Blot and densitometry. Quantitative real-time polymerase chain reaction for TSP-1, hyaluronic acid synthase 2 (HAS2), and transforming growth factor beta 2 (TGFß2) was performed. Statistical analysis was performed with analysis of variance (P < .05). RESULTS: Inhibition of miR-21 blocked TSP-1-induced VSMC migration, proliferation, and ERK 1/2 phosphorylation (P < .05) and had no effect on TSP-1-stimulated expression of genes for TSP-1, HAS2, or TGFß2 (P > .05). CONCLUSION: Acute inhibition of miR-21 led to a decrease in VSMC migration and proliferation caused by TSP-1. The decrease in TSP-1's activation of ERK 1/2 after acute miR-21 inhibition indicates an active role for miR-21 in TSP-1's cell signaling cascade. No effect on TSP-1-induced expression of the pro-stenotic genes thbs1, tgfb2, or has2, occurred after acute miR-21 inhibition. These data indicate that miR-21 directly modulates cell function and signaling pathways in ways other than inhibition of protein translation.

Thrombospondin-1-induced smooth muscle cell chemotaxis and proliferation are dependent on transforming growth factor-ß2 and hyaluronic acid synthase.

Angioplasty causes local vascular injury, leading to the release of thrombospondin-1 (TSP-1), which stimulates vascular smooth muscle cell (VSMC) migration and proliferation, important steps in the development of intimal hyperplasia. Transforming growth factor beta 2 (TGF-ß2) and hyaluronic acid synthase (HAS) are two pro-stenotic genes upregulated in VSMCs by TSP-1. We hypothesized that inhibition of TGF-ß2 or HAS would inhibit TSP-1-induced VSMC migration, proliferation, and TSP-1 signaling. Our data demonstrate that Inhibition of either TGF-ß2 or HAS inhibited TSP-1-induced VSMC migration and proliferation. Activation of ERK 1 was decreased by TGF-ß2 inhibition and unaffected by HAS inhibition. TGF-ß2 and HAS are not implicated in TSP-1-induced thbs1 expression, while they are each implicated in TSP-1-induced expression of their own gene. In summary, TSP-1-induced VSMC migration and proliferation rely on intact TGF-ß2 signaling and HAS function. TSP-1 activation of ERK 1 is dependent on TGF-ß2. These data further expand our understanding of the complexity of TSP-1 cellular signaling and the involvement of TGF-ß2 and HAS.