Trauma pancreaticoduodenectomy (TP) remains a challenging operation with morbidity and mortality rates as high as 80% and 50%. Many trauma surgeons consider it surgical dogma to avoid performing a TP during the index operation for patients with severe pancreatic or duodenal injuries. However, there is no modern analysis evaluating this belief. Therefore, we hypothesized no difference in risk of mortality between patients with severe pancreatic or duodenal injury undergoing a TP for penetrating trauma to propensity-matched controls undergoing laparotomy without TP. The Trauma Quality Improvement Program (2010-2016) was queried for adults with severe penetrating pancreatic or duodenal injuries undergoing laparotomy. A 1:2 propensity-matching including demographics/comorbidities, injury severity score, vitals on admission, Glasgow Coma Scale and concomitant injuries for laparotomy with or without TP was performed. Risk of mortality was reported using a univariable logistic regression model. Of 2182 patients with severe pancreatic or duodenal injuries undergoing laparotomy, 54 (2.5%) underwent TP and 2128 (97.5%) underwent laparotomy without TP. There were no differences in propensity-matching characteristics. Patients undergoing TP had a similar mortality rate (20.0% vs. 28.7%, p = 0.302) but a longer length of stay (LOS) (27.5 vs. 16.5 days, p = 0.017). The TP group had a similar associated risk of mortality (OR = 0.62, p = 0.302) but higher risk of major complications (OR 3.44, CI 1.35-17.47, p = 0.015). In appropriately selected penetrating trauma patients with severe pancreatic/duodenal injuries, TP is associated with a similar risk of mortality compared to laparotomy without TP. However, TP patients did have an increased associated risk of major complications and longer LOS.

Objectives

The Centers for Disease Control disclosed over 600,000 cases of child abuse or neglect in 2016. Single-institution studies have shown that nonaccidental trauma (NAT) has higher complication rates than accidental trauma (AT). Nonaccidental trauma is disproportionately represented in infants. We hypothesized that NAT would increase the risk of mortality in infants. This study aims to provide a contemporary descriptive analysis for infant trauma patients and determine the association between NAT and mortality.

Methods

Infants (<1 year of age) within the Pediatric Trauma Quality Improvement Program database (2014-2016) were identified. Descriptive statistics (χ2 and t test) were used to compare NAT infants to AT infants. A multivariable logistic regression was used to determine the risk of mortality associated with select variables including NAT.

Results

From 14,965 infant traumas, most presented to a level I pediatric trauma center (53.5%) with a median injury severity score of 9. The most common mechanism was falls (48.6%), followed by NAT (14.5%). Overall mortality was 2.1%. Although most NAT infants were white (60.2%), black infants were overrepresented (23.6% vs 18.3%; P < 0.0001) compared with AT infants. The incidence of mortality was higher in NAT infants (41.6% vs 13.9%; P < 0.0001), and they were more likely to have traumatic brain injury (TBI) (63.1% vs 50.6%; P < 0.001). Nonaccidental trauma [odds ratio (OR), 2.48; P < 0.001], hypotension within 24 hours (OR, 8.93; P < 0.001), injury severity score (OR, 1.12; P < 0.001), and severe abbreviated injury scale-head (OR 1.62, P = 0.014) had the highest association with mortality.

Conclusions

This study confirms the incidence of TBI and NAT in infants. Although providers should be vigilant for NAT, suspicion of NAT should prompt close surveillance, as there is a 2-fold increased risk of mortality independent of injury or TBI.

Objectives

Trauma patients undergoing damage-control surgery may have a planned return to the operating room. In contrast, little is known about unplanned returns to the operating room (uROR) in trauma. The aim of this study was to identify risk factors for uROR in trauma patients. It is hypothesized that blunt trauma patients with uROR have higher mortality when compared to penetrating trauma patients with uROR. Additionally, it is hypothesized that trauma patients with uROR after thoracotomy have higher mortality than patients with uROR after laparotomy.

Material and methods

A retrospective analysis of the National Trauma Data Bank from 2011-2015 including any adult patient with an uROR was performed.

Results

From 3.447.320 patients, 9.269 (0.2%) were identified to have uROR. In a multivariable logistic regression analysis, 27 independent predictors were identified for risk of uROR with the strongest independent risk factor being compartment syndrome (OR= 10.50, CI= 9.35-11.78, p <0.001). Blunt (compared to penetrating) mechanism was associated with higher risk for mortality in patents with uROR (OR= 1.69, CI= 1.14-2.51, p <0.001) as was re-incision thoracotomy (RT) compared to re-incision laparotomy (RL) (OR= 2.22, CI= 1.29-3.84, p <0.001).

Conclusion

The strongest risk factor for uROR in trauma is compartment syndrome. Both a blunt (compared to penetrating) mechanism and RT (compared to RL) are independent risk factors for mortality in patients undergoing an uROR.

Nephroptosis is a rare complication in renal transplantation, but one with significant associated risk. Due to non-specific clinical features, there may be a substantial delay in diagnosis and loss of the transplanted kidney due to renal pedicle thrombosis. We present a case of post-transplantation nephroptosis after simultaneous pancreas and kidney transplant, which resulted in accelerated hypertension and reversible acute kidney injury >1 year after transplantation. Prompt detection of this rare entity leading to expeditious surgical intervention is necessary to preserve viability of the renal allograft.

Background

Given the growing number of people worldwide living with human immunodeficiency virus (HIV), a larger subset of these patients are now susceptible to sustaining a traumatic injury. However, the impact of HIV on outcomes in trauma with modern antiretroviral treatment remains unclear. We hypothesized mortality and rates of infectious and inflammatory complications would be higher in HIV positive (HIV+) trauma patients.

Methods

The Trauma Quality Improvement Program was queried to identify trauma patients  ≥ 18 years of age with HIV. Due to the imbalance between HIV+ and HIV negative (HIV-) trauma patients, a 1:2 propensity-matched model was utilized. Matched variables included age, injury severity score, mechanism of injury, systolic blood pressure, pulse rate, Glasgow Coma Scale score, and patient comorbidities.

Results

84 HIV+ patients were matched to 168 HIV- patients. Compared to HIV- patients, HIV+ patients had no significant differences in mortality rate (9.5% vs. 4.8%, p = 0.144) or infectious complications, including pneumonia (6.0% vs. 4.2%, p = 0.530), urinary tract infection (1.2% vs. 1.2%, p = 1.000), or severe sepsis (1.2% vs. 0.0%, p = 0.156). However, higher rates of acute respiratory distress syndrome (ARDS) (9.5% vs. 0.6%, p < 0.001) and acute kidney injury (AKI) (4.8% vs. 0.0%, p = 0.004) were observed.

Conclusion

HIV+ trauma patients are not at higher risk of mortality or infectious complications, likely due to the advent and prevalence of combination antiretroviral therapy. However, HIV positivity appears to increase the risk of AKI and ARDS in trauma patients. Further research is needed to confirm this finding to elucidate the etiology underlying this association.

UNLABELLED: We have shown that KRAS-TP53 genomic coalteration is associated with immune-excluded microenvironments, chemoresistance, and poor survival in pancreatic ductal adenocarcinoma (PDAC) patients. By treating KRAS-TP53 cooperativity as a model for high-risk biology, we now identify cell-autonomous Cxcl1 as a key mediator of spatial T-cell restriction via interactions with CXCR2+ neutrophilic myeloid-derived suppressor cells in human PDAC using imaging mass cytometry. Silencing of cell-intrinsic Cxcl1 in LSL-KrasG12D/+;Trp53R172H/+;Pdx-1Cre/+(KPC) cells reprograms the trafficking and functional dynamics of neutrophils to overcome T-cell exclusion and controls tumor growth in a T cell-dependent manner. Mechanistically, neutrophil-derived TNF is a central regulator of this immunologic rewiring, instigating feed-forward Cxcl1 overproduction from tumor cells and cancer-associated fibroblasts (CAF), T-cell dysfunction, and inflammatory CAF polarization via transmembrane TNF-TNFR2 interactions. TNFR2 inhibition disrupts this circuitry and improves sensitivity to chemotherapy in vivo. Our results uncover cancer cell-neutrophil cross-talk in which context-dependent TNF signaling amplifies stromal inflammation and immune tolerance to promote therapeutic resistance in PDAC. SIGNIFICANCE: By decoding connections between high-risk tumor genotypes, cell-autonomous inflammatory programs, and myeloid-enriched/T cell-excluded contexts, we identify a novel role for neutrophil-derived TNF in sustaining immunosuppression and stromal inflammation in pancreatic tumor microenvironments. This work offers a conceptual framework by which targeting context-dependent TNF signaling may overcome hallmarks of chemoresistance in pancreatic cancer. This article is highlighted in the In This Issue feature, p. 1275.