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Background Trauma leads to a complex inflammatory cascade that induces both immune activation and a refractory immune state in parallel. Although both components are deemed necessary for recovery, the balance is tight and easily lost. Losing the balance can lead to life-threatening infectious complications as well as long-term immunosuppression with recurrent infections. Neutrophils are known to play a key role in these processes. Therefore, this review focuses on neutrophil characteristics and function after trauma and how these features can be used to identify trauma patients at risk for infectious complications. Results Distinct neutrophil subtypes exist that play their own role in the recovery and/or development of infectious complications after trauma. Furthermore, the refractory immune state is related to the risk of infectious complications. These findings change the initial concepts of the immune response after trauma and give rise to new biomarkers for monitoring and predicting inflammatory complications in severely injured patients. Conclusion For early recognition of patients at risk, the immune system should be monitored. Several neutrophil biomarkers show promising results and analysis of these markers has become accessible to such extent that they can be used for point-of-care decision making after trauma.

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Nowadays, more trauma patients develop chronic critical illness (CCI), a state characterized by prolonged intensive care. Some of these CCI patients have disproportional difficulties to recover and suffer from recurrent infections, a syndrome described as the persistent inflammation, immunosuppression and catabolism syndrome (PICS). A total of 78 trauma patients with an ICU stay of ≥14 days (CCI patients) between 2007 and 2017 were retrospectively included. Within this group, PICS patients were identified through two ways: (1) their clinical course (≥3 infectious complications) and (2) by laboratory markers suggested in the literature (C-reactive protein (CRP) and lymphocytes), both in combination with evidence of increased catabolism. The incidence of PICS was 4.7 per 1000 multitrauma patients. The sensitivity and specificity of the laboratory markers was 44% and 73%, respectively. PICS patients had a longer hospital stay (median 83 vs. 40, p < 0.001) and required significantly more surgical interventions (median 13 vs. 3, p = 0.003) than other CCI patients. Thirteen PICS patients developed sepsis (72%) and 12 (67%) were readmitted at least once due to an infection. In conclusion, patients who develop PICS experience recurrent infectious complications that lead to prolonged hospitalization, many surgical procedures and frequent readmissions. Therefore, PICS forms a substantial burden on the patient and the hospital, despite its low incidence.

At homeostasis the vast majority of neutrophils in the circulation expresses CD16 and CD62L within a narrow expression range, but this quickly changes in disease. Little is known regarding the changes in kinetics of neutrophils phenotypes in inflammatory conditions. During acute inflammation more heterogeneity was found, characterized by an increase in CD16dim banded neutrophils. These cells were probably released from the bone marrow (left shift). Acute inflammation induced by human experimental endotoxemia (LPS model) was additionally accompanied by an immediate increase in a CD62Llow neutrophil population, which was not as explicit after injury/trauma induced acute inflammation. The situation in sub-acute inflammation was more complex. CD62Llow neutrophils appeared in the peripheral blood several days (&gt;3 days) after trauma with a peak after 10 days. A similar situation was found in the blood of COVID-19 patients returning from the ICU. Sorted CD16low and CD62Llow subsets from trauma and COVID-19 patients displayed the same nuclear characteristics as found after experimental endotoxemia. In diseases associated with chronic inflammation (stable COPD and treatment naive HIV) no increases in CD16low or CD62Llow neutrophils were found in the peripheral blood. All neutrophil subsets were present in the bone marrow during homeostasis. After LPS rechallenge, these subsets failed to appear in the circulation, but continued to be present in the bone marrow, suggesting the absence of recruitment signals. Because the subsets were reported to have different functionalities, these results on the kinetics of neutrophil subsets in a range of inflammatory conditions contribute to our understanding on the role of neutrophils in health and disease.

Coronavirus disease 2019 (COVID‐19) is a rapidly emerging pandemic disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). Critical COVID‐19 is thought to be associated with a hyper‐inflammatory process that can develop into acute respiratory distress syndrome, a critical disease normally mediated by dysfunctional neutrophils. This study tested the hypothesis whether the neutrophil compartment displays characteristics of hyperinflammation in COVID‐19 patients. Therefore, a prospective study was performed on all patients with suspected COVID‐19 presenting at the emergency room of a large academic hospital. Blood drawn within 2 d after hospital presentation was analyzed by point‐of‐care automated flow cytometry and compared with blood samples collected at later time points. COVID‐19 patients did not exhibit neutrophilia or eosinopenia. Unexpectedly neutrophil activation markers (CD11b, CD16, CD10, and CD62L) did not differ between COVID‐19‐positive patients and COVID‐19‐negative patients diagnosed with other bacterial/viral infections, or between COVID‐19 severity groups. In all patients, a decrease was found in the neutrophil maturation markers indicating an inflammation‐induced left shift of the neutrophil compartment. In COVID‐19 this was associated with disease severity.

BackgroundNonoperative management for blunt splenic injury is the preferred treatment. To improve the outcome of selective nonoperative therapy, the current challenge is to identify factors that predict failure. Little is known about the impact of concomitant injury on outcome. Our study has two goals. First, to determine whether concomitant injury affects the safety of selective nonoperative treatment. Secondly we aimed to identify factors that can predict failure.MethodsFrom our prospective trauma registry we selected all nonoperatively treated adult patients with blunt splenic trauma admitted between 01.01.2000 and 12.21.2013. All concurrent injuries with an AIS ≥ 2 were scored. We grouped and compared patients sustaining solitary splenic injuries and patients with concomitant injuries. To identify specific factors that predict failure we used a multivariable regression analysis.ResultsA total of 79 patients were included. Failure of nonoperative therapy (n = 11) and complications only occurred in patients sustaining concomitant injury. Furthermore, ICU-stay as well as hospitalization time were significantly prolonged in the presence of associated injury (4 versus 13 days,p < 0.05). Mortality was not seen. Multivariable analysis revealed the presence of a femur fracture and higher age as predictors of failure.ConclusionsNonoperative management for hemodynamically normal patients with blunt splenic injury is feasible and safe, even in the presence of concurrent (non-hollow organ) injuries or a contrast blush on CT. However, associated injuries are related to prolonged intensive care unit- and hospital stay, complications, and failure of nonoperative management. Specifically, higher age and the presence of a femur fracture are predictors of failure.

BackgroundSelective non-operative management (NOM) for the treatment of blunt splenic trauma is safe. Currently, the feasibility of selective NOM for penetrating splenic injury (PSI) is unclear. Unfortunately, little is known about the success rate of spleen-preserving surgical procedures. The aim of this study was to investigate the outcome of selective NOM for penetrating splenic injuries.MethodsA dual-centre study is performed in two level-one trauma centres. All identified patients treated for PSI were identified. Patients were grouped based on the treatment they received. Group one consisted of splenectomised patients, the second group included patients treated by a spleen-preserving surgical intervention, and group three included those patients who were treated by NOM.ResultsA total of 118 patients with a median age of 27 and a median ISS of 25 (interquartile range (IQR) 16–34) were included. Ninety-six patients required operative intervention, of whom 45 underwent a total splenectomy and 51 underwent spleen-preserving surgical procedures. Furthermore, 22 patients (12 stab wounds and 10 gunshot wounds) were treated by NOM. There were several anticipated significant differences in the baseline encountered. The median hospitalization time was 8 (5–12) days, with no significant differences between the groups. The splenectomy group had significantly more intensive care unit (ICU) days (2(0–6) vs. 0(0–1)) and ventilation days (1(0–3) vs. 0(0–0)) compared to the NOM group. Mortality was only noted in the splenectomy group.ConclusionsSpleen-preserving surgical therapy for PSI is a feasible treatment modality and is not associated with increased mortality. Moreover, a select group of patients can be treated without any surgical intervention at all.