Delirium in trauma ICUs: a review of incidence, risk factors, outcomes, and management.

PURPOSE OF REVIEW: This article reviews the impact and importance of delirium on patients admitted to the ICU after trauma, including the latest work on prevention and treatment of this condition. As the population ages, the incidence of geriatric trauma will continue to increase with a concomitant rise in the patient and healthcare costs of delirium in this population. RECENT FINDINGS: Recent studies have further defined the risk factors for delirium in the trauma ICU patient population, as well as better demonstrated the poor outcomes associated with the diagnosis of delirium in these patients. Recent trials and meta-analysis offer some new evidence for the use of dexmedetomidine and quetiapine as preferred agents for prevention and treatment of delirium and add music interventions as a promising part of nonpharmacologic bundles. SUMMARY: Trauma patients requiring admission to the ICU are at significant risk of developing delirium, an acute neuropsychiatric disorder associated with increased healthcare costs and worse outcomes including increased mortality. Ideal methods for prevention and treatment of delirium are not well established, especially in this population, but recent research helps to clarify optimal prevention and treatment strategies.

Preperitoneal pelvic packing in isolated severe pelvic fractures is associated with higher mortality and venous thromboembolism: A matched-cohort study.

INTRODUCTION: Preperitoneal pelvic packing (PPP) has been advocated as a damage control procedure for pelvic fracture bleeding, despite of weak evidence. METHODS: Matched cohort study, TQIP database. Patients with isolated severe blunt pelvic fractures (pelvis abbreviated injury score [AIS] â€‹≥ â€‹3, AIS ≤2 in all other body regions) were included. Patients who underwent PPP were matched to patients with no PPP, 1:3 nearest propensity score. Matching was performed based on demographics, vital signs on admission, comorbidities, injury characteristics, type and timing of initiation of VTE prophylaxis, and additional procedures including laparotomy, REBOA, and angioembolization. RESULTS: 64 patients with PPP were matched with 182 patients with No-PPP. PPP patients had higher in-hospital mortality (14.1 â€‹% vs 2.2 â€‹% p â€‹< â€‹0.001) and higher rates of VTE and DVT (VTE: 14.1 â€‹% vs 4.4 â€‹% p â€‹= â€‹0.018, DVT: 10.9 â€‹% vs 2.2 â€‹% p â€‹= â€‹0.008). CONCLUSION: PPP is associated with worse survival outcomes and increased rate of VTE and DVT complications.

Precious cargo: Modulation of the mesenteric lymph exosome payload after hemorrhagic shock.

BACKGROUND: Trauma/hemorrhagic shock (T/HS) causes a release of proinflammatory mediators into the mesenteric lymph (ML) that may trigger a systemic inflammatory response and subsequent organ failure. Recently, we showed that exosomes in postshock ML are biologically active mediators of this inflammation. Because the specific inflammatory mediators in postshock ML exosomes have yet to be characterized, we hypothesized that T/HS would lead to a distinct ML proinflammatory exosome phenotype that could be identified by proteomic analysis. We further hypothesized that their regulation by the neuroenteric axis via the vagus nerve would modify this proinflammatory profile. METHODS: Male rats underwent an established T/HS model including 60 minutes of HS followed by resuscitation. Mesenteric lymph was collected before HS (preshock) and after resuscitation (postshock). A subset of animals underwent cervical vagus nerve electrical stimulation (VNS) after the HS phase. Liquid chromatography with tandem mass spectroscopy (LC-MS/MS) followed by protein identification, label free quantification, and bioinformatic analysis was performed on exosomes from the pre-shock and post-shock phases in the T/HS and T/HS + vagus nerve electrical stimulation groups. Biological activity of exosomes was evaluated using a monocyte nuclear factor kappa B (NF-κB) activity assay. RESULTS: ML exosomes express a distinct protein profile after T/HS with enrichment in pathways associated with cell signaling, cell death and survival, and the inflammatory response. Stimulation of the vagus nerve following injury attenuated the transition of ML exosomes to this T/HS-induced inflammatory phenotype with protein expression remaining similar to pre-shock. Monocyte NF-κB activity was increased after exposure to ML exosomes harvested after T/HS, while ML exosomes from preshock had no effect on monocyte NF-κB expression. CONCLUSION: Postshock ML exosomes carry a distinct, proinflammatory protein cargo. Stimulating the vagus nerve prevents the T/HS-induced changes in ML exosome protein payload and suggests a novel mechanism by which the neuroenteric axis may limit the systemic inflammatory response after injury.

AMPK regulates the circadian clock by cryptochrome phosphorylation and degradation.

Circadian clocks coordinate behavioral and physiological processes with daily light-dark cycles by driving rhythmic transcription of thousands of genes. Whereas the master clock in the brain is set by light, pacemakers in peripheral organs, such as the liver, are reset by food availability, although the setting, or "entrainment," mechanisms remain mysterious. Studying mouse fibroblasts, we demonstrated that the nutrient-responsive adenosine monophosphate-activated protein kinase (AMPK) phosphorylates and destabilizes the clock component cryptochrome 1 (CRY1). In mouse livers, AMPK activity and nuclear localization were rhythmic and inversely correlated with CRY1 nuclear protein abundance. Stimulation of AMPK destabilized cryptochromes and altered circadian rhythms, and mice in which the AMPK pathway was genetically disrupted showed alterations in peripheral clocks. Thus, phosphorylation by AMPK enables cryptochrome to transduce nutrient signals to circadian clocks in mammalian peripheral organs.