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Abstract Background Severe chest wall injuries are potentially life-threatening injuries which require a standardized multidisciplinary management strategy for prevention of posttraumatic complications and adverse outcome. Case presentation We report the successful management of a 55-year old man who sustained a complete “bony disruption” of the thoracic cage secondary to an “all-terrain vehicle” roll-over accident. The injury pattern consisted of a bilateral “flail chest” with serial segmental rib fractures, bilateral hemo-pneumothoraces and pulmonary contusions, bilateral midshaft clavicle fractures, a displaced transverse sternum fracture with significant diastasis, and an unstable T9 hyperextension injury. After initial life-saving procedures, the chest wall injuries were sequentially stabilized by surgical fixation of bilateral clavicle fractures, locked plating of the displaced sternal fracture, and a two-level anterior spine fixation of the T9 hyperextension injury. The patient had an excellent radiological and physiological outcome at 6 months post injury. Conclusion Severe chest wall trauma with a complete “bony disruption” of the thoracic cage represents a rare, but detrimental injury pattern. Multidisciplinary management with a staged timing for addressing each of the critical injuries, represents the ideal approach for an excellent long-term outcome.

Abstract Experiments show that upon traumatic injury the composition of mesenteric lymph changes such that it initiates an immune response that can ultimately result in multiple organ dysfunction syndrome (MODS). To identify candidate protein mediators of this process we carried out a quantitative proteomic study on mesenteric lymph from a well characterized rat shock model. We analyzed three animals using analytical 2D differential gel electrophoresis. Intra-animal variation for the majority of protein spots was minor. Functional clustering of proteins revealed changes arising from several global classes that give novel insight into fundamental mechanisms of MODS. Mass spectrometry based proteomic analysis of proteins in mesenteric lymph can effectively be used to identify candidate mediators and loss of protective agents in shock models.

Background Temporary abdominal closure (TAC) may be performed for cirrhotic patients undergoing emergent laparotomy. The effects of cirrhosis on physiologic parameters, resuscitation requirements, and outcomes following TAC are unknown. We hypothesized that cirrhotic TAC patients would have different resuscitation requirements and worse outcomes than noncirrhotic patients. Methods We performed a 3-year retrospective cohort analysis of 231 patients managed with TAC following emergent laparotomy for sepsis, trauma, or abdominal compartment syndrome. All patients were initially managed with negative pressure wound therapy (NPWT) TAC with intention for planned relaparotomy and sequential abdominal closure attempts at 24- to 48-h intervals. Results At presentation, cirrhotic patients had higher incidence of acidosis (33% versus 17%) and coagulopathy (87% versus 54%) than noncirrhotic patients. Forty-eight hours after presentation, cirrhotic patients had a persistently higher incidence of coagulopathy (77% versus 44%) despite receiving more fresh frozen plasma (10.8 units versus 4.4 units). Cirrhotic patients had higher NPWT output (4427 mL versus 2375 mL) and developed higher vasopressor infusion rates (57% versus 29%). Cirrhotic patients had fewer intensive care unit-free days (2.3 versus 7.6 days) and higher rates of multiple organ failure (64% versus 34%), in-hospital mortality (67% versus 21%), and long-term mortality (80% versus 34%) than noncirrhotic patients. Conclusions Cirrhotic patients managed with TAC are susceptible to early acidosis, persistent coagulopathy, large NPWT fluid losses, prolonged vasopressor requirements, multiple organ failure, and early mortality. Future research should seek to determine whether TAC provides an advantage over primary fascial closure for cirrhotic patients undergoing emergency laparotomy. [ABSTRACT FROM AUTHOR]

Mesenteric lymph is the mechanistic link between splanchnic hypoperfusion and acute lung injury (ALL), but the culprit mediator(s) remains elusive. Previous work has shown that administration of a phospholipase A2 (PLA2) inhibitor attenuated postshock ALT and also identified a non-ionic lipid within the postshock mesenteric lymph (PSML) responsible for polymorphonuclear neutrophil (PMN) priming. Consequently, we hypothesized that gut-derived leukotriene B4 (LTB4) is a key mediator in the pathogenesis of ALT. Trauma/hemorrhagic shock (TIHS) was induced in male Sprague-Dawley rats and the mesenteric duct cannu- lated for lymph collection/diversion. PSML, arachidonic acid (AA), and a LTB4 receptor antagonist were added to PMNs in vitro. LCIMSIMS was employed to identify bioactive lipids in PSML and the lungs. TIHS increased AA in PSML and increased LTB4 and PMNs in the lung. Lymph diversion decreased lung LTB4 by 75% and PMNs by 40%. PSML stimulated PMN priming (11.56 ± 1.25 vs. 3.95 ± 0.29 nmol O,2~/min; 3.75 X iO~ cells/mi; P < 0.01) that was attenuated by LTB4 receptor blockade (2.64 ± 0.58; P < 0.01). AA stimulated PMNs to produce LTB4, and AA-induced PMN priming was attenuated by LTB4 receptor antagonism. Collectively, these data indicate that splanchnic ischemia/reperfusion activates gut PLA2-mediated release of AA into the lymph where it is delivered to the lungs, provoking LTB4 production and subsequent PMN-mediated lung injury. [ABSTRACT FROM AUTHOR]

Background: Gelsolin is a plasma protein that functions to depolymerize actin filaments preventing capillary plug formation following tissue injury. It also functions to mediate the inflammatory response by binding proinflammatory lipids such as lysophosphatidic acid, sphingosine-1-phosphate and phosphoinositides. Clinically, reduced gelsolin concentrations have been associated with increased mortality in critically ill, trauma, and burn patients. We have previously shown that following hemorrhagic shock with splanchnic hypoperfusion, mesenteric lymph contains lipid components that cause neutrophil and EC activation and that protein concentrations are severely diluted due to resuscitation. We hypothesized that lipid binding proteins such as gelsolin may be depleted after trauma/hemorrhagic shock leading to increased lipid bioactivity. Methods: Shock was induced in SD rats by controlled hemorrhage and the mesenteric duct cannulated for lymph collection. Resuscitation was performed by infusing 2× SB volume in NS over 30 min, followed by 1/2 SB volume over 30 min, then 2× SB volume in NS over 60 min. Pre and post-shock lymph was loaded at equal protein concentrations on 2D-gels, followed by trypsin digestion and identification with mass spectrometry (MS-MS). Proteomics data were confirmed with Western blotting then quantitated by densitometry. Analysis of variance was used evaluate statistical data. Results: Gelsolin decreased in mesenteric lymph following hemorrhagic shock. Conclusions: Gelsolin is found at high levels (comparable to plasma) in mesenteric lymph. Following hemorrhagic shock, gelsolin levels decrease significantly, possibly due to consumption by the actin scavenging system. The magnitude of this change in concentration could release lipid bioactivity and predispose the lung and other organs to capillary injury. [Copyright &y& Elsevier]

Incidence of venous thromboembolism (VTE) in adult trauma patients is high despite mechanical and pharmacologic prophylaxis. We hypothesized that thrombin formation capacity as measured by calibrated automated thrombogram (CAT) is increased early in hospitalization and is associated with the development of VTE. Methods We conducted a prospective study in adult, critically ill trauma patients. Plasma was generated from whole blood samples collected within the first 3 days of hospital admission. CAT was used to determine lag time, thrombin peak, time to thrombin peak, endogenous thrombin potential (ETP), and velocity index in plasma samples from patients, and in control samples of platelet-poor, pooled normal plasma. Results There were 35 trauma patients and 35 controls included in this pilot analysis. Patients were a mean (SD) age of 45 (19) years, and 23 (66%) were male. The most common mechanism of injury was motor vehicle crash followed by falls, and the median (IQR) injury severity score was 17 (12–27). Three patients (8.6%) had deep vein thrombosis (DVT) confirmed by Doppler ultrasound on median hospital day 7. Compared to control samples, patients had significantly longer lag times (3.1 min vs. 2.7 min, p = 0.02) and significantly higher ETP (1136 nM ∗ min vs. 1019 nM ∗ min, p = 0.007), peak thrombin generation (239 nM vs. 176 nM, p < 0.001), and velocity index (108 nM/min vs. 57 nM/min, p < 0.001) (Fig. 1). There was no difference in the time to peak thrombin generation between the two groups (5.5 min vs. 5.7 min, p = 0.22). In the 3 patients with VTE compared to controls, lag times were shorter and velocity index was higher while ETP and peak thrombin generation were similar. There were no statistically significant differences in thrombin generation parameters in patients with or without VTE, but lag time was numerically shorter, and thrombin peak, time to peak and area-under-the-curve (ETP) were numerically lower in patients with DVT. Conclusions We observed a thrombin generation profile in critically ill trauma patients consistent with an early hypercoagulable state; however, thrombin generation parameters did not discriminate patients with VTE. [ABSTRACT FROM AUTHOR]

Background The prognosis for patients with severe acute lower intestinal bleeding (ALIB) may be assessed by complex artificial neural networks (ANNs) or user-friendly regression-based models. Comparisons between these modalities are limited, and predicting the need for surgical intervention remains elusive. We hypothesized that ANNs would outperform the Strate rule to predict severe bleeding and would also predict the need for surgical intervention. Methods We performed a 4-y retrospective analysis of 147 adult patients who underwent endoscopy, angiography, or surgery for ALIB. Baseline characteristics, Strate risk factors, management parameters, and outcomes were analyzed. The primary outcomes were severe bleeding and surgical intervention. ANNs were created in SPSS. Models were compared by area under the receiver operating characteristic curve (AUROC) with 95% confidence intervals. Results The number of Strate risk factors for each patient correlated significantly with the outcome of severe bleeding ( r = 0.29, P < 0.001). However, the Strate model was less accurate than an ANN (AUROC 0.66 [0.57-0.75] versus 0.98 [0.95-1.00], respectively) which incorporated six variables present on admission: hemoglobin, systolic blood pressure, outpatient prescription for Aspirin 325 mg daily, Charlson comorbidity index, base deficit ≥5 mEq/L, and international normalized ratio ≥1.5. A similar ANN including hemoglobin nadir and the occurrence of a 20% decrease in hematocrit was effective in predicting the need for surgery (AUROC 0.95 [0.90-1.00]). Conclusions The Strate prediction rule effectively stratified risk for severe ALIB, but was less accurate than an ANN. A separate ANN accurately predicted the need for surgery by combining risk factors for severe bleeding with parameters quantifying blood loss. Optimal prognostication may be achieved by integrating pragmatic regression-based calculators for quick decisions at the bedside and highly accurate ANNs when time and resources permit. [ABSTRACT FROM AUTHOR]

Background Our objective was to identify predictors of successful nonoperative management (NOM) of uncomplicated appendicitis. We hypothesized that the absence of diabetes, absence of an appendicolith, short duration of symptoms, absence of systemic inflammation, and low modified Alvarado score would predict successful NOM. Methods We performed a retrospective cohort analysis of 81 consecutive patients who underwent NOM of uncomplicated appendicitis. Successful NOM was defined as resolution of appendicitis with antibiotics alone and no recurrent appendicitis within 180 days. Patients with successful NOM ( n = 36) were compared with patients who failed NOM ( n = 45). Multivariable logistic regression was used to identify predictors of successful NOM, expressed as odds ratios (ORs) with 95% confidence intervals. Model strength was assessed by calculating area under the receiver operating characteristic curve (AUC). Results Patient age (35 years), the American Society of Anesthesiologists class (2.0), and Charlson comorbidity index (0.0) were similar between groups. Independent predictors of successful NOM were duration of symptoms prior to admission >25 hours: OR 4.17 (1.42-12.24), maximum temperature within 6 hours of admission <37.3°C: OR 8.07 (1.79-36.38), modified Alvarado score <4: OR 9.06 (1.26-64.93), and appendiceal diameter <13 mm: OR 17.55 (1.30-237.28); model AUC: 0.81 (0.72-0.90). Conclusions Patients with a longer duration of symptoms prior to admission were more likely to have successful NOM. Other independent predictors of successful NOM included lower temperature, lower modified Alvarado score, and smaller appendiceal diameter. These findings provide a framework for clinical decision-making and large-scale derivation and validation of a model to predict successful NOM of uncomplicated appendicitis. [ABSTRACT FROM AUTHOR]

Early events triggered by posttrauma/hemorrhagic shock currently represent a leading cause of morbidity and mortality in these patients. The causative agents of these events have been associated with increased neutrophil priming secondary to shock-dependent alterations of mesenteric lymph. Previous studies have suggested that unknown soluble components of the postshock mesenteric lymph are main drivers of these events. In the present study, we applied a label-free proteomics approach to further delve into the early proteome changes of the mesenteric lymph in response to hemorrhagic shock. Time-course analyses were performed by sampling the lymph every 30 min after shock up until 3 h (the time window within which a climax in neutrophil priming was observed). There are novel, transient early post-hemorrhagic shock alterations to the proteome and previously undocumented postshock protein alterations. These results underlie the triggering of coagulation and proinflammatory responses secondary to trauma/hemorrhagic shock, metabolic deregulation and apoptosis, and alterations to proteases/antiproteases homeostasis, which are suggestive of the potential implication of extracellular matrix proteases in priming neutrophil activation. Finally, there is a likely correlation between early postshock mesenteric lymph-mediated neutrophil priming and proteomics changes, above all protease/antiproteases impaired homeostasis (especially of serine proteases and metalloproteases).

Mesenteric lymph is the mechanistic link between splanchnic hypoperfusion and acute lung injury (ALI), but the culprit mediator(s) remains elusive. Previous work has shown that administration of a phospholipase A(2) (PLA(2)) inhibitor attenuated postshock ALI and also identified a non-ionic lipid within the postshock mesenteric lymph (PSML) responsible for polymorphonuclear neutrophil (PMN) priming. Consequently, we hypothesized that gut-derived leukotriene B(4) (LTB(4)) is a key mediator in the pathogenesis of ALI. Trauma/hemorrhagic shock (T/HS) was induced in male Sprague-Dawley rats and the mesenteric duct cannulated for lymph collection/diversion. PSML, arachidonic acid (AA), and a LTB(4) receptor antagonist were added to PMNs in vitro. LC/MS/MS was employed to identify bioactive lipids in PSML and the lungs. T/HS increased AA in PSML and increased LTB(4) and PMNs in the lung. Lymph diversion decreased lung LTB(4) by 75% and PMNs by 40%. PSML stimulated PMN priming (11.56 +/- 1.25 vs. 3.95 +/- 0.29 nmol O(2)(-)/min; 3.75 x 10(5) cells/ml; P < 0.01) that was attenuated by LTB(4) receptor blockade (2.64 +/- 0.58; P < 0.01). AA stimulated PMNs to produce LTB(4), and AA-induced PMN priming was attenuated by LTB(4) receptor antagonism. Collectively, these data indicate that splanchnic ischemia/reperfusion activates gut PLA(2)-mediated release of AA into the lymph where it is delivered to the lungs, provoking LTB(4) production and subsequent PMN-mediated lung injury.