Splenosis is a common benign condition that occurs after splenic rupture via trauma or surgery. Splenosis is usually found incidentally and unless symptomatic, therapy is not indicated. However, since radiographically it can mimic malignancy, most patients have an extensive workup. The diagnostic method of choice is nuclear scintigraphy, specifically, a heat-damaged red blood cell scan. Splenosis usually occurs within the abdominal and pelvic cavities, but patients have been described with intrathoracic, subcutaneous, intrahepatic and intracranial lesions.

Background The diagnosis of acute lung injury (ALI) is based on a consensus clinical definition. Despite the simplicity of this definition, ALI remains underdiagnosed and undertreated. Severe trauma is a well-described cause of ALI that represents a relatively homogeneous subset of ALI patients. The goals of this study were to develop a panel of plasma biomarkers to facilitate diagnosis of trauma-induced ALI and to enhance our understanding of the pathogenesis of human ALI. Methods A retrospective nested case control of 192 patients admitted to the trauma intensive care unit (ICU) at a university hospital between 2002 and 2006. We compared 107 patients with ALI to 85 patients without ALI. Plasma was collected within 72 h of ICU admission. Twenty-one plasma biomarkers were measured in duplicate in each plasma sample. Results Patients with ALI had higher severity of illness scores, more days of mechanical ventilation, longer hospital stays and higher mortality versus controls. Seven biomarkers (RAGE, PCPIII, BNP, ANG2, IL10, TNF-α, and IL8) had a high diagnostic accuracy as reflected by the area under the receiver operating characteristic curve of 0.86 (95% CI 0.82 – 0.92) in differentiating ALI from controls. Conclusions A model utilizing seven plasma biomarkers had a high diagnostic accuracy in differentiating patients with trauma-induced ALI from trauma patients without ALI. In addition, use of a panel of biomarkers provides insight into the likely importance of alveolar epithelial injury in the pathogenesis of early acute lung injury.

Background: Pulmonary venous hypertension (PVH) is a well-described cause of pulmonary hypertension (PH) in patients with left heart disease associated with elevated left heart filling pressure. PVH results from a number of processes, including left-sided valvular disease, constrictive pericardial disease, restrictive cardiomyopathies, and left ventricular (LV) systolic dysfunction. PVH in patients with normal LV systolic function, commonly referred to as diastolic dysfunction, is not well characterized. We observed that many patients with PH due to PVH have obesity, hypertension, diabetes mellitus, and hypercholesterolemia, which are clinical features of the metabolic syndrome (MS), a previously identified cause for systemic vascular disease. Methods: We evaluated 122 consecutive patients referred for diagnosis and treatment of PH and compared the prevalence of features of the MS between patients with PVH and those with pulmonary arterial hypertension (PAH). We also compared clinical and hemodynamic characteristics between these two groups.

LB. Procoagulant alveolar microparticles in the lungs of patients with acute respiratory distress syndrome.

Background: Acute lung injury (ALI) and ARDS are common clinical syndromes that are underdiagnosed. Clara cell secretory protein (CC16) is an antiinflammatory protein secreted by the Clara cells of the distal respiratory epithelium that has been proposed as a biomarker of lung epithelial injury. We tested the diagnostic and prognostic utility of CC16 in patients with non-trauma-related ALI/ARDS compared to a control group of patients with acute cardiogenic pulmonary edema (CPE). Methods: Plasma and pulmonary edema fluid samples were obtained from medical and surgical patients with ALI/ARDS or CPE requiring intubation for mechanical ventilation. The etiology of pulmonary edema was determined using consensus clinical criteria for ALI/ARDS and CPE and the edema fluid-to-plasma protein ratio. Plasma and edema fluid CC16 levels were measured by sandwich enzyme-linked immunosorbent assay. CC16 levels were log transformed for analysis, and comparisons were made by the Student t test or 2 as appropriate. Results: Compared to patients with CPE (n ‫؍‬ 9), patients with ALI/ARDS (n ‫؍‬

Objectives To determine if prehospital statin use is associated with a lower risk of sepsis, ALI/ARDS, and mortality in critically ill patients. We also investigated the effect of combined prehospital use of both statins and aspirin. Design Cross-sectional analysis of a prospective cohort Patients 575 critically ill patients admitted to the medical or surgical ICU of an academic tertiary-care hospital Measurements and Main Results Of 575 patients, 149 (26%) were on statin therapy prior to hospitalization. A multivariable analysis including age, gender, current tobacco use, prehospital aspirin use, race, and APACHE II score revealed that patients on statin therapy prior to hospitalization were less likely to have or develop severe sepsis (OR 0.62, 95% CI 0.40 to 0.96) or ALI/ARDS (OR 0.60, 95% CI 0.36 to 0.99) during the first four ICU days. In-hospital mortality for patients with and without prehospital statin use (OR 1.06, 95% CI 0.62 to 1.83) was similar. Patients who had prehospital use of both statins and aspirin had the lowest rates of severe sepsis, ALI/ARDS and mortality. Conclusions Prehospital use of statins may be protective against the sepsis and ALI. This effect may be potentiated by prehospital aspirin use.

Most patients with acute lung injury (ALI) have reduced alveolar fluid clearance that has been associated with higher mortality. Several mechanisms may contribute to the decrease in alveolar fluid clearance. In this study, we tested the hypothesis that pulmonary edema fluid from patients with ALI might reduce the expression of ion transport genes responsible for vectorial fluid transport in primary cultures of human alveolar epithelial type II cells. Following exposure to ALI pulmonary edema fluid, the gene copy number for the major sodium and chloride transport genes decreased. By Western blot analyses, protein levels of ␣ENaC, ␣1Na,K-ATPase, and cystic fibrosis transmembrane conductance regulator decreased as well. In contrast, the gene copy number for several inflammatory cytokines increased markedly. Functional studies demonstrated that net vectorial fluid transport was reduced for human alveolar type II cells exposed to ALI pulmonary edema fluid compared with plasma (0.02 ؎ 0.05 versus 1.31 ؎ 0.56 l/cm 2 /h, p < 0.02). An inhibitor of p38 MAPK phosphorylation (SB202190) partially reversed the effects of the edema fluid on net fluid transport as well as gene and protein expression of the main ion transporters. In summary, alveolar edema fluid from patients with ALI induced a significant reduction in sodium and chloride transport genes and proteins in human alveolar epithelial type II cells, effects that were associated with a decrease in net vectorial fluid transport across human alveolar type II cell monolayers. Impaired alveolar fluid clearance (AFC;2 i.e. the resolution of alveolar edema) is a common characteristic among patients with acute lung injury (ALI) and acute respiratory distress syndrome. The level of AFC impairment has significant prognostic value in determining morbidity and mortality (1, 2). Multiple clinically relevant experimental studies have tried to uncover the underlying mechanisms that reduce AFC in ALI, and several pathways have been implicated (3, 4).In the alveolar environment, basal AFC is determined predominately by amiloride-sensitive (epithelial sodium channel (ENaC)) and -insensitive sodium channels and the activity of the Na,K-ATPase (3, 5-8). Several stimuli can up-regulate AFC including ␤-adrenergic agonists via cAMP-dependent mechanisms (3, 4). In the mouse and human lung, cAMP-dependent alveolar epithelial fluid transport is dependent on CFTR activity, especially in mediating ␤-adrenergic receptor-driven alveolar epithelial fluid transport (9 -11).We and others have reported that, in the early phase of ALI, pulmonary edema fluid contains high levels of several proinflammatory cytokines, including IL-1␤, TNF␣,. Several of these proinflammatory cytokines have been studied in experimental fluid transport experiments. For example, during short in vitro exposures, TNF␣ increases AFC, which is mediated predominantly by both TNF␣ receptor-dependent and -independent effects (15, 16). In contrast, for exposures up to 24 h, TNF␣ decreases the expression of ENaC (␣, ␤, and ␥ subunit...

Objective The acute respiratory distress syndrome (ARDS) is a pro-inflammatory condition that often complicates trauma and critical illness. Animal studies have shown that both gender and sex hormones play an important role in inflammatory regulation. Human data is scant regarding the role of gender and sex hormones in developing ARDS. Our objective was to describe gender and hormonal differences in patients who develop ARDS in a large cohort of critically injured adults. Methods A prospective cohort study of adult trauma patients requiring ICU admission for at least 48 hours was performed. Demographic and clinical data was collected prospectively, and sex hormones were assayed at study entry (48 hours). The primary outcome was the development of ARDS. Multivariate logistic regression was used to determine the adjusted odds of death associated with differences in gender. Results 648 patients met entry criteria and 180 patients developed ARDS (31%). Females were more likely to develop ARDS (35 % versus 25%, p=0.02). This association remained after adjusting for age, mechanism of injury, injury severity and blood product transfusion (OR 1.6 95% CI 1.1 – 2.4, p=0.02). Of patients with ARDS, there was no difference in mortality related to gender (22% mortality in females with ARDS versus 20% in males, p=NS). A pro-inflammatory sex hormone profile (low testosterone, high estradiol) was associated with ARDS in both males and females. Conclusion Females are more likely than males to develop ARDS following critical injury. Despite the increased incidence in ARDS, the mortality in patients with ARDS does not differ according to gender. The inflammatory properties of sex hormones may contribute to ARDS, but they do not fully explain observed gender differences.