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: 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.

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.

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

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.

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 ‫؍‬

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...

We hypothesised that the oedema fluid-to-plasma protein (EF/PL) ratio, a noninvasive measure of alveolar capillary membrane permeability, can accurately determine the aetiology of acute pulmonary oedema.390 mechanically ventilated patients with acute pulmonary oedema were enrolled. A clinical diagnosis of acute lung injury (ALI), cardiogenic pulmonary oedema or a mixed aetiology was based on expert medical record review at the end of hospitalisation. The EF/PL ratio was measured from pulmonary oedema fluid and plasma samples collected at intubation.209 patients had a clinical diagnosis of ALI, 147 had a diagnosis of cardiogenic pulmonary oedema and 34 had a mixed aetiology. The EF/PL ratio had an area under the receiver-operating curve of 0.84 for differentiating ALI from cardiogenic pulmonary oedema. Using a predefined cutoff of 0.65, the EF/PL ratio had a sensitivity of 81% and a specificity of 81% for the diagnosis of ALI. An EF/PL ratio o0.65 was also associated with significantly higher mortality and fewer ventilatorfree days.Noninvasive measurement of the EF/PL ratio is a safe and reliable bedside method for rapidly determining the aetiology of acute pulmonary oedema that can be used at the bedside in both developed and developing countries.KEYWORDS: Acute lung injury, acute pulmonary oedema, acute respiratory distress syndrome, alveolar capillary membrane permeability, diagnosis A cute pulmonary oedema may be either due to increased permeability of the alveolar capillary barrier, in the case of acute lung injury (ALI) [1][2][3], or to increased pulmonary microvascular hydrostatic pressure [4], in the case of cardiogenic pulmonary oedema (CPE). Accurate determination of the aetiology of acute pulmonary oedema is of major clinical importance because the treatments for ALI and CPE are fundamentally different [4,5]. The shift in the practice of clinical medicine in both academic and nonacademic medical centres away from invasive measures, such as the pulmonary artery catheter, emphasises the need for other approaches to determine the clinical cause of pulmonary oedema.Accurate and rapid determination of the cause of acute pulmonary oedema at the bedside can be challenging. Although history, physical examination and laboratory testing are useful, the aetiology of pulmonary oedema remains unclear in a significant number of patients even after initial diagnostic testing is completed [4], and clinical definitions are imperfect [6]. Echocardiography can provide information about left ventricular performance and filling pressures but is not rapidly available in many centres. The gold standard for determining the aetiology of acute pulmonary oedema is measurement of the pulmonary arterial occlusion pressure by pulmonary artery catheterisation [7,8]. However, pulmonary artery catheterisation is invasive and has become much less common in the USA [9] with the publication of a number of studies suggesting that routine use of pulmonary artery catheterisation for the management of critically ill patients is ass...