Chest
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Abdominal compartment syndrome (ACS) is the end point of a process whereby massive interstitial swelling in the abdomen or rapid development of a space-filling lesion in the abdomen (such as ascites or a hematoma) leads to pathologically increased pressure. This results in so-called intraabdominal hypertension (IAH), causing decreased perfusion of the kidneys and abdominal viscera and possible difficulties with ventilation and maintenance of cardiac output. These effects contribute to a cascade of ischemia and multiple organ dysfunction with high mortality. ⋯ There is minimal primary literature on the pathophysiological underpinnings of IAH and ACS and few prospective randomized trials evaluating their treatment or prevention; this concise review therefore provides only brief summaries of these topics. Many modern studies nominally dealing with IAH or ACS are simply epidemiologic surveys on their incidence, so this paper summarizes the incidence of IAH and ACS in a variety of disease states. Especially emphasized is the fact that modern critical care paradigms emphasize rational limitations to fluid resuscitation, which may have contributed to an apparent decrease in ACS among critically ill patients.
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Accumulating evidence suggests that extracellular vesicles (EVs) play a role in the pathogenesis of lung diseases. These vesicles include exosomes, ectosomes (ie, microparticles, extracellular vesicles, microvesicles, and shedding vesicles), and apoptotic bodies. Exosomes are generated by inward budding of the membrane (endocytosis), subsequent forming of multivesicular bodies, and release by exocytosis. ⋯ EVs contain several molecules, including proteins, mRNA, microRNA, and DNA; they transfer these molecules to distant recipient cells. Circulating EVs modify the targeted cells and influence the microenvironment of the lungs. For this unique capability, EVs are expected to be a new drug delivery system and a novel therapeutic target.
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Emphysema has considerable variability in its regional distribution. Craniocaudal emphysema distribution is an important predictor of the response to lung volume reduction. However, there is little consensus regarding how to define upper lobe-predominant and lower lobe-predominant emphysema subtypes. Consequently, the clinical and genetic associations with these subtypes are poorly characterized. ⋯ Subgroups of smokers defined by upper-lobe or lower-lobe emphysema predominance exhibit different functional and radiological disease progression rates, and the upper-lobe predominant subtype shows evidence of association with known COPD genetic risk variants. These subgroups may be useful in the development of personalized treatments for COPD.
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Sirolimus reduces serum levels of vascular endothelial growth factor D (VEGF-D); the size of chylous effusions, lymphangioleiomyomas, and angiomyolipomas; and stabilizes lung function in patients with lymphangioleiomyomatosis (LAM). ⋯ Sirolimus therapy stabilizes lung function over many years of therapy while producing a sustained reduction in VEGF-D levels in patients with elevated levels preceding therapy. An association was not demonstrated between the magnitude of VEGF-D decline and the beneficial effect of sirolimus on lung function. Persistent improvement in lung function was observed in patients with lymphatic disease.
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Severe sepsis is a common, deadly, and diagnostically vexing condition. Recent recommendations for diagnosing sepsis, referred to as consensus guidelines, provide a definition of sepsis and remove the systemic inflammatory response syndrome (SIRS) as a component of the diagnostic process. A concise definition of sepsis is welcomed. ⋯ Emphasis is placed on mortality prediction rather than on early diagnosis. Diagnostic criteria are recommended to replace current criteria without evidence of any effect that their use would have on mortality. SIRS is a prevalent feature of patients with sepsis, should remain an important component of the diagnostic process, and remains a valuable term for discussing patients with life-threatening organ dysfunction caused by infection.