Seminars in respiratory and critical care medicine
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Coccidioidomycosis refers to the spectrum of disease caused by the dimorphic fungi Coccidioides immitis and Coccidioides posadasii. Clinical manifestations vary depending upon both the extent of infection and the immune status of the host. ⋯ The majority of patients with coccidioidomycosis resolve their initial infection without sequelae; however, several patients develop complications of disease ranging in severity from complicated pulmonary coccidioidomycosis to widely disseminated disease with immediately life-threatening manifestations. This review focuses on complications of pulmonary coccidioidomycosis with an emphasis on the management of primary coccidioidal infection, solitary pulmonary nodules, pleural effusions, cavitary disease, acute respiratory distress syndrome (ARDS), miliary disease, and sepsis.
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Aspergillosis remains a significant cause of morbidity and mortality. The spectrum of disease is diverse and ranges from noninvasive disease with an excessive immune response, such as in allergic bronchopulmonary aspergillosis (ABPA), to a lack of an immune response as seen in patients with quantitative or qualitative granulocyte deficits and subsequent invasive pulmonary aspergillosis. ⋯ Voriconazole remains the preferred agent in the treatment of invasive pulmonary aspergillosis, and recent data have increased interest in the potential of combination therapy against this often lethal infection. The role of host genetics in selecting patients that may benefit from more aggressive antifungal prophylaxis or treatment practices remains unclear but is likely to guide therapeutic choices as newer data become available.
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Cardiac alterations may be defined as changes that lead to abnormal cardiac function. They include decrease in preload, increase in afterload, and depressed cardiac contractility. Cardiac dysfunction differs from cardiac failure: cardiac performance is altered, but this does not necessarily mean that the cardiovascular system is failing. ⋯ Only when there is an imbalance between oxygen demand and oxygen transport is correction of cardiac alterations required. But the truth is that no study supports the use of one treatment rather than another. Changes in respiratory settings or in respiratory mechanics induce changes in cardiac function and must then be considered in the strategy.
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Cardiovascular system failure is commonly faced by the intensivist. Heart failure can occur due to a host of predisposing cardiac disorders or as secondary effects of systemic illness. When the heart is unable to provide an adequate cardiac output to maintain adequate tissue perfusion, cardiogenic shock ensues. ⋯ Accurate and rapid identification of cardiogenic shock as a medical emergency, with expeditious implementation of appropriate therapy, can lead to improved clinical outcomes. In this review, we discuss optimal strategies for diagnosis and monitoring of cardiogenic shock. We discuss the diverse therapeutic strategies employed for cardiogenic shock, including pharmacological (e.g., vasoactive agents, fibrinolytic agents), mechanical (e.g., intraaortic balloon pumps, left ventricular assist devices, percutaneous coronary intervention [PCI]), and surgical approaches such as coronary artery bypass graft (CABG), valvular repair or replacement (e.g., for acute mitral regurgitation, ventricular septal rupture, or free wall rupture).
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The role of dysfunction of the gastrointestinal tract in the pathogenesis of multiple organ failure (MOF) complicating the course of critically ill patients has been suspected for more than 40 years. However, several hypotheses have been proposed and sometimes refuted to establish a link. This review summarizes the current knowledge on gastrointestinal physiology and recapitulates existing evidence on the link between gastrointestinal dysfunction and MOF. ⋯ It produces hormones with local and systemic effects, plays a major role in immunological function, and serves as a barrier against antigens within its lumen. Gastrointestinal dysfunction or gut failure is frequently encountered in critical care patients and is associated with bacterial translocation, which can lead to the development of sepsis, initiation of a cytokine-mediated systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), and death. The aim of this manuscript is to define gut failure, to review physiopathological mechanisms and clinical implications, and, finally, to suggest preventive measures.