Articles: function.
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To discuss the role of echocardiography for the hemodynamic evaluation of critically ill patients. ⋯ Echocardiography has now become an important tool for hemodynamic evaluation of the critically ill patient. Echocardiography should be performed in most patients with circulatory and respiratory failure.
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While numerous treatments for mitochondrial disorders have been suggested, relatively few have undergone controlled clinical trials. Treatment of these disorders is challenging, as only symptomatic therapy is available. In this review we will focus on newer drugs and treatment trials in mitochondrial diseases, with a special focus on medications to avoid in treating epilepsy and ICU patient with mitochondrial disease, which has not been included in such a review. ⋯ Treatment of epilepsy, which is a common feature in many mitochondrial phenotypes, warrants special consideration due to the added toxicity of certain medications, and we provide a discussion of these unique treatment challenges. Interesting, however, with only a few exceptions, the treatment strategies for epilepsy in mitochondrial cytopathies are the same as for epilepsy without mitochondrial dysfunction. We also discuss intensive care management, building upon similar reviews, adding new dimensions, and demonstrating the complexity of overall care of these patients.
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Critical care medicine · Jun 2014
Observational StudyMicrocirculatory Alterations in Traumatic Hemorrhagic Shock.
Microcirculatory dysfunction has been well reported in clinical studies in septic shock. However, no clinical studies have investigated microcirculatory blood flow behavior in hemorrhagic shock. The main objective of this study was to assess the time course of sublingual microcirculation in traumatic hemorrhagic shock during the first 4 days after trauma. ⋯ Alterations of microcirculation in traumatic hemorrhagic shock patients result from the interplay among hemorrhage-induced tissue hypoperfusion, trauma injuries, inflammatory response, and subsequent resuscitation interventions. Despite restoration of the macrocirculation, the sublingual microcirculation was impaired for at least 72 hours. The initial proportion of perfused vessels appears to be a good predictor of high Sequential Organ Failure Assessment score at D4. Further studies are required to firmly establish the link between microvascular alterations and organ dysfunction in traumatic hemorrhagic shock patients.
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Management of ischemic stroke is targeted on four therapeutic objectives: limitation of neurological deficit, prevention of earyl stroke recurrence, protection against complications, and secondary prevention. Intravenous thrombolysis within 4.5h of stroke onset is the only proven therapy to improvefunctional outcome. ⋯ Subcutaneous heparin/low molecular weight heparin, mobilisation, nasogastric tube, and decompressive craniectomy may protect from venous thromboembolism, aspiration pneumonia, and malignant brain edema, respectively. Secondary prevention is guided by stroke etiology, e.g. oral anticoagulation in the presence atrial fibrillation or endarterectomy in case of sympomatic high-grade carotid stenosis.
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A consensus statement found in most peer-reviewed literature on sarcoidosis is that the etiology of sarcoidosis is unknown. It is timely to review whether this statement should be revised. Many infectious agents meet the basic requirements of inducing granulomatous inflammation and immunologic responses consistent with sarcoidosis including oligoclonal expansion of CD4+ T cells, polarized Th1 and possibly Th17 responses, and dysregulated regulatory T-cell function. ⋯ The hypothesis that chronic sarcoidosis is caused by a viable, replicating mycobacterial or other infection has no direct pathologic, microbiologic, or clinical evidence. A novel hypothesis links microbial triggers to a sarcoidosis outcome from the accumulation of aggregated proinflammatory serum amyloid A within granulomas, providing a mechanism for chronic disease in the absence of any viable tissue infection. Further studies are needed to provide more definitive evidence for these competing hypotheses before the statement that the etiology of sarcoidosis is unknown becomes obsolete.