Critical care : the official journal of the Critical Care Forum
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Multicenter Study
Impact of emergency intubation on central venous oxygen saturation in critically ill patients: a multicenter observational study.
Central venous oxygen saturation (ScvO2) has emerged as an important resuscitation goal for critically ill patients. Nevertheless, growing concerns about its limitations as a perfusion parameter have been expressed recently, including the uncommon finding of low ScvO2 values in patients in the intensive care unit (ICU). Emergency intubation may induce strong and eventually divergent effects on the physiologic determinants of oxygen transport (DO2) and oxygen consumption (VO2) and, thus, on ScvO2. Therefore, we conducted a study to determine the impact of emergency intubation on ScvO2. ⋯ ScvO2 increases significantly in response to emergency intubation in the majority of septic and non-septic patients. When interpreting ScvO2 during early resuscitation, it is crucial to consider whether the patient has been recently intubated or is spontaneously breathing.
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Early structured resuscitation of severe sepsis has been suggested to improve short term mortality; however, no previous study has examined the long-term effect of this therapy. We sought to determine one year outcomes associated with implementation of early goal directed therapy (EGDT) in the emergency department (ED) care of sepsis. ⋯ Implementation of EGDT for the treatment of ED patients with severe sepsis and septic shock was associated with significantly lower mortality at one year.
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Eleven papers on trauma published in Critical Care during 2008 addressed traumatic brain injury (TBI), burns, diagnostic concerns and immunosuppression. In regard to TBI, preliminary results indicate the utility of either magnetic resonance imaging (MRI) or ultrasound in measuring optic nerve sheath diameter to identify elevated intracranial pressure (ICP) as well as the potential benefit of thiopental for refractory ICP. Another investigation demonstrated that early extubation of TBI patients whose Glasgow Coma Scale score was 8 or less did not result in additional incidence of nosocomial pneumonia. ⋯ One literature review described the disadvantages of prolonged immobilization or additional use of MRI for ruling out cervical spine injuries in obtunded TBI patients already cleared by computerized tomography scans. Other investigators found that higher N-terminal pro B-type natriuretic peptide (NT-proBNP) levels may be useful markers for post-traumatic cardiac impairment. Finally, an experimental model showed that both splenic apoptosis and lymphocytopenia may occur shortly after severe hemorrhage, thus increasing the threat of immunosuppression in those with severe blood loss.
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Delirium occurs frequently in critically ill patients and has been associated with both short-term and long-term consequences. Efforts to decrease delirium prevalence have been directed at identifying and modifying its risk factors. One potentially modifiable risk factor is sleep deprivation. ⋯ However, studies have demonstrated many similarities between the clinical and physiologic profiles of patients with delirium and sleep deprivation. This article aims to review the literature, the clinical and neurobiologic consequences of sleep deprivation, and the potential relationship between sleep deprivation and delirium in intensive care unit patients. Sleep deprivation may prove to be a modifiable risk factor for the development of delirium with important implications for the acute and long-term outcome of critically ill patients.
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Severe burn injury remains a major burden on patients and healthcare systems. Following severe burns, the injured tissues mount a local inflammatory response aiming to restore homeostasis. With excessive burn load, the immune response becomes disproportionate and patients may develop an overshooting systemic inflammatory response, compromising multiple physiological barriers in the lung, kidney, liver, and brain. ⋯ Copious amounts of reactive oxygen species, reactive nitrogen species, proteases, cytokines/chemokines, and complement proteins are being released by these inflammatory cells, resulting in additional neuronal damage and life-threatening cerebral edema. Despite the correlation between cerebral complications in severe burn victims with mortality, burn-induced neuroinflammation continues to fly under the radar as an underestimated entity in the critically ill burn patient. In this paper, we illustrate the molecular events leading to blood-brain barrier breakdown, with a focus on the subsequent neuroinflammatory changes leading to cerebral edema in patients with severe burns.