Critical care : the official journal of the Critical Care Forum
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Case Reports
Licorice consumption as a cause of posterior reversible encephalopathy syndrome: a case report.
A 49-year-old woman was admitted to our hospital because of thunderclap headache and blurred vision. At the time of presentation, her blood pressure was 219/100 mmHg, her arterial pH was 7.64 and her potassium level was 2.7 mM/l. ⋯ To the best of our knowledge, this is the first case report describing licorice consumption as a cause of PRES. Glycyrrhizic acid, a component of licorice, inhibits 11β-hydroxysteroid dehydrogenase and subsequently causes mineralocorticoid excess. Mineralocorticoid excess in turn causes high blood pressure and ultimately gives rise to malignant hypertension. Physicians should remember that licorice use is a very easy-to-treat cause of hypertension, hypertensive encephalopathy and PRES.
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Mechanical ventilation (MV) could prime the lung toward an inflammatory response if exposed to another insult such as bacterial invasion. The underlying mechanisms are not so far clear. Toll-like receptors (TLRs) allow the host to recognize selectively bacterial pathogens and in turn to trigger an immune response. We therefore hypothesized that MV modulates TLR2 expression and in turn modifies responsiveness to agonists such as bacterial lipopeptide (BLP). ⋯ Mild-stretch MV increases lung expression of TLR2 and sensitizes the lung to bacterial TLR2 ligands. This may account for the propensity of mechanically ventilated patients to develop acute lung injury in the context of airway bacterial colonization/infection.
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Cytomegalovirus (CMV) is a ubiquitous virus present in approximately two-thirds of the healthy population. This virus rarely causes an active disease in healthy individuals, but it is among the most common opportunistic infections in immunocompromised patients such as solid organ transplant recipients, patients receiving chemotherapy for cancer or patients with human immunodeficiency virus. Critically ill patients who are immunocompetent before intensive care unit admission may also become more prone to develop active CMV infection if they have prolonged hospitalizations, high disease severity, and severe sepsis. ⋯ The present issue of Critical Care brings a new study by Heininger and colleagues in which the authors found that patients with severe sepsis who developed active CMV infection had significantly longer intensive care unit and hospital stays, prolonged mechanical ventilation, but no changes in mortality compared to patients without CMV infection. We discuss the possible reasons for their findings (for example, selection bias and low (20%) statistical power to detect mortality endpoints), and also perform an update of our previous meta-analysis with the addition of Heininger and colleagues' study to verify whether the higher mortality rate with CMV holds. Our updated meta-analysis with approximately 1,000 patients shows that active CMV infection continues to be associated with a significant 81% higher mortality rate than that in critically ill patients without active CMV infection.
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Substantial basic and translational research has been directed to detect earlier and more sensitive acute kidney injury (AKI) biomarkers over the past decade. Much of the seminal AKI biomarker validation research has been performed in children undergoing cardiopulmonary bypass since they represent an ideal clinical model for AKI biomarker study: the timing of the injury is known and children do not have many of the co-morbidities seen in adult patient populations, which can confound the clinical situation. ⋯ They demonstrate that fenoldopam administration led to decreased postoperative urine NGAL and urine cystatin C concentrations, suggesting a renoprotective effect. Given the high sensitivity of NGAL for AKI post cardiopulmonary bypass, this study provides a model to use novel AKI biomarkers in a novel manner.
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Donnino and colleagues provide new insights into the field of oxidative stress and mitochondrial dysfunction during septic shock. These authors suggest a coenzyme Q10 (CoQ10) deficiency in patients with septic shock. Larger prospective observational trials measuring CoQ10 in patients with septic shock are required to confirm the possibility of CoQ10 depletion. This study is a new step toward a study testing CoQ10 as a potential therapeutic agent for patients with septic shock.