Critical Care Medicine

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IV Immunoglobulin: A Useful Tool for the Severe Pneumonia Toolbox?*

Vie, 01/01/2016 - 08:00
No abstract available

Online Editorial Board Acknowledgment

Vie, 01/01/2016 - 08:00
No abstract available

IV Immunoglobulin for Acute Lung Injury and Bacteremia in Pseudomonas aeruginosa Pneumonia*

Vie, 01/01/2016 - 08:00
Objectives: Virulent and multidrug-resistant Pseudomonas aeruginosa causes a lethal pneumonia, especially in patients who are artificially ventilated. It has been reported that the virulence mechanism used by P. aeruginosa, which is linked to acute lung injury, is strongly associated with the type III secretion system, and specific antibodies targeting this system have shown a protective effect in both experimental and clinical settings. We investigated the effect of administering IV immunoglobulins on P. aeruginosa pneumonia, including its associated bacteremia and mortality, although focusing especially on type III secretion system–associated P. aeruginosa virulence. Design: Prospective randomized and controlled animal study. Setting: University laboratory. Subjects: Male ICR mice. Interventions: Mice were infected intratracheally with a lethal dose of the virulent P. aeruginosa PA103 strain. IV immunoglobulin administration was examined in three different settings: 1) premixed; 2) pre-IV, prophylactic administration before bacterial infection; and 3) post-IV, therapeutic administration after bacterial infection. The effect of specific antigen titer depletion of IV immunoglobulins was also examined. Measurements and Main Results: Survival and body temperature were monitored for 24 hours. Bacteremia, cytokine concentration, myeloperoxidase activity, WBC counts in the blood, and lung bacterial load were evaluated. Survival improved significantly in mice that received IV immunoglobulins (p < 0.05). Lung edema, lung bacteriologic load, and bacteremia decreased significantly in the IV immunoglobulin–treated mice (p < 0.05). The mechanism of protection was associated with the presence of antibodies against both PcrV and some bacterial surface antigens in the IV immunoglobulins. Conclusions: IV immunoglobulin administration had a significantly protective effect against lethal infection from virulent P. aeruginosa. Prophylactic IV immunoglobulin administration at the highest dose was comparable with that achieved by administrating a specific anti-PcrV polyclonal IgG into the mice. The mechanism of protection is likely to involve the synergic action of anti-PcrV titers and antibodies against some surface antigen(s) that block the type III secretion system–associated virulence of P. aeruginosa.

Hyperbaric Oxygen Therapy Alleviates Carbon Monoxide Poisoning–Induced Delayed Memory Impairment by Preserving Brain-Derived Neurotrophic Factor–Dependent Hippocampal Neurogenesis

Vie, 01/01/2016 - 08:00
Objective: To test the hypothesis that hyperbaric oxygen therapy ameliorates delayed cognitive impairment after acute carbon monoxide poisoning by promoting neurogenesis through upregulating the brain-derived neurotrophic factor in the hippocampus. Design: Laboratory animal experiments. Setting: University/Medical center research laboratory. Subjects: Adult, male Sprague-Dawley rats. Interventions: Rats were divided into five groups: (1) non–carbon monoxide-treated control, (2) acute carbon monoxide poisoning, (3) acute carbon monoxide poisoning followed by 7-day hyperbaric oxygen treatment, (4) carbon monoxide + hyperbaric oxygen with additional intracerebroventricular infusion of Fc fragment of tyrosine kinase receptor B protein (TrkB-Fc) chimera, and (5) acute carbon monoxide poisoning followed by intracerebroventricular infusion of brain-derived neurotrophic factor. Acute carbon monoxide poisoning was achieved by exposing the rats to carbon monoxide at 2,500 ppm for 40 minutes, followed by 3,000 ppm for 20 minutes. Hyperbaric oxygen therapy (at 2.5 atmospheres absolute with 100% oxygen for 60?min) was conducted during the first 7 days after carbon monoxide poisoning. Recombinant human TrkB-Fc chimera or brain-derived neurotrophic factor was infused into the lateral ventricle via the implanted osmotic minipump. For labeling of mitotic cells in the hippocampus, bromodeoxyuridine was injected into the peritoneal cavity. Distribution of bromodeoxyuridine and two additional adult neurogenesis markers, Ki-67 and doublecortin, in the hippocampus was evaluated by immunohistochemistry or immunofluorescence staining. Tissue level of brain-derived neurotrophic factor was assessed by enzyme-linked immunosorbent assay. Cognitive behavior was evaluated by the use of eight-arm radial maze. Measurements and Main Results: Acute carbon monoxide poisoning significantly suppressed adult hippocampal neurogenesis evident by the reduction in number of bromodeoxyuridine-positive, Ki-67+, and doublecortin+ cells in the subgranular zone of the dentate gyrus. This suppression of adult neurogenesis by the carbon monoxide poisoning was appreciably alleviated by early treatment of hyperbaric oxygen. The hyperbaric oxygen treatment also promoted a sustained increase in hippocampal brain-derived neurotrophic factor level. Blockade of hippocampal brain-derived neurotrophic factor signaling with intracerebroventricular infusion of recombinant human TrkB-Fc chimera significantly blunted the protection by the hyperbaric oxygen on hippocampal neurogenesis; whereas intracerebroventricular infusion of brain-derived neurotrophic factor mimicked the action of hyperbaric oxygen and preserved hippocampal neurogenesis after acute carbon monoxide poisoning. Furthermore, acute carbon monoxide poisoning resulted in a delayed impairment of cognitive function. The hyperbaric oxygen treatment notably restored the cognitive impairment in a brain-derived neurotrophic factor–dependent manner. Conclusions: The early hyperbaric oxygen treatment may alleviate delayed memory impairment after acute carbon monoxide poisoning by preserving adult neurogenesis via an increase in hippocampal brain-derived neurotrophic factor content.

Failure to Improve the Oxygenation Index Is a Useful Predictor of Therapy Failure in Acute Respiratory Distress Syndrome Clinical Trials

Vie, 01/01/2016 - 08:00
Objective: Acute respiratory distress syndrome trials powered for mortality require significant resources, limiting the number of evaluable therapies. Validation of intermediate endpoints would enhance the feasibility of testing novel acute respiratory distress syndrome therapies in pilot studies and potentially reduce the frequency of failed large clinical trials. We sought to determine whether a change in the oxygenation index over the first 7 days of acute respiratory distress syndrome could discriminate between therapies likely or unlikely to show benefit in larger clinical trials. Design: A derivation cohort from three acute respiratory distress syndrome studies was used to estimate the 7-day change in oxygenation index. Receiver operating characteristic curves were used to calculate optimal thresholds and predictability of the change in oxygenation index for 28-day mortality and ventilator-free days. The thresholds were then validated in two cohorts. Then, for each individual acute respiratory distress syndrome study, the threshold 7-day oxygenation index change was tested as an outcome measure and compared with mortality and ventilator-free days as reported in the original study. Setting: Medical ICUs. Patients: Acute respiratory distress syndrome patients. Interventions: Various. Measurements and Main Results: Change in oxygenation index, 28-day mortality, and ventilator-free days. In the derivation cohort, the mean 7-day oxygenation index improved by 4.2 (± 11.7) in 28-day survivors compared with an increase of 2.4 (± 11.6) in 28-day nonsurvivors (p < 0.001). The mean 7-day oxygenation index decreased by 5.9 (± 8.4) in patients with more than 14 ventilator-free days, compared with a decrease of 1.9 (± 12.4) among those with less than 14 ventilator-free days (p = 0.001). The optimal 7-day oxygenation index threshold for predicting mortality was an increase of 1.71 and for predicting less than 14 ventilator-free days, a decrease of 2.34. When used as a surrogate endpoint, the optimal 7-day oxygenation index change closely approximated mortality and ventilator-free day outcomes in three Acute Respiratory Distress Syndrome Network studies used for the derivation cohort and a distinct study used for validation. The change in oxygenation index was a poor predictor of individual patient outcome. Conclusions: Failure to meet a threshold improvement in the oxygenation index over the first 7 days of therapy can be used to identify therapies unlikely to succeed in subsequent trials powered for mortality and ventilator-free days. By reducing trial time and costs, use of the 7-day oxygenation index change as an intermediate endpoint could increase the number of clinical trials of promising therapies for acute respiratory distress syndrome and reduce the number of large-scale trials of therapies unlikely to be of benefit.

Successful Extracorporeal Life Support in a Case of Severe Glyphosate-Surfactant Intoxication

Vie, 01/01/2016 - 08:00
Objective: To describe the experience of emergency extracorporeal membrane oxygenation in treating life-threatening glyphosate-surfactant intoxication. Design: Case report. Setting: Emergency department and ICU. Patient: A patient with cardiopulmonary failure after glyphosate-surfactant intoxication. Intervention: Extracorporeal membrane oxygenation. Case Report: A 47-year-old man presented with mildly decreased consciousness in our emergency department after ingesting approximately 100?mL of glyphosate-surfactant 1.5 hours previously. Respiratory failure, persistent ventricular tachycardia, profound shock refractory to inotropic agents, and metabolic acidosis developed in the patient within 2 hours. Extracorporeal membrane oxygenation was applied within 4 hours of cardiopulmonary failure. The patient’s condition improved considerably. He was transferred to the general ward on the eighth day with stable hemodynamic status and complete neurological recovery. Conclusions: On the basis of our research, this was the first case in which extracorporeal membrane oxygenation was used to treat severe glyphosate-surfactant intoxication. We recommend early initiation of extracorporeal membrane oxygenation therapy to mitigate cardiopulmonary compromise in patients with glyphosate-surfactant intoxication.

Designing Better, Not Just Bigger, Multicenter Critical Care Trials

Vie, 01/01/2016 - 08:00
No abstract available

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Vie, 01/01/2016 - 08:00
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Vie, 01/01/2016 - 08:00
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Vie, 01/01/2016 - 08:00
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Vie, 01/01/2016 - 08:00
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Vie, 01/01/2016 - 08:00
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Fast Facts for the Neonatal Nurse

Vie, 01/01/2016 - 08:00
No abstract available

Rationing Is Not a Four-Letter Word: Setting Limits on Healthcare

Vie, 01/01/2016 - 08:00
No abstract available

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