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31. |
SOCIETY OF CRITICAL CARE MEDICINE'S GRANT FUNDING OPPORTUNITIES |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1581-1581
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ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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32. |
Whatever happened to Reye's syndrome? Did it ever really exist? |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1582-1587
James P. Orlowski,
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摘要:
ObjectiveReye's syndrome (RS) appeared suddenly in the 1950s and disappeared almost as quickly in the late 1980s. A number of metabolic disorders were discovered in the 1980s that could completely mimic RS. This study was undertaken to reassess the original diagnosis of RS in light of newly described metabolic disorders.InterventionThe medical records of 26 patients who had survived RS and were originally studied in Australia in the 1980s were reexamined 10 yrs later, and families were interviewed to ascertain if the diagnosis had changed. The 49 original patients with RS from Australia were also reanalyzed using more precise diagnostic criteria for RS to ascertain how many of the patients would continue to fit the more precise diagnosis of RS.Measurements and Main ResultsOf 26 original patients with RS who had survived, 18 (69%) were subsequently diagnosed as having other diseases, most commonly inborn errors of metabolism. The most commonly diagnosed metabolic disorder was medium-chain acyl-coenzyme-A dehydrogenase deficiency. Of the 18 patients rediagnosed with diseases other than RS, 15 (83%) are now known to have metabolic disorders.By using more precise diagnostic criteria for RS, none of the original 49 patients with RS could be diagnosed as having certain RS.Only six patients had probable RS, two patients had possible RS, 23 patients had unlikely RS, and 18 patients were excluded as RS cases.ConclusionWith better diagnostic techniques and criteria, most patients originally diagnosed with RS are now known to have metabolic disorders. The disappearance of RS was probably related to the discovery and ability to diagnose inborn errors of metabolism that mimicked RS clinically, biochemically, and pathologically. (Crit Care Med 1999; 27:1582-1587)
ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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33. |
Financial impact of elimination of routine chest radiographs in a pediatric intensive care unit |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1588-1593
Mary B. Price,
Mary Jo Chellis Grant,
Katy Welkie,
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摘要:
ObjectiveTo determine the change in chest radiograph use if each chest radiograph requires a separate order and clinical indication.DesignProspective, nonrandomized, controlled design with an intervention.SettingThe pediatric intensive care unit (PICU) at Primary Children's Medical Center, Salt Lake City, UT.PatientsThe study comprised 3,727 PICU patients treated between 1992 and 1996.InterventionsA change in ordering practice: There will be no standing orders for routine daily morning chest radiographs. Each radiograph requires a written order and a clinical indication.Measurements and Main ResultsDuring a 29-month control phase when routine daily chest radiographs were obtained for all intubated patients, 1.026 chest radiographs per patients day were performed. After the intervention, the ratio dropped to 0.653 chest radiographs per patient day, a decrease of 36.4%. This resulted in a (projected) variable cost savings of $45,476. Data were also collected for quality assurance purposes.ConclusionsThese results demonstrate the impact of an evaluation and subsequent change in radiology ordering practice in our PICU. The change resulted in decreased variability in ordering practice, fewer chest radiographs per patient, and an accompanying cost savings to our patients and payors. (Crit Care Med 1999; 27:1588-1593)
ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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34. |
UPCOMING CRITICAL CARE MEETINGS |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1593-1593
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ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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35. |
Distribution and pathophysiology of acute lobar collapse in the pediatric intensive care unit |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1594-1597
Karen,
Thomas Parviz,
Habibi Joseph,
Britto Catherine M.,
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摘要:
ObjectiveThe high incidence of lower lobe collapse in adult intensive care patients is well described. We aimed to document the incidence and distribution of acute lobar collapse in the pediatric intensive care setting. The influence of anatomical and pathophysiological differences between the adult and pediatric respiratory tract will be considered.DesignRetrospective review of chest radiograph series.SettingTertiary referral center for pediatric intensive care and the Department of Diagnostic Radiology in a large teaching hospital in England.PatientsCohort of 160 patients receiving intensive care during a 2-yr period (age range, 6 days-18 yrs; median, 23 months).InterventionsNoneMeasurements and Main ResultsTwenty-four of 160 children (15%) developed acute lobar collapse during their intensive care unit admission. Isolated right upper lobe collapse occurred in 14 patients, right upper lobe in association with one or more other lobes in five patients, and lobar collapse other than the right upper lobe in five patients. The development of lobar collapse and, in particular, right upper lobe collapse was associated with a lower median age (no collapse, 26 months; lobar collapse, 8 months; right upper lobe collapse, 4 months). Lobar collapse was significantly associated with the requirement for mechanical ventilation during admission (chi-square, 12.18; p = .005). It was observed in association with both high and low endotracheal tube positions.ConclusionThe predominance of upper lobe and, in particular, right upper lobe collapse observed in pediatric intensive care patients contrasts with the high incidence of lower lobe collapse in their adult counterparts. Multiple interrelated factors are likely to be contributory and include the following: a) anatomical and physiological differences between adults and children; b) the pathophysiology of childhood respiratory disease; c) more critical positioning of endotracheal tubes in younger patients and their movement with patient positioning. (Crit Care Med 1999; 27: 1594-1597)
ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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36. |
Development of a percutaneous fiberoptic hepatic venous localization catheter |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1598-1602
Michael S.,
Dahn Ralph,
Ballerstadt M. Patricia,
Lange Jerome,
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摘要:
ObjectiveTo develop a liver-specific biosensor system/catheter assembly that can be used to localize and cannulate the hepatic venous system without the need for fluoroscopic imaging. This would permit the bedside placement of a hepatic venous catheter for monitoring purposes without radiographic guidance.DesignExperimental, in vitro.Study SettingExperimental laboratory at a university center.SubjectThis was a simulation study to evaluate the ability of a cardiovascular monitoring catheter mounted with a liver-specific biosensor to anatomically identify a side arm tributary. The experimental system used for this study mimics the hepatic vein draining into the inferior vena cava and allows its localization without the need for assisted imaging. The biosensor design and catheter/sensor assembly function were studied in this in vitro model.InterventionsA liver-specific biosensor was developed by housing a homogeneous affinity fluorescence assay system sensitive to galactose in a microdialysis hollow fiber receptacle. A polyvinyl chloride tube containing a side arm was constructed to mimic the confluence of a venous tributary (i.e., the hepatic vein) with a major vascular channel (i.e., the vena cava). In this simulation, the side arm was continuously perfused with a liver-sensitive analyte (galactose) and the main channel was perfused with galactose-free buffer. A cardiovascular catheter containing a fiberoptic waveguide mounted with a galactose-sensitive fluorescent probe was advanced along the main conduit to assess its ability to identify the location of the galactose side arm infusion site.Measurements and Main ResultsThe response of the fiberoptic sensor to different galactose concentrations was assessed and found to be almost linear over the concentration range of 0 to 2 mM, which encompasses the expected utilization range of this system. The variability in identifying the galactose infusion point (simulated hepatic vein) in a 15-cm conduit was 1.7 to 2.8 mm, or 1.1% to 1.9%.ConclusionsThe construction of a catheter/sensor system with the ability to provide accurate spatial/anatomical localization data for the hepatic venous system is feasible. This assembly will eliminate the need for ancillary imaging systems for catheter/sensor delivery to an individual organ system and potentially can be positioned at the bedside in a fashion similar to the pulmonary artery flotation catheter. (Crit Care Med 1999; 27:1598-1602)
ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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37. |
Effect of nitric oxide, perfluorocarbon, and heliox on minute volume measurement and ventilator volumes delivered |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1603-1607
Venu G.,
Devabhaktuni Adalberto,
Torres Sterling,
Wilson Minken P.,
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摘要:
ObjectiveTo determine the effect of heliox, nitric oxide (NO), and perfluorocarbon on differential pressure pneumotachometer characteristics and to determine the effect of heliox on volumes delivered by the Siemens S900C (S900C), and Servo Ventilator 300 (SV300) ventilators.DesignProspective, laboratory study.SettingPulmonary laboratory of a tertiary care, nonprofit children's hospital.ApparatusSV300, S900C ventilator, differential pressure pneumotachometer.InterventionsDual pneumotachometers were connected in series to a 0.5-L calibration syringe and a 1-L anesthesia bag creating a closed system. Calibration of the pneumotachometers was done in room air at ambient temperature with 100 strokes. Accepted accuracy of measured volumes is within 0.5%. Flow-conductance curves were constructed using 100 strokes each for heliox (70:30 mixture), NO, and perfluorocarbon. Expired gases of room air and a 70:30 mixture of heliox from the above ventilators were collected into a nondiffusing gas collection bag, and the volume was measured in a chain-compensated gasometer. Ten sets of 500-mL breaths (20 breaths each set) and 100-mL breaths (40 breaths each set) were collected. The paired Student's t-test was used to detect significant differences in measured volumes, with significance defined as p < .01.Measurements and Main ResultsVolumes measured with the pneumotachometer using 25 ppm of NO, 50 ppm of NO, and perfluorocarbon were within +0.25%, -0.7%, and +0.4%, respectively (p = .155, p = .001, p = .06). Heliox decreased the conductance of the pneumotachometer, thereby increasing the measured volume by 15% (p < .001). However, heliox did not affect its linearity. Heliox had no affect on volumes delivered by the S900C. However, the SV300 delivered 7.9% less volume of heliox at a set tidal volume of 500 mL and 10.8% less at a set tidal volume of 100 mL.ConclusionsA 70:30 mixture of heliox caused a significantly overestimated gas volume measured and, therefore, an underestimated gas volume delivered by SV300. NO at 25 ppm and perfluorocarbon did not interfere with the accuracy of a differential pressure pneumotachometer. However, at 50 ppm, NO caused a difference in measured gas volume that was statistically, but not clinically, significant. Application of pneumotachometers in critically ill children receiving heliox requires recalibration. Heliox did not affect volumes delivered with the S900C ventilator. Although volumes delivered with the SV300 were significantly reduced by heliox, the difference can be corrected easily by increasing minute ventilation until expired tidal volume equals desired tidal volume. (Crit Care Med 1999; 27:1603-1607)
ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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38. |
VISIT SCCM'S UPDATED WEB SITE |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1607-1607
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ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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39. |
Clinical Gram-positive sepsisDoes it fundamentally differ from Gram-negative bacterial sepsis? |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1608-1616
Steven M. Opal,
Jonathan Cohen,
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摘要:
ObjectiveTo review the basic differences between Gram-positive and Gram-negative sepsis and to assess the effect of these differences on current and future therapeutic strategies for sepsis.DesignLiterature review of the past 30 yrs of laboratory and clinical reports that analyze the microbial aspects of sepsis and the immunologic response to systemic infection.ResultsThe increasing prevalence of sepsis from Gram-positive bacterial pathogens necessitates reevaluation of many of the basic assumptions about the molecular pathogenesis of septic shock. It has been assumed that the initiation of the systemic inflammatory response with activation of the proinflammatory cytokine networks and other mediators results in a similar pathophysiologic process, regardless of the causative microbic pathogen. Yet, there is increasing experimental evidence that fundamental differences exist in the host response to Gram-positive bacterial pathogens compared with the host response to Gram-negative organisms. Systemic immune activation during sepsis may promote the clearance of the microbic pathogen; however, generalized inflammation also contributes to the pathogenesis of septic shock. The balance between these beneficial and deleterious effects may differ between Gram-positive and Gram-negative pathogens.ConclusionsResults of antimediator therapies in clinical trials in septic shock are inconclusive but suggest that the response may differ, depending on the type of microbic pathogen. The immune-mediated pathophysiologic mechanisms that underlie Gram-positive sepsis and the potential interactions between the infecting microorganism and efficacy of anticytokine therapies require further investigation. Treatment strategies that explain the causative organism may be necessary for optimal use of immunoadjuvants in the future. (Crit Care Med 1999; 27:1608-1616)
ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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40. |
ATTENTIONADVERTISERS |
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Critical Care Medicine,
Volume 27,
Issue 8,
1999,
Page 1616-1616
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ISSN:0090-3493
出版商:OVID
年代:1999
数据来源: OVID
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