Acute Respiratory Distress Syndrome Publications (25124)
Acute Respiratory Distress Syndrome Publications
Survival methods were used to determine the relationship among blood component ratios and inflammatory complications.
Patients were primarily male (68%), Caucasians (89%), aged 39 ± 14 years, involved in a motor vehicle collision (53%). Eighty-six percent of patients developed an inflammatory complication; 76% developed organ failure, 27% ventilator-associated pneumonia, and 24% acute respiratory distress syndrome. Injury severity, sex, and total PRBC transfusion volume, not blood component ratio, predicted inflammatory complications.
Increased understanding of factors associated with inflammation after trauma and PRBC transfusion is needed.
We included 4 ARDS patients with a partial arterial oxygen tension over the fraction of inspired oxygen (PaO2/FiO2) lower than 150 mmHg, receiving lung-protective ventilation and treated with the Abylcap® via a double lumen 13.5-Fr dialysis catheter in the femoral vein. Every 24 hours during 5 consecutive days, blood was sampled at the Abylcap® inlet and outlet for different blood flows (QB:200-300-400 mL/min) with 100% O2 gas flow (QG) of 7 L/min, and for different QG (QG: 0.5-1-1.5-3-6-8 L/min) with QB400 mL/min. CO2 and O2 transfer remained constant over 5 days for a fixed QB.
We found that, for a fixed QG of 7 L/min, CO2 transfer linearly and significantly increased with QB (i.e. from 58 ± 8 to 98 ± 16 mL/min for QB 200 to 400 mL/min). For a fixed QB of 400 mL/min, CO2 transfer non-linearly increased with QG (i.e. from 39 ± 9 to 98 ± 16 mL/min for QG 0.5 to 8 L/min) reaching a plateau at QG of 6 L/min.
Hence, when using the Abylcap® ECCO2R in the treatment of ARDS patients the O2 flow should be at least 6 L/min while QB should be set at its maximum.
Healthy volunteers were randomised to receive placebo or aspirin 75 or 1200 mg (1:1:1) for seven days prior to lipopolysaccharide (LPS) inhalation, in a double-blind, placebo-controlled, allocation-concealed study. Bronchoalveolar lavage (BAL) was performed 6 hours after inhaling 50 µg of LPS. The primary outcome measure was BAL IL-8. Secondary outcome measures included markers of alveolar inflammation (BAL neutrophils, cytokines, neutrophil proteases), alveolar epithelial cell injury, systemic inflammation (neutrophils and plasma C-reactive protein (CRP)) and platelet activation (thromboxane B2, TXB2). Human lungs, perfused and ventilated ex vivo (EVLP) were randomised to placebo or 24 mg aspirin and injured with LPS. BAL was carried out 4 hours later. Inflammation was assessed by BAL differential cell counts and histological changes.
In the healthy volunteer (n=33) model, data for the aspirin groups were combined. Aspirin did not reduce BAL IL-8. However, aspirin reduced pulmonary neutrophilia and tissue damaging neutrophil proteases (Matrix Metalloproteinase (MMP)-8/-9), reduced BAL concentrations of tumour necrosis factor α and reduced systemic and pulmonary TXB2. There was no difference between high-dose and low-dose aspirin. In the EVLP model, aspirin reduced BAL neutrophilia and alveolar injury as measured by histological damage.
These are the first prospective human data indicating that aspirin inhibits pulmonary neutrophilic inflammation, at both low and high doses. Further clinical studies are indicated to assess the role of aspirin in the prevention and treatment of ARDS.
The quantification of pulmonary molecular imaging data remains challenging due to variations in tissue, air, blood and water fractions within the lungs. The proportions of these components further differ depending on the lung disease. Therefore, different quantification approaches have been proposed to address these variabilities. However, no standardized approach has been developed to date. This article reviews the data evaluating (18)F-FDG PET quantification approaches in lung diseases, focusing on methods to account for variations in lung components and the interpretation of the derived parameters. The diseases reviewed include acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD) and interstitial lung disease such as idiopathic pulmonary fibrosis (IPF). Based on review of prior literature, ongoing research and discussions amongst the authors, suggested considerations are presented to assist with the interpretation of the derived parameters from these approaches and the design of future studies.
, elastance decrease during inflation, pressure-volume curve with upward curvature) or overdistension (i.e., elastance increase during inflation, downward curvature).
Secondary analysis of experimental cohort study.
University research facility.
Twelve mechanically ventilated pigs.
After induction of acute respiratory distress syndrome by hydrochloric acid instillation, animals underwent a decremental positive end-expiratory pressure titration (steps of 2 cm H2O starting from ≥ 26 cm H2O).
Electrical impedance tomography-derived maps were computed at each positive end-expiratory pressure-titration step, and whole-lung CT taken every second steps. Airway flow and pressure were recorded to compute driving pressure and elastance. Significant correlations between electrical impedance tomography-derived maps and positive end-expiratory pressure indicate that, expectedly, tidal recruitment increases in dependent regions with decreasing positive end-expiratory pressure (p < 0.001) and suggest that overdistension increases both at high and low positive end-expiratory pressures in nondependent regions (p < 0.027), supporting the idea of two different scenarios of overdistension occurrence. Significant correlations with CT measurements were observed: electrical impedance tomography-derived tidal recruitment with poorly aerated regions (r = 0.43; p < 0.001); electrical impedance tomography-derived overdistension with nonaerated regions at lower positive end-expiratory pressures and with hyperaerated regions at higher positive end-expiratory pressures (r ≥ 0.72; p < 0.003). Even for positive end-expiratory pressure levels minimizing global elastance and driving pressure, electrical impedance tomography-derived maps showed nonnegligible regions of presumed overdistension and tidal recruitment.
Electrical impedance tomography-derived maps of pressure-volume curve shapes allow to detect regions in which elastance changes during inflation. This could promote individualized mechanical ventilation by minimizing the probability of local tidal recruitment and/or overdistension. Electrical impedance tomography-derived maps might become clinically feasible and relevant, being simpler than currently available alternative approaches.
The primary indicators to assess the lung injury were infiltration of inflammatory cells; pulmonary edema; expression of proinflammatory cytokines, cyclo-oxygenase 2, and intracellular adhesion molecule 1; activation of nuclear factor-κB pathways; and cellular apoptosis. The results showed that LG evidently alleviated the inflammatory response, decreased the apoptosis of alveolar macrophages, and improved the lung injury in mice with LPS-induced ARDS. In conclusion, LG improved LPS-induced ARDS by anti-inflammation and anti-apoptosis and might be a promising pharmacological therapy for ARDS.
Mediation of the JHR in RF by the pro-inflammatory cytokines tumor necrosis factor (TNF), interleukin (IL)-6, and IL-8 has been proposed, consistent with measurements in patients' blood and inhibition by anti-TNF antibodies. Accelerated phagocytosis of spirochetes by polymorphonuclear (PMN) leukocytes before rise in cytokines is responsible for removal of organisms from the blood, suggesting an early inflammatory signal from PMNs. Rarely fatal, except in neonates and in pregnancy for African women whose babies showed high perinatal mortality because of low birth weight, the JHR can be regarded as an adverse effect of antibiotics, necessary for achieving a cure of spirochetal infections.
We conducted two web-based, cross-sectional surveys of ICU organizational practices in Pennsylvania acute care hospitals, in 2005 (chief nursing officer respondents) and 2014 (ICU nurse manager respondents).
Of 223 eligible respondents, nurse managers from 136 (61%) medical, surgical, mixed medical-surgical, cardiac, and specialty ICUs in 98 hospitals completed the 2014 survey, compared to 124 of 164 (76%) chief nursing officers in the 2005 survey. In 2014, daytime physician staffing models varied widely, with 23 of 136 (17%) using closed models and 33 (24%) offering no intensivist staffing. Nighttime intensivist staffing was used in 37 (27%) ICUs, 38 (28%) used non-intensivist attending staffing, and 24 (18%) had no nighttime attending physicians. Daily multidisciplinary rounds occurred in 93 (68%) ICUs. Regular participants included clinical pharmacists in 68 of 93 (73%) ICUs, respiratory therapists in 62 (67%), and advanced practitioners in 37 (39%). Patients and family members participated in rounds in 36 (39%) ICUs. Clinical protocols or checklists for mechanically ventilated patients were available in 128 of 133 (96%) ICUs, low tidal volume ventilation for Acute Respiratory Distress Syndrome (ARDS) in 54 of 132 (41%) ICUs, prone positioning for severe ARDS in 37 of 134 (28%) ICUs, and family meetings in 19 of 134 (14%) ICUs. Among 61 ICUs that responded to both surveys, there was a significant increase in the proportion of ICUs employing nighttime in-ICU attending physicians [23 (38%) in 2005 vs 30 (49%) in 2014, p=0.006].
The diffusion of evidence-based ICU organizational practices has been variable across the state of Pennsylvania. Only half of Pennsylvania ICUs have intensivists dedicated to the ICU. Variable numbers use clinical protocols for life-saving therapies, and few use structured family engagement strategies. In contrast, the diffusion of non-evidence-based practices, including overnight ICU attending physician staffing, is increasing. Future research should focus on promoting implementation of organizational evidence to promote high-quality ICU care.
In this regard, the assessment of genetic polymorphisms responsible for developing ARDS present as a challenge and are considered future biomarkers. Early detection of the specific polymorphic gene responsible for ARDS in critically ill patients can prove to be a useful tool in the future, able to help decrease the mortality rates in these cases. Moreover, identifying the genetic polymorphism in these patients can help in the implementation of a personalized intensive therapy scheme for every type of patient, based on its genotype.
Imaging suggested interstitial pneumonia and an iliopsoas abscess, and blood tests showed liver dysfunction and disseminated intravascular coagulation (DIC). Despite three-agent combined therapy for tuberculosis, she died 32 days after hospitalization. PMI showed multiple fresh cerebral and cerebellar infarctions and diffuse ground-glass shadows in bilateral lungs. On autopsy, the diagnosis of miliary tuberculosis was made, and non-bacterial thrombotic endocarditis that involved the aortic valve may have caused the cerebral infarctions. A 74-year-old man on steroid therapy for systemic lupus erythematosus presented with severe anemia, melena with no obvious source, and DIC. Imaging suggested intestinal perforation. The patient was treated with antibiotics and drainage of ascites. However, he developed adult respiratory distress syndrome, worsening DIC, and renal dysfunction and died 2 months after admission. PMI showed infiltrative lung shadow, ascites, an abdominal aortic aneurysm, a wide infarction in the right parietal lobe, and multiple new cerebral infarctions. Autopsy examination showed purulent ascites, diffuse peritonitis, invasive bronchopulmonary aspergillosis, and non-bacterial thrombotic endocarditis that likely caused the cerebral infarctions. A 65-year-old man with an old pontine infarction presented with a fever and neutropenia. Despite appropriate treatment, his fever persisted. CT showed bilateral upper lobe pneumonia, pain appeared in both femoral regions, and intramuscular abscesses of both shoulders developed. His pneumonia worsened, his level of consciousness decreased, right hemiplegia developed, and he died. PMI showed a newly diagnosed cerebral infarction in the left parietal lobe. The autopsy revealed bilateral bronchopneumonia, right-sided pleuritis with effusion, an intramuscular abscess in the right thigh, and fresh multiple organ infarctions. Systemic fibrin thrombosis and DIC were also found. Postmortem cultures showed E. coli and Burkholderia cepacia.
Cerebral infarction that is newly recognized on PMI might suggest the presence of severe systemic infection.