Background: Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are syndromes of severe respiratory failure that are associated with substantial mortality and morbidity. Artifical ventilatory support is commonly required and may exacerbate lung injury. Partial liquid ventilation (PLV) has been proposed as a less injurious form of ventilatory support for these patients. Although PLV has been shown to improve gas exchange and to reduce inflammation in experimental models of ALI, a previous systematic review did not find any evidence to support or refute its use in humans with ALI and ARDS.
Objectives: The primary objective of this review was to assess whether PLV reduced mortality (at 28 d, at discharge from the intensive care unit (ICU), at discharge from hospital and at one, two and five years) in adults with ALI or ARDS when compared with conventional ventilatory support.Secondary objectives were to determine how PLV compared with conventional ventilation with regard to duration of invasive mechanical ventilation, duration of respiratory support, duration of oxygen therapy, length of ICU stay, length of hospital stay, incidence of infection, long-term cognitive impairment, long-term health related quality of life, long- term lung function, long-term morbidity costs and adverse events. The following adverse events were considered: hypoxia (arterial PO2 <80 mm Hg), pneumothorax (any air leak into the pleural space requiring therapeutic intervention), hypotension (systolic blood pressure < 90 mm Hg sustained for longer than two minutes or requiring treatment with fluids or vasoactive drugs), bradycardia (heart rate < 50 beats per minute sustained for longer than one minute or requiring therapeutic intervention) and cardiac arrest (absence of effective cardiac output).
Search Methods: In this updated review, we searched the Cochrane Central Register of Controlled Trials (CENTRAL Issue 10, 2012, in The Cochrane Library; MEDLINE (Ovid SP, 1966 to November 2012); EMBASE (Ovid SP, 1980 to November 2012) and CINAHL (EBSCOhost,1982 to November 2012) for published studies. In our original review, we searched until May 2004.Grey literature was identified by searching conference proceedings and trial registries and by contacting experts in the field.
Selection Criteria: As in the original review, review authors selected randomized controlled trials that compared PLV with other forms of ventilation in adults (16 y of age or older) with ALI or ARDS, reporting one or more of the following: mortality; duration of mechanical ventilation, respiratory support, oxygen therapy, stay in the intensive care unit or stay in hospital; infection; long-term cognitive impairment or health-related quality of life; long-term lung function or cost.
Data Collection And Analysis: Two review authors independently evaluated the quality of the relevant studies and extracted the data from included studies.
Main Results: In this updated review, one new eligible study was identified and included, yielding a total of two eligible studies (including a combined total of 401 participants). Of those 401 participants, 170 received 'high'-dose partial liquid ventilation (i.e. a mean dose of at least 20 mL/kg), 99 received 'low-dose' partial liquid ventilation (i.e. a dose of 10 mL/kg) and 132 received conventional mechanical ventilation (CMV). Pooled estimates of effect were calculated for all those who received 'high'-dose PLV versus conventional ventilation. No evidence indicated that 'high'-dose PLV either reduced mortality at 28 d (risk ratio (RR) 1.21, 95% confidence interval (CI) 0.79 to 1.85, P = 0.37) or increased the number of days free of CMV at 28 d (mean difference (MD) -2.24, 95% CI -4.71 to 0.23, P = 0.08). The pooled estimate of effect for bradycardia in those who received PLV was significantly greater than in those who received CMV (RR 2.51, 95% CI 1.31 to 4.81, P = 0.005). Pooled estimates of effect for the following adverse events- hypoxia, pneumothorax, hypotension and cardiac arrest- all showed a nonsignificant trend towards a higher occurrence of these events in those treated with PLV. Because neither eligible study addressed morbidity or mortality beyond 28 d, it was not possible to determine the effect of PLV on these outcomes.
Authors' Conclusions: No evidence supports the use of PLV in ALI or ARDS; some evidence suggests an increased risk of adverse events associated with its use.
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http://dx.doi.org/10.1002/14651858.CD003707.pub3 | DOI Listing |
Burns Trauma
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Treatment Center for Traumatic Injuries, The Third Affiliated Hospital, Southern Medical University, No. 183, Zhongshan Avenue West, Tianhe District, Guangzhou, 510063, Guangdong, China.
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January 2025
Department of Burn, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Second Ruijin Road, Huangpu District, Shanghai, 200025, China.
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View Article and Find Full Text PDFClin Case Rep
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Pediatric Intensive Care Unit, Department of Maternal and Child Health and Urological Sciences Sapienza University of Rome Rome Italy.
Key Clinical Message: Although the symptoms of accidental chlorine inhalation are typically mild, severe exposure can result in acute respiratory distress syndrome (ARDS). We present a case of pediatric ARDS due to chlorine exposure in which lung lavage and exogenous surfactant were successful in avoiding more invasive and costly treatments.
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Phytomedicine
January 2025
Department of Integrative Biotechnology, and Biomedical Institute for Convergence at SKKU, Sungkyunkwan University, Suwon 16419, Republic of Korea; Department of Biocosmetics, Sungkyunkwan University, Suwon 16419, Republic of Korea. Electronic address:
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January 2025
Department of Pathology, Dokkyo Medical University School of Medicine and Graduate School of Medicine, 880 Kitakobayashi, Mibu, Shimotsugagun, Tochigi, 321-0293, Japan.
Although alveolar hyperoxia exacerbates lung injury, clinical studies have failed to demonstrate the beneficial effects of lowering the fraction of inspired oxygen (FO) in patients with acute respiratory distress syndrome (ARDS). Atelectasis, which is commonly observed in ARDS, not only leads to hypoxemia but also contributes to lung injury through hypoxia-induced alveolar tissue inflammation. Therefore, it is possible that excessively low FO may enhance hypoxia-induced inflammation in atelectasis, and raising FO to an appropriate level may be a reasonable strategy for its mitigation.
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