Articles: respiratory-distress-syndrome.
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Acute respiratory failure is commonly encountered in severe acute brain injury due to a multitude of factors related to the sequelae of the primary injury. The interaction between pulmonary and neurologic systems in this population is complex, often with competing priorities. Many treatment modalities for acute respiratory failure can result in deleterious effects on cerebral physiology, and secondary brain injury due to elevations in intracranial pressure or impaired cerebral perfusion. High-quality literature is lacking to guide clinical decision-making in this population, and deliberate considerations of individual patient factors must be considered to optimize each patient's care.
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Am. J. Respir. Crit. Care Med. · Apr 2024
Host and Microbe Blood Metagenomics Reveals Key Pathways Characterizing Critical Illness Phenotypes.
Rationale: Two molecular phenotypes of sepsis and acute respiratory distress syndrome, termed hyperinflammatory and hypoinflammatory, have been consistently identified by latent class analysis in numerous cohorts, with widely divergent clinical outcomes and differential responses to some treatments; however, the key biological differences between these phenotypes remain poorly understood. Objectives: We used host and microbe metagenomic sequencing data from blood to deepen our understanding of biological differences between latent class analysis-derived phenotypes and to assess concordance between the latent class analysis-derived phenotypes and phenotypes reported by other investigative groups (e.g., Sepsis Response Signature [SRS1-2], molecular diagnosis and risk stratification of sepsis [MARS1-4], reactive and uninflamed). Methods: We analyzed data from 113 patients with hypoinflammatory sepsis and 76 patients with hyperinflammatory sepsis enrolled in a two-hospital prospective cohort study. ⋯ Significant overlap was observed between these phenotypes and previously identified transcriptional subtypes of acute respiratory distress syndrome (reactive and uninflamed) and sepsis (SRS1-2). Analysis of data from the VANISH trial indicated that corticosteroids might have a detrimental effect in patients with the hypoinflammatory phenotype. Conclusions: The hyperinflammatory and hypoinflammatory phenotypes have distinct transcriptional and metagenomic features that could be leveraged for precision treatment strategies.
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Acute respiratory failure relies on supportive care using non-invasive and invasive oxygen and ventilatory support. Pharmacologic therapies for the most severe form of respiratory failure, acute respiratory distress syndrome (ARDS), are limited. ⋯ Treatment requires prompt recognition of ARDS and an understanding of which patients may benefit most from specific pharmacologic interventions. The key to finding effective pharmacotherapies for ARDS may rely on deeper understanding of pathophysiology and bedside identification of ARDS subphenotypes.
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Acute respiratory failure is a common clinical finding caused by insufficient oxygenation (hypoxemia) or ventilation (hypocapnia). Understanding the pathophysiology of acute respiratory failure can help to facilitate recognition, diagnosis, and treatment. The cause of acute respiratory failure can be identified through utilization of physical examination findings, laboratory analysis, and chest imaging.
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Respiratory failure may affect up to 1 in 500 pregnancies, due to pregnancy-specific conditions, conditions aggravated by the pregnant state, or other causes. Management during pregnancy is influenced by altered maternal physiology, and the presence of a fetus influencing imaging, and drug therapy choices. ⋯ Hypocapnia reduces uteroplacental circulation, and some degree of hypercapnia may be tolerated in pregnancy. Delivery of the fetus may be considered to improve maternal respiratory status but improvement does not always occur.