Long-term cognitive impairment after acute respiratory distress syndrome: a review of clinical impact and pathophysiological mechanisms
Open accessAbstract
Acute respiratory distress syndrome (ARDS) survivors experience a high prevalence of cognitive impairment with concomitantly impaired functional status and quality of life, often persisting months after hospital discharge. In this review, we explore the pathophysiological mechanisms underlying cognitive impairment following ARDS, the interrelations between mechanisms and risk factors, and interventions that may mitigate the risk of cognitive impairment. Risk factors for cognitive decline following ARDS include pre-existing cognitive impairment, neurological injury, delirium, mechanical ventilation, prolonged exposure to sedating medications, sepsis, systemic inflammation, and environmental factors in the intensive care unit, which can co-occur synergistically in various combinations. Detection and characterization of pre-existing cognitive impairment imparts challenges in clinical management and longitudinal outcome study enrollment. Patients with brain injury who experience ARDS constitute a distinct population with a particular combination of risk factors and pathophysiological mechanisms: considerations raised by brain injury include neurogenic pulmonary edema, differences in sympathetic activation and cholinergic transmission, effects of positive end-expiratory pressure on cerebral microcirculation and intracranial pressure, and sensitivity to vasopressor use and volume status. The blood-brain barrier represents a physiological interface at which multiple mechanisms of cognitive impairment interact, as acute blood-brain barrier weakening from mechanical ventilation and systemic inflammation can compound existing chronic blood-brain barrier dysfunction from Alzheimer’s-type pathophysiology, rendering the brain vulnerable to both amyloid-beta accumulation and cytokine-mediated hippocampal damage. Although some contributory elements, such as the presenting brain injury or pre-existing cognitive impairment, may be irreversible, interventions such as minimizing mechanical ventilation tidal volume, minimizing duration of exposure to sedating medications, maintaining hemodynamic stability, optimizing fluid balance, and implementing bundles to enhance patient care help dramatically to reduce duration of delirium and may help prevent acquisition of long-term cognitive impairment.
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Putative biological mechanisms underlying long-term cognitive impairment in ARDS patients include hypoxia, cytokine-mediated damage, cerebral autoregulation disruption, and blood-brain barrier damage-associated decrease in Amyloid-β clearance.
“Putative biological mechanisms underlying long-term cognitive impairment in ARDS patients include hypoxia, cytokine-mediated damage, cerebral autoregulation disruption, and blood–brain barrier damage-associated decrease in Amyloid-β clearance [124].”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [124]
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Bickenbach, J., Biener, I., Czaplik, M., Nolte, K. W., Dembinski, R., Marx, G., Rossaint, R., & Fries, M. (2011) · Respiratory Physiology & Neurobiology · doi:10.1016/j.resp.2011.08.003 · Cited by 37 · see citing works
Acute lung injury in head trauma patients
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Miskowiak, K., Johnsen, S., Sattler, S., Nielsen, S., Kunalan, K., Rungby, J., Lapperre, T., & Porsberg, C. (2021) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2021.03.019 · Cited by 365 · see citing works
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Investigating Ketone Bodies as Immunometabolic Countermeasures against Respiratory Viral Infections
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Rabinovitz, B., Jaywant, A., & Fridman, C. B. (2020) · The Clinical Neuropsychologist · doi:10.1080/13854046.2020.1803408 · Cited by 46 · see citing works
- Authors
- Sasannejad, C., Ely, E. W., & Lahiri, S.
- Affiliations
- Yale University (US)
- Vanderbilt University (US)
- Cedars-Sinai Medical Center (US)
- Corresponding author
- Lahiri, Shouri
- Venue
- Critical Care
- Published
- 2019-11-12
- Volume
- 23
- Issue
- 1
- Pages
- 352-352
- ISSN
- 1364-8535 (ISSN-L)
- PMC
- PMC6852966
- OpenAlex
- W2984454129
- Cited by
- 326
- References
- 89
- Citations by year
- 2026: 16 · 2025: 33 · 2024: 33 · 2023: 43 · 2022: 64 · 2021: 84 · 2020: 53
- FWCI
- 8.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Critical Care (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (R03AG064106)
- American Academy of Neurology (Career Development Award)
- Topics
- Health Sciences › Medicine › Critical Care and Intensive Care Medicine › Intensive Care Unit Cognitive Disorders
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Respiratory Support and Mechanisms
- Health Sciences › Medicine › Infectious Diseases › Infectious Encephalopathies and Encephalitis
- Keywords
- acute respiratory distress syndrome, long-term cognitive decline, delirium, brain injury, neurogenic pulmonary edema, mechanical ventilation, sedation, sepsis, systemic inflammation, blood-brain barrier, amyloid-beta, hippocampal lesions, positive end-expiratory pressure, vasopressors, fluid balance, ICU environment, risk factors, cognitive impairment prevention
- MeSH terms
- Hypoxia, Humans, Respiration, Artificial, Respiratory Distress Syndrome, Risk Factors, Cognitive Dysfunction
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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