Introduction
Background and epidemiology
Cognitive impairment in survivors of acute respiratory distress syndrome: clinical burden and long-term sequelae
Author(s) | Year | Methodology | Results/conclusions |
---|---|---|---|
Davidson et al. | 1999 | Prospective cohort (n = 146) | Patients who survived ARDS experience significantly reduced quality of life following discharge compared to critically ill patients without ARDS |
Hopkins et al. | 1999 | Prospective cohort (n = 62) | Survivors of ARDS demonstrate cognitive impairments in memory, attention, concentration, and processing speed: 100% at discharge and 78% at 1 year after discharge |
Contant et al. | 2001 | Observational (n = 161) | ARDS following severe head injury results in severe intracranial hypertension. Targeting intracranial pressure rather than cerebral blood flow improves outcomes |
Georgiadis et al. | 2001 | Prospective interventional (n = 20) | In patients with acute stroke receiving mechanical ventilation, changes in cerebral perfusion pressure are mediated by mean arterial pressure rather than by positive end-expiratory pressure. Positive end-expiratory pressure does not increase intracranial pressure as long as hemodynamic stability is maintained |
Holland et al. | 2003 | Prospective cohort (n = 137) | In patients with traumatic brain injury, ARDS independently predicts mortality and is associated with worse long-term neurological outcome |
Ely et al. | 2004 | Prospective cohort (n = 275) | Delirium independently predicts higher mortality and longer hospital stay among patients treated with mechanical ventilation |
Mascia et al. | 2005 | Prospective interventional (n = 12) | Positive end-expiratory pressure does not affect intracranial pressure when inducing alveolar recruitment, but does lead to significant increases in PaCO2 and intracranial pressure when inducing alveolar hyperinflation |
Muench et al. | 2005 | Prospective interventional (n = 10) | In hemodynamically unstable patients with severe subarachnoid hemorrhage, increases in positive end-expiratory pressure disturb cerebrovascular autoregulation, resulting in significant decreases in mean arterial pressure and regional cerebral blood flow |
Mascia et al. | 2007 | Observational (n = 82) | High-tidal-volume mechanical ventilation is associated with the development of ARDS after severe brain injury |
Fong et al. | 2009 | Secondary analysis of prospective cohort (n = 408) | Delirium accelerates cognitive decline in patients with probable or possible Alzheimer’s disease |
Taccone et al. | 2009 | Observational (n = 21) | Septic shock impairs cerebral autoregulation in patients with septic shock, particularly with concurrent hypercapnia |
Janz et al. | 2010 | Retrospective cohort (n = 7 from database of 379) | Brain autopsy of patients with ICU delirium shows hypoxic ischemic damage in the hippocampus, suggesting a link between ICU delirium and long-term cognitive impairment |
van den Boogard et al. | 2011 | Exploratory observational (n = 100) | The underlying mechanism of delirium may differ in patients with systemic inflammation versus patients without systemic inflammation and is mediated by different cytokines for each mechanism |
Mikkelsen et al. | 2012 | Prospective cohort (n = 102) | Survivors of ARDS 1 year following discharge demonstrate a confluence of cognitive impairment, psychiatric sequelae, and diminished quality of life. Hypoxemia and conservative fluid management are associated with these long-term impairments |
Elmer et al. | 2013 | Retrospective cohort (n = 697) | High-tidal-volume mechanical ventilation in patients with intracerebral hemorrhage is associated with the development of ARDS and increased mortality |
Pandharipande et al. | 2013 | Prospective cohort (n = 821) | At 12-month follow-up after discharge, 1/4 of patients who had been critically ill demonstrate cognitive impairment similar in severity to that seen in mild Alzheimer’s disease, and 1/3 similar in severity to that seen in traumatic brain injury |
Needham et al. | 2014 | Prospective cohort (n = 203) | At 6- and 12-month follow-up, ARDS survivors demonstrated impairments in 6-min walk distance and physical function outcomes. Minimizing the duration of intensive care and corticosteroid use may reflect modifiable risk factors |
Girard et al. | 2018 | Prospective cohort (n = 1040 enrolled, n = 586 follow-up) | Patients with ARDS, septic shock, or both experience multiple subtypes of delirium associated with long-term cognitive impairment at 3- and 12-month follow-up, including hypoxic, septic, unclassified, and sedative-associated delirium. The durations of these delirium subtypes predict worse cognitive function at 12-month follow-up, particularly sedative-associated delirium |
ARDS in brain injury
Risk factors for cognitive decline
Pre-existing cognitive impairment and the interface of delirium and dementia
Delirium subtypes and pathways
ARDS and hypoxemia: short-term and long-term effects
Inflammation and septic delirium
Mechanical ventilation and inflammatory and sedative-associated delirium
Putative biological mechanisms
Inflammation and hypoxemia
Author(s) | Year | Animal model | Results/conclusions |
---|---|---|---|
De la Torre et al. | 1992 | Rat | Chronic cerebrovascular insufficiency following ligation of the common carotid and left subclavian arteries in aged rats induces behavioral and cognitive impairments consistent with dementia |
Pappas et al. | 1996 | Rat | Rats exposed to chronic reduction of cerebral blood flow following carotid artery ligation develop memory dysfunction and cell loss in the CA1 region of the hippocampus |
Feldman et al. | 1997 | Rabbit | Positive end-expiratory pressure reduces intracranial compliance in rabbits |
Wilson et al. | 2003 | Mouse | High-tidal-volume mechanical ventilation upregulates cytokines in mouse lungs |
Altmeier et al. | 2005 | Mouse | Systemic inflammation simulated by lipopolysaccharide in mechanically ventilated mice induces cytokine-mediated lung injury in mechanically ventilated wild-type mice |
Fries et al. | 2005 | Pig | Mechanically ventilated pigs exposed to hypoxemia with lung injury develop histopathologic changes in the CA1 region of the hippocampus not when exposed to the same degree of hypoxemia alone, suggesting lung injury as a mechanism of damage independent from hypoxemia |
Semmler et al. | 2005 | Rat | Systemic inflammation induces apoptosis in the rat brain, particularly in the hippocampus |
Wilson et al. | 2005 | Mouse | Pulmonary inflammation following high-tidal-volume mechanical ventilation in mice without underlying lung injury is mediated by TNF-α |
Bickenbach et al. | 2009 | Pig | Low- versus high-tidal-volume mechanical ventilation improves cerebral tissue oxygenation in pigs |
Wolthuis et al. | 2009 | Mouse | Mechanical ventilation even at lower tidal volumes causes lung injury in wild-type mice without history of lung disease |
Bickenbach et al. | 2011 | Pig | Mechanically ventilated pigs exposed to hypoxemia with lung injury demonstrate trends toward elevated cytokines IL-6 and TNF-α in the CA1 region of the hippocampus versus mechanically ventilated pigs exposed to hypoxemia alone |
Heuer et al. | 2011 | Pig | In mechanically ventilated pigs, ARDS results in elevations in TNF-α, IL-6, and IL-1β, which further increase in pigs with acute intracranial hypertension. The combination of ARDS and acute intracranial hypertension results in hippocampal damage. Acute intracranial hypertension induces lung injury and extravascular lung water |
Imamura et al. | 2011 | Mouse | In a mouse model of septic encephalopathy, an IL-1β cytokine-mediated process disrupts the synaptic processing of long-term potentiation in the hippocampus |
Davis et al. | 2015 | Mouse | Baseline neurodegeneration in mice increases the risk, duration, and severity of delirium |
Shohami et al. | 2016 | Rat | TNF-α and IL-6 are detected in the contused hemisphere of rats soon after closed head injury, but not in healthy rats. TNF-α is detected as early as 1 h after injury and peaks at 4 h, whereas IL-6 is detected at 3–5 h and peaks at 8 h after injury |
Lahiri et al. | 2019 | Mouse | High-tidal-volume mechanical ventilation simulates Alzheimer’s disease pathophysiology in transgenic Alzheimer’s disease and wild-type mice |