Search strategies were developed based on the search interface, to ensure an appropriate balance between search sensitivity and specificity.
Searches were conducted using the following sources: Medline (1946-present), EMBASE (1974-present), Cochrane Database of Systematic Reviews, Cochrane Central Register of Controlled Trials, Cochrane Methodology Register, and the Database of Abstracts of Reviews and Effects (DARE). Searches were performed by a librarian at the Health Sciences Library at Fraser Health Authority, Royal Columbian Hospital (New Westminster, Canada). This study was conducted following the Preferred Reporting Items for Systematic Review and Meta-Analysis (PRISMA) protocol. Our secondary objective was to identify possible gaps in the literature that can inform the design of future studies for a better understanding of this complex problem. The primary objective of this systematic review was to identify published papers that assess any link between MV and either cognitive impairment or brain insult, independent of underlying medical conditions. We sought to explore the current knowledge in the literature regarding MV, delirium, cognitive impairment, and neuroinflammation, through a systematic review. However, it is likely that there are many factors beyond neuroinflammation that can contribute to cognitive impairment in the ICU, such as medications, immobility, overload of sensory input and lack of adequate sleep. This indicates that when neuroinflammation is triggered, by direct brain insult, aberrant systemic stress response, or some other mechanism, it may be associated with cognitive dysfunction. Taking as an example a case–control post-mortem study of deceased ICU patients without direct brain injury, higher levels of inflammatory cells were reported in the hippocampi of deceased patients with delirium than in patients without delirium. Regardless of the mechanism that triggers delirium, it is postulated that delirium is a result of an imbalance in neurotransmitters, specifically acetylcholine and dopamine, impairing the connection among several brain areas. Pathophysiologically, some authors have classified the mechanism that triggers delirium into two distinct categories, direct brain insult (such as hemorrhagic stroke), and aberrant stress response (such as systemic stress induced by MV, sepsis, septic shock, systemic inflammation post-surgery, etc.). Currently, direct links between MV, delirium, cognitive impairment, and neuroinflammation have not been established in the literature.ĭelirium is a complex disturbance of consciousness, characterized by acute changes in cognition, a direct consequence of a medical condition, medical treatment, or intoxicating substance. Preclinical experiments have, however, shown lower cognitive scores in subjects ventilated longer, and that these subjects had greater levels of brain insult, neuroinflammation, and neuronal apoptosis than subjects either mechanically ventilated less, or spontaneously breathing. Ventilation-induced brain injury (VIBI) is well known in neonatology, as a consequence of either hyperoxia or the use of intermittent positive pressure ventilation in adult patients, the existence of VIBI is still unknown. While it is undeniable that MV is a crucial life-support tool, it may also cause injury to distal organs, such as the lungs, diaphragm, and brain.
Mechanical ventilation (MV) is considered essential in the Intensive Care Unit (ICU). More studies should be designed to investigate ventilation-induced brain injury pathways as well as any causative linkage between MV, cognitive impairment, and brain insult.
The clinical literature suggests an association between MV and delirium, and that delirium in mechanically ventilated patients may be associated with greater likelihood of long-term cognitive impairment our systematic review found no clinical study that demonstrated a causal link between MV, cognitive dysfunction, and brain insult. The preclinical literature suggests that MV is associated with neuroinflammation, cognitive impairment, and brain insult, reporting higher neuroinflammatory markers, greater evidence of brain injury markers, and lower cognitive scores in subjects that were ventilated longer, compared to those ventilated less, and to never-ventilated subjects. Secondary objectives were to identify possible gaps in the literature that can be used to inform future studies and move toward a better understanding of this complex problem. We conducted a systematic review following the PRISMA protocol primarily to identify publications that assessed any links between mechanical ventilation (MV) and either cognitive impairment or brain insult, independent of underlying medical conditions.
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