Acute respiratory distress syndrome (ARDS) is characterized by pathological pulmonary edema caused by direct or indirect damage to the alveolar-capillary membrane.

Its management relies on etiological treatment, invasive mechanical ventilation, and the use of sedatives and neuromuscular blockers, depending on the patient's condition.

Improvements in patient care have led to an improved prognosis. However, in-hospital mortality remains high (between 35% and 45%). Notably, morbidity among surviving patients is very high and is largely dominated by neuropsychological sequelae. Attention and executive function disorders, confusion, disorientation, or memory impairment are thus found in 70 to 100% of patients following ARDS. These disorders are still present in 46 to 80% of surviving patients one year after ARDS and in 20% of them five years later.

Although essential to treatment, mechanical ventilation carries a risk of significant complications. Beyond the risk of infection and complications related to sedation and neuromuscular blockade, the use of mechanical ventilation is associated with a risk of ventilator-induced lung injury (VILI).

The use of so-called protective ventilation reduces the risk of VILI and improves patient outcomes. However, analysis of relevant physiological parameters shows that the risk of VILI may still exist even when ventilator settings comply with recommendations and the concept of protective ventilation. Driving pressure (which represents Strain) is a good marker of VILI; it represents the distension of the lung with each breath relative to the initial lung volume. Values above 14 cmH₂O are associated with high mortality in patients with ARDS. Inspiratory transpulmonary pressure represents Stress-that is, the pressure that distends the alveoli at the end of inspiration-and is also associated with the risk of VILI. Finally, mechanical power represents the amount of energy delivered to the lung by the ventilator and has been validated as a marker of VILI. The advantage of mechanical power over the other indices described is that it incorporates all components that can lead to VILI.

Among the various sources of neurological damage during ARDS, inflammatory processes appear to play a major role. Numerous inflammatory mediators (TNF-α, IL-6, IL-8, IL-1β) are secreted during ARDS, and animal studies have demonstrated a link between inflammation and hippocampal damage. Furthermore, cerebral ischemic lesions, exacerbated by systemic inflammation and endothelial activation leading to coagulation activation with thrombus formation, may also contribute to the development of cognitive impairments.

In addition to the inflammatory processes associated with ARDS, mechanical ventilation itself may have a significant impact on neuroinflammatory damage. Recently, the term "ventilator-associated brain injury" (VABI) has been proposed to describe these secondary neurological lesions induced by mechanical ventilation. Studies in mouse and pig models have demonstrated a relationship between the dose and duration of VILI, apoptosis, neuroinflammation, and neuronal damage. An animal study in mice also showed an association between the duration of mechanical ventilation and the onset of cognitive impairments.

During brain injury, proteins and neurotransmitters are released and serve as biomarkers of brain damage. Elevated plasma levels of S100B protein indicate astrocyte damage caused by traumatic, anoxic-ischemic, or inflammatory mechanisms. It correlates with neurological prognosis following cardiac arrest, in ischemic or hemorrhagic strokes, in neurodegenerative diseases, and in patients with traumatic brain injury.

Clinical studies have shown a negative correlation between elevated S100B protein levels, the MoCA (Montreal Cognitive Assessment) score, and the MMSE (Mini-mental state evaluation ) in patients with OSA (Obstructive Sleep Apnea) or COPD (chronic obstructive pulmonary disease), respectively, indicating an association between this protein and cognitive impairment.

The investigators therefore hypothesize that mechanical ventilation associated with high mechanical power is linked to a significant risk of brain injury, reflected by elevated serum S100B protein levels and the presence of neurocognitive disorders long after ARDS.

Inclusion Criteria:

• Adult patient

• Patient admitted to the intensive care unit less than 48 hours ago

• Patient diagnosed with mild, moderate or severe ARDS according to the Berlin classification based on the PaO₂/FiO₂ ratio, with a minimum PEEP set at 5 cmH₂O (16), of pulmonary aetiology:

  • Mild ARDS: 200 < PaO₂/FiO₂ < 300 mmHg
  • Moderate ARDS: 100 < PaO₂/FiO₂ < 200 mmHg
  • Severe ARDS: PaO₂/FiO₂ < 100 mmHg

• Patients fitted with an oesophageal pressure measurement catheter (Nutrivent, Sidam, San Giacomo Roncole, Italy)

• Patients registered with or covered by a social security scheme

• Free and informed consent from the patient or a trusted relative (where the patient is unable to give consent).

Exclusion Criteria:

• Patients with a history of central nervous system disorders resulting in cognitive impairment
• Patients on ECMO
• Patients admitted for symptomatic central nervous system disorders
• Patients admitted for acute respiratory distress syndrome following cardiorespiratory arrest.
• Patients being treated for a psychiatric condition, chronic heavy drinkers, or those undergoing long-term treatment with benzodiazepines, antidepressants or antipsychotics.
• Pregnant, breastfeeding or labouring patients
• Individuals subject to a legal protection order
• Individuals receiving compulsory psychiatric care
• Individuals deprived of their liberty by judicial or administrative decision

Data will be shared upon reasonable request. Only de-identified data will be shared. Any data collected during the study may be shared. The protocol will be shared initially. Other documents may be shared at a later date upon request (e.g., the CRF to allow a collaborator to select the data they wish to access). The recipients of the data will be researchers. The data will be available for any purpose deemed relevant by the study investigator, based on a protocol provided by the requester, after verification of the obtaining of regulatory approvals, including the favorable opinion of an ethics committee.

The data will be shared after signing a negotiated data transfer agreement ( data access agreement), for the duration specified in the agreement.

The data will be made available via secure transfer (sharing platform approved by the university hospital: BlueFiles or Oodrive).