Sepsis-associated encephalopathy, advances in pathophysiology understanding and in non-pharmacologic approaches

Sepsis-associated encephalopathy (SAE) is a complication of severe infections. Its diagnosis is based on clinical examination and is formalised by checklists or algorithms. Its incidence is estimated around 20-40% of patients admitted to intensive care for an infection. It results in abnormalities of clinical examination, such as consciousness disorders or coma associated with electroencephalographic or radiological abnormalities. The occurrence of generalised seizures is rare, although epileptic abnormalities are frequent at EEG. Neurological signs of localisation are sometimes observed, often related to ischemic or intracranial haemorrhagic events. The SAE is a provider of psychological disorders (anxiety, depression, suicide) and long-term cognitive decline impacting the quality of life of patients, but also excess mortality probably related to the persistence of disorders of swallowing. Its pathophysiology involves neuroinflammatory and ischemic processes associated with metabolic disturbances leading to a metabolic crisis and cell death. Disturbances of cerebral autoregulation have recently been highlighted. To date, there is no pharmacological strategy targeting neuroinflammation or neurotransmission (including a sedation strategy) to reduce the incidence of the duration or severity of SAE. Non-pharmacological interventions proposed for the prevention or treatment of delirium should be applied in septic patients, including early mobilisation, cessation of sedation and rehydration, management of physical and psychological discomfort and withdrawal of pro-delusional medication.