Hématome rétroplacentaire

Retroplacental haematoma (RPH) is a complication affecting 0.25 to 0.4% of all pregnancies and 4% of severe PEs. It is of acute onset, usually unpredictable and its symptoms are not specific: Isolated metrorrhagia, foetal distress, uterine hypertonicity. Clinical, biological and sonographic features suggesting a RPH can be early or late. Haemoconcentration and the forming of notches on Doppler examination of the uterus can appear weeks before the event, whereas raised D-Dimers and foetal tachycardia are identified within days of the event. Although Caesarian section reduces the perinatal death rate by 20 to 50% in a setting of RPH with a live foetus, vaginal delivery is indicated in cases of RPH with fetal demise, following the control of haemorrhagic shock, clotting disorders and uterine hypotonicity.     

Inflammation et lésions cérébrales aiguës en anesthésie réanimation

Patients with acute brain injuries or susceptibility to post-surgery stroke are a major therapeutic challenge for intensive care and anaesthesiology medicine. The control of systemic stress involved in brain damage is necessary to reduce the frequency and severity of secondary brain lesions. Inflammation is known to be directly involved in acute brain lesions. The brain is a major participant in inflammation control through activation or inhibition effects. The exact mechanisms involved in deleterious effects following acute brain injuries due to inflammation are still unknown. This non-exhaustive study will expose the principal processes involved in inflammatory brain disease and explain the consequences of peripheral inflammation for the brain. Neuroprotection strategies in acute neuroinflammation will be reported with a focus on anaesthetic agents and the inflammation cascade.     

Neurosédation en réanimation

The objectives for using sedation in neurointensive care unit (neuroICU) are somewhat different from those used for patients without severe brain injuries. One goal is to clinically reassess the neurological function following the initial brain insult in order to define subsequent strategies for diagnosis and treatment. Another goal is to prevent severely injured brain from additional aggravation of cerebral blood perfusion and intracranial pressure. Depending on these situations is the choice of sedatives and analgesics: short-term agents, e.g., remifentanil, if a timely neurological reassessment is required, long-term agents, e.g., midazolam and sufentanil, as part of the treatment for elevated intracranial pressure. In that situation, a multimodal monitoring is needed to overcome the lack of clinical monitoring, including repeated measurements of intracranial pressure, blood flow velocities (transcranial Doppler), cerebral oxygenation (brain tissue oxygen tension), and brain imaging. The ultimate stop of neurosedation can distinguish between no consciousness and an alteration of arousing in brain-injured patients. During this period, an elevation of intracranial pressure is usual, and should not always result in reintroducing the neurosedation.