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Table 2 Caring for the injured brain: specific management of severe acute cerebral pathologies

From: Update in Neurocritical Care: a summary of the 2018 Paris international conference of the French Society of Intensive Care

Disease

What is important

What is new

Hypoxic-ischaemic brain injury

In-hospital targeted temperature management (TTM)

Optimize blood pressure and ventilatory management (SaO2, CO2)

Multimodal neuro-prognostication

Pre-hospital TTM not effective

Use automated devices for TTM

Precise temperature target undefined

Quantitative tools (pupillometry, MRI) improve neuro-prognostication

Immune-mediated encephalitis

≈ 30% of encephalitis are of non-infectious origin

Anti-NMDAR encephalitis most common form

Two main patterns in the ICU:

(1) anti-NMDA-R encephalitis (psychiatric symptoms, seizures and abnormal movements)

(2), anti-NMDA, GABA-A or LGI-1-R (refractory status epilepticus)

CNS vasculitis

Two main forms: Primary (primary CNS angitis, PACNS) or Secondary to systemic diseases (infections, autoimmune vasculitis with or without anti-cytoplasmic antibodies (ANCA), connective tissue diseases, malignancies, lymphoma)

MRI is essential to diagnosis

Treatment of CNS vasculitis requires high-dose of steroids; cyclophosphamide and rituximab may be added (no consensus)

Refractory status epilepticus

Maintain general anaesthesia for at least 24 h

Continuous EEG monitoring

Ketamine is an alternative to barbiturates Novel anti-epileptic drugs available (levetiracetam, brivaracetam, lacosamide, perampanel, etc.)

Ischaemic stroke

Mechanical recanalization and alteplase

Therapeutic time window can be extended beyond 12 h

Tenecteplase as alternative to alteplase

Anticoagulation-associated intracerebral haemorrhage

Rapid reversal with the use of PCC

Idarucizumab for dabigatran reversal

Andexanet-alpha for reversal of other direct oral anticoagulants (available in the US only)

Cerebral venous thrombosis

Early anticoagulation with heparin

Endovascular therapy and/or decompressive craniectomy for severe forms

Favourable prognosis in the majority of cases if early intervention is applied

Delayed ischaemia after subarachnoid haemorrhage

Additional mechanisms other than vasospasm play a role

Diagnosis based on the combination of clinical, and neuroimaging data

Nimodipine prophylaxis

Management based on the combination of medical (BP augmentation) and endovascular (local vasodilatory drugs ± angioplasty) therapies

MMM may help in the diagnosis in comatose patients

TBI surgical management

Secondary decompressive craniectomy may increase dependency in survivors

Individualized multidisciplinary decisions are recommended

TBI prognosis

IMPACT and CRASH scores

Advanced MRI diffusion at least 1 week after injury (DWI and DTI)