Introduction
Caring for the injured brain: general aspects
Topic | What is important | What is new |
---|---|---|
Management of the comatose patient | GCS, brainstem reflexes, FOUR score Brain imaging (CT scan, MRI) Multimodal monitoring (ICP, brain oximetry, TCD) | Automated infrared pupillometry q-EEG Multimodal monitoring-based individualized therapy |
Management of the delirious patient | CAM-ICU, ICDSC scores Minimized targeted sedation Early active mobilization | ABCDEF, e-CASH bundles Alternative sedatives (dexmedetomidine) Prophylactic use of anti-psychotics not effective |
Management of ICU-acquired weakness | MRC muscle scale, ENMG Optimize nutrition and glycaemic control Early active mobilization | Assessment of diaphragmatic dysfunction Physical (electrical) therapy Mobilization protocols |
Assessment of the comatose patient
What is important
What is new
EEG monitoring of brain function in the comatose patient
What is important
What is new
Assessment of delirious patient
What is important
What is new
Sedative strategies and delirium management
Sedative strategies
What is important
What is new
Developing management approaches for delirium
What is important
What is new
ICU-acquired weakness
Pathophysiology
What is important?
What is new?
Clinical aspects
What is important
What is new
Early mobilization
What is important
What is new
Caring for the injured brain: management of specific pathologies
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) |