Sedating a patient

Patients with severe acute brain injury (ABI; including severe traumatic brain injury, poor-grade subarachnoid haemorrhage, severe ischaemic/haemorrhagic stroke, comatose cardiac arrest, status epilepticus) have traditionally been kept deeply sedated, at least in the early phase following ICU admission. First, sedation/analgesia is used for control of pain, anxiety, agitation and patient–ventilator synchrony.Second, sedation/analgesia has additional ‘neuro-specific’ indications in the acute phase that might significantly influence its use in this setting [3].Therefore, whether the new paradigm of minimal sedation can be translated to the neuro-ICU (NICU) is unclear.In patients with ABI, sedation has ‘general’ indications (control of anxiety, pain, discomfort, agitation, facilitation of mechanical ventilation) and ‘neuro-specific’ indications (reduction of cerebral metabolic demand, improved brain tolerance to ischaemia).First, they induce a reduction in CMRO and, consequently, in CBF, leading to a parallel decrease in cerebral blood volume.This decrease in cerebral blood volume will produce a reduction of intracranial volume and, therefore, ICP.

Even when CBF autoregulation is preserved, MAP reduction can lead to an increase in intracranial pressure (ICP) as a result of compensatory vasodilation [11].Titration and withdrawal of sedation in the NICU setting has to be balanced between the risk that interrupting sedation might exacerbate brain injury (e.g.intracranial pressure elevation) and the potential benefits of enhanced neurological function and reduced complications.Sedation also is an essential therapeutic component of intracranial pressure therapy, targeted temperature management and seizure control.Given the lack of large trials which have evaluated clinically relevant endpoints, sedative selection depends on the effect of each agent on cerebral and systemic haemodynamics.

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