Abstract
Daily interruption of sedative therapy and limitation of deep sedation have been shown in several randomized trials to reduce the duration of mechanical ventilation and hospital length of stay, and to improve the outcome of critically ill patients. However, patients with severe acute brain injury (ABI; including subjects with coma after traumatic brain injury, ischaemic/haemorrhagic stroke, cardiac arrest, status epilepticus) were excluded from these studies. 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). 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. 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. In this review, we provide a concise summary of cerebral physiologic effects of sedatives and analgesics, the advantages/disadvantages of each agent, the comparative effects of standard sedatives (propofol and midazolam) and the emerging role of alternative drugs (ketamine). We suggest a pragmatic approach for the use of sedation-analgesia in the NICU, focusing on some practical aspects, including optimal titration and management of sedation withdrawal according to ABI severity.
Highlights
It is well established, based on randomized trials conducted in the general ICU adult and paediatric populations, that minimizing or avoiding sedation provides a better outcome, including shorter duration of mechanical ventilation and length of hospital stay [1]
We provide a concise summary of the main cerebral physiologic effects of sedatives and analgesics, the advantages/disadvantages of each agent, the comparative effects of standard sedatives in patients with acute brain injury (ABI), and the emerging role of alternative sedatives, ketamine
We suggest a practical approach for the use of sedation and analgesia in the neuro-ICU (NICU), with specific attention on how to best initiate, titrate and stop sedation, according to ABI severity
Summary
It is well established, based on randomized trials conducted in the general ICU adult and paediatric populations, that minimizing or avoiding sedation provides a better outcome, including shorter duration of mechanical ventilation and length of hospital stay [1]. After ABI, interventions are targeted to both increase cerebral oxygen delivery and/or attenuate cerebral metabolic demand, aiming to provide adequate oxygen availability and energy balance at the neuronal level In this setting, sedative agents act by reducing CMRO2, improving cerebral tolerance to ischaemia and limiting supply/ demand mismatch in conditions of impaired autoregulation [6, 7]. Control of ICP Sedatives and analgesics may reduce ICP by different mechanisms [3] They induce a reduction in CMRO2 and, in CBF, leading to a parallel decrease in cerebral blood volume. A recent statement by the European Federation of Neurological Societies included propofol as a treatment of generalized convulsive status epilepticus [14] Both benzodiazepines and propofol can be selected in ABI patients to reduce the risk of secondary seizures. Since spreading depolarization is a potentially modifiable secondary injury mechanism, these findings make a strong case for a trial of ketamine containing sedative regimes in patients with ABI
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