HHE 2018 | Page 70

• Richmond Agitation Sedation Scale (RASS): examines cognition • Sedation Agitation Scale (SAS) and Motor Activity Assessment Scale (MAAS): monitor sedation and arousal. Their use can reduce the amount of sedatives given to achieve a specific sedation target, decreasing the number of days on mechanical ventilation and cost of hospital stay; however, no validation is available in the neuro-ICU environment. 2 The Nociception Coma Scale has emerged as a valid tool to assess pain in patients with disorders of consciousness. 9 When it is not possible to use these scales, for example, in patients who require muscular relaxation, then an electrophysiological endpoint must be used instead. One example is bispectral index (BIS) monitoring, 10 which has made adjustments of sedation possible. A study showed that BIS values significantly correlated with RASS and SAS scores in patients with acute brain injury. 11 In another study, the BIS reliably assessed sedation levels during continuous propofol infusion in the same type of patients. 12 BIS was initially developed for monitoring the depth of general anaesthesia in patients without brain pathology. It is thought that the ABI (acute brain injury) may influence the BIS algorithm because of EEG changes related to the pathology itself rather than to the sedative state. 1 The approach to sedation should first consider the severity of acute brain injury and the cerebral physiological state, mainly ICP. Figure 1 shows a possible algorithm for the management of sedation in neurointensive care units. 1 The first things to consider are appropriate control of pain, control of agitation and promoting ventilator synchrony. In patients with intracranial hypertension, the targets for sedation and analgesia should be titrated to control ICP and brain tissue oxygen pressure. 1 Need to wake up For the clinical assessment of neurocritical patients, interruption of continuous sedation (IS) is therefore necessary. This is usually short-term, aimed at evaluating the patients and planning further management strategies, including the definitive sedation interruption once the clinical concern and IS does not provoke patients’ distress and metabolic imbalance. 2 Withdrawal of sedation and IS by daily wake-up tests might appear beneficial to these patients by allowing clinical neuro-monitoring and timely detection of warning neurological signs. 13 Daily IS trials have the potential to reduce mechanical ventilation duration and the need for tracheostomy. 14 These potential benefits, however, must be balanced against the risk of further cerebral haemodynamic deterioration when sedation is stopped abruptly. 15 Cerebral hypoperfusion and raised ICP might result in an imbalance of energy supply and demand, especially for the injured brain and, therefore, aggravate the risk for metabolic distress and brain tissue hypoxia. 16–22 IS might lead to significant ICP elevation and CPP reduction, which are more relevant in the first days after ABI than after 4–5 days. 23 Avoidance of IS is recommended in all patients at risk of, or having, elevated ICP. In these patients, sedation should never be stopped abruptly but withdrawn progressively, titrating the sedation dose to ICP targets. In all other ABI patients, withdrawal should proceed as in the general ICU and daily IS in not contraindicated. 1 Given that little knowledge is available about the benefits of IS in ABI, it is important to implement multi-modal monitoring in neurocritical care in order to omit IS in those patients who will potentially be harmed by the procedure. 2 Sedative drugs available The ideal drug for sedation should have a rapid onset and rapid recovery, in order to evaluate the neurological state, as well as a predictable clearance independent of end-organ function (avoiding accumulation). It should be easy to achieve adequate levels of sedation and it would have to reduce ICP by reducing cerebral blood and cerebral vasoconstriction. As it reduces cerebral blood flow, it should decrease the metabolic rate of oxygen consumption at the same time. In addition, cerebral autoregulation should also be maintained, while having minimal cardiovascular depressant effects. 24 The ideal sedative drug should be able to decrease ICP and maintain an appropriate cerebral perfusion without interfering with its autoregulation Propofol Propofol has a rapid onset and cessation of sedation. However, it also can unpredictably accumulate after long-term use and cause prolonged sedation. 25 Cerebral blood flow and ICP are decreased. 26–28 Standard- and high-dose propofol infusion (2mg/kg induction bolus followed by 150–200mg/kg/min infusion) can be used as an anticonvulsivant. 29–32 Propofol infusion syndrome should be detected promptly in order to start adequate treatment. The hypotension related to propofol is multifactoral, and severe propofol-associated hypotension occurred in 26.2% of patients in some studies. 33–36 Weaning from mechanical ventilation occurs earlier than with midazolam. 37 Opioids In general, opioids decrease the cerebral metabolic rate of oxygen, cerebral blood flow and ICP, as long as normocapnia is maintained by mechanical ventilation. 2 However, Roberts et al found that morphine, fentanyl, sufentanil and alfentanil significantly increased ICP and decreased CPP and MAP after bolus administration. 38 Remifentanil Remifentanil is a mu-opioid agonist with analgesic effects and a rapid onset and a short duration of action. It can cause decreases in both cerebral metabolic rate and ICP, with minimal changes in CPP and cerebral blood flow. 39 It can facilitate frequent awakening to evaluate neurological and respiratory parameters. 40 Benzodiazepines Use of benzodiazepines increases the incidence of delirium significantly. Midazolam is an appealing sedative option for its rapid onset and short duration of effect with bolus administration, making it ideal for procedural sedation. It is also a very important drug in refractory status epilepticus. Benzodiazepines increase the seizure threshold and are useful antivonvulsivants. 41,42 Midazolam accumulates in adipose tissue 70 HHE 2018 | hospitalhealthcare.com