A patient’s self-report of pain is considered the “gold standard,” and clinicians should always attempt to have a patient rate his or her own pain first [12]. Chanques and colleagues demonstrated that a 0–10 visually enlarged horizontal numeric rating scale was the most valid and feasible of five pain intensity rating scales tested in over 100 ICU patients [13]. The Behavioral Pain Scale (BPS) and the Critical-Care Pain Observation Tool (CPOT) are the most valid and reliable behavioral pain scales for monitoring pain in medical, postoperative, or trauma adult ICU patients who are unable to self-report and in whom motor function is intact and behaviors are observable [12, 14–17]. Vital signs (or observational pain scales that include vital signs) should not be used alone for pain assessment in adult ICU patients.

Ongoing clinical evaluation is the most effective method of assessing sedation. In order to provide a more consistent and objective means of assessing the degree of sedation a number of sedation scales have been developed. Reliable sedation scales can enhance communication among caregivers, improve consistency in drug administration, be used in sedation protocols and improve precision of medication titration as patient needs change over time. The routine use of a sedation scale, including frequent adjustments of the sedation target as needed, is strongly endorsed by evidence-based guidelines [12].

The Glasgow Coma Scale (GCS) was developed to assess the level of consciousness of trauma patients. This scale is commonly used in neurosurgical ICU’s. The GCS is however essentially a measure of pathologic obtundation and cannot be recommended for monitoring the level of sedation in ICU patients. The Ramsay Sedation Scale and variations of this scale are frequently used method of assessing and documenting sedation in the ICU. The Ramsay scale was reported by Ramsey and colleagues in 1974 in a study which assessed the use of alphaxalone-alphadolone (Althesin) in 30 ICU patients [18]. The Ramsey scale has a number of significant limitations when used to assess the level of sedation in ICU patients and is not recommended

Observational and randomized trials have demonstrated that protocols directed at minimizing the use of sedative infusions shorten the weaning process. Specifically, approaches intended to avoid over-sedation by limiting the use of continuous infusions either through sedation assessment scoring or by daily cessation of sedation, decreases duration of mechanical ventilation and duration of ICU stay [22–24].

Girard et al. published the results of a trial that employed a “wake up and breathe” strategy (the ABC trial) [25]. Patients randomized to a daily awakening trial followed by a SBT (versus SBT alone) experienced increased time off of mechanical ventilation, decreased time in coma, decreased ICU and hospital length of stay and improved survival at 1 year. Based on this data, the sedation should be stopped (or the dose significantly reduced) each morning; this allows for neurological assessment of the patient, performance of a SBT, reassessment of the goals of sedation, and an individualized exercise/occupational program. Schweickert and colleagues performed a RCT in which patients who remained ventilator dependant for more than 3 days were randomized to early physical and occupational therapy which was coupled with daily awakenings [26]. Patients in the intervention group had shorter duration of delirium and more ventilator-free days with significantly more patients returning to an independent functional status.

Delirium is characterized by a disturbance of consciousness with accompanying change in cognition. Delirium typically manifests as a constellation of symptoms with an acute onset and a fluctuating course. Delirium in the ICU is very common, the incidence ranging from 45 to 87 %. The incidence appears to vary according to whether the studied population is composed exclusively of mechanically ventilated patients. The symptoms of delirium have been organized into cognitive and behavioral groups. Common cognitive symptoms include disorientation, inability to sustain attention, impaired short-term memory, impaired visuospatial ability, reduced level of consciousness, and perseveration. Common behavioral symptoms include sleep-wake cycle disturbance, irritability, hallucinations, and delusions. The manifestations of delirium can vary widely among patients. While some patients may manifest somnolence and even coma, others appear anxious, disruptive, or combative. Recognition of this symptom variability has led to the classification of delirium into motoric subtypes. One such subtype is hyperactive delirium, of which the manifestations include agitation, hypervigilance, irritability, lack of concentration, and perseveration. One the other hand, hypoactive delirium manifests as diminished alertness, absence of or slowed speech, hypokinesia, and lethargy. Mixed delirium, as the name implies, includes manifestations of both hyperactive and hypoactive delirium. The mixed and hypoactive forms of delirium are the most common in the ICU. Hypoactive delirium tends to occur more frequently in older patients and carries worse prognosis. While multiple clinical risk factors have been identified and numerous pathophysiologic pathways have been hypothesized, the pathophysiology of delirium remains poorly understood [27]. Studies using magnetic resonance imaging have shown a positive association between the duration of delirium in the ICU and both cerebral atrophy and cerebral white-matter disruption [28, 29]. These preliminary investigations indicate either that delirium in the ICU gives rise to alterations in brain structure or that the presence of such cerebral atrophy and white-matter disruption renders patients more susceptible to delirium. The major predisposing factors include respiratory failure, older age, alcohol abuse, dementia and medications. Classes of medications commonly associated with delirium include anticholinergic agents, benzodiazepines, and opiates. Benzodiazepines appear to be strongly associated with delirium in ICU patients [11].

Delirium is associated with increased ICU and hospital length of stay. The presence of delirium has important prognostic implications; in mechanically ventilated patients it is associated with a 2.5 fold increase in short-term mortality and a 3.2 fold increase in 6-month mortality. Furthermore, delirium is associated with the development of post-ICU cognitive impairment. Delirium is frequently undiagnosed unless specific diagnostic instruments are used. Therefore routine monitoring of delirium in all ICU patients is recommended [12]. The Confusion Assessment Method for the ICU (CAM-ICU) and the Intensive Care Delirium Screening Checklist (ICDSC) are the most valid and reliable delirium monitoring tools (see Fig. 15.2) [30]. Gusmao-Flores et al. performed a metaanalysis comparing the CAM-ICU with the ICDSC [31]. The CAM-ICU had a high sensitivity and specificity with a diagnostic odds ratio of 103.3 and a ROC of 0.97. The ICDSC has moderate sensitivity and good specificity (ROC 0.89). The available data suggest that both CAM-ICU and the ICDSC can be used as a screening tool for the diagnosis of delirium in critically ill patients. It is however not clear that the use of these scales is more sensitive than unstructured assessments made by trained bedside nurses who are prompted to look for delirium [32].

Non-pharmacological approaches such as physical and occupational therapy decrease the duration of delirium and should be encouraged. The use of pharmacologic agents to prevent delirium is not recommended, as there is no compelling data to demonstrate that this reduces the incidence or duration of delirium. Page and colleagues randomized 141 mechanically ventilated patients to receive haloperidol 2·5 mg or placebo intravenously every 8 h, irrespective of coma or delirium status [33]. Patients in the haloperidol group spent the same number of days alive, without delirium, and without coma as did patients in the placebo group.

Traditionally haloperidol has been used to treat delirium in the ICU. There is however no published evidence that treatment with haloperidol reduces the duration of delirium. Girard et al. randomized 101 mechanically ventilated patients with delirium/coma to receive haloperidol, ziprasidone, or placebo every 6 h for up to 14 days [34]. Treatment with antipsychotics did not improve the number of days alive without delirium or coma, nor did it increase adverse outcomes. Devlin et al. performed a double-blind, placebo controlled, multicenter study which evaluated the efficacy and safety of quetiapine in 36 ICU patients diagnosed with delirium [35]. Rescue intravenous haloperidol was allowed to be used in both groups. The results showed that quetiapine was associated with quicker resolution of delirium, reduced time of delirium and agitation, and reduced haloperidol requirement compared to placebo. There was however no difference in the duration of ICU stay, length of hospitalization, and hospital mortality. Two clinical trials have found that antipsychotics, compared with placebo, hasten the resolution of delirium in hospitalized patients without critical illness. Hu et al. found that haloperidol and olanzapine each led to earlier improvements in Delirium Rating Scales scores among 175 elderly patients, compared with placebo [36]. Similarly, Kalisvaart et al. found that haloperidol reduced the severity and duration of delirium among elderly patients undergoing hip surgery, compared with placebo [37]. These data suggest haloperidol has a limited role in the treatment of delirium. Atypical antipsychotics may reduce the duration of delirium (see Table 15.1). Dexmedetomidine has been demonstrated to reduce the duration of delirium and may be the agent of choice in these patients [38].