The management of pain, agitation/sedation and delirium is a fundamental part of the treatment received by patients admitted to Intensive Care Units (ICU). The use of different strategies for the prevention and treatment of pain, agitation and delirium is one of the bases in the management of these patients. Knowledge of the different techniques for monitoring pain and delirium, pharmacokinetic behavior and the dosage used in this population, as well as the adverse effects and their management, is essential in order to provide optimal pharmacotherapeutic validation by the ICU clinical pharmacist.
El manejo de la sedación, la analgesia y la relajación es parte fundamental del tratamiento que reciben los pacientes ingresados en unidades de cuidados intensivos. El empleo de diferentes estrategias para la prevención y tratamiento del dolor, la agitación y el delirio constituye una de las bases en el manejo de estos pacientes. Conocer las diferentes técnicas de monitorización del dolor y del delirio, el comportamiento farmacocinético y la posología utilizada en esta población, así como los efectos adversos y su manejo, es fundamental para poder proporcionar una validación farmacoterapéutica óptima por parte del farmacéutico clínico de la unidad de cuidados intensivos.
The effective management of sedation, analgesia, and relaxation is crucial in the care of patients admitted to intensive care units (ICUs), with strategies to prevent and treat pain, agitation, and delirium being central to their overall management. The aim of analgosedation is therefore to provide patients with optimal comfort with the minimum necessary sedation, as well as to reduce agitation, disorientation, and anxiety, promote sleep, ensure adequate pain control, and facilitate compliance with mechanical ventilation (MV).1 Insufficient sedation can result in poor compliance with MV, accidental extubations, and increased agitation, anxiety, and stress. By contrast, oversedation is associated with longer MV and ICU stays, an increased incidence of nosocomial infections, delirium, and long-term cognitive impairment, and impaired communication with patients.2 The most recent guidelines recommend the use of sedation strategies based on analgesia,1,3–5 proposing concepts such as early Comfort using Analgesia, minimal Sedatives, and maximal Human care. Effective analgesia should be prioritised, and the minimum sedative dose should then be used, always with a focus on patient care.6 Thus, the Spanish Society of Intensive Care Medicine and Coronary Units promotes strategies such as the Zero Oversedation Project, which provides a practical teaching and collective awareness tool aimed at optimising clinical outcomes and minimising the harmful effects of excessive sedation. The tool comprises a package of measures that includes monitoring pain, analgesia, agitation, sedation, delirium, and neuromuscular blockade, implementing dynamic sedation, and avoiding deep sedation when not clinically indicated.7
Recommended activities for clinical pharmacists working in ICUs include validating pharmacotherapeutic regimens (dosage, interactions, drug allergies, adverse effects), identifying and preventing medication errors and drug-related problems, monitoring pharmacokinetics, and providing drug-related information and education to other healthcare professionals. Therefore, ICU clinical pharmacists must have a thorough knowledge of pharmacotherapy management related to analgosedation and delirium, participate in multidisciplinary teams to agree on treatment guidelines, implement protocols, provide information related to these treatments, and promote the evaluation of the impact of pharmacotherapeutic protocols.8,9 Thus, the aim of this article was to provide a review of the strategies available for the assessment, prevention, and treatment of pain, agitation, and delirium in ICUs.
Monitoring analgosedation and delirium in critically ill patientsIt is recommended that the level of sedation and pain, as well as the presence of delirium, should be routinely assessed every 4–6 h in all patients admitted to critical care units. These assessments should be systematically documented in the patients' medical records.1,5 Although there are several validated scales that provide an approximate assessment of critically ill patients, few tools are available to objectively monitor analgesia levels, particularly in sedated patients who are unable to communicate.
Sedation scalesRichmond Agitation Sedation Scale (RASS): this tool assesses patients on a scale ranging from 5− to 4+, where 0 indicates an alert, calm patient with no signs of agitation or sedation (Table 1). A negative score indicates sedation, whereas a positive score indicates agitation. This scale is the preferred choice in ICUs, except when monitoring patients who are being treated with neuromuscular blockers.4
Richmond agitation-sedation scale.
| Score | Name | Description | Examination |
|---|---|---|---|
| 4+ | Combative | Combative, violent, immediate danger to staff | Observe patient |
| 3+ | Very agitated | Aggressive, pulls or removes tubes or catheters | |
| 2+ | Agitated | Frequent nonpurposeful movement, fights ventilator | |
| 1+ | Restless | Anxious, but movements not aggressive or vigorous | |
| 0 | Alert and calm | ||
| 1− | Drowsy | Not fully alert, but remains (≥10 s) awake (eye opening and contact) | Call patients by name and say “Open your eyes and look at me” |
| 2− | Light sedation | Wakes briefly (<10 s) with eye contact to voice | |
| 3− | Moderate sedation | Eye movement or opening to voice (but no eye contact) | |
| 4− | Deep sedation | No response to voice, but eye movement or opening in response to physical stimuli | Stimulate patients by shaking their shoulder or rubbing their chest |
| 5− | Unarousable | No response to voice or physical stimuli |
Sedation-Agitation Scale (SAS): this scale describes agitation and sedation in critically ill patients. It is valid for use with both intubated and non-intubated patients; however, it is not suitable for monitoring patients who are being treated with neuromuscular blockers. The SAS is scored on a scale ranging from 1 to 7, with 4 indicating a calm, cooperative patient5 (Table 2).
Sedation-agitation scale.
| Score | Level of sedation | Response |
|---|---|---|
| 7 | Dangerous agitation | Tries to remove endotracheal tube and catheters; attempts to get out of bed; strikes at staff |
| 6 | Very agitated | Does not calm down when spoken to, bites tube, needs physical restraint |
| 5 | Agitated | Anxious or moderately agitated, attempts to sit up, but calms down when spoken to |
| 4 | Calm and cooperative | Calm or easily awakened, follows commands |
| 3 | Sedated | Difficult to arouse, awakens to verbal stimuli or gentle shaking, but quickly falls asleep again Obeys simple commands |
| 2 | Very sedated | May awaken to physical stimulation, but does not communicate or follow commands May move spontaneously |
| 1 | Unarousable | May move or gesticulate slightly to noxious stimuli, but does not communicate or follow commands |
Ramsay scale: this scale assesses the patients' responses to stimuli. It is scored on a scale ranging from 1 to 6. A score of 1 to 3 indicates a state of wakefulness, whereas a score of 4 to 6 indicates a state of sleep (Table 3). One of its limitations is that it only includes 1 category of agitation, making it less useful for quantifying its severity.10 Furthermore, it is not suitable for monitoring patients who are being treated with neuromuscular blockers, since they are unable to respond to these stimuli.
Ramsay scale.
| Level | Description |
|---|---|
| Awake | |
| 1 | Anxious and agitated or restless |
| 2 | Cooperative, oriented, and calm |
| 3 | Drowsy Responds to normal verbal stimuli |
| Asleep | |
| 4 | Brisk response to loud noises or light glabellar tap |
| 5 | Sluggish response to loud noises or light glabellar tap |
| 6 | No response to loud noises or light glabellar |
Bispectral index (BIS): this index, derived from the analysis of electroencephalogram wave frequencies, estimates the level of brain electrical activity. The BIS scale ranges from 0 to 100, enabling continuous objective monitoring. It is indicated in patients who are being treated with neuromuscular blockers or who are deeply sedated. The goal is to maintain the BIS score within the range of 40–60.11
Pain scalesIn conscious and communicative patients, pain can be assessed using graphic scales such as the Visual Analogue Scale or the Visual Numeric Scale. Patients express their degree of pain on a scale ranging from 0 (no pain) to 10 (the worst pain imaginable).12
In noncommunicative patients or those on MV, indirect tools such as physiological indicators (e.g. high blood pressure, tachycardia, tachypnoea, sweating) or behavioural indicators (e.g. facial expression, presence of movement, or posture) can serve as an alert system for inadequate pain control.10 These indicators have been used to develop validated scales, such as the Behavioural Indicators of Pain Scale, as there is currently no technique available to objectively assess the presence and intensity of pain.13 This scale assesses pain on a scale of 0 to 10 based on facial expression, calmness, muscle tone, compliance with MV, and consolability. The aim is to maintain the pain level below 4 on the scale. It is recommended that pain is assessed before, during, and 15 min after any procedure is performed on noncommunicative patients on MV.1 However, there is limited evidence of its use in patients with quadriplegia, those receiving treatment with neuromuscular blockers, patients in deep coma due to metabolic or neurological causes, or those with haemodynamic or respiratory instability. This limitation arises because this scale has not been evaluated in these clinical contexts, where patients may exhibit diminished responses to stimuli or reduced motor responses. These patients were therefore excluded from ESCID scale validation studies.14
Campbell scale: this instrument has been validated for assessing the presence and degree of pain in patients who are unable to communicate. It is scored on a scale ranging from 0 to 10. The objective is to maintain the score below 3. A score above 6 is considered to be very intense5 (Table 4).
Campbell scale.
| Score | 0 | 1 | 2 |
|---|---|---|---|
| Facial expression | Relaxed | Tense, frowning, or grimacing | Regularly frowning or clenching teeth |
| Calmness | Calm, relaxed, normal movements | Occasional restless movements and shifting position | Frequent movement, including head or limbs |
| Muscle tonea | Normal | Increased. Flexion of fingers and toes | Rigid |
| Verbal responseb | Normal | Occasional complaints, crying, moaning, or grunting | Frequent complaints, crying, moaning, or grunting |
| Consolability | Comfortable and calm | Reassured by touch and voice. Easy to distract | Difficult to console by touch or talking |
Behavioural pain scale: this scale assesses the presence of pain on a 12-point scale (Table 5). The main limitation of this scale is that it only indicates whether the stimulus is painful, offering little value in quantifying pain.15
Behavioural pain scale.
| Item | Description | Points |
|---|---|---|
| Facial expression | Relaxed | 1 |
| Partially tightened | 2 | |
| Fully tightened | 3 | |
| Grimacing | 4 | |
| Upper limbs | No movement | 1 |
| Partially bent | 2 | |
| Fully bent. With finger flexion | 3 | |
| Permanently retracted | 4 | |
| Compliance with ventilation | Tolerates movement | 1 |
| Coughs, but tolerates ventilation most of the time | 2 | |
| Fighting ventilator | 3 | |
| Unable to control ventilation | 4 | |
The analgesia nociception index: this index measures heart rate variability based on electrocardiogram monitoring. It uses spectral analysis to generate an algorithm that converts nociception into an absolute value between 0 and 100. The target value is between 50 and 70, indicating a balance between analgesia and sedation.16
Nociception level index: this index measures nociception on a scale ranging from 1 to 100, based on the non-linear integration of physiological variables associated with pain perception (heart rate, photoplethysmogram amplitude, skin conductance, and skin conductance fluctuations along with their temporal derivatives). It has been used extensively during surgery, but its use in critical patients is limited.17
Scales for assessing deliriumConfusion assessment method for the intensive care unit scale: this scale assesses the state of consciousness, comprehension, memory, attention, and alertness. This dichotomous scale only detects the presence or absence of delirium (a positive or negative result) but does not distinguish between hypo- or hyperactive delirium or determine its severity.18
Intensive Care Delirium Screening Checklist (ICDSC): this checklist comprises an 8-item scale used to detect delirium over a period of 8 to 24 h. A score of 4 or higher on the ICDSC is positive and indicates the presence of delirium. It is particularly useful in sedated or uncommunicative patients.19
SedationSedation involves reducing the patients' level of consciousness and their response to external stimuli. The ideal sedative should have an immediate onset of action, enable rapid recovery and easy dose adjustment, and have a wide therapeutic margin. It should also not accumulate or interact with other drugs, have no adverse effects, and be low cost.20 However, as there is no ideal sedative, the choice of drug will depend on the patients' pathophysiological characteristics and any changes affecting pharmacokinetic and pharmacodynamic behaviour.
Sedation strategiesLight or conscious sedation (RASS 0 to −2): at this level of sedation, consciousness is minimally depressed. Patients are calm but not asleep, and still maintain their airway reflexes, spontaneous ventilation, and appropriate responses to stimuli. Drugs such as dexmedetomidine are recommended for use over alternatives such as fentanyl, remifentanil, or propofol.4
Deep sedation (RASS −4 to −5): for deep sedation, midazolam, propofol, or lorazepam are recommended as the sedatives of choice. This level may be accompanied by total or partial loss of defence reflexes, airway reflexes, or response to physical or verbal stimuli.
Sedative drugs (Table 6)Propofol: this drug is indicated for short-term sedation or when sedation windows are required (e.g. frequent neurological assessments or early extubation), due to its rapid onset and quick recovery time. Lipid levels should be monitored and caloric intake maintained at a rate of 1.1 kcal/mL (i.e. 0.1 g of lipids per mL of 1% propofol). Propofol infusion syndrome may develop at high doses (greater than 5 mg/kg/h) and during prolonged infusions (greater than 48 h). This syndrome is life-threatening with a high mortality rate and is characterised by the development of arrhythmias, metabolic acidosis, hyperkalaemia, kidney failure, and rhabdomyolysis.
Main drugs used for sedation, analgesia, and delirium in critically ill patients.
| Sedation | ||||||
|---|---|---|---|---|---|---|
| Drug | Mechanism of action | Dosage | Clinical effects | Indication/characteristics | Metabolism/elimination | Adverse effects |
| Midazolam | BenzodiazepineAction on GABAA receptor | IV bolus: 1–5 mgInfusion: 0.02–0.1 mg/kg/hDmax: 0.25 mg/kg/h | AnxiolyticHypnoticAmnesicMuscle relaxationAnticonvulsant | Status epilepticus, alcohol withdrawal syndrome, and prolonged sedation | Hepatic metabolism (CYP3A4)Active metabolite: α1-hydroxymidazolamRenal elimination | HypotensionTachycardiaRespiratory depressionToleranceParadoxical reactions |
| Propofol | GABAA receptor agonist | IV bolus: 0.5–1 mg/kgInfusion:5–50 μg/kg/min or0.3–3 mg/kg/hDmax: 4 mg/kg/h | SedativeHypnoticAntiemeticAnticonvulsant | Recommended administration routeCentralContraindicated in patients allergic to soy, peanuts, eggsPreferred choice if CRRT | Hepatic conjugation metabolismRenal elimination | HypotensionRespiratory depressionBradycardiaPropofol infusion syndromeHypertriglyceridaemia |
| Dexmedetomidine | Selective α-2 receptor agonist | 0.2–0.7 μg/kg/hDmax: 1.5 μg/kg/h | HypnoticAnalgesicImproves sleep quality | Light sedationControl of agitation during mechanical ventilation weaning | Hepatic metabolism (CYP2A6)Renal elimination | HypotensionBradycardiaFeverAvoid in cerebrovascular and cardiovascular disease |
| Ketamine | Noncompetitive NMDA receptor antagonist | Slow IV bolus: 0.25–1 mg/kgInfusion: 0.1–2.5 mg/kg/h | Dissociative anaesthesiaAnalgesicBronchodilatorVasodilation | Bronchospasm or asthmatic state | Hepatic metabolismRenal elimination | HypertensionSialorrhoeaArrhythmiasIncreased ICPHallucinations and delirium |
| Sodium thiopental | Barbiturate anaestheticPotentiates GABA receptor response | Bolus: 50–75 mgInfusion: 1–4 mg/kg/h | HypnoticAnxiolyticAnticonvulsant | Neurocritical: refractory intracranial hypertension or status epilepticus | Hepatic metabolismRenal elimination | HypotensionMyocardial dysfunctionRisk of infectionBronchospasmParalytic ileus |
| Remifentanil | μ-opioid receptor agonist | Infusion:0.5–15 μg/kg/h | SedativeAnalgesic | Dynamic sedation | Plasma esterases | BradycardiaRespiratory depressionMuscle rigidityParadoxical hyperalgesiaTolerance |
| Analgesia | ||||||
| Morphine | μ, ĸ, δ, σ opioid receptor agonist | IV bolus: 2–4 mg or0.05–0.1 mg/kgInfusion: 2–15 mg/h | Acute pain, postoperative painDyspnoeaLong-term analgosedation | Hepatic metabolismRequires adjustment in RF | Nausea, vomitingRespiratory depressionHypotensionIleus and urinary retentionTolerance, dependence, and withdrawal syndromeHistamine release | |
| Fentanyl | μ, ĸ, δ opioid receptor agonist | IV bolus: 50–100 μgInfusion: 0.7–5 μg/kg/hDmax: 10 μg/kg/h | Severe acute painPreferred in haemodynamically unstable patients | Hepatic metabolismRenal and biliary elimination | Respiratory depressionHypotensionMuscle rigidityDecreases ICP | |
| Sufentanil | μ-opioid receptor agonist | Induction: 5–20 μg or 0.1–2 μg/kgMaintenance: 0.2–2 μg/kg/h | Adjuvant analgesic during anaesthesiaInduction and maintenance of analgesic anaesthesia | Hepatic metabolism | Respiratory depressionBradycardia, hypotensionNausea, vomitingPruritus | |
| Methadone | μ-opioid receptor agonist | Analgesic dose: 10–40 mg every 6–12 h orally | Opioid withdrawal syndrome | Hepatic metabolismRenal elimination | QT interval prolongationSerotonergic effectDrowsinessRespiratory depression | |
| Tramadol | μ-opioid receptor agonistMinor centrally acting opioid | 50–100 mg every 6–8 hDmax: 400 mg/d | Acute postoperative painNeuropathic pain | Reduce dose in elderly patientsRequires adjustment in RF | TachycardiaNausea, vomitingOrthostatic hypotensionSeizuresTolerance, dependence, and withdrawal syndrome | |
| Paracetamol | Inhibits prostaglandin synthesis | IV: 1 g every 6–8 hDmax: 4 g/d | Mild to moderate painAntipyretic | Hepatic metabolismRenal elimination | HepatotoxicityHypotensionHypoglycaemia | |
| Metamizole | Pyrazolone derivative | IV: 1 g every 6–8 hDmax: 8 g/d | Severe acute painAntipyreticAnti-inflammatoryAntispasmodic | Hepatic metabolismRenal elimination | HypotensionAgranulocytosis, thrombocytopeniaAngioedemaBronchospasm | |
| Dexketoprofen | NSAID | IV: 50 mg every 8–12 h | Moderate to severe painAntipyreticAnti-inflammatory | Hepatic metabolismRenal elimination | NephrotoxicityHypertensionAbdominal pain, constipationPeptic ulcer | |
| Delirium | ||||||
| Haloperidol | Typical neurolepticDopamine D2 receptor agonist | IV, IM bolus: 2.5–5 mg every 20–30 minDmax: 30 mg/dContinuous infusion: 5–25 mg/hDmax: 40 mg/h oral: 0.5–2 mg/4–8 h | Agitation and psychosisHyperactive deliriumHypoactive delirium | Hepatic metabolism, CYP2D6CYP3A4 | QT interval prolongation (ventricular arrhythmias), Torsades de PointesMalignant neuroleptic syndromeExtrapyramidal symptomsHypotension | |
| Quetiapine | Atypical antipsychoticActs on serotonergic and dopaminergic D1 and D2 brain receptors | Oral: 12.5–25 mgDmax: 300 mg/dUse delayed-release tablets | Hyperactive delirium | Hepatic metabolismCYP3A4 | QT interval prolongationDrowsiness and sedationOrthostatic hypotensionHyperglycaemiaExtrapyramidal symptoms | |
| Olanzapine | Atypical antipsychotic. Acts on serotonergic, histamine, and muscarinic receptors and has a moderate effect on D2 dopaminergic receptors | Oral: 2.5–15 mg/d | Hyperactive deliriumPositive psychotic symptoms | Hepatic metabolismCYP1A2CYP2D6 | QT interval prolongationDrowsiness and sedationHyperglycaemiaIncreased appetiteMonitor liver functionSerotonin syndrome | |
| Risperidone | Atypical antipsychotic | 0.25–3 mg/12 hDmax: 6 mg/d | Mild–moderate hyperactive delirium with active psychotic symptoms | Hepatic metabolismCYP2D6CYP3A4 | DrowsinessHyperglycaemiaQT interval prolongationDrowsiness and sedationHyperglycaemiaMonitor liver functionIncreased risk of acute stroke in patients >65 years | |
| Dexmedetomidine | Selective α-2 adrenergic agonist | 0.2–0.7 μg/kg/hDmax: 1.5 μg/kg/h | Conscious sedation Better sleep qualityControl of agitation during mechanical ventilation weaning | Hepatic metabolism CYP2D6 | HypotensionBradycardiaFeverAvoid in cerebrovascular and cardiovascular disease | |
| Clonidine | α-2 adrenergic agonist | Oral: 0.2–0.5 mg every 6–8 h or0.15 mg every 12–24 hIV bolus: 300 μg(stable haemodynamics)Infusion: Dmax: 3 μg/kg/h | Hyperactive delirium | Renal elimination | Hypotension, bradycardiaDry mouthQT monitoring | |
NSAID, nonsteroidal antiinflammatory drug; Dmax, maximum dose; GABA, gamma-aminobutyric acid; IM, intramuscular; RF, renal failure; IV, intravenous; NMDA, N-methyl-D-aspartate; ICP, intracranial pressure; CRRT, continuous renal replacement therapy; MV, mechanical ventilation.
Midazolam: due to its high lipophilicity and strong binding to plasma proteins, there is a risk of accumulation in patients with hepatic failure, obesity, or hypoalbuminaemia. It should not be used in patients with cirrhosis. It has no analgesic effect. As it is a benzodiazepine, flumazenil can be used as an antidote to reverse its effects.
Dexmedetomidine: this drug is recommended for short-term sedation and patients at high risk of delirium. The advantages of dexmedetomidine for conscious sedation over other drugs include its lack of respiratory depression and its ability to reduce opioid requirements, shorten the duration of mechanical ventilation and ICU stays, and lower the incidence of delirium compared to propofol or midazolam4; however, due to its high risk of secondary cardiac block, it should be avoided in patients with cardiac decompensation.
Remifentanil: this drug is indicated for short-term dynamic and sequential sedation in cases where repeated therapeutic procedures are required, such as aggressive treatments that necessitate potent analgesia. As remifentanil is eliminated through plasma esterases, adjustment is not required in cases of renal or hepatic failure. It should not be administered as an intravenous (IV) bolus because of cardiovascular effects, such as the risk of bradycardia or hypotension.
Ketamine: this drug is an alternative for short-term sedation in patients with bronchospasm, as it preserves protective pharyngeal and laryngeal reflexes while avoiding respiratory depression. It has an analgesic effect by binding to sigma receptors. Due to its significant adverse effects, treatment should start with a low dose, which should then be increased gradually. Treatment should be monitored for the onset of persistent pain, haemodynamic instability, delirium, psychotic episodes, and tonic/clonic movements.
Inhaled gases: the use of inhaled anaesthetics in ICUs, such as isoflurane or sevoflurane, is increasing. They are a good alternative to IV anaesthesia, offering shorter recovery times and MV duration. These advantages are due to their excellent dose–response relationship and cardio- and neuroprotective properties, together with the availability of administration devices (AnaConDa or Mirus).21
AnalgesiaOpioids are the primary analgesics used for critical patients, with morphine and fentanyl being the preferred drugs for continuous IV administration. They act through μ, ĸ, δ, and σ opioid receptors at both central and peripheral levels, which mediate analgesic effects. These drugs interact synergistically with sedatives and require strict control due to their high inter- and intra-individual variability, their narrow therapeutic margin, and potential for adverse effects, such as respiratory depression, hypotension, decreased level of consciousness, urinary and gastric retention, ileus, nausea, and vomiting. Therefore, to minimise opioid consumption, strategies such as multimodal analgesia are recommended. This approach involves using nonopioid adjuvants, such as paracetamol (first step), metamizole (second step), or dexketoprofen (third step), as well as anticonvulsants or local anaesthetics.22Table 6 shows the main drugs used in ICUs for sedation, analgesia, and delirium in critically ill patients. The need for preventive analgesia should be assessed prior to handling patients or conducting routine procedures, such as patient care. In the event of opioid overdose, naloxone is the drug of choice as an antidote; it is a pure competitive opioid receptor antagonist.
DeliriumNeuropsychiatric syndrome is characterised by the onset of impaired consciousness and cognitive function, developing over a short period and following a fluctuating course. Its most characteristic manifestations include alterations in attention and perception of the environment (delusions or hallucinations) with agitation or hypoactivity.20 It affects about 40% of patients in ICUs, although it often goes unnoticed, particularly the hypoactive forms.23 Delirium in patients should be monitored every 8–12 h. It is associated with extended hospital stays, longer MV duration, higher costs, and increased mortality rates.24
Depending on the level of alertness and psychomotor activity, it is classified into 3 subtypes:
Hyperactive: agitation, aggression, restlessness, emotional instability, and a tendency to remove probes and catheters.
Hypoactive: decreased activity, lethargy, emotional indifference, apathy, and decreased response to external stimuli. The use of psychoactive drugs in ICUs makes hypoactive delirium more prevalent and harder to recognise than hyperactive delirium.
Mixed: this subtype is the most common. Patients alternate between the 2 subtypes described above.
Modifiable: use of benzodiazepines, immobility, sleep deprivation, low exposure to sunlight, dehydration, and malnutrition.
Non-modifiable: advanced age, a high APACHE-II score on admission, dementia, previous episodes of delirium, high blood pressure, metabolic acidosis, emergency surgery, and multiple trauma.
Prevention and treatment: delirium can have multifactorial causes. The first step in managing delirium is to identify and correct the underlying cause. Table 6 shows the drugs used in this setting.
Nonpharmacological measures: it has been shown that the onset of delirium in ICUs can be reduced by strategies such as early mobilisation, stimulating patient orientation, controlling ambient light, maintaining a higher level of communication with patients, providing cognitive stimulation, reducing noise in the environment, maintaining adequate hydration, promoting the early removal of catheters, and performing early tracheostomy.
Pharmacological treatment: the guidelines suggest that drugs such as typical neuroleptics (haloperidol) or atypical neuroleptics (olanzapine, risperidone, or quetiapine) should not be routinely used to treat delirium. Although several studies have attempted to demonstrate the efficacy of pharmacological treatment, the results have not been conclusive.1,4,10 If these drugs are used, they should be administered at the lowest possible concentration within their respective therapeutic range for this indication. The drugs should then be discontinued once clinical improvement or resolution has been achieved.
In conclusion, correctly implementing protocols for managing analgosedation and delirium in ICUs is crucial to individualise therapy in critically ill patients, improve safety, and optimise patient-centred health outcomes. Thus, clinical pharmacists can play a key role in selecting and individualising dosages, minimising medication errors and adverse events, and educating and training multidisciplinary teams to ensure continuous improvement in the quality of care for critically ill patients.
Declaration of authorshipAll authors are members of the FARMIC Working Group. All authors participated in developing the concept, designing the project, defining the intellectual content, preparing the project, and reviewing it. The manuscript was written by María Martín-Cerezuela, Esther Domingo-Chiva, and Fernando Becerril-Moreno. All of the authors have critically reviewed and approved the final version of the manuscript for publication.
CRediT authorship contribution statementMaría Martín Cerezuela: Writing – review & editing, Conceptualization. Esther Domingo Chiva: Methodology. Tatiana Betancor García: Writing – review & editing, Conceptualization. Irene Aquerreta González: Writing – review & editing. Carla Bastida Fernández: Writing – review & editing. Fernando Becerril Moreno: Writing – review & editing, Writing – original draft, Conceptualization.
FundingNone declared.
None declared.
