[The dose alone makes the poison]
Paracelsus (Swiss alchemist and physician, 1493-1541)

The rapid broad-based development of intensive care medicine now allows the treatment and recovery of patients who some decades ago would have been considered hopeless. At the basis of this achievement lies not only a better understanding of pathophysiological mechanisms or the introduction of new drugs but also the implementation of invasive diagnostic, therapeutic and monitoring techniques. The critically ill patient often faces several potential sources of pain as well as physical and psychological stressors. The relief of pain and suffering is one of our priorities within this setting. The establishment of adequate analgosedation contributes to this goal and influences the prognosis and stay of patients in the the intensive care unit (ICU). Hence, health care professionals need to be familiar with the use of specific groups of drugs and have a proper knowledge of their various pharmacological aspects.

67.1.1 Terminology

Analgesia. A deadening or absence of the sense of pain without loss of consciousness.

Sedation. A drug-induced depression of central nervous system (CNS) activity; its intensity may be minimal (anxiolysis), moderate or deep (Table 67.1). In practical terms, sedation is the process of establishing a state of calm.

Table 67.1. Sedation levels according to the American Society of Anesthesiologists (ASA).

(±) Swallow and gag

* Reflex withdrawal from a painful stimulus is NOT considered a purposeful response;

** Patients with restrictive or chronic obstructive pulmonary disease, sleep apnoea, pregnant women, elderly or obese individuals may develop respiratory failure and arterial oxygen desaturation during moderate sedation.

“Sedation”, analgosedation or sedoanalgesia. Terms used indistinctly in anesthesiology and intensive care medicine to define therapeutic interventions performed to relief pain or provide sedation to reduce the signs and symptoms of pain, anxiety/stress, agitation, and delirium. Additionally, these procedures may include the use of amnesic drugs to prevent the “memory” and subsequent recall of unpleasant experiences or particularly stressful episodes.

General anesthesia refers to a pharmacologically induced and reversible state of unconsciousness (hypnosis) and lack of sensation, with the eventual addition or coexistence of analgesia, muscle relaxation, depression of the autonomic nervous system activity (decreased stress response) and amnesia.

Few seconds following the intravenous (IV) administration of a hypnotic dose of a general anesthetic, the patient loses consciousness and stops breathing. At the same time, airway reflexes are suppressed or impaired (risk of aspiration). Under such circumstances, positive pressure ventilation should be established (i.e., with a face mask, laryngeal mask or tracheal intubation). A properly anesthetized patient cannot be aroused even by means of intense painful stimulation.

Artificial coma, pharmacological or barbiturate coma refer to deep sedation or general anesthesia established to help patients recover from injury, serious life-threatening conditions in the ICU, or to protect the brain during or after certain major neurosurgical procedures. Pharmacological coma can be induced by means of different general anesthetic agents; barbiturate coma, for instance, may be used to lower elevated intracranial pressure (ICP) in patients with severe traumatic brain injury (TBI). Other uses include the treatment of refractory status epilepticus, cerebral vasospasm after subarachnoid hemorrhage (SAH), comatose survivors of cardiac arrest, and patients with cerebral edema and elevated ICP of any etiology other than TBI.

Anesthetics. Like narcotics (from the Greek word narcosis meaning stupor), anesthetics is a broad term under which the most commonly used drugs in anesthesia are grouped, i.e., opioids, hypnotics and muscle relaxants. Many anesthesiologists prefer to reserve this term for hypnotic or inducing agents, which can be subdivided into two categories: those given intravenously (propofol, midazolam, thiopental, ketamine, etomidate, etc.) and those inhaled (sevoflurane, desflurane, etc.).

Opiates and opioids are two other terms used interchangeably. Opiates are naturally occurring substances derived from opium obtained from the poppy plant (morphine, codeine, thebaine, papaverine, noscapine). The term opioids refers strictly to endogenous (endorphins, encephalin, dynorphins) or exogenous (synthetic agents distantly related chemically to opium’s alkaloids) compounds with an intrinsic activity, either agonist or antagonist. Exogenous opioids are subdivided into semi-synthetic (heroin, oxycodone, tramadol, etc.) or synthetic (methadone, fentanyl, sufentanil, remifentanil, meperidine, etc.).

In the United States, the term narcotics are generally associated with opioids or opiates. The concept of narcotics includes any psychoactive compound with sleep-inducing properties which can also hinder the transmission of pain signals. Unfortunately, there is no anesthetic that fulfils these two requirements. It is true that the isolated administration of high doses of certain opioids can produce unconsciousness in humans. However, their effects are unpredictable and inconsistent. Furthermore, most currently available anesthetics (except ketamine) are simply hypnotics without an analgesic effect. Therefore, from a pharmacological standpoint, “narcotics” it is not an accurate term.

Muscle relaxation or neuromuscular blockade is the reversible paralysis of somatic striated muscle induced by the administration of pharmacological agents that interrupt the transmission of nerve impulses at the level of neuromuscular junction.

67.1.2 Analgesia in the Neurological ICU

Indications: to manage postoperative pain, traumatic injury, subacute or chronic pain, to facilitate tolerance to invasive diagnostic and therapeutic procedures, and to provide care and mobilization of patient by nursing and rehabilitation staff.

Monitoring of Pain

Pain intensity can be recorded on a variety of scales. Rating pain intensity allows the evaluation of the effect of analgesic regimens in individual patients. The numerical rating scale (NRS) is a good option when a patient preserves verbal communication. With this numerical scale, the user has the option to verbally rate the pain on a scale from 0 to 10 (where 0 indicates the absence of pain and 10 the worst pain possible). If verbal communication is not possible (i.e., due to tracheal intubation, speech or language disturbances), a 10 cm line with two end points (representing “no pain” and “worst pain imaginable”, respectively), can be drawn on paper (visual analogue scale [VAS]). Patients are asked to rate their pain by indicating or placing a mark on the line corresponding to their current level of pain. The VAS score is determined by measuring in centimetres from the left end of the line (“no pain”) to the point that the patient marks. A numerical score ≤3 on the NRS or VAS can be used as evidence of effective analgesia.

The use of surrogate signs of pain such as physiological parameters (e.g., blood pressure or heart rate) or elicited behaviors (e.g., facial expression, lacrimation) is an unproven and probably inappropriate practice.

In unconscious or paralyzed patients, such signs may include: a transient increase in blood pressure or heart rate; grimaces or running tears; tachypnea when spontaneous respiration is preserved; pupil size changes; or increased muscle tone when the patient is not paralyzed. Practitioners should have a high level of suspicion in front of severe critically ill patients. Routine administration of analgesics is not always a synonym of an effective analgesia. In fact, about 50% of patients discharged from the ICU remember pain as their worst experience while in the ICU.

Table 67.2. Pharmacologic options options for analgesia in the neurological ICU.

Pharmacological and Nonpharmacological Options

Pharmacological options are summarized in Table 67.2.

On the other hand, regional anaesthesia techniques encompass: continuous epidural anaesthesia (epidural catheter), plexus block, and peripheral nerve blocks. Other methods such: transcutaneous nerve stimulation, neuromodulation or neurostimulation, intrathecal pump implantation and other surgical procedures (i.e., rhizotomy) may eventually be considered.

Considerations and Precautions

The list of drugs included in the section on pharmacological options is partial. There are many others which for practical reasons will not be covered in this chapter. The availability and preferences for some of these drugs varies according to the country, institution, or personal experience. Similarly, the primary morbid nature of the disorder or the presence of certain accompanying conditions (renal failure, peptic ulcer, etc.) determine their selection and dosage.

• With few exceptions, opiates/opioids administration in hospitalized patients do not cause drug addiction. However, their withdrawal after prolonged administration may trigger rebound hyperalgesia.
  
• The effective dose of an opioid should be determined by patient response and not by a predetermined notion of what an effective dose should be (Table 67.3).
  
• Potent opioids induce severe respiratory and cardiovascular depression (Table 67.4).
  
• Chest wall rigidity, although rare, is another adverse reaction which can be triggered upon opioid administration.
  
• Potent opioids should administered by personnel familiar with these drugs and in an environment where all conditions for securing the airway and mechanically ventilate be readily available. .
  
• Use of background opioid infusion increases the risk of respiratory depression, especially when combined with sedative drugs.
  
• While pain antagonizes opioid-induced respiratory depression, sleep can intensify the depressant effects of opioids.
  
• Respiratory depression secondary to opioid use promotes the retention of carbon dioxide (CO₂).
  
• Hypercarbia related to respiratory depression may lead to cerebral vasodilatation increasing intracranial pressure (ICP) and thus impairing the condition in patients with poor intracranial compliance, or an acute brain catastrophe.
  
• When opioids are given intravenously, patients should be closely monitored (respiratory rate, pulse oximetry [SpO₂], ECG, blood pressure). Patients with severe hypercapnia may become somnolent (risk of CO₂ narcosis with respiratory acidosis and possible silent death consecutive to cardiac arrest).
  
• Caution: patients with respiratory depression and severe hypercarbia may show normal SpO₂ values!
  
• Fear of respiratory depression, however realistic or exaggerated, represents a major barrier to the most effective use of opioids in management of pain. Although serious complications or deaths from opioid-induced respiratory depression are rare, the risk is not zero, and a death or neurologic injury for a patient with an otherwise treatable illness is a great tragedy.
  
• Miosis is another side effect associated with opioids and an important sign to be taken into account during neurological examination.
  
• The anticholinergic effect of opioids, as well as several general anaesthetics, may cause delirium in some patients (see section on agitation and delirium).
  
• Opioid analgesics may disturb gastrointestinal motility; paralytic ileus can result when these agents are given continuously and in high doses.
  
• The appearance of tolerance (e.g. tachyphylaxis) is another problem associated with prolonged administration of some of these drugs, in such cases higher doses are needed to achieve the desired therapeutic effect. Dose increments may interfere at the time to perform the neurological examination, and ultimately trigger toxicity phenomena.
  
• The long-term administration of NSAIDs (mainly non-selective COX inhibitors) is often associated with a risk of bleeding dyscrasias or gastrointestinal bleeding (a relative contraindication in critically ill patients). Platelet aggregation disorders secondary to NSAIDs administration are an unwanted effect in patients with Intracranial bleeding.
  
• The use of selective COX-2 inhibitors occasionally provides significant pain relief in situations where other NSAIDs and even low-potency opioids are ineffective. This “superior” effect may be related to the particular mechanism of action inherent only to these specific drugs (see section on main drugs).
  
• Usually, NSAIDs provide good analgesia in neurosurgical patients; the rational use of these compounds can reduce opioid requirements or obviate the need for opioids altogether.
  
• An effective analgesia contributes to the maintenance of the sleep-wake cycle; pain and sleep deprivation are precipitating of delirium (see section on agitation and delirium).
  
• Analgesia is not only the act of blunting pain with drugs, but also through proper positioning of the patient, stabilising fractures and minimising harmful physical stimulation. For instance, proper patient positioning and frequent position changes help to prevent or decrease pain in the extremities or in support areas (i.e. back, sacrum, heels). Conscious patients, while intubated and paralyzed (i.e., Guillain-Barré syndrome), may be experiencing unbearable pains undetected by medical personnel.
  
• Although regional anaesthetic techniques are an important complement to the analgesia regimen in some critically ill patients, they may be not taken into consideration if the medical staff are not familiar with them.
  
• The quality and duration of analgesia provided by regional anaesthesia techniques is superior to that offered by opioids or NSAIDs. Epidural analgesia allows the earlier return of bowel function. In addition, regional anesthesia may facilitate mobilization and physiotherapy and often it does not require complementary sedation. Under the effects of regional anaesthesia (i.e., thoracic epidural anaesthesia) both early mobilization of patient and normal thoracic excursions are guaranteed. Facilitating early mobilization and normal respiratory function allows early rehabilitation treatments and helps to reduce the incidence of complications such as atelectasis, pneumonia and thromboembolic events consecutive to deep vein thrombosis.

Table 67.3. Initial dose and duration of analgesic effect of some opioids used in anesthesia and intensive care medicine.

* Required dose (in association with an hypnotic) to blunt the responses to airway stimulation (laryngoskopy, tracheal intubation);

** Time required to exert maximum effect;

^$ Duration of maximal analgesia;

^# Includes time of maximal analgesia plus residual effect;

(−) Not currently used during perioperative analgesia (anesthesia).

Table 67.4. Summary of pharmacological aspects of various opioid analgesics.

67.1.3 Sedation in the Neurological ICU

Anxiety, agitation and delirium represent diagnostic and therapeutic problems (see section on agitation and delirium). Increased physical activity during episodes of agitation increases oxygen consumption (VO₂) and the risk of self-harm (extubation, catheter dislocation, etc.). Moreover, sedation can interfere with the neurological examination. Talking to patients and making adjustments in the ICU environment should be the first steps to calm an anxious patient. However, in this setting drugs are often needed to calm patients. Anxiety and pain may be interrelated: pain is a major source of anxiety, and anxiety may lower the threshold for pain per¬ception. Sedation should only be performed by a qualified medical professional experienced in working with sedatives and who understands their potential side effects.

Chronic obstructive pulmonary disease patients or patient with obstructive sleep apnea are particularly prone to hypoxia during sedation treatments.

Patients with intracranial haemorrhage who preserve consciousness and may still rebleed need to be sedated. Sedation in these cases is aimed to ensure patient comfort but also to attenuate sympathetic activity. This simple measure can help to prevent unwanted events like tachycardia, sustained hypertension or systolic peaks. Similarly, patients at risk for secondary brain injury from cerebral edema and intracranial hypertension may benefit from sedation

Sedation in the neuro-ICU or general ICU as premedication is also an important component of the preoperative management for patients undergoing surgical procedures. Premedication should be reduced or withheld in the elderly, chronic obstructive pulmonary disease patients, or patients with obstructive sleep apnea, severe neurologic deterioration, or those candidates for awake or fiberoptic-assisted tracheal intubation e.g., cervical trauma, narrowed oral aperture (dermatomyositis, scleroderma, etc.). Indications for sedation are summarized in Table 67.5.

Table 67.5. Indications for sedation in the neurological ICU.

Monitoring

There is a wide variety of scoring systems to monitor sedation (Tables 67.7 and 67.8). These scores provide information about the grade of sedation but not about its quality, in addition, scoring indexes carry the potential for variability in measurements. Sedation scores are not intended for patients who are unconscious or receiving neuromuscular blocking agents.

In principle, most of these scores (see section on agitation and delirium) were created to evaluate patients admitted into general ICU, therefore, the inclusion of several important aspects of neurological evaluation were not included during their designs. These limitations should not be ignored considering how crucial neurological examination is to assess the effectiveness of treatment and the outcome of patients admitted to the neuro-ICU.

The bispectral index (BIS) is another alternative to monitor the depth of sedation. BIS monitors are noninvasive devices that reflect -into a single number- a signal-processed electroencephalogram (EEG). This technology was first developed as an adjunctive method of monitoring anesthesia states during surgery. Basically, it compares the patient’s frontal EEG to processed data set from over 5000 volunteer EEG samples to scale the output of the measured EEG to between 0 and 100. A “fully awake state” is scored 100, whereas 0 is an isoelectric EEG reading; a score < 60 rates a high probability of unconsciousness. The aim during intraoperative monitoring is to achieve a score between 40 and 60, while sedation targets are typified by ranges of 60-75. Whether the use of BIS reduces drug doses, costs, length of mechanical ventilation or the length of ICU stay is controversial. Its main disadvantage is that it is best used when administering a short acting anesthetic (i.e., thiopental, propofol) on which the processed EEG algorithm is based. Agents such benzodiazepines, opioids or other classes of sedatives differentially influence the EEG and BIS is not programmed to interpret such changes. The Narcotrend index is other monitoring tool based on EEG pattern recognition during anesthesia or sedation. This technology has been developed in Germany and at present it is being use to assess the depth of sedation in several ICUs.

67.1.4 Pharmacological and Non-pharmacological Options

Pharmacological options are summarized in Table 67.6.

Non pharmacological options include: psychotherapy, background music, establishing effective communication with patients, and allowing flexible visiting hours, etc.

Table 67.6. Sedation: pharmacological options.

Considerations and Precautions

• When possible, sedation treatments that may interfere with neurological examination should be avoided. The goal of sedation in the ICU is a patient who is calm but easily arousable. Non-pharmacological options decrease sedative and analgesic requirements.
  
• A prolonged amnesia is not desirable, since it may interfere with long-term neuropsychological recovery.
  
• With few exceptions (e.g. morphine, tramadol) , opioids are not first-line sedation drugs because their sedative effect is usually achieved at higher doses than those required to produce analgesia. Agitation secondary to pain justifies the use of these drugs as sedatives (caution: consider side effects).
  
• Unlike opioids, therapeutic doses of benzodiazepines do not cause respiratory depression in healthy subjects, but this effect can occur in select ICU patients (Table 67.1).
  
• Airway protection often becomes insufficient after deep sedation.
  
• Paradoxical effects may occur upon administration of benzodiazepines (see chapter on agitation and delirium).
  
• Consider that all major antidepressant drugs, except trimipramine, mirtazapine and nefazodone suppress rapid eye movement (REM) sleep.

67.1.5 Analgosedation

Pain and anxiety are frequently concurrent in critically ill patients. Analgosedation (or “sedation”) is an essential therapy in the ICU where patients may be sedated for many hours and even days, largely because of their dependence on mechanical ventilation but also because of their poor general condition, post surgical or traumatic injuries, high treatment and monitoring invasiveness, nursing maneuvers, sleep deprivation, etc. The relief of pain and anxiety is not only a humanitarian gesture but also serves to attenuate the stress response (tachycardia, hypertension, increase of VO₂), which may be poorly tolerated by some patients. Increased VO₂ can have deleterious effects on patients with ischemic stroke, ischemic heart disease, anaemia, or acute respiratory distress syndrome (ARDS). Furthermore, there is some evidence that optimising analgesia may prevent wound infection, by improving the subcutaneous oxygenation.

However, sedation poses many problems since it is difficult to titrate. Inadequate, light sedation may lead to hypertension, tachycardia, and poor ventilator synchrony, producing stressful experiences, which sometimes are responsible for long-term psychological effects and the so called “post-traumatic stress disorder”.

On the other hand, providing adequate and appropriate sedation for patients in prolonged or long-term mechanical ventilation is often a difficult task . Over-sedation, side effects, tolerance, ceiling effect and withdrawal symptoms are among the problems to be faced in this setting. Therefore, the medical personnel involved in this task should be aware to detect and treat such unwanted effects early.

When weaning neurological ICU patients from the ventilator and approaching extubation it has to be acknowledged that conventional ICU criteria for weaning and extubation can only have an orienting character and that dysphagia is much more frequent in these patients.

67.1.6 Peculiarities in Neurocritically Ill Patients

• In the setting of sedation, serious neurological events may be occurring and go undetected and untreated. For instance, in a neuro-ICU setting, the rates of nonconvulsive status epilepticus are as high as 35%.
  
• Certain specific aspects of brain-injured patients should be taken into account. These include interactions of drugs with intracranial pressure, disturbed autoregulation, a higher frequency of seizures and an increased risk of delirium.
  
• Patients with acute brain insult are mostly intubated, ventilated and sedated; neurological examination may be difficult, and the insult severity can be over-estimated.
  
• The lesions responsible for brain damage can evolve during the initial hours and, unfortunately, continuous sedation can mask important changes that can only be identified by clinical examination. For these reasons, the strategy of repeated wake up tests (WUt) is often used for reliable assessment.
  
• Patients with preexistent neurologic impairment are more sensitive to the sedative effects of multiple medications and may take a prolonged time to awaken from sedation or general anesthesia.
  
• When weaning neurological ICU patients from the ventilator and approaching extubation it has to be acknowledged that conventional ICU criteria for weaning and extubation can only have an orienting character and that dysphagia is much more frequent in these patients.

67.1.7 Key Points of Analgosedation

• Analgosedation is a combination therapy: a strong opioid analgesic plus a sedative, with the eventual addition of supportive drugs (e.g. clonidine). Drug combinations provide analgesia and anxyolisis, and reduce hypnotic dose requirements.
  
• Combine drugs according to patient’s disease and expected sedoanalgesia duration (see SeSAM).
  
• The administration of drugs must be individualized based on the patient’s response.
  
• Consider periodic dose adjustments: administer as much as is necessary, and as little as possible.
  
• Total pain suppression is not always desirable, since changes in pain intensity may be an indicator of illness course. A numerical score of 3 or less on the NRS or VAS can be considered as effective analgesia.
  
• Inadequate sedation complicates daily ICU tasks and management of ventilation; excessive sedation promotes difficulties in weaning and may delay enteral feeding.
  
• Whenever possible, etiological diagnosis should be addressed in case of pain and agitation. Does pain led to agitation, or does agitation obey to another disorder?
  
• Ideally, drug doses should be titrated to the minimum required to maintain patient comfort, and to allow a normal sleep pattern; promoting daily interruption of sedatives significantly improve clinical outcomes and reduce ICU stay. Nevertheless, it should be considered that, daily sedation holds (i.e., WUt) are not possible or appropriate in all patients.
  
• Avoid neuromuscular blocking agents whenever possible. However, neuromuscular relaxants may be required to treat certain conditions (e.g., refractory intracranial hypertension), or when IV sedatives and analgesics have proven ineffective in facilitating mechanical ventilation.
  
• Neuromuscular blocking agents do not produce analgesia or sedation and, because paralysis is an extremely frightening and even painful experience, it is imperative to establish the desired levels of sedation and analgesia before initiating drug-induced paralysis.
  
• Consider, some patients may require higher doses of sedatives and analgesics (e.g., alcoholics, drug addicts, smokers, patients undergoing hemofiltration). Conversely, opioid analgesic and sedative requirements can be less in elderly, renal failure or due to the synergism with other drugs.
  
• The potential for opioid, benzodiazepine, and propofol withdrawal should considered after high doses or more than seven days of continuous therapy. Doses should be tapered systematically to prevent withdrawal symptoms, e.g., 10-15% medication reduction every 6-8 h when sedation treatment lasted less than seven days, or 10-15% dose reduction per day by long-term sedation treatments (>10days).
  
• Consider, antidepressants may be required at the weaning time.
  
• According to a recent study, previous antidepressant use is associated with higher mortality in critically ill patients; however, the findings do not suggest the drugs cause deaths.

Sequential Analgosedation Management (SeSAM)

Category I (SeSAM I)

Sedation up to 24 h: e.g., short-term intubated patients including: drug overdose patients, short-term postoperative ventilation, etc. Drugs: 2% propofol (or midazolam IV by bolus), with a low potency opioid (i.e., piritramide 7.5 mg every 4-6 h), and the eventual addition of NSAIDs.

Category II (SeSAM II)

Sedation for 24-72 h (original concept), currently up to 7 days: e.g., patients who have not totally recovered within the first 24 hours; patients with multiple or serious underlying disease undergoing major surgery; patients in whom immediate weaning is unlikely (e.g., patients with extensive lung damage, patients undergoing brainstem surgery, etc.). Drugs: 2% propofol with sufentanil (separated infusion pumps). Regional anaesthetic techniques or clonidine may be added.

Category III (SeSAM III, stage 1 and 2)

Sedation for a period longer than 7 days.

Stage 1: e.g., for critically ill patients (severe TBI or polytrauma , sepsis, ARDS, etc.) in whom ventilation and sedation are essential components of treatment. During stage 1, patients undergo deep sedation (Ramsay Score 4-5). Drugs: midazolam and sufentanil IV (separated infusion pumps); ketamine/ketamine-S and sufentanil is an¬other alternative.

Stage 2: After stabilizing the patient, and when weaning is intended (Ramsay Score 2 during the day). Use drugs recommended for SeSAM II (propofol/sufentanil/clonidine).

Category IV (SeSAM IV)

Brief sedation (2-5 h): deep sedation (Ramsay Score 4-5) for few hours, striving to early spontaneous breathing. Drugs: e.g., propofol and remifentanil IV (separated infusion pumps).

Table 67.7. Ramsay Scale (1974) with sedation assessment (modified).

Table 67.8. AVRIPAS Scale (2001). Modified from [Avripas, 2001].

Sedation Using Inhalational Anesthetics

The ideal IV sedative does not exist. Inhalational anesthetics are a feasible alternative, which have often shown better performance when compared to IV drugs. Unfortunately, most ICU-settings do not have the proper devices or facilities to administer inhalational anesthetics, and in many cases, the ICU staff is not familiar with the pharmacology, physiologic effects, and handling of volatile anesthetics.

Volatile anesthetics, for instance, have usually a quick onset of action, and their emergence time are shorter and more predictable than IV sedation. Inhalational anesthetics accumulate very little, and elimination via the lungs is independent of liver and kidney function. Volatile anesthetics act primarily on the cerebral cortex, and even at low concentrations may completely depress consciousness while leaving many autonomic functions undisturbed (e.g., breathing, temperature control, and blood pressure regulation). These characteristics, and others like a cardiovascular protective effect, make inhalational anesthetics an almost ideal sedative in general ICU-settings. However, regarding neurocritically ill patients, it has to be taken into account that volatile anesthetics increase ICP, and may trigger malignant hyperthermia in the setting of myopathy. Therefore, studies have to be performed in order to evaluate the impact of this attractive sedation modality in neuro-ICU settings.

67.1.8 Muscular Relaxation in the Neuro-ICU

Optimal administration of analgesics and sedatives, as well as the application of certain modalities of mechanical ventilation (i.e., biphasic positive airway pressure [BiPAP]) have led to a substantial reduction in the use of muscle relaxants in the ICU settings. Currently, less than 10% of ICU patients receive neuromuscular blocking agents. These drugs are not devoid of side effects. Their long-term administration has been associated with the development of a group of neuromuscular disorders (i.e. critical illness myopathy, cachectic myopathy, or necrotizing myopathy, among others). The relationship between these my¬opathies and the administration of muscle relaxants and high-dose corticoesteroids remains controversial. At present, certain metabolic derangements like hyperglycemia are being considered as a major risk factor for ICU-acquired neuromuscular disorders. Indications are summarized in Table 67.9.

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