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FEATURE

The Sedation of Critically Ill Adults: Part 2Management

Pun, Brenda T. MSN, RN, ACNP; Dunn, Jan MSN, RN

Author Information
AJN, American Journal of Nursing: August 2007 - Volume 107 - Issue 8 - p 40-49
doi: 10.1097/01.NAJ.0000282293.72946.1f

In 2002 the Society of Critical Care Medicine (SCCM), along with the American Society of Health-System Pharmacists, updated recommendations in its clinical practice guidelines on the sustained use of sedatives and analgesics in adults, acknowledging that although sedatives often are used in the ICU to treat anxiety and agitation, indications for their use “are not well defined.”1 The updated recommendations—divided into three sections focusing on pain, sedation, and delirium—seek to clarify these murky waters. (The SCCM's guidelines were graded according to the strength of the supporting evidence; see Grading the Recommendations, page 42.)

This two-part series examines the SCCM recommendations and current literature pertinent to sedation, which is used primarily to relieve anxiety and agitation. In Part 1, published last month, we discussed the importance of using reliable tools to differentiate between pain, delirium, and anxiety and agitation; their signs and symptoms may look alike, but they can have different causes and require different treatments. In this article, Part 2, we present an algorithm for doing so and discuss specific recommendations for managing sedation when it's needed to treat anxiety and agitation.

MANAGING ANXIETY AND AGITATION IN THE ICU

Ideally, nonpharmacologic management should be considered first—as implied in the SCCM's algorithm (see Figure 1, page 44)—or at least concurrently with pharmacologic treatment, although this may be impractical when the need for sedation is urgent. In some cases, nonpharmacologic therapies may be effective enough that the use of sedatives can be reduced or avoided, although we could not find any studies that have investigated this specifically. Nonpharmacologic interventions may include one or more of the following2,3:

FIGURE 1
FIGURE 1:
Algorithm for the Sedation and Analgesia of Mechanically Ventilated Patients
FIGURE 1
FIGURE 1
  • establishing a method of nonverbal communication (for example, blinking or head nodding)
  • using a calm voice and gentle touch to convey reassurance
  • frequent repositioning
  • using distraction (such as listening to music, watching television)
  • making environmental changes (such as noise reduction)
  • using complementary therapies (such as aromatherapy and massage therapy)

Although few data supporting the use of nonpharmacologic therapies for managing agitation and anxiety in the ICU are available, a few studies have shown improved outcomes. In studies of cardiac patients and patients on mechanical ventilation, listening to music has been associated with a lowered heart rate and arterial blood pressure, reduced anxiety, and fewer cardiac complications.4–6 A pilot study subjecting volunteers to recorded ICU noise in a sleep laboratory found that earplugs may promote sleep in clinical settings.7 Back massage was found to promote sleep in critically ill older men, “lending indirect support to findings that back massage increases relaxation” and lowers anxiety.8 Although researchers found an association between aromatherapy and massage and improved mood and decreased anxiety, they found no link to physiologic stress indicators.3

Figure
Figure

Pharmacologic management. In choosing the appropriate sedative, it's important to understand how each agent works and what its limitations are. The ideal sedative has been described as one that works rapidly; provides anxiolysis, sedation, amnesia, or a combination of these; allows quick emergence when stopped; permits easy administration and adjustment of dosage; produces no active metabolites, significant adverse effects, or drug–drug interactions; and is inexpensive.9, 10 No drug meets all these criteria. Clinicians must therefore choose a sedative according to the patient's condition. The following are descriptions of the most commonly used sedatives.

Benzodiazepines (including diazepam [Valium], lorazepam [Ativan], and midazolam [Versed]) are the most widely used sedatives in the United States. The SCCM guidelines include the following recommendations (all recommendations from the SCCM guidelines used in this article are presented verbatim)1:

  • Midazolam or diazepam should be used for rapid sedation of acutely agitated patients. (Grade of recommendation = C)
  • Midazolam is recommended for short-term use only, as it produces unpredictable awakening and time to extubation when infusions continue longer than 48–72 hours. (Grade of recommendation = A)
  • Lorazepam is recommended for the sedation of most patients via intermittent IV administration or continuous infusion. (Grade of recommendation = B)

Drugs in this class produce sedation and anterograde amnesia by enhancing the effects of γ-aminobutyric acid (GABA), a potent inhibitory neurotransmitter. Because of their rapid onset (two to five minutes), midazolam and diazepam are recommended for treatment of acute agitation. Because midazolam has been associated with accumulation and prolonged sedation in critically ill patients who are obese or in kidney failure, it's only recommended for less than 24 hours; lorazepam is recommended for longer use.1,11 Benzodiazepines may produce adverse effects, including respiratory and cardiovascular depression, hypotension, tolerance, physical dependence, and paradoxical agitation, as well as prolonged sedation and unpredictable awakening resulting from accumulation of the drug or its active metabolites.1,11 The use of lorazepam has recently been reported to be an independent risk factor for ICU patients who develop delirium, with the risk of developing delirium increasing as the dosage increases.12

Because benzodiazepines pose a risk of accumulation, adjusting the dosage of these drugs can be difficult. It's important to establish a dosage end point and to frequently reassess the patient's needs and adjust the dosage accordingly, especially when administering a benzodiazepine by continuous infusion.1 For the same reason, when a benzodiazepine is given to elderly patients and patients with hepatic insufficiency, the lowest possible starting dose should be used and then adjusted upward as needed.1

Propofol (Diprivan) is a sedative–hypnotic agent used for anesthesia or sedation. The SCCM guidelines include the following recommendations for its use as a sedative1:

  • Propofol is the preferred sedative when rapid awakening (e.g., for neurologic assessment or extubation) is important. (Grade of recommendation = B)
  • Triglyceride concentrations should be monitored after two days of propofol infusion, and total caloric intake from lipids should be included in the nutrition support prescription. (Grade of recommendation = B)

How propofol works isn't completely understood, but it's believed to enhance GABA's affinity for its receptors, much like the benzodiazepines. Because propofol has a very rapid onset (one to two minutes) and its concentration in plasma falls quickly once the drug is discontinued, it's the sedative recommended when rapid awakening is needed (for example, for neurologic assessment or extubation).1 Propofol is a useful drug for patients with neurologic injury; it decreases intracranial pressure, cerebral blood flow, and cerebral metabolism.1, 13It can also be used in patients who are about to be weaned from mechanical ventilation and have been on long-term benzodiazepine therapy. Propofol can be started while the benzodiazepine is tapered to avoid withdrawal symptoms; the rapid awakening with propofol helps to facilitate extubation.

Adverse effects associated with propofol include dose-dependent hypotension, respiratory depression, and pain at the infusion site.1, 10, 11 The drug is prepared in a lipid emulsion, so long-term or high-dose infusion may lead to elevated triglyceride levels; serum triglyceride levels should be monitored and the emulsion considered a caloric source.1, 10, 11 Because the lipid emulsion can promote bacterial growth, strict aseptic technique and a dedicated IV catheter are essential to prevent infection. The manufacturers recommend that propofol infusion tubing and any unused product be discarded 12 hours after spiking the vial. If the drug is transferred to another container before administration, any unused product should be discarded and tubing changed after six hours. To help retard the growth of microorganisms, the manufacturers have added preservatives. One formulation (the brand name Diprivan) contains disodium edentate, a strong chelator of trace metals, including zinc. This manufacturer recommends a drug holiday after five days of continuous infusion, so that zinc lost through urination can be replaced. Another generic formulation contains sodium metabisulfite, a preservative that can cause allergic reactions (including symptoms of anaphylaxis) in susceptible patients, especially those with asthma.1

One review notes that high-dose propofol use has been linked to propofol infusion syndrome, a potentially fatal syndrome characterized by cardiac failure, rhabdomyolysis, severe metabolic acidosis, and renal failure.14 The reviewers “suggest caution when using prolonged [more than 48 hours] propofol sedation at doses higher than 5 mg/kg per hour, particularly in patients with acute neurological or inflammatory illnesses.” Reviews of studies comparing propofol with midazolam conclude that propofol is at least as effective as midazolam in achieving the desired level of sedation and results in faster extubation, but it's also associated with a higher incidence of hypotension.10, 15

Dexmedetomidine (Precedex) is an α-2 adrenergic receptor agonist that results in inhibition of norepinephrine and epinephrine centrally and peripherally.16 It has a rapid onset (five minutes) and results in both sedation and analgesia without respiratory depression.17, 18 It's believed to work by activating a sleep-promoting pathway, producing sedation and loss of consciousness that may closely resemble sleep.19 Patients on dexmedetomidine are easily roused, can follow commands, and fall back quickly into deeper sedation once the rousing stimulus is removed.1, 16 One research team has reported that dexmedetomidine was associated with a lower incidence of delirium after cardiac surgery than was propofol or midazolam.20 This drug's major adverse effects are hypotension and bradycardia,1, 17 and it has been approved by the Food and Drug Administration (FDA) for short-term use only (less than 24 hours); clinical trials are under way to evaluate its long-term use. Although the SCCM guidelines don't include dexmedetomidine in their recommendations, we believe it has many favorable attributes and may prove safe for extended use as a primary sedative in the ICU.

Antipsychotics are not classified as sedatives, but because they are often used to reduce anxiety and agitation in patients with hyperactive delirium, they are included in this discussion. Antipsychotics can control agitation without altering the level of consciousness. In patients with hyperactive delirium, treating with an antipsychotic first is usually best; often no additional sedation is needed. However, if the patient's agitation is severe and management is urgently needed, initial treatment with both an antipsychotic and a fast-acting sedative will probably be required, with the latter adjusted downward and then discontinued once the patient's agitation is controlled.

The SCCM guidelines include the following recommendations1:

  • Haloperidol is the preferred agent for the treatment of delirium in critically ill patients. (Grade of recommendation = C)
  • Patients should be monitored for electrocardiographic changes (QT-interval prolongation and arrhythmias) when receiving haloperidol. (Grade of recommendation = B)

Of the traditional antipsychotics, haloperidol (Haldol) is the most widely used in the ICU.21 How it works isn't completely known, but it acts as a potent dopamine-receptor antagonist, blocking impulse transmission of dopaminergic neurons.11 Adverse effects of haloperidol may include extrapyramidal symptoms (such as dyskinesia, akathisia), QT-interval prolongation (which can lead to torsade de pointes), and neuroleptic malignant syndrome. Monitoring for these adverse effects should be standard when this drug is used.

There are no studies to show that antipsychotics effectively treat anxiety and agitation—or for that matter, delirium. Although the SCCM guidelines recommend haloperidol as the preferred agent for treating delirium, this is an off-label use based on case series and anecdotal reports.1,22 Few rigorous studies have evaluated the efficacy of haloperidol and other strategies in treating delirium.23 One study found that prophylactic treatment of low-dose haloperidol in elderly hip-surgery patients reduced the duration and severity, but not the incidence, of delirium.24 Another large study found that the in-hospital death rate was significantly lower among patients who received haloperidol within two days of beginning mechanical ventilation than among those who did not receive haloperidol.25

The atypical, second-generation antipsychotics, which include olanzapine (Zyprexa, Zydis), quetiapine (Seroquel), and ziprasidone (Geodon), are FDA approved for the treatment of schizophrenia and other conditions, but they may also be helpful in the off-label use of treating delirium (as with haloperidol, evidence of their effectiveness for this use is limited).26 They work similarly to haloperidol, but instead of acting primarily on dopamine they affect a variety of neurotransmitters simultaneously.21, 23, 26 Adverse effects vary for each drug but generally include extrapyramidal symptoms, dry mouth, and constipation. A small study conducted with patients in a medical–surgical ICU found that although olanzapine and haloperidol showed comparable effectiveness in treating delirium, olanzapine was associated with fewer adverse effects.21

In 2005 the FDA issued a black-box warning for atypical antipsychotics based on a metaanalysis of data from elderly outpatients treated for dementia-related psychosis.27 The metaanalysis found that atypical antipsychotics were associated with a “small increased risk of death,” compared with placebos. Soon afterward, a study found that conventional antipsychotics, including haloperidol, carried a significantly higher risk of death than atypical antipsychotics.28 The alert and this study emphasize the need for more research on these drugs and underscore the importance of exercising caution when using them to treat delirium.

ADMINISTERING SEDATIVES: END POINTS AND AWAKENINGS

The SCCM guidelines include the following recommendations1:

  • Titrating the sedative dose to a defined end point is recommended, along with systematic tapering of the dose or daily interruption with retitration to minimize prolonged sedative effects. (Grade of recommendation = A)
  • The potential for opioid, benzodiazepine, and propofol withdrawal should be considered after high doses or more than approximately seven days of continuous therapy. Doses should be tapered systematically to prevent withdrawal symptoms. (Grade of recommendation = B)
  • The use of sedation guidelines, an algorithm, or a protocol is recommended. (Grade of recommendation = B)

Because sedatives vary widely in mechanism of action and in effect, nurses must understand each drug category to ensure that drugs are administered safely. Sedatives should be given only after the need for analgesia has been assessed.

The SCCM guidelines emphasize the importance of using the lowest dose to avoid oversedation. High doses of opioid, benzodiazepine, or propofol regimens longer than seven days may lead to “neuroadaptation or physiological dependence” and thus pose a risk for withdrawal symptoms.1

Nurses can use various methods to ensure good dosage control. One method, described earlier, is to taper the dosage of a sedative to a defined end point, preferably using a validated sedation-assessment scale, and frequent reevaluation and adjustment as needed. Another method involves interrupting sedation with daily awakening trials (also known as daily “wake-ups,” spontaneous awakening trials, and “sedation vacations”). One study found that such trials were associated with a shorter duration of mechanical ventilation, decreased lengths of stay in the ICU, and a reduced need for diagnostic tests, without an increase in complications.29

Daily awakening trials involve turning off the patient's sedation and analgesia and allowing the patient to awaken. (If pain management is clearly indicated, daily awakening trials may involve turning off sedation only.30) When the patient reaches a certain degree of awareness (for example, when she or he can respond to simple commands) or shows signs of needing sedation or pain management (such as agitation, increased respiratory rate, and increased heart rate), sedation and analgesia are restarted at half the previous doses and titrated as necessary.29, 31 This practice permits doses to be fine-tuned daily and may result in less medication being given to the patient over the course of the ICU stay, thus helping to prevent drug accumulation.31 This practice also provides an opportunity for nurses to reassess a patient's neurologic status and pain level, and may allow the patient to communicate with staff and family. For some patients, having and recovering from a critical illness is associated with long-term psychological disorders, including posttraumatic stress disorder (PTSD). There is evidence that over time, daily awakenings can reduce the severity of or prevent PTSD in such patients.32, 33

Daily awakenings are contraindicated in patients receiving neuromuscular blocking agents. Sedation should be discontinued in these patients only after paralytics have been stopped and a reversal of their effects is evident (as demonstrated, for example, through train-of-four stimulus—a method for assessing the depth of neuromuscular blockade—or the patient's spontaneous breathing and movement). There may be other contraindications, although none has been formally reported or tested; for example, patients in whom sedation has been steadily increasing and patients at high risk for myocardial ischemia may not be candidates for daily awakening trials.31 Modifications may include stopping sedatives only (as opposed to sedatives and analgesics) for patients likely to be in pain (such as those on postsurgical units).

Algorithms and protocols. For each patient, clinicians must choose from many assessment tools and sedatives. To help guide their choices, the SCCM recommends the use of sedation algorithms or protocols, such as an algorithm for the sedation and analgesia of mechanically ventilated patients (see Figure 1, page 44). Another algorithm can be found in an article by Sessler and colleagues published in Seminars in Respiratory and Critical Care Medicine in 2001 (volume 22, issue 2). Many institutions struggle with adherence to such protocols. In a recent survey of 448 critical care physicians in Canada, only 29% of 273 respondents reported that a sedation protocol, pathway, or guideline was in use in their ICUs.34 Forty-nine percent of the respondents used a sedation scoring system; 40% performed “daily interruption of continuous infusions of sedatives or analgesics.”34 When guidelines do exist, nurses' and physicians' adherence is often poor. One study reported that physicians rated themselves as being in compliance with clinical practice guidelines for sedation and neuromuscular blockade in 69% of cases but actually were in only 20% of cases.35 Another study found that after four months of use in a medical ICU, guidelines for the use of sedatives, analgesics, and neuromuscular-blocking agents were used with only 58% of patients.36

Why don't nurses and physicians adhere to protocols? Factors may include personal experience, differences in values between a protocol's developers and its users, ignorance of aspects of a protocol, and personal preferences for specific medications.35–37 It's recommended that sedation protocols be developed and reviewed by the members of multidisciplinary teams of critically ill patients and that all clinicians be educated in their use.

Managing Sedation: One Case

Day 1. Dorothy Arkady, a 69-year-old retired teacher, is admitted to the medical ICU in respiratory distress secondary to community-acquired pneumonia. (This case is a composite based on our experience.) On admission her vital signs were heart rate, 120 beats per minute; blood pressure, 170/108 mmHg; respiration, 35 breaths per minute; temperature, 97.1°; and oxygen saturation, 85% on room air. The bedside nurse assesses Ms. Arkady for pain, delirium, and anxiety and agitation using the Critical-Care Pain Observation Tool (CPOT), the Confusion Assessment Method for the ICU (CAM-ICU), and the Richmond Agitation–Sedation Scale (RASS), respectively. Ms. Arkady has a RASS score of +2, indicating agitation (patient makes frequent nonpurposeful movements, fights the ventilator), and a positive CAM-ICU score, indicating delirium. Her total CPOT score is 3, indicating that she's experiencing some pain and discomfort. (For more on these tools, see The Sedation of Critically Ill Adults: Part 1: Assessment, July.)

The health care team decides that she needs mechanical ventilation immediately to alleviate her respiratory distress. After successful intubation, mechanical ventilation is started. The following orders are written to manage her pain and anxiety and agitation:

  • Give morphine 2 mg IV as needed for pain. (The hospital's pain protocol recommends morphine for patients on mechanical ventilation when the CPOT score is greater than 2.)
  • Start lorazepam (Ativan) at 2 mg/hr IV and titrate the dose upward until the patient's RASS score is 0 (alert and calm) or –1 (drowsy; patient isn't fully alert but opens eyes in response to voice and sustains eye contact for at least 10 seconds).
  • Initiate the daily awakening trials protocol every morning at 9 AM. If management fails (if signs and symptoms of anxiety and agitation reappear), restart sedation at half the previous dose and titrate as necessary to reach the target RASS score.

The team believes that Ms. Arkady's delirium is probably caused by hypoxemia secondary to respiratory distress. No pharmacologic treatment of the delirium is ordered.

Day 2. At 7:30 AM the nurse reassesses Ms. Arkady. Her vital signs are stable and within normal limits, and oxygenation has improved (oxygen saturation levels have been greater than 98% for the past 24 hours). During the last 12-hour shift her RASS score fluctuated between –3, indicating moderate sedation (patient opens eyes in response to voice, but makes no eye contact), and –4, indicating deep sedation (patient is unresponsive to voice, but responds to physical stimuli); her current score is –3. Her CAM-ICU result remains positive for delirium. Her CPOT score is 0, indicating an absence of pain or discomfort. She is currently receiving lorazepam 4 mg/hr, and has received morphine twice in the past 24 hours (2 mg at 2 PM yesterday and 2 mg at 2 AM this morning).

Nursing actions. The nurse titrates the lorazepam down to 2 mg/hr in order to get the patient's RASS score back into the target range. The nurse now believes that the delirium is hypoactive secondary to possible oversedation and that decreasing the lorazepam dosage will alleviate it. Since the patient is not in any apparent pain or discomfort, no additional morphine is given.

At 9 AM, the nurse initiates the daily awakening trial, first checking whether Ms. Arkady meets the ICU's safety criteria for sedation cessation, which require that a patient demonstrate respiratory stability, show no evidence of myocardial ischemia within the past 24 hours, have needed no increase in sedation within the past four hours, and not be experiencing the effects of a neuromuscular blocking agent. After determining that Ms. Arkady meets these criteria, at 9:15 AM the nurse turns off the lorazepam drip. By 9:30 AM Ms. Arkady is breathing faster than 35 breaths per minute. Her RASS score has climbed to +2: she is moving frequently and without apparent purpose and coughing and gagging on the ventilation tube. Lorazepam is restarted at 1 mg/hr (half the previous dosage) and titrated upward as necessary until Ms. Arkady reaches her target RASS range.

Day 3. At 8 AM the nurse reassesses Ms. Arkady. Her vital signs are stable and within normal limits, and her oxygenation has improved further (oxygen saturation levels have been above 99% for the past 24 hours). During the last shift, her RASS score fluctuated between –1 and 0, and is currently –1. Her CAM-ICU result is negative and her CPOT score is 0. She is currently receiving lorazepam 1 mg/hr and has received no morphine within the past 24 hours.

Nursing actions. Because the patient's RASS score falls within the target range, the nurse makes no changes to sedation management. At 9 AM the nurse initiates the protocol for sedation cessation. Ms. Arkady again meets all safety criteria and is eligible for sedation cessation. The nurse turns off the lorazepam drip. Ms. Arkady tolerates this without showing any signs of agitation and anxiety, and her RASS score remains at –1 for the next hour. At 10:15 AM she passes a spontaneous breathing trial, and at 10:30 AM she is successfully extubated.

REFERENCES

1. Jacobi J, et al. Clinical practice guidelines for the sustained use of sedatives and analgesics in the critically ill adult. Crit Care Med 2002;30(1):119–41.
2. Yagan MB, et al. Sedation of the mechanically ventilated patient. Crit Care Nurs Q 2000;22(4):90–100.
3. Dunn C, et al. Sensing an improvement: an experimental study to evaluate the use of aromatherapy, massage and periods of rest in an intensive care unit. J Adv Nurs 1995;21(1):34–40.
4. Byers JF, Smyth KA. Effect of a music intervention on noise annoyance, heart rate, and blood pressure in cardiac surgery patients. Am J Crit Care 1997;6(3):183–91.
5. Guzzetta CE. Effects of relaxation and music therapy on patients in a coronary care unit with presumptive acute myocardial infarction. Heart Lung 1989;18(6):609–16.
6. Chlan L. Effectiveness of a music therapy intervention on relaxation and anxiety for patients receiving ventilatory assistance. Heart LungC 1998;27(3):169–76.
7. Wallace CJ, et al. The effect of earplugs on sleep measures during exposure to simulated intensive care unit noise. Am J Crit Care 1999;8(4):210–9.
8. Richards KC. Effect of a back massage and relaxation intervention on sleep in critically ill patients. Am J Crit Care 1998;7(4):288–99.
9. Sessler CN, et al. Multidisciplinary management of sedation and analgesia in critical care. Semin Respir Crit Care Med 2001;22(2):211–26.
10. Ostermann ME, et al. Sedation in the intensive care unit: a systematic review. JAMA 2000;283(11):1451–9.
11. Hassan E, et al. Therapeutic considerations in the management of agitated or delirious critically ill patients. Pharmacotherapy 1998;18(1):113–29.
12. Pandharipande P, et al. Lorazepam is an independent risk factor for transitioning to delirium in intensive care unit patients. Anesthesiology 2006;104(1):21–6.
13. Rhoney DH, Parker D, Jr. Use of sedative and analgesic agents in neurotrauma patients: effects on cerebral physiology. Neurol Res 2001;23(2–3):237–59.
14. Vasile B, et al. The pathophysiology of propofol infusion syndrome: a simple name for a complex syndrome. Intensive Care Med 2003;29(9):1417–25.
15. Hall RI, et al. Propofol vs midazolam for ICU sedation: a Canadian multicenter randomized trial. Chest 2001;119(4):1151–9.
16. Maze M, et al. New agents for sedation in the intensive care unit. Crit Care Clin 2001;17(4):881–97.
17. Pandharipande P, et al. Dexmedetomidine for sedation and perioperative management of critically ill patients. Seminars in Anesthesia, Perioperative Medicine and Pain 2006;25(2):43–50.
18. Venn RM, et al. Respiratory effects of dexmedetomidine in the surgical patient requiring intensive care. Crit Care 2000;4(5):302–8.
19. Nelson LE, et al. The alpha2-adrenoceptor agonist dexmedetomidine converges on an endogenous sleep-promoting pathway to exert its sedative effects. Anesthesiology 2003;98(2):428–36.
20. Maldonado JR, et al. Post-operative sedation and the incidence of ICU delirium in cardiac surgery patients. ASA Annual Meeting; 2003 Oct 13–17; San Francisco: American Society of Anesthesiologists; 2003. p. A465.http://www.asaabstracts.com/strands/asaabstracts/searchArticle.htm; jsessionid=E5ABDC626C759903584FECC670A6DA04?index=0&highlight=true&highlightcolor=0&bold=true&italic=false.
21. Skrobik YK, et al. Olanzapine vs haloperidol: treating delirium in a critical care setting. Intensive Care Med 2004;30(3):444–9.
22. Truman B, Ely EW. Monitoring delirium in critically ill patients. Using the confusion assessment method for the intensive care unit. Crit Care Nurse 2003;23(2):25–36.
23. Foreman MD, et al. Prevention and treatment strategies for delirium. Prim Psychiatry 2004;11(11):52–8.http://www.primarypsychiatry.com/aspx/articledetail.aspx?articleid=714.
24. Kalisvaart KJ, et al. Haloperidol prophylaxis for elderly hip-surgery patients at risk for delirium: a randomized placebo-controlled study. J Am Geriatr Soc 2005;53(10):1658–66.
25. Milbrandt EB, et al. Haloperidol use is associated with lower hospital mortality in mechanically ventilated patients. Crit Care Med 2005;33(1):226–9.
26. Tune L. The role of antipsychotics in treating delirium. Curr Psychiatry Rep 2002;4(3):209–12.
27. Schneider LS, et al. Risk of death with atypical antipsychotic drug treatment for dementia: meta-analysis of randomized placebo-controlled trials. JAMA 2005;294(15):1934–43.
28. Wang PS, et al. Risk of death in elderly users of conventional vs. atypical antipsychotic medications. N Engl J Med 2005;353(22):2335–41.
29. Kress JP, et al. Daily interruption of sedative infusions in critically ill patients undergoing mechanical ventilation. N Engl J Med 2000;342(20):1471–7.
30. Carson SS, et al. A randomized trial of intermittent lorazepam versus propofol with daily interruption in mechanically ventilated patients. Crit Care Med 2006;34(5):1326–32.
31. Kress JP, et al. Sedation and analgesia in the intensive care unit. Am J Respir Crit Care Med 2002;166(8):1024–8.
32. Kress JP, et al. The long-term psychological effects of daily sedative interruption on critically ill patients. Am J Respir Crit Care Med 2003;168(12):1457–61.
33. Misak CJ. The critical care experience: a patient's view. Am J Respir Crit Care Med 2004;170(4):357–9.
34. Mehta S, et al. Canadian survey of the use of sedatives, analgesics, and neuromuscular blocking agents in critically ill patients. Crit Care Med 2006;34(2):374–80.
35. Slomka J, et al. Influence of clinicians' values and perceptions on use of clinical practice guidelines for sedation and neuromuscular blockade in patients receiving mechanical ventilation. Am J Crit Care 2000;9(6):412–8.
36. Bair N, et al. Introduction of sedative, analgesic, and neuromuscular blocking agent guidelines in a medical intensive care unit: physician and nurse adherence. Crit Care Med 2000;28(3):707–13.
37. Weinert CR, et al. Sedating critically ill patients: factors affecting nurses' delivery of sedative therapy. Am J Crit Care 2001;10(3):156–65.

A Note on Pain Control

As one review has stated, “failure to recognize that pain frequently leads to agitation may result in excessive administration of sedatives.”1 And it's known that adequate pain management often reduces the need for sedation.1 Recent reports further suggest that, compared with traditional sedation (benzodiazepines plus analgesics for pain), narcotics-based sedation (such as fentanyl or morphine) may result in improved patient outcomes.2,3 Once the patient's pain is controlled adequately, sedative agents should be administered as needed. (For more information on ensuring adequate pain relief in patients who can't provide a report of pain, see Pain Control, “No Self-Report Means No Pain-Intensity Rating,” October 2005.)

Grading the Recommendations

How the SCCM guidelines were created.

In the mid-1990s the Society of Critical Care Medicine (SCCM), its affiliate the American College of Critical Care Medicine, and the American Society of Health-System Pharmacists created a task force to develop clinical practice guidelines on the sustained use of sedatives and analgesics in critically ill adults. A revised and updated version, often referred to as “the SCCM guidelines,” was published in 2001. Because these guidelines are based on the evidence, it's essential that the evidence be evaluated systematically.

After performing a literature search, the task force reviewed relevant studies and their reference lists, as well as abstracts from professional meetings. This literature, which varied widely in quality, was first classified by its type (see Table A, at right). Each article or abstract was then critically evaluated and scored to reflect the quality of its evidence. In doing so, the task force considered “research design, patient selection, medication dose, administration route, combination treatment, test measures, statistics, and results.”1

Table A
Table A:
Categories of Literature Evaluation

The SCCM guidelines include recommendations that were based on this literature review and were graded according to the strength and quality of the supporting evidence. This grading system (see Table B, at right) was itself devised by the task force, which reported that it made “a substantial effort … to adhere to the methodology for developing scientifically sound clinical practice guidelines as prescribed by the American Medical Association, the Institute of Medicine, and the Canadian Medical Association.”1

Table B
Table B:
Grades of Recommendations
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