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istorically, moderate to deep sedation has been used to decrease agitation and enhance compliance with ventilation modes.In the late 1990s, awareness of problems associated with excessive sedation began to surface; studies1,2

indicated that continuous sedation was associated with prolonged periods of mechanical ventilation and increased rates of pneumonia. Sub-sequently, results of randomized controlled trials3-5indicated improved outcomes with lighter

seda-tion and led to the widespread adopseda-tion of sedaseda-tion protocols or daily interrupseda-tions in sedaseda-tion. More recently, similar improvements occurred in a trial6

of analgosedation in patients treated with mechanical ventilation.

Sedation and Its

Association With

Posttraumatic Stress

Disorder

After Intensive Care

LORETTA F. ROCK, ACNP, CCRN

Feature

Overuse of sedation in patients treated with mechanical ventilation can increase duration of ventilation, dura-tion of delirium, and time to discharge. Although current principles of care include implementadura-tion of seda-tion protocols and/or daily interrupseda-tions in sedaseda-tion to improve patients’ outcomes, these strategies remain underused. Historically, a barrier to use of protocols has been a perception that being awake and aware while intubated is intrinsically distressing and could cause psychological harm. Evidence of a link between lighter sedation and decreased signs and symptoms of posttraumatic stress disorder has partially dispelled these fears and even prompted the adoption of no-sedation (eg, analgosedation) strategies. Published studies on posttrau-matic stress disorder and sedation are limited by small sample size, heterogeneous sedation practices, and inadequate follow-up. Despite limitations, current data suggest contemporary sedation practices to keep patients calm and comfortable but awake, as appropriate, are not associated with increased rates or severity of posttraumatic stress disorder. (Critical Care Nurse. 2014;34[1]:30-39)

This article has been designated for CNE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:

1. Summarize 2 research outcomes that can guide practice related to sedation in intubated patients 2. Discuss 3 limitations in the research studies associating sedation with posttraumatic stress disorder 3. Relate 3 qualifiers that must be considered when implementing practice changes in sedation protocols

©2014 American Association of Critical-Care Nurses doi: http://dx.doi.org/10.4037/ccn2014209

CNE

Continuing Nursing Education

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One early criticism of lighter sedation and interrup-tions in sedation was a concern that the experience of being awake while being treated with mechanical venti-lation would be psychologically harmful to patients. A 2003 follow-up study7

of patients who had interruptions in sedation indicated that this assumption was suspect and that deeper sedation might contribute to psycho-logical distress and the development of posttraumatic stress disorder (PTSD). Nevertheless, strategies to lighten sedation remain underused; in one survey,8

a total of 396 of 1355 respondents reported that they did not use sedation protocols.

Nurses’ resistance to sedation protocols or daily interruptions in sedation has been identified as a barrier to implementation.9

In a recent survey10

of 423 nurses, 48% reported an intent to sedate all patients receiving mechanical ventilation, a finding that correlated posi-tively with the nurses’ actual sedation practices. In addi-tion, 80% of the respondents agreed with the statement “Sedation is necessary for patient comfort” and charac-terized mechanical ventilation as “uncomfortable and stressful.” Because of the potential benefits of minimizing sedation, an examination of the impact of such sedation on psychological health, of which PTSD is one measure, is important. In this article, I review the literature on the influence of different sedation protocols on PTSD.

PTSD Definition and Prevalence

The Diagnostic and Statistical Manual of Mental Disorders(Fourth Edition, Text Revision)11

defines PTSD as the “development of characteristic symptoms follow-ing exposure to an extreme traumatic stressor” in which “the person’s response to the event must involve intense fear, helplessness, or horror.” A diagnosis of PTSD requires the presence of persistent signs and symptoms in each of 3 categories: hyperarousal, intrusive recollections, and avoidance/numbing. PTSD can be classified as acute (<3 months’ duration), chronic (≥3 months’ duration), or delayed onset. Practitioners have only recently become

aware that PTSD can occur after an ICU stay, and the etiology of the syndrome is not clearly understood.12

The reported prevalence13

of PTSD after ICU care is 19% to 22%, and occurrence of the syndrome is associated with a marked adverse effect on health-related quality of life.

Method

The population of interest was adult ICU patients treated with mechanical ventilation who were sedated. The intervention was any strategy that would decrease the level of sedation, either through daily interruptions in sedation, use of nursing protocols, or differences in sedation scores (Ramsay Sedation or Richmond Agitation-Sedation scales14,15

). Outcomes were rates of PTSD or PTSD-like signs or symptoms. The evidence was limited to controlled trials. A search of PUBMED conducted by using combinations of the MeSH terms “stress disorders, posttraumatic”; “intensive care unit”; “daily sedation inter-ruption”; and “sedation” yielded 322 articles. Narrowing the search by using the filters “humans” and “clinical trial” yielded 48 articles. Three prospective randomized controlled trials (RCTs) and 1 observational study were identified. A Web of Science search of articles that cited 1 or more of the 3 RCTs and references cited in 1 or more of the RCTs yielded a fourth trial that was nonrandom-ized. In total, 4 trials were reviewed and 1 observational study was included for citation in the discussion.

Terms

The term sedationrefers to the degree of consciousness along a continuum that extends from a state of unrespon-siveness (score of 6 on Ramsay scale) to agitation (score of 1 on Ramsay scale). Deep and light sedation are dis-cussed in terms of scores on the Richmond Agitation-Sedation Scale, the Ramsay scale, or the modified Ramsay scale. For clarity, the term sedative exposure is used to indicate differences in doses of administered sedatives. PTSD refers to diagnosis of PTSD, and scores on various tools used to evaluate PTSD are discussed in terms of PTSD symptoms.

Results

Effects of the Intervention on PTSD The first study7

to examine the relationship between sedation and PTSD was a follow-up to the findings of a landmark RCT published in 2000 by Kress et al4

on the Loretta Rock is a nurse practitioner in trauma services, Lancaster

General Hospital, Lancaster, Pennsylvania.

Corresponding author: Loretta Rock, 16 E New St, Lancaster, PA 17602 (e-mail: [email protected]).

To purchase electronic or print reprints, contact the American Association of Critical-Care Nurses, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, [email protected].

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impact of daily interruptions in sedation on the duration of mechanical ventilation and ICU stay. In this trial,4

patients randomized to the intervention group had daily interruptions in sedation with infusions restarted at half the rate after wakening. Sedation was then titrated to the goal Ramsay sedation score of 3 (following commands) or 4 (asleep, but easily arousable). The control group had standard sedation management with interruption only as per the ICU team. In a follow-up trial72 years later,

patients from the initial trial were evaluated for PTSD through psychological testing and their Impact of Events Score. Because the dropout rate was high, additional patients were recruited for comparison from a 2-year period after the study was concluded. The cohort stud-ied retrospectively received sedatives as in the original trial (daily spontaneous awakenings or standard care) but had not been randomized to these 2 groups. The

results of this study,7published in 2003, showed a

sur-prising trend toward increased incidence of PTSD in the control group; PTSD was diagnosed in 6 patients in the control group and in none in the intervention group (P= .06; see Table). A significant difference in Impact of Event Scores was also detected; compared with the interven-tion group, the control group had symptoms of PTSD more often (P=.02), particularly for the subscales of avoid-ance and intrusive thoughts. Interestingly, other markers of psychological health such as anxiety and depression did not differ between the groups. The study was limited by its small size (32 patients) and retrospective design.

In 2008 Girard et al5performed a similar study,

the Awake and Breathing Controlled (ABC) trial. They improved the quality of the study by using a randomized control design and a larger sample size. Interventions and assessment methods included daily interruptions in

Reference Kress et al,72003 Jackson et al,162010 Treggiari et al,172009 Strøm et al,182011 Design Retrospective, nonrandomized, controlled trial with historical comparison group; blinded observer Prospective randomized controlled trial; blinded observer Prospective randomized controlled trial; blinded observer Prospective randomized controlled trial; blinded observer Sample population

32 MICU patients from a single center in the United States

80 MICU patients from a single center in the United States

129 SICU and MICU patients from a single center in the United States

26 patients from a single center in Denmark with 1 to 1 nurse to patient ratios

Control

Usual care: Sedation man-agement per ICU team

Usual care: Sedation titrated to individual patients’ goals

Deep sedation group Continuous midazolam

infusion titrated to Ram-say score of 3-4 Morphine for pain

Sedation with continuous infusion of propofol or midazolam titrated to Ramsay score of 3-4 with daily sedation inter-ruption

Morphine bolus for pain Bedside sitter available as

needed

Intervention

Daily interruption of sedation by research team followed by adjust-ments to sedation dosage and titration to RASS score of 3-4

Sedation as in control group with spontaneous awakening trials (ie, sedation interruption) each morn-ing followed by adjustments in or cessation of sedation dosage, titrated to patient-specific goals Paired with spontaneous breathing

trials

Light sedation group

Bolus-dose midazolam titrated to Ramsay score of 1-2

Morphine for pain

Analgosedation

Morphine bolus for pain; haloperidol bolus for delirium

Bedside sitter available as needed

Table

Summary of studies of sedation and posttraumatic stress disorder

Abbreviations: ICU, intensive care unit; IES-R, Impact of Events Score; MICU, medical ICU; PTSD, posttraumatic stress disorder; PTSS-10, Posttraumatic Stress Scale-10; RASS, Richmond Agitation-Sedation Scale; SICU, surgical ICU.

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sedation similar to those used by Kress et al,7but with a

few marked differences. As in the study by Kress et al,7

patients in the control group received usual care, and those in the intervention group had daily interruptions in sedation. In both studies,5,7if the patients were agitated

or tachypneic upon awakening, they were returned to con-tinuous sedation with the dose adjusted to half the initial rate and then titrated to the goal rate or dose. However, in the trial by Girard et al,5patients who performed well

off sedation continued to receive no sedation for as long as they were not anxious or agitated. Another difference between the 2 studies5,7was that sedation for both groups

in the study by Girard et al was titrated to “patient com-fort” rather than to a score on the Ramsay scale.

In 2010, a prospective follow-up trial by Jackson et al16

was conducted to evaluate the impact of the ABC trial intervention on cognitive and psychological measures in

80 patients. The results indicated that although less seda-tion was achieved in the intervenseda-tion group (as measured by days in coma), the control group had only a slight, nonsignificant increase in the incidence of PTSD (P=.59) at 3 months and no difference at 12 months (P=.97) after discharge (see Table). In addition scores on the Posttraumatic Stress Scale-10 (another measure of PTSD symptoms) did not differ between the 2 groups at either evaluation (P=.83 and P=.60, at 3 and 12 months, respectively). As in the study by Kress et al,7depression

was unchanged at 12 months. Less cognitive impairment was observed in the intervention group than in the con-trol group at 3 months (P=.03), but this difference had disappeared by the 12 month follow-up.

In 2009, Treggiari et al17attempted to determine

the impact of sedation on psychological outcomes by randomizing patients to either light (score 1-2) or deep

Evaluation

IES15

Interview by clinical psychologist

PTSS-10 for the ICU administered by neuropsychologist IES-R or PTSD checklist by self-report PTSS-10 IES-R Interview with neuropsychologist Resultsa

IES15scores were lower in the intervention group (P= .02)

No patients in the intervention group had a diag-nosis of PTSD compared with 6 in the control group; a nonsignificant trend (P= .06) toward increased PTSD in the control group 14% of patients in the intervention group and

10% of patients in the control group had a test score suggestive of PTSD at 3 months (P= .59) 24% of patients in the intervention group and 24% of patients in the control group had a test score suggestive of PTSD at 12 months (P= .97)

Intervention group tended to have lower PTSD symptom scores (P= .07), particularly trouble remembering parts of the stressful experience (P= .01) and repeated, disturbing memories (P= .05)

10% of intervention group and 9% of control group had a test score suggestive of PTSD (P= .83) 2 patients in control group and 1 patient in

inter-vention group had PTSD diagnosed (P= .50) No patients in control group and 1 patient in

intervention group had a PTSS-10 score suggestive of PTSD (P= .14)

Comments

No power analysis, small sample size Most likely underpowered

Control group was a cohort of patients selected after the initial intervention was completed, introducing potential bias from retrospective comparison

RASS scores measured only daily and means not analyzed, mak-ing it difficult to identify true differences in alertness/sedation No power analysis

Strong design with intention-to-treat analysis and large, multicenter sample size

No formal clinical evaluation of PTSD No universal RASS goals for either group

RASS scores were measured only daily and means were not analyzed, making it difficult to identify true differences in alertness/sedation

Adequately powered to detect a difference of 10 points in score on IES-R or PTSD checklist.

Strong design with intention-to-treat analysis

Follow-up at only 4 weeks would have detected only acute form of PTSD, not delayed-type onset

No formal clinical evaluation of PTSD

Bolus vs continuous dosing may have influenced outcome Small sample size, no power analysis

Most likely underpowered to reject the null hypothesis (type II error)

Strong design with intention-to-treat analysis

Very low rates of PTSD suggest an effect of the trial itself or the particular clinical setting

Evaluation of patients at 2 years after ICU stay may have introduced a recall bias

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(score 3-4) sedation according a modified Ramsey scale in which a score of 0 indicated agitation. The study groups also differed in the method of administration of the sedative: the intervention group (light sedation) received intermittent boluses of midazolam, whereas the control group (deep sedation) received a continuous infusion. Daily interruptions in sedation were not used. The sam-ple size was large, and 129 of the 138 original patients completed follow-up. Similar to the findings of Kress et al,7

the results of Treggiari et al17showed a trend toward

fewer PTSD symptoms (as measured by Impact of Event Score-R) in the light-sedation group versus the deep-sedation group (P=.07; see Table). In particular, the 2

groups of patients in the study by Treg-giari et al differed significantly in their responses to “trouble remembering important parts of the stressful experi-ence” and the frequency of “repeated, disturbing memo-ries.” Despite these differences, the incidence of PTSD overall did not differ between the groups (P=.83). As in the other studies,7,16measurements of anxiety and

depression were similar between groups. Of note, the psychological assessments in the study by Treggiari et al17

were performed 4 weeks after patients’ discharge from the hospital, so the data provided information on the acute form of PTSD but not on the delayed-onset type.

The most recent evaluation of PTSD after sedation was a randomized control trial18in which patients had

either continuous infusion of midazolam for sedation with daily interruptions in sedation (control) or had analgose-dation (intervention). Patients in the intervention group received pain medication in the form of morphine boluses and haloperidol as needed for delirium but no sedative agents. Patients who were delirious and agitated in either group were assigned a bedside sitter. Of the 26 patients who completed follow-up, no significant differences in PTSD or symptoms were detected. One patient in the intervention group and no patients in the control group had a score on the Posttraumatic Stress Scale-10 sugges-tive of PTSD (P=.14). A total of 2 patients in the control group and 1 patient in the intervention group had an Impact of Events score suggestive of PTSD (P=.50). Over-all, the incidence (0%-8%) of PTSD in both groups in this study18was lower than the incidence in the other

studies7,16,17or in epidemiological data.13

Effect of the Intervention on Exposure to Sedatives

Despite differences in dosing strategy and sedative agents, interventions were consistently associated with a decrease in the use of midazolam or the broader category of benzodiazepines (values not reported). No difference was found in amounts of propofol or dexmedetomidine.

Limitations of Research

As a whole, the biggest limitation of these 4 studies is heterogeneity in protocols and measurements. Most strikingly, the sedation goal (Ramsay score 3-4) for the intervention group in the study by Kress et al7was the

same as the deep sedation control group in the 2 later studies by Treggiari et al17and Strøm et al.18Also,

differ-ent measures were use to assess PTSD or its symptoms; in an earlier study,7the investigators used scoring tools

based on definition of PTSD in the third edition of the

Diagnostic and Statistical Manual of Mental Disorders

(see Table). Timing of follow-up may also have confounded results; the time of evaluation was from 4 weeks to 2 years after ICU discharge. This lack of consistency across stud-ies prevents meta-analysis and may explain some differ-ences in results (see Discussion section).

Although the studies were well-designed, the one by Strøm et al18had several limitations that should be

con-sidered in evaluating the results. Differences in care such as the 1 to 1 staffing ratio in their study and standard staffing in US ICUs might affect the study’s external validity. This trial18also had a high rate of dropouts;

commenting on this, Griffiths19noted that patients who

declined to have psychological follow-up might represent a highly vulnerable population. Perhaps most importantly, the negative results of this trial18are not surprising given

the small sample size and low rates of PTSD, factors that could lead to a type II error.

Another possibility that should be considered in interpreting the results of all these studies7,16-18is that the

measurement of PTSD and its symptoms may be less specific after an episode of sedation. Mainly, the signs and symptoms of PTSD, which include difficulty remem-bering factual events as a defining feature, may be a reflec-tion of the intenreflec-tionally amnesic qualities of sedareflec-tion. This characteristic would partially explain the increased positive responses in the avoidance/numbing domain of PTSD symptom assessment, although not the questions about delirious or intrusive memories. The unaffected

The signs and symptoms of PTSD may be a reflection of the intentionally amnesic qualities of sedation.

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depression, cognitive capacity, and anxiety scores sup-port this line of reasoning to some degree.

Discussion

Despite differences in methods and outcomes in these studies,7,16-18the results can be used to guide practice and

research. Several statements are reasonably well-supported by the evidence.

First, lower levels of sedative exposure do not seem to increase the incidence of PTSD. Although this rela-tionship was not examined explicitly, patients in the intervention groups of all 4 studies7,16-18had less sedative

exposure than did patients in the control group. This finding is consistent with findings from an observational study by Weinert and Sprenkle,20who reported no

corre-lation between sedative exposure per body weight and PTSD incidence or symptoms.

In the studies7,16that included a variety of sedative

agents, the finding that sedative exposure differed only for those patients sedated with benzodiazepines sug-gests the possibility that use of midazolam alone, rather than sedation or sedatives in general, may be responsible for the increased PTSD symptoms in the control groups of the studies by Kress et al7and Treggiari et al.17Although

the link between benzodiazepines and PTSD is specula-tive, other investigators21,22have identified use of

benzo-diazepine as a risk factor for delirium, and delirium or delirious memories could plausibly lead more often to PTSD. Additionally, benzodiazepines can have a pro-longed half-life in critically ill patients.23Although the

findings from a recent meta-analysis24 raise questions

about the relationship between these medications and delirium, the Society of Critical Care Medicine 2013 guide-lines,25based on available evidence, state that “sedation

strategies using nonbenzodiazepine sedatives may be preferred over sedation with benzodiazepines.”

As a second point, increased alertness does not seem to increase incidence of PTSD or PTSD symptoms. Despite differences in sedation goals, this finding was consistent in all 4 studies I examined and has been incorporated into much of the literature in favor of sedation-interruption protocols.26-29Of note, the study6with the smallest sample

size, and the only study that included analgosedation, most likely was underpowered to confirm this assertion.

Results from the study by Weinert and Sprenkle20are

again largely consistent with the notion that increased alertness does increase incidence of PTSD or PTSD

symptoms, and may provide insight into the development of PTSD. Weinert and Sprenkle found that PTSD symp-toms were highest in the groups with intermediate or fluctuating levels of wakefulness (sedation scores not provided) and lower for patients who were more consis-tently deeply sedated or completely alert and that the alert group was the least affected. A possible explanation for the relationship between alertness and PTSD symp-toms in that study20and in the 4 studies I examined may

be related to findings by Myhren et al30that “memory of

pain, lack of control, and inability to express needs” were among the independent risk factors for PTSD. Similarly, in a qualitative study, Rattray et al31found that

patients who were less aware of the surroundings or who had frightening experiences had more PTSD symptoms after discharge than did other patients. A reasonable inference based on these various findings is that being moderately sedated may make expressing one’s needs and wishes more difficult without having a correspon-ding therapeutic effect, although this possibility was not explicitly investigated.

The question provoked by the earliest study,7“Does

decreased sedation prevent PTSD or its symptoms?” is still unanswered. Although the findings of Treggiari et al17

support this hypothesis to some extent, the findings of Jackson et al16and Strøm et al18do not. Some possible

reasons include differences in use of midazolam, PTSD measurement tools, follow-up, sampling, and mortality. However, a discussion of the reasons why Jackson et al16

were unable to replicate the findings of Kress et al7despite

overall similarity is important. One would expect that the interventions used by Jackson et al, awakening with the goal of stopping

sedation, would pro-duce a greater differ-ence in the sedation levels between the

control and intervention groups than the difference in sedation levels between the control and intervention groups seen in the Kress et al7trial. The most probable

explanation is that both Jackson et al16and Kress et al7

compared interventions with standard treatment. As Mehta et al32note in their discussion of a recent trial of

daily sedation interruption, “The effectiveness of any new intervention to minimize sedation likely depends on the local usual care.” Because lighter sedation strate-gies had not yet been popularized at the time of the study

Increased alertness does not seem to increase incidence of PTSD or PTSD symptoms.

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by Kress et al,7the difference in sedation they noted

most likely would have been more dramatic than the dif-ference in the later study by Jackson et al.16This change

in practice is important to keep in mind when evaluat-ing analgosedation; the potential psychological benefits of lighter sedation may have been already been realized with current sedation practices.

Current practice guidelines,25in agreement with the

evidence reported here, do reflect a goal of light sedation, which is defined as easily arousable and able to follow commands. Protocols with goals of light sedation or daily

interruptions in sedation should not be suspended to keep patients from consciously experiencing or remem-bering the ICU course. Education on the relationship between PTSD and sedation could increase acceptance of current sedation goals. Perhaps most importantly, ICU care should be performed with awareness of the potential for memory formation even in sedated or non-communicative patients.

Changes in Practice

No evidence yet suggests that trials of analgosedation are unethical from the standpoint of PTSD outcomes. In fact, the low overall rates of PTSD in the study by Strøm et al18 may have introduced a novel method of

reducing the occurrence of PTSD: the bedside sitter for patients with agitation. Although use of a sitter may seem impractical, it does suggest a potential role for psychoso-cial intervention. Training a patient’s family members and having their presence at the bedside, for example, may be one way to improve the patient’s autonomy and comfort. Caveats

A number of important qualifiers must be added to the previous statements. First, sedation goals should be adjusted according to both patient safety (including risk for injury, self-extubation, noncompliance with the ven-tilator, and increased intracranial pressure) and patient comfort. The investigators in the studies I examined did not evaluate the immediate consequences of lighter sedation. Agitation or anxiety should not be allowed to escalate in any patient. Importantly, practitioners should not assume that present distress off sedation will be bal-anced by a future free of PTSD, because such a balance

has not been demonstrated. In one study,33duration of

agitation in restrained, nonsedated patients was posi-tively associated with higher incidence of PTSD.

Second, adequate pain control is assumed. Third, adequate staffing to monitor and respond to patients with agitation or safety concerns is assumed. In studies7,16

of daily interruptions in sedation, additional monitoring was provided, and in the study18with analgosedation, in

addition to 1 to 1 staffing ratios, patients had an as-needed bedside sitter. Finally, the effects of sedation on PTSD have not been studied in subsets of patients (eg, neuro-surgical or burn patients), so the findings presented here may not hold true for such patients.

Gaps in Research

The links between sedation, delirious memories, and PTSD are not well established. A recent meta-analysis24

of 34 studies indicated that although delirium alone is not correlated with PTSD, whether or not memories of delirious episodes are contributory is unclear. As Wein-ert and Sprenkle20suggest, the character of the ICU

expe-rience may have a greater influence on psychological outcomes than the level of sedation does. More could be gleaned from an analysis of the subscale results in each PTSD symptom tool and from validation of these tools in patients after discharge from the ICU. Additionally, interventions that decrease delirium or helplessness in patients treated with mechanical ventilation could be evaluated for their effect on PTSD. Ongoing research on survivorship34,35has already begun to address the most

important outcomes from these studies7,16-18: the need to

decrease frightening and distressing events in the ICU. As in the study by Strøm et al,18evaluations of novel

sedation protocols should include psychological assess-ment and follow-up when possible.

Conclusion

The psychological effects of daily interruptions in sedation, lighter sedation, or analgosedation are not clear. The provocative relationship between PTSD symp-toms and sedation, in particular, use of midazolam, is an evidence-based challenge to the traditional practice of putting patients “to sleep.” Meanwhile, an intriguing new strategy, analgosedation, is being studied as an alternative to light-to-moderate sedation. Nurses remain the essen-tial providers in the assessment of and response to the constantly changing sedation needs of their patients;

Sedative exposure differed only for those patients receiving benzodiazepines.

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nurses are responsible for balancing goals for sedation with concerns about hemodynamic, neurological, and ventilatory compromise. While research on ICU sur-vivorship continues, current evidence shows no increased risk for PTSD in patients who have light sedation. CCN Acknowledgments

The author thanks Dr Deborah Becker for her support and Amelia Rogers for her assistance in the production of this article.

Financial Disclosures

None reported.

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23. Malacrida R, Fritz ME, Suter PM, Crevoisier C. Pharmacokinetics of midazolam administered by continuous infusion to intensive care patients. Crit Care Med.1992;20(8):1123-1126.

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29. Miller MA, Bosk EA, Iwashyna TJ, Krein SL. Implementation challenges in the intensive care unit: the why, who, and how of daily interruption of sedation. J Crit Care.2012;27:218.e1-218.e7

30. Myhren H, Toien K, Ekeberg O, Karlsson S, Sandvik L, Stokland O. Patients’ memory and psychological distress after ICU stay compared with expectations of the relatives. Intensive Care Med.2009;35(12):2078-2086. 31. Rattray J, Crocker C, Jones M, Connaghan J. Patients’ perceptions of and emotional outcome after intensive care: results from a multicentre study.

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32. Mehta S, Burry L, Cook D, et al. Daily sedation interruption in mechani-cally ventilated critimechani-cally ill patients cared for with a sedation protocol: a randomized controlled trial. JAMA.2012;308(19):1985-1992. 33. Jones C, Bäckman C, Capuzzo M, Flaatten H, Rylander C, Griffiths RD.

Precipitants of post-traumatic stress disorder following intensive care.

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34. Deja M, Denke C, Weber-Carstens S, et al. Social support during inten-sive care unit stay might improve mental impairment and consequently health-related quality of life in survivors of severe acute respiratory dis-tress syndrome. Crit Care.2006;10(5):R147.

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Now that you’ve read the article, create or contribute to an online discussion about this topic using eLetters. Just visit www.ccnonline.org and select the article you want to comment on. In the full-text or PDF view of the article, click “Responses” in the middle column and then “Submit a response.”

To learn more about sedation in the critical care setting, read “Sedation in Adults Receiving Mechanical Ventilation: Physiological and Comfort Outcomes” by Grap et al in the American Journal of Critical Care, 2012;21:e53-e64. Available at www.ajcconline.org.

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the article and has been incorporated into much of the literature in favor of sedation-interruption protocols.

• Current practice guidelines, in agreement with the evidence reported here, do reflect a goal of light sedation, which is defined as easily arousable and able to follow commands. Protocols with goals of light sedation or daily interruptions in sedation should not be suspended to keep patients from consciously experiencing or remembering the ICU course. Education on the relationship between PTSD and sedation could increase acceptance of current sedation goals. Perhaps most importantly, ICU care should be performed with awareness of the potential for memory formation even in sedated or noncom-municative patients.

• An intriguing new strategy, analgosedation, is being studied as an alternative to light-to-moderate seda-tion. Although use of a sitter may seem impractical, it does suggest a potential role for psychosocial intervention. Training a patient’s family members and having their presence at the bedside, for exam-ple, may be one way to improve the patient’s auton-omy and comfort.

• Nurses remain the essential providers in the assess-ment of and response to the constantly changing sedation needs of their patients; nurses are respon-sible for balancing goals for sedation with concerns about hemodynamic, neurological, and ventilatory compromise. While research on ICU survivorship continues, current evidence shows no increased risk for PTSD in patients who have light sedation. CCN

Facts

• A diagnosis of posttraumatic stress disorder (PTSD) requires the presence of persistent signs and symptoms in each of 3 categories: hyperarousal, intrusive recollections, and avoidance/numbing. The reported prevalence of PTSD after intensive care unit (ICU) care is 19% to 22%, and occurrence of the syndrome is associated with a marked adverse effect on health-related quality of life.

• In the most recent evaluation of PTSD after sedation, patients had either continuous infu-sion of midazolam for sedation with daily interruptions in sedation (control) or had anal-gosedation (intervention). No significant dif-ferences in PTSD or symptoms were detected. • Lower levels of sedative exposure do not seem

to increase the incidence of PTSD. Although this relationship was not examined explicitly, patients in the intervention groups of all stud-ies reviewed in the article had less sedative expo-sure than did patients in the control group. • In the studies reviewed in the article that

included a variety of sedative agents, the find-ing that sedative exposure differed only for those patients sedated with benzodiazepines suggests the possibility that use of midazolam alone, rather than sedation or sedatives in general, may be responsible for the increased PTSD symptoms in the control groups of 2 of the studies.

• Second, increased alertness does not seem to increase incidence of PTSD or PTSD symptoms. Despite differences in sedation goals, this find-ing was consistent in all 4 studies reviewed in

References

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