您当前的位置:首页 > 主题内容 > 临床麻醉 > 基础与临床研究

ASSESSMENT OF SEDATION IN THE ICU

时间:2010-08-24 11:38:55  来源:  作者:
Introduction
The routine assessment of sedation is a part of total care for the critically ill patients in the intensive care unit in a similar way that cardio-respiratory parameters are monitored. An appropriate level of sedation will not only avoid periods of excessive or undersedation, but also assist research into improved methods for the sedation of critically ill patients. However, the real difficulty in assessing sedation is that no simple, standard system for regular recording of its level is in regular clinical use.
In the last few decades, the combination of neuromuscular blocking agents with modern anaesthetic drugs has made it difficult to assess the depth of anaesthesia and the level of sedation in the ICU. Many techniques have been suggested for monitoring the depth of anaesthesia and the assessment of sedation. The techniques used to assess the depth of anaesthesia and sedation are so similar that most of the methods for assessing the depth of anaesthesia can also be used to assess the level of sedation. The methods which are suitable for assessing the level of sedation can be considered under two headings: subjective assessment and objective assessment, depending on whether the techniques require the application of a scoring system or an index derived from a quantifiable physiological variable respectively.

Subjective assessment

A number of methods of subjective assessment are available and generally require measurement of some variables which are influenced by the level of consciousness. They may include specific tests of performance. These tests often require a high level of patient co-operation and co-ordination.1 They are of three types: clinical tests, paper and pencil tests and psychomotor tests. Norris and Nisbett2 described subjective scores for measuring the level of sedation: 1. apprehensive, 2. fully awake, 3. drowsy. These scores are based on the patient's consciousness and they are added to objective measurements of changes in heart rate and blood pressure. Steward, who studied post-operative recovery in children, used three categories: consciousness, airway and movement. Each category was scored on a three-point scale. This method has been used to assess propofol sedation in adults during endoscopy and to assess clinical outcome.
Several scoring systems, which are useful for assessing critical illness, have been published. The APACHE II Scoring System5 and Glasgow Coma Score6 are the most notable ones among them. Their widespread use allows comparison between similar groups of patients in different intensive care units as well as allowing a prediction of outcome within individual units. The Glasgow Coma Score is helpful in assessing coma but it is not a sedation score. Furthermore, as the Glasgow Coma Score makes no allowance for agitation, distress or pain, patients may not be sedated appropriately.
Edbrooke et al.7 used a modified Glasgow Coma Score as a sedation scale. Ramsay et al.8 reported a six-point scorin system with three scores when awake and three others when asleep. The levels while asleep were determined by the patient's response to a light glabellar tap or a loud auditory stimulus. This scoring system, or a modification of it, has gained some acceptance, particularly in research. Both
Grounds9 and Kong10 used a modified version of this scoring system to assess sedation using propofol and isoflurane in intensive care. McMenemin and others" also used a six-point scale to assess sedation after cardiac surgery but reversed the scale to give distress as the highest score of six. However, these modifications all highlight the lack of consistency in the subjective assessment of sedation in critically ill patients.
In 1986, Bion described a scoring system using a linear analogue scale to determine a score for consciousness. The scale is divided to allow 10 scores, ranging from complete unarousability to fully awake and receptive. This system seems to have some attractions, but it is relatively complex and more suitable for research than routine clinical use. Another suitable sedation score system is Addenbrooke's sedation score system (Cambridge Sedation Score). This test was developed for the critically ill patient drawing from the experience of 2500 sedated patients over a ten year period. It is a simple, reproducible, purpose-built intensive care sedation score giving only a minimal workload and distraction for the staff. However, it has not yet been widely used.
Most of the subjective tests for assessing the level of sedation mentioned above have the same disadvantages:
1. It is impractical in a busy intensive care unit to repeat these tests on an hourly basis;
2. Some of the tests are too complex and time consuming;
3. Some of the tests are too disturbing for the patient;
4. The scores are subjective and, therefore, easily influenced by observer bias.
The disadvantages of subjective methods for assessing the level of sedation have led to more attention being paid during the past decade to developing objective methods, both to assess the depth of anaesthesia and the level of sedation.

Objective assessment
The development of objective assessment of the level of sedation has paralleled the development of methods for assessment of the depth of general anaesthesia. The following methods are currently employed in research.
Haemodynamic changes
The relationship between the haemodynamic measurements and the depth of anaesthesia is well recognized. In 1934, Guedel14 described his classification of clinical signs for ether anaesthesia. It relied almost completely upon skeletal muscle activity and pupil diameters. Since the use of muscle relaxants and opiate analgesics, the Guedel stages have become unreliable, bringing the possibility of patient awareness. Evans et al.15 described an integrated scoring system (PRST Score, table 1) for use in paralyzed, ventilated patients based on clinical signs. This scoring system seems a good indicator for assessing the depth of anaesthesia, but it has some limitations for assessing the depth of sedation in the ICU because the blood pressure and heart rates in ICU patients respond to not only the physical treatment, such as physiotherapy, but also drug therapy, disease and other factors. Most of the patients in the ICU suffer from one or multi-organ failures and some patients are even supported by vasoconstrictor. Therefore, the haemodynamic changes are more useful as vital signs rather than signs of the depth of sedation.
Lower oesophageal contractility (LOC)
Increased contractility of the oesophagus associated with psychological stress was first described by Faulkner in 1940.16 In 1987, Evans and colleagues17 found a progressive decrease in spontaneous lower oesophageal contractility (SLOC) and subsequently provoked lower oesophageal con- tractility (PLOC) with increasing depth of anaesthesia. These changes are partially reversed by surgical stimulation and the technique showed sufficient promise to lead to a commercial monitor becoming available.
The correlation between LOC and the clinical signs of anaesthesia was reported to be quite close. However, further evaluation18 has shown that there is wide interpatient variability and, furthermore, the effects are severely attenuated by atropine. This limits clinical use of LOC both during anaesthesia and in the ICU patient.

The electroencephalogram (EEG)
Since Gibbs19 first reported on the occurrence of EEC changes during the administration of general anaesthesia, many reports have been published which support its usefulness as an intraoperative monitor. Most anaesthetic agents cause a specific change in the EEC pattern. Peter2 and Martin and co-workers 1 studied EEC changes produced by fentanyl and anaesthetic agents. The results showed that all general anaesthetics yield a basically similar dose-dependent sequence of six different EEC patterns and suggested that the EEC could provide a general method of estimating the depth of anaesthesia for different agents.
However, monitoring the depth of anaesthesia using the EEC is fraught with problems. They include difficulty with standardization, reproducibility, interpretation of EEC pattern using routine techniques and interference from the many electrical devices. To help overcome these difficulties, other methods have been developed to monitor cerebral function using EEC signals. They are the Cerebral Function Monitor (CFM), the Cerebral Function Analyzing Monitor (CFAM), power spectrum analysis of the EEC (PSA) and sensory evoked potentials (auditory, visual and somatosensory evoked potentials).

Cerebral function monitor (CFM)
The Cerebral Function Monitor (CFM) uses a single EEC channel, and the amplitude changes in the EEC are integrated to provide a single strip recording. A series of strips are plotted with respect to time on one trace. The width of the trace is related to the level of variability in brain activity.

Several studies have been performed to evaluate the usefulness of the CFM as an indicator of depth of anaesthesia. Although these investigators did document the relationship between the changes in CFM recording and the
infusion rate of some intravenous anaesthetics, the correlation was poor. Thus, the applicability of the CFM in estimating the level of sedation appears to be limited.
Cerebral function analyzing monitor (CFAM)
The Cerebral Function Analyzing Monitor designed by Marynard is a microprocessor-based system with two input channels for the on-line analysis of the EEC. A plot of both the amplitude and frequency distribution of the EEC can be obtained from either channel using the CFAM. Sebel and others26 employed this technique in 5 patients for halothane anaesthesia. The results showed that deepening halothane anaesthesia was associated with a gradual decrease in weighted EEC amplitude and with changes in different frequency bands. They concluded that CFAM provides useful, easily interpreted EEC information. However, the use of CFAM in critically ill patients has not been reported.

Power spectral analysis of the EEG (PSA)
Power spectral analysis of the EEC uses a complex mathematical technique known as Fourier analysis to transform the raw EEC data into a distribution of varying frequencies which fall into clinically relevant frequencies: the delta, theta, alpha and beta bands. It requires 3 steps in the analysis of the EEC. The first step is to digitize the EEC at fixed epochs. Then the data in each epoch are processed using Fourier analysis. Finally, power spectral analysis is performed by squaring the amplitudes of the individual frequency components. It possesses several distinct advantages over the simpler analytic methods used for evaluating changes in the EEC.27 The EEC data is only transformed, therefore, more information is retained, and the identification of small changes in the EEC is simplified. Another advantage is that modern computer techniques can now allow the simultaneous, on-line analysis and display of four or more channels of EEC data, thereby allowing the localization of EEG changes in a way that cannot be obtained by
using a single channel device such as the CFM, Versalis and colleagues reported that the changes of Spectral Edge (the 95% quartile of EEC power distribution) of PSA correlates with the level of midazolam sedation in critically ill patients. Wang et al.29 used PSA to measure the depth of sedation in 10 ICU patients during physiotherapy. The results showed that the amplitude (power) was increased during physiotherapy and it returned to the previous level after physiotherapy. This suggests that PSA can be used for monitoring the depth of sedation in ICU patients. But, this technique has not yet been extensively evaluated in ICU patients.
Visual evoked potentials (VEP)

Visual evoked potentials (VEP) have been successfully used for monitoring the integrity of the optic nervous pathway during surgery and anaesthesia. The VEP is usually elicited by 2 Hz flashes from LED lights attached to a pair of goggles which are placed over the patient"s closed eyes.36 Since the first report on the effects of general anaesthetics on the VEP by Domino37 in 1963, many workers have investigated the relationship between VEP characteristics and the concen trations of anaesthetic agents during general anaesthesia. Sebel and others38 reported that nitrous oxide increased the latency of N70 and Chi et al.39,40 reported decreases in amplitudes and increases in latencies of N70 and P100 after administration of etomidate and thiopentone-fentanyl nitrous oxide anaesthesia. Uhl and colleagues41 found a progressive increase in latency of P100 with increase of alveolar concentration of halothane. Most of the reports confirmed the usefulness of VEP for monitoring cerebral function and the depth of anaesthesia during surgery, but it has not been tested for measuring the level of sedation in ICU patients.

Somatosensory evoked potentials (SSEP)
Somatosensory evoked potentials (SSEP) are the most intensively recorded of the three sensory evoked potentials. Studies have involved different kinds of anaesthetic agents, such as inhalation anaesthetic agents42 and intravenous agents. Most of the reports showed that both latency and amplitude change with increasing doses of anaesthetic agents. However, the changes varied with different agents. Etomidate increased both latency and amplitude,44 Thiopentone decreased amplitude and increased latency of SSEP, but in contrast, midazolam had no effect on amplitude but increased latency of the SSEP. Observations on the effects of fentanyl and morphine on SSEP during anaesthesia showed45 that the change in latency was more consistent than change in amplitude. However, all work reported so far was undertaken during anaesthesia. There are no reports on the use of Somatosensory evoked potentials for measuring the level of sedation in the ICU.

Heart rate-variation
Changes in the heart rate are a normal physiological phenomenon in response to physiological changes. A rhythmic variation of heart rate also occurs in association with breathing and is known as sinus arrhythmia.46 As early as 1935, Samann and others47 noticed that heart rate-variation disappeared during the induction of ether anaesthesia in experiments on dogs. Fifty years later, Donchin and others48 observed the changes of heart rate-variation in 10 females during isoflurane-nitrous oxide anaesthesia. They suggested that on-line analysis of heart rate-variation might provide a physiological index of the level of anaesthesia and the rate of recovery. Another study used on-line analysis of heart rate-variation during anaesthesia in 60 patients49 and all the patients showed a reduction in heart rate-variation during anaesthesia and an increase in heart rate-variation during the recovery period. We have performed a similar investigation on ICU patients using the same technique. The results showed that there is an increase in heart rate-variation when sedation becomes light. This suggests that heart rate-variation might be a good indicator of the depth of sedation in ICU patients although more studies are needed to confirm this conclusion.

Conclusion
Correct assessment of sedation can provide better care for the patients, and act as a guide for medical staff treating patients. It should be performed regularly. Because there is no single, objective, reliable monitoring system for assessing sedation commercially available at present, scoring systems are still popular for clinical assessment of sedation in the ICU. A technique suitable for use in the ICU for monitoring the level of sedation should satisfy the following requirements:
1. It must show graded changes corresponding with changes in the depth of sedation;
2. It must show similar changes for different sedative agents;
3. It must be consistent between patients under similar sedation regimens;
4. It must be easy to interpret;
5. It must be sensitive enough to show even small changes in sedation during observation;
6. It must cause no discomfort to the patient and be non-invasive;
7. It must work in the presence of neuromuscular blockingagents.
As computer and monitoring techniques become morepowerful and cost-effective, it is likely that conventional monitors will routinely incorporate at least one of the techniques discussed here, to ensure adequate sedation in the ICU.
Acknowledgement
I would like to thank Professor TEJ Healy, Dr CJD Pomfrett and Dr M Shelly for their helpful suggestions and encouragement during the writing of this paper.

1. Kortilla K. Recovery after intravenous sedation: A comparison of clinical and paper and pencil tests used in assessing late effects of diazepam. Anaesthesia 1976; 31: 724-31.
2. Nisbett HIA, Norris W. Objective measurement of sedation II, A simple scoring system. Br J Anaesth 1963; 35: 618-23.
3. Steward DJ. A simplified scoring system for the post-operative recovery room. Can Anesth Soc J 1975; 22: 111-13.
4. Dubois A, Balatoni E, Peeters JP, Baudaux M. Use of propofol for sedation during gastrointestinal endoscopies. Anaesthesia 1988; 43: 875-80.
5. Knaus WA, Draper EA, Wagner DP, Zimmerman JE . APACHE II, a severity disease classification system. Crit Care Mod 1985; 13: 818-29.
6. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. Lancet 1974; 2: 81.
7. Edbrook DL, Newby DM, Mather SJ, Dixon AM, Hebron BS. Safer sedation for ventilated patients. A new application for etomidate. Anaesthesia 1982; 37:765-71.
8. Ramsay MAE, Savege TM, Simpson BJR, Goodwin R. Controlled sedation with alphaxolone-alphadolone. Br Med J 1974; 2: 656-9.
9. Grounds RM, Lalor JM, Lumley J, Royston D, Morgan M. Propofol infusion for sedation in the Intensive Care Unit. Br Med J 1989; 294: 399-400.
10. Kong KL, Lalor JM, Lumley J, Royston D, Morgan M. Isoflurane compared with midazolam for sedation in the Intensive Care Unit. Br Med J 1989; 298:1277-99.
11. McMenemin IM. Sedation following cardiac surgery, evaluation of alfentanil and morphine in the presence of a computerized closed loop arterial pressure controller. Br J Anaesth 1988; 61: 669-74.
12. Bion JF. Sedation in Intensive Care, morphine and renal function. Intensive Care Med 1986; 12: 359-65.
13. Shelly M. Assessing sedation. Care of the Critically III 1986; 2 (4): 170.
14. Guedel AE. Inhalational anaesthesia — a fundamental guide. Macmillan, New York, 1937.
15. Evans JM. Computer controlled anaesthesia. In: 0 Prakash, ed. Computing in anaesthesia and intensive care. Boston: Martinus Nijhoff, 1983: 279-91.
16. Faulkner WB. Objective oesophageal changes due to psychic factors. American Journal of Medical Science 1940; 200: 796-803.
17. Evans JM, Bithell JF, Vlachonikolic IG. Relationship between lower oesophageal contractility, clinical signs and halothane concentration during general anaesthesia and surgery in man. Br J Anaesth 1987; 59: 1346-55.
18. Aitkenhead AR, Lin ES, Thomas D. Relationship between lower oesophageal contractility and clinical signs of light anaesthesia. Anesthesiology 1987; 67: A671.
19. Gibbs GA, Gibbs EL, Lennox WG. Effect on electroencephalogram of certain drugs which influence nervous activity. Arch Intern Med 1937; 60:154-66.
20. Peter S. Effects of high-dose fentanyl anesthesia on the electroencephalogram. Anesthesiology 1959; 20: 359-76.
21. Martin JT. Electroencephalogram in anesthesiology. Anesthesiology 1959; 20:359-76.
22. Dubois M, Savege TM, O'Carroll TM, Frank M. General anaesthesia and changes on the Cerebral Function Monitor. Anaesthesia 1978; 33: 157-64.
23. Frank M, Savege TM, Leigh M, Greenwood J, Holly JMP. Comparison of the Cerebral Function Monitor and plasma concentrations of thiopentone and alphaxalone during total I.V. anaesthesia with repeated bolus doses of thiopentone and althesin. Br J Anaesth 1982; 54: 609-16.
24. Prior PF, Scott DF. Device for continuous monitoring of cerebral activity in resuscitated patients. Br Med J 1969; 4: 545-6.
25. Marynard DE. Development of the CFM: the Cerebral Function Analyzing Monitor (CFAM). Ann Anesth Franc 1979; 3: 253.
26. Sebel PS, Marynard DE, Major E, Frank M. The Cerebral Function Analysis Monitor (CFAM), A new microprocessor-based device for the on-line analysis of the EEC and Evoked Potentials. Br J Anaesth 1983; 55: 1265-70.
27. Warren JL, Shapiro HM, Maruchak G, Meathe E. Automated EEG processing for intraoperative monitoring, A comparison of techniques. Anesthesiology 1980; 53:223-36.
28. Vesalis RA, Carlon GC, Bedford RF. Spectral edge frequency correlates with sedation level in ICU patients receiving continuous I.V. midazolam. Anesthesiology 1989; 71: A156.
29. Wang DY, Sneyd JR, Pomfrett CJD, Healy TEJ. The effect of physiotherapy on EEG spectral derivatives in sedated patients on the Intensive Care Unit. Br J Anaesth 1992:69:221.
30. Lader MH, Norris H. Effect of nitrous oxide on the Auditory Evoked Response in man. Nature 1968; 218: 1081-82.
31. Thornton C, Catley DM, Jordan C, LehaneJR, Royston D, Jones JG. Enflurane anaesthesia causes graded changes in the Brainstem and Early Cortical Auditory Evoked Potentials. Br J Anaesth 1983; 55: 479-86.
32. Thornton C, Henegan CPH, Navaratnarajah M, Jones JG. Sedative effect of Althesin on the Auditory Evoked Response in man. Br J Anaesth 1986; 58: 422-7.
33. Thornton C, Konieczko KM, Knight AB, Kaul B, Jones JG, Dore CJ, White DC. The effect of propofol on the Auditory Evoked Response and on oesophageal contractility. Br J Anaesth 1989; 63: 411-17.
34. Thornton C, Barowcliffe MP, Konieczko KM, Ventham P, Dore CJ, Newton DEF, Jones JG. The Auditory Evoked Response as an indicator of awareness. Br J Anaesth 1989; 63: 113-15.
35. Sneyd JR, Wang DY, Edwards D, Pomfrett CJD, Doran BRH, Healy TEJ, Pollard BJ. Does physiotherapy affect the auditory evoked potentials of sedated patients in the Intensive Care Unit? Br J Anaesth 1992; 68: 349-51.
36. Sebel PS. Somatosensory, visual and motor evoked potential in anaesthetized patients. Bailliere's Clinical Anaesthesiology 1989; 3 (3): 587-602.
37. Domino EF, Corssen G, Sweet RB. Effects of various general anesthetics on the visually evoked response in man. Anesth Analg (Cleve) 1963; 42: 735-47.
38. Sebel PS, Flynn PJ, Ingram DA. Effects of nitrous oxide on visual, auditory and somatosensory evoked potentials. Br J Anaesth 1984; 56: 1403-7.
39. Chi OZ, Ryterband S, Reegt CF. Visual evoked potentials during etomidate administration in humans. Can ] Anaesth 1989; 36: 637-40.
40. Chi OZ, Ryterband S, Reegt CF. Visual evoked potentials during thiopentone-fentanyl-nitrous oxide anaesthesia in humans. Can J Anaesth 1989; 36: 637-40.
41. Uhl RR, Squires KC, Bruce DL, Starr A. Effect of halothane anaesthesia on the human cortical visual evoked responses. Anesthesiology 1980; 53: 273-6.
42. Sebel PS, Erwin CW, Neville WK. Effects of halothane and enflurane on far and near field somatosensory evoked potentials. Br J Anaesth 1987; 59:1492-6.
43. McPherson RW, Sell B, Traystman RJ. Effects of thiopental, fentanyl and etomidate on upper extremity somatosensory evoked potentials in humans. Anesthesiology 1986; 65: 584-9.
44. Koht A, Schiitz W, Schmidt G, Schramm J, Watanabe E. Effects of etomidate, midazolam, and thiopental on median nerve somatosensory evoked potentials and the additive of fentanyl and nitrous oxide. Anesth Analg 1988; 67:435-41.
45. Pathak KS, Brown RH, Cascorbi HF, Nash Jr CL. Effects of fentanyl and morphine on intraoperative somatosensory cortical-evoked potentials. Anesth Analg 1984; 63:833-837.
46. Ganong WF. The heart: origin of the heartbeat & the electrical activity of the heart. In: Review of medical physiology. 9th Ed. Appleton & Lange Medical Publications, California. 1979: 415-31.
47. Samann A. The effect of adrenaline, atropine and ether anaesthesia on the heart rate of normal dogs and animals deprived of different parts of the autonomic nervous system. Arch Int Pharmacodyn Ther 1935; 50: 101.
48. Donchin Y, Feld FM, Porges SW. Respiratory sinus arrhythmia during recovery from isoflurane-nitrous oxide anaesthesia. Anesth Analg 1985; 64: 811-15.
49. Pomfrett CJD, Beech MJ, Healy TEJ. Variation in respiratory sinus arrhythmia may reflect levels of anaesthesia. Br J Anaesth 1991; 67: 646-7.

来顶一下
返回首页
返回首页

本周热点文章

站内搜索: 高级搜索
关于我们 | 主编信箱 | 广告查询 | 联系我们 | 网站地图 |