242.Moser KM, Fedullo PF, LittleJohn JK, Crawford R. Frequent asymptomatic pulmonary embolism in patients with deep venous thrombosis. JAMA. 1994;271:223. [erratum] J Am Med Assoc 1994;271(24):1908.

243.Collins R, Scrimgeour A, Yusuf S, Peto R. Reduction in fatal pulmonary embolism and venous thrombosis by perioperative administration of subcutaneous heparin, an overview of results of randomized trials in general, orthopedic and urologic surgery. N Engl J Med. 1988;318(18): 1162–73.

244.Prevention of venous thrombosis and pulmonary embolism. NIH consensus conference. JAMA. 1986;256(6):744–9.

245.Gallus A, Raman K, Darby T. Venous thrombosis after elective hips replacement-the influence of preventative intermittent calf compression on surgical technique. Br J Surg. 1983;70(1):17–9.

246.Bergqvist D, Lindblad B. A 30-year survey of pulmonary embolism verified at autopsy: an analysis of 1274 surgical patients. Br J Surg. 1985;72(2):105–8.

247.Gan TJ, Glass PS, Windsor A, Payne F, Rosow C, Sebel P, et al. Bispectral index monitoring allows faster emergence and improved recovery from propofol, fentanyl and nitrous oxide anesthesia. Anesthesiology. 1997;87(4):808–15.

248.Tonnesen AS. Crystalloids and colloids. In: Miller R, editor. Anesthesia. 4th ed. New York: Churchill Livingstone; 1994. p. 1595–618.

249.Linko K, Makelainen A. Cardiorespiratory function after replacement of blood loss with hydroxyethyl starch 120, Dextran-70, and Ringer’s lactate in pigs. Crit Care Med. 1989;17(10):1031–5.

250.Hankeln K, Radel C, Beez M, Laniewski P, Bohmert F. Comparison of hydroxyethyl starch and lactated Ringer’s solution in hemodynamics and oxygen transport of critically ill patients in prospective cross over studies. Crit Care Med. 1989;17(2):133–5.

255.Bennett GD. Anesthesia for liposuction and abdominoplasty. In: Shiffman MA, Mirrafati S, editors. Aesthetic surgery of the abdominal wall. Berlin: Springer; 2005. p. 29–54.

256.Natof HE, Gold B, Kitz DS. Complications. In: Wetcher BV, editor. Anesthesia of ambulatory surgery. 2nd ed. Philadelphia: Lippincott; 1991. p. 374–474.

257.Mecca RS. Postoperative recovery. In: Borash PG, Cullen BF, Stoelting RK, editors. Clinical anesthesia. Philadelphia: J.B. Lippincott; 1992. p. 1517–8.

258.Bailey PL, Egar TD, Stanley TH. Intravenous opioid anesthetics. In: Miller RD, editor. Anesthesia. 5th ed. Philadelphia: Churchill Livingstone; 2000. p. 273–376.

259.Jensen S, Knudsen L, Kirkegaard L, Kruse A, Knudsen EB. Flumazenil used for antagonizing the central effects of midazolam and diazepam in outpatients. Acta Anaesthesiol Scand. 1989;33(1):26–8.

260.Klotz U. Drug interactions and clinical pharmacokinetics of flumazenil. Eur J Anaesthesiol. 1988;2:103–8.

261.McCloy RF. Reversal of conscious sedation by flumazenil: current status and future prospects. Acta Anaesthsiol Scand Suppl. 1995;108:35–42.

262.Bourke DL, Rosenberg M, Allen PD. Physostigmine: effectiveness as an antagonist of respiratory depression and psychomotor effects caused by morphine or diazepam. Anesthesiology. 1984;61(5):523–8.

263.Hill GE, Stanley TH, Slentker CR. Physostigmine reversal of postoperative somnolence. Can Anaesth Soc J. 1977; 24(6):707–11.

Recommended Reading

Surg. 1988;155(3):425–34.

253.Leone BJ, Spahn DR. Anemia, hemodilution, and oxygen delivery. Anesth Analg. 1992;75(5):651–3.

254.American Society of Anesthesiologists Task Force on Blood Component Therapy. Practice guidelines for blood component therapy. Anesthesiology. 1996;84(3):732–47.

lem-oriented approach. Baltimore: Williams & Wilkins; 1995.

Miller RD. Anesthesia. 5th ed. Philadelphia: Churchill Livingstone; 2000.

White PF, editor. Ambulatory anesthesia & surgery. Philadelphia: W.B. Saunders; 1997.

7.1 Introduction

Multimodal anesthesia has been in the ascendency for some time. Chilvers [1] landmark paper gave this technique impetus by highlighting the merits of this approach as opposed to traditional epidural analgesia in colorectal surgery. This is old news! Office-based anesthetic practitioners have been using this approach, with opioid sparing if not outright exclusion, in spontaneously breathing patients since the late 1990s [2]. Emesis is the one outcome most feared by patients [3] and once again it has been the office-based practitioners who have redefined endpoints in this area.

7.2 Definition of Sedation

In 2002 the American Society of Anesthesiologists [4] assembled a Task Force and defined four specific levels of sedation/analgesia.

Minimal Sedation (Anxiolysis): A drug-induced state during which patients respond normally to verbal commands. Although cognitive function and coordination may be impaired, ventilatory and cardiovascular functions are unaffected.

Moderate Sedation/Analgesia (Conscious Sedation): A drug-induced depression of consciousness during which patients respond purposefully to verbal commands, either alone or accompanied by light tactile stimulation.

S.J. Gray

Papworth Hospital NHS Trust, Papworth Everard, Cambridge, CB23 3RE, UK

e-mail: sjgray@tiscali.co.uk

No interventions are required to maintain a patent airway and spontaneous ventilation is adequate. Cardiovascular function is usually maintained.

Deep Sedation/Analgesia: A drug-induced depression of consciousness during which patients cannot easily be aroused but respond purposefully following repeated or painful stimulation. The ability to independently maintain airway function may be impaired. Patients may require assistance in maintaining a patent airway and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained.

General Anesthesia: A drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to independently maintain ventilatory function is often impaired. Patients often require assistance in maintaining a patent airway and positive pressure ventilation may be required because of depressed spontaneous ventilation or drug-induced depression of neuromuscular function. Cardiovascular function may be impaired.

The Society rightly contends that sedation is a continuum and it is not always possible to gauge how a patient will respond. So where the intention was moderate sedation, it is always possible the patient may move into deep sedation and even general anesthesia. It behooves the practitioner to have the requisite skills to be able to rescue the situation. Undoubtedly, this has implications for personnel and facilities.

The situation in the UK is more polarized; deep sedation is regarded as general anesthesia. The demarcation being, moderate sedation can be given by nonanesthesiologists whereas deep sedation (general anesthesia) requires a physician trained in anesthesia.

The American Society of Anesthesiologists has recently examined Monitored Anesthesia Care (latest update September 2, 2008). The Society is emphatic that Monitored Anesthesia Care (MAC) is a physician-led

service facilitating the safe administration of a maximal depth of sedation/analgesia in excess of that provided by moderate sedation. The MAC provider must have the skills to convert to general anesthesia should the clinical need arise. The MAC provider has an extended role beyond that furnished by a practitioner of moderate sedation, namely, preoperative assessment, management concomitant medical problems, supervision of recovery, and pain relief.

7.3 Other Considerations

Sedation has inherent risks: hemodynamic instability [5], respiratory depression [6], and uncontrolled movements [7]. Elderly patients need less sedation [8] and are at greater risk of desaturation and cardiovascular lability [9]. Sedation can unmask obstructive sleep apnea [10].

7.4 Assessing Level of Sedation

The two most commonly used scales are Modified Wilson Sedation scale (Table 7.1) and Observer’s Assessment of Alertness/Sedation (OAA/S) (Table 7.2).

Table 7.1 Modified Wilson sedation scale

Score Description

1Oriented, eyes may be closed but can respond to “Can you tell me your name?” “Can you tell me where you are right now?”

2Drowsy, eyes may be closed, arousable only to command: “Please open your eyes?”

3 Arousable to mild physical stimulation (ear lobe tug)

4Unarousable to mild physical stimulation

The latter, though more detailed, produces a more accurate record and has an impressive inter-rater agreement of 85–96% [11].

A plethora of Level of Consciousness (LOC) monitors have appeared since Bispectral Index (BIS Aspect Medical) was granted FDA approval in 1996. These include Entropy (Datex-Ohmeda, Finland), Patient State Index (Physiometrix), Cerebral State Monitor (Danmeter), and Narcotrend (Schiller Medical). Auditory evoked potentials have created interest, in particular the mid-latency signal, though it has been Bispectral Index (BIS) and Spectral Entropy that have found their way into clinical practice.

BIS takes power-spectral analysis (relationship between power and frequency over time) a step further by examining the phase relationships between component waves of different frequencies that make up the composite EEG. The monitor generates a dimensionless number on a continuous scale of 0–100, with “100” representing awake normal cortical electrical activity and “0” signifying cortical electrical silence. Surgical anesthesia is deemed to occur between 60 and 40 (Table 7.3).

BIS correlates well with the hypnotic state and anesthetic drug concentration [12–14]. BIS can shorten recovery times [15]. The Australian “B-aware” trial [16] recruited 2,463 patients and elegantly established that BIS-guided anesthesia reduces awareness by 82% in an at-risk adult surgical population. However, BIS does not predict movement in response to surgical stimulation, such responses often stem from the spinal cord.

Interestingly, adding nitrous oxide to an inhalational agent has little effect on BIS in the absence