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Seminars in Anesthesia, Perioperative Medicine and Pain (2006) 25, 65-70

exmedetomidine sedation for awake fiberopticntubation

ichard J. Unger, MD,a and Christopher J. Gallagher, MDb

From the Scripps Memorial Hospital, La Jolla, California; and the

Department of Anesthesiology, University of Miami/Jackson Memorial Hospital, Miami, Florida

The awake fiberoptic intubation (AFI) is an important part of the anesthesiologist’s armamentarium. Aswell as being technically challenging, it is also uncomfortable and stressful for all involved. We discussthe use of an alpha-2 agonist, dexmedetomidine, to help the clinician and patient through this procedure.The advantages of dexmedetomidine are that it produces a unique “Cooperative Sedation,” whichreduces discomfort in the patient and assists in the topicalization of the airway. Most importantly,dexmedetomidine does not produce significant respiratory depression, so the airway may be secured inthe safest manner possible. We discuss the history of sedation for AFI, other medications, as well asguidelines and pitfalls in the use of dexmedetomidine.© 2006 Elsevier Inc. All rights reserved.

KEYWORDS:Dexmedetomidine;Awake intubation;Cooperative sedation;Conscious sedation;Fiberoptic intubation

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“In dreams begin responsibility.”William Butler YeatsResponsibilities, 1914

And as our patients face the dreamland of general anes-hesia, we take on the responsibility for keeping their airwayafe and secure. In case of doubt, the safest, surest route ishe awake intubation. Just look at the ASA Difficult Airwaylgorithm1 and the ASA Difficult Airway Algorithm Mod-

fied for Trauma.2 Awake intubation keeps popping upgain and again, like some beachball you try to push underhe water. There’s no keeping it down!

OK fine, so we do the awake intubation. No problem,ight? No sooner said than done?

Who hasn’t seen this scenario:“AAAAAAGH! GAAAAAAAAAAAAAAAAGH!”Damn! I thought he was topicalized.“Hold still Mr. Smith!” Turning to the cart, maybe just a

Address reprint requests and correspondence: Richard J. Unger, MD,372 Eads Avenue, La Jolla, CA 92037.

E-mail: richard.unger@gmail.com.

277-0326/$ -see front matter © 2006 Elsevier Inc. All rights reserved.oi:10.1053/j.sane.2006.01.004

ittle more midazolam. Just a touch, a touch of fentanyl, younow, zap that cough reflex.

“Gaaaaaaaaaaaaaaaak!”“Um, doctor, his heart rate is pretty. . .”“THANK YOU, I KNOW, LET ME JUST GET THIS!”Thank God, he’s finally quieted down. Where are those

ords, I saw them just a second ago.BOOPBOOPBOOPBOOP.“S#&�!!! Gimme the mask, gimme the mask!”Sound familiar?Telling someone, “Just intubate them awake” is like most

dvice. You can’t argue with it, and it just plain makesense. But then implementing this great advice can be a realeadache. On the tennis court, for example, people give mehis advice: “Just hit it in all the time.” Well, shucks, greatdvice. Wonderful advice. If I would just follow that advice,’d beat Roger Federer at Wimbledon every time.

But it’s hard to “hit it in every time.”And it’s hard to “just intubate them awake”.

Awake intubation can give you adverse hemodynamic

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66 Seminars in Anesthesia, Perioperative Medicine and Pain, Vol 25, No 2, June 2006

onsequences3 and cause trauma— epistaxis, for example.nd a number of scenarios make awake intubation nearly

mpossible: intoxicated and uncooperative patient, C-spinenjury where the patient may thrash around and worseneurologic injury. Some patients with difficult airways mayot cooperate due to developmental delays, closed headnjury sequelae, or chromosomal abnormalities.

Sedation for awake intubation has its own list of misery,s illustrated above.4 Mix and match some narcotic andenzodiazepine, and the synergistic effect may convert yourawake” intubation into an “asleep, oh hell, what do I doow?” intubation.

Any magic bullet out there?Is dexmedetomidine (who are we kidding, you read the

hapter title, what else were we going to talk about?) theagic bullet?Well, not exactly, but it gets pretty close to being that

agic bullet. Let’s see how.There are a multitude of indications for awake fiberoptic

ntubation (AFI)5 (Table 1): history of difficult airway,nticipated difficult direct visualization of larynx, trauma,ass, or infection in the upper airway, and need for neuro-

ogic assessment after intubation. There are but a few, butbsolute contraindications to AFI do exist (Table 2). Localnesthesia is an integral part of awake airway management,ut that will not be discussed in this essay. Instead, we willocus on the safe methods of sedating patients who havendications for AFI. Patient cooperation is paramount whenttempting to do AFI, and in addition to informed consentnd patient acceptance, judicial administration of intrave-ous agents can greatly and safely aid the anesthesiologisthen facing a patient in need of AFI.Typically, the better a patient understands and cooperates

ith topical and regional anesthesia of the airway, the moreffective will be the local anesthetics and the better theatient and staff will tolerate the procedure! Our focus inhis essay will be to explain the advantages of dexmedeto-idine to facilitate these procedures and explain its advan-

age over more traditional agents.How does dexmedetomidine compare with other seda-

ive agents? To better understand the advantages of dexme-etomidine, it will be useful to understand the other agentshich have been used before dexmedetomidine was avail-

Table 1 Site of action of Dexmedetomidine

History of difficult intubation or mask ventilationAnticipated difficult laryngoscopy on physical examinationAspiration risk in patients unsuitable for rapid sequence

inductionsNeed for neurological assessment after intubationPotential loss of airway secondary to mass effect, infection,

bleeding

ble.

remedication

Premedication is an essential component of AFI. We useremedicants to reduce secretions, enhance hemodynamictability, create amnesia, and reduce anxiety. Benzodiaz-pines including midazolam and lorazepam will effectivelyeduce anxiety and create amnesia. Caution’s the bywordhen you use these drugs along with dexmedetomidineecause dexmedetomidine is synergistic with all sedativeedications.6

How about narcotics? No need to use them. Dexmedeto-idine plus a little bit of benzodiazepine provides you all

he sedation your need. Plus, by avoiding narcotics, youvoid their respiratory depression.

Vagolytic and antisialogogues such as glycopyrrolate aressential premeds to patients undergoing AFI. A dry mouthnhances the efficacy of local anesthetics,7 enhances visu-lization of the airway, and helps prevent the bradycardiaeen with alpha-2 agonists. Recent work has shown thatounger patients with more predominant vagal tone willave a safer journey with alpha-2 agonists if pre-treatedith glycopyrrolate.8

Other antisialogogues such as hyoscine and atropineave been used, but in themselves have potent CNS sideffects. What is the one symptom of atropine poisoning?Mad as a hatter.” Atropine crosses into the brain and youet a central cholinergic effect. Now you’ve converted yourwake intubation into a “madhouse” intubation! Glycopyr-olate is a quaternary ammonium and does not cross thelood–brain barrier, therefore causing no sedation and CNSide effects. Typically, adults given 0.2-0.3 mg of glyco-yrrolate will have effective drying of the mucosal mem-ranes with no adverse effects on heart rate. That is, thelycopyrrolate will not cause a tachycardia and will notllow a bradycardia.

onscious sedation

Almost all patients require some form of intravenousedation before AFI. This makes the term AWAKE fiber-ptic intubation a bit of a misnomer. Sedation is needed fornxiety and pain associated with the procedure. Importantoals of intravenous sedation include maintenance of air-ay patency and ventilatory drive. Dexmedetomidine is aedication that provides these unique characteristics. The

erm “Cooperative Sedation” has been aptly coined in rela-ion to the unique sedation achieved with dexmedetomidine.

Table 2 Contraindications for awake fiberoptic intubation(AFI)

RefusalUncooperative patientBleeding (unable to visualize)Local anesthetic allergy or toxicity

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67Unger and Gallagher Dexmedetomidine Sedation

efore we discuss the specific advantages of alpha-2 ago-ists, let’s look at the older agents that have had someuccess.

lpha-2 agonist alternative pharmacologicherapies (Table 3)

etamine

No thanks! Ketamine increases secretions, causes tachy-ardia, and disorients patients. The one time ketamine mayome in handy is for the uncooperative and IV-less patientf whom you are trying to “get control.” The IM ketamineart is just the ticket in such a case.9

arcotics

Narcotics including morphine, fentanyl, alfentanil,emifentanil, and others have been used to help with seda-ion of patients undergoing AFI. Narcotics will slow venti-ation, cause muscle rigidity, have a delayed onset of action,nd alter the sensorium (ie, not “Cooperative Sedation”).he advantages of narcotics include reversibility and sup-ression of airway reflexes.10

ropofol

Propofol is a phenol derivative which often causes painn injection. Since propofol has been introduced, manyave used it as part of a cocktail for AFI. Propofol causesess respiratory depression than narcotics and is easily usedy intravenous infusion. The disadvantage of propofol ishat the airway reflexes may be blunted in a deeply sedatedatient, potentially leading to regurgitation, loss of airway,radypnea, and hypotension.11

roperidol

Droperidol is a butyrophenol derivative and does providexcellent sedation, especially when combined with fentanyl

Table 3 Comparative pharmacologic properties of drugs for co

Rapid onsetwith a short

half-life

Sedation withorientation and

arousability Analgesi

Narcotics ** *** ****Ketamine * * **Benzodiazepines * ** *Propofol **** ** **Droperidol * ** **Dexmedetomidine *** **** ***

nd midazolam. Innovar was a combination drug of fentanyl r

nd droperidol, and often made for a very cooperative pa-ient, but the patient often had bad recollections when In-ovar was used.12 In some circles Innovar became known as“chemical straight-jacket.” Droperidol should probably be

eserved for patients who won’t tolerate other sedatives dueo their cardiovascular condition. Using droperidol has an-ther potential headache, or should we say heartache: pro-ongation of the Q-T interval. This is an extremely cloudynd controversial issue, but potentially serious. In light ofecent FDA “Dear Doctor” letters warning of the dangers ofroperidol, you may encounter some resistance to using

his drug.13,14

enzodiazepines

Benzodiazepines are good choices for amnesia, anxioly-is, and sedation, but have no analgesic properties. Benzo-iazepines are associated with respiratory depression, andon’t have the cooperative component which is produced byexmedetomidine. Small amounts of midazolam (0.02-0.04cg/kg) may be a useful adjunct to dexmedetomidine to

roduce amnesia. In addition, there is a specific reversalgent for benzodiazepines. Let’s just come right out and sayt: a little bit of midazolam, 1-2 mg in your average adult, issually all the “additional stuff” you need when you do aexmedetomidine awake intubation!

exmedetomidine

Dexmedetomidine is an alpha-2 agonist. As such it hasnique properties, which makes it useful when you areaking care of patients with difficult airways. Other alpha-2gonists have been around for years, used both with humansnd animals. Since most of us aren’t vets and few of usemember those obscure compounds, let’s concentrate onhe “PLAYER” in the alpha-2 arena: DEXMEDETOMI-INE. Dexmedetomidine is the most specific agent avail-

ble to bind to the alpha-2 receptor.When alpha-2 agonists are present, there is stimulation of

he alpha-2 receptor, which causes a negative feedback,ausing less neurotransmitter (norepinephrine or epineph-

s sedation for AFI

xiolysisEasily

titratedLack of

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Useful inHypovolemic

patients

** *** *** * **** ** * *** ****

**** ** *** ** ***** **** ** ** *** * ** *** ***

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ine) at the postsynaptic receptor (alpha-1 receptor) (Figure

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68 Seminars in Anesthesia, Perioperative Medicine and Pain, Vol 25, No 2, June 2006

). The various central nervous system subclass of alpha-2eceptors block the CNS effects of catecholamines, whichnclude anxiolysis, sedation, and analgesia. Most of theseffects are mediated specifically at the locus coeruleus andpinal cord.15

Dexmedetomidine has the unique property of “Cooper-tive Sedation.”16 This allows patients to better work withhe medical staff to facilitate intubation. This includes co-peration while the airway is topicalized, the bronchoscopes passed, and after the endotracheal tube is in to verify anntact neurological system.

Dexmedetomidine does not have any direct effect on theeart. At low dose ranges (up to 0.7 mcg/kg/hour), there isirect vasodilation. Ramsay and Ebert have used higher doses;amsay advocates doses which are an order of magnitudeigher than in the package insert in patients with difficultirways. Unfortunately, Ebert and others have shown that theseigher doses lead to arterial and pulmonary hypertension, re-uced cardiac output, and obtundation. These issues makeigh-dose dexmedetomidine undesirable for AFI.17,18

Alpha-2 agonists have been shown to attenuate the peri-perative catecholamine response. AFI will produce an ob-ious catecholamine response from patient, staff, and phy-ician! Just look in an operating room when and AFI isn’toing well!

“HOLD STILL!”“KEEP YOUR HAND DOWN!”

igure 1 Site of action of alpha-2 agonists. (Color version ofgure is available online.)

“HOLD HIM DOWN!”

Who knows, perhaps dexmedetomidine will prove usefuln preventing cardiovascular complications in those of usoing AFI’s!

Dexmedetomidine will potentiate the effects of intrave-ous and inhaled anesthetic agents by between 20-80%.FTER a loading dose of dexmedetomidine, make sure youse less general anesthetic.15 You’re already halfway there!ince dexmedetomidine is a vasodilator and sympatholytic,uthors and practitioners alike have advocated fluid loadingnd vagolytic therapy with agents such as glycopyrrolate.

There have been many recent reports in the literature ofsing dexmedetomidine as part of the intravenous sedationf AFI.9,19-21 We will present a case typical of our ownxperience, which we hope will help you use dexmedeto-idine in a safe and effective manner.

ase study

he patient is a 37-year-old (80 kg, 178 cms) white maleho was involved in a motorcycle accident 2 days prior

Table 4). He had an unstable cervical spine fracture but waseurologically intact. The patient had no significant previ-us medical history except for social alcohol and marijuanase. Physical exam revealed a patient who was extremelynxious. Vital signs were as follows: BP 148/94, HR 112,R 24, SaO2 96%. There were no other significant injuriesr findings on physical examination. Laboratory and radio-ogic findings other than the cervical fracture were withinormal limits. The neurosurgeon requested an AFI so thate wouldn’t need to manipulate his neck and would be able

o do a quick neurological assessment after the endotrachealube was correctly positioned.

The patient had been NPO for 12 hours. He was broughtnto the pre-operative area. We rounded up all the usualuspects, including informed consent, detailing the need forFI. We explained that the patient will be sedated for thisrocedure, but his cooperation during this procedure wouldelp the intubation be accomplished more safely and com-ortably.

Table 4 Essential steps for safely using dexmedetomidinefor AFI

Monitor patients ECG, oxygen saturation, EtCO2, and bloodpressure

Have staff who are experienced in AFIHave all essential airway equipment, including suction and

oxygenAdminister glycopyrrolate 0.2–0.3 mg IVLoad dexmedetomidine 0.5–1.0 mcg/kg over 10–20 minutesUse continuous infusion of dexmedetomidine @ 0.2–0.7

mcg/kg/hour for as long as indicatedSparingly use benzodiazepines to assure amnesia, eg, 1–2 mg

midazolamUse regional and topical anesthesia as necessary to assure

patient comfort

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69Unger and Gallagher Dexmedetomidine Sedation

Non-invasive monitors were placed which included:CG, pulse-oximetry, and blood pressure monitors. The

hythm strip of ECG was examined to verify there was noresence of first degree or greater heart block. (Dexmedeto-idine should not be given in the presence of heart block

ecause of possible complications of life threatening heartlock.)

A free flowing 18-gauge IV was started, and the patientas then given a dose of glycopyrrolate 0.3 mg intrave-ously. A dexmedetomidine loading dose was then given.t the standard dilution of 4 mcg/ml, we loaded the patientith 80 mcg/10 minutes. This works out to a rate of 120l/hour � 10 minutes. Simultaneously, the patient was

iven 2 mg of midazolam IV, and we began to prep theatient for an AFI by application of topical anesthesia of theirway.

This was accomplished in the following manner: 1%eosynephrine drops were applied as well as 4% lidocaineintment that was applied to progressively larger nasalrumpets from 28-34 french. Supplemental oxygen was ad-inistered by nasal cannula at 4 liters/minute. By this time,

he dexmedetomidine infusion was nearly complete, and theatient was very sleepy but arousable [Ramsay Sedationcale (RSS) 2-3]. The dexmedetomidine infusion wastarted at 0.4 mcg/kg/hour (8 cc/hour). We then proceededo use nebulized and atomized 4% lidocaine. The patientas very cooperative, and we applied the local anesthetic to

he airway when the patient would inspire.A #7 Mallinckrodt endotracheal tube (ETT) was then

ently passed into the left nares after the tip was lubricatedith lidocaine ointment and softened with warmed saline.hen, the ETT was atraumatically passed into the hypophar-nx. After attaching oxygen to the working channel of theronchoscope, the fiberoptic bronchoscope was slowlyassed through the vocal cords on the first pass. The uniqueooperative sedation afforded by the dexmedetomidine al-ows the practitioner to more easily pass the bronchoscopento appropriate position in the trachea. This is due to theact that the patient can work with you and take deep breathss you advance the scope, facilitating correct placement!

After the bronchoscope was positioned, the endotrachealube was advanced over the bronchoscope and the pilotalloon was carefully inflated. The patient was then reas-ured that he wouldn’t be able to phonate, and would behortly going to sleep. The ETT was confirmed to be in theight location by fiberoptic visualization, auscultation of thehest, ballottement, and confirmation of EtCO2. Vital signsere stable throughout the induction. The neurosurgeonerformed a quick neurological examination, which in-luded having the patient move all four extremities andhecking sensation to light touch.

General anesthesia was then induced with a relativelymall dose of propofol (100 mg) and neuromuscular relax-tion was achieved with 50 mg of rocuronium. Anesthesiaas maintained with sevoflurane, nitrous oxide and 250

cg of fentanyl. The dexmedetomidine infusion was main- t

ained at 0.4 mcg/kg/hour. A brief episode of hypotensionas treated with two boluses of 5 mg of ephedrine.Three hours later, at the conclusion of the case, the

nesthetic vapors were turned off and recovery from neu-omuscular blockers was assured with the aide of the nervetimulator. The patient was then transported with the endo-racheal tube in situ and dexmedetomidine infusion runningt a rate of 0.4 mcg/kg/hour to the ICU. Once in the ICU, theatient was awake, adequate head lift was affirmed, and therachea was extubated. The patient maintained his vitaligns within a normal range and dexmedetomidine infusionas continued until the bag was empty about 3 hours later.he patient was intact neurologically, had minimal pain andvery successful outcome.Dexmedetomidine was extremely useful in this case be-

ause it calmed the patient before the procedure began,llowed us to toplicalize his airway, and the unique profilef the drug kept his oxygenation and ventilation intact. Inddition, after the tube was confirmed in correct position,he patient was comfortable and cooperative as we did aursory neurological evaluation.

At the conclusion of the case, the patient awoke com-ortably with the endotracheal tube in place, without unduemounts of coughing or agitation. Sometimes, airway com-romise can result after this surgical procedure because ofocal trauma. Pain, agitation, and coughing can further com-romise the airway. The analgesia, anxiolysis, and cooper-tive sedation associated with dexmedetomidine are veryseful in the post-operative period in this subset of patients.he combination of the unique sedative properties, natural

ype sleep, cooperation, anxiolysis, and beneficial sympa-hectomy make dexmedetomidine an ideal drug for mostwake fiberoptic intubations.

ractical tips for using dexmedetomidine forFI

ndications

Indications include conscious sedation in a patient whent is essential to maintain ventilatory drive and have theatient cooperate with the invasive procedure. The medica-ion also has the advantage of being sympatholytic creatingmore stable peri-induction period.

ontra-indications

Contra-indications include: hypovolemia, hypotension,ortic stenosis, cardiogenic shock, septic shock, idiopathicypertrophic sub-aortic stenosis (IHSS), pulmonary hyper-

ension, heart block (without back-up pacemaker present).

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70 Seminars in Anesthesia, Perioperative Medicine and Pain, Vol 25, No 2, June 2006

osing

Intravenously load 1 mcg/kg of dexmedetomidine over0-20 minutes (distribution T1/2 6 minutes). Follow loadingose with continuous infusion at 0.2-0.7 mcg/kg/hour.

aution

Dose other sedatives, anxiolytics, and analgesics withaution, as alpha-2 agonists are synergistic with these othergents. Typically a small amount of midazolam (1-2 mgsntravenously) will be useful.

iscussion

n the literature, research lab, and operating room, dexmedeto-idine is finding a place as a pharmacologic adjunct for AFI.bert and Maze wrote an editorial on Ramsay’s series ofexmedetomidine cases. In this editorial, Ebert and Maze el-quently sing the praises of this “wonder drug”22: Ramsay anduterman’s interesting series of cases provides another arrow

n the quiver of clinicians for the management of surgicalatients with compromised airways. We anticipate furtheromparative studies to establish the clinical role of dexmedeto-idine in difficult airway algorithms.In difficult airway workshops and academic research,

exmedetomidine is rapidly finding a place. There are at leastve separate reports in the literature discussing the utility ofexmedetomidine in this difficult clinical scenario.9,18-21 Theargest of these is by Avistsian et al. They retrospectivelyeport on 20 cases where dexmedetomidine was used to helpacilitate AFI. None of their patients had any desaturationpisodes. Thirteen patients developed post induction hypoten-ion (perhaps due to the fact that induction doses of intrave-ous agents weren’t altered enough?), which was promptlyorrected with boluses of ephedrine and phenylephrine. Oneatient needed a single small (10 mcg) bolus of epinephrine toreat more refractory hypotension. In all cases, the AFI wasecorded as “smooth,” with good patient tolerance and noirway obstruction during the procedure.

Dexmedetomidine is being discovered as a very useful drugn select patients for select procedures in both the operatingoom and intensive care unit. With well over 700 cases ofexmedetomidine use in our group, we have found the drugost useful. For us, the difficult airway and awake intubationeans dexmedetomidine. The unique sedation with arousabil-

ty, lack of respiratory depression, complete anxiolysis, andoderate analgesia make dexmedetomidine the best available

rug in this area. In addition, the sympatholytic effects ofexmedetomidine can be extremely useful during this proce-ure to blunt the hemodynamic and cardiac response to theesultant high catecholamine levels.

Caution is the word when using dexmedetomidine. Pa-ients should be euvolemic, have no evidence of inadequateerfusion, or have any evidence of impaired intra cardiaconduction. When faced with hypotension secondary to

exmedetomidine, the clinician can usually easily treat this

ith typically available vasopressor agents. Once used,exmedetomidine will nearly always make the awake fiber-ptic intubation easier for patient and clinician.

eferences

1. Miller CD: Management of the difficult intubation in closed malprac-tice claims. ASA Newsletter 64:13-16,19, 2000

2. Wilson WC: Trauma: airway management ASA difficult airway algo-rithm modified for trauma —and five common trauma intubationscenarios. ASA Newsletter 69:9-16, 2005

3. Ovassapian A, Yelich SJ, Dykes HM, et al: Blood pressure and heartrate changes during awake fiberoptic nsasotracheal intubation. AneshAnalg 62:951-954, 1983

4. Bailey PL, Pace NL, Ashburn MA, et al: Frequent hypoxemia andapnea with sedation with midazolam and fentanyl. Anesthesiology73:826-830, 1990

5. Batra YK, Mathewm PJ: Airway management with endotracheal in-tubation (including awake intubation and blind intubation.) Indian JAnaesth 49:263-268, 2005

6. Bol CJJ, Vogelaar JPW, Tang JP, et al: Quantification of pharmaco-dynamic interactions between dexmedetomidine and midazolam in therat. J Pharmacol Exp Ther 294:347-355, 2000

7. Watanabe H, Lindren L, Rosenberg P, et al: Glycopyrronium prolongstopical anaesthesia of the oral mucosal and enhances absorption oflignocaine. Br J Anaestha 70:94-95, 1993

8. Peden CJ, Cloote AH, Stratford N, et al: The effect of intravenousdexmedetomidine premedication on the dose requirement of propofolto induce loss of consciousness in patients receiving alfentanil. An-aesthesia 56:408-413, 2001

9. Scher C, Gitlin M: Dexmedetomidine and low-dose ketamine provideadequate sedation for awake fibreoptic intubation. Can J Anesth 50:607-610, 2003

0. Reusche MD, Talmage DE: Remifentanil for conscious sedation andanalgesia during awake fiberoptic tracheal intubation: a case reportwith pharmoacokinetic simulations. J Clin Anesth 11:64-68, 1999

1. Kakodkar P, Lua S, Sear J, et al: Target controlled propofol for awakefiberoptic intubation. Difficult Airway Society Abstracts Edinburgh,1999

2. Kallos T, Smith TC: The respiratory effects of Innovar given forpremedication. Br J Anaesth 41:303-306, 1969

3. Habib AS, Gan TJ: Food and drug administration black box warningon the perioperative use of droperidol: a review of the cases. AnesthAnalg 96:1377-1379, 2003

4. Scuderi PE: You (still) can’t disprove the existence of dragons. An-esthesiology 102:1081-1082, 2005

5. Gertler R, Brown C, Mitchell DH, et al: Dexmedetomidine: a novelsedative agent. Baylor University Medical Center Proceedings 14:13-21, 2001

6. Belleville JP, Ward DS, Bloor BC, et al: Effects of intravenousdexmedetomidine in humans. I. Sedation, ventilation and metabolicrate. Anesthesiology 77:1125-1133, 1992

7. Ebert TJ, Hall JE, Barney JA, et al: The effects of increasing plasmaconcentrations of dexmedetomidine in humans. Anesthesiology 93:382-394, 2000

8. Ramsay MAE, Luterman DL: Dexmedetomidine as a total intravenousanesthetic agent. Anesthesiology 101:787-790, 2004

9. Jooste E, Ohkawa S, Sun L: Fiberoptic intubation with dexmedetomi-dine in two children with spinal cord impingements. Anesth Analg101:1248, 2005

0. Avitsian R, Lin J, Lotto M, et al: Dexmedetomidine and awakefiberoptic intubation for possible cervical spine myelopathy. Neuro-surg Anesthesiol 17:97-99, 2005

1. Maroof M, Khan R, Jain D, et al: Dexmedetomidine is a useful adjunctfor awake intubation. Can J Anesth 52:776-777, 2005

2. Ebert T, Maze M: Dexmedetomidine: another arrow for the clinician’s

quiver. Anesthesiology 101:568-570, 2004