ADIS DRUG CLINICAL Q&A

Clin Drug Investig 2012; 32 (8): 561-567

1173-2563/12/0008-0561/$49.95/0
Adis 2012 Springer International Publishing AG. All rights reserved.

Dexmedetomidine: A Guide to Its Use

for Sedation in the US
Gillian M. Keating, Sheridan M. Hoy and Katherine A. Lyseng-Williamson
Adis, Auckland, New Zealand

Abstract

Intravenous dexmedetomidine (Precedex) provides both effective sedation in mechanically ventilated patients in an intensive care setting and effective procedural sedation. In these patient populations, it reduces the need
for rescue sedation with intravenous propofol or intravenous midazolam and
reduces opioid requirements. In addition, patients receiving dexmedetomidine
are calm and easy to arouse and manage. Intravenous dexmedetomidine is
generally well tolerated and is not associated with respiratory depression.
Although the utilization of dexmedetomidine is associated with hypotension
and bradycardia, both usually resolve without intervention.

What is the rationale for developing

the drug?
Sedation comprises a continuum represented
by four progressive stages: minimal sedation, moderate sedation, deep sedation and general anaesthesia.[1] Patients in an intensive care setting
commonly require sedation in order to improve
patient comfort by relieving pain and anxiety,
treat agitation, ameliorate the stress response and
optimize mechanical ventilation.[2,3] The desired
goal of sedation in these settings is usually a calm
patient who can be easily aroused.[4]
Thus, intravenous sedation is considered integral for patients in an intensive care setting,
particularly in those requiring mechanical ventilation, with its utilization for interventional procedures becoming more widespread.[4-6] A variety
of agents are used to achieve sedation, including benzodiazepines (e.g. midazolam), general anaesthetics (e.g. propofol), opioids and a2-adrenergic
receptor agonists such as dexmedetomidine
(Precedex) [table I].

How does the drug work?

Dexmedetomidine is a selective a2-adrenergic
receptor agonist with a broad range of pharmacological properties.[7,8] Its sympatholytic effects
are the result of decreased noradrenaline (norepinephrine) release in sympathetic nerve endings. The sedative effects of dexmedetomidine are
thought to be mediated through decreased firing
Table I. Adis Evaluation
What are the key clinical benefits and limitations of
dexmedetomidine in short-term sedation?
Clinical benefits
Provides effective short-term sedation in the intensive care
setting and effective procedural sedation
Reduces the need for rescue sedation with propofol or
midazolam and reduces opioid requirements
Patients receiving dexmedetomidine are calm and easy to
arouse and manage
Generally well tolerated; not associated with respiratory
depression
Limitations
Associated with hypotension and bradycardia (usually resolves
without intervention)

Keating et al.

562

of the locus coeruleus, the major site of noradrenergic innervation in the brainstem.[7]
For whom is the drug indicated?
Table II provides a summary of the US prescribing information[9] for dexmedetomidine in
the sedation of initially intubated and mechanically ventilated adult patients in an intensive care
setting and in non-intubated adult patients prior
to and/or during surgical and other procedures.

What is its therapeutic efficacy in

ventilated, intensive care patients?
The efficacy of intravenous dexmedetomidine
as a short-term sedative for post-surgical patients in an intensive care setting was evaluated in
two randomized, double-blind, placebo-controlled,
multinational trials.[10-12] Eligible patients had
undergone a surgical procedure (cardiac surgery,
head and neck surgery, laparotomy or other) that
was expected to require a minimum of 6 hours of

Table II. Prescribing summary of intravenous dexmedetomidine (Precedex) for adult patients requiring short-term sedation in
the US.[9] Consult local prescribing information for further details
What is its approved indication and how should it be administered in ventilated pts in an intensive care setting?
Indication
Sedation in initially intubated and mechanically ventilated pts during treatment in an intensive care setting
Administer by continuous infusion not to exceed 24 h
Dexmedetomidine has been continuously infused in mechanically ventilated pts prior to extubation, during
extubation, and post-extubation
It is not necessary to discontinue dexmedetomidine prior to extubation
Loading infusion
1 mg/kg infused over 10 min
Pts converting from alternate sedative therapy: loading infusion may not be required
Consider a dose reduction in pts aged >65 y and pts with impaired hepatic function
Maintenance infusion
0.20.7 mg/kg/h titrated to achieve the required level of sedation and infused for 24 h
Consider a dose reduction in pts aged >65 y and pts with impaired hepatic function
What is its approved indication and how should it be administered for sedation during procedures?
Indication
Sedation of non-intubated pts prior to and/or during surgical and other procedures
Loading infusion
1 mg/kg infused over 10 min (including for AFOI)
0.5 mg/kg infused over 10 min for less invasive procedures (e.g. ophthalmic surgery) and for pts aged >65 y
Consider a dose reduction in pts with impaired hepatic function
Maintenance infusion
Commence at 0.6 mg/kg/h and titrate from 0.2 to 1 mg/kg/h to achieve the desired level of sedation
0.7 mg/kg/h is recommended until the endotracheal tube is secured in pts undergoing AFOI
Consider a dose reduction in pts aged >65 y and pts with impaired hepatic function
What compatibility issues are associated with its administration?
Do not coadminister through the same intravenous catheter as blood or plasma
Incompatible when coadministered with amphotericin B or diazepam
How is it available?
100 mg/mL concentrate for solution for infusion; available in 2 mL vials containing 200 mg of dexmedetomidine
What is its pharmacokinetic profile?
Distribution
Rapid distribution phase with distribution half-life of 6 min
Volume of distribution at steady state of 118 L
Plasma protein binding of 94%
Metabolism and
Undergoes extensive hepatic metabolism
excretion
95% and 4% of the dose excreted in the urine and faeces after 9 d
No unchanged dexmedetomidine detected in urine
Terminal elimination half-life of 2 h
Are there any monitoring requirements and precautions?
Continuous monitoring is required in all pts
Administer with caution to pts with advanced heart block and/or severe ventricular dysfunction
What are its potential drug interactions?
When coadministered, a reduction in the dosage of dexmedetomidine or concomitant anaesthetics, sedatives, hypnotics or opioids
may be required because of enhanced effects
Coadminister dexmedetomidine and other vasodilators or negative chronotropic agents with caution
AFOI = awake fibre-optic intubation; pts = patients.

Adis 2012 Springer International Publishing AG. All rights reserved.

Clin Drug Investig 2012; 32 (8)

Dexmedetomidine: Adis Drug Clinical Q&A

563

Table III. Efficacy of intravenous dexmedetomidine vs placebo as a short-term sedative for post-surgical patients in an intensive care setting. Results of two randomized, double-blind, multinational trials[10-12] with supplemental data from the US
manufacturers prescribing information.[9] Efficacy endpoints relate to the utilization of rescue sedation with propofol or midazolam,a with results reported in the intent-to-treat population for the assisted ventilation period and across the entire study
drug administration period
Study
Treatmentb Assisted ventilation period
Study drug administration period
[no. of pts]
Mean total dose of
Pts not requiring
Mean rate of
Mean total dose of
Mean rate of
rescue sedation
rescue sedation
rescue sedation
rescue sedation
rescue sedation
required (mg)
(%)
(mg/h)
required (mg)
(mg/h)
Martin
et al.[10]
US
FDA[11,12]c
a

DEX [203]
PL [198]
DEX [178]

71.6***d
513.2d
4.8*d

60.1**
23.7
60.7**d

8.6**
65.6

80.0**
559.8

5.3**
39.1
0.29***

PL [175]
18.6d
24.6d
1.19
If the rate of study drug infusion was 0.7 mg/kg/h but sedation could not be maintained, a bolus of PRO 0.2 mg/kg[10] or MID
0.02 mg/kg[11] could be administered. If sedation remained inadequate following three bolus injections of PRO[10] or MID[11] within a 2 h
period,[11] a continuous infusion of PRO 0.54.0 mg/kg/h[10] or MID 0.010.02 mg/kg/h[11] could be initiated.

Pts initially received a loading dose of DEX 1 mg/kg or PL infused over 10 min followed by a maintenance infusion of DEX or PL
commencing at a rate of 0.4 mg/kg/h and titrated to a rate of 0.20.7 mg/kg/h to achieve and/or maintain a RSS score of 3.[9,10]

Data were obtained from the US FDA website,[11,12] supplemented by data from the US manufacturers prescribing information.[9]

Primary endpoint.

DEX = dexmedetomidine; MID = midazolam; PL = placebo; PRO = propofol; pt = patient; RSS = Ramsay Sedation Scale;
**
p < 0.001, *** p < 0.0001 vs PL.

post-surgical assisted ventilation.[10-12] The study

drug was started within 1 hour of entry to the
intensive care unit and continued for 6 hours of
assisted ventilation, through weaning and extubation, and for 6 hours post-extubation, with
a total treatment duration of up to 24 hours.[10-12]
Intravenous dexmedetomidine was an effective
short-term sedative in this setting. The mean total
dose of rescue sedation (intravenous propofol[10]
or midazolam[11,12]) required to achieve and/or
maintain a Ramsay Sedation Scale (RSS) score of
3 during the assisted ventilation period was significantly lower with dexmedetomidine than with
placebo (table III). Moreover, significantly more
dexmedetomidine than placebo recipients acquired
and/or maintained a RSS score of 3 without
rescue sedation with intravenous propofol[10] or
midazolam[9,11,12] (table III).
The mean rate of rescue sedation with intravenous propofol required to achieve and/or maintain a RSS score of 3 during the assisted ventilation
period was significantly lower with dexmedetomidine than with placebo (table III).[10] Moreover, the mean total dose[10] and/or mean rate[10,12]
Adis 2012 Springer International Publishing AG. All rights reserved.

p < 0.005,

of rescue sedation with intravenous propofol[10] or

midazolam[12] required over the entire study drug
administration period was significantly lower with
dexmedetomidine than with placebo (table III).
In addition, dexmedetomidine recipients required significantly (p < 0.05) less additional pain
medication (morphine; assessed as mean total
dose) than placebo recipients during the assisted
ventilation period and the period from extubation to the end of the administration of the study
medication.[10-12]
Mean Patient Management Index scores were
also significantly (p < 0.05) lower with dexmedetomidine than with placebo, with lower scores
corresponding to greater apparent calm, ease of
communication (i.e. easier to arouse to answer
questions or respond to neurological tests) and
overall manageability of care, and greater tolerance of the endotracheal tube, the ventilator and
the intensive care setting.[10-12]
Both dexmedetomidine and propofol provided
effective sedation in patients who had undergone
extensive cervical spine surgery and required overnight intubation and mechanical ventilation in a
Clin Drug Investig 2012; 32 (8)

Keating et al.

564

small, randomized, non-blind, single-centre study.[13]

Patients received loading doses of dexmedetomidine
0.1 mg/kg/min (n = 16) or propofol 0.1 mg/kg/min
(n = 16) over 10 minutes, followed by infusions
of dexmedetomidine 0.4 mg/kg/h or propofol
1 mg/kg/h adjusted to maintain a RSS score of 24.
All patients in both treatment groups achieved
adequate RSS scores and had an adequate pain
status and adequate movement in response to
verbal commands.[13]
What is its therapeutic efficacy during
procedural sedation?
Intravenous dexmedetomidine was effective as
a primary sedative in adult patients undergoing
awake fibre-optic intubation (AFOI)[14] or a variety
of diagnostic or surgical procedures requiring
monitored anaesthesia care (MAC),[15] according
to the results of two pivotal, randomized, doubleblind, multicentre trials. In the AFOI study,[14]
significantly fewer dexmedetomidine than placebo recipients required rescue sedation with intravenous midazolam to achieve and/or maintain
a RSS score of 2 during AFOI (table IV). In the
MAC study,[15] rescue sedation with intravenous
midazolam was not required to achieve and/or
maintain an OAA/S score of 4 during MAC by
significantly more dexmedetomidine than placebo recipients (table IV).[15]

The mean total midazolam dose was significantly lower in patients receiving dexmedetomidine
than in those receiving placebo in both studies
(table IV).[14,15] In addition, in the MAC study,
the median time to midazolam administration was
significantly longer with dexmedetomidine than
with placebo, and significantly fewer dexmedetomidine than placebo recipients required further
sedation (table IV).[15]
Small, randomized, controlled trials demonstrated that dexmedetomidine was generally associated with better outcomes than propofol[16]
or propofol plus alfentanil[17] in patients requiring procedural sedation. For example, in patients
with obstructive sleep apnoea syndrome who were
undergoing a coblation-assisted upper airway
procedure (n = 60), visual analogue scale scores
assessing pain, how well the procedure was tolerated
and satisfaction with the procedure significantly
favoured dexmedetomidine versus propofol recipients at most timepoints, in a randomized, singlecentre study (figure 1). In addition, significantly
fewer dexmedetomidine than propofol recipients
required supplemental analgesia (3% vs 23% of
patients; p < 0.05).[16]
In addition, the mean postoperative Iowa satisfaction with anaesthesia scale score (primary
endpoint) was significantly higher (indicating greater
patient satisfaction) with intravenous dexmedetomidine than with intravenous propofol plus

Table IV. Efficacy of sedation with intravenous dexmedetomidine in patients undergoing awake fibre-optic intubation[14] or a
variety of diagnostic or surgical procedures requiring monitored anaesthesia care.[15] Results of two randomized, double-blind,
placebo-controlled, multicentre studies; analyses are for the modified intent-to-treat population
Pts requiring
Median time to
No. of
Primary endpoint (% of pts)
Mean total
Study
Treatment
further
administration
pts
MID
(loading dose
Requiring
Not requiring
sedation (%)
of MID (min)
dose (mg)
[mg/kg])
MIDa
MIDa
DEXb
55
47.3**
1.07**
0
PLb
50
86.0
2.85
8.0
Candiotti et al.[15]
DEX 0.5 mg/kgc
134
40.3**
1.4**
40.0**
3.0*
DEX 1 mg/kgc
129
54.3**
0.9**
114.0**
1.6*
PLc
63
3.2
4.1
20.0
11.1
a A bolus of MID 0.5 mg could be administered as rescue medication.[14,15] MID administration was repeated until the RSS score was
2[14] or the OAA/S score was 4.[15]
Bergese et al.[14]

Pts received a loading dose of DEX 1 mg/kg or PL over 10 min followed by DEX 0.7 mg/kg/h or PL to achieve a RSS score of 2.

Pts received a loading dose of DEX 0.5 or 1 mg/kg or PL over 10 min followed by DEX or PL commencing at 0.6 mg/kg/h and titrated
from 0.2 to 1 mg/kg/h.[15]

DEX = dexmedetomidine; MID = midazolam; OAA/S = Observers Assessment of Alertness/Sedation Scale; PL = placebo; pts = patients;
RSS = Ramsay Sedation Scale; * p < 0.05, ** p < 0.001 vs PL.

Adis 2012 Springer International Publishing AG. All rights reserved.

Clin Drug Investig 2012; 32 (8)

Dexmedetomidine: Adis Drug Clinical Q&A

55

Dexmedetomidine
Propofol

50
Mean visual analogue scale scores (mm)

565

45
40
*

35

**

*
30

25
20

*
*

15
10

to experience oxygen desaturation (primary endpoint) [3% vs 29% of patients; p = 0.01] or require
oral suction (11% vs 37%; p = 0.03).[18] However,
dexmedetomidine plus propofol recipients had significantly longer recovery times, required topical
anaesthesia more frequently, and had poorer bronchoscopist cough and satisfaction scores than remifentanil plus propofol recipients (all p < 0.01).[18]
There were no significant between-group differences with regard to the level of sedation, oxygen
saturation during flexible bronchoscopy, patient
cough and satisfaction scores, and the proportion
of patients who were willing to undergo repeat
bronchoscopy.[18]

5
0
T1 T2 T3 T4
Pain score

T1 T2 T3 T4

T1 T2 T3 T4

Tolerability score Satisfaction score

Fig. 1. Efficacy of intravenous dexmedetomidine vs propofol for

procedural sedation. Results of a randomized, single-centre study in
which patients undergoing a coblation-assisted upper airway procedure received dexmedetomidine (1 mg/kg loading dose over 10 min
followed by 0.7 mg/kg/h adjusted to maintain a Ramsay Sedation
Scale score of 23) [n = 30] or propofol (n = 30).[16] Shown are patient-assessed visual analogue scales scores for pain, how well the
procedure was tolerated and satisfaction with the procedure; scores
ranged from 0 to 100 mm, with lower scores indicating better outcomes. Outcomes were assessed following radiofrequency volume
tissue reduction of the soft palate (T1), oropharyngeal region (T2),
tongue (T3) and inferior turbinate (T4). * p < 0.05, ** p < 0.01 vs propofol.

alfentanil in patients undergoing outpatient cataract surgery under MAC (50.3 vs 42.7; p < 0.001).[17]
In this randomized, crossover study, 15 patients
received dexmedetomidine 0.6 mg/kg/h and 16 patients received propofol 2 mg/kg/h plus alfentanil
20 mg/kg/h (both regimens were titrated to maintain a RSS score of 3) for the operation on the
first eye, with patients switching treatments for
the operation on the second eye; an interval of
12 weeks separated the operations.[17]
In another randomized, double-blind study,
patients undergoing diagnostic flexible bronchoscopy received dexmedetomidine (bolus dose of
0.2 mg/kg followed by an infusion of 0.42 mg/kg/h)
[n = 35] or remifentanil (bolus dose of 0.5 mg/kg,
followed by an infusion of 15 mg/kg/h) [n = 35].[18]
All patients received a bolus dose of propofol
0.5 mg/kg prior to study drug infusion.[18] Dexmedetomidine plus propofol recipients were significantly
less likely than remifentanil plus propofol recipients
Adis 2012 Springer International Publishing AG. All rights reserved.

What is its tolerability profile y

Intravenous dexmedetomidine was generally
well tolerated when used for sedation in mechanically ventilated patients in an intensive care
setting and for procedural sedation, with hypotension and/or bradycardia being the most commonly occurring adverse events.[9,10,14,15]
y versus placebo y

In postsurgical patients who were mechanically ventilated in an intensive care setting, sedation with dexmedetomidine was associated with a
significantly (p < 0.005) higher incidence of hypotension (30% vs 10%) and bradycardia (9% vs
2%) and a significantly (p < 0.05) lower incidence
of hypertension (12% vs 23%), atelectasis (0.5%
vs 5%) and rigours (0.5% vs 4%) than sedation
with placebo.[10] Hypotension and bradycardia
tended to occur during or shortly after infusion of
the dexmedetomidine loading dose. Hypotension
generally resolved either without treatment or with
changes in positioning and/or fluids, and bradycardia
resolved either spontaneously or with medication
(e.g. atropine). Dexmedetomidine did not appear
to affect respiratory rate or oxygen saturation.[10]
Similarly, hypotension was the most commonly
occurring adverse event in patients receiving
dexmedetomidine who underwent procedural sedation.[14,15] For example, in the AFOI study, the
incidence of hypotension was significantly higher
(27.3% vs 6.0%; p = 0.0042) and that of tachycardia
Clin Drug Investig 2012; 32 (8)

Keating et al.

566

significantly lower (7.3% vs 24.0%; p = 0.0277) in

dexmedetomidine than placebo recipients, with
no significant difference between dexmedetomidine
and placebo recipients in the incidence of bradycardia (7.3% vs 0%) or hypertension (23.6% vs
28.0%).[14] During the infusion period of the MAC
study, the incidence of respiratory depression was
significantly (p = 0.018) lower with dexmedetomidine
loading doses of 0.5 or 1 mg/kg than with placebo
(3.7% and 2.3% vs 12.7%).[15]
During infusion of the study drug in the AFOI
study, there was no significant difference between
dexmedetomidine and placebo recipients in the
proportion of patients requiring intravenous
fluids or medication to treat blood pressure or
heart rate changes (12.7% vs 8.0%).[14] The incidence of intervention (study drug titration, intravenous fluid boluses or pharmacological therapy)
for bradycardia, hypertension or tachycardia
during study drug infusion in the MAC study did
not significantly differ between patients receiving
a loading dose of dexmedetomidine 0.5 or 1 mg/kg
and those receiving placebo. However, the proportion of patients requiring intervention for
hypotension was significantly higher in dexmedetomidine 0.5 mg/kg recipients than in placebo recipients (11.9% vs 3.2%; p = 0.046).[15]
y or active comparators?

Dexmedetomidine recipients had a significantly

(p < 0.05) lower median heart rate than propofol
recipients for up to 6 hours after administration
of the loading dose in patients requiring overnight intubation and mechanical ventilation following extensive cervical spine surgery.[13] The
median dopamine dose was significantly (p < 0.05)
higher in dexmedetomidine than propofol recipients at 2 hours, but not at any other timepoint. In addition, atropine use was significantly
(p = 0.04) higher with dexmedetomidine than with
propofol.[13]
However, dexmedetomidine was better tolerated than propofol in patients requiring procedural sedation during a coblation-assisted upper
airway procedure.[16] Propofol recipients were significantly (p < 0.05) more likely than dexmedetomidine recipients to experience airway obstruction
Adis 2012 Springer International Publishing AG. All rights reserved.

or hypoxia, or to require esmolol for temporary

haemodynamic support.[16]
Significantly fewer patients experienced hypertension with dexmedetomidine than with propofol plus alfentanil during cataract surgery (3.2%
vs 25.8%; p < 0.05).[17] Systolic blood pressure was
significantly (p < 0.05) lower in dexmedetomidine
recipients than in propofol plus alfentanil recipients, with one case each of hypotension and
bradycardia occurring with dexmedetomidine.[17]
Among patients undergoing diagnostic flexible bronchoscopy, there were no significant differences between dexmedetomidine plus propofol
and remifentanil plus propofol in mean arterial
pressure or heart rate, apart from a significantly
(p < 0.05) higher heart rate with remifentanil plus
propofol than with dexmedetomidine plus propofol at the time the bronchoscope was passed
through the vocal cords.[18]
What is its current positioning?
Intravenous dexmedetomidine provides both
effective sedation in mechanically ventilated patients in an intensive care setting and effective
procedural sedation, and is generally well tolerated. In these patient populations, it reduces the
need for rescue sedation with intravenous propofol or intravenous midazolam and reduces opioid
requirements. Sedation with dexmedetomidine is
also effective in terms of patient management,
with dexmedetomidine recipients being calm and
easy to arouse and manage. Dexmedetomidine
is not associated with respiratory depression,
and although hypotension and bradycardia may
occur, both usually resolve without intervention.
Thus, intravenous dexmedetomidine provides a
further option as a short-term (<24 hours) primary sedative in mechanically ventilated adult
patients in an intensive care setting and in nonintubated adult patients requiring procedural
sedation.
Although dexmedetomidine is only indicated
in the US for infusions of <24 hours duration,
studies have also demonstrated the efficacy of
dexmedetomidine when used for longer-term sedation in mechanically ventilated patients in the
intensive care setting.[19] Moreover, a number
Clin Drug Investig 2012; 32 (8)

Dexmedetomidine: Adis Drug Clinical Q&A

of studies have examined the use of dexmedetomidine in paediatric patients, and as an adjunct
to anaesthesia during surgery.[8]
Acknowledgements and Disclosures
This article was updated from Drugs 2011: 71 (11): 1481501,[7] and was reviewed by J.L. Ard Jr, Department of Anesthesiology, NYU Medical Center, New York, NY, US;
S. Bergese, Departments of Anesthesiology and Neurological
Surgery, The Ohio State University Medical Center, Columbus, OH, USA; V.R. Belum, Departments of Anesthesiology and Neurological Surgery, The Ohio State University
Medical Center, Columbus, OH, USA; L. Liu, Department
of Anesthesia & Perioperative Care, UC San Francisco,
San Francisco, CA, USA.
The preparation of this article was not supported by any
external funding. During the peer review process, the manufacturer of the agent under review was offered an opportunity
to comment on the articles. Changes resulting from comments
received were made by the authors on the basis of scientific
and editorial merit.

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Correspondence: Gillian M. Keating, Adis, 41 Centorian

Drive, Private Bag 65901, Mairangi Bay, North Shore 0754,
Auckland, New Zealand.
E-mail: demail@springer.com

Clin Drug Investig 2012; 32 (8)