Table of Contents  
ORIGINAL ARTICLE
Year : 2015  |  Volume : 8  |  Issue : 2  |  Page : 223-229

Percutaneous endoscopic gastrostomy under conscious sedation


Department of Anesthesia and Surgical Intensive Care, Faculty of Medicine, Tanta University, Tanta, Egypt

Date of Submission16-Sep-2014
Date of Acceptance04-May-2015
Date of Web Publication8-May-2015

Correspondence Address:
Mohamed A Lotfy
Department of Anesthesiology and Surgical Intensive Care, Faculty of Medicine, Tanta University, El Gheish St, Tanta 31257, Gharbia
Egypt
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.156693

Rights and Permissions
  Abstract 

Background
Dexmedetomidine may be appropriate for painful procedures as a conscious sedation because of its sedative and analgesic properties. Percutaneous endoscopic gastrostomy (PEG) is mildly painful and thus may need conscious sedation. Hence, in this trial we aimed to evaluate the efficacy of propofol in comparison with dexmedetomidine for conscious sedation during PEG.
Patients and methods
Forty-four patients between 40 and 60 years old were included in the study. Patients undergoing elective PEG were randomly assigned to either the dexmedetomidine group or the propofol group. All patients received fentanyl 1 μg/kg, intravenous, 10 min before the procedure. An initial loading dose of 1 μg/kg dexmedetomidine was administered intravenously over 10 min to patients in group I (n = 22) before the procedure and as a continuous infusion dose of 0.2 μg/kg/h just before the procedure started. In group II (n = 22) propofol was infused at 4 mg/kg/h for 10 min, followed by infusion of 2 mg/kg/h. The visual analog scale was used to evaluate pain intensity at 5-min intervals during PEG (15-30 min). The Observer's Assessment of Alertness/Sedation was used to evaluate the sedation degree. Hemodynamic and respiratory variables and the Observer's Assessment of Alertness/Sedation scores were regularly recorded during PEG at 5-min intervals (35 min) and to 90 min after.
Results
Forty-four patients were evaluated. In the dexmedetomidine group, visual analog scale values were significantly lower than those in the propofol group at the 20-35 min assessments (P < 0.05). During sedation, the respiratory rate was significantly lower in the dexmedetomidine group; however, SpO 2 was significantly higher than that in the propofol group (P < 0.05).
Conclusion
Dexmedetomidine provides more efficient hemodynamic stability, higher Observer's Assessment of Alertness/Sedation, higher satisfaction scores, and lower visual analog scale scores. According to our results we believe that dexmedetomidine can be safely used as a sedoanalgesic agent in PEG.

Keywords: conscious sedation, dexmedetomidine, percutaneous endoscopic gastrostomy, propofol


How to cite this article:
Lotfy MA, Ayaad MG, El-Kalla RS. Percutaneous endoscopic gastrostomy under conscious sedation. Ain-Shams J Anaesthesiol 2015;8:223-9

How to cite this URL:
Lotfy MA, Ayaad MG, El-Kalla RS. Percutaneous endoscopic gastrostomy under conscious sedation. Ain-Shams J Anaesthesiol [serial online] 2015 [cited 2021 Oct 26];8:223-9. Available from: http://www.asja.eg.net/text.asp?2015/8/2/223/156693


  Introduction Top


Percutaneous endoscopic gastrostomy (PEG) is an endoscopic procedure through the abdominal wall in which a PEG tube is passed into a patient's stomach. This procedure is an alternative to surgery and does not need general anesthesia [1] .

There are two main indications for PEG: the first is to establish enteral access for feeding and the second is for gut decompression. Patients who are incapable of moving food from the mouth to the stomach are those who commonly need PEG tube placement. This includes those with neurological disorders such as stroke, cerebral palsy, brain injury, and impaired swallowing. Also, patients suffering from trauma or cancer or have undergone recent surgery of the upper gastrointestinal or respiratory tract may require this procedure to provide nutritional intake. Gut decompression may be needed in patients who have abdominal malignancies causing gastric outlet or small bowel obstruction or ileus [2] .

Midazolam, propofol, and fentanyl are commonly used drugs for monitored anesthesia care (MAC) [3],[4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33]. The most commonly reported side effects of these drugs are respiratory complications and variability of patient response [4] . The risk for hypoxia and apnea increases when midazolam is combined with fentanyl or other opioids for MAC [3] . Addition of propofol may worsen the respiratory depression [5] . A 2006 review of closed malpractice showed that respiratory depression due to oversedation had a prominent role in patient injuries during MAC [6] . The respiratory side effects of benzodiazepines, opioids, and propofol cause the requirement of a sedative drug that can be safely used during MAC with fewer adverse effects [7] .

Dexmedetomidine, which is an α2 receptor agonist that acts centrally, can be titrated to the required level of sedation with no significant respiratory depression [8],[9] . Dexmedetomidine's site of action is the locus coeruleus; therefore, its sedation action is characterized by an easy and quick arousal, resembling natural sleep. Further, dexmedetomidine causes an analgesic-sparing effect; thus, it significantly decreases the perioperative requirements of opioids [5,10-14]. Moreover, dexmedetomidine has an antisympathetic effect, reducing the stress response to surgery, hypertension, and tachycardia [10],[13] . Because of its cooperative sedation, analgesic effect, and absence of respiratory depression, dexmedetomidine usage as a sedative for MAC is increased [15] .

Many studies have reported that dexmedetomidine is an effective leading sedative for orthopedic, ophthalmic, dental, and plastic surgery, and for diagnostic procedures [13],[14],[16],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32] .

This randomized, double-blind study was planned to compare the sedative, analgesic, hemodynamic, and respiratory effects of propofol and dexmedetomidine, combined with fentanyl, during percutaneous endoscopic gastrostomy.


  Patients and methods Top


After obtaining approval from the local ethics committee, written consent was obtained from each patient to participate in the study. This study was performed between April 2012 and January 2013 in Tanta University Hospital. Randomization was done through computer-generated random numbers, and 44 patients were randomly divided into two groups of 22 patients each to receive either dexmedetomidine (Precedex; Hospira, Lake Forest, Illinois, USA) or propofol for sedation and analgesia during surgery. To follow the double-blind nature of the study, drugs were prepared by an independent anesthesia technician and diluted to a fixed volume for every single drug used. The anesthesiologist who attended the surgery and recorded the data was also blinded to both groups assigned. Forty-four patients aged 40-60 years who were selected for elective PEG and were of ASA physical status I-III were enrolled in this study. Patients were excluded if they had received general anesthesia within 10 days before study entry, an intake of α2-agonist or antagonist within 14 days before the procedure, or an opioid within 4 h of the start of the study drug administration. Also, patients were excluded if they had any of the following: a history of drug abuse, allergy to any of the study medications, a current respiratory or psychiatric disorder, acute unstable angina, acute myocardial infarction in the past 6 weeks, heart rate (HR) less than 50 bpm, systolic blood pressure less than 90 mmHg, and Glasgow coma score (GCS) less than 15.

An intravenous catheter was inserted; baseline HR, noninvasive mean arterial blood pressure (MAP), respiratory rate (RR), and oxygen saturation (SpO 2 ) were recorded. Evaluation of pain intensity was performed on a 0-100-mm visual analog scale (VAS). The Observer's Assessment of Alertness/Sedation (OAA/S) and VAS scores were assessed by an observer blinded to the patient group. Sedation level was assessed by using the modified OAA/S scale scores: 5, awake/alert (responds to name spoken in normal tone); 4, lethargic response to name spoken in normal tone; 3, responds to name spoken loudly or repeatedly; 2, responds after mild shaking; 1, asleep/unarousable (does not respond to mild shaking) [10] .

All patients received a local anesthetic block before gastrostomy puncture provided the OAA/S score was 3 or lower.

All patients received fentanyl 1 μg/kg, intravenous, 10 min before initiation of PEG. In group 1 (dexmedetomidine group), patients received an initial dose of dexmedetomidine intravenous infusion over 10 min at 1 μg/kg/h, followed by a maintenance infusion of 0.2 μg/kg/h. In group 2 (propofol group), propofol was infused intravenously over 10 min at 4 mg/kg/h, followed by a maintenance infusion of 2 mg/kg/h.

The baseline measurements were obtained just before the start of the study drug. The OAA/S scores, and respiratory (RR and SpO 2 ) and hemodynamic (MAP and HR) variables were recorded every 5 min after the baseline measurements until termination of the PEG procedure. If sedation was inadequate (OAA/S³4), we increased infusion doses of test drugs by 50%, and if patients were oversedated (OAA/S ≤3) we decreased them by 50%. If the OAA/S score was 2 or lower, we decreased the study drug infusion rate for 2 min; after the OAA/S score returned to 3 or above, we obtained a VAS score. It is an objective question and from after that we can judge or determine the patient VAS.

The OAA/S scores as well as hemodynamic (HR-MAP) and respiratory variables (RR-SpO 2 ) were recorded postoperatively at 45, 60, and 90 min from the original baseline measurement. The VAS scores were recorded at 5-min intervals during the PEG procedure. During the procedure, if bradycardia occurred (HR <45), 0.5-mg atropine was administered; if bradypnea (RR <10) or SpO 2 92% or less occurred, 4 l/min of supplemental oxygen was administered by means of a nasal cannula; and if hypotension (MAP <50) occurred, 0.9% saline was infused. Ephedrine 5-25 mg was administered as slow intravenous push (over at least 15 min; repeated in 5-10 min if necessary).

Patients were asked to answer the question 'How would you rate your experience with the sedation (or analgesia) you have received during surgery?' using a seven-point Likert-like verbal rating scale [30] . This assessment of patient satisfaction with sedation and analgesia was performed just before recovery room discharge to minimize the effects of sedation on patients' judgment. Moreover, the surgeons were asked to rate their satisfaction with patient sedation using the same method and scale at the end of surgery.

fx1

Seven-point Likert-like verbal rating scale for assessment of patient satisfaction with intraoperative sedation/analgesia.

Our sample size was based on our primary outcome measure of improved analgesia. We defined an average difference of 15 mm on a 100-mm VAS as clinically relevant. On the basis of our experience from our previous studies, it was expected that 95% of the reported VAS scores would range between 0 and 80 mm, resulting in a mean ± SD of 47 ± 19.7 mm. A sample size of 40 patients (20 in each arm of the study) was calculated to be necessary to detect a 15-mm reduction in VAS score with a power of 80% and an a-error of 5%. It was assumed that the study dropout rate would be ~10%, and therefore a sample of 44 patients was recruited and randomly allocated to one of the two study groups.

Randomization was achieved by using sequentially numbered, opaque, sealed envelopes containing computer-generated random allocations in a ratio of 1: 1 in balanced blocks of 8.

Statistical analysis

Data were collected and statistical presentation and analysis of this study was conducted using mean, SE, paired t-test, and analysis of variance (ANOVA) by SPSS (V 1.6; SPSS Inc., Chicago, Illinois, USA). Quantitative data are presented as mean and SD and qualitative data as frequency and percentage. Statistical analyses were performed using Statistica 7.0 software (Statsoft, Tulsa, Oklahoma, USA).

Demographics were compared with the t-test. The proportions of men/women, dose increase due to inadequate sedation, nausea, and oxygen supplementation of the study groups were compared with the χ2 -test. RR, SpO 2 , MAP, HR, and VAS were compared with repeated-measures ANOVA with the post-hoc Tukey's test. OAA/S was analyzed with Friedman's nonparametric repeated-measures ANOVA with the post-hoc Tukey's test. A P value of less than or equal to 0.05 was considered significant.


  Results Top


Both groups were comparable as regards age, weight, and male-to-female ratio (P > 0.05) ([Table 1]). The start of the PEG procedure was earlier in the dexmedetomidine group compared with the propofol group (the procedure was commenced in 17 patients in the dexmedetomidine group versus 11 patients in the propofol group in the first 10 min) ([Table 1]). VAS values in the propofol group at 25-35 min were significantly higher than those in the dexmedetomidine group at 20-35 min (P < 0.05). The rest of the VAS values at 10-20 min were similar (P > 0.05) ([Table 2] and [Figure 1]).
Figure 1: Visual analog scale values obtained during sedation. Data are expressed as mean ± SD. P ≤ 0.05 versus the propofol group. prop, propofol; dex, dex medetomidine.

Click here to view
Table 1 Demographic and selected clinical data of the study groups

Click here to view
Table 2 Visual analog scale values obtained during sedation

Click here to view


Patients in the propofol group achieved an Aldrete score of 10 faster and were thus ready for discharge sooner than those in the dexmedetomidine group (P < 0.01) ([Table 1]). Median [interquartile range (IQR)] times to readiness for discharge were 21 (10-32) versus 45 (36-54) min for groups P and D, respectively (P < 0.001).

On the other hand, median (IQR) satisfaction with sedation in group D was 6 (6-7) compared with 6 (5-7) in group M (P<0.05). In contrast, patients in both groups were similarly satisfied with their analgesia [median (IQR) 7 (5-7) vs. 7 (5-7)]. Further, surgeons' satisfaction with patients' sedation was similar in both groups [median (IQR) 5 (4-6) vs. 5 (4-6)].

The OAA/S values at 5-35 min were significantly lower than those at baseline in both groups (P < 0.05). At 35 min, the OAA/S value was significantly lower in the dexmedetomidine group compared with the propofol group (P < 0.05) ([Table 3] and [Figure 2]).
Figure 2: Observer's assessment alertness/sedation (OAA/S) values at baseline and during sedation and recovery. prop, propofol.

Click here to view
Table 3 Observer's assessment alertness/sedation values at baseline and during sedation and recovery

Click here to view


In the dexmedetomidine group, SpO 2 values at baseline and during sedation and recovery were 98.0 ± 0.7, 97.0 ± 0.9, and 98.1 ± 0.4, respectively. In the propofol group, SpO 2 values at baseline and during sedation and recovery were 97.0 ± 1.4, 95.0 ± 2.7, and 98.0 ± 0.6, respectively. During sedation, SpO 2 values of the dexmedetomidine group were significantly higher than those of the propofol group (P < 0.05). Also SpO 2 values during sedation were significantly lower than those at baseline and during recovery in both group (P < 0.05).

There were no differences in MAP values between the dexmedetomidine and propofol groups (P > 0.05). The MAP values during sedation were significantly lower than those at baseline and during recovery in both groups (P < 0.05) ([Table 4]). There were no differences in HR values between the dexmedetomidine and propofol groups (P > 0.05). In the dexmedetomidine and propofol groups, HR significantly decreased during sedation and recovery, compared with baseline (P < 0.05). The HR values during sedation were significantly lower than those during recovery in the dexmedetomidine group (P < 0.05) ([Table 4] and [Figure 3]a and b).
Figure 3: MAP (A)and HR(B) at baseline and during sedation and recovery of the study groups. Data are expressed as mean ±_sd. Baseline presents baseline measurements of MAP and HR. Sedation presents the mean of minimum MAP and HR during percutaneous endoscopic

Click here to view
Table 4 Mean arterial blood pressure and heart rate at baseline and during sedation and recovery in the study
groups


Click here to view


Significantly fewer patients required rescue fentanyl for pain during the infusion period in the dexmedetomidine group compared with the propofol group [2/22 (9%) versus 5/22 (22.7%), respectively; P < 0.001 for both comparisons].

In the dexmedetomidine group, RRs at baseline and during sedation and recovery were 16 ± 1.7, 12 ± 1.1, and 16 ± 1.1, respectively. In the propofol group, RRs at baseline and during sedation and recovery were 17 ± 3.0, 15 ± 3.0, and 18 ± 2.4, respectively. During sedation, RR values of the dexmedetomidine group were significantly lower than those in the propofol group (P < 0.05). Also during sedation, RR values were significantly lower than those at baseline and during recovery in both groups (P < 0.05).

The incidence of nausea, vomiting, dry mouth, and oxygen supplementation was similar between the two groups ([Table 1]). Bradycardia, hypotension, or respiratory depression (SpO 2 <92%) resulting from deep sedation was not observed in any patient.


  Discussion Top


This study aimed to compare the effect of dexmedetomidine and propofol in combination with fentanyl as a sedative and analgesic during PEG. Dexmedetomidine with fentanyl intravenously provided effective and safe analgesia. Dexmedetomidine and propofol were comparable as regards sedation, MAP, HR, satisfaction scores, and overall pain experience.

In this study, it was observed that patients in the dexmedetomidine group had slower RR, higher SpO 2 , and lower VAS. Our result suggested that dexmedetomidine in combination with fentanyl may offer more benefits compared with propofol as a sedative drug during PEG.

We found that dexmedetomidine provided better analgesic effects than propofol; this was in agreement with the results of both laboratory and human studies [20],[21] . Jalowiecki et al. [22] studied the analgesic and sedative effects of dexmedetomidine in outpatient colonoscopy. They found that the use of dexmedetomidine for colonoscopy is limited by its side effects, insufficient pain relief, pronounced hemodynamic instability, and a complicated administration regimen. Our study differed in adding fentanyl 1 μg/kg, intravenous, in both the dexmedetomidine and propofol groups to improve the analgesic effects of the studied drugs. Adding this low dose of fentanyl to the studied drugs provides good relief from pain during PEG.

At the same sedative doses, dexmedetomidine and propofol provided an equally mild decrease in MAP. However, no treatment was required in either group for this reduction in MAP. In this study, the frequent cardiovascular adverse effect seen before with the initial loading infusion of dexmedetomidine and propofol was not observed [23],[24] .

The respiratory effect of dexmedetomidine is controversial. Belleville et al. [25] reported a significant reduction in RR, whereas Hsu et al. [26] reported a significant rise in RR with dexmedetomidine. This discrepancy may be caused by the physiologic reactions of the arousal phenomenon (movements, and hemodynamic and respiratory changes induced by noxious stimuli). Also it could have been produced by the use of boluses in the study by Belleville et al. [25] , whereas Hsu et al. [26] used infusions resulting in constant and elevated dexmedetomidine concentrations. In our study, SpO 2 values did not decrease because of the initial infusion dose given over a much longer time (10 min).

Similar to Hsu et al. [26] , Ebert et al. [31] showed a significant increase in RR using similar dexmedetomidine infusion doses.

When propofol is administered in sedative doses, it produces negligible depressant effects on minute ventilation and tidal volume, with unchanged arterial blood gas and end-tidal CO 2 tension values [27] . However, when administered in larger doses, it can cause depression of the hypoxic ventilatory response [28] and more frequent and longer apnea than produced by barbiturates [29] . In our study, dexmedetomidine causes more reduction in RR compared with propofol.

However, in the dexmedetomidine group, the decrease in SpO 2 was less than that with propofol. This may be due to the effect on tidal volume: in the dexmedetomidine group, tidal volume probably remained unaffected or increased, although RR decreased, whereas in the propofol group tidal volume probably decreased, whereas RR did not change. Because fentanyl was added to the management of all patients in this study, its effect should also be taken into consideration to impact respiratory function. Moreover, the balance between pain and the effects of the administered sedatives/opioid may widely influence the effects of sedative drugs on respiratory depression. Many previous studies performed in mechanically ventilated patients comparing propofol with dexmedetomidine did not evaluate the effect of these drugs on RR [10],[11] . We found that, during this procedure, the respiratory depressant effect of dexmedetomidine was less notable compared with that observed with propofol.

The most suitable drug for PEG to achieve patient comfort should offer sufficient analgesia, enough sedation, rapid recovery, and minimal side effects. Alhashemi and Kaki [30] found that dexmedetomidine is an effective and safe drug for sedation during extracorporeal shock wave lithotripsy (ESWL). Our study is different from theirs, which evaluated only the effect of dexmedetomidine, whereas our study compared the effects of dexmedetomidine with those of propofol, the most commonly used intravenous sedative during PEG. Our study showed that equivalent sedation can be achieved with both propofol and dexmedetomidine during PEG.

An important finding in this study was the delayed readiness for recovery room discharge among patients in group dexmedetomidine. The importance of this observation is the cost implications of longer stay in the recovery room. This investigation, however, was not designed to address this issue. Another limitation is the method used for determining expired CO 2 and the inherent limitation of examining end-tidal CO 2 without establishing the gradient that normally exists between end-tidal and arterial CO 2 .

However, obtaining arterial blood gases to establish the end-tidal arterial CO 2 gradient could not be justified given that expired CO 2 was not the primary outcome variable in this study. In addition, the obtained CO 2 measurements lacked precision because of the inflow of oxygen through the nasal cannula. Another potential point of criticism in this study is the use of the OAA/S scale (OAA/S scores) as an endpoint for administering study drugs as opposed to the bispectral index. This was done because bispectral index is not a standard monitor during MAC and is not readily available in our hospital.

In conclusion, infusion of dexmedetomidine and propofol offers safe and adequate sedation, analgesia, and patient comfort during PEG. However, analgesic and respiratory variables (RR, tidal volume (Vt), and SpO 2 ) were better with dexmedetomidine than with propofol. Consequently, dexmedetomidine with a small dose of fentanyl can be useful during PEG and it may be a valuable substitute to propofol.

 
  References Top

1.
Current Opinion in Anesthesiology. 2011; 24:644-648.  Back to cited text no. 1
    
2.
Percutaneous Endoscopic Gastrostomy (PEG) Tube Placement Author: GauravArora, MS, MBBS; Chief Editor: Danny A Sherwinter, MD, Updated: May 9, 2011.  Back to cited text no. 2
    
3.
Bailey PL, Pace NL, Ashburn MA, Moll JW, East KA, Stanley TH. Frequent hypoxemia and apnea after sedation with midazolam and fentanyl. Anesthesiology 1990; 73:826-830.  Back to cited text no. 3
    
4.
ASA Task Force on Sedation and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology 2002; 96:1004-1017.  Back to cited text no. 4
    
5.
Herr DL, Sum-Ping ST, England M. ICU sedation after coronary artery bypass graft surgery: dexmedetomidine-based versus propofol-based sedation regimens. J Cardiothorac Vasc Anesth 2003; 17:576-584.  Back to cited text no. 5
    
6.
Bhananker SM, Posner KL, Cheney FW, Caplan RA, Lee LA, Domino KB. Injury and liability associated with monitored anesthesia care: a closed claims analysis. Anesthesiology 2006; 104:228-234.  Back to cited text no. 6
    
7.
Candiotti KA, Bergese SD, Bokesch PM, Feldman MA, Wisemandle W, Bekker AY. MAC Study Group. Monitored anesthesia care with dexmedetomidine: a prospective, randomized, double-blind, multicenter trial. Anesth Analg 2010; 110:47-56.  Back to cited text no. 7
    
8.
Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ. Sedative, amnestic, and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg 2000; 90:699-705.  Back to cited text no. 8
    
9.
Venn RM, Hell J, Grounds RM. Respiratory effects of dexmedetomidine in the surgical patient requiring intensive care. Crit Care 2000; 4:302-308.  Back to cited text no. 9
    
10.
Arain SR, Ebert TJ. The efficacy, side effects, and recovery characteristics of dexmedetomidine versus propofol when used for intraoperative sedation. Anesth Analg 2002; 95:461-466.  Back to cited text no. 10
    
11.
Venn RM, Grounds RM. Comparison between dexmedetomidine and propofol for sedation in the intensive care unit: patient and clinician perceptions. Br J Anaesth 2001; 87:684-690.  Back to cited text no. 11
    
12.
Elbaradie S, El Mahalawy FH, Solyman AH. Dexmedetomidine vs. propofol for short-term sedation of postoperative mechanically ventilated patients. J Egypt Natl Canc Inst 2004; 16:153-158.  Back to cited text no. 12
    
13.
Abdalla MIM, Mansouri FA, Bener A. Dexmedetomidine during local anesthesia. J Anesth 2006; 20:54-56.  Back to cited text no. 13
    
14.
Taghinia AH, Shapiro FE, Slavin SA. Dexmedetomidine in aesthetic facial surgery: improving anesthetic safety and efficacy. Plast Reconstr Surg 2008; 121:269-276.  Back to cited text no. 14
    
15.
Amornyotin S. Sedation and monitoring for gastrointestinal endoscopy. World J Gastrointest Endosc 2013; 5:47-55.  Back to cited text no. 15
    
16.
Demiraran Y, Korkut E, Tamer A, Yorulmaz I, Kocaman B, Sezen G, Akcan Y. The comparison of dexmedetomidine and midazolam used for sedation of patients during upper endoscopy: a prospective, randomized study. Can J Gastroenterol 2007; 21:25-29.  Back to cited text no. 16
    
17.
Alhashemi JA. Dexmedetomidine vs midazolam for monitored anaesthesia care during cataract surgery. Br J Anaesth 2006; 96:722-726.  Back to cited text no. 17
    
18.
Ustün Y, Gündü ZM, Erdoðan O, Benlidayi ME. Dexmedetomidine versus midazolam in outpatient third molar surgery. J Oral Maxillofac Surg 2006; 64:1353-1358.  Back to cited text no. 18
    
19.
Cooper L, Candiotti K, Gallagher C. Dexmedetomidine provides adequate sedation and homodynamic control for awake, diagnostic transesophageal echocardiography. Anesth Analg 2007; 104:S41.  Back to cited text no. 19
    
20.
Kayser V, Desmeules J, Guilbaud G. Systemic clonidine differentially modulates the abnormal reactions to mechanical and thermal stimuli in rats with peripheral mononeuropathy. Pain 1995; 60:275-285.  Back to cited text no. 20
    
21.
Jaakola ML, Salonen M, Lehtinen R, Scheinin H. The analgesic action of dexmedetomidine - a novel alpha 2-adrenoceptor agonist - in healthy volunteers. Pain 1991; 46:281-285.  Back to cited text no. 21
    
22.
Jalowiecki P, Rudner R, Gonciarz M, Kawecki P, Petelenz M, Dziurdzik P. Sole use of dexmedetomidine has limited utility for conscious sedation during outpatient colonoscopy. Anesthesiology 2005; 103:269-273.  Back to cited text no. 22
    
23.
McMurray TJ, Collier PS, Carson IW, Lyons SM, Elliott P. Propofol sedation after open heart surgery. A clinical and pharmacokinetic study. Anaesthesia 1990; 45:322-326.  Back to cited text no. 23
    
24.
Venn RM, Bradshaw CJ, Spencer R, Brealey D, Caudwell E, Naughton C, et al. Preliminary UK experience of dexmedetomidine, a novel agent for postoperative sedation in the intensive care unit. Anaesthesia 1999; 54:1136-1142.  Back to cited text no. 24
    
25.
Belleville JP, Ward DS, Bloor BC, Maze M. Effects of intravenous dexmedetomidine in humans. I. Sedation, ventilation, and metabolic rate. Anesthesiology 1992; 77:1125-1133.  Back to cited text no. 25
    
26.
Hsu YW, Cortinez LI, Robertson KM, Keifer JC, Sum-Ping ST, Moretti EW, et al. Dexmedetomidine pharmacodynamics: part I: crossover comparison of the respiratory effects of dexmedetomidine and remifentanil in healthy volunteers. Anesthesiology 2004; 101:1066-1076.  Back to cited text no. 26
    
27.
Rosa G, Conti G, Orsi P, D'Alessandro F, La Rosa I, Di Giugno G, Gasparetto A. Effects of low-dose propofol administration on central respiratory drive, gas exchanges and respiratory pattern. Acta Anaesthesiol Scand 1992; 36:128-131.  Back to cited text no. 27
    
28.
Blouin RT, Seifert HA, Babenco HD, Conard PF, Gross JB. Propofol depresses the hypoxic ventilatory response during conscious sedation and isohypercapnia. Anesthesiology 1993; 79:1177-1182.  Back to cited text no. 28
    
29.
Candela Toha AM, Benatar Hasserfaty J, Ascorve Domínguez A. Induction and maintenance of anesthesia with propofol and with thiopental-isoflurane. Comparative study. Rev Esp Anestesiol Reanim 1991; 38:218-221.  Back to cited text no. 29
    
30.
Alhashemi JA, Kaki AM. Dexmedetomidine in combination with morphine PCA provides superior analgesia for shockwave lithotripsy. Can J Anaesth 2004; 51:342-347.  Back to cited text no. 30
    
31.
Ebert TJ, Hall JE, Barney JA, Uhrich TD, Colinco MD. The effects of increasing plasma concentrations of dexmedetomidine in humans. Anesthesiology 2000; 93:382-394.  Back to cited text no. 31
    
32.
Tetzlaff JE, Vargo JJ, Maurer W. Nonoperating room anesthesia for the gastrointestinal endoscopy suite. Anesthesiol Clin 2014; 32:387-394.  Back to cited text no. 32
    
33.
Fagin A, Palmieri T, Greenhalgh D, Sen S. A comparison of dexmedetomidine and midazolam for sedation in severe pediatric burn injury. J Burn Care Res 2012; 33:759-763.  Back to cited text no. 33
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
   Abstract
  Introduction
  Patients and methods
  Results
  Discussion
   References
   Article Figures
   Article Tables

 Article Access Statistics
    Viewed1922    
    Printed71    
    Emailed3    
    PDF Downloaded151    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]