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The potential uses of dexmedetomidine (DEX), a highly selective α2 - adrenoceptor agonist are very diverse. DEX appears to mimic many of the actions of mythical ′ideal′ sedative/analgesic agent. Although not orally active, DEX shows good bioavailability when administered via various other routes like intranasal, buccal, IM than intra-venous. DEX ha...
Citations
... Dexmedetomidine is an alpha-2 agonist that is increasingly used off-label as part of an opioid minimisation strategy during general anaesthesia. [1][2][3] This drug was first approved by the US Food and Drug Administration in 1999 as a sedative medication for critically ill patients. 4 5 In the perioperative setting, however, clinical guidelines to inform ...
Introduction
Dexmedetomidine is a promising pharmaceutical strategy to minimise opioid use during surgery. Despite its growing use, it is uncertain whether dexmedetomidine can improve patient-centred outcomes such as quality of recovery and pain.
Methods and analysis
We will conduct a systematic review and meta-analysis following the recommendations of the Cochrane Handbook for Systematic Reviews. We will search MEDLINE, Embase, CENTRAL, Web of Science and CINAHL approximately in October 2023. We will include randomised controlled trials evaluating the impact of systemic intraoperative dexmedetomidine on patient-centred outcomes. Patient-centred outcome definition will be based on the consensus definition established by the Standardised Endpoints in Perioperative Medicine initiative (StEP-COMPAC). Our primary outcome will be the quality of recovery after surgery. Our secondary outcomes will be patient well-being, function, health-related quality of life, life impact, multidimensional assessment of postoperative acute pain, chronic pain, persistent postoperative opioid use, opioid-related adverse events, hospital length of stay and adverse events. Two reviewers will independently screen and identify trials and extract data. We will evaluate the risk of bias of trials using the Cochrane Risk of Bias Tool (RoB 2.0). We will synthesise data using a random effects Bayesian model framework, estimating the probability of achieving a benefit and its clinical significance. We will assess statistical heterogeneity with the tau-squared and explore sources of heterogeneity with meta-regression. We have involved patient partners, clinicians, methodologists, and key partner organisations in the development of this protocol, and we plan to continue this collaboration throughout all phases of this systematic review.
Ethics and dissemination
Our systematic review does not require research ethics approval. It will help inform current clinical practice guidelines and guide development of future randomised controlled trials. The results will be disseminated in open-access peer-reviewed journals, presented at conferences and shared among collaborators and networks.
PROSPERO registration number
CRD42023439896.
... The addition of Opioids to local anesthetics has its own disadvantages like, pruritus and respiratory depression. 1 Dexmedetomidine, an Alpha-2 Adrenoreceptor agonist, acts on the spinal cord and has been used as an effective adjuvant to Ropivacaine for regional and central neuraxial blocks. 2 Different local anesthetics are used for epidural anaesthesia, most popular in India being Lidocaine and Bupivacaine. The drawback of lidocaine is its intermediate duration of action and the drawback of bupivacaine though long acting, is increased incidence of fatal cardiac toxicity after accidental intravascular injection, because of narrow cardiovascular collapse/central nervous system toxicity (cc/cms). ...
Background: The regional anaesthesia has lot of benefits compared to general anaesthesia for lower abdominaland lower limb surgeries. Epidural anaesthesia is an ideal anesthetic technique for lower abdominal and lowerlimb surgeries. The additives are used with Anesthetics for Early onset of action, To prolong the duration ofaction, Analgesia and Improving the quality of block.Aims and Objectives: The aim of this study was to study the clinical efficacy of Dexmedetomidine versus Fentanylas an additive to Ropivacaine for lumbar epidural anaesthesia and post-operative analgesia.Materials and Methods: This study is a prospective randomised controlled study involving 90 patientsundergoing infraumbilical and lower limb surgeries who will be divided randomly into three groups Group R(n = 30): received 18 ml of 0.5% ropivacaine for epidural anaesthesia and 10 ml of 0.2% ropivacaine boluses forpostoperative analgesia; Group RF (n = 30): received 18 ml of 0.5% ropivacaine with 25μg fentanyl for epiduralanaesthesia and 10 ml of 0.2% ropivacaine with 10 μg fentanyl boluses for postoperative analgesia; and Group RD(n = 30): received 18 ml of 0.5% ropivacaine with 25 μg dexmedetomidine for epidural anaesthesia and 10 ml of0.2% ropivacaine with 5 μg dexmedetomidine boluses for postoperative analgesia.Results: Addition of additives have enhanced the onset of action, prolong duration of analgesia. Quality andduration of epidural anaesthesia provided by ropivacaine with dexmedetomidine is more effective than fentanyl.Better efficacy of analgesia evidenced with Dexmedetomidine than with Fentanyl.Conclusion: It can be concluded that RD (Ropivacaine and Dexmedetomidine) when given epidurally can be asafe and effective combination for epidural blockade in lower abdominal and lower limb surgeries.
... Such a decrease in pressures can be attributed to dexmedetomidine's highly selective α 2 agonistic action which causes a decrease in serum norepinephrine concentration thus leading to dose-dependent decrease in arterial blood pressure. [13][14][15] In agreement with our study results Sebastian B and coauthors [16] also showed a significant attenuation of hemodynamic stress response to laryngoscopy and intubation (0.001) with 0.75 µg/kg IV dexmedetomidine. ...
Background and aims:
Catheter-related bladder discomfort (CRBD) causes significant distress to the patient and requires great attention to analgesia and increases morbidity in the postoperative period. This study evaluated the efficacy of intramuscular dexmedetomidine in alleviating CRBD following percutaneous nephrolithotomy (PCNL) and postoperative inflammatory response.
Material and methods:
A prospective randomized double-blind study was conducted in a tertiary care hospital from December 2019- March 2020. Sixty seven of ASA I and II patients scheduled for elective PCNL were randomized and group I received 1 μg/kg dexmedetomidine intramuscularly and group II normal saline as control 30 minutes before induction of anesthesia. Standard anesthesia protocol was followed and patients were catheterized with 16 Fr Foleys after induction of anesthesia. Rescue analgesia was paracetamol if the score was moderate. Postoperatively CRBD score and inflammatory markers; total white cell count, erythrocyte sedimentation rate and temperature were noted for 3 days.
Results:
There was a significant low CRBD score in group I. Ramsay sedation score was 2 in group I with p 0.00 and rescue analgesia required was very low with p 0.00. Statistical Package for social Sciences software version 20 was used for analysis. Student ttest, analysis of variance, and Chisquare test were applied for quantitative and qualitative analysis respectively.
Conclusion:
Single dose intramuscular dexmedetomidine is effective, simple and safe in preventing the CRBD and the inflammatory response remained uninfluenced except ESR, the reason remains largely unknown.
... Atipamizole is the reversal drug for dexmedetomidine; it acts by increasing the central turnover of noradrenaline. Many studies have used intravenous dexmedetomidine to reduce the hemodynamic response to intubation; however, it has been found to cause hypotension and bradycardia [17]. Alternative routes for dexmedetomidine delivery are being investigated to avoid this. ...
Background and aim:
A variety of medications have been studied to reduce the hemodynamic response to laryngoscopy and intubation. Dexmedetomidine has been used intravenously in many studies to reduce the hemodynamic response to laryngoscopy and intubation. In high-risk patients, this pressor response can increase morbidity and mortality. As dexmedetomidine has a good bioavailability via the nebulisation route, we formulated this study to evaluate the effect of nebulised dexmedetomidine on the hemodynamic response to laryngoscopy and endotracheal intubation.
Methods:
This is a prospective, randomised controlled trial conducted on 100 patients with the American Society of Anesthesiologists grade I and II. The primary objective of the study was to see if nebulised dexmedetomidine at a dose of 1 microgram/kg could reduce the stress reaction to laryngoscopy and intubation. The secondary objective was to study the dose sparing effect of nebulised dexmedetomidine on the amount of propofol used during induction of general anaesthesia. The study population was randomly divided into two groups: group A (n = 50) included patients nebulised with dexmedetomidine 1 microgram/kg and group B (n = 50) included patients nebulised with 5 ml saline 30 minutes before induction of anaesthesia in a sitting position.
Results:
The demographics were similar in both groups. Following laryngoscopy and intubation, the systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and heart rate showed a significant increase in the control group B as compared to the treatment group A. In group A, there was attenuation in SBP (one minute = 113.2 ± 14.503, P < 0.001; five minutes = 109.86 ± 8.342, P < 0.001; 10 minutes = 114.24 ± 7.797, P = 0.010), DBP (one minute = 73.72 ± 10.986, P = 0.011; five minutes = 71.62 ± 9.934, P = 0.005; 10 minutes = 76.1 ± 8.006, P = 0.009), MAP (one minute = 86.80 ± 11.86, P = 0.001; five minutes = 84.44 ± 8.97, P = 0.006; 10 minutes = 88.72 ± 7.44, P = 0.018), and heart rate (one minute = 83.34 ± 12.325, P = 0.001; five minutes = 81.56 ± 13.33, P = 0.003; 10 minutes = 80.16 ± 14.086, P = 0.013) following laryngoscopy and intubation. Induction dose of propofol was significantly lower in the dexmedetomidine group (73 ± 19.509, P < 0.001).
Conclusion:
Nebulised dexmedetomidine effectively blunts the hemodynamic response to laryngoscopy and intubation and also has a dose sparing effect on the induction dose of propofol.
... efforts are made since long to control the pressor response to laryngoscopy through pharmacological methods. It has been shown that a selective α-2 adrenoreceptor agonist, the drug dexmedetomidine, a d-isomer of medetomidine imidazole, [5] decreases the levels of catecholamines in the perioperative period because the postsynaptic activation of α-2 receptors in the central nervous system decreases the sympathetic activity [6] and thus a favorable hemodynamic stability is obtained. [7] Aim and objectives ...
... [8] This evokes noxious stress responses and causes disturbance in hemodynamic parameters like tachycardia, hypertension, change in heart rhythm and evokes coughing, bronchospasm, raised intraocular, intracranial pressure and thus hazardous consequences in vulnerable patients [9] Dexmedetomidine, an alpha-2 adrenergic agonist possesses properties of sympatholysis, titratable sedation without respiratory depression, analgesia, benefit of reduced dosage of opioids. [10] It is a small molecule possessing an imidazole ring with distribution half-life of 6-8 minutes on intravenous administration [11,12] it possesses eight times more affinity for alpha-2 adrenoceptors as compared to clonidine, Hence a preferred agent as a full alpha-2 adrenoceptor agonist. [13] Activation of these presynaptic alpha 2 receptors inhibits release of norepinephrine and terminates transmission of noxious stimuli. ...
Background: Tracheal extubation causes autonomic nervous system disturbances which causes tachycardia, hypertension which are harmful in susceptible patients.so we conducted a study between iv Dexmedetomidine and iv Labetalol to assess their effectiveness in decreasing haemodynamic disturbances during extubation. Materials and Methods:we included 100 participants of age of 18-55 yrs with ASA grading I & II and divided them into 2 groups. Group D was given injection Dexmedetomidine 0.6mcg/kg iv and Group L was given injection Labetalol 0.25mg/kg body weight. We recorded Heart rate, systolic and diastolic blood pressure at baseline, 2,5,8 minutes post drug injection, at extubation and 1,3,5,8,10 and 15 minutes after extubation. Results: Group D had better decreased heart rate, systolic and diastolic blood pressure at the time of extubation, and also 15 minutes post extubation in comparison to Group L. Conclusion: Injection Dexmedetomidine 0.6µg/kg has showed a better attenuating effect on sympathoadrenal system during extubation than injection Labetalol 0.25mg/kg Keywords: Dexmedetomidine, labetalol, extubation,hemodynamics.
... Such a decrease in MAP can be attributed to dexmedetomidine's highly selective α 2 agonistic action that causes a decrease in serum norepinephrine concentration thus leading to a dose-dependent decrease in arterial blood pressure. [4,9] A literature review in this regard revealed three randomised controlled trials (RCTs) where there was a remarkable decline in SBP with intranasal dexmedetomidine administration. [10][11][12] However, all these RCTs entailed the use of dexmedetomidine for sedation in the paediatric population. ...
The process of laryngoscopy and endotracheal intubation is associated
with intense sympathetic activity, which may precipitate intra‑operative complications. Taking
the advantage of dexmedetomidine’s good bioavailability and rapid absorption through nasal
mucosa; we contemplated this study to evaluate the effects of nebulised dexmedetomidine as a
premedication in blunting the haemodynamic response to laryngoscopy and tracheal intubation.
Methods: This prospective, randomised, comparative study was conducted in 100 American
Society of Anesthesiologists (ASA) I, II patients. The primary outcome was to evaluate the effects
of dexmedetomidine nebulisation in blunting the stress response to laryngoscopy and intubation.
The secondary outcome was to study its adverse effects. The study population was divided
randomly into two groups. Control group C (n = 50) received nebulisation with 5 ml of normal
saline and group D (n = 50) received 1 μg/kg dexmedetomidine 5 ml 10 min before induction in
sitting position. Results: Demographics were comparable. Following laryngoscopy and intubation,
systolic (SBP), diastolic (DBP) and mean arterial pressure (MAP), response entropy (RE) and state
entropy (SE) were markedly increased in the control group whereas in group D there was a fall in
SBP (at 1 min‑126.64 ± 26.37; P 0.01, 5 min‑109.50 ± 16.83; P 0.02, 10 min‑106.94 ± 17.01; P 0.03),
DBP (at 1 min‑83.18 ± 17.89; P 0.001, 5 min‑66.40 ± 13.88; P 0.001, 10 min‑ 62.56 ± 14.91; P 0.01)
and MAP (at 1 min‑99.68 ± 19.22; P 0.001, 5 min‑ 84.08 ± 13.66; P 0.003, 10 min‑ 81.74 ± 14.79;
P 0.008), RE and SE which was statistically significant (P 0.002). There was a dose sparing effect
of propofol in group D; sedation score was comparable. Conclusion: Nebulised dexmedetomidine
effectively blunts the stress response to laryngoscopy and intubation with no adverse effects.
... Furthermore, dexmedetomidine (1 µg/kg) has been associated with the increased incidence of adverse effects like bradycardia and hypotension observed by Kartik et al 12 and Menda et al 13 . It has been established that the activation of post-synaptic á-2 receptors in CNS brings the decreased sympathetic activity which can lead to bradycardia as well as hypotension 14 . Furthermore dexmedetomidine (1 ìg/kg) is associated with increased incidence of adverse effects 13 . ...
Background: Laryngoscopic manipulation and endotracheal intubation are always a matter of concernwhich capable of producing tachycardia, arrhythmias and hypertension which is generally well tolerated inhealthy patient. In Hypertensive patient cardiovascular response to laryngoscopy and intubation is exaggerated. Aims: To assess the effectiveness in attenuation of haemodynamic responses to laryngoscopy andendotracheal intubation with different doses of intravenous dexmedetomidine in controlled hypertensivepatients with no adverse effects. Methods: This prospective Randomized controlled trial was carried out with 60 patients belonging toAmerican Society of Anesthesiologists (ASA) Physical Status II posted for elective general anaesthesia.Patients were randomly divided into three groups with fixed card sampling, where, patients who receivedIV dexmedetomidine 0.5 μg/kg diluted to 50 ml with normal saline as infusion over 10 min was consideredas group A, patients who received IV dexmedetomidine 0.75 μg/kg diluted to 50 ml with normal salinewas considered as group B and patients who received IV dexmedetomidine 1 μg/kg diluted to 50 ml withnormal saline was considered as group C. The primary outcome measures were haemodynamic responseat 1, 3 and 5 min after intubation. The secondary outcome measures were to note down any adverseeffects associated with drugs. Result: The groups were well matched for their demographic data . Male to female ratio was 1:1 in allthree group. The mean height, weight and BMI were almost similar among three groups. In this studybaseline readings of SBP, DBP, MAP and HR were almost similar in all three groups and statistically notsignificant. Maximum intubation response was seen at 1 min post intubation in all the three groups. Themean SBP of group A varied from 144.8±8.4 mmHg to 118.5±4.4 mmHg that of group B varied from134.8±4.1 to 122.0±4.2 mmHg and then group C varied from 126.5±15.5 mmHg to 103.8±8.4 mmHgduring different evaluation period (p<0.05). The mean DBP of group A varied from 91.8±7.6 mmHg to72.4±5.8 mmHg that of group B varied from 81.3±5.2 to 70.3±2.5 mmHg and then group C varied from80.9±6.7 mmHg to 63.4±2.4 mmHg during different evaluation period (p<0.05). The mean MAP of groupA varied from 109.0±5.6 mmHg to 87.5±4.4 mmHg that of group B varied from 98.7±2.5 to 86.3±3.4mmHg and then group C varied from 95.5±9.2 mmHg to 76.5±3.4 mmHg during different evaluationperiod (p<0.05). The mean heart rate of group A varied from 94.5±12.7 bpm to 75.2±10.5 bpm that ofgroup B varied from 87.3±8.3 to 75.0±6.6 bpm and then group C varied from 81.1±7.2 bpm to 66.2±8.1bpm during different evaluation period (p<0.05). Conclusion: Dexmedetomidine in doses of 0.75 μg/kg was more effective compared to 0.05 μg/kg and1μg/kg in attenuating haemodynamic response to laryngoscopy and endotracheal intubation withoutproducing adverse effects in control hypertensive patients. JBSA 2020; 33(2): 69-77
... 9 The chemical structure of dexmedetomidine contains a small molecule with an imidazole ring. 10 Since Dexmedetomidine exhibits eight times more affinity towards alpha-2 adrenoceptors compared to clonidine, it is often considered as a full alpha-2 adrenoceptor agonist. 11 On intravenous administration, the distribution half-life is 6-8 minutes. ...
Tracheal extubation evokes various degrees of disturbances in the autonomic nervous system in the form of tachycardia, hypertension which can cause deleterious consequences in susceptible patients.
Hence this study was conducted between iv Dexmedetomidine and iv Labetalol to compare their effectiveness in the suppression of haemodynamic response to tracheal extubation.
60 participants aged between 18-55 yrs belonging to ASA 1 or 2 were randomly allocated into 2 groups. Group Dd received injection Dexmedetomidine 0.6mcg/kg iv and Group Ll received injection Labetalol 0.25mg/kg body weight. Heart rate, systolic and diastolic blood pressure were recorded at baseline, 2,5,8 minutes after drug infusion, at extubation and 1,3,5,8,10 and 15 minutes post extubation.
Group Dd showed a better decrease in heart rate, systolic and diastolic blood pressure at extubation, and 15 minutes post extubation compared to Group Ll.
Injection Dexmedetomidine 0.6µg/kg showed a better attenuation of sympathoadrenal response to extubation compared to injection Labetalol 0.25mg/kg.
... IV dexmedetomidine produces analgesic effects at both spinal and supraspinal levels primarily from inhibition of locus ceruleus at the brain stem and may cause inhibition of nociceptive impulse transmission by increased activation of alpha-2 receptors at the spinal cord. [11] In our study, we noted prolongation in the duration of motor block and time for 2 segment regression with a dose of dexmedetomidine which was similar to Harsoor et al. [5] Our results are similar to the study done by Kumari et al., although the bolus of dexmedetomidine used by them was higher at 1 mcg/kg followed by infusion of 0.6 mcg/kg/h. [12] Additionally, both the above mentioned studies observed faster onset of sensorimotor block and prolonged duration of analgesia. ...
Background and Aims: Our aim was to study the effects of a low-dose bolus (0.5 mcg/kg) of dexmedetomidine followed by two different infusion doses (0.25, 0.5 mcg/kg/h) on spinal anesthesia, sedation, hemodynamics and side effects.
Material and Methods: Eighty consenting patients were randomized into two groups A and B with 40 patients each. Patients in both groups were administered intravenous (IV) dexmedetomidine 0.5 mcg/kg over 10 min prior to SAB followed by IV dexmedetomidine 0.25 mcg/kg/h infusion (A) and 0.5 mcg/kg/h infusion (B) throughout the duration of surgery. Time for onset of sensory and motor block, duration of motor block and analgesia, time for two segment regression, intra operative hemodynamics and sedation were assessed. P value less than 0.05 was taken as significant.
Results: Onset of sensory block to T10 was 2.1 ± 0.3 min in group A and group B. Onset of motor block was 4.6 ± 0.9 min in group A and 4.3 ± 0.9 min in group B. Duration of motor block in group A was 235.6 ± 12.4 min compared to group B which was 245.3 ± 9.3 min. Time for 2 segment regression in group A was 139.7 ± 29.7 min compared to group B which was 152.3 ± 18.7 min. Total duration of analgesia was 259.3 ± 92.4 min in group A and 273.8 ± 52.3 min in group B. There was a significant reduction in heart rate and mean blood pressure compared to the baseline within both the groups. Sedation was comparable in both the groups.
Conclusion: IV dexmedetomidine bolus of 0.5 mcg/kg prior to subarachnoid block followed by maintenance infusion of 0.5 mcg/kg/h significantly prolonged duration of motor block, time for two segment regression, along with stable hemodynamics and adequate sedation.
