Oral Clonidine Premedication Research Articles

ORAL TRANSMUCOSAL CLONIDINE PREMEDICATION REDUCES THE AWAKING CONCENTRATION (MAC-awake) OF SEVOFLURANE IN CHILDREN

S351 INTRODUCTION: Sevoflurane is a useful anesthetic for mask induction in children because of its low blood solubility and relative pleasant smell. Clonidine has sedative and anxiolytic properties and reduces the requirement for inhalation agents. Since the awaking concentration (MAC-awake) of sevoflurane in children has never been reported, we examined it. METHODS: Sixty-three patients, aged 2 to 10 yr, were randomly assigned one of three groups. They received no premedication (control, 2 [micro sign]g/kg (OTC-2 group) and 4 [micro sign]g/kg (OTC-4 group) of oral transmucosal clonidine OTC which made of the drug and candy matrix, respectively. Induction and maintenance of general anesthesia were obtained sevoflurane in oxygen. After the completion of surgery, end-tidal concentration of sevoflurane was decreased from 1.0%. Sevoflurane concentration was kept for 15 min and an investigator called the patient's name. If the patient failed to open his eyes, the end-tidal concentration was dfecreased by 0.2%, and the above process was repeated until the patient responded to call name. The concentration midway between the value permitting the response and that just preventing the response was defined as awaking concentration. RESULTS: There was no difference in patient's age, weight and height between the three groups (Table 1). The MAC-awake of sevoflurane were 0.78 +/- 0.02% (Mean +/- SE), 0.36 +/- 0.02% and 0.36 +/- 0.04% in control, OTC-2 and OTC-4 group, respectively. The MAC-awake values in OTC-2 and OTC-4 group were significantly less than control group, whereas no significant difference was seen in these variables between the OTC-2 and OTC-4 groups (Figure 1).Table 1: Demographic DataFigure 1: Awaking concentration of SevofluraneDISCUSSION: Oral transmucosal clonidine premedication with 2 [micro sign]g/kg and 4 [micro sign]g/kg reduced the MAC-awake of sevoflurane the same degree. Although this reason was not clear from this study, a ceiling effect of clonidine on the MAC-awake of sevoflurane was suspected.

The Effects of Pressor Response upon Intravenous Ephedrine Following Oral Clonidine Premedication in Anesthetized Patients

The Effects of Pressor Response upon Intravenous Ephedrine Following Oral Clonidine Premedication in Anesthetized Patients

The Effect of Oral Clonidine Premedication on Changes in Respiratory System Mechanics by Tracheal Intubation

The Effect of Oral Clonidine Premedication on Changes in Respiratory System Mechanics by Tracheal Intubation

Oral Clonidine Premedication Enhances the Pressor Response to Ephedrine During Spinal Anesthesia

Clonidine premedication enhances the pressor effects of ephedrine in awake and anesthetized patients.To test the hypothesis that clonidine augments the pressor response to ephedrine during spinal anesthesia, 48 ASA physical status I or II patients were randomly assigned to either the clonidine group (n = 23), receiving oral clonidine approximately 5 [micro sign]g/kg 90 min before spinal anesthesia, or the control group (n = 25), receiving no clonidine. Spinal anesthesia was performed at either the L2-3 or the L3-4 interspace using 0.5% hyperbaric tetracaine solution 1.4-3.0 mL. Blood pressure (BP), heart rate, and the upper dermatomal level of analgesia were determined at 1-min intervals with the patient in the supine position after tetracaine injections. When systolic BP decreased to <80% of the prespinal value or <100 mm Hg, IV ephedrine 0.2 mg/kg was administered as a bolus. There were no differences in the duration until the first dose of ephedrine after tetracaine injections, and the upper level of analgesia between groups (control group 8.5 +/- 3.7 min, T5; clonidine group 7.7 +/- 2.7 min, T6). Although prespinal and preephedrine BP values were higher in the control group, the magnitude of increases in mean BP after ephedrine was significantly greater in the clonidine group (P < 0.05). We conclude that oral clonidine premedication augments the pressor response to IV ephedrine during spinal anesthesia. Implications: The pressor effect of ephedrine is enhanced in patients given oral clonidine premedication during spinal anesthesia. (Anesth Analg 1998;87:1336-9)

Oral clonidine premedication does not prolong analgesia after herniorrhaphy under subarachnoid anesthesia

Study Objective: To determine the effect of oral clonidine premedication on duration of sensory and motor block, postoperative analgesia, hemodynamic stability, sedation, and respiratory parameters after subarachnoid anesthesia (SA). Design: Prospective, double blind, randomized, placebo-controlled study. Patients: 80 ASA physical status I patients were randomized into four equal groups to receive oral premedication with either clonidine 5 mcg/kg (C5), clonidine 2.5 mcg/kg (C2.5), diazepam 100 mcg/kg (D), or placebo (PL). Measurements and Main Results: The following parameters were measured: duration of motor and sensory block, requirement for postoperative analgesia; systolic (SBP), diastolic (DBP), and mean (MBP) blood pressures; heart rate (HR); sedation and anxiolysis scales; respiratory rate (RR); oxyhemoglobin saturation; and complications. (1) The duration of sensory and motor block did not differ significantly among the groups. (2) There were no differences in the time to first request for analgesia and in requirements for analgesia in the first 24 postoperative hours. (3) Clonidine premedication before SA did not produce episodes of significant hypotension. HR did not differ significantly among the groups. Baseline SBP was significantly higher ( p = 0.037) in group PL than in groups C5 and C2.5. Three minutes after SA significant decrease in the following parameters was observed: SBP in group PL compared with the other three groups ( p = 0.004), DBP in group PL vs. groups C5 and C2.5 ( p = 0.002), and MBP in group PL vs. groups C5 and C2.5 ( p = 0.003). (4) Sedation and anxiolysis were more pronounced ( p = 0.0001) in groups C5 and C2.5 than in groups D and PL and in group C5 than in group C2.5. (5) RR was significantly lower ( p = 0.0024) in group C5 than in groups D and PL. (6) Complications consisted of three episodes (15%) of bradycardia in the C5 group and two of bradypnea (10%) in the same group. Conclusions: In healthy patients, premedication with oral clonidine provided useful sedation and anxiolysis and stable hemodynamics, without prolongation of sensory and motor block. Side effects occurred only with clonidine 5 mcg/kg. Thus, a dose of 2.5 mcg/kg is recommended.

The Optimal Test Dose of Epinephrine for Epidural Injection with Lidocaine Solution in Awake Patients Premedicated with Oral Clonidine

We attempted to determine the optimal test dose of epinephrine for use with epidural anesthesia in awake patients premedicated with clonidine.Eighty-eight adult patients were randomized into two groups [oral premedication with clonidine 5 [micro sign]g/kg (CLON) or no premedication (CONT)]. Before induction of general anesthesia, heart rate (HR) and blood pressure (BP) were measured for 3 min after the IV injection of 3 mL of 1.5% lidocaine containing epinephrine (0, 1.25, 2.5, 5, 7.5, or 15 [micro sign]g) in a randomized, double-blind manner. We calculated 95% confidence intervals for the peak HR and BP increases induced by each dose of epinephrine. At 7.5 [micro sign]g, epinephrine induced a significantly greater increase in HR and BP in CLON than in CONT. The 95% confidence interval for the HR change induced by 7.5 [micro sign]g of epinephrine in CLON was nearly the same as the accepted standard dose of epinephrine (15 [micro sign]g) in CONT. We conclude that premedication with clonidine enhances HR and BP responses to the IV administration of epinephrine-containing epidural test solutions. Consequently, 7.5 [micro sign]g of epinephrine may be sufficient to enable detection of accidental injection into a blood vessel in awake patients premedicated with clonidine 5 [micro sign]g/kg. Implications: Clonidine, a commonly used preanesthetic medication, alters patients' cardiovascular responses to drugs such as epinephrine. Our randomized, double-blind study suggests that, in awake patients receiving oral clonidine premedication, 7.5 [micro sign]g of epinephrine (half the usual dose) is adequate as an indicator of accidental injection into the epidural vessels during epidural anesthesia. (Anesth Analg 1998;86:1010-4)

Oral Clonidine Premedication Reduces the Awakening Concentration of Isoflurane

Because clonidine has analgesic and sedative properties, it may influence the awakening concentration or dose of an anesthetic.To investigate the effects of oral clonidine premedication on emergence from isoflurane anesthesia, we studied 61 ASA physical status I or II patients undergoing superficial operations. They were randomly allocated to one of three groups according to the dose of clonidine they received: the clonidine-2.5 group (n = 21), clonidine-5 group (n = 20), and control group (n = 20) received approximately 2.5, 5, or 0 micro g/kg oral clonidine, respectively, in addition to 20 mg of famotidine 90 min before general anesthesia induction. Anesthesia was induced by thiamylal 5 mg/kg, and tracheal intubation was facilitated with succinylcholine 1.5 mg/kg IV. Anesthesia was maintained with a 1.1% end-tidal isoflurane concentration and 67% N2 O in oxygen, while ventilation was controlled to maintain end-tidal CO2 tension between 33 and 38 mm Hg. After surgery, N2 O was discontinued while the end-tidal isoflurane concentration was maintained at 1.1%. After confirming the end-tidal N2 O concentration of 0%, isoflurane was discontinued. The end-tidal isoflurane concentration at the time when patients responded to a standardized verbal command to open their eyes was recorded as MAC-Awake. The MAC-Awake values in the clonidine-5 group (0.22% +/- 0.09% [mean +/- SD]) was significantly less than those in the clonidine-2.5 and control groups (0.28% +/- 0.07% and 0.30% +/- 0.07%, respectively, P < 0.05). The wake-up time, from discontinuance of isoflurane until arousal, was longer in the clonidine-2.5 and clonidine-5 groups than in the control group (17.3 +/- 8.0, 16.9 +/- 7.0, and 10.6 +/- 5.3 min, respectively; P < 0.05). In conclusion, oral clonidine premedication 5 micro g/kg decreases the awakening concentration of isoflurane, and arousal from isoflurane anesthesia is prolonged with oral clonidine in a dose of 2.5-5 micro g/kg. Implications: Preanesthetic medication with oral clonidine, 2.5-5 micro g/kg, is associated with prolonged recovery from isoflurane anesthesia in adults. (Anesth Analg 1998;86:410-13)

Oral premedication of cloridine to reduce cerebrospinal pressure in patients with spinal anesthesia

S351 INTRODUCTION: Clonidine, an alpha2-agonist, has been reported to decrease cerebral blood flow [1,2]. The purpose of this study was to examine the effect of oral clonidine on cerebrospinal pressure. METHODS: The study protocol was approved by our Ethical Committee. We studied 40 ASA I or II adult patients scheduled for spinal anesthesia. The Queckenstedt's test was given to all patients to exclude spinal occlusion. They were randomly allocated to two groups. Group 1 (n=20) was the control group given no premedication. Group 2 (n=20) received 0.05 mg/kg of clonidine orally approximately 1 hr before the anesthesia. Each patient was given an intravenous infusion of lactated Ringer's solution 7-10 ml/kg 1 hr before anesthesia. After recording control blood pressure and heart rate, the patient was placed in a lateral recumbent position. After lumbar puncture, cerebrospinal pressure was measured through a 23G needle before the injection of local anesthetics. RESULTS: The mean age, weight and height of the patients were not significantly different between the two groups. The heart rate and mean blood pressure in the operation room and during the lumber puncture were significantly decreased in Group 2 (p < 0.05). Cerebrospinal pressure was significantly lower in Group 2 (p < 0.05). CONCLUSIONS: In this study, cerebrospinal pressure was reduced by oral clonidine administration. We assumed that reduction of cerebrospinal pressure was affected by the cerebral blood flow decreased which was affected by the use of clonidine. The anxiolysis effect of clonidine also supposed to reduce cerebrospinal pressure. We concluded that oral clonidine premedication reduced cerebrospinal pressure and that it is therefore useful for patients with intracranial hypertension. (Figure 1)Figure 1

Responses of Pro-Inflammatory and Anti-Inflammatory Cytokines with Clonidine Premedication in Patients Undergoing Spinal Surgery

Background : As immune mediators, cytokines are thought to regulate many biological functions. Changes in cytokine response were found in stressful conditions including surgery. Our aim was to study the effects of oral clonidine premedication on the proinflammatory and antiinflammatory cytokines in patients undergoing spinal fusion. Methods : Thirty patients (ASA I and II) were selected and randomly assigned to one of the three groups. Group 1, 2, and 3 received no premedication, clonidine 0.15 mg and 0.3 mg orally, respectively. Blood concentrations of proinflammatory cytokines, tumor necrosis factor- (TNF- ), Interleukin-1 (IL-1 ), IL-6, and antiinflammatory cytokines IL-10, IL-13 were determined as following intervals: before induction, immediate, 1 h, 3 h and 5 h after incision. For cytokines assay, commercially available ELISA kits were used. Results : Compared to baseline values, TNF- , IL-6 and IL-10 concnetrations at 3 h and 5 h after incision increased significantly in all the individual groups. IL-1 increased significantly at 3 h and 5 h after incision in group 1 and 3, and at immediate, 1 h and 3 h after incision in group 2. At the same times sampled, TNF- , IL-1 , IL-6, IL-13 concentrations were not statistically different among three groups. However, IL-10 concentration increased significantly at 5 h after incision in group 2 and 3 compared to group 1. In addition, IL-10 level at 5 h after incision in group 2 was significantly different from group 3. Conclusions : Oral clonidine premedication increased release of antiinflammatory cytokine IL-10 significantly during spinal fusion surgery. (Korean J Anesthesiol 1998; 35: 1080∼1088)

The Effect of Clonidine Premedication on Blood Pressure and Heart Rate during Endotracheal Intubation

Background : The endotracheal intubation for inhalational anesthesia induces hypertension and tachycardia and these hemodynamic changes cause many cardiovascular complications. Propofol has hemodynamic stability compared with thiopental sodium as an induction agent of general anesthesia. Clonidine, an 2-adrenergic receptor agonist, blunts hemodynamic changes when administered as premedicant. We evaluated the hemodynamic stability during endotracheal intubation after clonidine premedication and each induction with thiopental sodium or propofol. Methods : The 40 male and 40 female patients who scheduled for elective surgery, were randomly assigned in 4 groups (Group I, II, III and IV). In Group II and IV, the patients were administered 150 g of oral clonidine 90 minutes before induction of general anesthesia. Thiopental sodium was used as induction agents in Group I and II, propofol in Group III and IV. We measured systolic blood pressure, diastolic blood pressure, mean arterial pressure and heart rate at ward before administration of oral clonidine premedication (baseline value), before induction, after administration of induction agent, just after intubation, 1, 2, 3 and 5 minutes after endotracheal intubation. Results : The systolic, diastolic and mean arterial pressure and heart rate were increased significantly in all 4 groups (P＜0.05) when compared to baseline value of each group but lower in Group IV (P＜0.05) compared to Group I, II, III. Conclusion : Clonidine 150 g premedication and induction of general anesthesia with propofol blunts hemodynamic changes induced by endotracheal intubation. (Korean J Anesthesiol 1998; 35: 654∼661)

Oral clonidine premedication does not alter the efficacy of epidural test doses in adult patients anesthetized with isoflurane

Clonidine premedication has been increasingly used in clinical anesthesia. Though clonidine was found to alter pressor responses to various sympathomimetics, its effect on epidural test dose efficacy to detect intravascular injection has never been evaluated. Eighty healthy patients were randomly assigned to one of four groups, each of which was anesthetized with 1% end-tidal isoflurane and 67% nitrous oxide in oxygen after endotracheal intubation. The control-epinephrine group (n=20) given no clonidine premedication received 3 ml of 1.5% lidocain with 15 μg epinephrine (1:200000) intravenously to simulate an intravenously administered epidural test dose. The control-saline group (n=20) given no clonidine premedication received 3 ml of normal saline intravenously. The clonidine-epinephrine and clonidine-saline groups (n=20 each) were identical to the control groups, but were premedicated with oral clonidine, approximately 5 μg·kg(-1), 90 min before induction of general anesthesia. Heart rate (HR) and systolic blood pressure (SBP) were measured by a blinded observer at 20-s intervals for 4 min after intravenous injections of the test dose or saline. Following intravenous test dose injection, there were no significant diferences between the control-epinephrine and the clonidine-epinephrine groups in mean maximum increments of both HR (28±3vs 30±3 bpm, [mean±standard error], respectively) and SBP (46±6vs 45±4 mmHg, respectively). Six patients in the control-epinephrine and 4 in the clonidine-epinephrine group developed negative HR responses (HR increment <20 bpm). Since HR and SBP were essentially unchanged in the two groups receiving saline, sensitivities (negative predictive values) based on the HR criterion (positive if ≥20 bpm increase in HR) were 80% and 70% (83% and 77%) with and without clonidine premedication, respectively (P>0.05 between groups). However, when a modified HR criterion (positive if ≥10 bpm increase in HR) was used, sensitivities, specificities, and positive and negative predictive values were all 100% with or without clonidine. On the other hand, all of 20 patients in the control-epinephrine and the clonidine-epinephrine groups exhibited positive SBP responses (SBP increment ≥15 mmHg). Therefore, based on the SBP criterion, sensitivities, specificities, and positive and negative predictive values were all found to be 100% regardless of the presence of clonidine. We conclude that oral clonidine 5μg·kg(-1) premedication alters neither (a) hemodynamic responses to the intravenously administered epidural test dose containing 15 μg epinephrine, nor (b) the efficacy for detecting intravascular injection based on either criterion in adult patients under stable isoflurane anesthesia.

Oral clonidine premedication does not alter the efficacy of epidural test doses in adult patients anesthetized with isoflurane

Oral clonidine premedication does not alter the efficacy of epidural test doses in adult patients anesthetized with isoflurane

Hemodynamic effects of oral clonidine premedication in lumbar epidural anesthesia.

Clonidine, an α2-adrenergic agonist, has a potent sympatholytic effect and augments the pressor effect of ephedrine during general anesthesia. We evaluated whether oral clonidine premedication would alter the hemodynamic changes and enhance the pressor response to intravenous ephedrine during epidural anesthesia in 35 adult patients. They were randomly administered either premedication with clonidine approximately 5 μg·kg-1 po (n=17) or no clonidine medication (n=18). After establishment of epidural anesthesia, the hemodynamic response to ephedrine iv was measured in the awake state at 1-min intervals for 10 min. Then, the same hemodynamic measurement was repeated in the asleep state induced with midazolam iv. There were no differences in blood pressure (BP) and heart rate values between groups during the onset of epidural anesthesia, except that BP before epidural anesthesia was lower in the clonidine group than the control group (P<0.05). The magnitude and duration of pressor responses to ephedrine were comparable between groups in awake and asleep states. In conclusion oral clonidine premedication 5 μg·kg-1 alters neither the hemodynamic changes nor the pressor response to intravenous ephedrine during epidural anesthesia.

Hemodynamic effects of oral clonidine premedication in lumbar epidural anesthesia

Hemodynamic effects of oral clonidine premedication in lumbar epidural anesthesia

Oral Clonidine Premedication Blunts the Heart Rate Response to Intravenous Atropine in Awake Children

Comment Apparently two separate groups of Japanese researchers are simultaneously investigating the premedicating potential of oral clonidine, a centrally acting α-agonist. In awake adults, oral clonidine can cause bradycardia and hypotension and reduces the chronotropic response to intravenous atropine (Nishikawa et al.). In this investigation, high-dose (4 μg/kg) oral clonidine premedication in children, 10.8 ± 1.6 yr, also attenuated the increase in heart rate (HR) produced by intravenous atropine (10 μg/ kg) but did not cause significant changes in HR or blood pressure (BP) at the same or lower (2 M-g/kg) doses. No adverse effects of atropine were reported in this study, even though atropine doses as high as 30 μg/kg were required to increase HR 20 bpm in low-dose study patients, and atropine doses of 40 μg/kg were ineffective in 2 of 16 patients in the high-dose group. In addition, premedication with high-dose oral clonidine produced significandy higher (p <0.05, test statistic unreported) sedation scores than premedication with placebo or low-dose (2 μg/kg) oral clonidine. The authors concluded that effective (4 μg/kg) premedicating doses of oral clonidine can suppress the HR response to intravenous atropine in awake children; large doses (30–40+ μg/kg) of atropine may be required to increase HR 20 bpm in children

Oral Clonidine Premedication Enhances the Quality of Postoperative Analgesia by Intrathecal Morphine

Oral Clonidine Premedication Enhances the Quality of Postoperative Analgesia by Intrathecal Morphine

Effect of oral clonidine premedication on anesthetic requirement, hormonal response, hemodynamics, and recovery in coronary artery bypass graft surgery patients

Study Objective: To examine how premedication with clonidine affects opioid use, hemodynamic effects, hormonal responses, and recovery effects. Design: Double-blind, placebo-controlled study. Setting: Operating room and surgical intensive care unit of a university medical center. Patients: 54 patients undergoing elective coronary artery bypass graft (CABG) surgery. Interventions: Patients received approximately 5 μg/kg of oral clonidine or a placebo together with 40 μg/kg lorazepam 90 minutes prior to titrated sufentanil induction of anesthesia. Thirty minutes prior to cardiopulmonary bypass, a second dose of either approximately 5 μg/kg clonidine or placebo was given as a slurry via a nasogastric tube. Measurements and Main Results: Opioid use, hemodynamic effects, hormonal responses, and recovery effects were recorded. Values for ten hemodynamic variables were compiled on the evening prior to surgery, prior to induction, and during seven additional events and compared. Catecholamines and β-endorphins were measured prior to induction, after intubation, and after sternotomy. The amount of sufentanil used for induction, maintenance, and total opioid were compared. The times to awakening and response to verbal commands were compared. The two groups exhibited similar patient demographics, cardiopulmonary bypass time, and duration of surgery. Patients receiving clonidine required significantly (p < 0.04) less sufentanil for induction (clonidine: 2.19 ± 0.95 μg/kg vs. placebo: 2.93 ± 1.07 μg/kg) and total amount of sufentanil (clonidine: 9.1 ± 3.9 μg/kg vs. placebo: 11. 7 ± 4.6 μg/kg). Patients receiving clonidine required significantly (p < 0.01) less isoflurane (9.7 ± 6.8 MAC min vs. 19.7 ± 9.9 MAC min) to maintain heart rate (HR) and mean arterial pressure (MAP) to within 15% of baseline without significant differences in other vasoactive drugs. Catecholamine concentrations were significantly (p < 0.02) lower in patients receiving domaine without any difference in β-endorphin concentrations. Patients receiving clonidine had significantly (p < 0.02) lower HR, systolic arterial pressure, MAP, and systemic vascular resistance prior to induction than patients receiving placebo without differences in other hemodynamic variables. Conclusion: Clonidine decreases opioid use and lowers hormonal response while maintaining stable hemodynamics in patients undergoing CABG with sufentanil anesthesia.

Oral clonidine premedication reduces vomiting in children after strabismus surgery

This is a prospective randomized double-blind trial conducted to determine whether preoperative orally administered clonidine causes or potentiates postoperative vomiting in 140 children (3–12 yr) undergoing strabismus surgery. They were all inpatients and classified randomly into four groups (n = 35 each); placebo (control), diazepam 0.4 mg · kg−1, clonidine 2 μg · kg−1, and clonidine 4 μg · kg−1. These agents were administered 93–112 min (mean: 100 min) before the anticipated time of induction of anaesthesia. All children received inhalational anaesthesia with halothane and nitrous oxide in oxygen.’ Muscle relaxation in all patients was obtained with vecuronium and residual neuromuscular blockade was antagonized with neostigmine and atropine before tracheal extubation. Diclofenac suppository was prescribed to prevent postoperative pain. No opioids or postoperative antiemetics were administered. All children remained in hospital for two days postoperatively. The incidence and frequency of vomiting were compared in the groups with Kruskall-Wallis Rank test. Clonidine 4 μg · kg−1 caused a lower incidence and frequency of vomiting than did placebo and diazepam (incidence and frequency: 11% and 1,37% and 3, and 34% and 2 in clonidine 4 μg · kg−1, placebo, and diazepam, respectively; P < 0.05 for clonidine 4 μg · kg−1 vs placebo and diazepam). However, lowdose clonidine was ineffective. These data suggest that preanaesthetic medication with clonidine 4 μg · kg−1 may be useful for preventing emesis following strabismus surgery. This property of clonidine indicates that it may be superior to other sedative premedicants such as diazepam and midazolam.

Oral Clonidine Premedication Reduces Postoperative Pain in Children

Clonidine is an effective preanesthetic medication in children, providing a preoperative sedative effect. The analgesic properties of the drug have been well documented in adults. The current study was designed to investigate the effect of oral clonidine given preoperatively on postoperative pain in children undergoing minor surgery. In a prospective, randomized, controlled clinical trial, 90 children aged 5-12 yr undergoing elective ophthalmic, urologic, and otologic surgery received placebo (control), clonidine 2 micrograms/kg, or clonidine 4 micrograms/kg. These drugs were administered 105 min before the estimated time of induction of anesthesia and followed by treatment with oral atropine 0.03 mg/kg 60 min before anesthesia. Anesthesia was induced and maintained with halothane and nitrous oxide in oxygen. Postoperative pain was assessed by a blinded observer using an objective pain scale (OPS). Clonidine 4 micrograms/kg provided lower OPS (highest) scores during 12 h after surgery and reduced requirement for postoperative supplementary analgesic (diclofenac suppository) compared with the other two regimens. These data suggest that oral clonidine premedication (4 micrograms/kg) is a possible approach to facilitating postoperative analgesia in children undergoing minor surgery.

Oral Clonidine Premedication Reduces Postoperative Pain in Children

Oral Clonidine Premedication Reduces Postoperative Pain in Children