Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While the potent analgesic properties of clonidine, a centrally-acting antihypertensive agent, in humans is well described, its analgesic effect when administered into the pleural cavity is largely unknown. We have used intrapleural clonidine as a primary analgesic agent for postoperative pain control in two patients who had undergone cholecystectomy. Clonidine was instilled into the pleural space at the end of the operation via a silastic catheter placed through the seventh intercostal space. Oral pain medications were resumed within 48 hours after removal of the intrapleural catheter. In both patients, there was a substantial improvement in pulmonary function correlating with adequate pain control. No complications were noted secondary to the use of intrapleural clonidine. We conclude that intrapleurally administered clonidine is sufficient to provide adequate postoperative analgesia following abdominal surgery.
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PMID:The use of intrapleural clonidine for postoperative pain control. 867 28

Spasticity and pain are common disabling sequelae following spinal cord injury (SCI) and are often difficult to manage. The two problems are also not infrequently related. A variety of pharmacological and other approaches have been described for management of these problems in SCI. This case study reports a 32-year-old woman with an established incomplete C5 tetraplegia (anterior cord syndrome) who developed severe, intractable anal spasm following a hemorrhoidectomy, which persisted despite very good healing. This prevented evacuation of her bowels and resulted in severe rectal pain and episodes of autonomic dysreflexia. Attempts to modify the rate and mode of delivery of intrathecal baclofen through an existing programmable infusion pump failed to reduce anal sphincter spasm or improve symptoms. A right-sided pudendal block with lignocaine provided some relief. Clonidine was added to baclofen in the pump reservoir and both drugs were administered intrathecally in combination. This resulted in an immediate improvement in anal sphincter spasm and pain relief, allowing rapid reestablishment of her normal bowel pattern without need for any supplemental analgesia. It appears that intrathecal clonidine may have an important role in the treatment of spasticity, either as a single or an adjuvant agent, when intrathecal baclofen alone is ineffective or there is increasing tolerance to baclofen. Intrathecal clonidine may also prove useful in the management of intractable neuropathic pain.
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PMID:Intrathecal clonidine and baclofen in the management of spasticity and neuropathic pain following spinal cord injury: a case study. 870 79

Sympathetic nervous system stimulation, which releases noradrenaline, influences the nociceptor activity which develops after tissue injury. The alpha 2-adrenergic agonist, clonidine, produces analgesia through a central mechanism but also inhibits noradrenaline release at terminal nerve fibre endings. Clonidine may induce analgesia when administered at peripheral sites. This study assesses the potential analgesic effect of clonidine after intra-articular administration. Forty ASA I-III patients, scheduled for arthroscopic knee surgery under general anaesthesia were allocated randomly in 4 groups of 10 patients each, at the end of the surgical procedure. In the control group (group 1), the patients received 20 ml of intra-articular isotonic saline. In group 2, the patients received 150 micrograms of clonidine diluted in 20 ml of isotonic saline injected into the knee joint. In group 3, the patients were given 20 ml of intra-articular isotonic saline and clonidine 150 micrograms was injected subcutaneously. In group 4, morphine 1 mg, diluted in 20 ml of isotonic saline, was injected into the knee joint. Postoperative pain was assessed in a double-blind fashion using a visual analogue scale (VAS) at 1, 2, 3, 6 and 24 h after the end of surgery. VAS scores were significantly lower in groups 2 and 4, compared to groups 1 and 3, at 1 and 2 h after surgery. The delay between intra-articular injection and further postoperative analgesic administration was significantly longer (P < 0.05) in group 2 (533 +/- 488 min) compared to groups 1 and 3 (70 +/- 30 min and 132 +/- 90 min, respectively). The difference was not significant between group 4 (300 +/- 419 min) and the other groups. We conclude that a low dose of intra-articular clonidine produces analgesia unrelated to vascular uptake of the drug. This study further supports a peripheral analgesic effect of clonidine.
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PMID:Peripheral analgesic effect of intra-articular clonidine. 878 26

Sufentanil or a sufentanil-clonidine combination was evaluated to determine whether the basal rate in patient-controlled epidural analgesia (PCEA) might affect the daily consumption, quality of analgesia or incidence of side effects. Following Caesarean section delivery, 60 patients were randomly assigned to receive one of the four following PCA regimens (15 patients per group) for the relief of post-operative pain by the epidural route: sufentanil 2 micrograms mL-1 in 0.9% NaCl, demand dose 5 micrograms i.e. 2.5 mL, (group S+ with, group S without an infusion at 2.5 mL hr-1) or sufentanil 2 micrograms mL-1 + clonidine 3 micrograms mL-1, demand dose 5 micrograms sufentanil + 7.5 micrograms clonidine i.e. 2.5 mL (group SC+ with and SC without an infusion of 2.5 ml hr-1). The other PCA settings (Bard I PCA pump) were a lock out of interval of 10 min and a 1 h limit of 20 micrograms sufentanil and 30 micrograms clonidine i.e. 10 mL. The parameters measured were the analgesic drug consumption and number of dose demands during the first 24 h, pain scores at 6 h intervals, side effects and quality of sleep. The concurrent infusion increased the dose requirements regardless of the content of the syringe. Consumption of sufentanil was the highest in those patients receiving the plain solution with a basal infusion. Clonidine addition reduced the dose requirements but only significantly in those receiving the background infusion. Patients treated with the mixture tended to reach lower pain scores than those receiving sufentanil only without basal rate. Patients receiving the mixture with basal rate requested significantly fewer additional demands compared with the three other groups, but this did not influence the quality of sleep. Since side effects were more frequently registered in the patients in this group, it was concluded that the optimum regimen was the sufentanil-clonidine combination but with deletion of the basal rate.
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PMID:Potentiation of sufentanil by clonidine in PCEA with or without basal infusion. 895 87

The effect of the addition of clonidine 2 micrograms kg-1 to prilocaine 0.5% for intravenous regional anaesthesia (IVRA) in the arm was investigated in 56 healthy patients using a randomized, double-blind study. The characteristics of the sensory and motor block, quality of analgesia, development of post-operative pain sensations and haemodynamic variables were studied in three groups (IVRA with prilocaine, IVRA with prilocaine and clonidine, IVRA with prilocaine and systemic application of clonidine at tourniquet release). There were no significant differences between the groups concerning the onset and recovery characteristics of sensory and motor blockade, post-operative pain or side effects. In those patients receiving clonidine, mean arterial pressure decreased significantly (24-28%, respectively) after tourniquet release, while heart rate remained unchanged. Clonidine as an adjunct to prilocaine seems to be of limited benefit during and after intravenous regional anaesthesia.
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PMID:The addition of clonidine to prilocaine for intravenous regional anaesthesia. 904 57

The aim of this randomized, double-blind trial of postoperative thoracic epidural analgesic infusions was to determine whether clonidine at 10 microg/h (group C10, n = 22), 15 microg/h (Group C15, n = 24), or 20 microg/h (Group C20, n = 24) improved postoperative analgesia in patients undergoing abdominal gynecologic surgery, without side effects or hemodynamic changes, when added to a 5-mL/h infusion of 0.125% bupivacaine and fentanyl 2 microg/mL (Group CO, n = 22). The 24-h study infusion was supplemented, as required, by patient-controlled epidural fentanyl. Groups were similar for age, weight, duration, and type of surgery. Clonidine produced a dose-dependent improvement in analgesia at rest. Only 20 microg/h significantly increased the percentage of patients who experienced no pain with coughing (relative risk 1.44, 95% confidence interval 1.24-1.94), reduced pain scores with coughing (P < 0.05), and significantly lowered supplementary fentanyl requirements (P < 0.05). Groups were similar for sedation, pruritus, nausea, time to ambulation, and satisfaction with analgesia. Clonidine produced a dose-dependent decrease in blood pressure and pulse rate and an increase in vasopressor requirement (P < 0.01). Epidural clonidine infused at 20 microg/h improves analgesia during coughing when combined with epidural bupivacaine-fentanyl in patients undergoing lower abdominal surgery but is associated with hemodynamic changes and increased vasopressor requirement.
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PMID:Postoperative epidural infusion: a randomized, double-blind, dose-finding trial of clonidine in combination with bupivacaine and fentanyl. 917 14

Systemic opioids produce analgesia in part by activating bulbospinal noradrenergic pathways. Spinally released norepinephrine (NE) has been suggested to produce analgesia in part by stimulating alpha2-adrenoceptors on cholinergic spinal interneurons to release acetylcholine (ACh). We hypothesized that this spinally released ACh would stimulate synthesis of nitric oxide (NO), and that spinally released NO after intravenous (IV) opioid injection thus would depend on a cascade of noradrenergic and cholinergic receptor stimulation. To test these hypotheses, IV morphine was administered to anesthetized sheep, and neurotransmitters in dorsal horn interstitial fluid were measured by microdialysis. IV morphine increased NE and ACh in dorsal horn microdialysates, and these increases were inhibited by IV naloxone or cervical spinal cord transection. IV morphine also increased dorsal horn microdialysate concentrations of nitrite, a stable metabolite of NO. Increases in NE, ACh, and nitrite were antagonized by prior intrathecal injection of the alpha2-adrenergic antagonist idazoxan, the muscarinic antagonist atropine, or the NO synthase inhibitor N-methyl--arginine (NMLA). To examine the concentration-dependent effects of spinal adrenergic stimulation, isolated rat spinal cord tissue was perfused with the alpha2-adrenergic agonist clonidine. Clonidine increased nitrite in the spinal cord tissue perfusate, an effect blocked by coadministration of idazoxan, atropine, and NMLA. These data support a previously hypothesized cascade of spinally released NE and ACh after systemic opioid administration. These data also suggest that spinally released NO plays a role in the analgesic effects of systemic opioids. In addition, these data imply a positive feedback whereby spinally released nitric oxide increases NE release and that has not previously been described.
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PMID:Intravenous morphine increases release of nitric oxide from spinal cord by an alpha-adrenergic and cholinergic mechanism. 932 74

Opiates remain the most common form of analgesic therapy in the burn patient today. Because of increased opiate requirements, optimal relief of burn pain continues to be a problem for these patients. The purpose of this article is to summarize those alternative pain control methods that appear in the literature. For instance, in minor burns acetominophen continues to be a useful first line analgesic. Non-steroidal anti-inflammatory drugs (NSAID) and benzodiazepine are generally combined with opiates while entonox seems to be used commonly in the adolescent patients to relieve procedural pain. Antidepressants appear to enhance opiate-induced analgesia while anticonvulsants are useful in the treatment of sympathetically maintained pain following burns. Ketamine has been extensively used during burn dressing changes but its psychological side-effects have limited its use. Clonidine, however, has shown promise in reducing pain without causing pruritus or respiratory depression. Other forms such as transcutaneous electrical nerve stimulation (TENS), psychological techniques, topical and systemic local anaesthetics are also useful adjuncts.
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PMID:Adjunctive methods of pain control in burns. 942 10

In adults, clonidine when added to bupivacaine, results in no detectable respiratory depressant effect except when carbon dioxide challenge is performed. However, to date no investigations have quantified this in children. Twenty-four children (nine months to seven years) were randomized in a double-blind study into two groups. After induction, a caudal block was performed with 1 ml.kg-1 0.25% bupivacaine. Clonidine 1 microgram.kg-1 was added in the clonidine group, and 1 ml normal saline in the placebo group. Patients were monitored in the recovery room for three h from arrival to discharge with continuous pulse oximetry, respiratory rate, a transcutaneous CO2 tension (tcPCO2) every 15 min, and a four point sedation score every 30 min. Mean tcPCO2 and respiratory rate values were not different between the two groups. Apnoea and desaturation less than 97% were not observed. The sedation score decreased with time in both groups, and the score time interval was significantly higher in the clonidine group (P < 0.05). All the patients left the recovery room with a sedation score of 1, excepting four in the clonidine group with a sedation score of 2. Clonidine 1 microgram.kg-1 with 0.25% bupivacaine mixture in caudal analgesia in children did not induce an increase in tcPCO2 despite prolonged sedation.
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PMID:Transcutaneous CO2 tension effects of clonidine in paediatric caudal analgesia. 954 42

Caudal anaesthesia is indicated for surgical procedures lasting less than 90 min. Fentanyl and clonidine are known to prolong postoperative caudal analgesia, but there are no data on their effect on duration of surgical analgesia. We evaluated if the addition of clonidine or fentanyl to local anaesthetics prolonged the duration of surgical analgesia after single shot caudal block in children in a randomized, double-blind study. We studied 64 children, aged 6-108 months, undergoing bilateral correction of vesicoureteral reflux which was expected to last more than 90 min. Patients were allocated to one of four groups: group O received 1 ml kg-1 of a mixture of 0.25% bupivacaine with epinephrine and 1% lidocaine in equal parts; group F received the same mixture of local anaesthetics in addition to fentanyl 1 microgram kg-1; group C received the same mixture of local anaesthetics in addition to clonidine 1.5 micrograms kg-1; and group C + F received the same mixture of local anaesthetics in addition to fentanyl 0.5 microgram kg-1 and clonidine 0.75 microgram kg-1. Single shot caudal block was sufficient in only 57% of children in group O compared with 93% in groups C and F and 86% in group C + F (P = 0.035). Global assessment of anaesthesia, defined as the time from caudal injection to the first administration of analgesic (either during or after surgery), was significantly longer in the three groups of children who received additives compared with local anaesthetics alone (P = 0.035), but there were no differences between the three additive groups. Vomiting was observed only in children who received fentanyl. Addition of clonidine or fentanyl to local anaesthetics prolonged the duration of surgical analgesia of caudal block, allowing single shot caudal anaesthesia to be recommended for surgery lasting 90-150 minutes. Clonidine had some advantages over fentanyl as it did not produce clinically significant side effects.
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PMID:Addition of clonidine or fentanyl to local anaesthetics prolongs the duration of surgical analgesia after single shot caudal block in children. 962 26


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