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      Comparison of propofol–hydromorphone and propofol–dexmedetomidine in patients with intubation after maxillofacial plastic surgery

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          Abstract

          Objective

          To compare the sedation and analgesic effects between propofol–hydromorphone and propofol–dexmedetomidine in patients with postoperative intubation after maxillofacial plastic surgery.

          Methods

          Forty-two patients undertaking maxillofacial plastic surgery with intubation were randomly assigned into propofol plus hydromorphone (P–H) group or propofol plus dexmedetomidine (P–D) group, receiving intravenous infusion of P–H or P–D, respectively. Cerebral state index, Ramsay sedation score, arterial blood gas analysis, and physiology indices were recorded before admission (T0), 30 minutes (T1), 1 hour (T2), 2 hours (T3), 6 hours (T4), and 12 hours after admission (T5) to intensive care unit, and 10 minutes after extubation (T6). Blood interleukin-6 was measured with enzyme-linked immunosorbent assay.

          Results

          There was no significant difference in arterial blood gas analysis, oxygen saturation, mean arterial pressure, and respiratory rate between two groups at all time-points ( P>0.05). The changes of heart rate (at T4, T5, and T6), cerebral state index (T1, T2, T3, T4, and T5), and Ramsay score (at T3) in P–H group were significantly different from that in P–D group ( P<0.05). The plasma interleukin-6 at T4 in P–H group was significantly lower than that in P–D group ( P<0.05).

          Conclusion

          The P–H approach takes advantages over P–D approach in relieving the pain and discomfort, reducing the overstimulation of sympathetic nerve and the stress level, and enhancing the tolerance of postoperative intubation after maxillofacial plastic surgery.

          Related collections

          Most cited references 20

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          The pathophysiology of propofol infusion syndrome: a simple name for a complex syndrome.

          Propofol infusion syndrome (PRIS) is a rare and often fatal syndrome described in critically ill children undergoing long-term propofol infusion at high doses. Recently several cases have been reported in adults, too. The main features of the syndrome consist of cardiac failure, rhabdomyolysis, severe metabolic acidosis and renal failure. To date 21 paediatric cases and 14 adult cases have been described. These latter were mostly patients with acute neurological illnesses or acute inflammatory diseases complicated by severe infections or even sepsis, and receiving catecholamines and/or steroids in addition to propofol. Central nervous system activation with production of catecholamines and glucocorticoids, and systemic inflammation with cytokine production are priming factors for cardiac and peripheral muscle dysfunction. High-dose propofol, but also supportive treatments with catecholamines and corticosteroids, act as triggering factors. At the subcellular level, propofol impairs free fatty acid utilisation and mitochondrial activity. Imbalance between energy demand and utilisation is a key pathogenetic mechanism, which may lead to cardiac and peripheral muscle necrosis. Propofol infusion syndrome is multifactorial, and propofol, particularly when combined with catecholamines and/or steroids, acts as a triggering factor. The syndrome can be lethal and we suggest caution when using prolonged (>48 h) propofol sedation at doses higher than 5 mg/kg per h, particularly in patients with acute neurological or inflammatory illnesses. In these cases, alternative sedative agents should be considered. If unsuitable, strict monitoring of signs of myocytolysis is advisable.
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            Complications of cough: ACCP evidence-based clinical practice guidelines.

             R. John Irwin (2005)
            To review the spectrum and frequency of complications associated with coughing. Ovid MEDLINE literature review (through March 2004) for all studies published in the English language, including case series and case reports, since 1966 using the MeSH terms "cough" and "complications." The complications of cough appear to stem from physiologic events. The magnitude of pressures, velocities, and energy that is generated during vigorous coughing allow coughing to be an effective means of clearing the airways of excessive secretions and foreign material, and providing cardiopulmonary resuscitation; however, they can also cause a variety of profound physical and psychosocial complications. The adverse occurrences include cardiovascular, constitutional, GI, genitourinary, musculoskeletal, neurologic, ophthalmologic, psychosocial, respiratory, and skin complications, and a decrease in health-related quality of life. Knowledge of the spectrum of complications should enable clinicians to appreciate (1) the impact of cough on patients, (2) why it is imperative to exhaust all possible diagnostic and therapeutic options to eliminate cough, and (3) why it is inappropriate to minimize a patient's complaint of cough and/or advise him/her to "live with it."
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              The effects of dexmedetomidine on cardiac electrophysiology in children.

              Dexmedetomidine (DEX) is an alpha2-adrenergic agonist that is approved by the Food and Drug Administration for short-term (<24 h) sedation in adults. It is not approved for use in children. Nevertheless, the use of DEX for sedation and anesthesia in infants and children appears to be increasing. There are some concerns regarding the hemodynamic effects of the drug, including bradycardia, hypertension, and hypotension. No data regarding the effects of DEX on the cardiac conduction system are available. We therefore aimed to characterize the effects of DEX on cardiac conduction in pediatric patients. Twelve children between the ages of 5 and 17 yr undergoing electrophysiology study and ablation of supraventricular accessory pathways had hemodynamic and cardiac electrophysiologic variables measured before and during administration of DEX (1 microg/kg IV over 10 min followed by a 10-min continuous infusion of 0.7 microg x kg(-1) x h(-1)). Heart rate decreased while arterial blood pressure increased significantly after DEX administration. Sinus node function was significantly affected, as evidenced by an increase in sinus cycle length and sinus node recovery time. Atrioventricular nodal function was also depressed, as evidenced by Wenckeback cycle length prolongation and prolongation of PR interval. DEX significantly depressed sinus and atrioventricular nodal function in pediatric patients. Heart rate decreased and arterial blood pressure increased during administration of DEX. The use of DEX may not be desirable during electrophysiology study and may be associated with adverse effects in patients at risk for bradycardia or atrioventricular nodal block.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2016
                08 March 2016
                : 12
                : 373-377
                Affiliations
                [1 ]Department of Anesthesiology, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, People’s Republic of China
                [2 ]Department of Anesthesiology, School and Hospital of Stomatology, Wuhan University, Wuhan, Hubei, People’s Republic of China
                Author notes
                Correspondence: Yanlin Wang, Department of Anesthesiology, Zhongnan Hospital, Wuhan University, Donghu Street 169, Wuhan 430071, Hubei, People’s Republic of China, Tel +86 27 876 862 15, Fax +86 27 876 862 15, Email yanlin_wang98@ 123456sina.com
                Article
                tcrm-12-373
                10.2147/TCRM.S99262
                4789838
                27022268
                © 2016 Peng et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                Categories
                Original Research

                Medicine

                dexmedetomidine, maxillofacial plastic surgery, intubation, hydromorphone, propofol

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