Impact of clonidine administration on delirium and related respiratory weaning after surgical correction of acute type-A aortic dissection: Results of a pilot study

Cardiac Surgery Unit, Magna Graecia University of Catanzaro, Viale Europa, Località Germaneto, 88100 Catanzaro, Italy.
Interactive Cardiovascular and Thoracic Surgery (Impact Factor: 1.16). 10/2009; 10(1):58-62. DOI: 10.1510/icvts.2009.217562
Source: PubMed


Delirium and transient neurologic dysfunctions (TND) often complicate the postoperative course after surgery for acute type-A aortic dissection (AAD). We evaluated the role of clonidine on neurological outcome and respiratory function in 30 consecutive patients undergoing surgery for AAD. Patients were prospectively randomized to receive either clonidine (0.5 microg/kg bolus, followed by continuous infusion at 1-2 microg/kg/h) or placebo (NaCl 0.9%) in on starting and throughout the weaning period from the mechanical ventilation. Incidence of delirium and TND, Delirium Detection Score (DDS), weaning parameters [respiratory rate to tidal volume ratio - f/VT; pressure-frequency product (PFP); partial pressure of arterial oxygen to fractional inspired oxygen concentration (PaO(2)/FiO(2)); partial pressure of carbon dioxide (PaCO(2))], weaning duration and intensive care unit (ICU) length of stay were recorded. The two groups were similar for preoperative and operative variables and also for the incidence of postoperative complications. DDS was lower in the clonidine group (P<0.001). Patients weaned with clonidine showed lower f/VT and PFP, higher PaO(2)/FiO(2) and PaCO(2), lower DDS, weaning period and the related ICU length of stay (P<0.001). This was further confirmed in patients developing delirium/TND. Intravenous clonidine after surgery for AAD reduces the severity of delirium, improves the respiratory function, shortens the weaning duration and the ICU length of stay.

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Available from: Francesco Onorati, Aug 20, 2014
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    • "Inpatient time was reported in 22 studies [18,20,21,24-26,29,30,32,34-37,39-41,44,47,49,51,52,54]. The duration of postoperative delirium was reported in 10 studies [25,29,30,35,41,43-45,47,52] and the severity of delirium was reported in 11 studies [25,28,29,38,42,43,45,46,48,50,53]. "
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    ABSTRACT: Introduction The ideal measures to prevent postoperative delirium remain unestablished. We conducted this systematic review and meta-analysis to clarify the significance of potential interventions. Methods The PRISMA statement guidelines were followed. Two researchers searched MEDLINE, EMBASE, CINAHL and the Cochrane Library for articles published in English before August 2012. Additional sources included reference lists from reviews and related articles from 'Google Scholar'. Randomized clinical trials (RCTs) on interventions seeking to prevent postoperative delirium in adult patients were included. Data extraction and methodological quality assessment were performed using predefined data fields and scoring system. Meta-analysis was accomplished for studies that used similar strategies. The primary outcome measure was the incidence of postoperative delirium. We further tested whether interventions effective in preventing postoperative delirium shortened the length of hospital stay. Results We identified 38 RCTs with interventions ranging from perioperative managements to pharmacological, psychological or multicomponent interventions. Meta-analysis showed dexmedetomidine sedation was associated with less delirium compared to sedation produced by other drugs (two RCTs with 415 patients, pooled risk ratio (RR) = 0.39; 95% confidence interval (CI) = 0.16 to 0.95). Both typical (three RCTs with 965 patients, RR = 0.71; 95% CI = 0.54 to 0.93) and atypical antipsychotics (three RCTs with 627 patients, RR = 0.36; 95% CI = 0.26 to 0.50) decreased delirium occurrence when compared to placebos. Multicomponent interventions (two RCTs with 325 patients, RR = 0.71; 95% CI = 0.58 to 0.86) were effective in preventing delirium. No difference in the incidences of delirium was found between: neuraxial and general anesthesia (four RCTs with 511 patients, RR = 0.99; 95% CI = 0.65 to 1.50); epidural and intravenous analgesia (three RCTs with 167 patients, RR = 0.93; 95% CI = 0.61 to 1.43) or acetylcholinesterase inhibitors and placebo (four RCTs with 242 patients, RR = 0.95; 95% CI = 0.63 to 1.44). Effective prevention of postoperative delirium did not shorten the length of hospital stay (10 RCTs with 1,636 patients, pooled SMD (standard mean difference) = -0.06; 95% CI = -0.16 to 0.04). Conclusions The included studies showed great inconsistencies in definition, incidence, severity and duration of postoperative delirium. Meta-analysis supported dexmedetomidine sedation, multicomponent interventions and antipsychotics were useful in preventing postoperative delirium.
    Critical care (London, England) 03/2013; 17(2):R47. DOI:10.1186/cc12566 · 4.48 Impact Factor
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    • "desagonistesalpha-2danslapriseenchargedu syndromeconfusionnel(délirium)deréanimationonte´tée´tudiés. Audécoursdelachirurgiededissectiondel'aorte,l'incidencedu syndromeconfusionnele´taitsimilairedanslesdeuxgroupes (clonidinevsplacebo)avecunesévéritéetuneduréedusyndrome confusionneletuneduréedeséjourenréanimationréduitedansle groupeclonidine(placebovsclonidinebolus:0,5mg/kgpuis1– 2mg/kgparheure;n=15Â2;essairandomiséendoubleinsu)[75]. L'incidencedusyndromeconfusionnele´taitréduitede30% (n=103;essaibicentrique:groupelorazépam:92%;groupe dexmédétomidine:63%;p<0,01).L'agitatione´taitd'intensitéplus faibledanslegroupedexmédétomidine(p<0,04)[17].Cesdonnées onte´térépliquéesdansunessaimulticentrique(n=297)[18],ainsi quedansunessaicomparantdexmédétomidine,propofol,et midazolamenréanimationaprèschirurgiecardiaque(propofol: 50%d'incidencedesyndromeconfusionnel;midazolam:50%; dexmédétomidine:3%;n=30Â3;essaiouvertrandomisé)[76] "
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    ABSTRACT: Alpha-2 adrenergic agonists (“alpha-2 agonists”) present multiple pharmacodynamic effects: rousable sedation, decreased incidence of delirium in the setting of critical care, preservation of respiratory drive, decreased whole body oxygen consumption, decreased systemic and pulmonary arterial impedance, improved left ventricular systolic and diastolic function, preserved vascular reactivity to exogenous catecholamines, preserved vasomotor baroreflex with lowered set point, preserved kidney function, decreased protein catabolism. These pharmacodynamic effects explain the interest for these drugs in the critical care setting. However, their exact role for sedation in critically ill-patients remains open for further studies. Given the few double-blind randomized multicentric trials available, the present non exhaustive analysis of the literature aims at presenting the utilization of alpha-2 agonists as potential first-line sedative agents, in the critical care setting. Suggestions regarding the use of alpha-2 agonists as sedatives are detailed.
    Annales francaises d'anesthesie et de reanimation 11/2012; 31(11):876–896. DOI:10.1016/j.annfar.2012.07.018 · 0.84 Impact Factor
  • Anesthesiology 10/2010; 113(6):1439-46. DOI:10.1097/ALN.0b013e3181fcf5a7 · 5.88 Impact Factor
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