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Featured researches published by M. De Miguel.
European Journal of Anaesthesiology | 2007
A. Pelavski; M. I. Rochera; Miguel Roca; M. De Miguel; J. Roigé
preanesthesia (the only -2 agonist locally available at the moment) was compared to placebo. Materials and Methods: Two equivalent groups of 40 patients (ASA I–III) were randomised to receive Diazepam in the evening before and oral Clonidine 150 g or placebo in the morning of the surgery. They have received equivalent ballanced general anesthesia for medium amplitude abdominal procedures. Intraand postoperative haemodynamic was assesed, as well as opiod consumption during surgery, opioid antagonisation at emergence. Anxiety, sedation, postoperatory respiratory depression and analgesia were quantified at 5 min postoperatory, at 1 h, then each 3 h until 24 h. Patients’ satisfaction (pain control, side effects) was assesed by a self-administred questionnaire in day 4. The statistic significance of the differences observed in the evolution of these parameters was tested by T Student test. Results and Discussions: Haemodynamic was better in the Clonidine group (variation greater than 20% for arterial pressure and heart rate at induction and during surgery for placebo group, p 0.05). This was even stronger for hypertensive patients. Opioid consumption reported to the duration of the intervention was comparable in the two groups Sedation and respiratory depression was slightly higher in the Clonidine group during the first 12 hours (p 0.05), Analgetic consumption was not statistically different in the two groups, as well as the pain control, Postoperative satisfaction (pain control, sedation, other side effects) was equivalent in the two groups. Conclusion(s): Clonidine premedication for moderate amplitude abdominal surgery ensures a better haemodynamic both intraand postoperatively, with minor side effects concearning sedation and respiratory depression. References: Bonnet F, Houhou A, Aveline C, ESA Refresher Courses 2000. Foëx P, Sear JW Continuing Education in Anaesthesia, Critical Care & Pain 2004 4(5): 139–143. 182 Education, research and presentation
European Journal of Anaesthesiology | 2011
A. Bataller; L. Silva; M. De Miguel; Gastón Echaniz; A. Camps; M. de Nadal
Background and Goal of Study: Angiotensin converting enzyme (ACE) mediates inflammatory response in healthy lungs via angiotensin II and plasminogen activator inhibitor -1. Neutrophils play an important role in the development of acute lung injury associated with severe sepsis. However, the ability of ACE directly participating in LPS-induced neutrophil activation has not been fully examined. This study was performed to evaluate the ef fects of the ACE inhibitor captopril on lipopolysaccharide (LPS) induced neutrophil activation and mortality in LPS induced endotoxemic mice. Materials and Methods: To assess possible interactions between captopril and LPS on neutrophil activation, neutrophils from human blood were incubated with various concentrations of captopril (0, 1, 10, 50 and 100 nM) and LPS (100 ng/ml). The protein levels for interleukin (IL)-6, 8 and tumor necrosis factor (TNF)-α were measured using ELISA 4 hr af ter incubation period. To elucidate the intracellular signaling pathway, We measured the levels of phosphorylation of p38 mitogen activated protein kinases (p38), extracelluar signal-regulated kinase (ERK)1/2 and c-Jun amino-terminal kinases (JNK) with western blot analysis and nuclear levels of nuclear factor (NF)-κB with electrophoretic mobility shif t assays 0.5 hr af ter incubation period. We also examined the ef fect of captopril (30mg/kg, IP) on mortality of mice treated with LPS (20 mg/kg, IP) to determine whether these ef fects of captopril also have in vivo significance. Results and Discussion: Captopril at tenuated LPS induced neutrophils activation including expression of p38, JNK, NF-κB, IL-6, 8 and TNF-α. Captopril also at tenuated mortality in LPS induced endotoxemic mice. Conclusion(s): Captopril can at tenuate mortality in LPS induced endotoxemic mice via the at tenuation of neutrophil activation caused by LPS.
European Journal of Anaesthesiology | 2010
P. Galán; I. García; M. De Miguel; C. Puiggrós; M. de Nadal
1AP3-7 – Relationship between mortality risk and perioperative data Perioperative Data High Risk Intermediate Risk Intermediate Risk Low Risk (Charlson>0 + SRS≥8) (Charlson=0 + SRS≥8) (Charlson>0 + SRS<8) (Charlson=0 + SRS<8 Number of patients 241 128 73 37 <3 associate dis. 19% 44% (p<0.05) 25% 38% (p<0.05) Number of assoc.dis 4±2 2.9±1.8 (p<0.05) 3.9±1.9 3.3±1.8 (p<0.05) Urgent Surgery 81% 95% 18% (p=0.001) 43% (p<0.05) Surgery Time(hours) 2.7±2.1 2.6±1.8 2.1±1.5 (p<0.05) 2.6±1.7 Intraoperative Compl. 19% 14% 4% (p=0.002) 11% Intraoperative Deaths 34 2 0 0 Need of critical care 51% 55% 40% 68% (p<0.05) Re-operation 32% 26% 22% 57% (p=0.003) Multi-organic Failure 15% 26% (p=0.017) 15% 14% Cause of death Cardiac Death Cardiac Death Cardiac Death Sepsis Death
European Journal of Anaesthesiology | 2006
A. Camps; M. De Miguel; M. de Nadal; Carme Bosch; C. Cortés; Eloy Espín; A. Mora
PFA (2.89 1.22 U). No differences were seen between these two latter groups. Conclusion(s): Our study shows that patients with normal routine coagulation tests, but increased risk of bleeding can be identified by combining SBA questionnaire with PFA laboratory test. Further studies are needed to evaluate the impact of preoperative corrective therapy on postoperative morbidity, mortality and costs in this group of patients. Reference: 1 Koscielny J, et al. Clin Appl Thromb Hemost 2004; 10(3): 195–204.
European Journal of Anaesthesiology | 2006
M. I. Rochera; Carlos Cruz Vázquez; M. De Miguel; Aurelio González; Miguel Roca; B. Alvarez; M. de Nadal
A-105 Cerebral oxymetry monitoring after carotid endarterectomy or stenting M.I. Rochera1, C. Vazquez1, M. de Miguel1, A. Gonzalez1, M. Roca1, B. Alvarez2, M. de Nadal1 1Department of Anesthesiology, Vall d Hebron Universitary Hospital; 2Department of Angiology and Vascular Surgery, Vall d Hebron Universitary Hospital, Barcelona, Spain Background and Goal of Study: Hyperperfusion syndrome (HP) is a rare but potentially grave complication after carotid endarterectomy (CEA) or stenting (CS) (1). Intraoperative regional cerebral oxygen saturation (rSO2) monitoring can identify patients at risk for HP after CEA (2). The goal of this study was to determine whether intra or postoperative changes in rSO2 could help to identify patients at risk for HP after CEA or CS. Methods: 42 patients scheduled for elective severe carotid stenosis repair were studied; 24 underwent CEA and 18 CS. Bilateral rSO2, mean arterial blood pressure (MAP) and periferal oxygen saturation (SpO2) were continuously monitored intraoperatively, at arrival to postanesthesia care unit (PACU) and 12 hours postoperatively. All patients underwent strict control of postoperative blood pressure. Changes in rSO2 ( rSO2) were calculated between T1 (basal awake), T2 (after declamping), T3 (PACU arrival), 1, 6 and 12 hours postoperatively (T4 T6) and PACU discharge (T7). Changes in MAP and SpO2 were also recorded, as well as the postoperative incidence of cephalea, seizures or neurological events. Repeated measures ANOVA with post-hoc test and Pearson’s correlation coefficient were used for statistical analysis. Results: One patient had to be excluded because of intraoperative angina. From the remaining 41 patients (30 M, 11 W, mean age 73 10 years, 55–92), 11 (27%) had contralateral severe ICA stenosis. None of the patients had adverse neurological outcome. No significant changes in rSO2 were observed; however, patients with severe contralateral stenosis showed significant changes in rSO2 between T2–T3, T2–T4 and T2-T5. A positive correlation betweeen rSO2 and MAP for ipsilateral ICA (r2 0.244, p 0.001) was found. Conclusions: This study did not show significant changes in rSO2 immediately after repairing the carotid circulation or in the immediate postoperative period relative to preoperative values. Nevertheless none of the patients had symptoms of HP to be identified by cerebral oxymetry. References: 1 van Mook, Rennenberg RJ, Schuring GW. Lancet Neurol. 2005; 4:877–88. 2 Ogasawara K et al. Neurosurgery. 2003; 53:309–315.
European Journal of Anaesthesiology | 2014
G. Alcaraz; Villarino L. Vila; A. Pelavski; M. De Miguel; M. I. Rochera; Miguel Roca
European Journal of Anaesthesiology | 2014
L. Villarino; G. Alcaraz; M. De Miguel; A. Pelavski; A. Lacasta; Miguel Roca
European Journal of Anaesthesiology | 2014
I. Chocrón; Sabaté M. López; C. Mejía; A. Aponte; M. De Miguel; M. de Nadal
European Journal of Anaesthesiology | 2013
G. Alcaraz; A. Pelavski; M. De Miguel; A. Lacasta; M. I. Rochera; Miguel Roca
European Journal of Anaesthesiology | 2013
A. Camps; L. Villarino; E. Pelaez; M. De Miguel; M. de Nadal