72 research outputs found

    Ventricular fibrillation in six adults without overt heart disease

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    AbstractFindings are described in six patients with no clinical evidence of heart disease who had documented ventricular fibrillation (five patients) or ventricular flutter (one patient). The mean age of the six patients, all men, was 34 years (range 26 to 43). Cardiovascular collapse occurred in all and was followed by successful cardioversion. No patient had electrolyte or QT abnormalities. One patient had slight right ventricular enlargement on M-mode echocardiography, and another had a left ventricular pressure gradient at rest of 30 mm Hg with a normal two-dimensional echocardiogram. Holter electrocardiographic monitoring revealed incessant ventricular tachycardia in one patient and nonsustained ventricular tachycardia in three others. Exercise testing revealed nonsustained ventricular tachycardia in one patient.Ventricular fibrillation was induced at the time of programmed electrical stimulation in four of the six patients. Documented recurrence of ventricular fibrillation or ventricular flutter occurred in three patients, but in only one patient receiving antiarrhythmic drugs. Four patients were treated with amiodarone and one received an automatic implantable cardioverter-defibrillator. All patients are alive after a mean follow-up period of 78 months after the first documentation of their arrhythmia and 37 months after programmed electrical stimulation.Ventricular fibrillation can occur in the apparently structurally normal human heart. Antiarrhythmic treatment can provide effective control of this malignant arrhythmia

    Revisiting the loading dose of amikacin for patients with severe sepsis and septic shock

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    It has been proposed that doses of amikacin of >15 mg/kg should be used in conditions associated with an increased volume of distribution (Vd), such as severe sepsis and septic shock. The primary aim of this study was to determine whether 25 mg/kg (total body weight) of amikacin is an adequate loading dose for these patients.Clinical TrialJournal ArticleMulticenter StudyResearch Support, Non-U.S. Gov'tSCOPUS: ar.jinfo:eu-repo/semantics/publishe

    Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

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    Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

    Early severe acute pancreatitis : athogenic considerations and therapeutic perspectives

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    La pancréatite aiguë fulminante, caractérisée par l'apparition précoce d'une défaillance multiviscérale prolongée et une nécrose pancréatique étendue, représente encore un défi thérapeutique dans la mesure où elle est grevée d'une mortalité avoisinant 40 %. Ce travail aborde les mécanismes pathogéniques qui rendent compte des lésions tissulaires locales et à distance de la glande dans la pancréatite aiguë fulminante et envisage les stratégies thérapeutiques actuelles et futures dont pourrait bénéficier ce groupe à haut risque. Durant 14 ans, une stratégie thérapeutique conservatrice incluant le drainage du canal thoracique et le lavage péritonéal a été appliquée de manière consécutive chez 61 patients souffrant de pancréatite aiguë fulminante. Des échantillons d'ascite, de lymphe et de sang ont été prélevés lors de la mise en place du cathéter de lavage péritonéal et ensuite quotidiennement pendant le drainage de la lymphe thoracique. Nous avons montré qu'une attitude conservatrice peut être adoptée sans risque quelle que soit l'évolution de la défaillance multiviscérale, à condition d'y inclure une exploration précoce et itérative de la nécrose permettant de s'assurer qu'elle reste stérile. En effet, l'incidence de l'infection de la nécrose pancréatique et son poids pronostique sont considérables chez ces patients. La persistance de la défaillance multiviscérale au-delà de la première semaine d'évolution doit stimuler la recherche de l'infection de la nécrose mais ne peut justifier à elle seule le recours à la chirurgie. Tant le volume de la nécrose pancréatique que la sévérité de la défaillance multiviscérale sont associés à la concentration des médiateurs inflammatoires dans les divers compartiments testés. Ces médiateurs sont produits principalement dans le territoire splanchnique et gagnent le compartiment systémique par voie portale dans la mesure où leurs concentrations plasmatiques ne sont pas modifiées par le lavage péritonéal et le drainage de la lymphe thoracique. Bien qu'une balance pro-inflammatoire et protéolytique puisse être démontrée au voisinage de la glande pancréatique dès l'émergence de la défaillance multiviscérale, les mécanismes naturels de défense anti-inflammatoire et anti-protéolytique sont opérationnels dans la circulation systémique. Dans la mesure où l'infection pancréatique et la défaillance multiviscérale sont interdépendants, la prévention et le traitement de ces deux facteurs pronostiques majeurs doivent être pris en compte quel que soit leur poids pronostique relatif.Early severe acute pancreatitis still poses a major therapeutic challenge as it is characterized by persistent end-organ failure(s) from the outset, extended pancreatic necrosis and a mortality rate exceeding 40 %. This work deals with the pathogenic mechanisms underlying local and remote tissue injury in fulminant acute pancreatitis and addresses the question of the current and future therapeutic strategies in this high risk subgroup. A conservative therapeutic strategy incorporating thoracic duct drainage and percutaneous peritoneal lavage was consistently applied for 14 years in a cohort of 61 patients with early severe acute pancreatitis. Ascites was collected once at the time of insertion of the peritoneal lavage catheter whereas blood and lymph were sampled once daily during the course of early end-organ failure(s). We demonstrated that a conservative therapeutic strategy can be safely implemented regardless of the dynamic nature of end-organ failure(s) provided it includes an early and serial assessment of the microbiologic status of necrosis owing to the high incidence and the major prognostic importance of infected pancreatic necrosis in this subset of patients. Worsening end-organ failure(s) beyond the first week should trigger the search of infection, but is not predictive enough to be used as the sole indication for surgery. There is an association between inflammatory mediators and both the extent of necrosis and the magnitude of remote organ failures. These mediators are primarily produced within the splanchnic area and gain access to the systemic compartment via the splanchnic blood circulation. Hence, their circulating levels cannot be affected by peritoneal lavage and thoracic duct drainage. Whereas net pro-inflammatory activity and uninhibited protease are present in the vicinity of the necrotizing pancreas at the onset of end- organ failure(s), both natural antiprotease and anti-inflammatory defense mechanisms are fully operating in the systemic circulation. As pancreatic infection and end-organ failure(s) are interrelated, prevention and treatment of both prognostic factors must be tackled irrespective of their relative importance in determining outcome.Thèse de doctorat en sciences médicales (soins intensifs) (MED 3)--UCL, 200

    Influence of inspiratory flow pattern and nebulizer position on aerosol delivery with a vibrating-mesh nebulizer during invasive mechanical ventilation: An in vitro analysis

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    Background: Aerosol delivery during invasive mechanical ventilation (IMV) depends on nebulizer type, placement of the nebulizer and ventilator settings. The purpose of this study was to determine the influence of two inspiratory flow patterns on amikacin delivery with a vibrating-mesh nebulizer placed at different positions on an adult lung model of IMV equipped with a proximal flow sensor (PFS). Methods: IMV was simulated using a ventilator connected to a lung model through an 8-mm inner-diameter endotracheal tube. The impact of a decelerating and a constant flow pattern on aerosol delivery was evaluated in volume-controlled mode (tidal volume 500 mL, 20 breaths/min, inspiratory time of 1 sec, bias flow of 10 L/min). An amikacin solution (250 mg/3 mL) was nebulized with Aeroneb Solo® placed at five positions on the ventilator circuit equipped with a PFS: connected to the endotracheal tube (A), to the Y-piece (B), placed at 15 cm (C) and 45 cm upstream of the Y-piece (D), and placed at 15 cm of the inspiratory outlet of the ventilator (E). The four last positions were also tested without PFS. Deposited doses of amikacin were measured using the gravimetric residual method. Results: Amikacin delivery was significantly reduced with a decelerating inspiratory flow pattern compared to a constant flow (p<0.05). With a constant inspiratory flow pattern, connecting the nebulizer to the endotracheal tube enabled similar deposited doses than these obtained when connecting the nebulizer close to the ventilator. The PFS reduced deposited doses only when the nebulizer was connected to the Y-piece with both flow patterns or placed at 15 cm of the Y-piece with a constant inspiratory flow (p<0.01). Conclusions: Using similar tidal volume and inspiratory time, a constant flow pattern (30 L/min) delivers a higher amount of amikacin through an endotracheal tube compared to a decelerating inspiratory flow pattern (peak inspiratory flow around 60 L/min). The optimal nebulizer position depends on the inspiratory flow pattern and the presence of a PFS

    Défaillance multiviscérale précoce associée à la pancréatite aiguë: Stratégie thé rapeutique chirurgicale ou conservatrice?

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    The mortality of severe acute pancreatitis still ranges between 10% and 20%. Nowadays, infected pancreatic necrosis is the leading cause of death. Despite advances in intensive care therapy, however, early and worsening multi-system organ failure remains a source of substantial morbidity and still accounts for 20-50% of the deaths. News and hotspots - The three interrelated pathophysiological mechanisms underlying glandular necrosis include the premature intra-acinar activation of pancreatic pro-enzymes, an early pancreatic microcirculatory impairment, and the excessive stimulation of immune effector cells. In recent years, the systemic inflammatory response syndrome and the relevant cascades of inflammatory mediators have been implicated as the key factor in the emergence of remote tissue damage. Early multi-system organ failure that supervenes in the first week is typically associated with a sterile necrotizing process. The correlation between pathomorphological and clinical severity and the similarity between their respective pathophysiological mechanisms are not straightforward, however. There are no pathophysiological, clinical or economical data to support the practice of debridement of sterile necrosis to prevent or to control early multi-system organ failure. This issue has never been addressed in a controlled study. Besides intensive care support, non-surgical therapeutic modalities including urgent endoscopic sphincterotomy for impacted stones, antibiotic prophylaxis for the prevention of pancreatic infection and early jejunal nutrition have been specifically developed hopefully to attenuate multiple organ failure, to obviate the need of surgical drainage and to improve survival. Fine needle aspiration of necrotic areas must be incorporated in any conservative therapeutic strategy in order not to jeopardize those with infected necrosis that remains an absolute indication for drainage. Perspectives - There is ample experimental and pathophysiological evidence in favour of immunomodulatory therapy in severe acute pancreatitis. The administration of one or several antagonists of inflammatory mediators possibly combined with a protease inhibitor may at last provide the opportunity to interfere with the two major determinants of prognosis: the severity of multiple organ failure and the extent of necrotic areas that creates the culture medium for bacterial superinfection. These benefits remain to be substantiated in a controlled study, however. © 2003 Éditions scientifiques et médicales Elsevier SAS. Tous droits réservés

    Pronostic et réanimation des pancréatites aiguës sévères

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    [Prognosis and intensive care of severe acute pancreatitis]. Severe acute pancreatitis is morphologically characterized by an extensive and prolonged pancreatic and retroperitoneal inflammation with surimposed patchy or generalized areas of necrosis and hemorraghe in the pancreas and surrounding tissues. Clinical hallmarks include the early development of remote organ dysfunctions, notably cardiorespiratory failure and the late emergence of local complications (hemorraghe, acute pseudocyst and, most importantly, infection). The severity of the attack and the outcome of the patient are critically dependent on the presence and the extent of regional necrosis and are closely related to the casual bacterial contamination of these devitalized areas. The early identification of severe episodes is of therapeutic interest. This prognostic staging is best achieved with a combination of a set of clinical and laboratory data, initial CT findings and single biochemical indicators. Sequential assessment of severity, using biochemical markers and morphological data, is mandatory in order to monitor the fate of regional necrosis. Intensive care treatment includes supportive care of distant organ failures, prophylactic antibiotics and nutritional support
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