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Search Results: 1 - 10 of 29432 matches for " Jean-Louis Vincent "
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Is the Current Management of Severe Sepsis and Septic Shock Really Evidence Based?
Jean-Louis Vincent
PLOS Medicine , 2006, DOI: 10.1371/journal.pmed.0030346
Abstract:
Correction: Is the Current Management of Severe Sepsis and Septic Shock Really Evidence Based?
Jean-Louis Vincent
PLOS Medicine , 2006, DOI: 10.1371/journal.pmed.0030543
Abstract:
Obituary: Dr Max Harry Weil
Jean-Louis Vincent
Critical Care , 2011, DOI: 10.1186/cc10347
Abstract: Born in Switzerland, Dr Weil reached the US when he was just 10. He obtained his MD degree in New York in 1952, a PhD degree from the University of Minnesota in 1957, and an honorary ScD degree from the State University of New York in 2004. He worked for several years as a cardiologist before deciding to devote his time to critical care medicine.As early as 1959 Dr Weil created the famous Shock Unit at the University of Southern California, and then in 1974 started an Institute of Critical Care Medicine. He moved to the University of Health Sciences in 1981 before returning to California in 2007 to create his own Institute - The Weil Institute of Critical Care Medicine in Rancho Mirage.His major contributions are well known to all intensivists, and include improved understanding of the pathophysiology of shock states, of the importance of blood lactate levels, and of the mechanisms of lung edema including the role of colloid osmotic pressure. Many of today's management strategies and therapeutic approaches in critical care medicine are built on foundations put in place by Dr Weil, including the use of fluids (he developed the famous fluid challenge technique) and of vasoactive agents. In more recent years, his research focused on the microcirculation and on cardiopulmonary resuscitation, including monitoring techniques (for example, capnometry) and the role of various therapeutic agents. Not surprisingly, he was an important member of the Wolf Creek conferences on cardiopulmonary resuscitation.As a physiologist and a professor in clinical biomedical engineering, as well as a physician, Dr Weil managed to combine aspects of medicine, physiology, pharmacology, biochemistry and bio-engineering for the benefit of the critically ill. As an innovator and inventor, he owned more than 20 patents for medical equipment and devices he developed to help monitor and treat critically ill patients.Dr Weil trained many hundreds of intensivists from the five continents and remained
Understanding cardiac output
Jean-Louis Vincent
Critical Care , 2008, DOI: 10.1186/cc6975
Abstract: Cardiac output, expressed in liters/minute, is the amount of blood the heart pumps in 1 minute. Cardiac output is logically equal to the product of the stroke volume and the number of beats per minute (heart rate). Easy enough, one may think, but the term cardiac in cardiac output is potentially misleading – with clinician's sometimes assuming that to interpret cardiac output they must focus on the heart. The heart is just one part of the much larger cardiovascular system, however, and the amount of blood it pumps is dependent on both cardiac and extracardiac factors.Although most clinicians should/will be able to recite the four determinants of cardiac output – heart rate, contractility, preload, and afterload – understanding of the applicability and practical relevance of each of these four components is all too often less well ingrained. To try to clarify the individual roles and the combined roles of these four factors in generating cardiac output, and hence to facilitate our understanding of the effects of disease processes and therapies on cardiac output, I use a simple analogy that equates cardiac output (that is, the amount of blood pumped by the heart over a period of time) with the speed of a bicycle at a particular time point (Figure 1).The heart rate is perhaps the simplest determinant of cardiac output to visualize: the faster the heart beats, the more blood can be pumped over a particular period of time. Using our analogy, the faster the cyclist pedals, the faster the bicycle will go. But things are not quite so simple! Staying with the bicycle analogy, it is easy to imagine that if the cyclist pedals too fast for too long, he/she will get tired and be unable to maintain the rate of pedaling, so the bicycle will slow. There is an optimal rate of pedaling: too fast and the cyclist will tire too quickly and have to slow down; too slow and the bicycle will not move fast enough to cover the required distance. Similarly, if the heart rate is too slow, usual
Increasing awareness of sepsis: World Sepsis Day
Jean-Louis Vincent
Critical Care , 2012, DOI: 10.1186/cc11511
Abstract: So why is so little known about sepsis? Why is public awareness of other diseases so much greater than the awareness of sepsis. One key factor is that people suffering from asthma or AIDS or even cancer live with their disease from day to day, often long-term, and have the opportunity and time to speak out and to lobby politicians and others involved in health-care management for better facilities, treatments, research funding, and so on. Individuals with sepsis, in contrast, are critically ill in the intensive care unit (ICU) and unable to speak for themselves. The 50% to 60% of patients who survive could, of course, speak up when they have recovered, but these patients are often so happy to have survived that they want to move on and not look back. Alternatively, they may be unable to remember much of what happened during their ICU stay or they may suffer from ICU-related post-traumatic stress disorder [4] or depression [5], making it difficult for them to speak out. Patients with sepsis may also focus more on the primary disease process that caused their sepsis (for example, an underlying cancer, a pneumonia, or an episode of decompensated heart failure). They may even blame the hospital because their sepsis was hospital-acquired and caused by a multiresistant microorganism. Patients (and their families) often do not realize that it is the fact that they were already ill with an impaired immune status and required multiple invasive procedures that increased their risk of developing a nosocomial infection rather than the hospital or staff being at fault. Interestingly, the little support that sepsis does get tends to come from relatives of patients who die from sepsis, perhaps because they realize that we did our best for their loved one, but our best was not good enough, so it is important that treatments be improved or new therapies developed.Another key factor in the lack of public awareness of sepsis relates to the fact that there is still a lot of ambiguity a
Steroids in sepsis: another swing of the pendulum in our clinical trials
Jean-Louis Vincent
Critical Care , 2008, DOI: 10.1186/cc6861
Abstract: The search for effective interventions in sepsis has, in several cases, been associated with rather inconsistent results from clinical studies, as the pendulum seems to swing from a benefit effect through no effect to potential harm and all the way back to benefit, leaving the practicing clinician with a real therapeutic dilemma. This pendulum in clinical trial results is demonstrated well by the use of steroids in the treatment of patients with sepsis.Forty years ago, high-dose steroids were used in the belief that, because sepsis is an inflammatory response, the anti-inflammatory properties of steroids could be useful. Initial studies were encouraging, with Schumer demonstrating that treatment with one or two doses of intravenous dexamethasone (3 mg/kg) or methylprednisolone (30 mg/kg) was associated with reduced mortality compared with saline treatment in patients with septic shock [1]. Two large, double-blind, randomized controlled trials later failed to confirm these findings [2,3], however, and two meta-analyses in the mid 1990s concluded that steroids were ineffective [4] or indeed were potentially harmful [5] in sepsis.Then, in the late 1990s, several studies were published suggesting a role for much smaller, so-called stress, doses of steroids in reducing vasopressor requirements in patients with septic shock [6-8]. These results led to a study by Annane and colleagues in which patients with relative adrenal insufficiency – as assessed by nonresponse to a corticotropin test – who were treated with hydrocortisone (50 mg intravenously every 6 hours) and fludrocortisone (50 μg orally daily) for 7 days had a reduced mortality compared with nonresponders treated with placebo [9]. Despite concerns regarding the lack of statistical significance in overall mortality rates at 28 days, the results from this study led to steroids being recommended in the treatment of patients with septic shock [10]. Steroid use was also incorporated into the so-called sepsis bundles,
Withdrawing may be preferable to withholding
Jean-Louis Vincent
Critical Care , 2005, DOI: 10.1186/cc3486
Abstract: End-of-life decision making for the intensive care unit (ICU) patient has been a hot topic in recent years, with the acknowledgement that such practice is common worldwide [1] and with a new openness among doctors and laypersons regarding the once rather taboo subject of death. Indeed, because the majority of ICU deaths now occur following a decision to limit life-sustaining therapy [2-6], it is important that these often difficult ethical areas be discussed openly.Essentially, a decision to limit life-sustaining therapy can take one of two forms: withholding or withdrawing. Withdrawal of therapy is relatively easily defined as the removal of a therapy that was started in an attempt to sustain life but has become futile and is just prolonging the dying process. Withdrawal usually concerns therapies such as mechanical ventilation and administration of vasoactive agents. Withholding therapy, on the other hand, concerns the concept of no therapeutic escalation. Perhaps the most frequent example of this is the do not resuscitate (DNR) order (or DNAR – do not attempt to resuscitate). Withholding resuscitation efforts will almost inevitably result in death from a cardiac arrest should one occur. It is important to make this decision in advance because once the cardiac arrest occurs there is no time to think – each second counts. In many advanced cases the DNR order is not sufficient (e.g. the patient with terminal cancer or just very advanced age), and hence do not escalate (DNE) orders (e.g. no mechanical ventilation in respiratory failure or no extracorporeal support in terminal renal failure) may be used. However, it is important to define clearly what is included in a DNE order because less aggressive interventions such as antibiotic use or nasogastric tube feeding may not be seen as significant escalation and could still be given.The vast majority of doctors accept the principal and application of withholding; indeed, if life-sustaining therapies were not withheld fr
A reappraisal for the use of pulmonary artery catheters
Jean-Louis Vincent
Critical Care , 2006, DOI: 10.1186/cc4828
Abstract: However, in recent years, with the push to make medical care as noninvasive as possible and with the development of possible alternative, less invasive means of monitoring, the role of the PAC has come under close scrutiny. Intensivists are divided in their opinions, split into those who maintain that the haemodynamic data provided by the PAC aid in diagnosis and patient management, and those who believe that the complications and limitations outweigh the benefits. Increasingly, evidence does seem to suggest that patients managed with a PAC have similar outcomes to those without [3-7], although some studies have shown worse outcomes [8,9] and others improved outcomes [10]. The studies that have been conducted have used either complex statistical methodology to compare cohorts of patients [7,9,11] or have randomized patients to be managed with or without a PAC [3-6,12].In a recent observational study conducted across Europe and including 3147 patients, a cohort of 481 patients who had a PAC inserted was compared with a cohort of patients with no PAC [7]. PAC use was not an independent risk factor for 60-day mortality in multivariate analysis, and in 453 propensity-matched pairs ICU and hospital mortality rates were similar between groups (PAC use versus no PAC use: ICU mortality 26.7% versus 26.3%; hospital mortality 31.4% versus 32.8%; not significant). In the most recent randomized study, 1041 ICU patients were randomly assigned to treatment with or without a PAC [6]. Physicians managing patients without a PAC were allowed to use alternative monitoring equipment (selected for 79% of patients) if they wished. There were no differences in hospital mortality (68% versus 66%; P = 0.039), hospital length of stay, or days of organ support between patients managed with and those managed without a PAC, and in a cost-effectiveness analysis the authors concluded that there would be considerable savings if the PAC were to be withdrawn from clinical use.So, amidst all of these
The International Sepsis Forum's frontiers in sepsis: high cardiac output should be maintained in severe sepsis
Jean-Louis Vincent
Critical Care , 2003, DOI: 10.1186/cc2349
Abstract: Sepsis is associated with systemic, mediator-induced alterations in oxygen utilization, including increased oxygen demand, altered oxygen extraction, and decreased myocardial contractility (Fig. 1). Hence, despite a normal or high cardiac output, severe sepsis and septic shock are characterized by an inadequate organ oxygenation, leading ultimately to multiple organ failure and death. Almost 20 years ago, Abraham and colleagues [1] noted that survivors from septic shock had significantly higher cardiac indexes prior to the shock episode than did nonsurvivors, leading to the suggestion that pushing patients to reach high and even 'supranormal' levels of cardiac output could be beneficial. This early hypothesis has fueled an ongoing debate regarding the potential benefit or harm of this strategy in the patient with septic shock.Several groups have indicated increased survival in various groups of patients treated with a strategy to increase cardiac output or oxygen delivery (DO2) to so-called 'supranormal' values (cardiac index ≥ 4.5 l/min per m2, DO2 < 600 ml/min per m2 and oxygen consumption [VO2] >170 ml/min per m2) [2-9]. However, two notable studies conducted in mixed groups of critically ill patients by Hayes and coworkers [10] and Gattinoni and coworkers [11] showed that supranormal DO2 values do not result in improved outcomes. A possible explanation for those findings is that, unlike many of the other studies in this field, the heterogeneity of the critically ill patients included in the studies influenced the results. Thus, although some individuals might well have benefited from the trial strategy, these positive results may have been negated by harmful effects in other patients who perhaps had already been adequately resuscitated and therefore received excessive doses of vasopressor agents or fluids. There is little doubt that, in certain patients, achieving and maintaining high levels of cardiac output is associated with improved outcomes; the difficulty
Microvascular endothelial dysfunction: a renewed appreciation of sepsis pathophysiology
Jean-Louis Vincent
Critical Care , 2001, DOI: 10.1186/cc1332
Abstract: Sepsis, the host response to infection, involves a series of clinical, hematological, inflammatory and metabolic responses that can ultimately lead to organ failure. Severe sepsis is typically associated with activation of the coagulation system, leading to deposition of thrombin in the microvasculature. This process is associated first with activation, and then with inhibition of fibrinolysis. It is also associated with an inflammatory response and changes in microvascular permeability. These alterations, which are recognized by the clinician as disseminated intravascular coagulation (DIC), are commonly associated with multiple organ dysfunction, and have important prognostic implications. DIC, therefore, can be seen as both a thrombotic and a bleeding disorder, as an index of disease severity, or as an inflammatory disorder.It is now recognized that acute sepsis involves a complex interaction between the coagulation system and the inflammatory system that may result in organ dysfunction. The molecule that may be considered central to these effects is thrombin. In addition to its well-known procoagulation effects, thrombin may have anticoagulation effects through Protein C activation and induction of prostacyclin (Fig. 1). Thrombin may also cause cell proliferation and inflammation through induction of adhesion molecules and platelet-activating factor activation.The interaction between coagulation and inflammation has been demonstrated in a number of animal studies in which anticoagulant therapies, including heparin [1,2], antithrombin [3,4], tissue factor (TF) pathway inhibitor [5,6,7] and Activated Protein C [8], were shown to influence the inflammatory response. It is also now clear that both the coagulation and the fibrinolytic systems may be altered in acute sepsis, with the balance tipped in favour of procoagulation (through increased TF and thrombin expression, with decreased activation of thrombomodulin and Protein C) and antifibrinolysis (through plasminog
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