View clinical trials related to Shock.
Filter by:Anaphylaxis is an acute serious allergic reaction, with multi-organ system manifestations caused by the release of chemical mediators and it is potentially fatal . Between 5% and 14% of patients may experience a recurrence of anaphylaxis 8-12 hours after the initial presentation, called biphasic (late-phase) . The mainstay of treatment for children experiencing anaphylaxis remains adrenaline and H1-antihistamines. Corticosteroids are not life-saving and do not have an immediate effect on the symptoms of anaphylaxis but may help reduce or prevent a biphasic "late phase" reaction . The aim of this study is to compare the efficacy of oral glucocorticoids in prevention of the second phase or biphasic reaction of anaphylaxis, as compared to placebo in children, presenting to the pediatric emergency department (PEC Al-Sadd) with mild to moderate anaphylaxis (Prospective Study). Patients will be randomized to either one of the two treatment: Treatment 1: Dexamethasone 0.6mg/kg oral. Treatment 2 : Placebo All patients will be urgently treated for anaphylaxis according to guideline protocol. Enrolled patients will be given one of the study medications orally, and he /she will observe in the observation room with cardiac monitor and close monitoring by nurse. The treating physician will discharge patient when he/she looks well, breathing comfortably, has oxygen saturation >94%, stable blood pressure and no gastrointestinal or neurological manifestation. Discharge patients will be sent home on anti-histamine (cetirizine) for 5days. All patients will be followed up for one week post discharge by a phone call asking about the general condition, relapse of symptoms, or need for readmission.
The purpose of the present study is to evaluate the effect of vasopressin compared to norepinephrine on the clinical complications of patients with vasospastic shock after noncardiac surgeries.
In this study, we will explore the feasibility of a randomized controlled trial that will compare high protein dose from ICU day 6 to 14 with moderate protein intake.
Inaccurate monitoring of mean arterial pressure (MAP) could lead to improper treatment in the form of excessive fluid infusion or unnecessary vasopressor therapy; therefore, accurate hemodynamic monitoring is crucial in treatment of septic shock. In critically ill septic patients treated with vasoactive drugs, many studies reported that radial arterial pressure monitoring significantly underestimates central arterial pressure. Insertion of a femoral line allowed a substantial reduction of the infusion rate of vasoactive drugs in these patients. These findings might imply that femoral placement of arterial lines is the gold standard for invasive arterial blood pressure monitoring in shock patient. Our study aimed to determine the difference between radial (peripheral) and femoral (central) arterial pressures measured simultaneously in a group of critically ill patients receiving high dose noradrenaline therapy (≥ 0.1 mcg/kg/min).
Patients with septic shock in the intensive care unit have a high risk to develop acute kidney injury (AKI) and AKI is an independent risk factor of mortality. Given the absence of validated pharmacological treatments for limiting the progression of AKI or for accelerating recovery from AKI, early intervention and the restoration of the glomerular filtration rate (GFR) in this context of septic shock might improve the patients' prognosis. One major challenge is to determine whether or not the AKI is reversible (return to normal function KDIGO 0 within 72 hours). In this retrospective study the investigators will analyze all patients admitted for a septic shock in three French ICUs between the 1st january 2014 and 01st January 2017 who developed an AKI (KDIGO ≥1) at admission and who had a determination of the urine concentration of TIMP2*IGFBP7 at admission. The investigators will determine the best threshold of TIMP2*IGFBP7 to distinguish the population of patients who will return to normal kidney function within 72 hours (KDIGO 0).
During shock, arterial hypotension, inadequate cardiac output and microcirculatory alterations lead to tissue hypoxia, multiple organ failure and death. Arterial lactate is considered as the best marker of tissue hypoxia. A lactate decrease during the first 6 hour is strongly associated with better outcome and may be used as a target for assessing the efficiency of shock resuscitation. The EIRUS system (Maquet Critical Care AB, 17154, Solna, Sweden) is a new device allowing the continuous measurement of venous lactate through a central venous catheter. However, before being used extensively, such device needs to be evaluated concerning its accuracy. The aim of the present study is to assess the reliability of this device.
Many observational studies have highlighted an independent association between fluid overload and clinical outcomes during septic shock. To optimize fluid balance, clinician has several options to consider carefully fluid administration and avoid fluid overload. More than a general restrictive approach, a pragmatic, individual tailored approach should be considered to optimize patients' hemodynamics during acute circulatory failure. Many advances in hemodynamic monitoring were described. Mini-fluid challenge appears to be a sensible method to use for bedside assessment to optimize fluid infusion. The next step for hemodynamic management in the ICU should be to test a hemodynamic goal-directed approach to better control fluid management and eventually improve patient's outcome. The main objective of the GOAL study is to evaluate a pragmatic optimization fluid management protocol tailored to each patient's hemodynamic status based on mini-fluid challenges. This intervention will be compared to usual management based on the latest guidelines. This intervention aims to decrease organ dysfunction during septic shock. This is the first large clinical trial designed to test this hypothesis.
Fluid therapy is often used as first line treatment of acute circulatory failure, aiming an increase in cardiac output (by improving preload) and in tissue perfusion. Depending on left ventricular systolic function, fluid challenge could lead to an increase in cardiac ouput and tissue perfusion, or only detrimental consequences (by fluid overload and aggravation of lung and tissues oedema, increase of morbi-mortality). Patients are defined as responders to fluid therapy if one can observe an increase of cardiac output up to 15% after fluid therapy (500ml of crystalloids): gold standard test used in most of the studies on the subject. Literature reports on heterogenous populations a reproductible and constant response rate to this fluid challenge of 50%. It seems reasonable to dispose of indices allowing to predict fluid responsiveness without resulting in fluid intake. Statics markers have been abandonned for several years and dynamics methods have been developped. In front of arrythmia, validated methods are scarce. Passive leg rising method appears to be the only one and it's validity seems to be less well documented than in sinusal patients. The purpose of this study is to determine a new method to assess fluid responsiveness in arrythmic patients. In atrial fibrillation, RR interval varies widely between cardiac cylces. Systolic interval remain constant. Variations will occure at expense of diastolic interval, or ventricular filling interval. One can reliably assume that when RR is longer, preload is rising. If the patient is on the ascendant part of the Franck-Starling curve, a longer RR should cause au greater VTI (Vitess Time Integral, surrogate of cardiac output). The evaluation by transthoracic echocardiography of the indice delta ITV / delta RR should determine the degree of fluid responsiveness in arrhythmic patients. After decision of fluid expansion, patients will have haemodynamic and echocardiographic data measured, delta ITV / delta RR indice assessed, then passive leg rising and fluid expansion with 500 ml of cristalloids administered, with evaluation of VTI (as surrogate of cardiac output) at each time. Fluid responders will be compared to non-responders to evaluate the diagnostic performances of the indice delta ITV / delta RR.
Implantable cardioverter defibrillator (ICD) shocks are associated with a subsequent increased risk of death, and an elevation of cardiac enzymes has been measured after defibrillation testing (DFT). The aim of our study was to investigate the association between S-ICD vs T-ICD shocks and acute cardiac damage in humans, as evaluated by means of sensitive and highly specific circulating biomarkers
Atrial fibrillation (AF) is a cardiac rhythm disorder particularly common in intensive care patients. Some meta-analyzes report a prevalence of new onset AF ranging from 4.5% to 29.5% in polyvalent intensive care. In our department, a recent month-long survey showed that more than 30% of the patients who were unhealthy on admission suffer from an episode of new onset AF during their stay. The occurrence of AF in intensive care has a pejorative effect on the patient's outcome, and this through two factors. On the one hand, the decreasing of cardiac output by degradation of the ventricular filling in diastole time, on the other hand the FA is responsible for an over-risk of ischemic stroke. In fact, it has been shown that the occurrence of new onset AF in intensive care is associated with a higher level of severity and a higher mortality. It is also important to underline the medico-economic impact of this rhythmic disorder as complication of shock due to the frequent prescription of various anti-arrhythmic or anticoagulant medication. Various factors have been mentioned to explain the frequent occurrence of AF in shocked patients. The shock state, whatever its origin, is characterized by the occurrence of a systemic inflammatory response syndrome in which is observed a particularly important releasing of stress hormones and endogenous catecholamines involved in the occurrence of a rapid multi-organ failure without treatment. Systemic humoral elements are possibly involved in the occurrence of new onset AF, such as high level of inflammation that characterizes shock states. In addition, physiological factors such as hypoxia, hypovolemia, hyperthermia or ionic disorders are also implicated, but their non-systemic association with intensive care new onset FA suggests that humoral factors may play an important and independent role. Among these humoral factors, the proteins of chromogranin family particularly Vasostatin-I (VS-I) seem possibly involved in the genesis of AF in the aggressed intensive care patients. Several studies have highlighted the beneficial regulatory role of VS-I on the cardiovascular system, particularly in a study on a canine model Stavrakis and al. have shown the VS-I protective role on the FA occurrence. However, as has been demonstrated in a prospective study in intensive care, the rates of circulating VS-I were significantly higher in the most severe patients and those whose prognosis was the most pejorative, thus not supporting the thesis of the protective effect of VS-I. An explanation exists for this discrepancy: VS-I is present in two distinct forms in the circulating blood. In vitro work carried out within the U1121 INSERM team with has made it possible to highlight the coexistence of two forms of VS-1: an aggregated "inactive" form and an "active" disaggregated form. In our hypothesis, the inactive aggregated form would be predominant during the states of acute pathological aggressions such as the shock and thus would not exert the anti arrhythmic and cardio protector expected functions. The first aim of our study is therefore to confirm that the onset of new onset FA during the shock state is associated with a significant decrease in the VS-I plasma level in its monomeric form called "active", even when high levels of total VS-1 are detected by ELISA in the plasma of patients. Our project is a pilot and unpublished translational work. The link between VS-I and new onset AF in intensive care severe patients has never been studied in vivo, and the recent work of the associated INSERM team provides advances in understanding the function of VS-I over time shock conditions. Nevertheless, our experimental hypothesis require confirmation in humans. A better understanding of the factors influencing the occurrence of cardiac arrhythmias in intensive care patients is a major ambition as it would be a step forward in the development of a preventive strategy or new treatment for the benefit of patients.