View clinical trials related to Shock, Septic.
Filter by:The aim of the study was to investigate whether CVVH, in comparison to intermittent haemodialysis (IHD), is able to improve regional perfusion in septic shock patients studied by muscle microdialysis
Consecutive patients with cirrhosis and septic shock with AKI who give written informed consent will be included in this prospective trial. At baseline NT-Pro BNP, urine N-GAL will be done for all patients. A baseline serum blood sample (10 ml) and urine sample will be stored. Septic shock will be defined by the presence of two or more diagnostic criteria for the systemic inflammatory response syndrome, proven or suspected infection with hypotension non-responsive to adequate fluid resuscitation assessed by no evidence of stroke volume variation on flow track and need of a vasopressor to achieve a target mean arterial pressure (MAP) of ≥ 65 mm Hg. A record of CVP, IVC diameter and B-lines on ultrasound lung would also be done. Patients with age less than 18 years, severe known cardiopulmonary disease (structural or valvular heart disease, coronary artery disease, COPD) pregnancy, chronic kidney disease on hemodialysis, patients already meeting emergency criteria for immediate hemodialysis at the time of randomization as specified in the late group, patients transferred from other hospitals who have already been on hemodialysis before their arrival in the intensive care unit, extremely moribund patients with an expected life expectancy of less than 24 hours, failure to give informed consent from family members.
Persistence of a marked compensatory anti-inflammatory innate immune response after an insult is termed immunoparalysis. There is no biomarker available to determine the immune status of patient. Thus, the need for early and definite diagnosis of immune status of patient with sepsis, as well as the identification of patients at risk of evolving with severe organ dysfunctions, is crucial. Most important of all, speed is the key to survival. Therefore, it of crucial importance to identify which patient characteristic determines the poor prognosis. Early intervention can improve the prognosis. Investigators foresee an urgent need to identify predictors for mortality in severe sepsis, including clinical factors or immune status. Recently, the PIRO model has been proposed as a way of stratifying septic patients according to their Predisposing condition, the severity of Infection, the Response to therapy and the degree of Organ dysfunction. The immune status may be associated with above model. However, there is paucity data addressing this issue. In this study, investigators will also analyze the progression of patient condition during treatment and the associated immune status change. In the future, Investigators hope the determination of immune status may contribute to this model of classification rather than just being used as prognostic markers. Despite the advances in the knowledge of the basic processes that trigger and sustain the systemic inflammatory response in sepsis, the search for a "magic bullet" to treat this syndrome has been frustrating. The incidence of severe sepsis and septic shock still remains quite high, as does its mortality, which has decreased very little over the past decades.
In 2004, the Surviving Sepsis Campaign (SSC) introduced guidelines for the management of severe sepsis and septic shock, as well as strategies for bedside implementation. The treatment recommendations were organized in two bundles. In an international study, enrolling adult patients with severe sepsis admitted to these intensive care units, investigators found that while mortality from severe sepsis is high (44.5%), compliance with resuscitation and management bundles is generally poor in much of Asia. Investigators need to identify the patients at risk for high in-hospital mortality in order to take appropriate steps. From their past studies, investigators found that sepsis involved inflammation and coagulation. The multiple organ involvement was associated with interaction of novel biomarkers such as cytokines. There is limited data regarding comparing and application of biomarkers of different characteristic on sepsis treatment. A simultaneous detection of multiple cytokines may provide significant prognostic information. For other biomarkers, promising observation data have been put forward, but their potential needs to be evaluated in large-scale, well-designed prospective intervention studies before clinical use can be recommended. Besides many clinical studies on biomarkers were confounded by its lack of standard bundle care for severe sepsis patient. Here investigators performed a systematic study aimed at evaluating 1. the individual and combined diagnostic accuracy of biomarkers for predicting mortality; 2. whether trend change in biomarker level more useful for above prediction; 3. which biomarker or biomarker combination checked can predict patients at risk of evolving with severe organ dysfunctions.
After initial hemodynamic stabilization, 36 septic shock patients with heart rate > of 90 bpm and requiring norepinephrine to maintain mean arterial pressure (MAP) more than 65 mmHg will be randomised into two groups, esmolol group and control group. Patients allocated to esmolol group will receive a continuous esmolol infusion to maintain a lowering of heart rate of 10%. Norepinephrine will be titrated to achieve a MAP more than 65 mmHg. To investigate myocardial performance, the investigators will assess Tissue Doppler imaging by echocardiography and hemodynamic measures. Data will be obtained at baseline ,after esmolol infusion once achieved the predefined heart rate threshold and 72hours after esmolol infusion.
This study evaluates PK/PD of an extended-infusion protocol of meropenem, piperacillin-tazobactam and cefepime, in the early phase of septic shock.
Patients with septic shock in the intensive care unit have an elevated risk of developing acute kidney injury (AKI).
Septic syndromes (systemic inflammatory response associated with infection) remain a major although largely under-recognized health care problem and represent the first cause of mortality in intensive care units. While it has long been known that sepsis deeply perturbs immune homeostasis by inducing a tremendous systemic inflammatory response, novel findings indicate that sepsis indeed initiates a more complex immunologic response that varies over time, with the concomitant occurrence of both pro- and anti-inflammatory mechanisms. As a resultant, after a short pro-inflammatory phase, septic patients enter a stage of protracted immunosuppression. This is illustrated in those patients by reactivation of dormant viruses (CMV or HSV) or infections due to pathogens, including fungi, which are normally pathogenic solely in immunocompromised hosts. These alterations might be directly responsible for worsening outcome in patients who survived initial resuscitation as nearly all immune functions are deeply compromised. Both arms of immunity (innate and adaptive) are indeed markedly suppressed (including enhanced leukocyte apoptosis, lymphocyte anergy and deactivated monocyte functions). New promising therapeutic avenues are currently emerging from those recent findings such as adjunctive immunostimulation for the most immunosuppressed patients. The prerequisite for immunostimulation administration (IFNg, GM-CSF, IL-7) however relies on the investigators capacity in identifying the patients who could benefit from it, as there is no clinical sign of immune dysfunctions. The main objectives are: 1. to identify the best biomarkers for sepsis-induced immunosuppression and 2. to evaluate ex vivo whether drugs could rejuvenate immune functions.
The study aims at clarification of venous collapsibility measures with real venous flow measurements during dynamic maneuver testing fluid responsiveness in septic shock patients.
The primary objective of this study is to compare 28 day mortality rates between septic shock patients with acute renal insufficiency treated via L-Carnitine (as an adjunct therapy) versus a similar group of patients not receiving L-Carnitine adjunct therapy.