View clinical trials related to Toxemia.
Filter by:Children treated with intensive chemotherapy are at increased risk for life-threatening infections (sepsis). As the survival of oncology patients increased with the use of aggressive treatment protocols, there was also an increase in the need for hospitalization in intensive care units (ICU) due to sepsis.Several prognostic factors are known to affect the survival of these patients, including the number and type of damaged systems, the type of oncology disease and the duration of neutropenia. With the development of the treatment of ICU, the survival of the oncology patients hospitalized for sepsis has also increased. We will collect demographic details, details of their oncology and infections, laboratory tests and imaging. The goal is to identify prognostic factors in oncologic children hospitalized in ICU due to sepsis, as well as clinical and laboratory parameters that characterize this group of patients.
Maternal and neonatal infections are among the most frequent causes of maternal and neonatal deaths, and current antibiotic strategies have not been effective in preventing many of these deaths. Recently, a randomized clinical trial conducted in a single site in The Gambia showed that treatment with oral dose of 2 g azithromycin vs. placebo for all women in labor reduced selected maternal and neonatal infections. However, it is unknown if this therapy reduces maternal and neonatal sepsis and mortality. The A-PLUS trial includes two primary hypotheses, a maternal hypothesis and a neonatal hypothesis. First, a single, prophylactic intrapartum oral dose of 2 g azithromycin given to women in labor will reduce maternal death or sepsis. Second, a single, prophylactic intrapartum oral dose of 2 g azithromycin given to women in labor will reduce intrapartum/neonatal death or sepsis.
This study is an open-label, multi-center, interventional trial in which children with sepsis-induced MODS undergo surveillance immune function testing beginning on Day 2 of MODS. Those children who demonstrate immunoparalysis (TNF-alpha response <200 pg/ml) will receive a 7-day course of GM-CSF at a dose of 125 or 250 mcg/m2/day by either the intravenous (IV) or subcutaneous (SQ) route. The goal of the study is to establish the dose and route of delivery that results in resolution of immunoparalysis (TNF-alpha response >=200 pg/ml) by the morning after the 3rd scheduled dose with persistent resolution of immunoparalysis on the morning after the 7th scheduled dose. Resolution of immunoparalysis in 8 out of the first 10 subjects in a study treatment arm represents a successful dose and route. The goal of this study will be achieved through the following Specific Aims: Specific Aim 1. Establish the immunologic efficacy of GM-CSF administered by the IV and SQ routes in children with immunoparalysis in the setting of sepsis-induced MODS. Specific Aim 2. Estimate the pharmacokinetic parameters by the IV and SQ GM-CSF administered in pediatric sepsis-induced MODS. Specific Aim 3. Demonstrate the feasibility of screening, enrollment, drug delivery, and sample collection for a multi-center immunostimulation trial in children with sepsis-induced MODS.
Patients with sepsis (2 or more systemic inflammatory response syndrome criteria and suspected infection) assessed in the emergency department have blood cultures obtained to identify potential blood stream infections (BSI). Blood cultures are expensive, sometimes inaccurate, and only positive about 10% of the time in the emergency department. This study evaluates the effect of physician knowledge of C-reactive protein (CRP) levels on ordering rates of blood cultures in emergency department patients with sepsis. All patients with sepsis will have CRP levels measured using a point-of-care device, prior to blood tests being ordered. Half of participants will have their CRP level available to the emergency physician and half will not. Blood culture ordering rate and safety outcomes will be compared between these two groups.
Many biomarkers have been evaluated in sepsis, especially for prognostic purposes, but none has yet been shown to have sufficient sensitivity or specificity for routine use in clinical practice. However, highlighting a biomarker facilitating the evaluation of the severity of sepsis remains relevant in a pathology where survival is largely conditioned by the initiation of an early and adapted treatment. Recent evidence suggests that hepcidin, which is the key hormone for systemic regulation of iron metabolism, may be an interesting prognostic biomarker. The synthesis of this peptide is regulated by the iron stocks of the body, erythropoiesis, but also inflammation. The mechanisms inducing the expression of hepcidin during inflammation are multiple: interleukin-6 (IL-6) in particular, pro-inflammatory cytokine is a strong inducer of hepcidin. In addition, its expression is increased by the effect of lipopolysaccharide via Toll-like receptors . In septic patients, elevated levels of hepcidin or pro-hepcidin have been reported . A new role for hepcidin in the control of inflammatory and / or immune response has recently been reported. Thus, in a model of murine septic shock, the deleterious character of a lack of expression of hepcidin could be demonstrated . In humans, hepcidinemia has been shown to be a predictive factor in the development of immunotolerance in hepatic transplant patients. Hepcidin therefore plays a major role in the regulation of the inflammatory and / or immune response and in particular during sepsis. The investigators therefore hypothesize that hepcidin could be the marker of an adverse prognosis in septic patients expressing this
Sepsis associated encephalopathy (SAE) is a poorly understood acute cerebral dysfunction that frequently appears in the setting of sepsis induced systemic inflammation. In fact, altered mentation is recognized as an independent predictor of death and poor outcomes in patients with sepsis. SAE may be manifested by a number of symptoms characterized by a change in baseline behavior, attention, alertness, cognition, or executive functioning. It occurs in the absence of direct Central Nervous System (CNS) infection, and the exact pathophysiology is of SAE is unknown, but theoretically seems to encompass a constellation of mechanisms such as impairment of the blood brain barrier (BBB), endothelial dysfunction, alteration in cerebral blood flow and neurotransmission, circulating inflammatory mediators, cellular hypoxia, and metabolic disturbances, that ultimately result in neuronal dysfunction and cell death. SAE is characterized by an altered mental status (AMS) that ranges from delirium to coma, and can lead to long-term cognitive impairment. SAE may appear early in the course of sepsis, and is often underestimated as an independent factor of mortality, yet the pathophysiology of SAE remains unknown, and there is a lack of specific investigations available to clinicians. Studies have evaluated biomarkers as prognostic tools. The Investigator propose to measure neuron specific enolase (NSE), S-100B, glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase L1 (UCH-L1), Tau protein, Copeptin, spectrin breakdown products (SBDP 145, SBDP150), αII-spectrin N-terminal fragment (SNTF), neurofilament light and heavy chains (NF-L, NF-H), myelin basic protein (MBP), secretoneurin (SN), and other peptide levels in the serum of sepsis patients who develop altered mental status, to evaluate the kinetics of said biomarkers for 72 hours. The Investigator will monitor the course of the patients' hospitalization to determine whether there are biomarker correlates with survival and outcomes, including neurologic impairment. Finally, this investigation may provide a mechanistic pathway that defines the development of AMS in septic patients.
The purpose of this prospective, non-interventional, multi-centre clinical study is to assess the clinical validity of the Heparin Binding Protein (HBP) assay for indicating the presence, or outcome, of severe sepsis (including septic shock), over 72 hours, in patients with suspected infection following emergency department admission.
Comparison of noninvasive cardiac output monitor (NICOM, Cheetah Medical) with Edwards FloTrac minimally-invasive cardiac output monitor in predicting fluid responsiveness in sepsis and septic shock.
The purpose of this study is to determine the value of urine sTREM-1 on early predicting secondary acute kidney injury in sepsis
Presepsin (formerly CD14), is a glycoprotein receptor occurring at the surface of monocytes/macrophages. CD14 binds to lipopolysaccharide (LPS) complexes and LPS binding protein (LPB), which triggers the activation of toll-like receptor 4 (TLR4), resulting in the production of numerous pro-inflammatory cytokines. Following Presepsin activation by bacterial products, the CD14 complex is released in the circulation as its soluble form (sCD14), which in turn is cleaved by a plasma protease to generate a sCD14 fragment called sCD14-subtype (sCD14- ST). Plasma levels of sCD14 can be measured using an automated chemo-luminescent assay (PATHFAST).