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Shock clinical trials

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NCT ID: NCT06140147 Recruiting - Septic Shock Clinical Trials

Protocolized Reduction of Non-resuscitation Fluids Versus Usual Care in Septic Shock Patients

REDUSE
Start date: November 27, 2023
Phase: N/A
Study type: Interventional

The objective of this trial is to assess the beneficial and harmful effects of a restrictive strategy for administration of non-resuscitation fluids in adult patients with septic shock.

NCT ID: NCT06127927 Recruiting - Cardiogenic Shock Clinical Trials

Evaluation the Efficacy and Safety of an Interventional Left Ventricular Assist System for Hemodynamic Support in Patients With Cardiogenic Shock

Start date: November 8, 2023
Phase: N/A
Study type: Interventional

Imported Impella The price is relatively expensive and difficult for ordinary patients to afford. In order to better meet the growing clinical needs in China, Anhui Tongling Bionic Technology Co., Ltd. has developed an interventional left ventricular assist system. The test device was tested in preclinical animals It has shown good effectiveness and safety. Through the implementation of this clinical trial, the interventional left ventricular assist system The safety and effectiveness of the system for hemodynamic support in patients with cardiogenic shock have led to further development of this product in the country.

NCT ID: NCT06126263 Active, not recruiting - Clinical trials for Infection, Bacterial

Adjunctive Clindamycin Versus Linezolid for β-lactam Treated Patients With Invasive Group A Streptococcal Infections

iGASAntitox
Start date: January 1, 2023
Phase:
Study type: Observational

This study aims to emulate a hypothetical target pragmatic multi-center, non-blinded trial of adult inpatients in the PINC AITM dataset with B-lactam treated culture confirmed monomicrobial invasive Group A streptococcus (GAS) between the years 2015-2021

NCT ID: NCT06124599 Recruiting - Clinical trials for Toxic Shock Syndrome Staphylococcal

Prodromes of Menstrual Staphylococcal Toxic Shock

IPro-CTSm
Start date: December 21, 2021
Phase:
Study type: Observational

Menstrual staphylococcal toxic shock is a rare but severe disease, requiring intensive care in over 80% of cases. Menstrual staphylococcal toxic shock develops during the peri-menstrual period, in healthy young women colonized by a vaginal strain of Staphylococcus aureus secreting the Toxic shock syndrome toxin 1 (TSST-1) and not immune to it, in a favorable environment, i.e. wearing intravaginal menstrual protection (tampon, menstrual cup). The rarity of the syndrome, its polymorphous clinical presentation and the absence of a totally specific biological examination make menstrual staphylococcal toxic shock a difficult pathology to diagnose. The reference clinical criteria correspond to the advanced picture of multivisceral failure, making it possible to classify cases a posteriori, but contribute to diagnostic delay and lack sensitivity. Patient accounts suggest the presence of symptoms in the days preceding the development of toxic shock, and also during previous menstrual cycles. The identification of prodromal symptoms could enable earlier management of menstrual staphylococcal toxic shock by removal of intra-vaginal sanitary protection, the main risk factor, before the disease becomes permanently established and requires intensive care.

NCT ID: NCT06122987 Recruiting - Sepsis Clinical Trials

Hemodynamic Response to Angiotensin-II When Used as the Second Vasopressor Agent for Septic Shock

Start date: December 4, 2023
Phase: Phase 4
Study type: Interventional

Norepinephrine is a catecholamine that is the first-line vasopressor for septic shock. The addition of non-catecholamine vasopressors, including vasopressin and angiotensin-II may be used in adults with septic shock that have inadequate mean arterial pressure while on norepinephrine. Uncertainty exists regarding the timing of initiation of these agents and there is a lack of data comparing their safety and efficacy. The current literature suggests that earlier initiation of angiotensin-II will have a more significant reduction on norepinephrine-equivalent dose compared to later initiation. In addition, approximately half of patients initiated on vasopressin do not have an early hemodynamic response 6 hours after initiation. The purpose of this study is to evaluate the efficacy of angiotensin-II when used as the second vasopressor agent for septic shock.

NCT ID: NCT06122909 Recruiting - Septic Shock Clinical Trials

The Effect Of Resuscitation Guided By Two Different Dynamic Parameters On Time To Normalization Of The Capillary Refill Time In Adult Patients With Septic Shock

Start date: July 21, 2023
Phase: Phase 3
Study type: Interventional

The aim of this study is to compare the effect of resuscitation guided by Left ventricular outflow tract-velocity time integral (LVOT-VTI) variation versus the effect of resuscitation guided by inferior vena cava (IVC) variation on time to normalization of the capillary refill time in adult patients with septic shock, amount of resuscitation fluids, rate of vasopressor and ICU length of stay.

NCT ID: NCT06121115 Completed - Septic Shock Clinical Trials

Norepinephrine Administration Through a Midline Catheter in an Intermediate Care Unit

Start date: October 3, 2023
Phase:
Study type: Observational

This is a single-center study retrospectively evaluating a local clinical routine to administer norepinephrine in midline catheters, with regard to complications and patient outcomes

NCT ID: NCT06119815 Recruiting - Septic Shock Clinical Trials

CO2 Gap Changes Versus Inferior Vena Cava Collapsibility in Relation to Cardiac Index as a Prognostic Value in Septic Shock

Start date: October 10, 2023
Phase: N/A
Study type: Interventional

In 2016, sepsis and septic shock was redocumented as fatal organ dysfunction caused by infection-induced host response disorders (Singer et al. 2016). Infectious shock is a subtype of sepsis; its circulation abnormalities significantly increase the mortality rate. The definition was updated to facilitate rapid identification and timely treatment. Despite the continuous progress of awareness and intervention, the mortality rate of septic shock is approaching 40% or more (Gasim et al. 2016, Karampela et al. 2022). Infectious shock exists in the presence of imbalance of oxygen supply and demand as well as tissue hypoxia, early improvement of tissue hypoperfusion is key to the treatment, a specific cluster treatment program was recommended in the guidelines of sepsis rescue action (Rhodes et al. 2017). Severe sepsis remains associated with high mortality, and the early recognition of the signs of tissue hypoperfusion is crucial in its management. The effectiveness of oxygen-derived parameters as resuscitation goals has been questioned, and the latest data have failed to demonstrate clinical advantage (Rudd et al. 2020). Prompt diagnosis and appropriate treatment of sepsis are of ulmost importance and key to survival. However, routinely used biomarkers, such as C-reactive protein and procalcitonin, have shown moderate diagnostic and prognostic value. Of note, the recent consensus definition for sepsis is based on clinical criteria, implying the paucity of reliable sepsis biomarkers. The new diagnostic criteria also incorporate the use of the SOFA score, a composite prediction tool, which is derived by a combination of clinical signs and biomarkers of organ dysfunction, leaving aside classic inflammatory biomarkers (Pierrakos et al. 2020, Karampela et al. 2022). The venous oxygen saturation (SvO2) is <70% in the majority of patients with severe sepsis on admission to the intensive care unit (ICU). The central venous-to-arterial carbon dioxide difference or only carbon dioxide gap (PCO2 gap) has gained relevance as a measure of assessment of several parameters (Mallat et al. 2015). The balance of dioxide carbon (CO2) production by the tissues and its elimination through the lungs can be reflected by the difference between the mixed venous content (CvCO2) and the arterial content (CaCO2). This venous-arterial difference in CO2 content (CCO2) can be estimated by the following equation: ΔPCO2 = PvCO2 - PaCO2, denominated PCO2 gap and in physiological conditions it ranges from 2 to 5 mmHg. In a few words, it indicates the difference between partial pressure of carbon dioxide in central venous blood (PvCO2) and arterial blood (PaCO2) (Janotka et al. 2021). The venous-to-arterial carbon dioxide difference (Pv-aCO2) can indicate the adequacy of microvascular blood flow in the early phases of resuscitation in sepsis (Ospina-Tascon et al. 2016, de Sá 2022). Hence, other resuscitation goals, such as PCO2 gap, have been suggested, due to their ability to predict adverse clinical outcomes and simplicity in patients achieving normal oxygen derived parameters during the early phases of resuscitation in septic shock. The PCO2 gap can be a marker of cardiac output adequacy in global metabolic conditions that are less affected by the impairment of oxygen extraction capacity (Bitar et al. 2020).

NCT ID: NCT06118775 Not yet recruiting - Septic Shock Clinical Trials

Evaluating Dynamic Arterial Elastance in Septic Shock Patients.

EaDyn
Start date: July 1, 2024
Phase: N/A
Study type: Interventional

Assess the effectiveness and safety of using dynamic arterial elastance as a tool for weaning vasopressor support in patients with septic shock, compared to a control group

NCT ID: NCT06115473 Recruiting - Shock Clinical Trials

Epinephrine to Prevent Postintubation Collapse in Shocked ICU Patients

Start date: August 1, 2023
Phase: N/A
Study type: Interventional

Endotracheal intubation is a lifesaving procedure that is performed in various settings within the hospital or even in the pre-hospital field. However, it can result in serious hemodynamic complications, such as post-intubation hypotension (PIH) and cardiac arrest. Push-dose pressor (PDP) is common practice for rapid hemodynamic correction in post-intubation hypotension. In this study the investigators will use intravenous Epinephrine bolus for prevention of post intubation collapse in septic patients predicted by shock index in intensive care unit.