Ignite Creation Date:
2024-10-26 @ 3:39 PM
Last Modification Date:
2024-10-26 @ 3:39 PM
Study NCT ID:
NCT06586346
Status:
NOT_YET_RECRUITING
Last Update Posted:
None
First Post:
2024-09-04
Brief Title:
Frequency Predictors and Outcome of Sepsis Induced Coagulopathy in Critical Care Unit
Sponsor:
None
Organization:
None
Study Overview
Official Title:
Frequency Predictors and Outcome of Sepsis Induced Coagulopathy in Critical Care Unit
Status:
NOT_YET_RECRUITING
Status Verified Date:
2024-09
Last Known Status:
None
Delayed Posting:
No
If Stopped, Why?:
Not Stopped
Has Expanded Access:
No
If Expanded Access, NCT#:
N/A
Has Expanded Access, NCT# Status:
N/A
Acronym:
None
Brief Summary:
In intensive care units sepsis remains one of the common causes of mortality and morbidity The average hospital length of stay for sepsis is twice as long as any other fatal condition Furthermore sepsis survivors are at an increased risk of death or a reduced health related quality of life even after discharge from the hospital Sepsis induces multiple and complex derangements in many systems including the coagulation cascade The vast majority of septic patients present with hemostatic abnormalities ranging from subclinical coagulopathy to fulminant disseminated intravascular coagulation During the initial stages of infection coagulation operates as a natural defense mechanism attempting to confine the responsible pathogen and prevent its spread into systematic circulation However in advanced and severe infections as in sepsis mass inflammatory cytokine production and release into the circulation lead to significantly deranged hemostatic balance The coagulation process is activated while anticoagulant mechanisms including fibrinolysis and anticoagulant factors are suppressed Consequently septic patients are prone to a prothrombotic state through four main mechanisms extrinsic pathway activation cytokine induced coagulation amplification anticoagulant pathways suppression and fibrinolysis impairment
Detailed Description:
Sepsis is defined as a life-threatening syndrome associated with physiological pathological and biological abnormalities caused by a dysregulated host response to infections Globally there are 489 million sepsis cases leading to 11 million deaths annually
In intensive care units sepsis remains one of the common causes of mortality and morbidity The average hospital length of stay for sepsis is twice as long as any other fatal condition and the in-hospital mortality remains as high as 20 Furthermore sepsis survivors are at an increased risk of death or a reduced health-related quality of life even after discharge from the hospital
Sepsis induces multiple and complex derangements in many systems including the coagulation cascade The vast majority of septic patients present with hemostatic abnormalities ranging from subclinical coagulopathy to fulminant disseminated intravascular coagulation DIC During the initial stages of infection coagulation operates as a natural defense mechanism attempting to confine the responsible pathogen and prevent its spread into systematic circulation However in advanced and severe infections as in sepsis mass inflammatory cytokine production and release into the circulation lead to significantly deranged hemostatic balance The coagulation process is activated while anticoagulant mechanisms including fibrinolysis and anticoagulant factors are suppressed Consequently septic patients are prone to a prothrombotic state through 4 main mechanisms extrinsic pathway activation cytokine-induced coagulation amplification anticoagulant pathways suppression and fibrinolysis
In intensive care units sepsis remains one of the common causes of mortality and morbidity The average hospital length of stay for sepsis is twice as long as any other fatal condition and the in-hospital mortality remains as high as 20 Furthermore sepsis survivors are at an increased risk of death or a reduced health-related quality of life even after discharge from the hospital
Sepsis induces multiple and complex derangements in many systems including the coagulation cascade The vast majority of septic patients present with hemostatic abnormalities ranging from subclinical coagulopathy to fulminant disseminated intravascular coagulation DIC During the initial stages of infection coagulation operates as a natural defense mechanism attempting to confine the responsible pathogen and prevent its spread into systematic circulation However in advanced and severe infections as in sepsis mass inflammatory cytokine production and release into the circulation lead to significantly deranged hemostatic balance The coagulation process is activated while anticoagulant mechanisms including fibrinolysis and anticoagulant factors are suppressed Consequently septic patients are prone to a prothrombotic state through 4 main mechanisms extrinsic pathway activation cytokine-induced coagulation amplification anticoagulant pathways suppression and fibrinolysis
Study Oversight
Has Oversight DMC:
None
Is a FDA Regulated Drug?:
None
Is a FDA Regulated Device?:
None
Is an Unapproved Device?:
None
Is a PPSD?:
None
Is a US Export?:
None
Is an FDA AA801 Violation?:
None