Pathophysiology of Disseminated Intravascular Coagulation in Sepsis: A Clinically Focused Overview

Abstract

Sepsis is a major global health problem that results from a dysregulated and uncontrolled host response to infection, causing organ failure. Despite effective anti-infective therapy and supportive treatments, the mortality rate of sepsis remains high. Approximately 30–80% of patients with sepsis may develop disseminated intravascular coagulation (DIC), which can double the mortality rate. There is currently no definitive treatment approach for sepsis, with etiologic treatment being the cornerstone of therapy for sepsis-associated DIC. Early detection, diagnosis, and treatment are critical factors that impact the prognosis of sepsis-related DIC. Over the past several decades, researchers have made continuous efforts to better understand the mechanisms of DIC in sepsis, as well as improve its quantitative diagnosis and treatment. This article aims to provide a comprehensive overview of the current understanding of sepsis-related DIC, focusing on common causes and diagnoses, with the goal of guiding healthcare providers in the care of patients with sepsis.

Gene Dosage of F5 c.3481C>T Stop-Codon (p.R1161Ter) Switches the Clinical Phenotype from Severe Thrombosis to Recurrent Haemorrhage: Novel Hypotheses for Readthrough Strategy

“…This genetic-based model might be analogous to a complex and challenging complication in blood coagulation called disseminated intravascular coagulation (DIC). The coexistence of thrombosis and haemorrhages due to factor consumption/shortage assigns to DIC peculiar characteristics, revealing the double vulnerability of a coagulation balance [51,52]. Similarly, in our research, these concepts perfectly match and adequately paint the multifaceted architecture of haemostasis and thrombosis.…”

A Review of the Use of Extracellular Vesicles in the Treatment of Neonatal Diseases: Current State and Problems with Translation to the Clinic

“…Moreover, the acute, rare thrombotic reactions observed in patients after MSC administration in clinical trials are attributed to side effects associated with vascular thrombosis and the subsequent inflammatory response [ 262 ]. It is also a crucial factor to consider during the development of sepsis-related disseminated intravascular coagulation (DIC), in which tissue factor on the surfaces of platelets plays a leading role [ 263 ]. Tissue factor is recognized as a critical regulator of hemostasis capable of initiating localized thrombosis under specific circumstances, thereby eliciting an inflammatory immune response [ 264 ].…”

Revolution in sepsis: a symptoms-based to a systems-based approach?

“…4 ) [ 46 , 74 , 99 , 163 ]. Clinically, DIC continues to be diagnosed using a scoring system involving PT, platelet count, fibrinogen, and D-dimer levels [ 13 , 167 , 172 ]. However, without evidence of intravascular fibrin deposition, diagnosis may not be DIC and impact on optimal patient treatment.…”

“…Inflammasome-activated pyroptotic macrophages [181], microbial agents, cytokines and complement factors can further increase TF levels, which can activate the endothelial-glycocalyx and aggravate coagulopathy [177][178][179]. Wu and colleagues further showed in their mouse sepsis model that inhibition of TF abolishes inflammasome-mediated blood clotting and protects against death [172,181].…”