Disseminated Intravascular Coagulopathy and Persistent Inflammation, Immunosuppression, and Catabolism Syndrome: Pathophysiology, shared pathways, and clinical implications.

BACKGROUND

Disseminated Intravascular Coagulopathy (DIC) and Persistent Inflammation, Immunosuppression, and Catabolism Syndrome (PICS) are critical care syndromes that frequently coexist in critically ill patients, but mechanisms underlying their shared pathways are not well understood.

OBJECTIVE

This review discusses the pathophysiology of DIC and PICS and explores the shared mechanisms behind DIC and PICS and their implications for clinical management.

FINDINGS: DIC and PICS share a common pathophysiological foundation of endothelial dysfunction, coagulation dysregulation, and inflammation, leading to a vicious cycle of microvascular injury and systemic inflammation, culminating in organ dysfunction. DIC has also been identified as an independent risk factor for PICS. Anticoagulation therapies such as antithrombin, recombinant human soluble thrombomodulin (rhTM), and heparin attenuates inflammation, a mechanism underlying both syndromes, thereby improving outcomes in PICS.

CONCLUSION

DIC and PICS share critical pathophysiological pathways that exacerbate outcomes in critically ill patients. Recognizing these interconnections is essential for developing targeted therapies. Standardizing PICS definitions and advancing research to clarify mechanisms, interplay, and causality between DIC and PICS are crucial next steps.