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The diagnosis and management of disseminated intravascular coagulation
Fletcher B Taylor1, Gary T Kinasewitz
1Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, 825 NE 13th Street, Oklahoma City, OK 73104, USA.
Insights
Disseminated intravascular coagulation (DIC) involves hemostatic factor activation, ranging from compensated (nonovert) to decompensated (overt) states. Biomarkers can detect early nonovert DIC, aiding intervention before organ failure.
Area of Science:
- Hematology
- Pathophysiology
- Critical Care Medicine
Background:
- Disseminated intravascular coagulation (DIC) is a complex syndrome characterized by systemic activation of hemostatic factors.
- DIC exists on a spectrum from subclinical compensated (nonovert DIC) to overt, decompensated coagulopathy.
- The endothelium plays a crucial role in regulating hemostasis via anticoagulant and anti-inflammatory mechanisms.
Observation:
- The endothelium's microvascular network, with regulatory factors like protein C and thrombomodulin, controls hemostasis.
- Procoagulant and proinflammatory disorders, such as sepsis and amniotic fluid embolism, can overwhelm these regulatory mechanisms.
- Inflammatory processes targeting the microvasculature can induce systemic changes detectable by hemostatic biomarkers.
Findings:
- Non-overt DIC represents a compensated response to microvascular inflammatory stress.
- Diagnosing non-overt DIC using established criteria can identify at-risk patients before progression to overt DIC and organ failure.
- Biomarkers are crucial for diagnosing non-overt DIC and monitoring therapeutic responses.
Implications:
- Early detection of non-overt DIC via biomarkers can facilitate timely intervention, potentially preventing severe outcomes like organ failure.
- Understanding the interplay between microvascular endothelium and hemostasis is key to managing DIC.
- Biomarker-guided management strategies offer promise for improving patient outcomes in DIC.
Abstract:
This review describes disseminated intravascular coagulation (DIC) as a syndrome in which hemostatic factors are activated. The syndrome ranges in severity from a decompensated coagulopathy (overt-DIC) to the subclinical compensated activation of hemostatic factors (nonovert DIC). The first part of this review emphasizes two points. First, activation of the hemostatic system is controlled by a vast network of capillaries and venules through anticoagulant and anti-inflammatory regulatory factors that operate from the endothelium (e.g., protein C and thrombomodulin, tissue factor pathway inhibitor). These hemostatic regulators can be overridden by procoagulant disorders such as amniotic fluid embolism or degraded by proinflammatory disorders such as sepsis. Second, because this link between the microvascular endothelium and circulating hemostatic factors is so close, even a relatively mild disturbance of the microvasculature targeted by the inflammatory process may be reflected systemically by changes in molecular biomarkers of hemostatic activity. Therefore, application of criteria for the diagnosis of nonovert DIC should be of value in detecting a compensated response to inflammatory stress of the microvasculature in patients who are at risk before they develop an uncompensated over DIC response and organ failure. The second part of this review covers the recent experience investigators have had in diagnosing and following the response of patients to treatment with biomarkers.