Disseminated intravascular coagulation

Levi, Marcel

doi:10.1097/01.ccm.0000281468.94108.4b

Cited by 296 publications

(189 citation statements)

References 50 publications

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“…Overall the function of protein C is reduced in sepsis and DIC which results in significant compromise of in regulation of coagulation. APC is down-regulated during the host response to sepsis through cytokines and TM loss on the endothelium as well as a decrease in its primary cofactor protein S [3] . This down-regulation may reflect a conserved part of immunothrombosis and theoretically may be protective in localized tissue infection.…”

Section: Cascade Response To Severe Sepsismentioning

confidence: 99%

“…However, once the infection spreads to the blood stream and sepsis develops, the formation of thrombi within the microvasculature acts counterproductively and increases organ damage which may lead to organ failure. Significant coagulation disturbances are thought to complicate approximately 35% of all severe sepsis cases [3] . Small and medium size vessels show fibrin deposition that has been found during autopsy studies of patients with DIC and sepsis.…”

Section: Introductionmentioning

confidence: 99%

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Anticoagulant modulation of inflammation in severe sepsis

Allen

Sawheny

Kinasewitz

2015

WJCCM

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Inflammation and coagulation are so tightly linked that the cytokine storm which accompanies the development of sepsis initiates thrombin activation and the development of an intravascular coagulopathy. This review examines the interaction between the inflammatory and coagulation cascades, as well as the role of endogenous anticoagulants in regulating this interaction and dampening the activity of both pathways. Clinical trials attempting to improve outcomes in patients with severe sepsis by inhibiting thrombin generation with heparin and or endogenous anticoagulants are reviewed. In general, these trials have failed to demonstrate that anticoagulant therapy is associated with improvement in mortality or morbidity. While it is possible that selective patients who are severely ill with a high expected mortality may be shown to benefit from such therapy, at the present time none of these anticoagulants are neither approved nor can they be recommended for the treatment of sepsis.

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Section: Cascade Response To Severe Sepsismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Anticoagulant modulation of inflammation in severe sepsis

Allen

Sawheny

Kinasewitz

2015

WJCCM

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“…Microvascular thrombus formation due to PAI-1 with subsequent occlusion of microvessels and hypoperfusion is a major contributor to organ dysfunction in critically ill patients [1,25,26]. When oxygen delivery fails to meet the tissue oxygen demand in a critical situation, there is a compensatory increase in oxygen extraction.…”

Section: Discussionmentioning

confidence: 99%

<i>4G/5G</i> Polymorphism of the Plasminogen Activator Inhibitor-1 Gene Is Associated with Multiple Organ Dysfunction in Critically Ill Patients

et al. 2011

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Objective: Impaired fibrinolysis is associated with a higher incidence of both multiple organ dysfunction and mortality in the intensive care unit (ICU). Plasminogen activator inhibitor (PAI)-1 is the chief inhibitor of fibrinolysis. We investigated the influence of the 4G/5G polymorphism (rs1799768) of the PAI-1 gene on the plasma PAI-1 level and the outcome of critically ill patients. Methods: In 41 consecutive patients admitted to the ICU, PAI-1 gene polymorphism was assessed, plasma PAI-1 and arterial lactate concentrations were measured and clinical severity scores were recorded. Results: Homozygotes for the 4G allele had higher plasma levels of PAI-1 antigen. The mean ± SD PAI-1 antigen level was 193.31 ± 167.93 ng/ml for the 4G/4G genotype, 100.67 ± 114.16 ng/ml for the 4G/5G genotype and 0.43 ± 0.53 ng/ml for the 5G/5G genotype. There was a significant correlation between plasma PAI-1 and arterial lactate concentrations, as well as between PAI-1 and severity scores. The mortality rate was 63, 33 and 0% for patients with the 4G/4G, 4G/5G and 5G/5G genotypes, respectively. Conclusions: These results demonstrate that the 4G/5G polymorphism of the PAI-1 gene affects the plasma PAI-1 concentration, which could impair fibrinolysis and cause organ failure, and thus the presence of the 4G allele increases the risk of death.

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“…In some cases, the formation of a macroscopic thrombus takes only a few minutes (Levi 2007). Under normal conditions, blood coagulation stops the bleeding.…”

Section: (B ) Bcs Monitoring In Medicinementioning

confidence: 99%

“…In cases of BCS dysfunctions, its activation may lead to intravascular blood coagulation, thromboses and embolization. For instance, such well-known pathologies as cardiac infarction, thrombotic pulmonary embolism and disseminated intravascular coagulation result from dysfunctions of the BCS (Furie & Furie 2007;Levi 2007).…”

Section: (B ) Bcs Monitoring In Medicinementioning

confidence: 99%

Acoustic determination of early stages of intravascular blood coagulation

Uzlova

Guria

2008

Phil. Trans. R. Soc. A.

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The blood coagulation system (BCS) is a complex biological system playing a principal role in the maintenance of haemostasis. Insufficient activity of the BCS may lead to bleeding and blood loss (e.g. in the case of haemophilia). On the other hand, excessive activity may cause intravascular blood coagulation, thromboses and embolization. Most of the methods currently used for BCS monitoring suffer from the major disadvantage of being invasive. The purpose of the present work is to demonstrate the feasibility of using ultrasonic methods for noninvasive registration of the early stages of blood coagulation processes in intensive flows. With this purpose, a special experimental set-up was designed, facilitating the simultaneous detection of optical and acoustic signals during the clotting process. It was shown that (i) as microemboli appear in the flow during the early stage of blood coagulation, the intensity of the Doppler signal increases twofold, and (ii) microemboli formation in the early stages of blood clotting always reveals itself through an acoustic contrast. Both of these effects are well defined, so we hope that they may be used for non-invasive BCS monitoring in clinical practice.

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Disseminated intravascular coagulation

Abstract: Insight into the pathogenesis of DIC has resulted in better strategies for clinical management, including straightforward diagnostic criteria and potentially beneficial supportive treatment options.

Cited by 296 publications

References 50 publications

Anticoagulant modulation of inflammation in severe sepsis

Anticoagulant modulation of inflammation in severe sepsis

<i>4G/5G</i> Polymorphism of the Plasminogen Activator Inhibitor-1 Gene Is Associated with Multiple Organ Dysfunction in Critically Ill Patients

Acoustic determination of early stages of intravascular blood coagulation

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