A Short Contemporary History of Disseminated Intravascular Coagulation

Levi, Marcel; Poll, Tom van der

doi:10.1055/s-0034-1395155

Cited by 59 publications

(12 citation statements)

References 83 publications

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“…68–70 Four-factor formulations appear to be more effective as compared to three factor PCCs for correcting the PT (2.5 s reduction vs. 0.6 s reduction in PT in a head-to-head comparison in healthy, rivaroxaban-treated volunteers), but less effective for correcting thrombin generation indices in patients taking rivaroxaban. 70, 71 Data on efficacy for restoration of hemostasis are limited, but reduced bleeding duration was demonstrated with PCC as compared to placebo in edoxaban-treated healthy volunteers undergoing punch biopsy. 72 Data on use of PCC in DOAC-treated bleeding patients are currently lacking, as are data on risk of thromboembolism, although a 4% incidence of VTE has been reported with the use of PCC for reversal of VKA.…”

Section: 0 Anti-xa Agentsmentioning

confidence: 99%

Measurement and reversal of the direct oral anticoagulants

2017

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Direct oral anticoagulants (DOACs) offer non-inferior efficacy and improved safety compared to vitamin K antagonists (VKAs) for prevention and treatment of venous thromboembolism and prevention of stroke and systemic embolism in non-valvular atrial fibrillation. Unlike VKAs, DOACs do not require routine laboratory monitoring of anticoagulant effect and dose adjustment. In certain situations, however, laboratory assessment of anticoagulant effect may be desirable. Here we review the utility of currently available assays for assessment of DOAC effect and recommend an optimal assessment strategy for each drug, including calibrated dilute thrombin time or ecarin-based assays for dabigatran and calibrated anti-Xa activity assays for the factor Xa inhibitors. We also discuss reversal strategies, both specific and non-specific, for each drug, including the preferential use of idarucizumab for reversal of dabigatran and two agents, andexanet and ciraparantag, currently under development for reversal of rivaroxaban, apixaban and edoxaban.

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Section: 0 Anti-xa Agentsmentioning

confidence: 99%

Measurement and reversal of the direct oral anticoagulants

2017

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“…TF triggers fibrinogenesis via activation of FVII. On the other hand, “DIC”, which occurs in critical illnesses, has also been named as DIC based on the same TF-initiated coagulation (thrombotic) disorder [ 89 , 90 ]. However, the clinical and hematologic features are very different between APL and critical illnesses.…”

Section: Introductionmentioning

confidence: 99%

“…The concept of microthrombogenesis clearly supports that “microthrombi” in DIT are exclusively composed of platelet-ULVWF complexes [ 1 , 2 , 4 – 6 ]. In contrast, the ironclad concept of “microthrombi” in “DIC” has been “micro blood clots” made of fibrin clots with participation of platelets via TF-initiated coagulation cascade [ 89 – 91 ].…”

Section: Introductionmentioning

confidence: 99%

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TTP-like syndrome: novel concept and molecular pathogenesis of endotheliopathy-associated vascular microthrombotic disease

Chang

2018

Thrombosis J

145

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TTP is characterized by microangiopathic hemolytic anemia and thrombocytopenia associated with brain and kidney dysfunction. It occurs due to ADAMTS13 deficiency. TTP-like syndrome occurs in critically ill patients with the similar hematologic changes and additional organ dysfunction syndromes. Vascular microthrombotic disease (VMTD) includes both TTP and TTP-like syndrome because their underlying pathology is the same disseminated intravascular microthrombosis (DIT). Microthrombi are composed of platelet-unusually large von Willebrand factor multimers (ULVWF) complexes. TTP occurs as a result of accumulation of circulating ULVWF secondary to ADAMTS13 deficiency. This protease deficiency triggers microthrombogenesis, leading to “microthrombi” formation in microcirculation. Unlike TTP, TTP-like syndrome occurs in critical illnesses due to complement activation. Terminal C5b-9 complex causes channel formation to endothelial membrane, leading to endotheliopathy, which activates two different molecular pathways (i.e., inflammatory and microthrombotic). Activation of inflammatory pathway triggers inflammation. Activation of microthrombotic pathway promotes platelet activation and excessive endothelial exocytosis of ULVWF from endothelial cells (ECs). Overexpressed and uncleaved ULVWF become anchored to ECs as long elongated strings to recruit activated platelets, and assemble “microthrombi”. In TTP, circulating microthrombi typically be lodged in microvasculature of the brain and kidney, but in TTP-like syndrome, microthrombi anchored to ECs of organs such as the lungs and liver as well as the brain and kidneys, leading to multiorgan dysfunction syndrome. TTP occurs as hereditary or autoimmune disease and is the phenotype of ADAMTS13 deficiency-associated VMTD. But TTP-like syndrome is hemostatic disorder occurring in critical illnesses and is the phenotype of endotheliopathy-associated VMTD. Thus, this author’s contention is TTP and TTP-like syndrome are two distinctly different disorders with dissimilar underlying pathology and pathogenesis.

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“…In the clinical course of sepsis, coagulation/fibrinolytic abnormalities are identified early on, and the risk of death due to multiple organ failure increases markedly when complicated by disseminated intravascular coagulation (DIC) [ 382 , 383 ]. DIC in sepsis manifests primarily as a state of severe systemic activation of the blood coagulation cascade, and it is believed that microcirculatory damage caused by intravascular coagulation can become a cause of organ damage [ 384 ]. In DIC, although fibrinolytic function also increases in response to the activation of the coagulation cascade, the extent of this increase varies depending on the underlying disease, and thus, DIC can occur with suppressed fibrinolysis or with enhanced fibrinolysis.…”

Section: Cq16: Diagnosis and Treatment Of Disseminated Intravascular mentioning

confidence: 99%

The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2016 (J-SSCG 2016)

et al. 2018

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Background and purposeThe Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2016 (J-SSCG 2016), a Japanese-specific set of clinical practice guidelines for sepsis and septic shock created jointly by the Japanese Society of Intensive Care Medicine and the Japanese Association for Acute Medicine, was first released in February 2017 and published in the Journal of JSICM, [2017; Volume 24 (supplement 2)] 10.3918/jsicm.24S0001 and Journal of Japanese Association for Acute Medicine [2017; Volume 28, (supplement 1)] http://onlinelibrary.wiley.com/doi/10.1002/jja2.2017.28.issue-S1/issuetoc.This abridged English edition of the J-SSCG 2016 was produced with permission from the Japanese Association of Acute Medicine and the Japanese Society for Intensive Care Medicine.MethodsMembers of the Japanese Society of Intensive Care Medicine and the Japanese Association for Acute Medicine were selected and organized into 19 committee members and 52 working group members. The guidelines were prepared in accordance with the Medical Information Network Distribution Service (Minds) creation procedures. The Academic Guidelines Promotion Team was organized to oversee and provide academic support to the respective activities allocated to each Guideline Creation Team. To improve quality assurance and workflow transparency, a mutual peer review system was established, and discussions within each team were open to the public. Public comments were collected once after the initial formulation of a clinical question (CQ) and twice during the review of the final draft. Recommendations were determined to have been adopted after obtaining support from a two-thirds (> 66.6%) majority vote of each of the 19 committee members.ResultsA total of 87 CQs were selected among 19 clinical areas, including pediatric topics and several other important areas not covered in the first edition of the Japanese guidelines (J-SSCG 2012). The approval rate obtained through committee voting, in addition to ratings of the strengths of the recommendation, and its supporting evidence were also added to each recommendation statement. We conducted meta-analyses for 29 CQs. Thirty-seven CQs contained recommendations in the form of an expert consensus due to insufficient evidence. No recommendations were provided for five CQs.ConclusionsBased on the evidence gathered, we were able to formulate Japanese-specific clinical practice guidelines that are tailored to the Japanese context in a highly transparent manner. These guidelines can easily be used not only by specialists, but also by non-specialists, general clinicians, nurses, pharmacists, clinical engineers, and other healthcare professionals.Electronic supplementary materialThe online version of this article (10.1186/s40560-017-0270-8) contains supplementary material, which is available to authorized users.

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A Short Contemporary History of Disseminated Intravascular Coagulation

Cited by 59 publications

References 83 publications

Measurement and reversal of the direct oral anticoagulants

Measurement and reversal of the direct oral anticoagulants

TTP-like syndrome: novel concept and molecular pathogenesis of endotheliopathy-associated vascular microthrombotic disease

The Japanese Clinical Practice Guidelines for Management of Sepsis and Septic Shock 2016 (J-SSCG 2016)

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