Evidence map›Paper›PMID 32467443›Full record

ReviewCritical care medicine2020

Coagulopathy of Coronavirus Disease 2019.

Toshiaki Iba, Jerrold H Levy, Marcel Levi, Jean Marie Connors, Jecko Thachil

Open access · greenAbstract readReview
In one paragraph

Review in Critical care medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 281 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
281citing papers in PubMed, 5 pooled it
12.8field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

281 citing papers in PubMed, 5 syntheses or guidelines pooled it, 562 citations in OpenAlex.

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221 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 4 institutions in 3 countries.

Toshiaki IbaDepartment of Emergency and Disaster Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Jerrold H LevyDepartment of Anesthesiology, Critical Care, and Surgery, Duke University School of Medicine, Durham, NC.
Marcel LeviDepartment of Medicine and Cardio-metabolic Programme-NIHR UCLH/UCL BRC, University College London Hospitals NHS Foundation Trust, London, United Kingdom.
Jean Marie ConnorsHematology Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Jecko ThachilDepartment of Haematology, Manchester Royal Infirmary, Manchester, United Kingdom.
Duke University · USHarvard University · USJuntendo University · JPManchester Royal Infirmary · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesRecent studies have reported a high prevalence of thrombotic events in coronavirus disease 2019. However, the significance of thromboembolic complications has not been widely appreciated. The purpose of this review is to provide current knowledge of this serious problem.

designNarrative review. DATA SOURCES: Online search of published medical literature through PubMed using the term "COVID-19," "SARS," "acute respiratory distress syndrome," "coronavirus," "coagulopathy," "thrombus," and "anticoagulants." STUDY SELECTION AND DATA EXTRACTION: Articles were chosen for inclusion based on their relevance to coagulopathy and thrombosis in coronavirus disease 2019, and anticoagulant therapy. Reference lists were reviewed to identify additional relevant articles. DATA SYNTHESIS: Coronavirus disease 2019 is associated with a strikingly high prevalence of coagulopathy and venous thromboembolism that may contribute to respiratory deterioration. Monitoring coagulation variables is important, as abnormal coagulation tests are related to adverse outcomes and may necessitate adjuvant antithrombotic interventions. In the initial phase of the infection, D-dimer and fibrinogen levels are increased, while activated partial prothrombin time, prothrombin time, and platelet counts are often relatively normal. Increased D-dimer levels three times the upper limit of normal may trigger screening for venous thromboembolism. In all hospitalized patients, thromboprophylaxis using low-molecular-weight heparin is currently recommended. The etiology of the procoagulant responses is complex and thought to be a result of specific interactions between host defense mechanisms and the coagulation system. Although the coagulopathy is reminiscent of disseminated intravascular coagulation and thrombotic microangiopathy, it has features that are markedly distinct from these entities.

conclusionsSevere acute respiratory syndrome coronavirus 2/coronavirus disease 2019 frequently induces hypercoagulability with both microangiopathy and local thrombus formation, and a systemic coagulation defect that leads to large vessel thrombosis and major thromboembolic complications, including pulmonary embolism in critically ill hospitalized patients. D-dimers and fibrinogen levels should be monitored, and all hospitalized patients should undergo thromboembolism prophylaxis with an increase in therapeutic anticoagulation in certain clinical situations.

Indexed as

BetacoronavirusAnticoagulantsBlood Coagulation DisordersCoronavirus InfectionsCOVID-19Disseminated Intravascular CoagulationFemaleHumansMalePandemicsPlatelet Aggregation InhibitorsPneumonia, ViralPregnancyPrevalenceSARS-CoV-2ThromboembolismAnticoagulantsPlatelet Aggregation Inhibitors

Identifiers

PMID32467443
PMCPMC7255402
OpenAlexW3028615142

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.