Evidence map›Paper›PMID 32841919›Full record

ReviewThrombosis research2020

COVID-19 versus HIT hypercoagulability.

Theodore E Warkentin, Scott Kaatz

Abstract readReview
In one paragraph

Review in Thrombosis research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

27 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Prognostic markers in patients with COVID-19 requiring intensive care support.Journal of Taibah University Medical Sciences · 2023
    Article
  6. Article
  7. FcFrontiers in cardiovascular medicine · 2023
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. COVID-19-related laboratory coagulation findings.International journal of laboratory hematology · 2021
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Theodore E WarkentinDepartment of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada; Department of Medicine, McMaster University, Hamilton, Ontario, Canada; Hamilton Regional Laboratory Medicine Program (Transfusion Medicine), Hamilton, Ontario, Canada; Service of Clinical Hematology, Hamilton Health Sciences (Hamilton General Hospital), Canada. Electronic address: twarken@mcmaster.ca.
Scott KaatzDivision of Hospital Medicine, Henry Ford Hospital, Detroit, MI, United States of America.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A striking feature of COVID-19 is the high frequency of thrombosis, particularly in patients who require admission to intensive care unit because of respiratory complications (pneumonia/adult respiratory distress syndrome). The spectrum of thrombotic events is wide, including in situ pulmonary thrombosis, deep-vein thrombosis and associated pulmonary embolism, as well as arterial thrombotic events (stroke, myocardial infarction, limb artery thrombosis). Unusual thrombotic events have also been reported, e.g., cerebral venous sinus thrombosis, mesenteric artery and vein thrombosis. Several hematology abnormalities have been observed in COVID-19 patients, including lymphopenia, neutrophilia, thrombocytopenia (usually mild), thrombocytosis, elevated prothrombin time and partial thromboplastin times (the latter abnormality often indicating lupus anticoagulant phenomenon), hyperfibrinogenemia, elevated von Willebrand factor levels, and elevated fibrin d-dimer. Many of these abnormal hematologic parameters-even as early as the time of initial hospital admission-indicate adverse prognosis, including greater frequency of progression to severe respiratory illness and death. Progression to overt disseminated intravascular coagulation in fatal COVID-19 has been reported in some studies, but not observed in others. We compare and contrast COVID-19 hypercoagulability, and associated increased risk of venous and arterial thrombosis, from the perspective of heparin-induced thrombocytopenia (HIT), including the dilemma of providing thromboprophylaxis and treatment recommendations when available data are limited to observational studies. The frequent use of heparin-both low-molecular-weight and unfractionated-in preventing and treating COVID-19 thrombosis, means that vigilance for HIT occurrence is required in this patient population.

Indexed as

SARS-CoV-2COVID-19Disseminated Intravascular CoagulationHeparinHumansThrombocytopeniaThrombophiliaThrombosisHeparinCOVID-19Disseminated intravascular coagulationHeparinThrombocytopeniaThrombosis

Identifiers

PMID32841919
PMCPMC7416717

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.