COVID-19 versus HIT hypercoagulability

Warkentin, Theodore E.; Kaatz, Scott

doi:10.1016/j.thromres.2020.08.017

Cited by 47 publications

(64 citation statements)

References 129 publications

(230 reference statements)

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“…This may be attributed to the increased exposure to heparin based thromboprophylaxis, increased hospital length of stay, and the hyperin ammation and heightened immune response in COVID-19 patients. 14,22,23 Diagnosing HIT is complex and requires 4Ts score calculation, EIA testing, and functional assay testing like SRA. 18 Our data, supported by the literature analysis, showed that 4Ts score was not predictive of either EIA + or patient mortality.…”

Section: Discussionmentioning

confidence: 99%

“…11,12 Many COVID-19 patients have prolonged hospital stays leading to extended duration of heparin exposure, which increases risk for heparin induced thrombocytopenia (HIT). 13,14 HIT occurs when IgG antibodies form against platelet factor 4-Heparin complex, resulting in platelet activation, subsequently leading to a prothrombotic state. 15,16 HIT is suspected when there is a platelet count decrease of more than 50% after 5-10 days of heparin exposure, along with evidence of hypercoagulability.…”

Section: Introductionmentioning

confidence: 99%

“…21 Treatment of HIT includes discontinuation of all heparin-based products and transitioning to a therapeutic dose of non-heparin anticoagulation. 14,18 This study was performed to analyze incidence, e cacy of testing, and adverse effects such as thrombosis and mortality associated with HIT in COVID-19 patients. and hospitalized at Rush University System for Health Hospitals were included in the study.…”

Section: Introductionmentioning

confidence: 99%

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Heparin Induced Thrombocytopenia in Patients with COVID-19

Warrior

Behrens

Gezer

et al. 2021

Preprint

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Background Acute respiratory and renal failure as well as systemic coagulopathy are critical aspects of the morbidity and mortality in patients with COVID-19. Heparin Induced Thrombocytopenia (HIT) occurs when IgG antibodies form against platelet factor 4-Heparin complex, resulting in platelet activation and removal, leading to a prothrombotic state. Studies have shown that only 6% who are investigated serologically for HIT actually have the diagnosis. Methods A retrospective analysis was performed on all COVID-19 positive patients hospitalized between March and June 2020. Patients with suspicion for HIT were tested for HIT antibodies with IgG-specific platelet factor 4(PF4)-dependent enzyme immunoassay (EIA). Confirmatory testing with serotonin release assay (SRA) and heparin-induced platelet aggregation were used in cases with intermediate or low optical density (OD) with EIA positivity (EIA+). Due to rarity of disease, a through literature review on HIT in COVID-19 patients was also analyzed. Results Incidence of EIA + in COVID-19 patients was 0.6%, significantly higher than in the general population 0.2% (p < 0.0001). The incidence of thromboembolic events in EIA + patients was 87.5%, significantly higher than the rate of 10.90% in all COVID-19 patients (p < 0.0001). The mortality rate in EIA + patients was 50%, significantly greater than the mortality rate of 12% in all hospitalized COVID-19 patients (p = 0.0011). Serological confirmation of HIT diagnosis was 37.5% which is significantly higher than confirmation of HIT in nonCOVID-19 patients 6% (p < 0.0001). Of 39 HIT antibody positive patients in the literature, 23.07% had positive confirmatory testing (6 SRA, 3 HIPAA) which is significantly higher than 5.6% in the general population (p = 0.00001). The incidence of thrombosis in EIA + COVID-19 patients in the literature was 56.4% which is significantly higher than reported rates of thrombotic events in in all COVID-19 patients in the literature at 4.8%1 (p = 0.00001). Conclusion Our study indicates incidence of HIT is higher in the COVID-19 population. This can be attributed to the cytokine storm and severe sepsis seen in critically ill COVID-19 patients. Our study also suggests that development of HIT can contribute to increased risk for thromboembolic events as well as mortality of COVID-19 patients, however, our study is limited due to small sample size.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Heparin Induced Thrombocytopenia in Patients with COVID-19

Warrior

Behrens

Gezer

et al. 2021

Preprint

View full text Add to dashboard Cite

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“…127,135,136 Some patients may suddenly deteriorate as a consequence of thromboembolism of large blood vessels, including pulmonary embolism. 137 In this setting, some robust, though preliminary, evidence indicates that low molecular weight heparin helps to prevent and treat this hypercoagulation syndrome. 138 To counter the systemic inflammation cascade before it causes multiorgan failure and death, therapy hinges on the use of immunomodulatory agents.…”

Section: Clinical Findings and Outcomes Of Covid-19mentioning

confidence: 99%

Coronavirus 2019 Infectious Disease Epidemic: Where We Are, What Can Be Done and Hope For

Carbone

Lednicky²,

Xiao

et al. 2021

Journal of Thoracic Oncology

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spreads mainly by means of aerosols (microdroplets) in enclosed environments, especially those in which temperature and humidity are regulated by means of airconditioning. About 30% of individuals infected with SARS-CoV-2 develop coronavirus disease 2019 (COVID-19) disease. Among them, approximately 25% require hospitalization. In medicine, cases are identified as those who become ill. During this pandemic, cases have been identified as those with a positive SARS-CoV-2 polymerase chain reaction test, including approximately 70% who were asymptomatic-this has caused unnecessary anxiety. Individuals more than 65 years old, those affected by obesity, diabetes, asthma, or are immune-depressed owing to cancer and other conditions, are at a higher risk of hospitalization and of dying of COVID-19. Healthy individuals younger than 40 years very rarely die of COVID-19. Estimates of the COVID-19 mortality rate vary because the definition of COVID-19-related deaths varies. Belgium has the highest death rate at 154.9 per 100,000 persons, because it includes anyone who died with symptoms compatible with COVID-19, even those never tested for SARS-CoV-2. The United States includes all patients who died with a positive test, whether they died because of, or with, SARS-CoV-2. Countries that include only patients in which COVID-19 was the main cause of death, rather than a cofactor, have lower death rates. Numerous therapies are being developed, and rapid improvements are anticipated. Because of disinformation, only approximately 50% of the U.S. population plans to receive a COVID-19 vaccine. By sharing accurate information, physicians, health professionals, and scientists play a key role in addressing myths and anxiety, help public health officials enact measures to decrease infections, and provide the best care for those who become sick. In this article, we discuss these issues.

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“…One of the explanations is the hypercoagulation state, due to rises in interleukin-6 (IL-6) and C reactive protein (CRP) levels [7]. Evidence of coagulation abnormalities has been observed in some patients with COVID-19, including thrombocytosis, hyperfibrinogenemia, elevated prothrombin time (PT) and partial thromboplastin time (PTT), elevated fibrin D-dimer, and elevated von Willebrand factor levels [8]. Cardiac and peripheral arteries, as well as cerebral arteries, are at risk for thrombosis.…”

Section: Introductionmentioning

confidence: 99%

Cerebral Sinus Thrombosis Secondary to SARS-CoV-2 Infection

Khazaei

Karimi

Sedighi

et al. 2021

Case Reports in Neurological Medicine

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Coronavirus disease-19 (COVID‐19) is a novel infectious disease and every day we are learning more about its various clinical features and complications. Different studies during the pandemic have shown various neurological manifestations secondary to the infection such as stroke due to cerebral vessel thrombosis. Herein, we presented a 57-year-old man admitted to our hospital with gradual headache, seizure, and decreasing level of consciousness. Three weeks earlier, he was diagnosed with COVID-19 and mild to moderate respiratory problems. Decreased level of consciousness made physicians intubate the patient and initiate mechanical ventilation in the intensive care unit (ICU). Treatment was initiated with phenytoin. Brain CT scan showed right transverse sinus and cortical vein thrombosis with subarachnoid hemorrhage. He received successful anticoagulant therapy, with further improvement in oxygenation, and discharged with a good general condition. This case is important because several neurological complications of COVID-19 should be noticed and managed by appropriate treatment according to the patient’s condition.

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COVID-19 versus HIT hypercoagulability

Cited by 47 publications

References 129 publications

Heparin Induced Thrombocytopenia in Patients with COVID-19

Heparin Induced Thrombocytopenia in Patients with COVID-19

Coronavirus 2019 Infectious Disease Epidemic: Where We Are, What Can Be Done and Hope For

Cerebral Sinus Thrombosis Secondary to SARS-CoV-2 Infection

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