• Critical care
• Factor Xa
• LMWH
• Nadroparin
• Thrombosis

• Humans
• Nadroparin/administration & dosage
• Nadroparin/therapeutic use
• Female
• Male
• Middle Aged
• Retrospective Studies
• Aged
• Dose-Response Relationship, Drug
• Intensive Care Units
• Anticoagulants/administration & dosage
• Anticoagulants/therapeutic use
• Factor Xa Inhibitors/blood
• Venous Thromboembolism/prevention & control
• Venous Thromboembolism/drug therapy
• Critical Illness
• Heparin, Low-Molecular-Weight/administration & dosage
• Adult
• Factor Xa

• VTE
• pneumatic compression
• risk assessment model
• thromboprophylaxis

• Humans
• Male
• Female
• Critical Illness/therapy
• Risk Assessment/methods
• Middle Aged
• Venous Thromboembolism/prevention & control
• Venous Thromboembolism/epidemiology
• Intermittent Pneumatic Compression Devices
• Aged
• Anticoagulants/therapeutic use
• ROC Curve
• Risk Factors

• Anticoagulation
• Chemoprophylaxis
• Traumatic brain injury
• Vte

• Humans
• Brain Injuries, Traumatic/complications
• Brain Injuries, Traumatic/drug therapy
• Anticoagulants/therapeutic use
• Venous Thromboembolism/prevention & control
• Venous Thromboembolism/etiology
• Heparin, Low-Molecular-Weight/therapeutic use
• Risk Factors

• Varicose veins
• caprini score
• deep vein thrombosis
• endovenous radiofrequency ablation
• ultrasound-guided foam sclerotherapy

• Deep vein thrombosis (DVT)
• Major trauma
• Pulmonary Embolus (PE)
• Trauma
• Venous thromboembolism (VTE)

• Humans
• Venous Thromboembolism/epidemiology
• Venous Thromboembolism/prevention & control
• Venous Thromboembolism/etiology
• Risk Factors
• Wounds and Injuries/complications
• Anticoagulants/therapeutic use

• Arterial thrombosis
• COVID-19
• Thromboembolism
• Venous thrombosis

• Aged
• Female
• Humans
• Male
• COVID-19/epidemiology
• COVID-19/complications
• COVID-19/mortality
• Hospital Mortality/trends
• Incidence
• Inpatients/statistics & numerical data
• Retrospective Studies
• Risk Factors
• SARS-CoV-2
• Thrombosis/epidemiology
• United States/epidemiology
• Venous Thromboembolism/epidemiology
• Venous Thromboembolism/etiology
• Venous Thrombosis/epidemiology

• Bioinformatics analysis
• COVID-19
• Pathogenic mechanisms
• VTE

• Humans
• COVID-19/genetics
• Venous Thromboembolism/genetics
• Computational Biology/methods
• Gene Regulatory Networks
• Protein Interaction Maps/genetics
• SARS-CoV-2/genetics
• MicroRNAs/genetics
• Signal Transduction/genetics
• Transcription Factors/genetics
• Transcription Factors/metabolism
• Gene Expression Profiling
• Transcriptome/genetics

• ERAS
• Enhanced recovery
• compliance
• multi‐institutional
• predictive
• regression

• Humans
• Enhanced Recovery After Surgery
• Postoperative Complications/epidemiology
• Postoperative Complications/etiology
• Perioperative Care/methods
• Cystectomy/adverse effects
• Cystectomy/methods
• Length of Stay
• Retrospective Studies

• Deep vein Thrombosis
• In-hospital Thrombosis
• Pulmonary thromboembolism
• Thromboprophylaxis
• Thromboprophylaxis failure

• Incidence
• Intensive care unit
• Mortality
• Predictors
• Surgical

• Humans
• Ethiopia/epidemiology
• Anticoagulants
• Follow-Up Studies
• Retrospective Studies
• Venous Thromboembolism
• Intensive Care Units
• Hypoxia
• Critical Care

• bleeding
• cost analyses
• enoxaparin
• medical inpatients
• obesity
• thromboprophylaxis
• unfractionated heparin
• venous thromboembolism (VTE)

• COVID-19
• bleeding
• thromboprophylaxis
• thrombosis

• VTE chemoprophylaxis
• VTE prophylaxis
• enoxaparin
• trauma
• venous thromboembolism

• Humans
• Anticoagulants/therapeutic use
• Venous Thromboembolism/prevention & control
• Venous Thromboembolism/drug therapy
• Palliative Care
• Critical Care

• Acute pulmonary embolism
• Deep vein thrombosis
• Guidelines
• Intensive care unit mortality

The coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was declared as pandemic by World Health Organization (WHO) in March 2020. The outbreak has caused 5,232,562 deaths worldwide until December 3rd, 2021. Though primarily affecting the respiratory system, involvement of other organ systems have been reported in severe disease. Venous thromboembolism (VTE) has been recognized as an important complication. Previous studies have reported the prevalence of VTE in intensive care unit (ICU) patients between 7 and 85% and in non-ICU patients between 0 and 19%. COVID-19 patients that are at high risk for VTE are also at increased risk for bleeding. In such cases, anticoagulation may potentially be harmful. Thereby, it is important to understand the risk factors for VTE predisposition in the COVID-19 patients, timing of VTE, and the rate of occurrence of VTE in hospitalized patients post-discharge. Comparison of the rate of occurrence of VTE in COVID-19 patients with the non-COVID-19 patients with similar disease severity is required to truly interpret the reportedly high rates of VTE in COVID-19 patients. Several pathophysiological mechanisms have been reported for the development of VTE in COVID-19. Autopsy-based studies have contributed to the existing knowledge. d-dimer, presently, seems to be the most suitable investigation for risk-identification of VTE supported by Doppler studies and overall clinical context. Further, prospective studies and clinical trials are essentially required to fill the gaps in evidence for occurrence, risk prediction and management of VTE in COVID-19 patients.

• COVID-19
• Coronavirus
• Epidemiology
• Thrombosis
• Venous thromboembolism
• d-dimer

Anti-factor Xa activity has been suggested as a surrogate parameter for judging the effectiveness of pharmacological thromboprophylaxis with low molecular weight heparins in critically ill patients. However, this practice is not supported by evidence associating low anti-factor Xa activity with venous thromboembolism.

We performed a retrospective observational study including 1,352 critically ill patients admitted to 6 intensive care units of the Medical University of Vienna, Austria between 01/2015 and 12/2018. Included patients received prophylactically dosed enoxaparin (≤100 IU/kg body weight per day). We analyzed median peak, 12-h trough and 24-h trough anti-factor Xa activity per patient and compared anti-factor Xa activity between patients without vs. with venous thromboembolic events.

19 patients (1.4%) developed a total of 22 venous thromboembolic events. We did not observe a difference of median (IQR) anti-factor Xa activity between patients without venous thromboembolism [peak 0.22 IU/mL (0.14–0.32); 12-h trough 0.1 IU/mL (<0.1–0.17), 24-h trough < 0.1 IU/mL (<0.1– <0.1)] vs. patients with venous thromboembolism [peak 0.33 IU/mL (0.14–0.34); 12-h trough 0.12 IU/mL (<0.1–0.26); 24-h trough < 0.1 IU/mL (<0.1–<0.1)].

Patients who developed venous thromboembolism had anti-factor Xa activities comparable to those who did not suffer from venous thromboembolism.

• Ascorbic acid
• Heparin
• MATH plus
• Methylprednisolone
• Thiamine

Venous thromboembolism (VTE) in patients with COVID-19 in intensive care units (ICU) is frequent, but risk factors (RF) remain unidentified. In this meta-analysis (CRD42020188764) we searched for observational studies from ICUs reporting the association between VTE and RF in Medline/Embase up to 15 April 2021. Reviewers independently extracted data in duplicate and assessed the certainty of the evidence using the GRADE approach. Analyses were conducted using the random-effects model and produced a non-adjusted odds ratio (OR). We analysed 83 RF from 21 studies (5296 patients). We found moderate-certainty evidence for an association between VTE and the D-dimer peak (OR 5.83, 95%CI 3.18–10.70), and length of hospitalization (OR 7.09, 95%CI 3.41–14.73) and intubation (OR 2.61, 95%CI 1.94–3.51). We identified low-certainty evidence for an association between VTE and CRP (OR 1.83, 95% CI 1.32–2.53), D-dimer (OR 4.58, 95% CI 2.52–8.50), troponin T (OR 8.64, 95% CI 3.25–22.97), and the requirement for inotropic drugs (OR 1.67, 95% CI 1.15–2.43). Traditional VTE RF (i.e., history of cancer, previous VTE events, obesity) were not found to be associated to VTE in COVID-19. Anticoagulation was not associated with a decreased VTE risk. VTE RF in severe COVID-19 correspond to individual illness severity, and inflammatory and coagulation parameters.

• COVID-19
• critical care
• meta-analysis
• risk factors
• venous thromboembolism

Introduction: Thrombosis and bleeding are recognized complications of the novel coronavirus infection (COVID-19), with a higher incidence described particularly in the critically ill. Methods: A retrospective review of COVID-19 patients admitted to our intensive care units (ICU) between 1 January 2020 and 31 December 2020 was performed. Primary outcomes included clinically significant thrombotic and bleeding events (according to the ISTH definition) in the ICU. Secondary outcomes included mortality vis-a-vis the type of anticoagulation. Results: The cohort included 144 consecutive COVID-19 patients with a median age of 64 years (IQR 54.5–75). The majority were male (85 (59.0%)) and Caucasian (90 (62.5%)) with a median BMI of 30.5 kg/m² (IQR 25.7–36.1). The median APACHE score at admission to the ICU was 12.5 (IQR 9.5–22). The coagulation parameters at admission were a d-dimer level of 109.2 mg/mL, a platelet count of 217.5 k/mcl, and an INR of 1.4. The anticoagulation strategy at admission included prophylactic anticoagulation for 97 (67.4%) patients and therapeutic anticoagulation for 35 (24.3%) patients, while 12 (8.3%) patients received no anticoagulation. A total of 29 patients (20.1%) suffered from thrombotic or major bleeding complications. These included 17 thrombus events (11.8%)—8 while on prophylactic anticoagulation (7 regular dose and 1 intermediate dose) and 9 while on therapeutic anticoagulation (p-value = 0.02)—and 19 major bleeding events (13.2%) (4 on no anticoagulation, 7 on prophylactic (6 regular dose and 1 intermediate dose), and 8 on therapeutic anticoagulation (p-value = 0.02)). A higher thrombosis risk among patients who received remdesivir (18.8% vs. 5.3% (p-value = 0.01)) and convalescent serum (17.3% vs. 5.8% (p-value = 0.03%)) was noted, but no association with baseline characteristics (age, sex, race, comorbidity), coagulation parameters, or treatments (steroids, mechanical ventilation) could be identified. There were 10 pulmonary embolism cases (6.9%). A total of 99 (68.8%) patients were intubated, and 66 patients (45.8%) died. Mortality was higher, but not statistically significant, in patients with thrombotic or bleeding complications—58.6% vs. 42.6% (p-value = 0.12)—and higher in the bleeding (21.2%) vs. thrombus group (12.1%), p-value = 0.06. It did not significantly differ according to the type of anticoagulation used or the coagulation parameters. Conclusions: This study describes a high incidence of thrombotic and bleeding complications among critically ill COVID-19 patients. The findings of thrombotic events in patients on anticoagulation and major bleeding events in patients on no or prophylactic anticoagulation pose a challenging clinical dilemma in the issue of anticoagulation for COVID-19 patients. The questions raised by this study and previous literature on this subject demonstrate that the role of anticoagulation in COVID-19 patients is worthy of further investigation.

• COVID19
• ICU
• SARS-CoV-2
• bleeding mortality
• thrombosis

• COVID-19
• SARS-CoV-2
• coagulopathy
• coronavirus
• thromboembolism

• Anticoagulants/therapeutic use
• Blood Coagulation Disorders/drug therapy
• Blood Coagulation Disorders/etiology
• Blood Platelets/cytology
• Blood Platelets/metabolism
• COVID-19/complications
• COVID-19/pathology
• COVID-19/virology
• Heparin, Low-Molecular-Weight/therapeutic use
• Humans
• Inflammation/etiology
• SARS-CoV-2/isolation & purification
• Thromboembolism/drug therapy
• Thromboembolism/etiology

• unfractionated heparin
• venous thromboembolism prophylaxis

• COVID-19
• anticoagulation
• coagulopathy
• immunomodulatory
• immunothrombosis

• Animals
• Blood Coagulation
• COVID-19/blood
• COVID-19/complications
• COVID-19/immunology
• COVID-19/therapy
• Disease Management
• Humans
• Immunogenic Cell Death
• Inflammation/blood
• Inflammation/etiology
• Inflammation/immunology
• Inflammation/therapy
• SARS-CoV-2/immunology
• Thrombosis/blood
• Thrombosis/etiology
• Thrombosis/immunology
• Thrombosis/therapy

• PG/16/65/32313 British Heart Foundation

• anti-Xa activity
• anticoagulation monitoring
• intensive care unit
• venous thromboembolism

In December 2019, a disease attributed to a new severe acute respiratory syndrome coronavirus 2, and named coronavirus disease 2019 (COVID-19), broke out in Wuhan, China and has spread rapidly throughout the world. CT has been advocated in selected indications as a tool toward rapid and early diagnosis. The CT patterns of COVID-19 include ground glass opacities GGO, consolidation, and crazy paving. Additional signs include a “rounded morphology” of lesions, vascular enlargement sign, nodules, and fibrous stripe. Signs of healing and organization include subpleural bands, a reticular pattern, reversed halo sign and traction bronchiectasis. Cavitation and tree in bud signs are absent and pleural effusions are rare. There is a high incidence of pulmonary embolism associated with COVID-19. CT findings in COVID-19 appear to follow a predictable timeline with maximal involvement approximately 6–11 days after symptom onset. The stages of evolution include early stage (days 0–4) with GGO being the predominant abnormality, progressive stage (days 5–8) with increasing crazy paving; and peak stage (days 9–13) with predominance of consolidation and absorption phase (after day 14) with gradual absorption of consolidation with residual GGO and subpleural bands. CT findings in COVID-19 have a high sensitivity and low specificity, determined to be 98% and 25% in a retrospective study of 1014 patients. The low specificity of CT for the diagnosis of COVID-19 pneumonia is due to the overlap of CT findings with other viral pneumonias and other infections, lung involvement in connective tissue disorders, drug reaction, pulmonary edema, and hemorrhage.

• Consolidation
• Crazy paving
• Ground glass opacities
• Rounded consolidation
• Vascular enlargement sign

Purpose: Severe COVID-19 is associated with inflammation, thromboembolic disease, and high mortality. We studied factors associated with fatal outcomes in consecutive COVID-19 patients examined by computed tomography pulmonary angiogram (CTPA).

Methods: This retrospective, single-center cohort analysis included 130 PCR-positive patients hospitalized for COVID-19 [35 women and 95 men, median age 57 years (interquartile range 51–64)] with suspected pulmonary embolism based on clinical suspicion. The presence and extent of embolism and parenchymal abnormalities on CTPA were recorded. The severity of pulmonary parenchymal involvement was stratified by two experienced radiologists into two groups: lesions affecting ≤50% or >50% of the parenchyma. Patient characteristics, radiological aspects, laboratory parameters, and 60-day mortality data were collected.

Results: Pulmonary embolism was present in 26% of the patients. Most emboli were small and peripheral. Patients with widespread parenchymal abnormalities, with or without pulmonary embolism, had increased main pulmonary artery diameter (p < 0.05) and higher C-reactive protein (p < 0.01), D-dimer (p < 0.01), and troponin T (p < 0.001) and lower hemoglobin (p < 0.001). A wider main pulmonary artery diameter correlated positively with C-reactive protein (r = 0.28, p = 0.001, and n = 130) and procalcitonin. In a multivariant analysis, D-dimer >7.2 mg/L [odds ratio (±95% confidence interval) 4.1 (1.4–12.0)] and ICU stay were significantly associated with embolism (p < 0.001). The highest 60-day mortality was found in patients with widespread parenchymal abnormalities combined with pulmonary embolism (36%), followed by patients with widespread parenchymal abnormalities without pulmonary embolism (26%). In multivariate analysis, high troponin T, D-dimer, and plasma creatinine and widespread parenchymal abnormalities on CT were associated with 60-day mortality.

Conclusions: Pulmonary embolism combined with widespread parenchymal abnormalities contributed to mortality risk in COVID-19. Elevated C-reactive protein, D-dimer, troponin-T, P-creatinine, and enlarged pulmonary artery were associated with a worse outcome and may mirror a more severe systemic disease. A liberal approach to radiological investigation should be recommended at clinical deterioration, when the situation allows it. Computed tomography imaging, even without intravenous contrast to assess the severity of pulmonary infiltrates, are of value to predict outcome in COVID-19. Better radiological techniques with higher resolution could potentially improve the detection of microthromboses. This could influence anticoagulant treatment strategies, preventing clinical detoriation.

• C-reactive protein
• computed tomography
• critical care
• mortality
• pulmonary thromboembolism
• pulmonary trunk

• COVID-19
• Clinical features
• Liver injury
• Potential mechanism
• Treatment

• COVID-19/complications
• China/epidemiology
• Humans
• Liver Diseases/virology
• SARS-CoV-2

COVID-19 is associated with a high incidence of thrombotic complications, which can be explained by the complex and unique interplay between coronaviruses and endothelial cells, the local and systemic inflammatory response, and the coagulation system. Empirically, an intensified dose of thrombosis prophylaxis is being used in patients admitted to hospital with COVID-19 and several guidelines on this topic have been published, although the insufficiency of high quality and direct evidence has led to weak recommendations. In this Viewpoint we summarise the pathophysiology of COVID-19 coagulopathy in the context of patients who are ambulant, admitted to hospital, and critically ill or non-critically ill, and those post-discharge from hospital. We also review data from randomised controlled trials in the past year of antithrombotic therapy in patients who are critically ill. These data provide the first high-quality evidence on optimal use of antithrombotic therapy in patients with COVID-19. Pharmacological thromboprophylaxis is not routinely recommended for patients who are ambulant and post-discharge. A first ever trial in non-critically ill patients who were admitted to hospital has shown that a therapeutic dose of low-molecular-weight heparin might improve clinical outcomes in this population. In critically ill patients, this same treatment does not improve outcomes and prophylactic dose anticoagulant thromboprophylaxis is recommended. In the upcoming months we expect numerous data from the ongoing antithrombotic COVID-19 studies to guide clinicians at different stages of the disease.

• Acute Disease
• COVID-19/complications
• COVID-19/epidemiology
• COVID-19/ethnology
• COVID-19/therapy
• Cardiovascular Diseases/epidemiology
• Cardiovascular Diseases/therapy
• Humans
• Patient Advocacy
• SARS-CoV-2
• Syndrome
• Systemic Inflammatory Response Syndrome/epidemiology
• Systemic Inflammatory Response Syndrome/therapy
• Venous Thromboembolism/epidemiology
• Venous Thromboembolism/prevention & control

• PR181960 U.S. Department of Defense (United States Department of Defense)
• K23 DK111847 NIDDK NIH HHS
• U01 DK116066 NIDDK NIH HHS
• R03 HL146881 NHLBI NIH HHS
• R01-DK114893 U.S. Department of Health & Human Services | National Institutes of Health (NIH)
• T32 HL007854 NHLBI NIH HHS
• R01 DK114893 NIDDK NIH HHS
• P30 DK063608 NIDDK NIH HHS
• 5T32 NS007153 U.S. Department of Health & Human Services | National Institutes of Health (NIH)
• T32 NS007153 NINDS NIH HHS
• U01-DK116066 U.S. Department of Health & Human Services | National Institutes of Health (NIH)
• P30 AG066462 NIA NIH HHS
• R01 MD014161 NIMHD NIH HHS
• R01 DK064819 NIDDK NIH HHS
• R01 HL152236 NHLBI NIH HHS
• K08 HL122526 NHLBI NIH HHS
• 2032726 National Science Foundation (NSF)
• R01-MD014161 U.S. Department of Health & Human Services | National Institutes of Health (NIH)

Anticoagulant drugs have been used to prevent and treat thrombosis. However, they are associated with risk of hemorrhage. Therefore, prior to their clinical use, it is important to assess the risk of bleeding and thrombosis. In case of older anticoagulant drugs like heparin and warfarin, dose adjustment is required owing to narrow therapeutic ranges. The established monitoring methods for heparin and warfarin are activated partial thromboplastin time (APTT)/anti-Xa assay and prothrombin time – international normalized ratio (PT-INR), respectively. Since 2008, new generation anticoagulant drugs, called direct oral anticoagulants (DOACs), have been widely prescribed to prevent and treat several thromboembolic diseases. Although the use of DOACs without routine monitoring and frequent dose adjustment has been shown to be safe and effective, there may be clinical circumstances in specific patients when measurement of the anticoagulant effects of DOACs is required. Recently, anticoagulation therapy has received attention when treating patients with coronavirus disease 2019 (COVID-19). In this review, we discuss the mechanisms of anticoagulant drugs—heparin, warfarin, and DOACs and describe the methods used for the measurement of their effects. In addition, we discuss the latest findings on thrombosis mechanism in patients with COVID-19 with respect to biological chemistry.

• activated partial thromboplastin time
• direct oral anticoagulants
• heparin
• prothrombin time
• warfarin

• Critical illness
• Drug dosing
• Obesity
• Pharmacokinetics

• Adrenal Cortex Hormones/administration & dosage
• Adrenal Cortex Hormones/therapeutic use
• Body Weight/drug effects
• Body Weight/physiology
• Critical Illness/epidemiology
• Critical Illness/therapy
• Dose-Response Relationship, Drug
• Hemodynamics/drug effects
• Humans
• Obesity/complications
• Obesity/physiopathology
• Pre-Exposure Prophylaxis/methods
• Pre-Exposure Prophylaxis/standards
• Vasoconstrictor Agents/administration & dosage
• Vasoconstrictor Agents/therapeutic use

• COVID‐19
• adult health
• novel coronavirus
• stroke

• breathlessness
• lung infection
• respiratory failure
• thrombin

• Ascorbic Acid/therapeutic use
• COVID-19/epidemiology
• Clinical Protocols
• Drug Therapy, Combination
• Heparin/therapeutic use
• Hospitalization
• Humans
• Intensive Care Units/organization & administration
• Methylprednisolone/therapeutic use
• Pneumonia, Viral/drug therapy
• Pneumonia, Viral/epidemiology
• Respiration, Artificial
• SARS-CoV-2
• Thiamine/therapeutic use
• COVID-19 Drug Treatment

• Cohort studies
• Critical care
• Critical illness
• Embolism
• Venous thromboembolism

• Aged
• Anticoagulants/therapeutic use
• Cohort Studies
• Critical Illness/mortality
• Female
• Humans
• Incidence
• Logistic Models
• Male
• Middle Aged
• Prevalence
• Prognosis
• Prospective Studies
• Risk Factors
• Venous Thromboembolism/complications
• Venous Thromboembolism/mortality

• COVID-19
• SARS-COV-2
• deep venous thrombosis
• pulmonary embolism
• thromboembolism

• COVID-19/diagnosis
• COVID-19/epidemiology
• Hospitalization
• Humans
• Incidence
• Intensive Care Units
• Pulmonary Embolism/diagnosis
• Pulmonary Embolism/epidemiology
• Risk Assessment
• Risk Factors

• COVID-19 associated coagulopathy
• COVID-19 pandemic
• Doppler ultrasound
• Four-points compression ultrasound
• Pulmonary embolism
• Venous thromboembolism
• Wells score

• Biomarkers/blood
• COVID-19/diagnosis
• COVID-19/epidemiology
• COVID-19/therapy
• Clinical Decision-Making
• Fibrin Fibrinogen Degradation Products/analysis
• Hospitalization
• Humans
• Incidence
• Predictive Value of Tests
• Risk Factors
• Ultrasonography, Doppler
• Venous Thrombosis/diagnostic imaging
• Venous Thrombosis/epidemiology

Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has led to a worldwide pandemic, and patients with the infection are referred to as having COVID‐19. Although COVID‐19 is commonly considered a respiratory disease, there is clearly a thrombotic potential that was not expected. The pathophysiology of the disease and subsequent coagulopathy produce an inflammatory, hypercoagulable, and hypofibrinolytic state. Several observational studies have demonstrated surprisingly high rates of venous thromboembolism (VTE) in both general ward and intensive care patients with COVID‐19. Many of these observational studies demonstrate high rates of VTE despite patients being on standard, or even higher intensity, pharmacologic VTE prophylaxis. Fibrinolytic therapy has also been used in patients with acute respiratory distress syndrome. Unfortunately, high quality randomized controlled trials are lacking. A literature search was performed to provide the most up‐to‐date information on the pathophysiology, coagulopathy, risk of VTE, and prevention and treatment of VTE in patients with COVID‐19. These topics are reviewed in detail, along with practical issues of anticoagulant selection and duration. Although many international organizations have produced guidelines or consensus statements, they do not all cover the same issues regarding anticoagulant therapy for patients with COVID‐19, and they do not all agree. These statements and the most recent literature are combined into a list of clinical considerations that clinicians can use for the prevention and treatment of VTE in patients with COVID‐19.

• COVID-19
• SARS-CoV-2
• anticoagulation
• thrombosis
• venous thromboembolism

• Anticoagulation
• COVID-19
• Coronavirus 2019
• Critically ill
• Venous thromboembolism

• Aged
• Anticoagulants/administration & dosage
• Anticoagulants/adverse effects
• Betacoronavirus/pathogenicity
• Blood Coagulation/drug effects
• COVID-19
• Coronavirus Infections/blood
• Coronavirus Infections/drug therapy
• Coronavirus Infections/epidemiology
• Coronavirus Infections/virology
• Critical Illness
• Female
• Fibrinolytic Agents/administration & dosage
• Fibrinolytic Agents/adverse effects
• Host-Pathogen Interactions
• Humans
• Male
• Middle Aged
• Pandemics
• Pneumonia, Viral/blood
• Pneumonia, Viral/drug therapy
• Pneumonia, Viral/epidemiology
• Pneumonia, Viral/virology
• Risk Factors
• SARS-CoV-2
• Time Factors
• Treatment Outcome
• Venous Thromboembolism/blood
• Venous Thromboembolism/epidemiology
• Venous Thromboembolism/prevention & control
• Venous Thromboembolism/virology