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1.
J Cardiothorac Vasc Anesth ; 36(8 Pt B): 2961-2967, 2022 Aug.
Article in English | MEDLINE | ID: covidwho-1795642

ABSTRACT

OBJECTIVES: To compare heparin-based anticoagulation and bivalirudin-based anticoagulation within the context of critically ill patients with a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. DESIGN: An observational study. SETTING: At the intensive care unit of a university hospital. PARTICIPANTS AND INTERVENTIONS: Critically ill patients with a SARS-CoV-2 infection receiving full anticoagulation with heparin or bivalirudin. MEASUREMENTS AND MAIN RESULTS: Twenty-three patients received full anticoagulation with bivalirudin and 60 with heparin. Despite patients in the bivalirudin group having higher mortality risk scores (SAPS II 60 ± 16 v 39 ±7, p < 0.001) and a higher need for extracorporeal support compared to the heparin group, hospital mortality was comparable (57% v 45, p = 0.3). No difference in thromboembolic complications was observed, and bleeding events were more frequent in patients treated with bivalirudin (65% v 40%, p = 0.01). Similar results were confirmed in the subgroup analysis of patients undergoing intravenous anticoagulation; in addition to comparable thrombotic complications occurrence and thrombocytopenia rate, however, no difference in the bleeding rate was observed (65% v 35%, p = 0.08). CONCLUSIONS: Although heparin is the most used anticoagulant in the intensive care setting, bivalirudin-based anticoagulation was safe and effective in a cohort of critically ill patients with SARS-CoV-2. Bivalirudin may be given full consideration as an anticoagulation strategy for critically ill patients with SARS-CoV-2, especially in those with thrombocytopenia and on extracorporeal support.


Subject(s)
COVID-19 , Extracorporeal Membrane Oxygenation , Thrombocytopenia , Anticoagulants , Antithrombins/therapeutic use , COVID-19/complications , Critical Illness/therapy , Extracorporeal Membrane Oxygenation/methods , Fibrinolytic Agents , Hemorrhage/chemically induced , Heparin/adverse effects , Hirudins , Humans , Recombinant Proteins/therapeutic use , Retrospective Studies , SARS-CoV-2 , Thrombocytopenia/chemically induced
4.
Crit Care Med ; 49(9): e870-e873, 2021 09 01.
Article in English | MEDLINE | ID: covidwho-1455369

ABSTRACT

OBJECTIVES: To describe the successful recovery from multiple and life-threatening venous thrombosis after ChAdOx1 nCoV-19 vaccination. DESIGN: Case report. SETTING: University Hospital. PATIENT: Few days after the first dose of the ChAdOx1 nCoV-19 vaccine, a 21-year-old woman experienced massive thrombosis in the deep and superficial cerebral veins together with seizures, neurologic focal deficit, and thrombocytopenia. In the neurointensive care unit, her condition worsened despite early decompressive craniectomy. She developed bilateral segmental pulmonary embolism, left hepatic, and left external iliac venous thrombosis. INTERVENTION: Argatroban (0.5-2.2 µg/kg/min) and high-dose IV immunoglobulin (1 g/kg/d for 2 consecutive days) were initiated on day 6 after admission. With these therapies, there was a gradual resolution of multiple sites of venous thrombosis, and platelet count returned to normal. The patient left the ICU with full consciousness, expressive aphasia, and right hemiparesis. CONCLUSIONS: This case of vaccine-induced immune thrombotic thrombocytopenia shows that a good outcome can be obtained even with multiple and life-threatening venous thrombotic lesions. Argatroban and high-dose IV immunoglobulin along with management of severe cerebral venous thrombosis played a major role in this epilogue.


Subject(s)
Antithrombins/therapeutic use , Arginine/analogs & derivatives , COVID-19 Vaccines/adverse effects , Pipecolic Acids/therapeutic use , Sulfonamides/therapeutic use , Thrombocytopenia/drug therapy , Venous Thrombosis/drug therapy , Arginine/therapeutic use , Cerebral Veins/diagnostic imaging , Drug Therapy, Combination , Female , Fondaparinux/therapeutic use , Humans , Immunoglobulins, Intravenous , Thrombocytopenia/etiology , Tomography, X-Ray Computed , Venous Thrombosis/etiology , Young Adult
8.
Int J Mol Sci ; 22(8)2021 Apr 20.
Article in English | MEDLINE | ID: covidwho-1299445

ABSTRACT

Antithrombin (AT) is a natural anticoagulant that interacts with activated proteases of the coagulation system and with heparan sulfate proteoglycans (HSPG) on the surface of cells. The protein, which is synthesized in the liver, is also essential to confer the effects of therapeutic heparin. However, AT levels drop in systemic inflammatory diseases. The reason for this decline is consumption by the coagulation system but also by immunological processes. Aside from the primarily known anticoagulant effects, AT elicits distinct anti-inflammatory signaling responses. It binds to structures of the glycocalyx (syndecan-4) and further modulates the inflammatory response of endothelial cells and leukocytes by interacting with surface receptors. Additionally, AT exerts direct antimicrobial effects: depending on AT glycosylation it can bind to and perforate bacterial cell walls. Peptide fragments derived from proteolytic degradation of AT exert antibacterial properties. Despite these promising characteristics, therapeutic supplementation in inflammatory conditions has not proven to be effective in randomized control trials. Nevertheless, new insights provided by subgroup analyses and retrospective trials suggest that a recommendation be made to identify the patient population that would benefit most from AT substitution. Recent experiment findings place the role of various AT isoforms in the spotlight. This review provides an overview of new insights into a supposedly well-known molecule.


Subject(s)
Antithrombins/pharmacology , Disease Resistance/drug effects , Disease Susceptibility , Host-Pathogen Interactions , Inflammation/etiology , Inflammation/metabolism , Animals , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Antithrombins/therapeutic use , Biomarkers , Disease Management , Host-Pathogen Interactions/drug effects , Humans , Immunomodulation/drug effects , Inflammation/drug therapy , Inflammation/pathology , Organ Specificity , Signal Transduction/drug effects
9.
Sci Prog ; 104(2): 368504211025927, 2021.
Article in English | MEDLINE | ID: covidwho-1268172

ABSTRACT

With over 600 million coronavirus (COVID-19) vaccine doses administered globally, adverse events are constantly monitored. Recently however, reports of thrombosis and thrombocytopenia following vaccination with the ChAdOx1 nCoV-19 vaccine have emerged. This paper aims to review the available literature and guidelines pertaining to vaccine-induced immune thrombotic thrombocytopenia (VITT) and the proposed guidelines, while offering a potential approach that unifies the available evidence. While the risk of VITT remains extremely low and the benefits outweigh the risks, experimental studies are needed to clarify the pathophysiology behind VITT and possibly decrease the risk of thrombosis and other adverse events occurring. However, treatment should not be delayed in suspected cases, and IV immunoglobulin and non-heparin anticoagulation should be initiated.


Subject(s)
Anticoagulants/therapeutic use , COVID-19 Vaccines/adverse effects , COVID-19/prevention & control , Immunoglobulins, Intravenous/therapeutic use , Purpura, Thrombocytopenic, Idiopathic/drug therapy , Thrombosis/drug therapy , Antithrombins/therapeutic use , Autoantibodies/blood , Biomarkers/blood , COVID-19/epidemiology , COVID-19/immunology , Factor Xa Inhibitors/therapeutic use , Fibrin Fibrinogen Degradation Products/metabolism , Fondaparinux/therapeutic use , Heparin/adverse effects , Humans , Practice Guidelines as Topic , Purpura, Thrombocytopenic, Idiopathic/blood , Purpura, Thrombocytopenic, Idiopathic/chemically induced , Purpura, Thrombocytopenic, Idiopathic/pathology , SARS-CoV-2/immunology , SARS-CoV-2/pathogenicity , Thrombosis/blood , Thrombosis/chemically induced , Thrombosis/pathology
11.
Turk J Haematol ; 38(1): 15-21, 2021 02 25.
Article in English | MEDLINE | ID: covidwho-1045314

ABSTRACT

Objective: The defective interplay between coagulation and inflammation may be the leading cause of intravascular coagulation and organ dysfunction in coronavirus disease-19 (COVID-19) patients. Abnormal coagulation profiles were reported to be associated with poor outcomes. In this study, we assessed the prognostic values of antithrombin (AT) activity levels and the impact of fresh frozen plasma (FFP) treatment on outcome. Materials and Methods: Conventional coagulation parameters as well as AT activity levels and outcomes of 104 consecutive critically ill acute respiratory distress syndrome (ARDS) patients with laboratory-confirmed COVID-19 disease were retrospectively analyzed. Patients with AT activity below 75% were treated with FFP. Maximum AT activity levels achieved in those patients were recorded. Results: AT activity levels at admission were significantly lower in nonsurvivors than survivors (73% vs. 81%). The cutoff level for admission AT activity was 79% and 58% was the lowest AT for survival. The outcome in those patients who had AT activity levels above 75% after FFP treatment was better than that of the nonresponding group. As well as AT, admission values of D-dimer, C-reactive protein, and procalcitonin were coagulation and inflammatory parameters among the mortality risk factors. Conclusion: AT activity could be used as a prognostic marker for survival and organ failure in COVID-19-associated ARDS patients. AT supplementation therapy with FFP in patients with COVID-19-induced hypercoagulopathy may improve thrombosis prophylaxis and thus have an impact on survival.


Subject(s)
Antithrombins/blood , COVID-19/blood , COVID-19/therapy , Critical Illness/mortality , Aged , Aged, 80 and over , Antithrombins/physiology , Antithrombins/therapeutic use , Blood Coagulation Tests/methods , C-Reactive Protein/analysis , COVID-19/diagnosis , COVID-19/mortality , Case-Control Studies , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/prevention & control , Female , Fibrin Fibrinogen Degradation Products/analysis , Humans , Male , Middle Aged , Multiple Organ Failure/etiology , Multiple Organ Failure/prevention & control , Plasma , Procalcitonin/analysis , Prognosis , Retrospective Studies , SARS-CoV-2/genetics , Thrombophilia/complications , Thrombophilia/physiopathology , Turkey/epidemiology
13.
Med Hypotheses ; 146: 110394, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-919589

ABSTRACT

No definitive treatment for COVID-19 exists although promising results have been reported with remdesivir and glucocorticoids. Short of a truly effective preventive or curative vaccine against SARS-CoV-2, it is becoming increasingly clear that multiple pathophysiologic processes seen with COVID-19 as well as SARS-CoV-2 itself should be targeted. Because alpha-1-antitrypsin (AAT) embraces a panoply of biologic activities that may antagonize several pathophysiologic mechanisms induced by SARS-CoV-2, we hypothesize that this naturally occurring molecule is a promising agent to ameliorate COVID-19. We posit at least seven different mechanisms by which AAT may alleviate COVID-19. First, AAT is a serine protease inhibitor (SERPIN) shown to inhibit TMPRSS-2, the host serine protease that cleaves the spike protein of SARS-CoV-2, a necessary preparatory step for the virus to bind its cell surface receptor ACE2 to gain intracellular entry. Second, AAT has anti-viral activity against other RNA viruses HIV and influenza as well as induces autophagy, a known host effector mechanism against MERS-CoV, a related coronavirus that causes the Middle East Respiratory Syndrome. Third, AAT has potent anti-inflammatory properties, in part through inhibiting both nuclear factor-kappa B (NFκB) activation and ADAM17 (also known as tumor necrosis factor-alpha converting enzyme), and thus may dampen the hyper-inflammatory response of COVID-19. Fourth, AAT inhibits neutrophil elastase, a serine protease that helps recruit potentially injurious neutrophils and implicated in acute lung injury. AAT inhibition of ADAM17 also prevents shedding of ACE2 and hence may preserve ACE2 inhibition of bradykinin, reducing the ability of bradykinin to cause a capillary leak in COVID-19. Fifth, AAT inhibits thrombin, and venous thromboembolism and in situ microthrombi and macrothrombi are increasingly implicated in COVID-19. Sixth, AAT inhibition of elastase can antagonize the formation of neutrophil extracellular traps (NETs), a complex extracellular structure comprised of neutrophil-derived DNA, histones, and proteases, and implicated in the immunothrombosis of COVID-19; indeed, AAT has been shown to change the shape and adherence of non-COVID-19-related NETs. Seventh, AAT inhibition of endothelial cell apoptosis may limit the endothelial injury linked to severe COVID-19-associated acute lung injury, multi-organ dysfunction, and pre-eclampsia-like syndrome seen in gravid women. Furthermore, because both NETs formation and the presence of anti-phospholipid antibodies are increased in both COVID-19 and non-COVID pre-eclampsia, it suggests a similar vascular pathogenesis in both disorders. As a final point, AAT has an excellent safety profile when administered to patients with AAT deficiency and is dosed intravenously once weekly but also comes in an inhaled preparation. Thus, AAT is an appealing drug candidate to treat COVID-19 and should be studied.


Subject(s)
COVID-19/drug therapy , Models, Biological , alpha 1-Antitrypsin/therapeutic use , Acute Lung Injury/drug therapy , Anti-Inflammatory Agents/therapeutic use , Antithrombins/therapeutic use , Antiviral Agents/therapeutic use , Apoptosis/drug effects , COVID-19/physiopathology , Extracellular Traps/drug effects , Host Microbial Interactions/drug effects , Host Microbial Interactions/physiology , Humans , Leukocyte Elastase/antagonists & inhibitors , Pandemics , SARS-CoV-2/drug effects , SARS-CoV-2/pathogenicity , SARS-CoV-2/physiology , Serine Endopeptidases/drug effects , Serine Endopeptidases/physiology , Virus Internalization/drug effects , alpha 1-Antitrypsin/administration & dosage
14.
J Cardiovasc Pharmacol ; 76(4): 369-371, 2020 10.
Article in English | MEDLINE | ID: covidwho-835200

ABSTRACT

The use of heparin has been shown to decrease the mortality in hospitalized patients with severe COVID-19. The aim of our study was to evaluate the clinical impact of venous thromboembolism prophylaxis with fondaparinux versus enoxaparin among 100 hospitalized COVID-19 patients. The incidence of pulmonary embolism, deep venous thrombosis, major bleeding (MB), clinically relevant non-MB, acute respiratory distress syndrome, and in-hospital mortality was compared between patients on fondaparinux versus enoxaparin therapy. The 2 groups were homogeneous for demographic, laboratory, and clinical characteristics. In a median follow-up of 28 (IQR: 12-45) days, no statistically significant difference in venous thromboembolism (14.5% vs. 5.3%; P = 0.20), MB and clinically relevant non-MB (3.2% vs. 5.3%, P = 0.76), ARDS (17.7% vs. 15.8%; P = 0.83), and in-hospital mortality (9.7% vs. 10.5%; P = 0.97) has been shown between the enoxaparin group versus the fondaparinux group. Our preliminary results support the hypothesis of a safe and effective use of fondaparinux among patients with COVID-19 hospitalized in internal medicine units.


Subject(s)
Antithrombins/therapeutic use , Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Factor Xa Inhibitors/therapeutic use , Fondaparinux/therapeutic use , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , Venous Thrombosis/etiology , Venous Thrombosis/prevention & control , Aged , Anticoagulants/adverse effects , Anticoagulants/therapeutic use , Antithrombins/adverse effects , COVID-19 , Enoxaparin/adverse effects , Enoxaparin/therapeutic use , Factor Xa Inhibitors/adverse effects , Female , Fondaparinux/adverse effects , Hemorrhage/chemically induced , Hospital Mortality , Humans , Incidence , Male , Middle Aged , Pandemics , Pulmonary Embolism/complications , Retrospective Studies , Venous Thromboembolism/epidemiology , Venous Thromboembolism/prevention & control , Venous Thrombosis/epidemiology
15.
Trials ; 21(1): 769, 2020 Sep 07.
Article in English | MEDLINE | ID: covidwho-748922

ABSTRACT

OBJECTIVES: To assess the effect of anticoagulation with bivalirudin administered intravenously on gas-exchange in patients with COVID-19 and respiratory failure using invasive mechanical ventilation. TRIAL DESIGN: This is a single centre parallel group, superiority, randomized (1:1 allocation ratio) controlled trial. PARTICIPANTS: All patients admitted to the Hamad Medical Corporation -ICU in Qatar for COVID-19 associated respiratory distress and in need of mechanical ventilation are screened for eligibility. INCLUSION CRITERIA: all adult patients admitted to the ICU who test positive for COVID-19 by PCR-test and in need for mechanical ventilation are eligible for inclusion. Upon crossing the limit of D-dimers (1.2 mg/L) these patients are routinely treated with an increased dose of anticoagulant according to our local protocol. This will be the start of randomization. EXCLUSION CRITERIA: pregnancy, allergic to the drug, inherited coagulation abnormalities, no informed consent. INTERVENTION AND COMPARATOR: The intervention group will receive the anticoagulant bivalirudin intravenously with a target aPTT of 45-70 sec for three days while the control group will stay on the standard treatment with low-molecular-weight heparins /unfractionated heparin subcutaneously (see scheme in Additional file 1). All other treatment will be unchanged and left to the attending physicians. MAIN OUTCOMES: As a surrogate parameter for clinical improvement and primary outcome we will use the PaO2/FiO2 (P/F) ratio. RANDOMISATION: After inclusion, the patients will be randomized using a closed envelope method into the conventional treatment group, which uses the standard strategy and the experimental group which receives anticoagulation treatment with bivalirudin using an allocation ratio of 1:1. BLINDING (MASKING): Due to logistical and safety reasons (assessment of aPTT to titrate the study drug) only the data-analyst will be blinded to the groups. NUMBERS TO BE RANDOMISED (SAMPLE SIZE): We performed a sample size calculation and assumed the data for P/F ratio (according to literature) is normally distributed and used the mean which would be: 160 and SD is 80. We expect the treatment will improve this by 30%. In order to reach a power of 80% we would need 44 patients per group (in total 88 patients). Taking approximately 10% of dropout into account we will include 100 patients (50 in each group). TRIAL STATUS: The local registration number is MRC-05-082 with the protocol version number 2. The date of approval is 18th June 2020. Recruitment started on 28th June and is expected to end in November 2020. TRIAL REGISTRATION: The protocol is registered before starting subject recruitment under the title: "Anticoagulation in patients suffering from COVID-19 disease. The ANTI-CO Trial" in ClinicalTrials.org with the registration number: NCT04445935 . Registered on 24 June 2020. FULL PROTOCOL: The full protocol is attached as an additional file, accessible from the Trials website (Additional file 2). In the interest in expediting dissemination of this material, the familiar formatting has been eliminated; this Letter serves as a summary of the key elements of the full protocol.


Subject(s)
Antithrombins/therapeutic use , Coronavirus Infections/drug therapy , Peptide Fragments/therapeutic use , Pneumonia, Viral/drug therapy , Respiration, Artificial , Respiratory Distress Syndrome/therapy , Anticoagulants/therapeutic use , Betacoronavirus , COVID-19 , Coronavirus Infections/blood , Critical Illness , Fibrin Fibrinogen Degradation Products/metabolism , Heparin/therapeutic use , Heparin, Low-Molecular-Weight/therapeutic use , Hirudins , Humans , Pandemics , Partial Thromboplastin Time , Pneumonia, Viral/blood , Qatar , Recombinant Proteins/therapeutic use , SARS-CoV-2
18.
J Emerg Med ; 60(2): 223-225, 2021 02.
Article in English | MEDLINE | ID: covidwho-693267

ABSTRACT

BACKGROUND: Coronavirus disease 2019 (COVID-19) is associated with endothelial inflammation and a hypercoagulable state resulting in both venous and arterial thromboembolic complications. We present a case of COVID-19-associated aortic thrombus in an otherwise healthy patient. CASE REPORT: A 53-year-old woman with no past medical history presented with a 10-day history of dyspnea, fever, and cough. Her pulse oximetry on room air was 84%. She tested positive for severe acute respiratory syndrome coronavirus 2 infection, and chest radiography revealed moderate patchy bilateral airspace opacities. Serology markers for cytokine storm were significantly elevated, with a serum D-dimer level of 8180 ng/mL (normal < 230 ng/mL). Computed tomography of the chest with i.v. contrast was positive for bilateral ground-glass opacities, scattered filling defects within the bilateral segmental and subsegmental pulmonary arteries, and a large thrombus was present at the aortic arch. The patient was admitted to the intensive care unit and successfully treated with unfractionated heparin, alteplase 50 mg, and argatroban 2 µg/kg/min. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Mural aortic thrombus is a rare but serious cause of distal embolism and is typically discovered during an evaluation of cryptogenic arterial embolization to the viscera or extremities. Patients with suspected hypercoagulable states, such as that encountered with COVID-19, should be screened for thromboembolism, and when identified, aggressively anticoagulated.


Subject(s)
COVID-19/complications , Pneumonia, Viral/complications , Pulmonary Embolism/drug therapy , Pulmonary Embolism/etiology , Thrombosis/drug therapy , Thrombosis/etiology , Anticoagulants/therapeutic use , Antithrombins/therapeutic use , Aorta, Thoracic , Arginine/analogs & derivatives , Arginine/therapeutic use , Biomarkers/blood , Female , Heparin/therapeutic use , Humans , Middle Aged , Pipecolic Acids/therapeutic use , Pneumonia, Viral/virology , Pulmonary Embolism/diagnostic imaging , SARS-CoV-2 , Sulfonamides/therapeutic use , Thrombosis/diagnostic imaging
19.
J Cardiothorac Vasc Anesth ; 35(4): 1149-1153, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-650635

ABSTRACT

In its severe manifestation, coronavirus disease 2019 (COVID-19) compromises oxygenation in a manner that is refractory to maximal conventional support and requires escalation to extracorporeal membrane oxygenation (ECMO). Maintaining ECMO support for extended durations requires a delicately balanced anticoagulation strategy to maintain circuit viability by preventing thrombus deposition while avoiding excessive anticoagulation yielding hemorrhage-a task that is complicated in COVID-19 secondary to an inherent hypercoagulable state. Bivalirudin, a member of the direct thrombin inhibitor drug class, offers potential advantages during ECMO, including to its ability to exert its effect by directly attaching to and inhibiting freely circulating and fibrin-bound thrombin. Herein, the successful use of an anticoagulation strategy using the off-label use of a continuous infusion of bivalirudin in a case of severe hypoxemic and hypercarbic respiratory failure caused by COVID-19 requiring venovenous ECMO is reported. Importantly, therapeutic anticoagulation intensity was achieved rapidly with stable pharmacokinetics, and there was no need for any circuit interventions throughout the patient's 27-day ECMO course. In COVID-19, bivalirudin offers a potential option for maintaining systemic anticoagulation during ECMO in a manner that may mitigate the prothrombotic nature of the underlying pathophysiologic state.


Subject(s)
Anticoagulants/administration & dosage , Antithrombins/administration & dosage , COVID-19/diagnosis , COVID-19/therapy , Extracorporeal Membrane Oxygenation/adverse effects , Hirudins/administration & dosage , Peptide Fragments/administration & dosage , Thrombosis/prevention & control , Aged , Anticoagulants/therapeutic use , Antithrombins/therapeutic use , COVID-19/complications , COVID-19 Nucleic Acid Testing , Female , Humans , Peptide Fragments/therapeutic use , Polymerase Chain Reaction , Recombinant Proteins/administration & dosage , Recombinant Proteins/therapeutic use , Respiratory Insufficiency/etiology , Respiratory Insufficiency/therapy , SARS-CoV-2/genetics , SARS-CoV-2/isolation & purification , Treatment Outcome
20.
Paediatr Respir Rev ; 35: 20-24, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-593671

ABSTRACT

Since the initial description in 2019, the novel coronavirus SARS-Cov-2 infection (COVID-19) pandemic has swept the globe. The most severe form of the disease presents with fever and shortness of breath, which rapidly deteriorates to respiratory failure and acute lung injury (ALI). COVID-19 also presents with a severe coagulopathy with a high rate of venous thromboembiolism. In addition, autopsy studies have revealed co-localized thrombosis and inflammation, which is the signature of thromboinflammation, within the pulmonary capillary vasculature. While the majority of published data is on adult patients, there are parallels to pediatric patients. In our experience as a COVID-19 epicenter, children and young adults do develop both the coagulopathy and the ALI of COVID-19. This review will discuss COVID-19 ALI from a hematological perspective with discussion of the distinct aspects of coagulation that are apparent in COVID-19. Current and potential interventions targeting the multiple thromboinflammatory mechanisms will be discussed.


Subject(s)
Acute Lung Injury/blood , Coronavirus Infections/blood , Inflammation/blood , Pneumonia, Viral/blood , Thrombosis/blood , Acute Lung Injury/drug therapy , Acute Lung Injury/immunology , Acute Lung Injury/physiopathology , Anticoagulants/therapeutic use , Antithrombins/therapeutic use , Betacoronavirus , Blood Coagulation Disorders/blood , Blood Coagulation Disorders/immunology , Blood Coagulation Disorders/physiopathology , COVID-19 , Capillaries/immunology , Capillaries/physiopathology , Coronavirus Infections/drug therapy , Coronavirus Infections/immunology , Coronavirus Infections/physiopathology , Endothelium, Vascular/immunology , Endothelium, Vascular/physiopathology , Factor Xa Inhibitors/therapeutic use , Humans , Inflammation/drug therapy , Inflammation/immunology , Inflammation/physiopathology , Pandemics , Platelet Activation , Platelet Aggregation Inhibitors/therapeutic use , Pneumonia, Viral/drug therapy , Pneumonia, Viral/immunology , Pneumonia, Viral/physiopathology , Pulmonary Embolism/blood , Pulmonary Embolism/immunology , Pulmonary Embolism/physiopathology , SARS-CoV-2 , Thrombin/immunology , Thrombin/metabolism , Thrombosis/drug therapy , Thrombosis/immunology , Thrombosis/physiopathology
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