As described more thoroughly in the articles below, Covid-19 generates clot related complications that very frequently and very significantly increase the morbidity and mortality of patients with Heparin administration clinically demonstrating itself as a life saver for many patients. 

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Unfortunately, doctors have been in the dark about in which cases should it be administered.

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Update: Fairly comprehensive data about anticoagulant use in Covid-19 and their respective contraindications and adverse drug reactions are covered on an individual basis in a study here. 

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That is until now. Early publication data from the Cleveland Clinic Journal of Medicine reveals very reliable data about what marker should indicate immediate administration of Heparin to patients.  

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 A critical blood biomarker that indicates that your body is undergoing abnormal clotting events is a measure called D-dimer. Specifically, it means clots, made up critically of fibrin, are forming and breaking down in the body, and D-dimer measures the end product of the breakdown of fibrin. 

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The study asserts that "aggressive" anti-coagulation therapy is needed for all Covid-19 patients.

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However, in patients with "very high D-dimer levels (6 times the upper limit of normal, greater than 3,000 ng/mL) have the greatest risk of thrombosis and may benefit from active screening and more intensive VTE prophylaxis."

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This is absolutely critical because the study noted that other common biological alarm systems for coagulation (like platelet count, fibrinogen, and prothrombins) in the blood were oddly silent even when thrombotic incidents were present in Covid-19 patients. 

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In all Covid-19 patients measured by another study the rate of incidence of either deep-vein thrombosis (DVT), pulmonary embolism, or arterial thrombosis was 31%.

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Cleveland Clinic corroborated this study with a similar 25-30% detection of DVT alone, in addition "slowed venous flow" was common in patients, which is a similarly lethal symptom in terms of its ability to cause oxygen starvation in organ systems. 

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As a result the initial study concluded the following:

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"Heparin anticoagulation seems to be the obvious response to such a hypercoagulable process. In addition to its antithrombotic effect, heparin may have anti-inflammatory, anti-complement, and direct antiviral effects that may be beneficial in COVID-19. Heparin inhibits neutrophil activation, binds inflammatory cytokines, and reduces endothelial activation. Experimental models have also shown that heparin directly binds to SARS-CoV spike-protein1, which acts as the viral anchor site for SARS-CoV–ACE2 interaction, and thereby blocks cell entry."

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It should be made clear that heparin has mainly had substantial validation in mortality improvement only in severe covid-19 cases and as a result the physicians created a protocol for heparin introduction based on patient symptomology, which is copied below.

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"Our current approach is based on POCUS screening for VTE and intensified prophylaxis in high-risk patients (Figure 2, Table 1). We divide patients into 3 categories:

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• Category 1: D-dimer greater than 3,000 ng/mL FEU and no evidence of VTE. Patients in category 1 receive standard DVT prophylaxis and are monitored using serial D-dimer testing.

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• Category 2: D-dimer greater than 3,000 ng/mL FEU, POCUS-negative. Patients in category 2 receive intensified DVT prophylaxis.

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• Category 3: Patients with confirmed thrombosis receive full anticoagulation."

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