Abstract
All autopsy studies demonstrated widespread thrombosis and alveolar-capillary microthrombi as the cause of death among patients with COVID-19. The autopsy studies are the gold-standard for diagnostic accuracy and therapeutic strategies for any clinical scenarios. The author initially observed that patients already taking therapeutic dose of oral direct factor Xa inhibitors for an unrelated reason, have significantly better survival rates than those not taking any anticoagulants. This influenced the author to conduct a retrospective chart review of the hospitalized patients in Jackson Hospital (Alabama) to evaluate the effect of variable doses of anticoagulation among COVID-19 patients. The study found that serum inflammatory bio-marker D-dimer trends are associated with changes in oxygen requirement among patients with COVID-19, if patients present at an early stage, and titration of Enoxaparin (anticoagulation) dose based on D-dimer trends leads to increased patient survival.
Highlights
How does the widespread coagulation cascade gets initiated in the case of COVID-19? The COVID-19 infects cells through the upregulation of angiotensin-converting enzyme 2, which is considered to be the functional receptor for COVID-19 cellular entry [1]
The study considered the patients who received traditional treatments with Remdesivir, convalescent plasma, Plaquenil, intravenous steroids, and prophylaxis dose of Enoxaparin as a control group. Those patients who received a variable dose of anticoagulation (Apixaban, Enoxaparin, and Heparin) plus the IV Dexamethasone for treating COVID-19 were considered the treatment group
Kabir investigators found that among noncritically ill patients with Covid-19, an initial strategy of therapeutic dose of anticoagulation with heparin increased the probability of survival to hospital discharge with reduced use of cardiovascular or respiratory organ support as compared with usual-care thromboprophylaxis [8]
Summary
The COVID-19 infects cells through the upregulation of angiotensin-converting enzyme 2, which is considered to be the functional receptor for COVID-19 cellular entry [1]. How does the widespread coagulation cascade gets initiated in the case of COVID-19? This endothelial cell entry may cause microscopic cellular injury, possibly causing the endothelitis needed to initiate the cascade for anticoagulation. Shortness of breath, and chest pain may be due to microthrombi in the heart and lungs capillary bed. Abdominal pain, diarrhea, and ischemic colitis may be due to microthrombi in the intestinal capillary bed. While the ARDS and PE may be due to the alveolar-capillary microthrombi and larger thrombi, stroke, seizures, and loss of sense of smell may be due to microthrombi in the capillary bed of the brain
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