News

The pandemic caused by the Coronavirus in 2020, responsible for approximately 1,235,000 deaths so far, is not the first to affect humanity, being preceded over time by other global infections caused by influenza viruses:

• In 1918 the Influenza A virus (H1N1 strain) caused the Spanish flu, causing about 50 million deaths worldwide;
• In 1957 Influenza A virus (H2N2 strain) the etiological agent of the Asian flu was responsible for 1.5 million deaths;
• In 1968 the Influenza A virus (H3N3 strain) caused the Hong Kong flu epidemic with 1 million deaths:
• In 2009, a new flu epidemic (H1N1 strain) caused 300,000 deaths worldwide.

A brief classification of human coronaviruses and their involvement in the occurrence of pneumonia manifested by fever, cough, fatigue accompanied by dyspnea and hypoxemia includes:

• HCOV 229E discovered in 1966 - mild lung damage;
• HCOV OC43 discovered in 1967 - mild lung damage;
• SARS-CoV discovered in 2003 - severe acute lung damage;
• SARS-CoV-2 discovered in 2019 - severe acute lung damage.

Content

• Thrombotic events and COVID-19
• What are the mechanisms of thrombosis associated with COVID-19
• Laboratory investigations
• The treatment used in COVID-19 coagulopathy

Thrombotic events and COVID-19

In patients infected with the new coronavirus, a close link has been identified between COVID-19 and the frequency of thrombotic episodes, especially in patients who develop severe respiratory complications and require hospitalization in intensive care units.

These thrombotic events are represented by pulmonary thrombosis, deep vein thrombosis (which causes pulmonary embolism) and arterial thrombosis (especially damage to the pulmonary arteries). Depending on their location, thrombi can lead to stroke, acute myocardial infarction, or arterial limb thrombosis, a lower incidence of mesenteric arterial or venous thrombosis and venous thrombosis of the cerebral sinuses.

Wich are the mechanisms of thrombosis associated with COVID-19

Patients diagnosed with SARS-CoV2 have a state of systemic hypercoagulability that favours the appearance of micro and macro embolisms (the formation of a larger or smaller blood clot) that lead to thrombosis.

The virus attaches via the M spike surface protein to ACE2 receptors (angiotensin convertase), an enzyme found mainly in endothelial cells (which line blood vessels) but also in the alveoli of the lungs, hepatocytes, enterocytes, cardiomyocytes or epithelial cells. Damage to vascular endothelial cells by viral invasion causes inflammation in a process called endotheliitis, with a specific blockade of angiotensin convertase and thrombo-inflammation being the main pathophysiological mechanisms involved in the occurrence of thrombotic episodes in COVID-19 positive patients.

Prolonged immobilization, systemic inflammation, platelet aggregation (platelet aggregation), endothelial dysfunction, and blood stasis promote thrombotic complications in patients severely affected by COVID-19 infection and may lead to the development of pulmonary embolism with a poor prognosis.

Although there are currently no screening methods for pulmonary embolism, it has been shown that the occurrence of pulmonary thrombotic microangiopathy in COVID-19 patients is not caused by an episode of deep vein thrombosis, with different pathophysiological mechanisms of occurrence.

Laboratory investigations

From a paraclinical point of view, laboratory tests indicate a series of changes specific to COVID-positive patients:

• The blood count highlights lymphopenia (decrease in the number of lymphocytes) with neutrophils (decrease in the number of polymorphonuclears), mild thrombocytopenia (decrease in the number of platelets);
• Coagulogram indicates hyperfibrinogenemia (increased fibrinogen), prothrombin time and slightly elevated APTT;
• Increase of von Willebrand factor;
• The presence of plasma DD-dimers in large quantity (a marker of thrombotic processes);
• Increased levels of procalcitonin, C-reactive protein, ferritin (pro-inflammatory markers).

Systemic inflammation accompanied by the increase of the plasminogen activator inhibitor PAI similar to sepsis states is frequently found in COVID-19 patients along with the "cytokine storm" (the immune system produces large amounts of cytokines and chemokines with a role in the nonspecific defence of the organism - interferon-gamma, tumour necrosis factor TNF alfa, interleukins, lysozyme, lactoferrin).

Most of the listed haematological abnormalities can be highlighted since the patient's hospitalization and indicate an unfavourable prognosis of the evolution of the disease towards severe acute respiratory syndrome SARS, disseminated intravascular coagulation CID and increased risk of death.

The treatment used in coagulopathy associated with COVID-19

The current therapeutic guidelines emphasize the importance of paraclinical monitoring of confirmed cases by monitoring the markers of inflammation and implementing as quickly as possible a prophylactic antithrombotic treatment with low molecular weight heparin, due to the anti-inflammatory and anticoagulant effect of the compound that can improve the long-term prognosis of COVID-19 patients.

However, there is no optimal treatment for coagulopathy associated with COVID 19, for this purpose being necessary elaborate studies to help to fully understand the pathophysiological mechanisms involved in the appearance of thrombotic phenomena within the disease.

The article was written by Dr. Toni Feodor - Md. General Surgery / Vascular Surgery Specialist