Introduction:
WHO received an alert on several new cases of pneumonia of unknown cause in China on December 31, 2019. Chinese authorities identified a novel coronavirus as the cause on January 7, 2020, and it was temporarily named "2019-nCoV." Coronaviruses (CoV) are a large virus family that cause illnesses ranging from the common cold to more serious diseases. A novel coronavirus (nCoV) is a strain of coronavirus that has not previously been identified in humans. The new virus was later called the "COVID-19 virus."
Coronaviruses are a type of virus that causes respiratory illness in humans. The virus is called a "corona" because it has crown-like spikes on its surface. Coronaviruses that cause illness in humans include severe acute respiratory syndrome (SARS), Middle East respiratory syndrome (MERS), and the common cold. SARS-CoV-2, a new coronavirus strain, was first identified in December 2019 in Wuhan, China. Since then, it has spread to every country on the planet. Coronaviruses are frequently discovered in bats, cats, and camels. The viruses live in the animals but do not infect them. These viruses can then spread to other animal species. Viruses may change (mutate) as they spread to new species. The virus can eventually jump between animal species and infect humans. The first people infected with SARS-CoV-19 are thought to have contracted the virus at a food market that sold meat, fish, and live animals.
In terms of disease manifestation, it is clear that some infected people suffer from a potentially fatal severe acute respiratory syndrome, while others suffer from a mild respiratory illness and still others are completely asymptomatic. While respiratory symptoms are the primary symptom of the disease, evidence is emerging that the disease is associated with coagulation dysfunction, which predisposes patients to an increased risk of both venous and arterial thromboembolism (TE) and potentially increased mortality risk. The reported rate of TE in the literature varies. Some studies have reported TE rates ranging from 20 % to 30 %, while others have reported rates ranging from 40 % to 70 %.
The presence of hypercoagulation and thromboembolic complications has been linked to a more severe course of the disease, requiring admission to intensive care units and, potentially, death. However, the relationship between COVID-19's increased thrombotic risk and mortality is not well understood. While some studies discovered a higher risk of mortality in COVID-19 patients with TE, others did not.
With studies reporting varying rates of TE in COVID-19 patients, the overall rate of venous and arterial TE, as well as the extent to which TE in COVID-19 may increase mortality, are unknown. However, the overall rates of COVID-19 TE can be determined and used to suggest a link between TE and mortality among COVID-19 patients.
What Is the Risk of VTE With COVID-19?
COVID-19 patients have a relatively long disease, with a duration ranging from 17 to 25 days. Although the majority of patients have a good prognosis, older patients and those with chronic underlying conditions may fare worse. As of April 17, 2020, the global death rate was approximately 6.6 percent. Complications such as respiratory failure and acute respiratory distress syndrome affect approximately one-third of the worsened patients and up to 41.8 percent (ARDS). They may also suffer from heart failure, secondary bacterial infections, and septic shock.
Patients may require high-flow oxygen, inhalations, vasopressors, mechanical ventilation, and even ECMO (extracorporeal membrane oxygenation) during their illness. To deal with these unique challenges, the complexity of disease in many patients necessitates a large number of highly qualified medical personnel.
How Can VTE Be Diagnosed in COVID Patients?
COVID-19 patients typically have a long course of disease that can last several weeks. Some will require supplemental oxygen, while others will be intubated or treated with vasopressors. Signs, symptoms, and laboratory tests pointing to the diagnosis of VTE can be masked and attributed to COVID-19 or other complications occurring during the lengthy and sometimes complex hospitalization. Most patients have elevated D-dimer levels, which cannot rule out the presence of VTE. As a result, timely diagnosis of VTE is expected to be a significant challenge.
Acute pulmonary embolism (PE), the most dangerous VTE event, has nonspecific clinical signs and symptoms. Some patients are asymptomatic, while others experience dyspnea, chest pain, hemoptysis, presyncope or syncope, and even hemodynamic instability. They may be confused with COVID-19 infection symptoms or complications such as ARDS, pleural effusion, or myocarditis.
Having one or more of the VTE risk factors can provide a clue to the diagnosis that would otherwise go unnoticed. COVID-19 patients may have these factors at the start of their illness or acquire them during their hospitalization: elevated CRP (C-reactive protein), older age, D-dimer, tachypnea, fibrinogen levels, fever, infectious etiology, critical illness, and immobility. When predicting low risk for VTE, risk scores such as the Wells score or the Geneva clinical prediction score may be useful in avoiding unnecessary tests. Hypoxemia, electrocardiogram (ECG) changes indicating right ventricular (RV) strain, sinus tachycardia, or atrial fibrillation may occur, but they are not specific to PE and can be attributed to other COVID-19 complications.
What Is the COVID-19 VTE Prophylaxis?
Patients hospitalized with moderate-to-severe COVID-19 should be carefully screened for VTE. In the absence of contraindications, those found to be at high risk, including those admitted to the intensive care unit should receive pharmacologic VTE prophylaxis with unfractionated heparin (UFH) and low-molecular-weight heparin (LMWH). There is currently insufficient evidence to recommend the routine use of intermediate-dose or fully-therapeutic heparin-based regimens for VTE prevention in high-risk patients, such as those admitted to the ICU. Despite standard-dose thromboprophylaxis, many reports have described breakthrough VTE events in COVID-19 patients. As a result, alternative drug and dosing strategies, such as escalated-dose heparin-based regimens or the use of adjunct antithrombotic agents, must be investigated further.
How Can VTE Be Treated?
COVID-19 VTE prophylaxis without prior anticoagulation indications:
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Pharmacologic prophylaxis with low-molecular-weight heparin or unfractionated heparin in all patients hospitalized for COVID-19.
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Patients with moderate-to-high risk, unless otherwise contraindicated.
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In high-risk patients, consider intermediate-dose or fully-therapeutic anticoagulation. Prospective data collection is encouraged in this area.
Pre-existing anticoagulation management in COVID-19:
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Unless otherwise indicated, continue the previous anticoagulation regimen.
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Consider switching to unfractionated heparin if the patient has renal dysfunction.
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Consider potential drug interactions between anticoagulation and COVID-19 therapies.
VTE treatment in COVID-19:
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Unless otherwise indicated, begin therapeutic anticoagulation.
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When selecting anticoagulants, keep end-organ dysfunction and drug interactions in mind.
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In severe or refractory cases, advanced therapies should be considered.
Conclusion:
VTE is a common problem in hospitalized patients, and it is a preventable cause of death. VTE presents a unique challenge in patients with COVID-19. First, despite the wide range of respiratory entities and causes of hemodynamic deterioration in these patients, such as ARDS, secondary bacterial infection, heart failure, and septic shock, one must suspect the diagnosis. Following that, if the suspicion is high enough, consider initiating full-dose anticoagulation and the risk associated with the diagnostic workup in terms of the risk of contamination and the mobilization of the hemodynamic or respiratory unstable patient out of the ICU.
