Severe systemic inflammatory processes and hypercoagulability with COVID-19 disease increase the risk for atherosclerotic plaque disruption and acute myocardial infarction (AMI). Patients with a previous history of coronary heart disease and / or other underlying comorbidities are particularly prone to heart complications with COVID-19 infection.1 In this installment, we will discuss a patient with COVID-19 and venous thromboembolism.
Presentation of the Case
A 61-year-old woman presented to a rural emergency department with complaints of gradually increasing dyspnea over the past 24 hours and pleuritic chest pain. In the introductory presentation, the patient was hypoxic with an oxygen saturation of 92% with 5 L / min supplemental oxygen through the nasal cannula and showed sinus tachycardia (130–140 beats per minute).
The patient’s COVID-19 polymerase chain reaction (PCR) test was positive. Blood work revealed that D-dimer was 3 times higher than normal (<0.4 mcg / mL), initial troponin within normal limits (0–0.1 ng / mL), hemoglobin 10.7 g / dL , hematocrit 33.1%, and platelet count 172 × 10 / µL.
A large saddle pulmonary emboli (PE) is present on spiral compute tomography (CT) arteriography with intravenous differentiation of the pulmonary arteries. Echocardiogram showed acute cor pulmonale with a right ventricular (RV) to left ventricular (LV) diameter ratio of 1.4. Venous ultrasound revealed a nonocclusive popliteal venous thromboembolism.
The patient was given a full dose of enoxaparin and transferred to an acute care specialist at the cardiac hospital for further treatment. Arriving at the specialist hospital, he was taken to the catheterization laboratory where a right and left pulmonary angiogram was performed with thrombectomy of the right and left pulmonary arteries.
Important Medical History
The patient’s medical history included type 2 diabetes mellitus, hypertension, dyslipidemia, hypothyroidism, and a 60-pack / year history of smoking.
The patient was a middle -aged obese woman who was with severe difficulty breathing. She was short of breath and tachypneic, with a respiratory rate of between 30. Lung examination revealed slow expiratory wheezing bilaterally; a heart -bound satisfaction was noticed.
Electrocardiography (ECG) monitoring may show findings of cor pulmonale (failure of the right side of the heart) identified by a newly incomplete or complete right ventricular ligament, right axis deviation, or right ventricular ischemia with ST-segment depression of right pericardial lead. ECG monitoring can also help evaluate for atrial arrhythmia such as atrial fibrillation commonly found in PE.1
Spiral CT arterography of the chest with variance was ordered to rule out pulmonary embolus, which can cause respiratory symptoms, elevated biomarkers, and a follow-up to COVID-19 infection.3
Ultrasound of the lower extremity (bilaterally) is used to prevent deep vein thrombosis (DVT) of the lower extremity.
The gold standard for confirming a PE is a spiral CT with arteriography. In this case, the test confirmed that there was a widespread saddle pulmonary embolus. Minimal invasive intervention is indicated if the patient is found to have the correct ventricular strain on the echocardiogram (Table 1).
Table 1. Recommended Diagnostic / Laboratory Tests
|Combination: increase in PT / INR, D-dimer, platelet count, fibrinogen|
|Cardiac biomarkers: troponin|
|The cause of the Leiden mutation|
|Modification of the Prothrombin gene|
|Anticardiolipin antibodies (including lupus anticoagulant)|
|Hyperhomocysteinemia (usually due to folate deficiency)1,2|
A radionuclide lung scan, commonly known as a ventilation-perfusion (VQ) scan, can serve as a diagnostic tool for inpatients with elevated bladder indices and unable to undergo various studies. A VQ scan with high clinical suspicion confirms the diagnosis of PE in 40% of cases.1
The Echocardiogram is a useful tool for determining risk assessment. The presence of right ventricular wall akinesis or hypokinesis with apex retention has a high suitability for acute PE. Similarly, in cases of PE, the ratio of right ventricular end-diastolic area (RVEDA) to left ventricular end-diastolic area (LVEDA) exceeded the upper limit of normal, which was 0.6 mm.1
This article originally appeared Clinical Advisor