Case presentation

A 29-year-old man presented with retrosternal chest pain for five days with associated fatigue, dyspnea on exertion, left upper extremity numbness, and left calf pain. Initial history and physical exam did not reveal any risk factors for venous thromboembolism. Of note, his mother had an ischemic stroke and was discovered to have a PFO. He was tachypneic and had mild tachycardia. His vital signs showed oxygen saturation of 92% on room air, blood pressure of 129/73 mmHg, heart rate of 98 beats per minute, temperature of 36.6°C, and a respiratory rate of 28 breaths per minute. Laboratory testing on admission is presented in hematology (Table 1) and chemistry (Table 2) panels.

Test name | Measured value | Reference range | Units
White blood cell | 8.7 | 4.5-11.0 | × 10³/μL
Hemoglobin | 16.0 | 13.5-17.5 | g/dL
Hematocrit | 46.6 | 41.0-53.0 | %
Platelet | 197 | 146-390 | × 10³/μL

Test name | Measured value | Reference range | Units
Sodium | 138 | 136-144 | mmol/L
Potassium | 4.0 | 3.6-5.1 | mmol/L
Chloride | 104 | 102-110 | mmol/L
Carbon dioxide | 24 | 22-32 | mmol/L
Blood urea nitrogen | 16 | 8-20 | mg/dL
Creatinine | 1.32 | 0.6-1.10 | mg/dL
eGFR | 64 | >60 | mL/min/1.73 m2
Glucose | 145 | 60-99 | mg/dL
Anion gap | 10 | 2-11 | mmol/L
Calcium | 9.8 | 8.7-10.3 | mg/dL
Total protein | 7.3 | 6.4-8.2 | g/dL
Albumin | 4.2 | 3.5-4.8 | g/dL
Total bilirubin | 0.9 | 0.4-2.0 | mg/dL
Alkaline phosphatase | 74 | 38-126 | U/L
AST | 17 | 15-41 | U/L
ALT | 18 | 14-54 | U/L
B-type natriuretic peptide | 80 | <100 | pg/mL
Troponin | 51 | <14 | ng/L
D-Dimer | >10 | <0.50 | µg/mL

Pertinent findings were significantly elevated D-dimer at >10 µg/mL (reference range <0.50 µg/mL), increasing serial serum troponin levels (51, 71, 409, 4,627 ng/L; normal<14 ng/L), and normal B-type natriuretic peptide 80 pg/mL (normal<100 pg/mL). Electrocardiography and chest radiography were nonrevealing. Contrast-enhanced computed tomography angiogram of the chest revealed multiple bilateral acute distal pulmonary emboli, and a saddle PE with findings consistent with right heart strain (Figure 1). Given the right ventricular (RV) injury, as reflected by elevated troponin levels and RV dysfunction on cross-sectional imaging, this patient was evidently in the intermediate-high risk category as per the American Heart Association (AHA) classification of PE. Coronal reconstructed images showed the extent of the clot burden in the pulmonary artery and its subsequent branches. A representative image is shown in Figure 2.

Figure 1: Cross-sectional imaging showing clot burden in the main pulmonary trunk, right and left pulmonary arteries (blue arrows)

Figure 2: Coronal reconstructed imaging partially showing the extent of the single clot within the pulmonary trunk and the right ventricle (blue arrows)

A thrombophilia panel including evaluation for protein C, protein S, factor V Leiden, homocysteine, antithrombin II deficiencies, and anti-cardiolipin/beta-2 glycoprotein antibodies was considered but deferred for a later stage as testing during acute thrombosis and/or while on anticoagulation can distort these results.

The patient was admitted, and initial plans were made for interventional radiology to proceed with CDT. However, these plans were aborted due to the risk for clot fragmentation, paradoxical embolism, and stroke risk when the primary physician performed a bedside echocardiogram revealing a mobile intracardiac, interatrial clot. This was confirmed with a formal echocardiogram demonstrating a large embolus traversing the PFO, extending from the tricuspid valve through the right atrium across the septal defect through the left atrium and the mitral valve (Figure 3).

Figure 3: Apical four-chamber echocardiographic image demonstrating the single clot straddling the bilateral atrioventricular (AV) valves. The clot was mobile across both AV valves (arrows pointing at the free ends in each ventricle)

Systemic anticoagulation was initiated and continued without thrombolysis due to the risk of further clot breakdown and dislodgement. The case was discussed with cardiothoracic surgery as surgical embolectomy was felt to be the only viable option with the least risk of clot fragmentation and stroke risk in a young man. The patient underwent emergent pulmonary embolectomy with simultaneous closure of PFO, intracardiac embolectomy, and pulmonary arteriotomy with thrombectomy, where the clot was removed en bloc with closure of the PFO (Figure 4). A follow-up echocardiogram two days later did not reveal any residual clot; however, it showed persistent RV dysfunction.

Figure 4: Intraoperative image of the clot that was removed

Postoperative hypercoagulable workup was completed, including lupus anticoagulant and factor V Leiden mutation analysis, which was unrevealing. The patient was started on Coumadin and was subsequently discharged home.