A middle-aged man was diagnosed with thromboembolic disease just weeks after COVID-19 infection. The disease was more extensive than would have been expected given the patient's risk profile.
A man in his fifties was admitted to a local hospital with pain, pallor, coldness and reduced sensation in both lower extremities. He had had COVID-19 three weeks earlier, with fever, sore throat, chest pain and cough, but no dyspnoea. Following his recovery and quarantine, he had been back at work full-time for a week.
The patient had hypercholesterolaemia, and seven years earlier he had undergone a percutaneous coronary intervention following a myocardial infarction. He had subsequently stopped smoking and had reported no further health issues.
A PCR test on admission was negative for COVID-19 and the patient had no respiratory symptoms. CT angiography showed a filling defect from both popliteal arteries in the knee joint (Figure 1). He also had occlusions distally with localised refilling in the calf arteries, consistent with thrombosis in both lower extremities. The patient was given 5 000 IU dalteparin before being transferred to a regional hospital.
Upon arrival at the regional hospital, the patient had stable respiration and circulation. His lower left extremity was showing signs of acute ischaemia, with pain and reduced sensation, but preserved motor function. The symptoms in his lower right extremity had gradually improved over the course of the day, and the patient now had normal sensation and motor function, but continuing peripheral coldness. An acute bilateral mechanical thromboembolectomy of the popliteal artery and tibiofibular trunk was performed under general anaesthesia. Good circulation was achieved in both lower limbs postoperatively.
A few hours later, however, the patient again reported coldness and pain in his right foot, and no Doppler signal could be detected in the arteries of the foot. The patient was therefore operated on again to clear the arteries in the calf, resulting in the discovery of abundant thrombi.
Postoperatively, all symptoms in the lower extremities improved, but the patient's oxygen saturation was noticeably low with SpO2 of 94.5 % (reference range > 99 %). Blood gas analysis while the patient was receiving 3 L O2 via nasal catheter showed pH 7.47 (7.36−7.44), pCO2 4.5 kPa (4.5−6.1) and pO2 8.9 kPa (> 9.6). CT angiography of the thoracic aorta was performed, which revealed several pulmonary emboli in both lower lobes as well as ground-glass opacities typical of previous COVID-19 pneumonia (Figure 2). In addition, a 7 mm pendulating thrombus was seen in the distal aortic arch (Figure 3). Dalteparin was increased to 10 000 IU × 2, and the patient received non-invasive respiratory support in the intensive care unit.
Echocardiography two days later revealed an apical thrombus 1 cm in diameter. Mild apical hypokinesia was observed, but contractility of the left ventricle was otherwise good. There was no evidence of cardiac arrhythmia or of a previous myocardial infarction. Haematological testing for possible antiphospholipid syndrome (including testing for lupus anticoagulant, anti-cardiolipin antibodies and beta-2 glycoprotein I antibodies) revealed no pathology that could explain the emboli. A normal platelet count was seen, along with slightly elevated fibrinogen at 5.3 g/L (1.9–4) and D-dimer at 14.8 mg/L (< 0.57), as would be expected with thrombosis. It was concluded that treatment with dalteparin 10 000 IU × 2 was sufficient, and that the patient should be followed up by a haematologist and eventually switched to a direct oral anticoagulant or warfarin. Nine days after admission, the patient was discharged in good health and able to walk normally. He was referred to the medical department at his local hospital for further follow up.
The patient has consented to the publication of this article. The article has been peer-reviewed.