Cystic lung destruction distal to pulmonary emboli/immunothrombosis in COVID-19

A 53-year-old male with a heavy smoking history presented following 8 days of feeling generally unwell with fever and worsening dyspnoea. He had oxygen saturations of 90% on 15L of oxygen via a non-rebreather mask. He tested positive for SARS-Cov-2 on RT-PCR, and was intubated and treated with IV steroids and antibiotics on intensive care.

An initial CT pulmonary angiogram on admission revealed features in keeping with severe COVID-19 pneumonitis but no pulmonary emboli. The patient had repeat imaging one week into his admission following a further increase in oxygen requirement and a D-Dimer of >20000, which revealed pulmonary thrombi in the lingular artery and right lower lobe lateral segmental artery (Figure 1(a)). Although there was evidence of worsening COVID-19 pneumonitis, there were no bullae or cysts seen within the lungs (Figure 1(b)). Further high resolution CT 18 days later showed two new, large thin walled, air-filled cysts in the lung segments distal to the pulmonary thrombi demonstrated on the previous images (Figure 2).

Patients with COVID-19 are at increased risk of developing pulmonary thrombosis, with various studies revealing incidences of between 20 and 30% of thrombotic complications in critically ill COVID-19 patients [1,2]. Patients being treated in intensive care already have a high risk of developing pulmonary thrombosis [3], but in addition to this, increased hypercoagulability in patients with COVID-19 can lead to immunothrombosis, which has a different pathophysiological mechanism to conventional pulmonary emboli [4]. Although not yet fully understood, immunothrombosis is a result of increased production of immunologically mediated thrombi that predominantly form within the microvasculature [5].  There is emphasis on prompt initiation of prophylactic dose anticoagulation in order to decrease mortality in patients with severe COVID-19, with an argument for therapeutic anticoagulation for high risk patients [6]. It is not possible to determine whether the thrombi were secondary to pulmonary emboli or immunothrombosis on imaging alone, but nonetheless cystic lung destruction as a sequelae of these events should be an important consideration when imaging patients with COVID-19 due to potential complications such as pneumothorax. Pulmonary infarction is a possible mechanism of cystic lung destruction in this case. Another theory published in a previous case report by Caviezel et al is that the cysts formed as a result of air leak secondary to severe vascular inflammation and focal endolethitis [7].

The patient received treatment dose clexane following confirmation of PEs on CT. Despite treatment with broad spectrum antibiotics, antifungals, pulsed steroids and mechanical ventilation, the patient continued to deteriorate, becoming increasingly hypoxic and acidotic. Unfortunately the patient passed away about 5 weeks after admission. The reversibility of these changes could therefore not be assessed on follow-up imaging.

Learning points:

1. COVID-19 patients being treated in critical care are proven to be at increased risk of not only conventional pulmonary emboli, but also immunothrombosis.
2. The potential for pulmonary emboli/immunothrombosis to lead to cystic lung destruction should be an essential consideration when imaging patients with COVID-19.