CASE 17483 Published on 27.10.2021

Post-Covid pulmonary artery pseudoaneurysm



Case Type

Clinical Cases


Heena Soni, Annu Sareen, Swati Naik


40 years, male

Area of Interest Cardiovascular system, Pulmonary vessels ; Imaging Technique CT-Angiography
Clinical History

A 40-year-old male who recovered from COVID-19 infection 5 weeks ago presented with complaints of hoarseness and change in voice with multiple episodes of hemoptysis and severe weakness since 2 weeks. Initial workup revealed negative RT-PCR, Hb <7 gm/dl, mild leucocytosis, increased d-dimer, and C reactive proteins. A bronchoscopy was done at some other hospital for the above complaints which revealed left vocal cord palsy and Left lower lobe bronchus mass.

Imaging Findings

HRCT chest done elsewhere during the time that the patient had active COVID-19 infection revealed features of covid pneumonitis evidenced as peripheral and subpleural ground-glass opacities (GGO) in bilateral lung fields without any evidence of vasculitis or any focal area of consolidation (Fig. 1 a,b). An urgent CECT chest was performed in our hospital to look for the cause of hemoptysis which revealed an enhancing lesion with the same attenuation as that of the aorta in the posterobasal segment of the left lower lobe (Fig. 2a) causing mass effect and obstructing the left lower lobe bronchus (Fig. 2b) with surrounding consolidation (Fig. 2a). Further CT Pulmonary Angiography (CTPA) was done which revealed a saccular pseudoaneurysm arising from the posterobasal segment of the left lower lobe pulmonary artery measuring 2.2×2.6cm (Fig. 3a,b,c). Incidental finding of patent ductus arteriosus (PDA) noted (Fig4a) with a small non-occlusive main pulmonary artery thrombus (Fig. 4b).  The patient underwent pulmonary angiogram which confirmed the findings of CTPA (Fig. 5a) and the pseudoaneurysm was successfully stented (Fig. 5b).

An interval CTPA demonstrated the reduced size of pseudoaneurysm with stent in-situ (Fig. 6).


Pulmonary artery pseudoaneurysms (PAPs) are uncommon but potentially lethal. These are defined as the focal dilatation of a segment of the pulmonary artery, involves only the external layers of the arterial wall (the media and adventitia), and thus associated with a higher risk of rupture [1]. PAPs can be congenital or acquired. The common causes of acquired PAPs are trauma, infection, vasculitis, and neoplasm [2]. In the pre-antibiotic era, tuberculosis and syphilis were major causes of PAPs [3].

CTPA is the initial investigation of choice in which a focal dilatation of a branch of the pulmonary artery can be demonstrated with the appropriate timing of intravenous contrast [4].

Research into COVID-19 infection and its systemic effects has demonstrated increased risk of mortality secondary to diffuse alveolar damage and the development of immunothrombi in the vasculature. In addition, COVID-19 infection has been directly linked to inflammatory and vasculitic processes affecting the skin, pulmonary vasculature, and Kawasaki like disease phenomenon [5].

The destruction of the vessel wall in COVID-19 could be explained by the direct insult to the artery by viral infection or through the release of the inflammatory cytokines [6]. COVID-19 infection is known to induce cytokine storm leading to elevated systemic inflammation with high levels of IL-6, IL- 1β, and TNF-α which causes vascular injury including the breakdown of collagen [7]. Furthermore, the ACE2 Receptors are highly expressed in the endothelial cells of the artery [6].

In our case, the patient had no previous history of tuberculosis, joint pains, rash and there was no history of trauma, I.v. drug abuse or evidence of endocarditis. Rheumatology workups were all negative. No bacterial or fungal growth was detected in either his blood or urine culture. Sputum analysis was normal. There was no evidence of overt neoplasm, features of tuberculosis or previous vasculitis on the CT.

We, therefore, postulate that severe inflammation and pulmonary vasculitis secondary to COVID-19 may have contributed to the development of PAP in our case.

The patient was treated for PAP by stenting of the pseudoaneurysm. Intravenous (i/v) and oral antibiotics were given for the secondary obstructive pneumonia.

Our case also showed incidental finding of PDA which appears non-related to COVID-19 infection. A small non-occlusive thrombus in the main pulmonary artery could be likely associated as post covid vascular complication.

To our knowledge, only one case of PAP secondary to COVID-19 infection has been reported in the medical literature. However, there have been case reports of intracerebral aneurysm formation in patients with COVID-19 infections.

Clinical presentation of PAPs varies, ranging from no symptoms to massive life-threatening hemoptysis. Clinicians should therefore recognise PAP as a complication of COVID-19 infection and aim to identify and treat this early. An individualised and judicial approach of anticoagulants should be followed in COVID-19 patients as it may increase the risk of bleeding tendencies especially in case of underlying PAP.

Written informed patient consent for publication has been obtained.

Differential Diagnosis List
Post COVID-19 pulmonary artery pseudoaneurysm with secondary obstructive pneumonia
Mycotic aneurysm
Pulmonary artery aneurysm secondary to Behcet’s disease
Rasmussen aneurysm
Final Diagnosis
Post COVID-19 pulmonary artery pseudoaneurysm with secondary obstructive pneumonia
Case information
DOI: 10.35100/eurorad/case.17483
ISSN: 1563-4086