Pulmonary arteriovenous malformations (PAVMs) are rare congenital vascular anomalies of the lung in which abnormally dilated vessels provide a direct capillary-free communication between the pulmonary and systemic circulations with three main clinical consequences:(1) pulmonary arterial blood passing through these rightto-left shunts cannot be oxygenated, which may lead to arterial hypoxemia;(2) the absence of normally filtering capillary bed allows thromboembolic material to reach the systemic circulation (paradoxical embolism), which can result in transient ischaemic attack and stroke, while bacterial embolisation has been reported to result in brain abscess;(3) rupture of the thin-walled PAVMs can lead to haemoptysis or haemothorax, particularly during pregnancy when hormonal changes may induce a rapid enlargement of PAVMs.

Churton first described PAVMs in 1897 following the autopsy of a cyanotic boy who suffered from recurrent episodes of haemoptysis [1]. In 1938, Rodes described the association between PAVMs and hereditary haemorrhagic telangiectasia (HHT)[2], which is an autosomal dominant inherited vascular disease. PAVMs are about twice as common in women, with a male-to-female ratio of