Discussion

Takayasu arteritis is a vasculitis entity divided into two stages, the generalised inflammatory state and the pulseless stage. During the first stage, patients will complain of systematic symptoms, such as low-grade fever and weakness. Arterial stenosis and aneurysms can be observed during the late stage also called the pulseless or vascular inflammatory stage. ^{Reference de Souza, Machado and Pereria5} Most patients with Takayasu arteritis have stenotic or occlusive changes; aneurysmal degeneration is relatively rare and is related to the destruction of the arterial media during the acute progression phase. Although Takayasu arteritis has been extensively researched among the adult population, ^{Reference Piyachon6} small number of reports has been published regarding its manifestation in children. ^{Reference Mendiola Ramirez, Portillo Rivera, Gralicia Reyes, García Montes, Maldonado Velázquez Mdel and Faugier Fuentes7}

Takayasu arteritis is related to other autoimmune disorders among which are juvenile rheumatoid arthritis, systemic lupus erythematosus, and Crohn’s disease. ^{Reference Opastirakul, Chartapisak and Sirivanichai8} The association of pyoderma gangrenosum and Takayasu arteritis has rarely been reported in the Western literature, but is well known in the Japanese population. ^{Reference Ujiie, Sawarmura, Yokota, Nishie, Shichinohe and Shimizu9} Our patient presented initially with pyoderma gangrenosum and further investigations revealed the diagnosis of Takayasu arteritis. Upper extremity aneurysms are rare and often detected at the time of onset of symptoms. To our knowledge, axillary aneurysm secondary to Takayasu arteritis has been reported only once in the literature. ^{Reference Kim and Roche-Nagle10} Management of Takayasu arteritis varies between steroids and tumour necrosis factor alpha inhibitors depending on the disease’s stage. It is quite possible that our patient improved at first on steroids and infliximab from reduction of the inflammatory process surrounding the axillary aneurysm; nevertheless, this did not prevent later expansion and further brachial plexus compression. Duplex ultrasound was instrumental in confirming the pathology and documenting expansion compared to the previous studies. It showed an irregular shape with thickening of the wall that was severely tender under the probe raising the possibility of a contained rupture (Supplementary Fig S1). Since duplex findings correlated perfectly with the clinical diagnosis, no further imaging was done. There was no need at that point to control the old aortic repair. Although the conventional treatment approach would have been exploration and repair of the axillary artery, in this particular situation, with the subclavian artery being occluded and well collateralised all what was needed was to exclude the pressurised aneurysm sac and stop the leak. Thus, an embolisation procedure without revascularisation was contemplated. After several unsuccessful attempts at percutaneous embolisation, we decided to try the transcutaneous approach. The use of thrombin injections that are commonly done in peripheral pseudo-aneurysms was debated, but decided against since the behaviour of the thrombin in this setting and possible collaterals occlusion could not be predicted.