ABSTRACT
Bronchial artery embolization (BAE) is a procedure that aims to control bleeding from bronchial arteries in massive and chronic haemoptysis. It is considered to be a life-saving measure in severe life-threatening haemoptysis. Although it is minimally invasive and has a high success rate, it still carries a list of complications. These include post-embolisation syndrome, chest pain, back pain, dysphagia, vascular injury at the site of the embolisation leading to dissection, perforation, pseudoaneurysm and, very rarely, embolic infarction to non-target vessels. Stroke is one of the rare complications post BAE, and it can be severe and fatal. Few cases of stroke post BAE have been reported in the literature, and they were mainly due to posterior cerebral circulation infarction. Here, we report a case of a stroke post BAE due to massive middle cerebral artery (MCA) infarction and to our knowledge it seems to be the first reported case of MCA infarction post BAE. The discussion will cover the possible mechanisms of embolic passage, the outcome of the case including rehabilitation perspectives and the learning points. These will also highlight the importance of early recognition, which can save patients from a disabling stroke in the future. LEARNING POINTS: Bronchial artery embolisation (BAE) carries a high risk of significant complications such as transverse myelitis, bronchial infraction, ischaemic colitis and stroke. While stroke remains one of the rarest complication post BAE, it may be under-reported or unrecognised.Close monitoring in post-BAE patients for any abnormal neurological signs that warrant urgent brain imaging, and early recognition can save patients from a disabling stroke by having the appropriate hyperactive stroke management plan including mechanical thrombectomy.
ABSTRACT
Protein kinase Cζ (PKCζ) is highly expressed in the lung, where it plays several regulating roles in the pathogenesis of acute lung injury (ALI). Proliferation and differentiation of integrin ß4+ distal lung epithelial progenitor cells seem to play a key role in proper lung regeneration. We investigated the effects of a myristoylated PKCζ inhibitor (PKCζi) in a murine model of bleomycin-induced ALI. After intratracheal injury, we treated mice three times a week with PKCζi or its vehicle, DMSO. We found that mice injured with bleomycin and then treated with PKCζi for one week showed decreased activation of PKCζ, improved lung compliance, and decreased lung protein permeability compared to injured mice treated with DMSO. Mice treated continuously with PKCζi for 6 weeks showed reduced evidence of lung fibrosis by computed tomographic images, decreased lung collagen deposition, and decreased active transforming growth factor-ß in the bronchoalveolar lavage fluid. In addition, we found an increased number of lung ß4+ cells compared to DMSO at Week 6. Therefore, we grew isolated integrin ß4+ lung progenitor cells in the presence of PKCζi or DMSO and found that ß4+ cells treated with PKCζi proliferated more in vitro compared to DMSO. We conclude that the use of a PKCζi promotes resolution of lung fibrosis in a bleomycin ALI model and increases the number of ß4+ progenitor cells with regenerative potential in the lung.
