Paradoxical embolization secondary to acquired veno-venous m
A 53-year-old lady was admitted with an asthma exacerbation requiring intravenous hydrocortisone and aminophylline. She had a background of severe eosinophilic asthma with recurrent admissions for intravenous treatment via a long-standing port-a-cath. Her other medical history included steroid-induced osteopenia, gastro-oesophageal reflux disease, and a Grade 2 patent foramen ovale (PFO), treated with subcutaneous enoxaparin for thromboprophylaxis. The PFO was initially diagnosed on bubble study 4 years prior; however, subsequent imaging had been unable to identify the shunt defect. During admission, she developed left-sided weakness diagnosed as acute ischaemic stroke and was thrombolysed.

Common cardiovascular risk factors for stroke were explored. Electrocardiogram showed normal sinus rhythm as did 24-h Holter monitor and continuous inpatient telemetry. Carotid Doppler examination was normal. Transthoracic echocardiography showed normal biventricular size and function and we were unable to identify the PFO.

A further bubble contrast study demonstrated bubbles appearing in the left atrium and ventricle, prior to arrival to the right atrium, highly suggestive of an extracardiac right-to-left shunt. Subsequent computed tomographic pulmonary angiogram showed complete superior vena cava (SVC) occlusion below the central line with two tortuous veno-venous malformations (VVMs) arising from the dilated azygous vein and SVC communicating directly with the right upper pulmonary vein.

These anomalous connections were thought to be the cause of her stroke via paradoxical embolization. The patient underwent successful percutaneous coil embolization of the VVMs with no obvious residual shunt. During the coil embolization procedure, an attempt was made to identify the suspected PFO, but the operators were unable to visualize any PFO on intraprocedural bubble study nor successfully cross it with a guidewire.

She recovered well from her hemiplegia. She also noticed an improvement in peripheral oxygen saturations following VVM embolization (baseline 94% on room air to 98% post-embolization).

VVMs can occur in patients with congenital heart defects, irrespective of palliative surgical intervention. These malformations can develop due to the increasing venous pressure and in her case, secondary to obstructed systemic veins. VVMs also need to be suspected when one or more of the systemic veins are interrupted, especially in the presence of a prolonged use of central catheters. Diagnosis requires multimodality imaging and treatment is either by intraoperative ligation or, more recently, coil embolization.

Source: https://academic.oup.com/ehjcr/article/5/6/ytab136/6289837
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