Nonaccidental Arterial Cerebral Air Embolism: A Ten-Year Stroke Center Experience

Patient 1: A 77-year-old woman was diagnosed with platypneaorthodeoxia syndrome due to massive patent foramen ovale (PFO). During the control transthoracic echocardiography (showing moderate residual shunt) the day after PFO closure, immediately after the microbubble injection (bubbles produced by injecting 0.5–1.0 ml of ambient air in 10 ml of a mixture of a 0.9% saline/5% glucose solution which is shaken manually for 1 min; residual visible air on top of the solution was evacuated before injection), the patient developed mutism, somnolence and right hemiparesis. The patient improved rapidly with hyperbaric oxygen therapy (HOT) and became asymptomatic 2 days later. Patient 2: A 49-year-old man had a right middle cerebral artery TIA 14 years earlier, attributed to a massive PFO with atrial septal aneurysm. The patient now decided to close the PFO. Thirty seconds after the microbubble injection (for method, see patient 1) during a transthoracic echocardiography to confirm the PFO, the patient presented with bilateral transient visual loss and a left hemisyndrome. HOT was started immediately after hospital arrival and before neuroimaging. After HOT, only a left-sided hyperreflexia was present and the MRI taken 7 h after stroke onset was normal. The PFO was closed 3 weeks later. Patient 3: A 67-year-old woman with chronic superior vena cava syndrome was dialyzed for diabetic nephropathy through a central venous catheter (CVC). Fifteen minutes after the beginning of a dialysis session, she developed acute right eye deviation and left hemiparesis. Right frontal intracortical air bubbles were found on acute CT, and focal cerebral edema was found 5 days later ( fig. 1 a, b). A moderate-sized PFO was detected. She initially had partial recovery but died 6 weeks later from sepsis. Patient 4: A 34-year-old man with Rendu-Osler-Weber disease had multiple pulmonary arteriovenous malformations (PAVMs) embolized 13 years earlier. Over a period of 5 days he now experienced multiple episodes of transitory left hemiparesis, followed by a stroke with a left hemisyndrome. After partial improvement over 2 days, he developed multiple episodes of chest pain and secondarily generalized seizures. Ischemic ECG changes and cardiac enzyme elevation occurred, but coronary angiography was normal. After partial embolization of the PAVMs, he developed another acute left hemisyndrome, followed by cardiorespiratory arrest, cardiac massage and intubation. Cerebral CT showed parenchymal air emboli ( fig. 2 b), MRI revealed ischemic strokes ( fig. 2 c), and transcranial Doppler detected multiple spontaneous embolic signals. More PAVMs were embolized ( fig. 2 a), and the patient recovered progressively. Patient 5: A 74-year-old man with chronic liver cancer developed syncope 30 min after a needle biopsy of a lung nodule, followed by dysarthria and gait ataxia. The thoracic CT at the end of the biopsy retrospectively showed air bubbles in the left ventricle ( fig. 3 a). MRI confirmed ischemic strokes. A minor-sized PFO was also detected ( fig. 3 b). The patient recovered completely spontaneously within 48 h. Introduction Arterial air embolism can result from the introduction of air directly into the arterial system, incomplete filtration of venous air emboli by the pulmonary capillaries, or paradoxical right-to-left embolization [1] . It is a medical emergency as it can lead to cerebral ischemic events (CIE) such as ischemic stroke or transient ischemic attack (TIA), or to acute coronary syndrome. The incidence of cerebral air embolism (CAE) in a stroke population remains unknown [2–5] . We aim to present the incidence, causes, treatment and course of nonaccidental CAE-related CIE in an academic center over a 10-year period.