Daily Radiology Case

Explanation

Cerebral air embolism (CAE) is a rare but life-threatening condition in which air enters the arterial cerebral circulation, causing focal ischemia and infarction. It most commonly occurs as a iatrogenic complication — CVC insertion or removal, barotrauma, neurosurgery in the sitting position, or pulmonary procedures. Air enters the venous system and reaches the cerebral arterial circulation either directly (via pulmonary arteriovenous shunts or barotrauma) or paradoxically through a PFO, which is present in approximately 25–30% of the population. CT is the first-line imaging modality and demonstrates intravascular or intraparenchymal air, distinguishing it from thrombotic stroke where you would instead see a hyperdense artery sign, loss of gray-white differentiation, or diffusion restriction on MRI. Management centers on positioning (left lateral decubitus + Trendelenburg to trap air in the right heart apex away from the pulmonic valve), 100% oxygen (accelerates nitrogen reabsorption by creating a diffusion gradient), and hyperbaric oxygen therapy, which both reduces bubble size via Boyle's Law and reverses ischemia. It is distinguished from venous air embolism, which causes obstructive shock and cor pulmonale rather than focal neurological deficits, and does not require the paradoxical transit step to cause harm.

Source: rID:185679

Hints

• A 67-year-old man is brought to the emergency department with sudden onset confusion, focal neurological deficits, and hypotension immediately following removal of a central venous catheter from his right internal jugular vein.
• Non-contrast CT of the head is obtained urgently and demonstrates hypodense foci within the cerebral vasculature and sulci, distributed in a pattern inconsistent with any single arterial territory.
• The patient was sitting upright at 30 degrees when the catheter was removed, and the nurse notes the dressing was not immediately occlusive — a maneuver that is a well-known predisposing factor for this complication.
• The CT also demonstrates air within the right heart chambers and pulmonary vasculature, suggesting the embolic material crossed into the systemic circulation via a paradoxical mechanism through a patent foramen ovale.
• Immediate management includes placing the patient in the left lateral decubitus (Durant's maneuver) and Trendelenburg position, administering 100% high-flow oxygen to accelerate reabsorption of the embolic material, and preparing for hyperbaric oxygen therapy
• The mechanism of injury is cytotoxic and ischemic — intravascular air obstructs cerebral arterioles, triggers inflammatory endothelial injury, and causes downstream infarction in a distribution that mimics stroke but with CT findings of intravascular gas rather than hyperdense artery sign or early ischemic changes.