30 January 2025: Articles
Cerebral Air Embolism Risks in TAVR Procedures: Insights from a 75-Year-Old Patient Case
Rare coexistence of disease or pathology
Anudeep Surendranath

DOI: 10.12659/AJCR.946254
Am J Case Rep 2025; 26:e946254
Abstract
BACKGROUND: Transcatheter aortic valve replacement (TAVR) is a minimally invasive procedure increasingly used to treat severe aortic stenosis, especially in elderly patients and those with significant comorbidities who are at high risk for surgical intervention. While TAVR is generally safe and effective, rare complications can occur, including cerebral air embolism, which can result in acute neurological deficits. This report presents the case of a 75-year-old man who developed a cerebral air embolism following TAVR.
CASE REPORT: A 75-year-old man with severe aortic stenosis and comorbidities, including atrial fibrillation, prior stroke, diabetes mellitus, and coronary artery disease, underwent transfemoral TAVR. After the procedure, he experienced sudden neurological symptoms, including left-sided visual field loss, facial droop, and limb weakness. Neurological evaluation revealed an NIHSS score of 10, with dysarthria and right gaze preference. Imaging studies identified an air embolism in the right posterior cerebral artery, resulting in an infarction in the posterior cerebral artery territory. Supportive care was provided, and the patient was later transferred to a rehabilitation service for further recovery.
CONCLUSIONS: Cerebral air embolism is a rare but potentially serious complication of TAVR. Prompt recognition, the use of advanced imaging techniques, and appropriate management are critical in minimizing neurological damage and improving clinical outcomes. This case highlights the importance of procedural vigilance, strict adherence to air-purging protocols, meticulous device handling, and increased awareness among clinicians performing TAVR. Awareness of such rare but significant complications is essential to ensure optimal patient safety.
Keywords: Embolism, Air, Stroke, Transcatheter Aortic Valve Replacement
Introduction
Cerebral air embolism, although rare, is a potentially serious complication of transcatheter aortic valve replacement (TAVR), a minimally invasive procedure increasingly used to treat severe aortic stenosis, particularly in patients with significant comorbidities or those at high surgical risk. This procedure involves introducing catheters and devices into the vasculature, where even small air bubbles inadvertently introduced can obstruct blood flow, leading to ischemic events such as stroke. The reported incidence of clinical stroke following TAVR ranges from 2.3% to 3.3%, with silent cerebral embolism being even more prevalent, detected in up to two-thirds of patients via diffusion-weighted magnetic resonance imaging [1–3].
Despite advancements in TAVR techniques and protocols, complications such as air embolism remain a concern. These events highlight the need for procedural vigilance, meticulous device handling, and adherence to strict air-purging protocols, to mitigate risks. Advanced imaging techniques play a crucial role in identifying and managing such complications.
This report describes a 75-year-old man who developed a posterior cerebral artery (PCA) infarction due to an air embolism following transfemoral TAVR. Imaging confirmed the presence of an air embolus in the right PCA, underscoring the importance of procedural safeguards and early recognition in mitigating neurological damage. This case aims to raise awareness about this rare but significant complication and emphasizes strategies for prevention and timely management.
Case Report
A 75-year-old man with a complex medical history, including atrial fibrillation, prior cerebral infarction (without residual deficits), hypertension, hyperlipidemia, diabetes mellitus, congestive heart failure, with a pacemaker, coronary artery disease, with multiple stents, chronic kidney disease, and previous abdominal aortic aneurysm repair, presented with worsening chest pain and shortness of breath. Severe aortic valve stenosis was diagnosed, and he underwent transfemoral TAVR, using a balloon-expandable valve. The procedure was uneventful, and the patient was monitored in the recovery area.
Approximately 5 h after the procedure, the patient’s wife observed left lower facial droop, left-sided weakness, and an absent blink-to-threat response on the left side. A stroke alert was activated. Neurological evaluation revealed a National Institutes of Health Stroke Scale (NIHSS) score of 10, with additional findings of dysarthria and right gaze preference. Given the time elapsed since the patient was last seen normal, tissue plasminogen activator was not administered.
A computed tomography (CT) angiogram of the head identified an air embolus in the P2 segment of the right PCA. A subsequent non-contrast CT of the head confirmed a moderatesized infarction in the PCA distribution, without evidence of hemorrhagic transformation. By the time of this imaging, the air embolus was no longer visualized.
Axial non-contrast computed tomography (CT) scan of the brain (Figure 1) and a computed tomography angiogram of the head (Figure 2) identified an air embolus in the P2 segment of the right posterior cerebral artery (PCA). A subsequent non-contrast CT of the head on day 3 (Figure 3) confirmed a moderate-sized infarction in the PCA distribution without evidence of hemorrhagic transformation. By the time of this imaging, the air embolus was no longer visualized.
The patient was treated with supportive care. Hyperbaric oxygen therapy was not available. Neurological symptoms stabilized, and the patient was transferred to a rehabilitation facility for continued recovery and physical therapy.
Discussion
This case underscores the importance of recognizing cerebral air embolism as a rare but serious complication of TAVR. It highlights the critical role of advanced imaging techniques in its diagnosis and emphasizes the need for stringent procedural vigilance and adherence to air-purging protocols to prevent such complications. TAVR is increasingly favored over traditional surgical aortic valve replacement, especially in high-risk patients, due to its less invasive nature and comparable outcomes regarding health-related quality of life and cerebrovascular complications in the long term [4,5]. Despite its advantages, TAVR is not without risks. Stroke is a major risk during the periprocedural period of TAVR, with most events occurring within the first 48 h [6–8]. Studies comparing the transfemoral and transapical approaches have found that silent cerebral embolism, as detected by diffusion-weighted magnetic resonance imaging, is prevalent in both approaches, affecting approximately two-thirds of patients. The incidence of clinical stroke within the first 30 days ranges from 2.3% to 3.3%, with no statistically significant difference between the 2 approaches [2,3]. Research using transcranial Doppler to assess cerebral embolic exposure indicates that it is unable to reliably distinguish between solid and air emboli. The cerebral embolic risk during TAVR varies by phase of the procedure and approach used, with the highest risk occurring during wire manipulation and valve insertion. Solid emboli, often dislodged during these stages, pose a greater risk of stroke, particularly with the transfemoral approach, which involves retrograde passage through the aortic arch. In contrast, the transapical approach, carries a higher potential for air embolism due to antegrade passage of devices directly through the heart, wire and sheath manipulation through the left ventricular apex. Despite the limitations of transcranial Doppler in differentiation, solid emboli remain the predominant cause of clinically significant strokes in both approaches [9,10]. While various studies have proposed air embolism as a potential cause of stroke, this has largely been based on indirect evidence. To the best of our knowledge, no reported case has directly demonstrated air embolism as the cause of a major stroke in the context of TAVR.
Arterial air embolism occurs when air enters the systemic arterial circulation, which can arise during medical procedures such as percutaneous lung biopsy and tumor ablation, arterial catheterization (as in TAVR), and cardiopulmonary bypass. The mechanism involves air being introduced into the vasculature, which then travels through the bloodstream. Arterial air embolism is caused by the entry of air into the pulmonary veins or directly into the arteries of the systemic circulation [11,12]. There have been reports of fatal cerebral arterial embolism secondary to large venous emboli without any demonstration of intracardiac defects or shunt mechanisms [13]. Celli et al describe a case of venous air embolism leading to cardiopulmonary collapse during TAVR, managed successfully with mechanical circulatory support [14]. In the context of TAVR, air embolism can happen during catheter and sheath insertion, wire manipulation, contrast injection, valve deployment, balloon aortic valvuloplasty, or improper flushing of devices, where air bubbles are not fully removed before insertion. Air bubbles can travel retrograde from peripheral arteries to central arteries in the setting of arterial puncture, potentially causing ischemia in vital organs. such as the brain or heart. In our patient’s case, the femoral artery puncture site, created during the arterial puncture, was the likely entry point for the air embolism, which subsequently traveled retrograde to the cerebral circulation, leading to the infarction in the right PCA. In an experimental model, Schaefer et al demonstrated that air emboli originating from the ascending aorta can enter the cerebral circulation, causing infarctions with a distribution and size influenced by the embolus origin and volume. These findings underscore the relevance of procedural factors in TAVR, where improper device flushing or air bubble introduction can result in emboli traveling to the brain via similar mechanisms. Incorporating strategies to minimize air emboli during TAVR, such as enhanced flushing techniques and intraoperative imaging for bubble detection, could mitigate risks identified in experimental and clinical settings [15].
The effects of air embolism vary depending on the location and volume of air. Arterial emboli can obstruct blood flow, causing myocardial ischemia, arrhythmias, or neurological deficits like stroke. Venous emboli can lead to pulmonary obstruction, right heart failure, or systemic complications in cases of paradoxical embolism. The clinical presentation of cerebral air embolism can be dramatic and includes symptoms such as altered mental status, focal neurological deficits, and seizures. These symptoms can mimic those of a thromboembolic stroke, making prompt and accurate diagnosis crucial. Imaging study modalities, such as transesophageal echocardiography, computed tomography, and Doppler ultrasound, are instrumental in identifying air emboli [11,12]. In our patient, CT angiography revealed an air embolus in the right PCA, a finding that underscores the importance of advanced imaging techniques in the diagnosis of air embolism.
Preventive strategies to reduce the risk of arterial air embolism during procedures are critical, given the potential for severe complications. Ensuring meticulous flushing of vascular catheters and devices to eliminate air before insertion is essential to minimize the risk of air introduction. The use of airtight connections and hemostatic valves during catheter exchanges can further reduce the chance of air entrainment. Avoiding prolonged exposure of catheters to the atmosphere and promptly sealing any open vascular access points are key procedural safeguards. Additionally, maintaining vigilance during high-risk phases of the procedure, such as balloon inflation or device deployment, is vital. Using intraoperative imaging, such as transesophageal echocardiography or fluoroscopy, can aid in early detection of air bubbles, enabling immediate intervention. Adherence to standardized protocols and proper operator training are paramount in reducing the incidence of arterial air embolism and its devastating consequences [11,12]. The use of bubble filters can further aid in preventing air emboli during catheterization procedures [16].
The management of air embolism involves prompt intervention tailored to the type of embolism – arterial or venous. For arterial air embolism, the right lateral decubitus position is recommended, as it traps air in the non-dependent apex of the left ventricle, away from the left ventricular outflow tract, reducing the risk of systemic embolization. In venous air embolism, the left lateral decubitus (Durant’s position) and Trendelenburg positions are used to prevent air from entering the pulmonary circulation and causing right ventricular obstruction. Ensuring the patient is well hydrated to maintain a central venous pressure of 10 to 15 mm Hg helps to reduce the pressure gradient, thereby minimizing further air entry and promoting effective perfusion. Administration of 100% high-flow oxygen is crucial in both cases, to reduce the size of the embolus and mitigate ischemic damage. Definitive treatment often involves hyper-baric oxygen therapy, which accelerates the dissolution of air bubbles, improves tissue oxygenation, and reduces ischemiareperfusion injury. Supportive measures, such as fluid resuscitation, inotropes, or catheter-based air aspiration, can also be necessary depending on the severity. Continuous monitoring with imaging modalities, such as echocardiography or computed tomography, facilitates assessment of embolus resolution and guides further management. Rapid recognition and intervention are essential to improving outcomes in air embolism [11,12,17].
The prognosis of cerebral air embolism depends on the amount of air embolized, the promptness of diagnosis, and the effectiveness of the treatment. Early intervention with supportive care and hyperbaric oxygen therapy significantly improves outcomes. However, delays in diagnosis and treatment can lead to significant morbidity, including permanent neurological deficits or death.
Conclusions
Air embolism, although rare, remains a potentially serious complication of TAVR and other invasive procedures. This case highlights the need for vigilance during TAVR, to prevent air embolism, as even small volumes of air can lead to significant complications. Prompt diagnosis and appropriate management are essential to minimize neurological damage and improve patient outcomes. Preventive measures, such as ensuring meticulous device flushing and careful monitoring during high-risk phases of the procedure, are crucial to reducing the risk of air embolism. Given the increasing use of TAVR, awareness of such rare complications should be heightened among healthcare providers to ensure early recognition and treatment.
Figures
References:
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