Cerebral venous air embolism, a hidden precursor of arterial ischemia: a case report

Abstract

Background

Cerebral venous air embolism is a rare but potentially fatal complication of central venous catheter insertion and removal. Although most venous air emboli remain clinically silent or cause only transient symptoms, they may exceptionally lead to extensive arterial cerebral ischemia, particularly in patients with impaired pulmonary filtration or pre-existing lung disease. We report a distinctive sequence of computed-tomography-demonstrated cortical venous air followed by extensive right middle and posterior cerebral artery infarction on magnetic resonance imaging despite a negative saline-contrast echocardiography for intracardiac shunt, occurring after elective internal jugular central venous catheter removal in a frail patient with idiopathic pulmonary fibrosis.

Case presentation

We report the case of a 68-year-old Lebanese, right-side dominant, cachectic man with multiple comorbidities, including coronary artery disease, heart failure with reduced ejection fraction, pulmonary fibrosis on long-term oxygen therapy, chronic kidney disease, and a history of nephrectomy for metastatic renal carcinoma. He was admitted for weight loss and hypotension, diagnosed with cardiogenic shock, and managed with vasopressor support in the intensive care unit. After stabilization and transfer to the ward, removal of a right internal jugular central venous catheter led to the sudden onset of acute paraplegia, altered consciousness, and left-sided neurological deficits. A non-contrast brain computed tomography scan revealed multiple cortical venous air emboli, and magnetic resonance imaging confirmed extensive ischemic lesions in the right-middle and posterior cerebral artery territories. Despite immediate supportive measures and antiseizure treatment, the patient developed refractory status epilepticus. Given his advanced comorbidities, extensive cerebral injury, and poor pre-morbid status, a shared decision was made with the family to limit further aggressive treatment, and the patient died a few hours later.

Conclusion

This case suggests that venous cortical air embolism can be a hidden precursor of extensive arterial ischemia even without an intracardiac right-to-left shunt, particularly when pulmonary filtration reserve is limited. Clinicians should maintain a high index of suspicion when new neurological deficits appear after central venous catheter manipulation, ensure meticulous preventive measures and close observation after removal, and rapidly initiate appropriate supportive treatment if venous air embolism is suspected.

Introduction

Central venous catheters (CVCs) are widely used in critically ill patients for vasoactive drug infusion, hemodynamic monitoring, and difficult venous access. Although generally safe, their insertion, manipulation and removal can lead to complications, including infection, thrombosis, and venous air (gas) embolism.

Venous air embolism is a rare complication of CVC use, but it can be catastrophic when a clinically significant gas volume is entrained or when cardiopulmonary “filtering” is impaired. Reported rates vary across settings and catheter types, and the true incidence is likely underestimated because many events are clinically silent [1–3] Beyond cardiopulmonary compromise, cerebral involvement may occur and present abruptly with seizures, focal deficits, coma, or death [4–6].

Gas can reach the brain through at least two major mechanisms: by a retrograde ascent from the central venous system into the cranial venous circulation (particularly with internal jugular access) or passage into the arterial circulation (arterial gas embolism) via intracardiac right-to-left shunts or transpulmonary passage when pulmonary capillary filtration is bypassed or overwhelmed [4, 6–9]. Patients with chronic lung disease, pulmonary fibrosis, or pulmonary hypertension may be particularly vulnerable [7, 10]. In addition, prolonged catheter dwell time (fibrin tract formation) and low central venous pressure states (for example, dehydration and cachexia) may increase the risk of air entry during removal [3, 11–15].

Uniquely, imaging in our patient captured cortical venous air on computed tomography (CT) followed by extensive middle and posterior cerebral arterial territory infarction on magnetic resonance imaging (MRI) with a negative bubble study, supporting a venous-to-arterial injury pathway in a high-risk idiopathic pulmonary fibrosis (IPF)/frail context.

Case presentation

We report the case of a 68-year-old Lebanese, right-side dominant, and cachectic man (body mass index 17.63 kg/m²). His medical history included arterial hypertension, diabetes mellitus, dyslipidemia, coronary artery disease with left ventricular aneurysm, heart failure with a reduced ejection fraction (HFrEF) of 40%, atrial fibrillation, and left carotid endarterectomy. He was a former heavy smoker with idiopathic pulmonary fibrosis (IPF) requiring continuous oxygen therapy, and he had chronic kidney disease with a baseline creatinine of 136 µmol/L (glomerular filtration rate 46 mL/minute/1.73 m², CKD-EPI). Twelve years earlier, he had undergone nephrectomy for clear cell carcinoma of the right kidney, followed by nivolumab for lung and left adrenal metastases.

He was admitted to the emergency department for a 1-month history of anorexia and weight loss, complicated by arterial hypotension. On arrival, his oxygen saturation (SpO₂) was 95% on room air, but he rapidly developed systolic blood pressure of 80 mmHg despite 1.5 L of isotonic crystalloid infusion. Laboratory tests showed acute-on-chronic kidney injury (creatinine 236 µmol/L), hemoglobin 14.1 g/dL, mild thrombocytopenia (126,000/µL), low procalcitonin and C-reactive protein, and modest elevations of cardiac biomarkers compatible with cardiogenic shock. Arterial blood gas revealed a pH of 7.33, PaCO₂ of 44 mmHg, PaO₂ of 69 mmHg, bicarbonate 23.2 mmol/L, and SaO₂ of 92%.

A right internal jugular CVC was inserted under ultrasound guidance, and he was admitted to the medical intensive care unit. Bedside cardiac ultrasound confirmed an ejection fraction of 30%, a pulmonary artery systolic pressure of 35 mmHg, an undilated inferior vena cava with reduced compliance, and septal hypokinesia. Hemodynamically, he required noradrenaline support for 10 days, with a maximum dose of 3 µg per minute. After clinical stabilization, he was transferred to the ward on day 11 with a final diagnosis of cardiogenic shock.

Seven days after transfer to the ward, with resolution of shock and no ongoing vasoactive therapy, the right internal jugular CVC was electively removed. Removal was performed by an experienced physician according to the unit’s protocol: the patient was placed in a strict supine position with slight Trendelenburg tilt, all catheter lumens were clamped, the dressing was removed and securing sutures were cut, the patient was instructed to avoid deep inspiration or coughing, and the catheter was withdrawn in a single smooth movement while manual pressure was applied over the insertion site. Continuous manual compression was maintained for approximately 10 minutes, followed by application of an occlusive sterile dressing. The patient remained under bedside monitoring in the supine position.

Shortly after catheter removal, while still supine, the patient developed sudden, severe headache, tachycardia, and a brief loss of consciousness. Within minutes, he regained consciousness but then exhibited acute paraplegia, headache, left hemineglect and altered mental status. Neurological examination revealed an alert but confused patient with reactive pupils, left-sided lower motor neuron facial palsy, left-sided sensory extinction, motor strength of 0/5 in the lower limbs and 4/5 in the upper limbs, tongue deviation to the left, and a positive Babinski sign. Cerebellar testing could not be performed owing to poor cooperation.

Given the temporal relationship between CVC removal and the abrupt onset of neurological deficits, venous air embolism with cerebral involvement was immediately suspected. The patient was placed in a Trendelenburg position and received high-flow oxygen via a non-rebreather mask. Continuous ECG and noninvasive blood pressure monitoring were initiated, and the neurology and intensive care teams were urgently called. The patient remained hemodynamically stable, without hypotension or hypoxemia, and therefore did not require cardiopulmonary resuscitation, vasopressor escalation, or endotracheal intubation. An urgent non-contrast brain CT scan revealed multiple very low-attenuation foci outlining the right frontoparietal sulci, suggestive of air emboli, as well as subtle hypodensities in the right centrum semiovale and juxtacortical areas (Fig. 2A, B). Subsequent brain MRI showed ischemic lesions in the right central and precentral regions, absence of flow in the right Sylvian artery branches, and low flow in the right frontoparietal and parieto-occipital cortices (Fig. 2C–E). An emergency cardiac ultrasound with bubble test did not reveal any right-to-left intracardiac shunt.

Fig. 2.

Imaging findings of a 68-year-old male patient with sudden onset of acute paraplegia, headache, hemineglect, and altered mental status after jugular CVC removal. (A and B) Noncontrast computed tomography scan showing several structures with negative density (gaseous, less likely fatty) outlining the vascular structures in the right frontoparietal sulci of the convexity, suggestive of air emboli (white arrows). (C and D) Magnetic resonance imaging diffusion sequence and Apparent Diffusion Coefficient (ADC) showing a magnetic susceptibility artifact outlining the right frontoparietal cortical vessels and extending toward the right parieto-occipital gyrus. This marked hypointensity extends intraparenchymal toward the ependymal wall of the right lateral ventricle, associated with diffusion restriction in a junctional area as well as in the territory of the central and precentral branches of the right Sylvian artery. (E) Magnetic resonance imaging brain axial diffusion sequence showing occipital cortex air bubbles

Two hours later, the patient developed status epilepticus, requiring initiation of antiseizure medications. He received an intravenous loading dose of valproic acid (40 mg/kg, 1600 mg) and 1 mg of intravenous clonazepam, followed by an oral loading dose of 1 g of levetiracetam administered via a nasogastric tube, then maintenance levetiracetam 250 mg every 8 hours with 1 mg of clonazepam. Lacosamide was not administered because of prolonged QT interval on the electrocardiogram (ECG).

Despite these measures, the patient’s neurological status deteriorated, with refractory seizures and progressive coma. Taking into account his advanced comorbidities, his marked frailty and poor pre-morbid functional status, the extensive bilateral ischemic lesions with malignant edema on MRI, and the rapid occurrence of refractory status epilepticus, the multidisciplinary team considered further aggressive interventions (including ICU readmission and potential transfer for hyperbaric oxygen therapy) to be futile. After several discussions with his family, in line with his previously expressed wishes, a decision was made to limit therapeutic effort and to focus on comfort measures. Palliative care protocols were initiated, and the patient died a few hours later (Figs. 1, 2).

Fig. 1.

Timeline of the patient’s clinical course

Discussion

This case illustrates that catastrophic cerebral venous air embolism can occur even when CVC removal follows standard precautions, and that venous cerebral air can be complicated by secondary arterial ischemic injury. The immediate temporal relationship between catheter removal and abrupt neurological deficits, together with CT evidence of cortical venous air, supports the diagnosis of cerebral venous air embolism after jugular CVC removal.

Several patient- and catheter-related factors likely converged. First, low central venous pressure states increase the pressure gradient favoring air entrainment when the venous tract is open to atmosphere. Dehydration and marked cachexia (BMI 17.63 kg/m²) plausibly contributed to low venous pressure and delayed closure of the puncture track [2, 3, 11, 15]. Second, prolonged catheter dwell time (18 days) increases the probability of a persistent fibrin tract, which can behave as a conduit for air entry after catheter removal, even when the skin site is covered, particularly if tract closure is incomplete [13, 14]. Third, the catheter caliber and lumen size matter because larger lumens can permit rapid air entrainment under favorable gradients, making meticulous occlusion and sustained pressure critical [4, 16]. Finally, the presence of idiopathic pulmonary fibrosis with probable pulmonary hypertension could have reduced the lung’s capacity to filter venous bubbles and thereby facilitated downstream cerebral injury even without a demonstrable intracardiac shunt [7, 10].

Plausible mechanism(s) linking venous air to cerebral injury in this case

Retrograde cerebral venous air embolism

The cerebral CT pattern (multiple serpiginous, very low-attenuation foci outlining cortical veins/sulci) strongly supports cortical venous air rather than primary arterial emboli. Retrograde ascent from the internal jugular vein into intracranial venous structures has been described after CVC removal and is probably underrecognized [9, 10]. Anatomically, jugular access provides a direct pathway to cranial venous channels, and gas (being buoyant) may travel against venous blood flow under certain conditions [9].

Secondary arterial ischemia after venous air embolism

MRI later demonstrated ischemia in the right middle cerebral artery (MCA) and posterior cerebral artery (PCA) territories. Several mechanisms can reconcile venous air on CT with arterial ischemia:

• Paradoxical/transpulmonary passage of bubbles into the arterial circulation when pulmonary filtration is overwhelmed or bypassed. Even if saline contrast echocardiography excludes an intracardiac shunt, transpulmonary passage can occur, particularly when pulmonary vascular reserve is limited [7, 8, 10].

• Microvascular obstruction and endothelial injury from intravascular gas leading to impaired perfusion, inflammatory activation, and vasogenic edema processes described in cerebral gas embolism pathophysiology [6, 17].

• Large venous gas loads may impair pulmonary circulation and promote functional intrapulmonary shunting, enabling systemic embolization even without a fixed anatomical defect [7, 8].

In this patient, the negative bubble study makes an intracardiac right-to-left shunt unlikely, so the most plausible unifying explanation is a primary retrograde cerebral venous air embolism with concurrent (or subsequent) arterial compromise, potentially amplified by limited pulmonary filtration capacity related to IPF [7, 9, 10, 18].

Diagnostic considerations

The key diagnostic clue was the abrupt neurological syndrome occurring minutes after catheter removal, paired with CT evidence of venous air. Typical imaging features of cerebral gas embolism on noncontrast CT include multiple small, serpiginous, very low-attenuation foci outlining cortical veins and cerebral sulci, and, occasionally, air–fluid levels or punctate gas bubbles within the venous sinuses. In our patient, the CT scan showed several such negative-density structures following the right frontoparietal sulci, which is highly suggestive of cortical venous air emboli [4, 5, 19]. These findings, together with the subsequent MRI evidence of ischemic lesions in the right middle and posterior cerebral artery territories, support the diagnosis of cerebral gas embolism complicated by arterial ischemic stroke. This description allows us to eliminate a carotid origin of the embolism given the absence of imaging of a well-described arterial territory.

Our patient’s imaging is consistent with a massive Venous Gas Embolism (VGE), which led to arterial ischemia and significant vasogenic edema. This pattern may reflect an unusually large venous gas load with overwhelmed pulmonary capillary filtration and/or functional intrapulmonary right-to-left passage, allowing some bubbles to enter the arterial circulation despite the absence of an intracardiac shunt. In advanced IPF with probable pulmonary hypertension, reduced pulmonary vascular reserve may further limit bubble filtration and amplify downstream cerebral injury.

Initial management, high-flow oxygen, and immediate positioning measures were appropriate and align with standard recommendations to reduce bubble size (nitrogen washout) and mitigate ongoing embolic effects [2, 3, 6]. High-FiO₂ oxygen via non-rebreather mask, continuous ECG and blood pressure monitoring, and urgent involvement of neurology/ICU teams were appropriate. Rapid neuroimaging confirmed cortical venous air, and saline-contrast echocardiography did not demonstrate an intracardiac right-to-left shunt, which helped refine the mechanistic hypothesis. Seizures were treated promptly with antiseizure therapy. Hyperbaric oxygen therapy is often recommended for significant neurologic gas embolism when feasible, but in this case, the patient’s rapid progression to refractory status epilepticus, extensive ischemic injury, severe comorbidity burden, and poor pre-morbid status guided a goals-of-care discussion and limitation of aggressive measures.

Lessons learned and prevention

From a systems perspective, this case illustrates how several risk factors can converge despite adherence to standard CVC removal recommendations. Our patient was male, markedly cachectic and dehydrated, with a prolonged catheter dwell time of 18 days and underlying idiopathic pulmonary fibrosis with probable pulmonary hypertension, all elements that can facilitate air entrainment and impair pulmonary filtration. CVC removal was performed on the ward, with appropriate positioning and occlusive dressing, but the event occurred within minutes of the procedure. This underscores the need to: (i) identify high-risk patients (frailty, chronic lung disease, pulmonary hypertension, prolonged catheterization), (ii) optimize volume status before elective removal, (iii) ensure meticulous, airtight closure of the puncture site with sustained manual pressure and occlusive dressing, and (iv) maintain close clinical observation and continuous monitoring for at least 30–60 minutes after removal in such patients. Regular staff training and clear written protocols may help reduce the incidence of this rare, but potentially devastating, complication.

Conclusion

Cerebral gas embolism should be systematically considered when acute neurological symptoms occur immediately after insertion, manipulation, or removal of a central venous catheter. This case shows that massive cerebral involvement with secondary arterial ischemic stroke can develop even when CVC removal is performed according to standard precautions, particularly in frail patients with chronic lung disease and prolonged catheter dwell times. Prevention relies on careful risk stratification, meticulous removal technique, airtight closure of the puncture site, and close post-removal monitoring. Awareness of this complication and prompt supportive management are essential to reduce its morbidity and mortality.

Author contributions

HE, MR, RH, and CM: conceptualization and design of the study, data collection, interpretation, and manuscript writing. MR and KAK: critical revision of the manuscript, contribution to the interpretation of the data, and final approval of the version to be published. RH: assistance with data collection, drafting of sections of the manuscript, and review of literature. MR, HE, and KAK: supervision of the project, expert clinical guidance, and review of the manuscript for important intellectual content.

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Availability of data and materials

The data supporting the findings of this case report are included within the article. Due to patient confidentiality, additional detailed information (such as medical records or raw data) is not publicly available but can be shared upon reasonable request.

Declarations

Ethics approval and consent to participate

Ethics approval was not required for this case report. Informed consent for publication was obtained from the patient’s legal guardian, and the report was anonymized to protect patient identity.

Informed consent

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors declare that they have no competing interests.