Mingzhe Song
Wenxiang Wang1,2*- 1The Second Department of Thoracic Surgery, The Affiliated Cancer Hospital of Xiangya School of Medicine/Hunan Cancer Hospital, Central South University, Changsha, China
- 2The Second Department of Thoracic Surgery, Hunan Clinical Medical Research Center of Accurate Diagnosis and Treatment for Esophageal Carcinoma, Changsha, China
Background: Cerebral air embolism following the removal of a central venous catheter is a rare and often fatal complication, resulting in severe neurological deficits and potentially death.
Case presentation: We report a unique case involving a 57-year-old male, where the postoperative removal of a central venous catheter resulted in cerebral air embolism in a patient with esophageal cancer who had no intracardiac structural abnormalities. Following treatment that included low-temperature brain protection and the reduction of cerebral edema, a favorable prognosis was achieved.
Conclusions: This case underscores the efficacy of prompt low-temperature brain protection in managing cerebral air embolism. Additionally, it examines potential mechanisms underlying cerebral air embolism in the absence of intracardiac structural abnormalities.
Background
The central venous catheter (CVC) is widely utilized for fluid management, drug infusion, and hemodynamic monitoring in critically ill, oncological, and postoperative patients. Despite its clinical value, CVC-related complications, such as infection, thrombosis, catheter malposition, and air embolism, cannot be overlooked. Among these complications, while the incidence of air embolism (AE) is relatively low, ranging from 0.1% to 2%, its occurrence, particularly cerebral air embolism (CAE), can result in severe neurological deficits and potentially death (1–4).
Here, we report a postoperative esophageal cancer patient who self-removed his internal jugular central venous catheter and developed a catheter-related air embolism. He was successfully managed with comprehensive treatment and made a full recovery.
Case report
A 57-year-old male patient was diagnosed with lower esophageal squamous cell carcinoma and underwent esophageal cancer radical surgery at our hospital. On the fourth day after the operation, the patient suddenly lost consciousness and had decreased blood oxygen when going to the toilet after removing the Internal jugular vein CVC catheter connector by himself. This was considered CAE according to clinical manifestations and behavior. After performing an emergency tracheal intubation, the anesthesiologist conducted a brain CT scan, revealing scattered small air shadows in both frontal lobes, indicating the presence of gas embolism within a brain blood vessel (Figure 1). CTA of the head and neck showed no vascular abnormalities (Figure 2A). Cardiac ultrasound did not show any heart structural abnormalities (Figure 3). Following the diagnosis of venous air embolism, the patient was immediately placed in a left lateral decubitus and Trendelenburg position. Sedation, hypothermia, and reduced cerebral edema treatment were administered to the patient. The following day, a brain MRI showed swelling in the bilateral frontal and parietal cortex, indicating ischemic and hypoxic brain (Figures 2B,C). Additionally, edema of soft tissue beneath the scalp in the left hemisphere of the brain was noted. At the same time, hyperbaric oxygen therapy was considered. However, it was not administered as the patient remained hemodynamically stable and exhibited rapid neurological improvement with supportive care alone. Thus, we continued sedation with propofol and administered methylprednisolone and mannitol to reduce cerebral edema. After three days, the patient's consciousness recovered; their pupils were reactive to light; upper limb muscle strength returned to normal; and lower limb muscle strength returned to 2–3 levels. Continue treatment for one week and be discharged (Table 1).
Figure 1. Brain computed tomography (A, B) revealed scattered small air shadows in both frontal lobes, suggesting gas embolism (arrows) in both cerebral hemisphere.
Figure 2. Head MRI shows swelling in the frontal and parietal lobes, indicating ischemic hypoxic encephalopathy. FLAIR imaging shows that brain edema is located in both frontal and parietal lobes, indicating the extent of cerebral ischemia and hypoxia (A),The high signal of DWI sequence indicates ischemic areas in brain tissue (B),The dark signal of the ADC sequence confirms the location of the ischemic and hypoxic regions in the brain (C).
Figure 3. Normal apical four chamber echocardiography (A), normal four chamber aortic valve blood flow spectrum (B). Cardiac ultrasound did not show any structural abnormalities in the heart.
Table 1. Timeline of clinical events and management.
Disscussion
Venous air embolism is a known complication associated with the insertion, maintenance, and removal of central venous catheters (CVCs). However, CAE following CVC removal remains a rare yet severe event, with reported mortality rates as high as 23% (5). Typically, air entering the venous circulation is filtered by the pulmonary capillary bed. However, in the presence of a right-to-left shunt, such as a patent foramen ovale (PFO), air can bypass this filtration, entering the systemic circulation and potentially causing embolisms in critical organs like the brain (6–8). This mechanism, known as paradoxical air embolism, is a well-documented pathway for CAE.
Notably, clinical observations indicate that some patients with CAE show no evidence of intracardiac shunting, suggesting alternative pathways. These may include a massive air burden overwhelming the pulmonary filter or the opening of bronchopulmonary anastomoses, allowing air to enter the pulmonary venous system directly. Notably, the case reported by Teifurova et al. highlights the potential for retrograde venous flow as another plausible mechanism for cerebral infarction in the absence of a shunt. Thus, this concept warrants greater clinical attention (7, 9, 10).
This case also highlights the potential therapeutic value of hypothermia in managing CAE. Standard management includes high-flow oxygen to promote nitrogen washout, hyperbaric oxygen therapy (HBO), and neuroprotective strategies (11, 12).
Although our patient did not receive HBO, significant neurological recovery was achieved through targeted temperature management (maintained at 34°C for 24 h, 0.25°C/h rewarming, bladder temperature monitoring) and measures to reduce intracranial pressure. This outcome suggests that therapeutic hypothermia may confer neuroprotection by reducing cerebral metabolic rate, mitigating oxidative stress, and suppressing inflammatory cascades (9, 11, 13–14). However, it is crucial to acknowledge the potential risks of therapeutic hypothermia, particularly during the rewarming phase. Rapid rewarming can lead to a significant increase in the number of cerebral gas microemboli. Therefore, we implemented a strictly controlled slow rewarming protocol (0.25°C per hour) to minimize the risk of emboli expansion and secondary brain injury potentially induced by overly rapid rewarming. Nevertheless, due to the rarity and acute nature of CAE, robust evidence to guide optimal treatment remains limited.
Finally, this case reinforces the critical importance of preventing CVC-related CAE, particularly in high-risk patients with postoperative delirium or impaired consciousness. Preventive strategies should include securing the catheter meticulously, employing appropriate sedation or physical restraints when necessary, and adhering strictly to standardized removal protocols—such as placing the patient in the Trendelenburg position and removing the catheter at end-exhalation (7, 15).
In conclusion, further research is essential to elucidate the non-shunt pathogenic mechanisms of CAE and to refine its treatment protocols, including the role of adjuvant therapies like hypothermia.
Conclusion
A rare case of a patient with esophageal cancer who underwent successful recovery from CAE caused by CVC removal after surgery was reported. Through hypothermic brain protection and administered methylprednisolone and mannitol to reduce cerebral edema, the patient achieved a favorable prognosis. The study also analyzed the potential mechanisms of CAE, including the possibility of air embolism under intracardiac shunt and non-shunt conditions. Moreover, it highlights the critical role of hypothermia therapy in neuroprotection. Thus, this study provides important insights into the treatment and prevention of CAE, emphasizes the importance of standardized operation and timely intervention, and lays the foundation for future research.
Data availability statement
The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.
Ethics statement
Written informed consent was obtained from the individual(s) for the publication of any potentially identifiable images or data included in this article.
Author contributions
MS: Writing – original draft, Visualization, Methodology, Data curation, Investigation, Conceptualization, Writing – review & editing. WW: Visualization, Resources, Supervision, Conceptualization, Writing – review & editing. JW: Writing – review & editing, Funding acquisition, Supervision, Resources, Project administration, Validation.
Funding
The author(s) declare financial support was received for the research and/or publication of this article.Science and technology innovation Program of Hunan Province (Grant No. 2021SK51109), the Hunan Cancer Hospital Climb Plan (Grant No. ZX2020005), and the High-level Talent Program of Hunan Health Commission (Grant No. 20230227-1001).
Acknowledgments
The authors thank AiMi Academic Services (https://www.aimieditor.com) for English language editing and review services.
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Keywords: case report, esophageal cancer, cerebral air embolism, central venous catheter, air embolism
Citation: Song M, Wang W and Wu J (2025) Case Report: A rare successful case of treating cerebral air embolism following the removal of a central venous catheter without intracardiac structural abnormalities. Front. Surg. 12:1673766. doi: 10.3389/fsurg.2025.1673766
Received: 26 July 2025; Accepted: 10 November 2025;
Published: 21 November 2025.
Edited by:
Savvas Lampridis, Imperial College London, United KingdomReviewed by:
Zhouxiong Xing, Zunyi Medical University, ChinaArturs Balodis, Riga Stradiņš University, Latvia
Stephanus Andy Prakasa Kaligis, Primaya Hospital Bekasi Utara, Indonesia
Copyright: © 2025 Song, Wang and Wu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Wenxiang Wang, d2FuZ3dlbnhpYW5nQGhuY2Eub3JnLmNu; Jie Wu, d3VqaWVAaG5jYS5vcmcuY24=