Zhang and Bian BMC Neurology
(2020) 20:16
https://doi.org/10.1186/s12883-020-1602-1

CASE REPORT

Open Access

Cerebral arterial air embolism secondary to
iatrogenic left atrial-esophageal fistula: a
case report
Ping Zhang1 and Yi Bian2*

Abstract
Background: Cerebral arterial air embolism is a life-threatening complication that can result in neurologic deficits
or death. Sometimes it is iatrogenic, presented as a complication of invasive medical procedures. Here we describe
a case of cerebral arterial air embolism secondary to iatrogenic left atrial-esophageal fistula, of which the diagnosis
might be covered up by the complicated pathophysiologic changes.
Case presentation: A 68-year-old man presented with unconsciousness hours after aphasia and right hemiplegia,
accompanied with hematemesis and fever. He had a history of atrial fibrillation, treated by radiofrequency catheter
ablation 1 month ago. Brain CT displayed massive air embolism in left hemisphere, as well as right parietal lobe.
Chest CT demonstrated a focus of air in the left atrium, which highly suggested an atrial-esophageal fistula. The
patient received high flow (6 L/min) oxygen therapy. Intravenous antibiotics including imipenem and vancomycin
were administered together with crystalloid rehydration. Supportive therapies were given including intubation,
mechanical ventilation and vasopressor use. Because of the patient’s unstable condition and poor prognosis,
surgical repair was considered but not pursued. The patient presented a very fast deterioration of cardiac function
and circulatory failure, and finally died from cardiac arrest.
Conclusions: Clinicians must have a high index of suspicion for atrial-esophageal fistula for patients presenting
with chest discomfort, new onset of stroke, upper gastrointestinal bleeding, and development of sepsis as long as
50 days after the ablation for atrial fibrillation. Urgent CT can ultimately establish the diagnosis in most cases.
Keywords: Cerebral arterial air embolism, Atrial-esophageal fistula, Iatrogenic, Atrial fibrillation ablation

Background
Cerebral vascular air embolism occurs when air enters a
patient’s cerebral circulation, which may occur either in
artery or in vein. It most commonly results from arterial
air embolism [1]. Cerebral arterial air embolism is a lifethreatening complication that can result in neurologic deficits or death, depending on the volume and scope of gas
entry into the cerebral circulation. Sometimes it is iatrogenic, presented as a complication of invasive medical
procedures, mechanical ventilation, or anesthesia [1, 2].
The diagnosis is mainly based on the neurologic symptoms and the performance history of an invasive
* Correspondence: bianyi2526@163.com
2
Department of Emergency, Tongji Hospital, Tongji Medical College,
Huazhong University of Science and Technology, No.1095 Jiefang Road,
Wuhan 430030, China
Full list of author information is available at the end of the article

procedure. Here we describe a patient who suffered from
cerebral arterial air embolism secondary to iatrogenic left
atrial-esophageal fistula, of whom the diagnosis might be
covered up by the complicated pathophysiologic changes.

Case presentation
A 68-year-old man was admitted to the emergency room
due to hematemesis and fever, accompanied with palpitation and chest distress. He spit blood twice, with the
total volume of 500 ml. His body temperature was
39.5 °C, presented with chills. Twenty hours later, he
presented with new symptoms of aphasia and right
hemiplegia. And very soon he became unconscious. He
had a history of atrial fibrillation, treated by radiofrequency catheter ablation 1 month ago. However after
the interventional therapy, he still felt palpitation
intermittently.

© The Author(s). 2020 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0
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(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Zhang and Bian BMC Neurology

(2020) 20:16

General examination was unremarkable. On neurological examination, he appeared stupor, mixed aphasia
and central paralysis of the right side. Blood routine indicated infection and anemia, with leukocyte count
23.23*109/L, neutrophil count 21.59*109/L, hemoglobin
93 g/L, and hematocrit 28%. His C-reactive protein (CRP)
level was 140 mg/L, with blood lactate 2.22 mmol/L,
serum procalcitonin (PCT) 32.51 ng/mL, which supported
the diagnosis of sepsis. His amino-terminal pro-brain
natriuretic peptide (NT-proBNP) was 8445 pg/mL, with
hypersensitive cardiac troponin I (CTnI) 862.5 pg/mL.
Cardiac color ultrasound revealed enlargement of the left
atrium (40 mm) and the left ventricle (61 mm), and impairment of the left ventricular systolic function (Ejection
Fraction: 30%). Then computer tomography (CT) of the
brain was performed, displaying massive air embolism in
left hemisphere, as well as right parietal lobe (Fig. 1).
Chest CT demonstrated a focus of air in the left atrium
(Fig. 1), which highly suggested an atrial-esophageal fistula
[3]. The patient received high flow (6 L/min) oxygen therapy since diagnosis. He didn’t receive hyperbaric oxygen
therapy because of hemodynamic instability. Intravenous
antibiotics including imipenem and vancomycin were administered together with crystalloid rehydration. Supportive therapies were given including intubation, mechanical
ventilation and vasopressor use. Because of the patient’s
unstable condition and poor prognosis, surgical repair was
considered but not pursued. The patient presented a very
fast deterioration of cardiac function and circulatory failure, and finally died from cardiac arrest.

Page 2 of 4

Discussion and Conclusions
Arterial air embolism can be an iatrogenic complication
of numerous invasive medical procedures which performed in almost all clinical specialties when an entry of
air into the arterial circulation is created [2]. The entry
of air can happen through the pulmonary veins or directly into the arteries of the systemic circulation. Among
all vulnerable areas, obstruction of either the coronary
or the cerebral arteries is especially critical, which sometimes can be fatal [2]. Cerebral arterial air embolism typically involves the small arteries, the average diameter of
which ranges from 30 to 60 μm [4]. One the one hand,
the reduction in perfusion distal to the obstruction
causes hypoxia; on the other hand, the secondary inflammatory response to the air bubble aggravates brain damage [2]. Clinical symptoms of cerebral arterial air
embolism can be decreased consciousness, headache,
dizziness, seizures and focal neurological defects, which
vary with the location and size of the air bubbles [5].
The most important criterion for the diagnosis is the patient’s history, which reveals the temporal relation between the initial neurologic symptoms and the
performance of an invasive procedure [2]. CT scan and
magnetic resonance imaging (MRI) of the brain can
sometimes help making the diagnosis.
Atrial-esophageal fistula after radiofrequency catheter
ablation is a rare but fatal complication. This complication
was first described in the surgical literature in 2001 [6]
and in the medical literature in 2004 [7]. The incidence is
estimated to be less than 0.1 to 0.25% of atrial fibrillation

Fig. 1 CT scanning. Brain CT shows massive air embolism in the left frontal, parietal, temporal, and occipital lobe (a, b, c), the left basal ganglion
(b), as well as the right parietal lobe (c). Chest CT plain scan (d) and contrast-enhanced scan (e) show the enlargement of the left atrium, and a
focus of air in the left atrium (arrows), which highly suggests an atrial-esophageal fistula

Zhang and Bian BMC Neurology

(2020) 20:16

ablation procedures [8]. Its mortality has been reported to
be 67 to 100% [9, 10]. Its clinical manifestations mainly include neurologic symptoms, bacteremia and cardiac complications [11]. Neurologic symptoms include encephalopathy,
seizures, transient ischemic attack (TIA), septic embolic
stroke, and air embolism [3], which can appear alone or in
combination. In 2017, Fatula et al. [12] reviewed all reported
cases of atrial-esophageal fistula to date (N = 75). The authors reported that fevers (76.7%) and neurological deficits
(69.9%) were the most common presenting symptoms. Successively, our patient presented almost all common symptoms, including fever, neurological deficits, chest pain,
hematemesis, and altered mental status. Esophageal injury
during the ablation procedure is the leading cause of the formation of atrial-esophageal fistula. Autopsy studies have
demonstrated that the distance between the left atrium and
the esophagus can be as small as 5 mm [13]. The ablative
damage and perforation of the atrial wall and adjacent
esophagus can lead to the development of an abnormal anatomic passage between the left atrium and the esophagus
[14]. The time course of the presentation of atrial-esophageal

Page 3 of 4

fistula after the ablation procedure has been reported from
within a few days to as long as 50 days [15]. In our patient,
the prolonged timeframe of 1 month and the nonspecific
symptoms at the very beginning might greatly mislead the
diagnosis. But ultimately the diagnostic clues were manifested through the air embolism and the consequent neurologic symptoms. The cerebral air embolism, sepsis and
“hematemesis” (blood loss from the left atrium to the
esophagus through the fistula) all supported the diagnosis
of atrial-esophageal fistula. The iatrogenic left atrialesophageal fistula secondary to atrial fibrillation ablation
formed abnormal anatomic communication tract between
the esophagus and the circulation. The air was introduced
through the fistula to the arterial circulation, resulting in
multiple cerebral arterial air embolism. The food and bacteria in the esophagus got into the blood, causing sepsis
and fever. The “hematemesis” originated in blood loss
from the left atrium to the esophagus through the fistula
(Fig. 2). Our patient demonstrated the complexities of establishing the diagnosis. For the diagnosis of atrialesophageal fistula, the optimal evaluation method is not

Fig. 2 Schematic diagram of atrial-esophageal fistula formation and consequent pathogenetic conditions. a Histological section diagram shows the distance
between the left atrial wall and the esophageal wall, which can be as small as 5 mm. b Thermal injury to the atrial esophageal junction is produced during the
ablation procedure. This leads to esophageal injury and atrial-esophageal fistula formation. c The air and bacteria in the esophagus can be introduced through
the fistula to the arterial circulation. d The blood is lost from the left atrium to the esophagus through the fistula

Zhang and Bian BMC Neurology

(2020) 20:16

transthoracic echocardiogram but chest CT [16]. When
chest CT shows air in the mediastinum or pericardium, or
intracardiac air, an atrial-esophageal fistula is strongly suggested [3]. Transesophageal echocardiography or endoscopy is relatively contraindicated, because of the potential
risk of developing air embolism [9].
Considering the high mortality rate and the poor prognosis,
neurologists need to be aware of this rare but fatal complication in patients with new neurological deficits and recent history of ablation for atrial fibrillation. Unfortunately,
neurological deficits tend to be a late finding, which often result in substantial sequelae and increased mortality. The variability in both timing and clinical presentation often leads to
delayed diagnosis of atrial-esophageal fistula. Clinicians must
have a high index of suspicion for this diagnosis for patients
presenting with chest discomfort, new onset of stroke, upper
gastrointestinal bleeding, and development of sepsis as long as
50 days after the ablation. Urgent CT can ultimately establish
the diagnosis in almost all patients. Even though mortality is
extremely high, earlier recognition and multidisciplinary collaboration (including cardiology, anesthesiology, cardiothoracic
surgery, gastroenterology, and neurology) may provide an opportunity for improving outcomes.
Abbreviations
CRP: C-reactive protein; CT: Computer tomography; CTnI: Cardiac troponin I;
MRI: Magnetic resonance imaging; NT-proBNP: Amino-terminal pro-brain
natriuretic peptide; PCT: Procalcitonin; TIA: transient ischemic attack
Acknowledgements
Not applicable.
Authors’ contributions
PZ interpreted the patient data and drafted the manuscript; YB reviewed the
literatures and revised the manuscript. Both authors read and approved the
final manuscript.
Funding
This study was supported by the Hubei Provincial Natural Science
Foundation of China (Grant No. 2018CFB115, 2019CFB107), the Hubei
Provincial Higher Education Research Foundation (Grant No. 2017043), and
the Teaching Research Project of Huazhong University of Science and
Technology (Grant No. 2017103).
Availability of data and materials
All data generated or analyzed during this study are included in this
published article.
Ethics approval and consent to participate
This study was approved by the ethics committee of Tongji Hospital, Tongji
Medical College, Huazhong University of Science and Technology, China.
Consent for publication
Written informed consent was obtained from the patient’s son.
Competing interests
The authors declare that they have no competing interests.
Author details
1
Department of Neurology, Tongji Hospital, Tongji Medical College,
Huazhong University of Science and Technology, Wuhan, China.
2
Department of Emergency, Tongji Hospital, Tongji Medical College,
Huazhong University of Science and Technology, No.1095 Jiefang Road,
Wuhan 430030, China.

Page 4 of 4

Received: 24 July 2019 Accepted: 6 January 2020

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