[Cerebral gas embolism as a complication of diffuse interstitial lung disease] / Embolismo gaseoso cerebral como complicación de una enfermedad pulmonar intersticial difusa.

Introduction: Cerebral gas embolism is an unusual but extremely serious condition that occurs when air is introduced into the arterial or venous circulation of the brain. Although rare, it can lead to significant neurological deficits and even the death of the patient. Clinical Case: 76-year-old patient with pre-existing diffuse interstitial lung disease, who experienced a massive stroke due to spontaneous pneumomediastinum. Her presentation included confusion, seizures, and motor weakness. Imaging tests revealed air bubbles in the cerebral sulci and hypodense areas in the cerebellum and parietooccipitals. In addition, pneumothorax and air in the upper mediastinum were noted on chest radiographs and chest CT scan. Despite therapeutic measures such as hyperbaric oxygen, the patient unfortunately died due to multiple organ failure. Discussion: The diagnosis of cerebral gas embolism generally involves performing a cerebral computed tomography, which is highly sensitive for detecting the presence of air in the cerebral vessels. Management includes monitoring of vital and neurological signs, as well as specific measures such as airway closure, venous catheter aspiration, Trendelenburg positioning, and hyperbaric oxygen. Conclusion: Cerebral gas embolism is a potentially fatal condition that requires a brain computed tomography for diagnosis and it is vitally important to know the prevention measures to avoid the appearance of this complication and also to know the general measures to adopt when it occurs.

Introducción: La embolia gaseosa cerebral es una afección inusual pero extremadamente grave que se produce cuando se introduce aire en la circulación arterial o venosa del cerebro. Aunque poco común, puede derivar en déficits neurológicos significativos e incluso la muerte del paciente. Caso Clínico: Paciente de 76 años con una enfermedad pulmonar intersticial difusa preexistente, que experimentó un ictus masivo debido a un neumomediastino espontáneo. Su presentación incluyó confusión, convulsiones y debilidad motora. Las pruebas de imagen revelaron burbujas de aire en los surcos cerebrales y áreas hipodensas en el cerebelo y parietooccipitales. Además, se observó neumotórax y aire en el mediastino superior en las radiografías de tórax y la tomografía torácica. A pesar de las medidas terapéuticas como el oxígeno hiperbárico, la paciente lamentablemente falleció debido al fallo multiorgánico. Discusión: El diagnóstico de embolia gaseosa cerebral generalmente implica la realización de una tomografía computarizada cerebral, que es altamente sensible para detectar la presencia de aire en los vasos cerebrales. El manejo incluye el control de las constantes vitales y neurológicas, así como medidas específicas como cierre de la entrada de aire, aspiración de catéteres venosos, posicionamiento de Trendelenburg y oxígeno hiperbárico. Conclusión: La embolia gaseosa cerebral es una afección potencialmente mortal que requiere una tomografía computarizada cerebral para el diagnóstico y de vital importancia conocer las medidas de prevención para evitar la aparición de esta complicación y así mismo conocer las medidas generales a adoptar cuando ésta se presenta.

A portent of catastrophic carbon dioxide embolism in laparoscopic hepatectomy: A case report.

INTRODUCTION: Laparoscopic hepatectomy (LH) poses a high risk of carbon dioxide embolism due to extensive hepatic transection, long surgery duration, and dissection of the large hepatic veins or vena cava. PATIENT CONCERNS: A 65-year-old man was scheduled to undergo LH. Following intraperitoneal carbon dioxide (CO2) insufflation and hepatic portal occlusion, the patient developed severe hemodynamic collapse accompanied by a decrease in the pulse oxygen saturation (SpO2). DIAGNOSIS: Although a decrease in end-tidal carbon dioxide (ETCO2) was not observed, CO2 embolism was still suspected because of the symptoms. INTERVENTIONS AND OUTCOMES: The patient was successfully resuscitated after the immediate discontinuation of CO2 insufflation and inotrope administration. CO2 embolism must always be suspected during laparoscopic surgery whenever sudden hemodynamic collapse associated with decreased pulse oxygen saturation occurs, regardless of whether ETCO2 changes. Instant arterial blood gas analysis is imperative, and a significant difference between PaCO2 and ETCO2 is indicative of carbon dioxide embolism. CONCLUSION: Instant arterial blood gas analysis is imperative, and a significant difference between PaCO2 and ETCO2 is indicative of carbon dioxide embolism.

Retained intracardiac air in cardiovascular surgery: a re-visited problem.

Intracardiac air remains an unsolved problem in the realm of cardiac surgery, leading to embolic events encompassing conduction disturbance, heart failure, and stroke. Transesophageal echocardiography allows the visualization of three distinct types of retained intracardiac air: pooled air, coarse bubbles, and microbubbles. The former two predominantly manifest in the right upper pulmonary vein, left atrium, and left ventricle, exhibiting passive movement along the vessel walls by buoyancy. De-airing, involving "eradication" of air from circulation and "expulsion" of air from the heart into the systemic circulation assumes paramount importance in averting embolic events. Optimal de-airing strategies necessitate the thorough elimination of air during the static phase before the resumption of cardiac activity, achieved through aspiration or guided exit leveraging buoyancy. While the dynamic phase, characterized by active cardiac beating, presents challenges for air eradication, the majority of air expulsion occurs towards the aorta during this period. In this latter phase, collaborative efforts among the surgeon, anesthesiologist, and clinical engineer are pivotal to mitigate the risk of bolus air embolism. The efficacy of carbon dioxide insufflation is limited, as it is rapidly aspirated by wall suction or absorbed into the bloodstream. Consequently, the "air" identified by TEE is acknowledged as conventional air. Understanding the distinctive properties of air as well as timely and judicious collaboration for detection and removal, with the ultimate goal of eradication, emerges as an essential prerequisite for successful de-airing in the evolving era of cardiac surgery.

Can Intracardiac Echocardiography Reduce Steam Pops During Half-Normal Saline Irrigated Radiofrequency Ablation?

BACKGROUND: Irrigated radiofrequency ablation with half-normal saline can potentially increase lesion size but may increase the risk of steam pops with the risk of emboli or perforation. We hypothesized that pops would be preceded by intracardiac echocardiography (ICE) findings as well as a large impedance fall. METHODS: In 100 consecutive patients undergoing endocardial ventricular arrhythmia radiofrequency ablation with half-normal saline, we attempted to observe the ablation site with ICE. Radiofrequency ablation power was titrated to a 15 to 20 Ohm impedance fall and could be adjusted for tissue whitening and increasing bubble formation on ICE. Steam pops were defined as audible or a sudden explosion of microbubbles on ICE. RESULTS: Of 2190 ablation applications in 100 patients (82% cardiomyopathy, 50% sustained ventricular tachycardia), pops occurred during 43 (2.0%) applications. Sites with pops had greater impedance decreases of 18 [14, 21]% versus 13 [10, 17]% (P<0.001). ICE visualized 1308 (59.7%) radiofrequency sites, and fewer pops occurred when ICE visualized the radiofrequency ablation site (1.4%) compared with without ICE visualization (2.8%; P=0.016). Of the 18 ICE-visible pops, 7 (39%) were silent but recognized as an explosion of bubbles on ICE. With ICE, 89% of pops were preceded by either tissue whitening or a sudden increase in bubbles. In a multivariable model, tissue whitening and a sudden increase in bubbles were associated with steam pops (odds ratio, 7.186; P=0.004, and odds ratio, 29.93; P<0.001, respectively), independent of impedance fall and power. There were no pericardial effusions or embolic events with steam pops. CONCLUSIONS: Steam pops occurred in 2% of half-normal saline radiofrequency applications titrated to an impedance fall and are likely under-recognized without ICE. On ICE, steam pops are usually preceded by tissue whitening or a sudden increase in bubble formation, which can potentially be used to adjust radiofrequency application to help reduce pops.

Arterial Gas Embolism in Breath-Hold Diver.

An arterial gas embolism (AGE) is a potentially fatal complication of scuba diving that is related to insufficient exhalation during ascent. During breath-hold diving, an arterial gas embolism is unlikely because the volume of gas in the lungs generally cannot exceed the volume at the beginning of the dive. However, if a diver breathes from a gas source at any time during the dive, they are at risk for an AGE or other pulmonary overinflation syndromes (POIS). In this case report, a breath-hold diver suffered a suspected AGE due to rapidly ascending without exhalation following breathing from an air pocket at approximately 40 feet.

In-field use of I-VED electrical impedance sensor for assessing post-dive decompression stress in humans.

Purpose: Ultrasound imaging is commonly used in decompression research to assess venous gas emboli (VGE) post-dive, with higher loads associated with increased decompression sickness risk. This work examines, for the first time in humans, the performance of a novel electrical impedance spectroscopy technology (I-VED), on possible detection of post-dive bubbles presence and arterial endothelial dysfunction that may be used as markers of decompression stress. Methods: I-VED signals were recorded in scuba divers who performed standardized pool dives before and at set time points after their dives at 35-minute intervals for about two hours. Two distinct frequency components of the obtained signals, Low-Pass Frequency-LPF: 0-0.5 Hz and Band-Pass Frequency-BPF: 0.5-10 Hz, are extracted and respectively compared to VGE presence and known flow-mediated dilation trends for the same dive profile for endothelial dysfunction. Results: Subjects with VGE counts above the median for all subjects were found to have an elevated average LPF compared to subjects with lower VGE counts, although this was not statistically significant (p=0.06), as well as significantly decreased BPF standard deviation post-dive compared to pre-dive (p=0.008). Conclusions: I-VED was used for the first time in humans and operated to provide qualitative in-vivo electrical impedance measurements that may contribute to the assessment of decompression stress. Compared to ultrasound imaging, the proposed method is less expensive, not operator-dependent and compatible with continuous monitoring and application of multiple probes. This study provided preliminary insights; further calibration and validation are necessary to determine I-VED sensitivity and specificity.

[Air Embolism of the Left Ventricle due to Pulmonary Stab Wound].

A man in his 50s was stabbed deeply in the back with a knife and brought to the emergency room. He was found to have a significant left hemopneumothorax. He was planned to undergo hemostatic surgery under general anesthesia. However, shortly after the change in a right lateral decubitus position, he experienced ventricular fibrillation. Hemostasis of the intercostal artery injury, the source of bleeding, and suture of the injured visceral pleura were performed under extracorporeal membrance oxgenation( ECMO). Although sinus rhythm was resumed, when positive pressure ventilation was applied to the left lung for an air leak test, ST elevation on the electrocardiogram and loss of arterial pressure occurred. A transesophageal echo revealed air accumulation in the left ventricle. It was determined that air had entered the damaged pulmonary vein from the injured bronchi due to the stab wound, leading to left ventricular puncture decompression and lower left lower lobectomy. Subsequently, his circulatory status stabilized, and ECMO was weaned off. He recovered without postoperative neurological deficits postoperatively. The mortality rate for chest trauma with systemic air embolism is very high. In cases of deep lung stab wounds, there is a possibility of systemic air embolism, so treatment should consider control of airway and vascular disruption during surgery.

Air Embolism-Induced Ischemic Stroke Following Orthognathic Surgery in a Patient With Goldenhar Syndrome.

Goldenhar syndrome, a rare congenital anomaly, manifests as craniofacial malformations often necessitating intricate surgical interventions. These procedures, though crucial, can expose patients to diverse postoperative complications, including hemorrhage or infection. A noteworthy complication is stroke, potentially linked to air embolism or local surgical trauma. We highlight a case of a male patient, aged 20 years, who experienced a significant postoperative complication of an ischemic stroke, theorized to be due to an air embolism, after undergoing orthognathic procedures for Goldenhar syndrome. The patient was subjected to LeFort I maxillary osteotomy, bilateral sagittal split ramus osteotomy of the mandible, and anterior iliac crest bone grafting to the right maxilla. He suffered an acute ischemic stroke in the left thalamus post-surgery, theorized to stem from an air embolism. Advanced imaging demonstrated air pockets within the cavernous sinus, a rare and concerning finding suggestive of potential air embolism. This case underscores the intricate challenges in treating Goldenhar syndrome patients and the rare but significant risk of stroke due to air embolism or surgical trauma. Limited literature on managing air embolism complications specific to Goldenhar syndrome surgeries exists. Generally, management includes immediate recognition, positional adjustments, air aspiration via central venous catheters, hyperbaric oxygen therapy, hemodynamic support, and high-flow oxygen administration to expedite air resorption. Our patient was conservatively managed post-surgery, and at a 3-month neurology follow-up, he showed significant improvement with only residual right arm weakness. It emphasizes the imperative of a comprehensive, multidisciplinary approach.

Air embolism caused by peripheral superficial vein catheterization: A case report.

BACKGROUND: Air embolization is usually an iatrogenic complication that can occur in both veins and arteries. Intravenous air embolization is mainly associated with large central vein catheters and mechanical ventilation. A 59-year-old woman was sent to our hospital with spontaneous cerebral hemorrhage and treated conservatively with a left forearm peripheral venous catheter infusion drug. After 48 hours, the patient's oxygen saturation decreased to 92 % with snoring breathing. Computer tomography of the head and chest revealed scattered gas in the right subclavian, the right edge of the sternum, the superior vena cava, and the leading edge of the heart shadow. METHODS: She was sent to the intensive care unit for high-flow oxygen inhalation and left-side reclining instantly. As the patient was at an acute stage of cerebral hemorrhage and did not take the Trendelenburg position. RESULTS: The computed tomography (CT) scan after 24 hours shows that the air embolism subsides. CONCLUSION SUBSECTIONS: Air embolism can occur in any clinical scenario, suggesting that medical staff should enhance the ability to identify and deal with air embolism. For similar cases in clinical practice, air embolism can be considered.

Investigation of air bubble behaviour after gas embolism events induced in a microfluidic network mimicking microvasculature.

Gas embolism is a medical condition that occurs when gas bubbles are present in veins or arteries, decreasing blood flow and potentially reducing oxygen delivery to vital organs, such as the brain. Although usually reported as rare, gas embolism can lead to severe neurological damage or death. However, presently, only limited understanding exists regarding the microscale processes leading to the formation, persistence, movement, and resolution of gas emboli, as modulated by microvasculature geometrical features and blood properties. Because gas embolism is initially a physico-chemical-only process, with biological responses starting later, the opportunity exists to fully study the genesis and evolution of gas emboli using in vitro microfluidic networks mimicking small regions of microvasculature. The microfluidics networks used in this study, which aim to mimic microvasculature geometry, comprise linear channels with T-, or Y-junction air inlets, with 20, 40, and 60 µm widths (arterial or venous), and a 30 µm width honeycombed network (arterial) with three bifurcation angles (30°, 60°, and 90°). Synthetic blood, equivalent to 46% haematocrit concentrations, and water were used to study the modulation of gas embolism-like events by liquid viscosity. Our study shows that (i) longer bubbles with lower velocity occur in narrower channels, e.g., with 20 µm width; (ii) the resistance of air bubbles to the flow increases with the higher haematocrit concentration; and lastly (iii) the propensity of gas embolism-like events in honeycomb architectures increases for more acute, e.g., 30°, bifurcation angles. A dimensionless analysis using Euler, Weber, and capillary numbers demarcated the conditions conducive to gas embolism. This work suggests that in vitro experimentation using microfluidic devices with microvascular tissue-like structures could assist medical guidelines and management in preventing and mitigating the effects of gas embolism.

Intrapulmonary Shunting and Paradoxical Air Embolism in Liver Transplantation: A Case Report.

BACKGROUND A paradoxical air embolism (PAE) occurs when air entering the central venous circulation reaches the systemic circulation, occurring through an intracardiac shunt or intrapulmonary shunting. Patients presenting for liver transplantation often have intrapulmonary shunting due to pulmonary arterial vasodilation, even in the absence of hepatopulmonary syndrome. Here, we present a case of hemodynamic collapse believed to be caused by a PAE, which was diagnosed intraoperatively with transesophageal echocardiography (TEE). CASE REPORT A 60-year-old man who was diagnosed with non-alcoholic steatohepatitis cirrhosis presented for deceased donor orthotopic liver transplantation with utilization of normothermic machine perfusion. Following reperfusion of the liver allograft, TEE detected intrapulmonary shunting resulting in air within the left atrium, left ventricle, and ascending aorta. The patient developed severe biventricular dysfunction with ST-segment changes on electrocardiography monitoring and became acutely hypotensive with significant hepatic congestion 5 min after liver reperfusion. High doses of inotropic and vasopressor support were used as well as inhaled nitric oxide. The patient recovered after 30 min of medical management. The liver transplantation operation was successfully completed and the patient was discharged home on postoperative day 7. CONCLUSIONS Intracardiac air at the time of reperfusion during liver transplantation can originate from the donor allograft and result in PAE in the setting of intrapulmonary shunting. PAE can result in intracoronary air and should be considered in cases of hemodynamic instability in liver transplantation, especially if air is seen within the left atrium, left ventricle, and ascending aorta.

Decompression illness: a comprehensive overview.

Decompression illness is a collective term for two maladies (decompression sickness [DCS] and arterial gas embolism [AGE]) that may arise during or after surfacing from compressed gas diving. Bubbles are the presumed primary vector of injury in both disorders, but the respective sources of bubbles are distinct. In DCS bubbles form primarily from inert gas that becomes dissolved in tissues over the course of a compressed gas dive. During and after ascent ('decompression'), if the pressure of this dissolved gas exceeds ambient pressure small bubbles may form in the extravascular space or in tissue blood vessels, thereafter passing into the venous circulation. In AGE, if compressed gas is trapped in the lungs during ascent, pulmonary barotrauma may introduce bubbles directly into the pulmonary veins and thence to the systemic arterial circulation. In both settings, bubbles may provoke ischaemic, inflammatory, and mechanical injury to tissues and their associated microcirculation. While AGE typically presents with stroke-like manifestations referrable to cerebral involvement, DCS can affect many organs including the brain, spinal cord, inner ear, musculoskeletal tissue, cardiopulmonary system and skin, and potential symptoms are protean in both nature and severity. This comprehensive overview addresses the pathophysiology, manifestations, prevention and treatment of both disorders.

[A case of hepatic portal venous gas and upper gastrointestinal mucosal injury due to accidental ingestion of hydrogen peroxide].

A 40-year-old woman was admitted to our hospital by ambulance due to accidental ingestion of 100ml of 35% hydrogen peroxide. Although the patient suffered from frequent vomiting, abdominal distension, and abdominal pain, signs of peritonitis were not observed. An abdominal computed tomography examination demonstrated obvious gas images in the gastric wall and intrahepatic portal veins. Upper gastrointestinal endoscopy revealed mucosal redness, swelling, and erosion from the lower part of the esophagus to the duodenum. Portal venous gas and upper gastrointestinal mucosal injury due to accidental hydrogen peroxide ingestion were suspected. As the vital signs were stable and there were no signs peritoneal irritation or neurological symptoms, she was treated medically with vonoprazan, rebamipide, and sodium alginate. The next day, abdominal symptoms immediately improved and 3 days later, hepatic portal venous gas had disappeared on ultrasonography. She was discharged on the 5th day after admission. Two months later, upper gastrointestinal endoscopy showed improvement in inflammatory findings. We report a remarkable case of hepatic portal venous gas and upper gastrointestinal mucosal injury and elucidate the endoscopic findings associated with hydrogen peroxide ingestion.

Chemotherapy-induced pneumatosis intestinalis followed by hepatic portal venous gas. A case report.

Pneumatosis intestinalis (PI) is a rare disease, and there are many theories about its pathogenesis. Hepatic portal venous gas (HPVG), is thought to occur secondary to intramural intestinal gas emboli migrating through the portal venous system via the mesenteric veins. PI accompanied by HPVG is usually a sign of bowel ischaemia and is associated with a high mortality rate. We report here, a patient with liver metastases from colorectal cancer who developed PI followed by HPVG after treatment with 5-Fluorouracil, leucovorin, and oxaliplatin (mFOLFOX6). Timely attention and management of gastrointestinal symptoms following chemotherapy are essential in the treatment of this type of patient.

Chain of events analysis in diving accidents treated by the Royal Netherlands Navy 1966-2023.

Introduction: Diving injuries are influenced by a multitude of factors. Literature analysing the full chain of events in diving accidents influencing the occurrence of diving injuries is limited. A previously published 'chain of events analysis' (CEA) framework consists of five steps that may sequentially lead to a diving fatality. This study applied four of these steps to predominately non-lethal diving injuries and aims to determine the causes of diving injuries sustained by divers treated by the Diving Medical Centre of the Royal Netherlands Navy. Methods: This retrospective cohort study was performed on diving injuries treated by the Diving Medical Centre between 1966 and 2023. Baseline characteristics and information pertinent to all four steps of the reduced CEA model were extracted and recorded in a database. Results: A total of 288 cases met the inclusion criteria. In 111 cases, all four steps of the CEA model could be applied. Predisposing factors were identified in 261 (90%) cases, triggers in 142 (49%), disabling agents in 195 (68%), and 228 (79%) contained a (possible-) disabling condition. The sustained diving injury led to a fatality in seven cases (2%). The most frequent predisposing factor was health conditions (58%). Exertion (19%), primary diver errors (18%), and faulty equipment (17%) were the most frequently identified triggers. The ascent was the most frequent disabling agent (52%). Conclusions: The CEA framework was found to be a valuable tool in this analysis. Health factors present before diving were identified as the most frequent predisposing factors. Arterial gas emboli were the most lethal injury mechanism.

Secondary deterioration in a patient with cerebral and coronary arterial gas embolism after brief symptom resolution: a case report.

Introduction: Hyperbaric oxygen treatment (HBOT) is recommended for arterial gas embolism (AGE) with severe symptoms. However, once symptoms subside, there may be a dilemma to treat or not. Case presentation: A 71-year-old man was noted to have a mass shadow in his left lung, and a transbronchial biopsy was performed with sedation. Flumazenil was intravenously administered at the end of the procedure. However, the patient remained comatose and developed bradycardia, hypotension, and ST-segment elevation in lead II. Although the ST changes spontaneously resolved, the patient had prolonged disorientation. Whole- body computed tomography revealed several black rounded lucencies in the left ventricle and brain, confirming AGE. The patient received oxygen and remained supine. His neurological symptoms gradually improved but worsened again, necessitating HBOT. HBOT was performed seven times, after which neurological symptoms resolved almost completely. Conclusions: AGE can secondarily deteriorate after symptoms have subsided. We recommend that HBOT be performed promptly once severe symptoms appear, even if they resolve spontaneously.

Low Pneumoperitoneum Pressure Reduces Gas Embolism During Laparoscopic Liver Resection: A Randomized Controlled Trial.

OBJECTIVE: To compare the effect of low and standard pneumoperitoneal pressure (PP) on the occurrence of gas embolism during laparoscopic liver resection (LLR). BACKGROUND: LLR has an increased risk of gas embolism. Although animal studies have shown that low PP reduces the occurrence of gas embolism, clinical evidence is lacking. METHODS: This parallel, dual-arm, double-blind, randomized controlled trial included 141 patients undergoing elective LLR. Patients were randomized into standard ("S," 15 mm Hg; n = 70) or low ("L," 10 mm Hg; n = 71) PP groups. Severe gas embolism (≥ grade 3, based on the Schmandra microbubble method) was detected using transesophageal echocardiography and recorded as the primary outcome. Intraoperative vital signs and postoperative recovery profiles were also evaluated. RESULTS: Fewer severe gas embolism cases (n = 29, 40.8% vs n = 47, 67.1%, P = 0.003), fewer abrupt decreases in end-tidal carbon dioxide partial pressure, shorter severe gas embolism duration, less peripheral oxygen saturation reduction, and fewer increases in heart rate and lactate during gas embolization episodes was found in group L than in group S. Moreover, a higher arterial partial pressure of oxygen and peripheral oxygen saturation were observed, and fewer fluids and vasoactive drugs were administered in group L than in group S. In both groups, the distensibility index of the inferior vena cava negatively correlated with central venous pressure throughout LLR, and a comparable quality of recovery was observed. CONCLUSIONS: Low PP reduced the incidence and duration of severe gas embolism and achieved steadier hemodynamics and vital signs during LLR. Therefore, a low PP strategy can be considered a valuable choice for the future LLR.

[Air embolism after biliary stent removal during endoscopic retrograde cholangiopancreatography for cholangitis after biliary reconstruction: a case report].

A 62-year-old male patient underwent pancreaticoduodenectomy with modified Child reconstruction for distal cholangiocarcinoma. After eight years, a contrast-enhanced computed tomography (CT) revealed a recurrent lesion at the biliojejunal anastomosis, and a biliary stent was placed for obstructive cholangitis in the right posterior segment of the liver. A right hepatectomy was planned for a local recurrent lesion;thus, percutaneous transhepatic portal embolization was performed on the portal vein's right branch to enlarge the left liver. However, he was referred to our department for endoscopic retrograde biliary drainage for the subsequent cholangitis and liver abscess appearance. A double-balloon enteroscope under CO2 insufflation was used to reach the bile duct-jejunal anastomosis. After removing the bile duct stent with grasping forceps, his general condition suddenly deteriorated, causing cardiopulmonary arrest. He was diagnosed with air embolism based on the findings of air in the heart, aorta, and brain on CT after the return of spontaneous circulation. Treatment for the air embolism and subsequent complications continued in the intensive care unit, but he eventually died 114 days after the onset of the air embolism due to his deteriorating general condition. Pathological autopsy revealed cholangiocarcinoma that extends from the porta hepatis to the posterior segment. Additionally, the proximity between the bile duct and vein extended by the adenocarcinoma and the fibrous obstruction of the vein were revealed, indicating the possibility of a bile duct-vein shunt.