Intra-arterial Air Thrombogenesis after Cerebral Air Embolism Complicating Lower Extremity Sclerotherapy

Background  Cerebral arterial gas embolism is a potentially life-threatening event. Intraarterial air can occlude blood flow directly or cause thrombosis. Sclerotherapy is an extremely rare cause of cerebral arterial gas embolism. Method  Case-report. Results  A 38-year-old female suffered acute onset of a left middle cerebral artery (LMCA) syndrome with an NIH stroke score of 11 approximately ten minutes after lower extremity sclerotherapy. CT angiogram demonstrated LMCA intraarterial air. Patient fully recovered after hyperbaric oxygen treatment with complete resolution of intraarterial air. However, thrombus replaced intraarterial air despite anticoagulation with heparin. Conclusion  We provide radiological evidence of hyperbaric oxygen therapy resolving intraarterial air but also demonstrate the thrombogenic potential of this procedural complication.     

大脑空气栓塞2例报告

正1病例介绍病例1,女,61岁。主因"发现意识不清5 h"经急诊以"急性脑梗死"于2017年3月27日19:50收入院。入院5 h前,患者在飞机上(睡眠中)被家属发现意识不清,呼之不应,伴汗出、口角流涎,有发作性双上肢肢体不自主抖动。120接诊途中患者出现呕吐,呕吐物为胃内容物,无四肢抽搐、口吐白沫等症状。至入院前,患者神志不清,大便未解,小便正常。既往史:"乳腺癌术后"3年,否认高血压     

Paradoxical Cerebral Air Embolism after Cardiac Ablation in Williams-Beuren Syndrome: A Clinico-Pathological Correlation

Non-traumatic neurological deterioration is a medical emergency that may arise from diverse causes, to include cerebral infarction or intracranial hemorrhage, meningoencephalitis, seizure, hypoxic-ischemic or toxic/metabolic encephalopathy, poisoning, or drug intoxication. We describe the abrupt onset of neurological deterioration in a 53-year-old man with Williams-Beuren syndrome, a sporadically occurring genetic disorder caused by chromosomal microdeletion at 7q11.23. The clinical phenotype of Williams-Beuren syndrome is suggested by distinctive elfin facies, limited intellect, unique personality features, growth abnormalities, and endocrinopathies. The causative microdeletion of chromosomal material will frequently involve loss of the elastin gene, ELN, with resulting arteriopathy, supravalvular aortic stenosis, non-ischemic cardiopathy, and atrial fibrillation. Our patient sustained acute neurological decline within one month after undergoing a cardiac ablative procedure to convert atrial fibrillation to sinus rhythm. We present our findings in the setting of a clinico-pathological correlation, in which we reveal the cause of the abrupt neurological deterioration and discuss how our patient was affected by an uncommon stroke disorder.     

Spontaneous Cerebral Air Embolism Associated with Remote Lung Surgery

Introduction  Airembolism without obvious trauma or surgery is rare. Methods  Case report. Results  Four years after resection of a non-small cell lung cancer, a 57-year-old man presented with recurrent episodes of sudden onset neurological deficits. Head computer tomographic (CT) scans suggested air embolism, and further investigations showed a potential anastomosis between a pulmonary air cavity and a pulmonary vein. He was treated surgically by debridement of the bronchovascular bundles surrounding the air cavity. The patient had no further neurologic deficits during 10 months of post-surgical follow-up. Conclusion  In the absence of trauma, sinus disease, recent surgery, or vascular procedures, the presence of air in the brain is unusual, and pulmonary sources of air embolism should be considered.     

Cerebral Air Embolism after Esophagogastroduodenoscopy: Insight on Pathophysiology,Epidemiology, Prevention and Treatment

BackgroundAir embolism is an extremely rare complication that can follow gastrointestinal endoscopy. The most accepted treatment of cerebral air embolism (CAE) is hyperbaric oxygen (HBO). Limited evidence suggests that lidocaine may have a neuroprotective effect. The exact mechanism does not appear to be well elucidated.MethodsWe conducted a literature search using multiple combinations of keywords from PubMed and Ovid Medline databases according to the PRISMA guidelines. We included articles with cases of air embolism caused by an esophagogastroduodenoscopy (EGD). We excluded cases related to other procedures e.g. colonoscopy, endoscopic retrograde cholangiopancreatography, cholangioscopy, Kasai procedure, bronchoscopy, laparoscopy or thoracoscopy. We were able to identify 30 cases of CAE associated with EGD. We included our experience in treating one patient with CAE after elective EGD.ResultsGiven the results of our literature search and this patient's characteristics, we chose to treat our patient with HBO and lidocaine infusion. Our case series consists of 31 patients of post EGD CAE, the mean age was 63.7 ± 11.14 years, 38.7% of the patients were women (n = 12). 38.7% of the cases underwent esophageal dilatation (n = 12), while 19.35% had EGD biopsy (n = 6), 9.6% had variceal ligation (n = 3), and 3.22% had variceal banding (n = 1). In 20 out of 31 cases, echocardiography has been documented, 20% of those patients (n = 4) had patent foramen ovale. HBO was used in treatment of 48% of cases (n = 15), among the included patients, 61% survived (n = 19). Our patient showed significant neurological improvement.ConclusionsDespite the rare incidence of CAE during or after EGD, physicians should be aware of this potential complication. In patients who develop sudden acute neurological symptoms, early diagnosis and intervention may prevent devastating neurological injury and death. The most accepted emergent treatment for CAE includes HBO, consideration of lidocaine, and work-up of source of the air embolism.     

Kinetics of Elimination and Acute Consequences of Cerebral Air Embolism

The pathophysiology of arterial air embolism inducing brain injuries remains unclear. Previous experiments demonstrated the usefulness of computed tomography (CT) in the detection of air emboli in canine brain. This canine study investigates CT's ability to detect small air bubbles and to determine the kinetics of air elimination from cerebral arteries and it's relationship with clinical, electroencephalographic (EEG), and histological manifestations. CT detects small air embolism, and intracerebral air volume strongly correlates with injected air dose (r² = 0.86, p = 2 × 10 ³) Air clearance time significantly depends on intracerebral air volume (r² = 0.86, p = 0 04) and on the number of bubbles (r² = 0.71, p = 0 03), whereas half–life of air elimination does not. No relationship was found between injected air dose, air clearance time, intracerebral volume of air, and clinical, EEG, and histological findings. The data indicate that CT accurately detects small air bubbles in the early course of cerebral air embolism, that air elimination from cerebral arteries follows a first–order compartment model, and that early CT findings do not correlate with clinical, EEG, and histological manifestations.     

Involvement of Jugular Valve Insufficiency in Cerebral Venous Air Embolism

BACKGROUND: Cerebral venous air entrapment is a rare finding on cranial computed tomography (CT) scan. Peripheral air embolism is discussed as a potential cause. However, the mechanism of retrograde passage through internal jugular valves and veins is unclear. CASE REPORT: The case of a patient is reported, who had air entrapment in the left cavernous sinus. Prior to CT scanning, a peripheral intravenous line had been placed. Ultrasound revealed excessive insufficiency of the left internal jugular valve. To further study the mechanism of embolism, an echo contrast agent was injected into the cubital vein. A Valsalva maneuver resulted in retrograde transition of microbubbles across the insufficient valve. Valvular function on the unaffected right side was intact. CONCLUSIONS: This case report gives insight into the mechanism of cerebral venous air embolism. This is the firstcase describing jugular valve insufficiency as the missing link between peripheral air embolism and cerebral venous air entrapment.     

Fatal Massive Cerebral Air Embolism in a Lung Transplant Patient

Introduction  

Massive air embolism has been described in multiple clinical scenarios, especially in critical ill patients who undergo invasive procedures. Nevertheless, air embolism is often unrecognized and a high index of suspicion is required to diagnose this entity. Two previous cases of air embolism in lung transplant patients have been described in the literature; we describe a third case of fatal massive air embolism and cardiovascular collapse in a lung transplant patient.     

航空旅行诱发脑空气栓塞1例报道

正1病例介绍患者男性,63岁,主因被发现意识不清4小时于2020年5月20日就诊于首都医科大学附属北京天坛医院神经内科急诊。患者入院前7 h独自乘坐飞机,登机时正常。4 h前(下飞机前)被发现意识不清,具体发病时间及情况不详。当时无肢体抽搐、二便失禁。下机后被送至附近医院,头颅CT检查未见出血。为求进一步诊治转来我院。     

Diffuse Cerebral Air Embolism Treated With Hyperbaric Oxygen: A Case Report

A 54-year-old woman presented for cardiac evaluation of atypical chest pain. Workup included coronary angiography and a left ventriculogram, during which air was inadvertently injected, resulting in the development of an acute right hemisphere syndrome. Right carotid angiography was immediately performed, yielding only a delayed diffuse venous phase without focal vessel cutoffs. Within 60 minutes, the patient underwent hyperbaric oxygen therapy for the suspected cerebral air emboli. After removal from the chamber for technical reasons, she had a generalized tonic-clonic seizure, and further hyperbaric oxygen therapy was withheld. Initial computed tomography imaging obtained approximately 8 hours after symptom onset showed signs of early right hemispheric edema. Subsequent magnetic resonance imaging studies were markedly abnormal and suggestive of diffuse bilateral but predominantly right-sided parietal lobe edema with mildly positive diffusion-weighted imaging. Follow-up magnetic resonance imaging at 6 months was normal, and the patient's neurological examination returned to normal.     

缺血性卒中患者餐后高血糖与下肢静脉血流动力学相关性的研究

目的 探讨缺血性卒中患者餐后高血糖与下肢静脉血流动力学的相关性。 方法 筛选前循环轻度缺血性卒中住院患者,根据口服葡萄糖耐量试验（oral glucose tolerance test, OGTT）中2 h血糖水平（2-h plasma glucose,2hPG）将餐后高血糖患者设为实验组（90例）,血糖正常患 者设为对照组（72例）。采用彩色多普勒超声检查两组患者下肢深静脉的形态、结构,测量下肢静脉 管径及峰值流速,采用全自动生化分析仪测定两组生化指标。 结果 两组患者性别、年龄、吸烟、饮酒、高血压、美国国立卫生研究院卒中量表评分（National Institutes of Health Stroke Scale,NIHSS）、体质指数（body mass index,BMI）、总胆固醇（total cholesterol, TC）、甘油三酯（triglyceride,TG）、低密度脂蛋白胆固醇（low density lipoprotein-cholesterol,LDL-C）、高密 度脂蛋白胆固醇（high density lipoprotein-cholesterol,HDL-C）水平比较,差异无统计学意义;实验组2hPG 水平高于对照组,实验组髂总静脉、髂内静脉、股总静脉、腘静脉的内径大于对照组,实验组髂总静 脉、髂内静脉、股总静脉、腘静脉的峰值流速低于对照组,比较差异均有统计学意义（P＜0.05）。 结论 缺血性卒中伴餐后高血糖患者下肢静脉血流速度变慢,内径也相应变大,会增加下肢静脉 血栓发生风险,不利于患者预后。     

Cerebral Air Embolism Resulting in Fatal Stroke in an Airplane Passenger with a Pulmonary Bronchogenic Cyst

Introduction  Cerebral air embolism is a rare cause of stroke, but may occur in patients undergoing invasive cardiac and pulmonary procedures, as well as in divers suffering pulmonary barotrauma from rapid ascent. Cerebral air embolism during air travel, however, is particularly rare. Case  We present a case of a previously healthy gentleman who presented with an acute stroke after a commercial flight; the stroke was initially felt to be of cardioembolic origin. A large intrapulmonary cyst was noted on his imaging studies, but thought to be an incidental finding. During a return flight, he suffered another stroke and was found to have cerebral air emboli. Conclusion  This case suggests the importance of considering cerebral air embolism in patients with stroke associated with air travel; restricting air travel in patients with intrapulmonary cysts may be prudent.     

Cerebral Embolism of Iodized Oil (Lipiodol) after Transcatheter Arterial Chemoembolization for Hepatocellular Carcinoma

Cerebral lipiodol embolism is a rare complication of transcatheter arterial chemoembolization (TACE). Its pathological mechanism remains ambiguous despite several investigations. In Case 1, a 67-year-old man with hepatocellular carcinoma (HCC) experienced neurological deficits soon after undergoing a fourth session of TACE. Computed tomography (CT) scan showed multiple hyperdense lesions along the gyrus of frontal lobes and in the subcortical white matter. Transcranial Doppler (TCD) and transesophageal echocardiogram performed during the intravenous injection of agitated saline documented the presence of a right-to-left shunt (RLS) by demonstrating microbubbles in the left middle cerebral artery and left atrium. In Case 2, a 63-year-old woman underwent a third TACE due to a large HCC. After the procedure, her mental status deteriorated. Brain CT showed multiple hyperdense lesions on the cerebral and cerebellar cortex. TCD with agitated saline showed multiple microembolic signals shortly after the injection of agitated saline. The risk of cerebral lipiodol embolism may increase with recurrence and progression of HCC in patients who have a pre-existing RLS in the heart or lung. A test for the detection of an RLS may be necessary to identify patients with a heightened risk of cerebral embolism when multiple TACE procedures are required. TACE for HCC can cause pulmonary embolism or infarction. ^1,2 However, cerebral lipiodol embolism is rare after TACE. There have been several reports of cerebral embolism after TACE, but their exact mechanism has not yet been fully elucidated. We report herein 2 patients who developed cerebral lipiodol embolism after undergoing multiple TACE procedures for remnant HCC through a pre-existing RLS.