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.

Air Medical Transport of a 12-Year-Old Girl With Cerebral Gas Embolism Due to Helium Inhalation.

This case report describes the initial care and transport considerations of a pediatric patient who suffered from cerebral gas embolism sustained after inhalation of helium from a pressurized tank. The patient demonstrated neurologic symptoms necessitating hyperbaric oxygen therapy and required fixed wing air transport across a mountain range from a rural community hospital to a tertiary center for the treatment. We review the pathophysiology of cerebral gas embolism and strategies for transporting patients with cerebral gas embolism and other trapped gas.

Systemic Venous Air Emboli After Emergent Hyperbaric Therapy for Carbon Monoxide Poisoning.

BACKGROUND A venous air embolism is a rare condition but could have a disastrous effect on vital organs. It usually occurs due to iatrogenic sources, such as central venous catheter insertion, neurosurgery, and other invasive procedures. In most cases, hyperbaric oxygen therapy (HBOT) is the best treatment for those conditions. However, multiple venous air emboli after hyperbaric oxygen therapy has not been reported in the literature. CASE REPORT An 82-yr-old woman came to the Emergency Department after inhalation of fumes at the scene of a house fire. She had dizziness and nausea. Her vital signs were normal at the time of presentation. She received HBOT for carbon monoxide poisoning. Soon after the HBOT, the patient started to have dizziness, abdominal pain, and leg pains. Computed tomography scans showed multiple systemic venous air emboli throughout the portal venous system and femoral veins. The air emboli totally disappeared after HBOT with a longer ascent time. CONCLUSIONS To the best of our knowledge, this is the first case of multiple systemic venous air bubbles after emergent HBOT. Physicians should be aware of any kind of complications when treating patients who need HBOT in the emergent setting. Although decompression sickness following HBOT is extremely rare, it should not be ignored by emergency physicians.

Clinical Characteristics, Imaging Findings, and Outcomes of Cerebral Air Embolism.

BACKGROUND: Arterial cerebral air embolism (CAE) is an uncommon but potentially catastrophic event. Patients can present with focal neurologic deficits, seizures, or coma. They may be treated with hyperbaric oxygen therapy. We review the causes, radiographic and clinical characteristics, and outcomes of patients with CAE. METHODS: We performed a retrospective chart review via an existing institutional database at Mayo Clinic to identify patients with arterial CAE. Demographic data, clinical characteristics, and diagnostic studies were extracted and classified on predefined criteria of diagnostic confidence, and descriptive and univariate analysis was completed. RESULTS: Fifteen patients met criteria for inclusion in our study. Most presented with focal deficits (80%) and/or coma (53%). Seven patients (47%) had seizures, including status epilepticus in one (7%). Five presented with increased muscle tone at the time of the event (33%). Computed tomography (CT) imaging was insensitive for the detection of CAE, only identifying free air in 4 of 13 who underwent this study. When obtained, magnetic resonance imaging typically showed multifocal areas of restricted diffusion. Six patients (40%) were treated with hyperbaric oxygen therapy. Age, Glasgow Coma Scale score at nadir, and use of hyperbaric oxygen therapy were not associated with functional outcome at 1 year in our cohort. Twenty-six percent of patients had a modified Rankin scale score of 0 one year after the event, and functional improvement over time was common after discharge. CONCLUSIONS: A high index of clinical suspicion is needed to identify patients with CAE because of low sensitivity of free air on CT imaging and nonspecific clinical presentation. Acute alteration of consciousness, seizures, and focal signs occur frequently. Because improvement over time is possible even among patients with severe presentation, early prognostication should be approached with caution.

Massive cerebral air embolism following percutaneous transhepatic biliary drainage: A case report.

RATIONALE: Cerebral air embolism from portal venous gas rarely occurs due to invasive procedures (e.g., endoscopic procedures, liver biopsy, or percutaneous transhepatic biliary drainage) that disrupt the gastrointestinal or hepatobiliary structures. Here, we report a rare case of fatal cerebral air embolism following a series of percutaneous transhepatic biliary drainage tube insertions. PATIENT CONCERNS: A 50-year-old woman with a history of cholecystectomy, liver wedge resection, and hepaticojejunostomy for gallbladder cancer presented with altered mental status 1 week after percutaneous transhepatic biliary drainage tube placement. DIAGNOSES: Extensive cerebral air embolism and acute cerebral infarction. INTERVENTIONS: Brain computed tomography and magnetic resonance imaging, hyperbaric oxygen therapy, medical therapy. OUTCOMES: Despite the use of hyperbaric oxygen therapy and medical treatment including vasopressors, the patient eventually died due to massive systemic air embolism. LESSONS: To date, there have been no reports of cerebral air embolism due to percutaneous transhepatic biliary drainage with pronounced radiologic images. We reviewed previously reported fatal cases associated with endoscopic hepatobiliary procedures and assessed the possible mechanisms and potential causes of air embolism.

Air embolism during lumbar surgery in the prone position.

Only a few clinical cases of cerebral arterial gas embolism during spinal surgery are published. It seems important not to overlook this diagnosis in order to initiate rapid appropriate treatment. This was a suspected case of paradoxical gas embolism revealed postoperatively by neurological deficits and whose recovery was noted during hyperbaric oxygen treatment. Unfortunately, no complementary examination showed gas embolism and only the context, the clinical picture and the case evolution evoke this diagnosis. The diagnostic difficulty in the immediate postoperative period is highlighted.

Cerebral arterial air embolism after endobronchial electrocautery: a case report and review of the literature.

BACKGROUND: Endobronchial electrocautery is a common and safe therapeutic endoscopic treatment for malignant airway obstruction. Cerebral arterial air embolism (CAAE) is a rare but potentially fatal complication of endobronchial electrocautery. CASE PRESENTATION: We present the first case of cerebral arterial air embolism after endobronchial electrocautery. A 56-year-old male with a pulmonary tumour in the right upper lobe received repeated endobronchial electrocautery. During the procedure, he experienced unresponsiveness, hypoxemia and bradycardia, and he developed tetraplegia. Brain computed tomography showed several cerebral arterial air emboli with low-density spots in the right frontal lobe. He received hyperbaric oxygen therapy with almost full recovery, except for residual left-sided weakness. CONCLUSIONS: General physicians should realize that CAAE may be a possible complication of endobronchial electrocautery. Several measures, including avoiding positive pressure, lowering ventilatory pressures if possible, avoiding advancing the bronchoscope to occlude the bronchus and using the non-contact technique, should be used to prevent this devastating complication.

Pulmonary barotrauma with cerebral arterial gas embolism from a depth of 0.75-1.2 metres of fresh water or less: A case report.

During underwater vehicle escape training with compressed air, a fit 26-year-old soldier suffered pulmonary barotrauma with cerebral arterial gas embolism after surfacing from a depth of 0.75-1.2 metres of freshwater or less. She presented with an altered level of consciousness. Rapid neurological examination noted slurred speech, a sensory deficit and right hemiparesis. Eleven hours after the accident, hyperbaric oxygen treatment was initiated using US Navy Treatment Table 6. The soldier almost completely recovered after repeated hyperbaric oxygen treatment. Given the very shallow depth this is an unusual case with only two similar case reports published previously.

Variability in venous gas emboli following the same dive at 3,658 meters.

Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the Cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver presented with symptoms of DCS following the dive or two hours post-dive at altitude. Despite inter- and intra-diver variability of VGE grade following the dives, the majority (11/20 dives) presented a peak VGE Grade 0, three VGE Grade 1, one VGE Grade 2, four VGE Grade 3, and one VGE Grade 4. Using the Cross correction method for a 66-fsw dive at 12,000 feet of altitude resulted in a relatively low decompression stress and no cases of DCS.

Application of a new hyperbaric oxygen therapy protocol in patients with arterial and venous gas embolism due to hydrogen peroxide poisoning.

Hydrogen peroxide (H2O2) ingestion can cause vascular gas embolism (GE). Hyperbaric oxygen therapy (HBO2) is known to improve neurological abnormalities in patients with arterial gas embolism (AGE). Previously, HBO2 based on the U.S. Navy Table 6 diving protocol has been adopted for treating AGE and preventing the progression of portal venous GE, caused by H2O2 ingestion, to AGE. However, the indication and protocol for HBO2 have not been established for GE related to H2O2 ingestion. Herein, we describe a case in which GE caused by H2O2 ingestion was treated using HBO2 with a short protocol. A 69-year-old female patient presented with abdominal pain, vomiting, and transient loss of consciousness after ingesting 35% H2O2. Computed tomography revealed gastric wall and portal venous gas. She was administered an HBO2 protocol with 2.8-atmosphere absolute (ATA) compression for 45 minutes. This was followed by a 2.0-ATA treatment for 60 minutes with a five-minute air break, after which all gas bubbles disappeared. After HBO2 treatment, brain magnetic resonance imaging revealed focal cytotoxic edema lesions; however, the patient was discharged without additional symptoms.

Cerebral arterial gas embolism in a patient with hypoplastic left heart syndrome treated with emergent hyperbaric oxygen: case report.

A 30-year-old female with a history of seizure disorder and hypoplastic left heart syndrome treated with a Norwood procedure in 1986 followed by a modified non-fenestrated Fontan (Left SVC to IVC to pulmonary arteries) with a known baffle leak presented to the emergency department. On day of presentation, the patient became unresponsive, with perioral cyanosis, rightward gaze and a left facial droop near the end of a platelet transfusion. An emergent non-contrast head CT revealed intracranial air in the right MCA distribution. She was taken to the hyperbaric chamber and was treated with a U.S. Navy Table 6 in a multiplace chamber with no extensions. Ten minutes into the treatment patient became more alert and spontaneously asked questions. The following day she was treated with a U.S. Navy Table 5. Patient had repeat CT of the head, which showed resolution of intracerebral gas and small areas of ischemia in right frontal lobe and right caudate. On hospital day five neurologic exam was normal, with 5/5 strength and no residual deficits. Treating the patient was a concern because patient has a single ventricle, in which the pulmonary artery is connected directly to the vena cava. There is very little data regarding the effects of hyperbaric oxygen (HBO2)therapy on single-ventricle physiology. Only two case reports of three pediatric patients treated with HBO2 for CAGE in a similar setting are known. In these cases the patients had improvements in their symptoms following HBO2. These cases and ours indicate HBO2 is feasible and indicated for CAGE in patients with cyanotic congenital heart disease.

Review of Thoracic Causes of Systemic Arterial Air Embolism on Computed Tomography.

Systemic arterial air embolism (SAAE) is a rare but potentially life-threatening condition that may occur when air enters into pulmonary veins or directly into the systemic circulation after pulmonary procedures (biopsy or resection) or penetrating trauma to the lung. While venous air embolism is commonly reported, arterial air embolism is rare. Even a minor injury to the chest along with positive-pressure ventilation can cause SAAE. Small amounts of air may cause neurological or cardiac symptoms depending on the affected arteries, while massive embolism can result in fatal cardiovascular collapse. We discuss the various causes of SAAE, including trauma, computed tomography-guided lung biopsy, and various intervention procedures such as mechanical circulatory support device implantation, coronary catheterization, and atrial fibrillation repair. SAAE diagnosis can be overlooked because its symptoms are not specific, and confirmation of the presence of air in the arterial system is difficult. Although computed tomography is the optimal imaging tool for diagnosis, patient instability and resuscitation often precludes its use. When imaging is performed, awareness of the causes of SAAE allows the radiologist to promptly diagnose the condition and relay findings to the clinicians so that treatment, namely hyperbaric oxygen therapy, may be started promptly.

Systemic air embolism in a fungal pneumonia patient with lung cavities formation and review of literature.

Systemic air embolism is a rare but potentially fatal complication related to many factors. The purpose of this article is to alert clinicians once patients occurs an abnormal neurological and cardiovascular status, following minor traumatic treatment, air embolism should be considered. A 20-year-old man who presented with fungal pneumonia with lung cavities formation was admitted to an intensive care unit (ICU) and received positive airway pressure ventilation. Four days later, the fungal pneumonia was improved, but the patient's blood pressure and arterial oxygen saturation deteriorated, so computed tomography (CT) scans were preformed to reevaluate him. The scans detected air embolism in the left atrium and ventricle, ascending aorta, aortic arch and its branches (right brachiocephalic, bilateral common carotid and right subclavian arteries), descending aorta and right coronary artery. A CT scan of the abdomen revealed air in the spleen, cauda pancreatic, superior mesenteric artery and right external iliac artery. The patient died two days later from multiple organ dysfunction. We suggest that vascular air embolism should be considered under mechanical ventilation when patients' neurologic and cardiovascular status deteriorates, and hyperbaric oxygen therapy should be conducted immediately.

Multifocal Stroke From Ozone Gas Emboli.

A 34-year-old man with chronic neck pain was treated with regular cervical paravertebral ozone injections. After his last injection, he experienced a syncopal episode and, upon awakening, was found to have ataxia, aphasia, hemiparesis, and left sixth nerve palsy. Computed tomographic angiography demonstrated intra-arterial gas in the right vertebral artery; multiple posterior circulation infarcts were seen on brain MRI. This case illustrates the potential dangers of paravertebral injections of ozone.

Venous air embolism: ultrasonographic diagnosis and treatment with hyperbaric oxygen therapy.

A man with neuromuscular respiratory failure requiring intubation and ventilation suffered a venous air embolism during inadvertent administration of 5 ml of air. Ultrasound (US) imaging confirmed an air embolus in the left subclavian vein, which was only partially treated by US-guided aspiration. The embolus completely resolved on US imaging during hyperbaric oxygen therapy, and the patient recovered with no complications secondary to the embolism. Venous air embolism is under-recognised, and can cause siginificant neurological morbidity and death if untreated. When available, urgent hyperbaric oxygen therapy appears to be an effective approach.

A Rare Case of Cerebral Air Embolism Caused by Pulmonary Arteriovenous Malformation After Removal of a Central Venous Catheter.

Cerebral air embolism following central venous catheter (CVC) removal is extremely rare. We report a case of cerebral air embolism with loss of consciousness after removal of CVC caused by pulmonary arteriovenous malformation (PAVM). Computed tomography revealed air bubbles in the internal carotid arteries along the sulci in the cerebral hemispheres, as well as a PAVM. The cerebral air embolism was treated with hyperbaric oxygen and intravenous thrombolytic therapy, and transcatheter embolization of the PAVM was performed. When inserting/removing CVC in a patient with a small PAVM, treatment of the PAVM, irrespective of its size, could prevent the type of complication that occurred in our present case.

Implementation of Targeted Temperature Management in a Patient with Cerebral Arterial Gas Embolism.

Cerebral arterial gas embolism (CAGE) shows various manifestations according to the quantity of gas and the brain areas affected. The symptoms range from minor motor weakness, headache, and confusion to disorientation, convulsions, hemiparesis, unconsciousness, and coma. A 46-year-old man was transferred to our emergency department due to altered sensorium. Immediately after a controlled ascent from 33 m of seawater, he complained of shortness of breath and rigid extremities, lapsing into unconsciousness. He was intubated at another medical center, where a brain computerized axial tomography scan showed no definitive abnormal findings. Pneumothorax and obstructing lesions were apparent in the left thorax of the computed tomography scan. Following closed thoracostomy, we provided hyperbaric oxygen therapy (HBOT) using U.S. Navy Treatment Table (USN TT) 6A. A brain magnetic resonance imaging diffusion image taken after HBOT showed acute infarction in both middle and posterior cerebral arteries. We implemented targeted temperature management (TTM) to prevent worsening of cerebral function in the intensive care unit. After completing TTM, we repeated HBOT using USN TT5 and started rehabilitation therapy. He fully recovered from the neurological deficits. This is the first case of CAGE treated with TTM and consecutive HBOTs suggesting that TTM might facilitate salvage of the penumbra in severe CAGE.

Cerebral Artery Gas Embolism Following Navigational Bronchoscopy.

INTRODUCTION: Cerebral artery gas embolism (CAGE) is a rare but serious adverse event with potentially devastating neurologic sequelae. Bronchoscopy is a frequently performed procedure but with only a few reported cases of CAGE. METHODS: We report the first documented case of CAGE associated with electromagnetic navigational bronchoscopy. RESULTS: A 61-year-old man with a left lower lobe nodule underwent electromagnetic navigational bronchoscopy. The target lesion underwent transbronchial biopsy, brushing and an end-procedure lavage. Following the procedure, he developed seizures, evidence of hypoxic injury and cerebral edema, and air emboli were seen on computed tomography imaging. He then underwent treatment with hyperbaric oxygen with a full and complete neurologic recovery. Review of other cases reported in the literature suggests improved neurologic outcomes with hyperbaric oxygen treatment. CONCLUSIONS: Biopsy techniques performed during bronchoscopy and electromagnetic navigational bronchoscopy can result in CAGE. Comparison with other reported cases suggests improved neurologic outcomes in those treated with hyperbaric oxygen. Prompt recognition of this complication and timely treatment with hyperbaric oxygen are the cornerstones to recovery.