Arterial Gas Embolism

Etiology

As mentioned, air entry into the systemic circulation is an air embolism. Introducing air into the venous system results in a pulmonary embolism, whereas when air enters the arterial circulation system, it is referred to as an arterial gas embolism. Air can enter the bloodstream through two main methods. Firstly, it can directly pass from the atmosphere into the blood vessels, often occurring during surgical procedures involving incisions. Secondly, air can indirectly enter the circulation due to pressure gradients, such as during diving activities. 

Air can cause arterial embolism through direct entry into the arterial circulation or indirect transfer from the venous circulation. The table below provides an outline of these mechanisms[3][4]:

An arterial gas embolism can arise from various causes. One common etiology is severe decompression sickness during the ascent phase of diving.[4] However, it can also result from ruptured alveoli caused by lung barotrauma or the migration of gas from the venous circulation through a pre-existing right-to-left shunt, such as ventricular septal defect (VSD) or atrial septal defect (ASD).[25] In addition to environmental factors, arterial gas embolisms can also result from iatrogenic causes related to medical and surgical procedures. Examples include percutaneous lung biopsy, tumor ablation, and arterial catheterization. These procedures can inadvertently introduce air into the arterial circulation, contributing to the development of arterial gas embolism.

Factors such as improper catheter flushing and balloon rupture during arterial catheterization can be potential causes.[26] Blunt and penetrating thoracic trauma have also been reported as causes, likely resulting from bronchial injury and associated pulmonary vein injury.[27] Additionally, there have been cases related to catheter ablation procedures for atrial fibrillation.[28] Awareness of these iatrogenic causes is crucial for healthcare providers to minimize the risk and promptly address arterial gas embolism during procedures.

Epidemiology

The entry of air into the arterial circulation is typically rare due to the protective nature of the high pressures of the arterial vascular system. Due to the varying clinical presentations, the potential failure to recognize and document cases, and different disease etiologies, the true incidence of arterial gas embolism remains unknown. In scuba diving, the incidence of air gas embolisms can range from 0.4 to 1 per 100,000 dives.[29] It is important to note that the frequency of occurrence may increase with deeper and longer dives. In patients undergoing cardiac bypass surgery, the prevalence of arterial gas embolisms can be as low as 0.003% and 0.007%; however, approximately 50% of these incidences can result in serious adverse outcomes.[30] Prospective cohort studies have reported the incidence to be 2.65 per 100,000 hospitalizations.[31] In addition to arterial gas embolism, other types of embolism, such as intracoronary embolism, can also occur. The overall incidence of significant air embolism is approximately 0.2%, and it can vary depending on the specific procedure, such as percutaneous transluminal coronary angioplasty versus diagnostic coronary angiography. It can also be affected by the years of training of the healthcare professionals involved.[32]

Pathophysiology

The pathophysiological effects of an arterial gas embolism are determined by the specific location of the embolism within the arterial system. The degree of impairment is influenced by several factors, including the type of gas involved (such as room air, carbon dioxide, helium, or nitrous oxide), the volume of the gas, the rate at which the embolism occurs, the presence of collateral circulation, and the presence of intracardiac or intrapulmonary shunts. The detrimental effects of an arterial gas embolism extend beyond the reduction of blood flow to the affected areas. Air bubbles initiate an inflammatory cascade, contributing to additional damage. A lethal volume of an air embolism is reported to be 3 to 5 ml/kg.[30] Furthermore, estimates suggest that introducing 300 ml to 500 ml of gas at a rate of 100 ml/sec is considered a fatal dose.[30]

Arterial gas embolisms resulting from iatrogenic procedures refer to air entry into the arterial circulation during medical or surgical interventions, potentially leading to significant complications and adverse outcomes. During iatrogenic procedures, an arterial gas embolism migrates from the venous to the arterial circulation, resulting in tissue ischemia, including conditions such as cardio-cerebral infarction.[33] The presentation can be similar to the features of a pulmonary embolism. The air in the pulmonary artery will lead to an increased pulmonary artery and right ventricular pressure. Increased pressures in the right ventricle may lead to right-sided heart failure, reduction in cardiac output, and even arrhythmias. Additionally, the air in the pulmonary artery will cause a ventilation-perfusion mismatch, which leads to intrapulmonary shunting, and increased alveolar dead space. The air in the left ventricle will impede diastolic filling leading to complete cardiovascular compromise. Air can also be pumped from the left ventricle into the coronary vasculature, leading to myocardial ischemia.[34]

Numerous processes contribute to forming arterial gas embolisms in diving-associated air gas embolisms. Lung barotrauma during rapid ascent can cause alveoli to burst.[35] During rapid ascension from deep water diving or sea level to high altitude, dissolved gas can expand and form bubbles that block small vessels.[36] If these bubbles form in the arterial circulation, they can cause end-organ damage. In addition, venous gas emboli can develop during rapid ascent from sea level to high altitude. The resulting venous gas emboli are usually very small (<700 μm)[37] and hence can be filtered by pulmonary capillaries.[38] However, some larger venous gas emboli can reach the arterial circulation through right-left shunts or septal wall heart defects such as patent foramen ovale (PFO) and atrial septal defects (ASD).[39] The presence of ASD or PFO increases the possibility of decompression sickness presentations, circulation disruption, and impaired cerebral blood flow resulting in brain hemorrhage and ischemia.[39][40] Unlike thrombotic stroke, stroke related to arterial gas embolism can resolve spontaneously or after compression therapy as the gas is reabsorbed, leading to inflammation and endothelial injury.

Histopathology

An arterial gas embolism occurs when gas bubbles directly injure the endothelium of postcapillary vessels, activating cellular and humoral responses. This injury triggers a cascade of events that contribute to the pathogenesis of the gas embolism.

History and Physical

The signs and symptoms of arterial gas embolisms can vary depending on the underlying causes and the affected organ systems. An arterial gas embolism commonly occurs during ascent from diving or within a few minutes (<10 minutes) of reaching the surface.[41] Classically the presentation of the arterial gas embolism is often catastrophic due to obstruction of blood vessels by gas bubbles, leading to infarction and sudden collapse. The severity of symptoms can vary depending on the affected organ system, but when the central nervous system is involved, the symptoms can be particularly pronounced and mimic a stroke. 

In severe cases, an arterial gas embolism can lead to cardiovascular collapse, characterized by a sudden drop in blood pressure, irregular heartbeat, and shock-like symptoms. The gas bubbles may also affect pulmonary circulation, causing respiratory symptoms to also be present, including shortness of breath, rapid breathing, chest pain, and coughing up blood.

If the affected individual does not die suddenly, the initial symptoms can be minor and easily missed. However, the symptoms become more pronounced and distinctive whenever the central nervous system is affected, often presenting as multifocal deficits involving multiple cerebrovascular territories. These symptoms may include hemiparesis and abnormal coordination. The most common initial manifestation of arterial gas embolism is loss of consciousness (39%), confusion (37%), or dizziness (30%).[41] Other potential manifestations are hemiplegia (27%), visual changes (21%), headache (20%), dysphasia (11%), and seizures (11%). Therefore, if divers or individuals who have been exposed to situations prone to gas embolism develop symptoms such as loss of consciousness, altered mental status, hemiparesis, seizures, or focal neurological deficits, within minutes of surfacing, an arterial gas embolism is very likely to be the primary etiology. 

When evaluating a patient with a suspected arterial gas embolism, history should aim to gather information about the onset, location, and duration of symptoms and any potential inciting events and factors that may worsen or alleviate the symptoms. Obtaining a detailed history may be challenging for patients with cerebral involvement secondary to an arterial gas embolism due to neurological symptoms and potential loss of consciousness. Many cases of arterial gas emboli are of iatrogenic etiology. Therefore it should be considered during invasive medical procedures such as central venous catheter placement, invasive monitoring, endoscopic procedures, and surgical interventions.[42]

In patients with a delayed presentation of symptoms, the history should primarily focus on identifying any recent procedures or events that may be associated with an arterial gas embolism. This includes lung biopsy, tumor ablation, recent arterial catheterization, or any recent lung or chest trauma that could lead to fistulas forming between airways and pulmonary vasculature.

Additionally, it is essential to inquire about symptoms that began following rapid ascent during diving. For example, a diving-related arterial gas embolism can occur when ascending too quickly, leading to the formation and release of gas bubbles in the bloodstream.

The physical examination should be thorough but not interfere with emergency intervention for airway compromise, breathing, or circulation. Monitor the patient's vital signs, including blood pressure, heart rate, respiratory rate, and oxygen saturation, as they can provide essential clues to the overall hemodynamic stability and respiratory function. A complete cardiovascular evaluation is warranted to assess for murmurs, signs of heart failure, bradycardia, hypotension, or pulse deficits. A comprehensive pulmonary examination should focus on listening for abnormal breath sounds, diminished lung sounds, or any signs of respiratory distress. A neurological exam should focus on cranial nerve deficits, motor weakness, and sensory loss. The Glasgow coma scale (GCS) assessment is also important to assess the level of consciousness in patients with altered mental status. GI exam should look for any signs of mesenteric ischemia. This includes peritoneal symptoms, such as abdominal tenderness, guarding, rebound tenderness, and abnormal bowel sounds. Other examination components can be performed as necessary by the patient's chief complaint. 

Evaluation

An arterial air embolism diagnosis is based primarily on clinical presentation and the patient's history. Therefore, no specific lab test can confirm the presence of an arterial air embolism. However, laboratory testing can help assess the affected organ system or systems and provide supportive information. Some examples of relevant laboratory investigations include:

• Blood gas analysis: Arterial blood gas (ABG) analysis can help evaluate the patient's oxygen and carbon dioxide levels and acid-base status. ABG results may show hypoxemia and respiratory alkalosis due to impaired gas exchange caused by the embolism.
• Cardiac enzymes: Measurement of cardiac enzymes, such as troponin, may be considered to assess for cardiac injury or myocardial infarction, particularly in cases where there is suspected involvement of the coronary arteries.
• Complete blood count (CBC): A CBC may be ordered to assess for evidence of infection or anemia, which could be associated with specific causes or complications of arterial gas embolism.
• Coagulation profile: Coagulation studies, including prothrombin time (PT), activated partial thromboplastin time (aPTT), and platelet count, may be considered to evaluate for any coagulopathy that could contribute to or result from the embolic event. 

Imaging studies, such as magnetic resonance imaging (MRI) and computed tomography (CT), can provide valuable information in evaluating an arterial gas embolism. Still, it is essential to note that these modalities are not highly sensitive for directly detecting air embolism.[43]

• MRI: While MRI can help assess organ damage and detect secondary effects of arterial gas embolism, such as ischemic changes or infarction, it is not sensitive to directly visualizing air bubbles. MRI is beneficial in evaluating the central nervous system (CNS) involvement and can identify areas of cerebral infarction or edema
• CT: CT scans can reveal indirect signs of arterial gas embolism, such as gas in blood vessels or air in unusual locations. However, the sensitivity of CT for directly detecting small air bubbles is limited. CT angiography may assess the vasculature and identify potential gas embolism causes, such as vascular injury or iatrogenic sources.

In addition, obtaining CT in these patients can be challenging as they require extensive resuscitation and stabilization before a definitive diagnosis.[27] 

Other imaging techniques, such as bedside transthoracic echocardiography, may be used to evaluate the presence of air bubbles, assess cardiac function, and detect abnormal blood flow patterns. A chest X-ray (CXR) may be helpful in cases involving invasive thoracic procedures to ensure symptoms are unrelated to lung collapse. Likewise, CXR in the supine position or chest ultrasonography is recommended to rule out pneumothorax.[44] A chest X-ray may show rare findings, such as air in the cardiac chambers and hepatic circulation. Intraoperatively, transesophageal echocardiography (TEE) is the most sensitive modality to detect air embolism in the cardiovascular system.[45]

ECG may reveal signs of coronary infarction or ischemia, bradycardia, and ventricular arrhythmia.[46]

Treatment / Management

The treatment approach for arterial gas embolism involves three main goals: maintaining hemodynamic stability, terminating the source of air, and decreasing the gas bubble size. In any unstable patient with arterial gas embolism, the immediate priority should be stabilizing the airway, ensuring adequate breathing, and maintaining circulation.

In the case of arterial gas embolism, the recommended positioning of patients differs from that of venous air embolism. Patients with arterial gas embolism are advised to be supine instead of the Trendelenburg or left lateral decubitus position commonly used in venous air embolism.[47][48] The positioning of patients with arterial gas embolism in the supine position is primarily based on the understanding that, unlike in venous circulation, the force of arterial circulation propels air forward. Placing patients in the Trendelenburg position (head down, feet up), commonly done in venous air embolism, can potentially worsen cerebral edema and prevent air transmission throughout the circulatory system.(B3)

Oxygen treatment is a crucial component of patients with suspected arterial gas embolism. Administering oxygen with a high fraction of inspired oxygen (FiO2) serves multiple purposes in arterial gas embolism. High FiO2 administration increases the partial pressure of oxygen in the blood. This helps improve the oxygenation of tissues and counteract the hypoxemia resulting from impaired gas exchange caused by gas bubbles. Providing a high FiO2 diminishes the partial pressure of nitrogen in the blood. This promotes the reabsorption of nitrogen gas from the bubbles, helping to reduce the size of the gas bubbles. Oxygen therapy can facilitate the resolution of gas bubbles by promoting gas elimination through the lungs. The increased oxygen concentration in the blood can enhance the diffusion of gases across the alveolar-capillary membrane, facilitating the elimination of nitrogen and other gases trapped within the bubbles.[49] Patients who require anesthesia and have suspected air embolism or are at risk for it should not be given nitrous oxide, which can increase the size of gas bubbles.[50]

Hemodynamic support is crucial in managing arterial gas embolism, particularly in cases where hypotension or cardiovascular collapse occurs. In cases of hypotension, intravenous (IV) fluids may be administered to restore intravascular volume and improve cardiac output. Vasopressors may also be indicated if adequate fluid resuscitation fails to restore hemodynamic stability.[45] The choice of IV fluids in cases of arterial gas embolisms may depend on various factors, including the patient's clinical condition and underlying comorbidities.

Crystalloid solutions, such as normal saline or balanced electrolyte solutions, are commonly used to maintain euvolemia and optimize hemodynamic status. Vasopressors are reserved for those who do not respond despite adequate intravenous fluid administration. These medications help to increase systemic vascular resistance and improve blood pressure. The selection and dosing of vasopressors should be individualized and guided by the patient's response to fluid therapy, ongoing hemodynamic monitoring, and the expertise of the healthcare team.

Hyperbaric Oxygen (HBO) treatment is an important therapeutic modality in managing an arterial gas embolism. HBO involves the administration of 100% oxygen at higher than atmospheric pressure, typically in a hyperbaric chamber. It serves multiple purposes in the reduction of air emboli size and the promotion of air emboli reabsorption.[45] HBO is the preferred treatment method for patients when available and feasible.[28][51] HBO works in the following ways:(B3)

• Increased oxygenation: HBO provides higher FIO2 compared to standard atmospheric conditions. This helps to improve tissue oxygenation, especially in areas affected by ischemia or compromised blood flow due to air emboli.
• Increased oxygen dissolution: The increased pressure during HBO facilitates oxygen dissolution in the bloodstream. This can help diminish the gas bubbles' size, as oxygen replaces the nitrogen or other gases trapped within the bubbles. 
• Promotion of gas bubble elimination: The elevated oxygen partial pressure and increased oxygen content in the blood during HBO promotes the elimination of gas bubbles through enhanced gas diffusion across the alveolar-capillary membrane. This aids in the reabsorption and clearance of the air emboli from circulation.

HBO should be administered to the following groups of patients:[52]

• Evidence of hemodynamic or cardiopulmonary compromise
• Presence of neurologic deficits
• Evidence of end-organ damage

In unstable patients with a pulse experiencing an arterial gas embolism, considering closed cardiac massage as part of cardiopulmonary resuscitation (CPR) can be crucial. It is performed as a last resort when the patient's condition deteriorates rapidly, and other interventions have not successfully stabilized the patient.

Additional interventions may be considered for patients with an arterial gas embolism and concurrent coronary artery involvement. For example, nitrates, such as nitroglycerin, can help dilate coronary arteries and improve blood flow to the heart muscle. This can be beneficial in relieving any potential coronary artery spasm or ischemia associated with the embolic event.

An attempt at aspiration through thrombectomy catheters may be considered when an arterial gas embolism occurs during coronary angiography. Thrombectomy catheters are designed to remove blood clots or emboli from blood vessels. This approach aims to remove or reduce the size of the gas emboli and restore blood flow through the affected coronary artery.[46](A1)

Differential Diagnosis

The differential diagnosis for arterial air embolism is extensive, as signs and symptoms are consistent with arterial occlusion. In addition, the clinical presentation of arterial gas embolism can vary depending on the specific location and affected organ system. 

• Central nervous system: Vestibular migraine, alternobaric vertigo, seizure, cerebrovascular vascular accident (CVA), TIA, syncope, altered mental status, spinal cord infarction, decompression sickness, and carotid or vertebral dissection.[4]
• Inner ear barotrauma: ear pain during descent
• Cardiovascular: myocardial infarction, cardiac arrest, ventricular arrhythmia, acute limb ischemia, cardiac tamponade
• Gastrointestinal: mesenteric ischemia.
• Renal: renal infarction, acute kidney injury.
• Metabolic: hypoglycemia, respiratory or metabolic acidosis.[53]

Prognosis

The prognosis for patients with an arterial gas embolism is based on limited evidence from studies that primarily rely on case series of patients selected for hyperbaric oxygen treatment. These studies have shown that patients with venous gas embolism who receive HBO therapy within 6 hours of symptom onset tend to have a better prognosis. However, the use of HBO therapy for an arterial gas embolism remains a topic of debate and controversy. While some studies have reported no significant benefit regarding the time to recovery, sequelae, or mortality when considering the timing of HBO therapy initiation, other retrospective case studies have documented cases where patients achieved complete neurological recovery following HBO treatment.[31][54]

Certain factors have been identified as potential indicators of a poor prognosis in patients with arterial gas embolism. These factors include: 

1. Positive Babinski test on presentation
2. Focal neurological deficits
3. Acute kidney failure
4. Cardiac arrest on presentation
5. Advanced Age
6. Mechanical ventilation for greater than 5 days

Complications

Complications associated with arterial gas embolism can vary depending on the specific organ systems involved. In a case series involving 119 patients with venous or arterial gas embolisms who received hyperbaric oxygen treatment, the long-term outcomes were assessed at 6 months and again at 1 year. Among those patients who survived, 43% had neurological sequelae at discharge.[55] The most commonly reported complications included visual field deficits, motor deficits, cognitive issues, and seizures. However, it is worth noting that most patients improved their functional outcomes over time. At the end of 6 months, three-fourths of the patients had mild or no disability.[55] This highlights the potential for recovery and rehabilitation following arterial gas embolism, especially with appropriate management and treatment.