Paradoxical Air Embolism

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Srijith Kambala

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Andrew Go Lee, MD, Srijith Kambala, Saif Aldeen Alryalat, MD, Osama Al Deyabat, MBBS, Sanjana Jaiswal

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Paradoxical air emboli pose a significant risk to patients with right-left shunts, with the potential to lead to stroke, acute vision loss, and end-organ failure. Importantly, paradoxical emboli can lead to acute vision loss if the posterior cerebral arteries become occluded. They are diagnosed clinically and collecting a detailed patient history is essential to screen for right-left shunts before cannulation procedures or surgeries are conducted. Air emboli should be prevented through Durant’s maneuver during venous cannulation procedures, and be managed rapidly through hyperbaric oxygen therapy.

Disease Entity

Definition

A vascular air embolism (VAE) is a potentially life-threatening event that occurs when air is introduced to circulation with a pressure gradient that enables entry. The physiological consequence of an air embolism depends on the rate at which the air enters, the volume of the bolus, and the route it takes through circulation. While small air bubbles are often absorbed in the capillary bed, larger bubbles can result in severe sequelae. A venous embolism routinely results in pulmonary embolism and may present with the associated symptoms of pulmonary artery hypertension, arrhythmias, and hypotension. Arterial air emboli may result from accessing the arterial circulation in procedures such as an arteriogram, or through a connection between venous and arterial circulation such as a patent foramen ovale, causing a paradoxical air embolism. While these emboli are less common, they are often more severe due to their ability to cause ischemia in end organs. Due to the potential for venous emboli to become paradoxical emboli in patients with a right-to-left shunt, a detailed history is essential for all practitioners before a cannulation procedure is attempted.

Etiology

While an air embolus may occur through multiple mechanisms that allow for a gas bubble to enter the bloodstream, for an embolism to be perpetuated, certain conditions must be met. Importantly, a negative pressure gradient must exist which enables airflow into the vessel. The existence of such physiological gradients is what makes a venous air embolism more common than an arterial embolism. The venous system has lower pressure than the arterial system, and baseline central venous pressure is lower than atmospheric pressure in 40% of patients ¹. This becomes clinically important during cannulation procedures. A central line is a common source of VAE due to the line terminating in the superior vena cava which is characterized by low central venous pressure, creating a favorable gradient for air entry.

Similarly, air can also enter during ophthalmic procedures such as vitrectomy, where an improperly positioned infusion line may result in pressurized air entering the suprachoroidal space, tearing the vortex veins, and entering systemic venous circulation ². This gradient in venous circulation further increases during inspiration due to negative intrathoracic pressure as the chest wall expands, or when the patient is seated in an upright position due to the antigravitational rise of air ³. On the other hand, the higher pressure in the arterial system is typically protective of air embolism formation. Yet, arterial air emboli may occur in the event of direct insertion of air into the arterial tree during procedures such as angiography, or if there is a connection between the two systems - resulting in a paradoxical air embolism. If a right-to-left pressure gradient or shunt exists, such as a patent foramen ovale, which is present in 30% of the population, then air could travel from the venous to the arterial circulation ⁴.

Pathogenesis

The physiological outcome of an air embolism depends significantly on whether the air was introduced into venous or arterial circulation. Venous emboli routinely result in pulmonary embolism and may present with the associated symptoms of pulmonary artery hypertension, arrhythmias, and hypotension. Commonly, air introduced through central venous catheterization travels through the internal jugular vein, brachiocephalic vein, superior vena cava, and right atrium, and then lodges in the pulmonary vasculature. Such an embolism would trigger elevated pulmonary and right ventricular pressures and could disrupt diastolic filling of the left ventricle ⁵. It should be noted that in patients with a connection between the two circulatory systems, the path of the air embolus is often more complicated. If a patient has a patent foramen ovale or atrial septal defect, when the bubble reaches the right atrium it may bypass pulmonary circulation and cross to the left atrium and ventricle. From there, there is a significant risk for stroke, as the bubble has the potential to travel up the aorta, along the brachiocephalic artery, right subclavian artery, right vertebral artery, basilar artery, and ultimately lodge in the Circle of Willis. Importantly, paradoxical emboli can lead to acute vision loss if the posterior cerebral arteries become occluded. As such, arteriolar emboli, including paradoxical emboli, have significant potential to cause end-organ ischemia and can lead to irreversible damage. Furthermore, the severity of symptoms resulting from air embolism also depends on the amount of air that enters circulation. Small bubbles often diffuse into circulation during their travel along capillaries and are asymptomatic, yet larger bubbles can lead to significant complications and even death. 2 mL of air that reaches cerebral circulation can be fatal, while as little as 0.5mL of air occluding the left anterior descending coronary artery can trigger ventricular fibrillation ⁶.

Diagnosis

Proving an air embolism has occurred requires imagining such as MRI, CT, or angiography to demonstrate the presence of air in the intravascular space or end-organs. However, by the time imaging is done, it is not uncommon for the air to have been absorbed by circulation ⁷. As such, the diagnosis of an air embolism is typically a retrospective clinical one that requires the exclusion of other disease processes. The diagnosis is made with a high degree of suspicion after a patient experiences sudden decompensation during or shortly after an invasive procedure. This temporal aspect of the diagnosis makes the patient’s history an extremely important diagnostic criterion. While waiting on diagnostic imaging, certain markers may help elucidate that the cause of decompensation was an air embolism. Reduced end-tidal CO2 may be noted as one of the earliest indicators of air embolism ⁸. This is caused by an increase in dead space ventilation, and inefficient gas exchange following pulmonary thromboembolism ⁹. Arterial, or paradoxical emboli, would not demonstrate immediate reduced end-tidal CO2 and can thus be harder to diagnose. While hypoxemia found on arterial blood gas can aid the diagnosis, this test lacks sensitivity ⁸. Ultimately, diagnosing an arterial air embolism involves MRI or CT imaging of the air. Diagnosing a paradoxical embolism requires confirmation of a right-left shunt, which is typically diagnosed early in life, or even in adulthood through echocardiography ¹⁰. This contributes to the diagnosis of air embolism being a clinical one which depends heavily on patient history.

Prognosis

As discussed previously, arterial air embolism, including paradoxical embolism, can lead to rapid ischemia of critical organs and cause serious complications or even death. Prognosis depends heavily on the amount of air injected and the organs affected, but also on certain comorbid conditions, and how quickly management is done. Risk factors for death or persistent neurologic sequelae include cardiac arrest at the time of air embolization, Simplified Acute Physiology II (SAPS II) score ≥33 at ICU admission, increasing age, prolonged mechanical ventilation for more than five days, and acute kidney failure ¹¹. Immediate management to improve prognosis, further discussed below, involves hyperbaric oxygen therapy. In a case series of 119 patients with venous or arterial gas embolisms treated with hyperbaric oxygen, long-term outcomes were evaluated at 6 months and 1 year. Of the patients who survived, 43% experienced neurological sequelae at discharge. The most frequently reported complications were visual field deficits, motor deficits, cognitive issues, and seizures ¹².

Management

Prevention

Air emboli have the potential to become lethal within minutes, and thus taking precautions to prevent them from occurring is essential. Following guidelines for central venous line placement can significantly reduce the risk of embolism. Adjusting central lines while patients are seated in an upright position or standing increases the risk of embolus formation via a favorable pressure gradient. It is most optimal to place the patient in the left lateral decubitus position (Durant’s maneuver) before cannulation to prevent embolism ¹³. Durant’s maneuver consists of placing the patient in the left lateral decubitus or Trendelenburg position to prevent a venous air embolism from lodging in the lungs. This maneuver allows for the air bubble to rise and stay within the heart until it reduces in size via diffusion, reducing the risk for ischemic events ⁸. This is essential in patients at higher risk for arterial emboli, such as those with right-left shunts. Additionally, intraoperative timeouts are another precaution that can be effective in reducing the likelihood of air emboli during procedures such as vitrectomy. Pausing to properly position the infusion cannula before fluid-gas exchange can prevent choroidal detachment ¹⁴.

Treatment

In the event of an air embolism occurring, immediate management should involve hyperbaric oxygen therapy. 100% oxygen increases the partial pressure of O2 in the blood, thereby promoting the diffusion of nitrogen out of the air bolus which allows it to shrink in size and reduces ischemic risk ¹⁵. In addition, as soon as an arterial embolism is suspected, the patient should be placed in a supine position. A supine position is preferred in arterial embolism, as in the Trendelenburg position, the force of arterial circulation may push the air forward and worsen cerebral edema ¹⁶. Finally, hemodynamic support is crucial in arterial air embolism, and IV fluids or vasopressors should be administered in the event of hypotension or cardiovascular collapse ¹⁷. Imaging is recommended based on the suspected location of the air bubble and can include transthoracic echocardiography or transesophageal echocardiography if intracardiac air is suspected, contrast-enhanced CT of the brain if cerebral embolism is suspected, and CT abdomen or pelvis if ischemia is suspected in these organs.

Conclusion

Paradoxical air emboli pose a significant risk to patients with right-left shunts, with the potential to lead to stroke, acute vision loss, and end-organ failure. They are diagnosed clinically and collecting a detailed patient history is essential in order to screen for any right-left shunts before cannulation procedures or surgeries are conducted. Air emboli should be prevented through Durant’s maneuver during venous cannulation procedures, and be managed rapidly through hyperbaric oxygen therapy.

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