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Air embolism

Air embolism
Literature review current through: Jan 2024.
This topic last updated: Jul 07, 2023.

INTRODUCTION — Air embolism is an uncommon, but potentially catastrophic, event that occurs as a consequence of the entry of air into the vasculature.

The etiology, pathophysiology, clinical features, diagnosis, treatment, and prognosis of air embolism are reviewed here. Embolization of thrombi, amniotic fluid, fat, or tumor is discussed separately. (See "Epidemiology and pathogenesis of acute pulmonary embolism in adults" and "Amniotic fluid embolism" and "Fat embolism syndrome" and "Pulmonary tumor embolism and lymphangitic carcinomatosis in adults: Diagnostic evaluation and management".)

TERMINOLOGY AND PATHOPHYSIOLOGY — Air embolism can be classified in to two types:

Venous air embolism – Venous air embolism (also called pulmonary air embolism) occurs when air enters the systemic venous circulation and travels to the right ventricle and pulmonary circulation. (See 'Venous air embolism' below.)

Arterial air embolism – Arterial air embolism occurs when air enters the arterial circulation. Arterial air embolism can produce ischemia in any organ that has insufficient collateral circulation. It is typically a more serious occurrence than venous embolism. (See 'Arterial air embolism' below.)

As a general rule of thumb, air embolism can occur when the following is present [1-4]:

Direct communication between a source of air and the vasculature

A pressure gradient favoring the passage of air into the circulation rather than bleeding from the vessel

As an example, surgical incision (communication between atmospheric air and the vasculature) in neurosurgical and otolaryngological procedures is usually located superior to the heart at an elevation that is higher than the central venous pressure. This sets up a condition of negative venous pressure relative to the atmosphere, which favors the passage of air into the circulation, especially when the patient is in a sitting position (ie, Fowler's position) [5,6]. This explains why these surgeries are at higher risk than others for venous air embolism. (See 'Surgery and trauma' below and "Patient positioning for surgery and anesthesia in adults".)

As another example, hypovolemia causes subatmospheric pressure in veins (ie, collapsible veins) such that when they are incised during venous catheter insertion, the pressure gradient is in favor of air moving from the atmosphere into the vein. (See 'Intravascular catheters' below.)

Venous air embolism — Venous air embolism is a consequence of air being introduced into the venous circulation, traveling to the right heart, and lodging in the pulmonary circulation. The pathophysiologic effects can be direct or indirect:

Direct – Small amounts of air can be removed from the pulmonary vascular bed by gas diffusion across the arteriolar wall and into the alveolar spaces. However, when the capacity of the lung to remove gas is exceeded (eg, 50 mL or more) pulmonary outflow tract obstruction with or without concomitant arterial embolization can occur [7]:

Obstruction – The pulmonary outflow tract, pulmonary arterioles, and/or pulmonary microcirculation become obstructed resulting in circulatory collapse (ie, obstructive shock) (see "Definition, classification, etiology, and pathophysiology of shock in adults", section on 'Obstructive'):

-Large bubbles tend to obstruct the pulmonary outflow tract (known as "air lock"). This diminishes blood flow from the right heart, resulting in increased central venous pressure, decreased pulmonary arterial pressure, and decreased systemic arterial pressure.

-Smaller bubbles tend to lodge within the pulmonary arterioles or pulmonary microcirculation, directly impeding blood flow and inducing vasoconstriction. As a result, the following hemodynamic effects may be observed: increased pulmonary vascular resistance, increased pulmonary arterial pressure, and increased right ventricular pressure. There may be an initial brief increase in the cardiac output and systemic arterial pressure due to tachycardia followed by a decrease in cardiac output and systemic arterial pressure, as well as myocardial ischemia due to hypoxia, right ventricular overload, and/or air emboli to the coronary arterial circulation [1].

Arterial embolization – Venous air may pass through the pulmonary capillaries, enter the arterial circulation, and cause arterial air embolization with organ ischemia. (See 'Arterial air embolism' below.)

Detrimental effects of venous gas embolism are determined by the total volumes of air injected as well as the rate and the final location. It is estimated that 300 to 500 mL of gas introduced at a rate of 100 mL/sec can be acutely fatal for humans [2]. This flow rate can be attained through a 14-gauge catheter with a pressure gradient of only 5 cm H2O. Other estimates suggest that 50 mL of venous air can also be fatal.

Indirect – Secondary effects of air embolism can also result in end organ damage. As an example, air bubbles in the pulmonary microcirculation are associated with local endothelial damage and the accumulation of neutrophils, platelets, fibrin, and lipid droplets at the gas-fluid interface. Additional endothelial damage may be caused by the activation of complement and the release of mediators and free radicals from neutrophils and other inflammatory cells. Consequences of the endothelial damage may include noncardiogenic pulmonary edema (ie, adult respiratory distress-like picture), bronchoconstriction, and physiological changes, such as hypoxemia (due to alveolar flooding and ventilation-perfusion mismatching), increased physiologic dead space (with a rise in PaCO2 if ventilation is held constant), decreased lung compliance (secondary to pulmonary edema), and increased airway resistance (may be due to release of bronchoconstrictive mediators such as serotonin and histamine from damaged endothelium) [1,8-10]. (See "Acute respiratory distress syndrome: Epidemiology, pathophysiology, pathology, and etiology in adults".)

Arterial air embolism — Arterial air embolism can be associated with three distinct processes [1]:

The incomplete filtration of venous air emboli by the pulmonary capillaries. (See 'Venous air embolism' above.)

The direct introduction of air into the arterial system, usually through a breech in an arterial vascular bed (eg, trauma or surgery, barotrauma). Reduced alveolar permeability to gas is also thought to result in the increased risk of arterial air embolism that can worsen during anesthesia [3].

The paradoxical embolization of air through a septal defect, patent foramen ovale, or pulmonary arteriovenous malformation (including hepatopulmonary syndrome). In patients with a left-to-right shunt, significant volumes of air in the right heart/pulmonary circulation can raise right heart pressures and reverse the direction of the shunt, also allowing paradoxical embolism to occur. (See "Patent foramen ovale", section on 'Decompression sickness and air embolism' and "Pulmonary arteriovenous malformations: Clinical features and diagnostic evaluation in adults".)

Similar to venous air embolism, the downstream pathophysiologic effects can be direct or indirect:

Direct – Air in the arterial circulation can occlude the microcirculation and cause ischemic end organ damage. Organs that are most vulnerable to arterial ischemia from microbubbles are the brain and the heart. Other organs are likely to receive air emboli but are less sensitive to end-organ ischemia; however, damage to other organs including the spinal cord and the skin has been reported [2,11]. It is believed that 2 mL of air in the cerebral arteries and 0.5 to 1 mL in the coronary circulation can be fatal [3].

Indirect – Organs may also be damaged indirectly by the release of ischemia-induced inflammatory mediators, and air embolism-induced endothelial damage similar to that described above. (See 'Venous air embolism' above.)

ETIOLOGY — Air embolism can be venous or arterial. Surgery, trauma, vascular interventions, and barotrauma from mechanical ventilation and diving are the most common causes of air embolism [1,2,11,12]. These and other less common causes are listed in the table (table 1). The causes of venous and arterial embolism differ depending on the portal of entry of air. The etiology, definition, and pathophysiology of venous and arterial embolism, are discussed in the sections below. (See 'Surgery and trauma' below and 'Intravascular catheters' below and 'Barotrauma' below and 'Other' below and 'Terminology and pathophysiology' above.)

Surgery and trauma

Neurosurgical and otolaryngological procedures — Venous air embolism complicates neurosurgical and otolaryngological procedures more often than other types of surgical procedures. The estimated incidence of venous air embolism during neurosurgical procedures ranges from 10 percent (for surgical patients in the prone position) to 80 percent (for patients undergoing repair of cranial synostosis in Fowler's position, ie, sitting upright) [1,5,13-15].

Other surgical or procedural interventions — Venous air embolism has been reported as a rare complication in the following surgeries or procedures:

Neodymium-yttrium-aluminum-garnet (Nd:YAG) laser treatment of endobronchial lesions [2,16] (see "Bronchoscopic laser in the management of airway disease in adults", section on 'Complications')

Bronchoscopic and percutaneous needle biopsy of the lung (ipsilateral-dependent position may reduce the risk for percutaneous aspirations) [17-20] (see "Diagnostic evaluation of the incidental pulmonary nodule", section on 'Transthoracic needle biopsy' and "Flexible bronchoscopy in adults: Overview" and "Flexible bronchoscopy in adults: Preparation, procedural technique, and complications", section on 'Complications')

Lung resection [21] (see "Overview of minimally invasive thoracic surgery")

Arthroscopy and total joint arthroplasty [22,23] (see "Surgical management of end-stage rheumatoid arthritis", section on 'General surgical complications')

Hysteroscopy and laparoscopy [24-29] (see "Complications of laparoscopic surgery" and "Hysteroscopy: Managing fluid and gas distending media" and "Hysteroscopy: Managing fluid and gas distending media", section on 'Gas embolism')

Cesarean section [30] (see "Cesarean birth: Postoperative care, complications, and long-term sequelae")

Colonoscopy [31] (see "Overview of colonoscopy in adults", section on 'Adverse events')

Cardiopulmonary bypass [32] (see "Early noncardiac complications of coronary artery bypass graft surgery")

Endoscopic retrograde cholangiopancreatography [33] (see "Adverse events related to endoscopic retrograde cholangiopancreatography (ERCP) in adults", section on 'Gas embolism')

Radiofrequency ablation of lung cancer [34] (see "Image-guided ablation of lung tumors", section on 'Radiofrequency ablation')

Pacemaker or defibrillator placement [35,36] (see "Cardiac implantable electronic devices: Periprocedural complications")

Cardiac ablation procedures [37] (see "Overview of catheter ablation of cardiac arrhythmias", section on 'Complications')

Ophthalmological and dental procedures [38,39]

Endovenous foam sclerotherapy [40]

Trauma — Venous air embolism can occur with penetrating (eg, venous lacerations) or blunt trauma to the chest (eg, bronchus fracture resulting in bronchovenous or atrioesophageal fistula) or abdomen [41,42]. However, arterial air embolism has also been described following trauma (particularly head and neck injuries, penetrating or blunt chest trauma, and blunt abdominal trauma), which can be lethal. In a series of nine patients who were found to have air in their coronary arteries, left ventricle, and/or aortic root following penetrating chest trauma, six patients (66 percent) died [43]. The presentation of air embolism may sometimes be delayed (eg, possible air entry via wounds) [44].

Intravascular catheters — Venous air embolism is a serious and under-recognized complication associated with the insertion of central venous catheters [11,45-47], hemodialysis catheters [48,49], pulmonary artery catheters [50], and with intravenous injections, particularly contrast injection [51,52]. Arterial embolism can occur with the insertion of arterial catheters [53,54], angioplasty catheters, or other arterial interventions (eg, intra-aortic balloon pump) [55].

Air emboli can occur at the time of catheter insertion, while the catheter is in place, or at the time of catheter removal [56]. The risk of catheter-related venous air embolism appears to be increased by the following factors [2,11,56,57]:

Fracture or detachment of catheter connections (which accounts for 60 to 90 percent of episodes)

Failure to occlude the needle hub and/or catheter during insertion or removal

Dysfunction of self-sealing valves in plastic introducer sheaths

Presence of a persistent catheter tract following the removal of a central venous catheter

Deep inspiration during insertion or removal, which increases the magnitude of negative pressure within the thorax

Hypovolemia, which reduces central venous pressure

Upright positioning of the patient, which reduces central venous pressure to below atmospheric pressure and places the patient at particular risk for entraining air very rapidly into the venous circulation [2]

The prevention of air embolism from intravascular catheters is discussed below. (See 'Prevention' below.)

Barotrauma

Positive pressure ventilation — Patients requiring positive pressure ventilation are at risk for pulmonary barotrauma and, as a consequence, air emboli. Gas may enter the circulation if the pulmonary vascular integrity is disrupted concomitantly with alveolar rupture from overdistention of the airspaces. This complication has been reported most frequently in adults who are mechanically ventilated for the acute respiratory distress syndrome and in premature neonates with respiratory distress syndrome (hyaline membrane disease), but it can also occur in patients with other diagnoses including those who are mechanically ventilated during anesthesia [2,58-61]. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults".)

Although air embolism can theoretically complicate noninvasive positive pressure ventilation (NPPV), rare case reports suggest that the occurrence may relate to the presence of concurrent risk factors other than NPPV [62,63].

Rapid ascent in scuba divers — Divers are also at risk for pulmonary barotrauma. One retrospective series estimated that pulmonary barotrauma and air embolism complicates approximately 7 of every 100,000 dives [64]. Rapid ascent without exhalation can result in expansion of gas in the lungs and consequent alveolar rupture. If the pulmonary veins tear as the alveoli rupture, air can return to the left heart with the oxygenated blood and then embolize through the arterial system to produce tissue ischemia [65,66]. Alternatively, air bubbles may form in the venous system during ascent and embolize to the systemic circulation via a patent foramen ovale [67]. (See "Complications of SCUBA diving", section on 'Arterial gas embolism'.)

Other — Rare case reports of air embolism have been reported during sexual intercourse (including orogenital sex), pregnancy, labor and delivery, and autoerotic practices (eg, vaginal insufflation of cocaine) [68-71]. Venous air embolism has also been described following insufflation of the urethra [72]. With the advent of plastic equipment and closed blood delivery systems, entry of large volumes of air into the venous system is no longer a problem with routine transfusions. However, significant amounts of air may be inadvertently transfused following the use of more complex transfusion systems, such as apheresis and blood salvage equipment [73-75]. One case of air embolism has been reported as a complication of pneumatosis intestinalis from retrograde flow of air from the mesenteric veins and portal vein [76].

CLINICAL FEATURES — Air embolism should always be suspected when patients experience sudden-onset respiratory distress (venous air embolism) and/or experience a neurological event (arterial embolism) in the setting of a known risk factor (eg, intravenous catheter insertion, trauma). The spectrum of findings depends upon the degree of severity of embolism, end-organs affected, and underlying comorbidities (table 2). The portal of entry for air into the vasculature is usually apparent but occasionally remains speculative.

History and examination — Minor cases of venous air embolism are common and cause minimal or no symptoms. Such cases are often transient and self-resolving. In more severe cases, dyspnea is almost a universal finding that may be accompanied by substernal chest pain, lightheadedness, or dizziness. Immediately life-threatening cases are characterized by acute-onset right-sided heart failure, an acute sense of impending doom, sudden-onset loss of consciousness, hemodynamic collapse (from obstructive shock), or cardiac arrest.

Signs of venous air embolism include a gasp or cough when the bolus of air enters the pulmonary circulation, a sucking noise as air is sucked into the intravascular space, and a mill wheel murmur (a churning sound heard throughout the entire cardiac cycle). Additional signs include tachypnea, tachycardia, bradycardia, hypotension, wheezing, crackles, elevated jugular venous pressure, and hypoxemic respiratory failure.

The symptoms and signs of arterial embolism vary depending in the organ affected (usually the brain) so that many present with a change in mental status, and/or focal neurological deficits. Severe cases associated with the entry of large volumes of air may present with loss of consciousness, coma, and cardiac arrest. Additional features include the signs of acute ischemia of affected organs, including the heart, and skin resulting in chest pain, wheeze, crepitus over superficial vessels, livedo reticularis, and bubbles within retinal arteries [1,2,11,65].

Electrocardiography and laboratory — Typical electrocardiographic and laboratory findings include the following (table 3):

Electrocardiography – The electrocardiogram of patients with air embolism typically reveals sinus tachycardia. Right heart strain (eg, peaked p-waves, right bundle branch block, right axis deviation) may be evident in those with venous air embolism, and non-specific ST-segment and T-wave changes, ST depression or elevation consistent with acute myocardial ischemia or infarction, respectively, may be apparent in those with arterial embolism [1,2].

Arterial blood gases – Typical arterial blood gas abnormalities due to air embolism include hypoxemia and hypercarbia [1,2]. The hypoxemia may be severe especially in those with severe venous (ie, pulmonary) air embolism.

Laboratory tests – Air embolism may be associated with a fall in the platelet count and/or an elevation in the serum creatine kinase activity [1,2,77]. In one study, 22 divers with arterial air embolism all had significant elevations in serum creatine kinase activity, whereas 22 divers without arterial air embolism did not [77]. The sensitivity of an elevated serum creatine kinase activity has not been studied in other populations with arterial air embolism.

Imaging — Imaging is typically normal because air is rapidly absorbed, often within 24 hours and consequently, is missed by the time that imaging is performed. Abnormalities include the following:

Chest radiography – Pulmonary edema due to arterial embolism-related ischemia may be observed. Additional rare findings of venous air embolism include air in the main pulmonary artery, focal oligemia, pulmonary artery enlargement, and atelectasis, and of unusual findings of arterial air embolism include intracardiac air and air in the hepatic circulation (table 3) [1,2,78].

Ventilation-perfusion scan – Rarely, ventilation-perfusion (V/Q) scan abnormalities that mimic those seen in pulmonary thromboembolism may be seen in the setting of massive venous air embolism [79].

Computed tomography – Chest computed tomography (CT) of the chest may detect air emboli in the central venous system (especially the axillary and subclavian veins), right ventricle, pulmonary artery, or heart. Computed tomography of the brain may reveal intraparenchymal gas and diffuse edema (image 1) [80].

Magnetic resonance imaging – Magnetic resonance imaging of the brain may also reveal locules of gas within cerebral arteries and veins [81,82].

Pulmonary angiography – Although pulmonary angiography is not routinely performed for diagnosis, patients with venous air embolism may have a filling defect or vascular occlusion (ie, similar to venous thromboembolism) and/or findings consistent with vasoconstriction. Additional findings include corkscrewing, tapering, and delayed emptying of the vessels in the affected lung, compared to the unaffected lung [1].

Echocardiography — Transthoracic and transesophageal echocardiography have been used to document the presence of air in cardiac chambers as well as air in the great veins. They may also show evidence of acute right ventricular dilation and pulmonary artery hypertension [3,83]. Continuous monitoring with echocardiography or transcranial Doppler has been used during high-risk surgical procedures to detect air embolism in the preclinical phase [84-86].

End-tidal carbon dioxide — The increase in physiologic dead space and worsening of ventilation-perfusion mismatching that occur with venous air embolism produce a fall in end-tidal CO2 that can be detected with capnography during anesthesia. (See "Carbon dioxide monitoring (capnography)".)

Pulmonary artery catheterization — In patients who have a pulmonary artery catheter (PAC) in position, a rise in the pulmonary artery pressure may be observed when venous air embolism occurs. Additional findings may include an increase in the central venous pressure, increase in the right ventricular pressure, decrease in the cardiac output, and decrease in the mean arterial pressure (table 3). Importantly, PAC is not routinely placed for diagnostic purposes as these findings are nonspecific with an estimated sensitivity of only 45 percent [85].

DIFFERENTIAL DIAGNOSIS — Air embolism should be considered in any patient who has sudden onset cardiopulmonary or neurologic decompensation in a clinical setting where the patient has a risk factor for air embolism (eg, central venous catheterization, neurosurgery) (table 1).

Disorders that should be considered in the differential diagnosis of such patients include all those that can cause the following (table 4):

Acute pulmonary decompensation (pulmonary embolism, pneumothorax, bronchospasm, pulmonary edema)

Acute cardiovascular decompensation (hypovolemia, cardiogenic shock, myocardial infarction, septic shock, and electromechanical dissociation, amniotic fluid embolism, fat embolism)

Acute neurological decompensation (cerebral hypoperfusion, stroke, intraparenchymal or subarachnoid hemorrhage, hypoxic brain injury, head trauma, blunt cerebrovascular injury, and metabolic disorders)

There are no pathognomic features of air embolism that distinguish it from other forms of embolism or acute decompensation other than the demonstration of air on imaging, particularly if air is visualized within the main pulmonary artery. Most of the other competing diagnoses will have different associated presenting clinical manifestations and imaging findings. As an example, a patient with pneumothorax will have an abnormal chest radiograph, and a patient with fat embolism may have lipemic serum.

DIAGNOSIS

Diagnosis — The diagnosis is best made by demonstrating air in the intravascular space or organs in a patient with a known risk factor for air embolism. However, because air may be rapidly absorbed from the circulation while waiting for diagnostic imaging, air embolism is typically a retrospective clinical diagnosis, based upon a high index of suspicion and the exclusion of other life-threatening processes. (See 'Differential diagnosis' above.)

Diagnostic approach — When air embolism is suspected, following immediate oxygenation, repositioning (see 'Positioning the patient' below), and supportive life-saving maneuvers (see 'Supportive therapy' below), the following diagnostic tests should be performed immediately (see 'Electrocardiography and laboratory' above and 'Imaging' above and 'Echocardiography' above and 'End-tidal carbon dioxide' above):

Routine laboratory tests including complete blood count, differential, and serum chemistries

Creatine phosphokinase, serum troponin-I or -T, and brain natriuretic peptide

Arterial blood gas analysis

Chest radiography

Electrocardiography

Additional testing depends upon the suspected source of air and location of potential end organ damage and may include:

Transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) (if intracardiac air is suspected)

Contrast enhanced computed tomography (CT) of the chest and/or pulmonary arteries (if venous embolism is suspected)

Contrast-enhanced CT of the brain (if cerebral embolism is suspected)

CT abdomen or pelvis (if ischemia is suspected in these organs)

Further testing may be performed in select patients or in those in whom the suspicion remains including the following:

Magnetic resonance imaging (MRI) of the brain (if air or infarct is suspected and CT is non diagnostic)

Transcranial Doppler (often used in the operating room for surgical cases that are at high risk of embolism)

Ventilation perfusion scanning (in suspected venous embolism if CT pulmonary angiography is contraindicated)

Capnography (if air embolism is suspected during anesthesia)

This approach is supported by our experience and by small retrospective case series.

Although the sensitivity and specificity of laboratory and electrocardiographic findings have not been formally studied, they are nonspecific as many of these abnormalities can be found in other pathological states that present similarly. (See 'Electrocardiography and laboratory' above and 'Differential diagnosis' above.)

Bedside TTE is the test of first choice for demonstrating intracardiac air; however, mild cases may be easily missed. TEE is often used in the operating room for neurosurgical and otolaryngological cases that are at high risk of air embolization but can also be used at the bedside if TTE is non diagnostic. (See 'Echocardiography' above.)

CT of the chest is often performed in cases of suspected venous air embolism and CT brain in suspected cerebral arterial air embolism. CT chest, particularly CT pulmonary angiography is frequently performed to determine the cause of dyspnea and rule out venous thromboembolism. CT is probably more sensitive than chest radiography for the detection of air, but because it is often delayed, bedside chest radiography should be done first in every case of suspected venous air embolism. In general, the sensitivity and specificity of radiologic imaging findings are poor. This is because imaging is often normal (ie, falsely negative) due to the rapid absorption of air as testing is being arranged. As an example, one study of 17 patients with cerebral arterial gas embolism reported a sensitivity of 25 percent for imaging (mostly CT and MRI) in detecting cerebral air and 50 percent for the detection of secondary effects of cerebral air (ie, infarcts) [82]. The sensitivity and specificity of CT are greatest when large defects are detected because small (<1 mL), asymptomatic air emboli of uncertain clinical significance (from contrast material) are detectable in 10 to 25 percent of contrast-enhanced CT scans if carefully sought [51,87]. False positive studies may be more common when higher resolution or electron beam CT scanners are used [87]. (See 'Imaging' above.)

For patients in the operating room, transcranial Doppler is a portable means of detecting intracerebral air. Consequently, it is often used during neurosurgical procedures for the preclinical detection of cerebral air. It has not been formally compared with CT or MRI of the brain. In addition, capnography can be readily used to detect a reduction in end-tidal CO2; however, end-tidal CO2 is also nonspecific and can occur with pulmonary embolism, massive blood loss, circulatory arrest, or disconnection from the anesthesia circuit [88]. The combination of intraoperative echocardiography and end-tidal CO2 monitoring may increase the intraoperative sensitivity of detecting preclinical air emboli in high-risk patients [85,89]. (See 'End-tidal carbon dioxide' above.)

TREATMENT

Overview — Once air embolism is suspected, the patient should be assessed for airway stability, breathing, and circulation (see 'Identify the need for definitive therapy' below) and appropriate supportive therapies should be administered immediately (eg, high flow oxygen, mechanical ventilation, volume resuscitation, vasopressors, advanced cardiac life support) while diagnostic tests are underway (see 'Supportive therapy' below). Simultaneously, the patient should be positioned to avoid further embolization (ie, the left lateral decubitus with or without head down or Trendelenburg, for patients with suspected venous air embolism, or the supine position when arterial embolism is suspected) (see 'Positioning the patient' below). Once a diagnosis is made, definitive therapy, usually hyperbaric oxygen, can be administered to those in whom it is indicated (ie, those who are hemodynamically unstable and those with evidence of cardiopulmonary compromise and/or end-organ damage due to air embolism). (See 'Definitive therapy' below.)

Identify the need for definitive therapy — When air embolism is suspected, simultaneous with repositioning, the airway and breathing should be stabilized with high flow oxygen and/or mechanical ventilation, when necessary. Intravenous access should be secured so that patients can be treated with intravenous fluids and/or vasopressors to restore adequate tissue perfusion (table 5). While diagnostic tests are pending, the clinician should stratify the patient according to the presence or absence of hemodynamic instability and/or end organ damage to identify those that may be candidates for definitive therapy (ie, hyperbaric oxygen).

Hemodynamically unstable patients — Most patients with persistent hemodynamic instability (eg, hypotension, need for vasopressors) due to air embolism should be treated with aggressive support and definitive therapy, usually hyperbaric oxygen. (See 'Supportive therapy' below and 'Definitive therapy' below.)

Patients with neurologic deficits or end-organ damage — Most patients with evidence of end-organ damage (eg, neurologic deficit, myocardial infarction) should be treated with supportive and definitive therapy, usually hyperbaric oxygen. (See 'Supportive therapy' below and 'Definitive therapy' below.)

Hemodynamically stable patients without end organ damage — Most patients who are hemodynamically stable, have mild or minimal symptoms only, and/or patients without end organ damage can be treated with high flow oxygen and repositioning only. Definitive therapy is not indicated in this population unless symptoms progress or signs of instability or ischemia ensue. (See 'Supportive therapy' below.)

Supportive therapy — The first priorities are to stabilize the airway and breathing with high-flow oxygen and/or mechanical ventilation, when necessary. Intravenous access should be secured so that patients can be immediately treated with intravenous fluids and vasopressors can be administered, when needed.

Oxygen – For all patients suspected of having air embolism, the administration of supplemental oxygen with a high fraction of inspired oxygen (FiO2) is critical. Although the optimal FiO2 or oxyhemoglobin saturation level is unknown, we prefer to start with the highest level of FiO2 to achieve the highest saturation as tolerated by the patient.

High-flow supplemental oxygen increases the rate with which the embolized air resorbs. The supplemental oxygen increases the partial pressure of oxygen and decreases the partial pressure of nitrogen in blood [90]. This causes diffusion of nitrogen from inside the air bubble (which has a high nitrogen content) into the blood (which has a low nitrogen concentration), which reduces bubble size and accelerates bubble resorption.

For patients who develop air embolism intraoperatively, in addition to the administration of high flow oxygen, nitrous oxide (N2O) should be discontinued because N2O causes the gas bubbles to enlarge and may worsen the embolism [89,91]. Alternative anesthetic agents should be administered. (See "Induction of general anesthesia: Overview".)

Mechanical ventilation – Patients with respiratory distress and/or marked hemodynamic instability are frequently intubated. Rapid sequence intubation, typically with etomidate (0.3 mg/kg intravenously) or ketamine (1 to 2 mg/kg intravenously), and a rapidly acting neuromuscular blocker, typically succinylcholine (1 mg/kg intravenously) or rocuronium (1 to 1.5 mg/kg intravenously) is the preferred approach; agents that worsen hypotension (eg, propofol, midazolam) should be avoided. (See "Rapid sequence intubation in adults for emergency medicine and critical care" and "Induction agents for rapid sequence intubation in adults for emergency medicine and critical care".)

Intravenous fluids and vasopressors – Rapid resuscitation with volume expansion (usually, crystalloids) should be performed to elevate venous pressure and avoid further entry of gas into the venous system. (See 'Terminology and pathophysiology' above.)

The optimal volume or type of fluids for patients with suspected air embolism is unknown. Although studies in animals suggest that hemodilution reduces cerebral edema, we prefer an approach that avoids and/or corrects hypovolemia, and maintains normovolemia. The choice and volume of administered fluids should be determined by factors including the type of shock if present, the presence of cerebral edema, and the degree of hypoxemia. Vasopressors should be administered to those who fail resuscitation with intravenous fluids.

Intravenous access – Peripheral venous access (14 to 18 gauge catheters) is typically sufficient for the initial evaluation and management of many patients with suspected air embolism. Central venous access should be obtained in those in whom peripheral access cannot be obtained, in those who need infusions of large volumes of fluids, or for the ongoing infusion of vasopressors. Central venous access may also be useful in patients who require frequent blood draws for laboratory studies and for hemodynamic monitoring (eg, central venous pressure, central venous oxyhemoglobin saturation). Regardless of the form of access, care during placement and use should be taken such that new air is not introduced into the vascular space.

Treatment of generalized seizures and secondary effects of embolism – The approach to treating seizures and other secondary effects of air embolism, (eg, acute lung or kidney injury) is the same as for other general medical patients, which are discussed in detail separately.

Positioning the patient — A patient with venous air embolization should be immediately placed into the left lateral decubitus position (Durant's maneuver), Trendelenburg position, or left lateral decubitus head down position [4]. These positions place the right ventricular outflow tract inferior to the right ventricular cavity, causing the air to migrate superiorly into a position within the right ventricle from which air is less likely to embolize [1,2]. The potential benefit of appropriate positioning was suggested by an animal experiment in which 40 percent of animals in the left lateral decubitus position survived the venous injection of a lethal amount of air (the experiment did not assess the left lateral decubitus head down or Trendelenburg position) [92].

In contrast, a patient with arterial air embolism should be placed in the supine position [4]. The reason that the optimal position differs for arterial and venous air embolism is that arterial blood flow is more forceful than venous blood flow and air bubbles are propelled forward by the arterial blood flow even if the patient is in a head down position. Since the head down positions have the potential to exacerbate the cerebral edema that is typically induced by cerebral air embolism, a flat supine position is also favored for this reason [4,93].

Definitive therapy — Specific interventions (hyperbaric oxygen, withdrawal of air from the right atrium, cardiac massage) can be used in select cases to reduce bubble size (hyperbaric oxygen) or remove air [1,2,94].

Hyperbaric oxygen — Hyperbaric oxygen therapy (HBO) is not routinely administered in patients with air embolism but is a useful adjunct in severe cases, which often occurs in those with arterial air embolization. When available, HBO should be administered to patients with evidence of hemodynamic or cardiopulmonary compromise, as well as those with neurologic deficits, or other evidence of end-organ damage [95-97]. We prefer that HBO be administered within the first four to six hours after symptom onset but continued benefit has been reported when HBO therapy is delayed for up to 30 hours [98,99]. The potential benefits of HBO must be weighed against the potential risks of transport to the HBO facility where it is administered [100]. (See "Hyperbaric oxygen therapy".)

The potential clinical benefits of HBO are mostly derived from small retrospective case series that examine patients with neurologic deficit from air embolism [98,99,101-103]. These studies are limited by small sample size, their retrospective design and lack of adjustment for severity of illness. Nonetheless, collectively they report benefit particularly when HBO is administered within the first four to six hours after symptom onset. As examples:

In one retrospective cohort study of 86 patients with venous or arterial air embolism, patients treated with HBO within six hours of presentation were more likely to recover than patients who received HBO after six hours or more (68 versus 40 percent), with outcomes best in those who underwent HBO within three hours [98].

In another case series of 17 patients treated with HBO for air embolism that developed during cardiac surgery, all five patients who were treated within three hours from the operation and half (two out of four) of those treated three to five hours from operation experienced a full neurologic recovery [101]. With a delay of 9 to 20 hours, only one (out of eight) patients had a full neurologic recovery.

HBO provides oxygen at pressures higher than atmospheric pressure and at 100 percent concentration such that a "supra" physiologic level of systemic hyperoxia can be achieved (ie, greater than that provided by 100 percent oxygen). Typically, a partial pressure of oxygen >2000 mmHg can be achieved with HBO (compared with <600 mmHg with 100 percent oxygen via face mask). This degree of hyperoxia allows enormous gradients for nitrogen to be displaced from inside the air bubble, which in turn, reduces air bubble size and the degree of mechanical obstruction to end arterial blood flow. In addition, the increase in the arterial oxygen tension improves oxygen delivery and ameliorates tissue ischemia. The mechanisms and clinical applications of HBO therapy are discussed separately. (See "Hyperbaric oxygen therapy".)

HBO is of limited availability and only highly specialized centers have expertise in the provision of this therapy. It is an intermittent therapy that often requires physical transfer of patients which can infer risk of cardiac arrest or death during transfer. Thus, the benefits of HBO therapy should be weighed against the risk of death during transfer and discussed with the patients and caregivers in every case.

Manual removal of embolized air — Air has been successfully aspirated from the right ventricle via a central venous catheter, pulmonary artery catheter, or percutaneously introduced needle, according to case reports and experimental models [92]. However, these maneuvers are of limited benefit because the volume of air recovered is usually less than 20 mL [3,85]. Given the limited benefit, most clinicians only attempt to aspirate air if a central venous catheter is already in place and the patient is in extremis [2,3].

Closed chest cardiac massage — In patients with shock who are severely hemodynamically unstable, closed-chest cardiac massage (ie, chest compressions) can be performed as a last-resort therapy. The goal is to force air out of the pulmonary outflow tract and into smaller pulmonary vessels, improving forward blood flow. Animal studies suggest that closed-chest cardiac massage is as effective as either left lateral decubitus positioning or intracardiac aspiration of air [92,104].

Therapies of unproven benefit — Therapies of uncertain benefit that are not routinely administered include the following:

Anticoagulation – Although there is evidence that systemic anticoagulation with heparin may be beneficial in rabbit models of air embolism [105], we do not routinely anticoagulate this population given the risk of bleeding into infarcted regions and lack of evidence in humans to support it.

Glucocorticoids – The use of corticosteroids is controversial [3,106]. However, we do not suggest their use as they may aggravate neuronal ischemic injury and have no proven role in other cerebral injuries.

Lidocaine – Similarly, lidocaine in animal models has been shown to have a protective effect on cerebral ischemia due to gas embolism [107,108], but it has no proven benefit in humans and is not routinely administered in this population, likely due to its potential cardiac toxicity.

PROGNOSIS — Accurate reports of the prognosis of patients with air embolism are limited to case series that have selected patients for therapy with hyperbaric oxygen (HBO). While in the past mortality rates as high as 90 percent were reported, case series since then suggest rates that range from 12 to 30 percent [104,109]. As examples:

One 2010 case series reported outcomes in 119 patients with either arterial or venous air embolism who were treated with HBO [109]. The series reported ICU, hospital, six-month, and one-year mortality rates of 12, 16, 18, and 21 percent, respectively. Among the survivors, 43 percent had neurological sequelae at the time of discharge from the ICU. These included visual field restriction (16 percent), persistent vegetative states (9 percent), focal motor deficits (7 percent), cognitive problems (7 percent), and seizures (4 percent). By six months, however, 75 percent of survivors had mild or no disability.

In one retrospective cohort study of 17 patients with venous or arterial air embolism who were treated with HBO, eight patients (48 percent) experienced a complete neurologic recovery, six patients (35 percent) remained unconscious at discharge, and three patients (18 percent) died [98].

Risk factors for death or persistent neurologic sequelae include the following [109,110]:

Cardiac arrest at the time of air embolization

Simplified Acute Physiology II (SAPS II) score ≥33 at ICU admission

Increasing age

The presence of focal motor deficits or a Babinski sign at ICU admission

Acute kidney failure

Prolonged mechanical ventilation for more than five days

Gyriform air on brain imaging

PREVENTION — Efforts should be made to reduce the risk of air embolism in the following at-risk populations:

For neurosurgical and procedures of the head and neck – For patients in whom cervical spine procedures or a craniotomy is performed in the sitting position (which is rare), the patient should be monitored for venous air embolism with transthoracic or transesophageal echocardiography, and a central venous catheter should be placed for possible air aspiration. A similar approach may be warranted on a case-by-case basis for other neurosurgical and otolaryngological surgeries that are assessed by the operating surgeon and anesthesiologist to be at high risk for air embolism. In addition, anesthesia with nitrous oxide should be discontinued as it can worsen air embolism. (See 'Terminology and pathophysiology' above and "Intraoperative venous air embolism during neurosurgery", section on 'Monitoring for venous air embolism'.)

Patients on mechanical ventilation – For patients who are mechanically ventilated, airway pressures should be minimized to prevent pulmonary barotrauma (ie, lung protective ventilation), the details of which, are discussed separately. (See "Diagnosis, management, and prevention of pulmonary barotrauma during invasive mechanical ventilation in adults", section on 'Prevention'.)

For patients with central intravascular catheters – The Trendelenburg position is preferred for central venous catheter insertion and removal from jugular and subclavian vein sites; the supine position is sufficient for the femoral site. Additional preventative maneuvers include treating hypovolemia prior to catheter placement, occluding the hub of the central venous catheter during insertion, keeping all connections to a central line closed and locked when not in use, withdrawing blood and injecting medications with the patient supine (ie, below the level of the heart), and asking the patient to Valsalva or exhale during removal [1,111]. Similar principles apply to the insertion, removal, use, and manipulation of arterial catheters. (See "Central venous catheters: Overview of complications and prevention in adults", section on 'Venous air embolism'.)

SUMMARY AND RECOMMENDATIONS

Definition – Air embolism is an uncommon, but potentially catastrophic, event that occurs as a consequence of the entry of air into the vasculature. Surgery, trauma, vascular interventions, and barotrauma from mechanical ventilation and diving are the most common causes of air embolism. These and other less common causes are listed in the table (table 1). (See 'Introduction' above.)

Terminology and pathophysiology – Air embolism requires direct communication between a source of air and the vasculature, as well as a pressure gradient favoring the passage of air into the circulation. Venous air embolism is a consequence of air being introduced into the venous circulation, traveling to the right heart, and lodging in the pulmonary circulation. Arterial air emboli may be a consequence of incomplete filtration of venous air emboli by the lung, the introduction of air directly into the arterial system, or paradoxical embolization. (See 'Terminology and pathophysiology' above.)

Clinical presentation – Air embolism should always be suspected when patients experience sudden-onset respiratory distress (venous air embolism) and/or experience a neurological event (arterial embolism) in the setting of a known risk factor (eg, intravenous catheter insertion, trauma). The spectrum of clinical findings depends upon the degree of severity of embolism, end-organs affected, and underlying comorbidities (table 2) (see 'Clinical features' above):

Venous – Minor cases of venous air embolism are common, cause minimal or no symptoms, and are often transient and self-resolving. In more severe cases, dyspnea is almost a universal finding and may be accompanied by substernal chest pain, lightheadedness, or dizziness. Immediately life-threatening cases are characterized by acute-onset right-sided heart failure, an acute sense of impending doom, sudden-onset loss of consciousness, hemodynamic collapse (from obstructive shock), or cardiac arrest. Signs include a gasp, cough, or sucking noise, a mill wheel murmur, tachypnea, tachycardia, bradycardia, hypotension, wheezing, crackles, elevated jugular venous pressure, and hypoxemic respiratory failure.

Arterial – The symptoms and signs of arterial embolism vary depending on the organ affected (usually the brain) so that many patients present with an acute change in mental status and/or focal neurological deficits. Severe cases may present with loss of consciousness, coma, and cardiac arrest. Additional features include the signs of acute ischemia of affected organs, including the heart and skin, resulting in chest pain, wheeze, crepitus over superficial vessels, livedo reticularis, and bubbles within retinal arteries.

Differential diagnosis – Disorders that should be considered in the differential diagnosis of patients with suspected air embolism include all those that can cause acute pulmonary, cardiovascular, or neurological decompensation (table 4). There are no pathognomic features of air embolism that distinguish it from other forms of embolism or acute decompensation other than the demonstration of air on imaging. (See 'Differential diagnosis' above.)

Diagnosis and initial management – For patients with suspected air embolism, we suggest the following strategy:

Initial supportive therapy – Patients should be rapidly assessed for airway stability, breathing, and circulation, and appropriate supportive therapies should be administered (eg, high flow oxygen, mechanical ventilation, volume resuscitation, vasopressors, advanced cardiac life support). For all patients suspected as having air embolism, we recommend the administration of supplemental oxygen with a high fraction of inspired oxygen (FiO2) (Grade 1C). Although the optimal FiO2 or oxyhemoglobin saturation level is unknown, we prefer to start with the highest level of FiO2 to achieve the highest saturation as tolerated by the patient. (See 'Supportive therapy' above.)

Positioning – For patients with suspected venous air embolism, we recommend placing the patient in the left lateral decubitus head down position, rather than leaving the patient supine (Grade 1C). The left lateral decubitus and Trendelenburg positions are acceptable alternatives. Conversely, for patients with arterial air embolism, we suggest placing the patient in the supine position rather than head down positions. (See 'Positioning the patient' above.)

Diagnostic evaluation – For patients with suspected air embolism, simultaneous with initial assessment, the following diagnostic tests should be performed (table 3): complete blood count and differential, serum chemistries, creatine phosphokinase, serum troponin-I or -T, brain natriuretic peptide, arterial blood gas analysis, chest radiography, and electrocardiography. Additional testing depends upon the suspected source of air and location of potential end organ damage and may include transthoracic or transesophageal echocardiography (if intracardiac air is suspected), contrast enhanced computed tomography (CT) of the chest and/or pulmonary arteries (if venous air embolism is suspected), and contrast-enhanced CT of the brain (if cerebral embolism is suspected). (See 'Diagnostic approach' above.)

Diagnosis – The diagnosis is best made by demonstrating air in the intravascular space or organs in a patient with a known risk factor for air embolism. However, because air may be rapidly absorbed from the circulation while waiting for diagnostic imaging, air embolism is typically a retrospective clinical diagnosis, based upon a high index of suspicion and the exclusion of other life-threatening processes. (See 'Diagnosis' above.)

Definitive therapy – For most patients with air embolism, hyperbaric oxygen (HBO) therapy is not routinely administered (Grade 2C). When available, HBO should be administered to patients with evidence of hemodynamic or cardiopulmonary compromise, as well as to those with neurologic deficits or other evidence of end-organ damage. We prefer that HBO be administered within the first four to six hours after symptom onset but continued benefit has been reported when HBO therapy is delayed for up to 30 hours. The potential benefits of HBO must be weighed against the potential risks of transport to the HBO facility where it is administered. The aspiration of air from the right ventricle using a preexisting central venous catheter and closed-chest cardiac massage (ie, chest compressions) are last resort therapies that may be attempted in patients who are in extremis due to air embolism. (See 'Treatment' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Liza C O'Dowd, MD, who contributed to earlier versions of this topic review.

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Topic 8263 Version 28.0

References

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