Intraoperative venous air embolism during neurosurgery

INTRODUCTION — Venous air embolism (VAE) may occur during any procedure in which an opening in a vascular structure is above the level of the heart, and has been reported to occur in many types of surgery. In neurosurgical procedures, VAE occurs most commonly in those that are performed in the sitting position. VAE rarely occurs when air is inadvertently injected into the vasculature. Clinically significant VAE is very rare but can have devastating consequences.

This topic will discuss the incidence and pathophysiology of VAE, monitoring for VAE, and management of VAE during neurosurgical procedures.

General principles of anesthesia for craniotomy are discussed separately. (See "Anesthesia for craniotomy in adults".)

General principles, physiologic effects, and complications of patient positioning for surgery are also discussed separately. (See "Patient positioning for surgery and anesthesia in adults".)

INCIDENCE OF VAE — The reported incidence of VAE during neurosurgery varies widely, depending on the method of detection and the procedure performed. Minor, clinically insignificant VAE is common in patients in the sitting position, and may occur in up to 76 percent of patients who undergo suboccipital craniotomy, monitored with transesophageal echocardiography (TEE) [1]. Severe or extreme VAE (variably defined) is rare, reported in up to 3 percent of cases [2-4].

Much of what is known about the incidence of VAE comes from case series. In these studies, intraoperative VAE was detected by precordial Doppler ultrasonography, transesophageal echocardiography, or a combination of the two monitors.

●Sitting position – The incidence of any intraoperative VAE is highest during craniotomy, reported at rates as high as 15 to 76 percent. Cervical spine procedures and cervical denervation for torticollis management have a lower but significant rate of VAE at 0.7 to 25 percent [1-7]. The reported incidence of VAE during deep brain simulator (DBS) procedures is between 0.3 to 4.8 percent [2,5].

●Other positions – VAE during non-sitting neurosurgery is probably less common than in the sitting position, reported in 0 to 12 percent of monitored patients during craniotomy [6-8]. The true incidence of VAE in non-sitting positions is unknown, since most patients in horizontal positions are not monitored specifically for VAE. There are isolated case reports and case series of VAE during prone spine surgery [9-11].

•In one single institution retrospective study of 580 patients who had posterior fossa craniotomy, precordial Doppler monitoring was used for all patients in the sitting position, and in 30 percent of patients in horizontal positions (ie, supine, prone, lateral, or park bench) [6]. VAE was detected in 45 percent of patients in the sitting position, compared with 12 percent of the monitored patients in horizontal positions.

•In another single institution retrospective review of approximately 430 patients who had vestibular schwannoma resection, VAE was detected by any method in 28 percent of patients in the sitting position, compared with 5 percent of patients in the supine position [7]. Precordial Doppler monitoring was used in all but one patient in the sitting position, and in 85 percent of non-sitting patients. TEE was used in 74 percent of sitting patients and in 2 percent of supine patients.

●Incidence of severe VAE – Clinically significant VAE has been reported in 1 to 3 percent of seated craniotomies [2,3]. In a single institution review of 1700 neurosurgical procedures performed in the sitting position, severe VAE (ie, requiring an urgent change in patient position) occurred in 1.5 percent of suboccipital craniotomies [4]. There were two cases of severe VAE during awake DBS placement (0.6 percent), and none occurred during cervical spine or torticollis denervation procedures.

VAE is a less common complication of a variety of other types of surgery. (See "Air embolism", section on 'Other surgical or procedural interventions'.)

PATHOPHYSIOLOGY — VAE occurs when air or gas is entrained or pushed into a venous structure, embolizing into the right heart and pulmonary vasculature. Air can enter the left heart through intracardiac (eg, patent foramen ovale [PFO]) or intrapulmonary shunts, and can then embolize to coronary, cerebral, or other organ arterial vessels.

Mechanism of air entry — VAE is possible when there is a pressure gradient across an opening in a vein, particularly in noncollapsible venous structures (eg, major intracerebral venous sinuses). During neurosurgery this can occur when a venous opening occurs at a point where venous pressure is negative relative to ambient pressure. Spontaneous ventilation may increase the risk of VAE due to the intermittent negative intrathoracic pressure that is transmitted to the venous system at the surgical site.

The most likely site of air entry is the surgical field during incision or dissection around vascular structures. Air embolism has also occurred during durotomy for deep brain stimulator placement (DBS; presumably by puncture of diploic or emissary veins), and has been reported from Mayfield pin sites [12].

Risk factors for VAE during neurosurgery include the following:

●Surgical incision or dissection at a height above the level of the heart when intravenous (IV) pressure is subatmospheric.

●Sudden release of positive end-expiratory pressure (PEEP). Sudden release of PEEP may theoretically embolize previously undetected air within intrathoracic vessels or intracranial air trapped after wound closure [13].

●Spontaneous ventilation, due to intermittent negative intrathoracic pressure that is transmitted to venous system at the surgical site [14].

●High-pressure mechanical ventilation risking barotrauma. (See "Air embolism", section on 'Positive pressure ventilation'.)

Mechanical and physiologic effects — The clinical effects of VAE may be determined by the volume and rate of air entrainment, both of which relate to the size of the vascular opening and the height of the opening above the heart. The mechanisms for the clinical effects of VAE are not fully understood. In addition to the mechanical effects of air bubbles or pockets, intravascular air may cause release of endothelin and inflammatory mediators, platelet aggregation, and hypoxic vasoconstriction, which can cause some of the physiologic responses that occur in severe VAE (eg, increased pulmonary pressures, bronchospasm, pulmonary edema) [14]. (See "Air embolism", section on 'Venous air embolism'.)

●Volume of air – The lethal volume of air embolism is unknown, and may depend on the patient's baseline cardiac status. Patients have died after estimated or known embolism of 200 to 300 mL of air [15-18], though it is likely that smaller amounts can be lethal in some patients.

●Rate of air entrainment – The lethal rate of entrainment is also unknown. High rates of air entry can quickly result in a lethal volume, and would need to be terminated quickly to avoid cardiovascular collapse. In contrast, very low rates of air entry may be well tolerated as the pulmonary circulation can act as a buffer. In animal models "lethal," volumes of air were tolerated at a slow infusion rate over several hours [19].

●Pulmonary vasoconstriction – Air within the pulmonary circulation can cause local and widespread pulmonary hypertension via pulmonary vasoconstriction [20].

●Air lock – A large amount of air accumulating quickly in the right heart and pulmonary arterial system can cause an air lock, with complete obstruction of right ventricular output. This can cause right ventricular overdistention and failure, and loss of left ventricular output due to lack of preload. This mechanism for cardiovascular deterioration during VAE is thought to be rare, and requires rapid embolism of large amounts of air.

●Cardiac ischemia – Cardiac ischemia after VAE can result from increased afterload, hypotension, and via embolism into the coronary arteries, and can cause ventricular dysfunction and/or arrhythmias.

●Pulmonary edema – Chemical and pro-inflammatory mediators released after acute VAE can cause pulmonary edema [14].

CLINICAL MANIFESTATIONS OF VAE — Clinical manifestations of VAE vary from no signs or symptoms to severe cardiopulmonary and/or neurologic events. Many instances of minor VAE detected by transesophageal echocardiography (TEE), or precordial Doppler monitoring are of no clinical consequence. In case reports of VAE, the sequence of the typical presentation of clinically relevant VAE is a reduction in end-tidal carbon dioxide (ETCO₂), followed by reduced blood pressure and/or increase in heart rate, and finally significant hemodynamic compromise which could include cardiac arrest [4,21]. Hypoxia is a late manifestation of VAE, and may not occur, even in patients with extreme VAE [4].

In awake patients (eg, during deep brain stimulator [DBS] placement), cough may be a clinical sign of VAE [12,22,23]. Focal neurologic deficits may indicate paradoxical air embolism, and hemodynamic compromise as a result of severe VAE can cause mental status changes.

The monitoring findings for VAE are discussed below. (See 'Monitoring for venous air embolism' below.)

RISK OF PARADOXICAL EMBOLISM — Patients with intracardiac shunt (eg, patent foramen ovale [PFO], atrial septal defect, ventricular septal defect) are theoretically at increased risk of paradoxical embolism with VAE, and therefore at increased risk of stroke, coronary artery embolism, or other end-organ arterial air embolism. Thus, in some institutions, the presence of an intracardiac shunt is a relative contraindication to high-risk procedures (ie, sitting position, surgery near cerebral venous sinuses).

We do not routinely obtain a preoperative echocardiogram before high-risk procedures specifically to rule out an intracardiac shunt. However, we do routinely perform a bubble test for shunt detection if we place a transesophageal echocardiography (TEE) probe. For patients with a known PFO, we discuss the choice of position for surgery with the surgeon (see 'Patient positioning' below). In consultation with the patient's cardiologist, we may obtain a preoperative echocardiogram for patients with known cardiovascular conditions that may increase the risk of decompensation with air embolism (eg, pulmonary hypertension, hypertrophic cardiomyopathy, right ventricular dysfunction, moderate to severe valvular disease).

Existing limited observational studies have not reported severe neurologic or cardiac sequelae following VAE in patients with PFO [24].

●In a single institution prospective study of 52 patients with a PFO who had neurosurgery in the semi-sitting position (ie, posterior fossa, pineal, or occipital procedures), air bubbles were observed on TEE in 29 patients (55.7 percent), however there were no cases of right to left shunting of air bubbles on TEE, no detected cardiac ischemia or arrhythmias, no brain ischemia, and no mortality [25]. All patients were monitored with routine physiologic monitors, TEE, continuous intra-arterial blood pressure, and a central venous catheter (CVC). If air bubbles were visualized on TEE, bilateral jugular venous pressure was applied to facilitate finding and repairing a venous leak site.

●In the study described above that included patients who experienced extreme VAE requiring intraoperative position change, three patients had demonstrated PFOs on intraoperative TEE; none of them had persistent adverse effects after VAE [4].

ANESTHETIC MANAGEMENT FOR AT RISK PATIENTS — Important management decisions for patients who are at high risk of VAE involve monitoring for VAE, patient position for surgery, and whether to place a central venous catheter (CVC) for air aspiration, which are discussed here. Other aspects of anesthesia for neurosurgical procedures are discussed separately.

●(See "Anesthesia for craniotomy in adults".)

●(See "Anesthesia for elective spine surgery in adults".)

●(See "Anesthesia for deep brain stimulator implantation".)

Patient positioning — We discuss the plan for patient positioning with the neurosurgical team preoperatively. The discussion includes the risk of VAE for the planned procedure (eg, proximity to cerebral venous sinuses), surgical factors that may make controlling VAE difficult, as well as the patient-specific risks should VAE occur (eg, pulmonary hypertension, right ventricular dysfunction, intracardiac shunts).

The semi-sitting or sitting position offers surgical advantages for some procedures, including improved exposure, reduced intracranial pressure, and reduced bleeding. In some cases, these advantages must be balanced against the risk of VAE when deciding on the position for surgery.

Monitoring for venous air embolism — Monitors for VAE include precordial Doppler, transesophageal echocardiography (TEE), and capnography (which is a standard physiologic monitor during anesthesia). For patients who have general anesthesia for procedures with a high risk of VAE, we use all three monitoring modalities. For patients who have contraindications to TEE or who have awake procedures, we use precordial Doppler and capnography (table 1).

The first signs of VAE on monitoring devices are typically visible air bubbles on TEE, and simultaneously a whirring sound on the precordial Doppler. Depending on the rapidity of progression and the patient's ability to compensate, a drop in end-tidal carbon dioxide (ETCO₂) will occur next; a significant drop in ETCO₂ usually precedes a drop in arterial blood pressure. Oxygen desaturation and cardiac arrythmias are later signs in most patients.

Capnography — Capnography is a standard anesthesia monitoring modality, used for almost all patients during anesthesia. A sudden flattening of the capnography waveform and reduction in ETCO₂ (>5 mmHg) during seated neurosurgery may suggest VAE in mechanically ventilated patients, though this finding is nonspecific [26]. ETCO₂ drops during VAE if air obstructs pulmonary vasculature, and results in areas of the lung that do not exchange gas, thereby increasing total (anatomic + physiologic) deadspace and reducing expired CO₂.

The magnitude of a drop in ETCO₂ cannot be used to diagnose or predict the severity of VAE. Although larger decreases in ETCO₂ are associated with greater severity of hemodynamic changes during VAE, this is only a fair to moderate association [27]. This means that some patients with VAE will have a minimal decrease in ETCO₂ but may go on to experience significant hemodynamic changes.

In addition, changes in ETCO₂ are nonspecific. If there are CO₂ changes without evidence of air on TEE, other diagnoses for a drop in ETCO₂ should be explored (eg, reduced cardiac output from reduced left ventricular preload, cardiac dysfunction due to coronary artery air embolism, or arrhythmia).

Precordial Doppler — A precordial Doppler placed along the sternal border can detect up to 0.015 cc/kg/minute of air [28]. Importantly, unless a massive rapid embolism occurs, Doppler is sensitive enough to detect embolism early and allow the surgeon and anesthesiologist to respond before cardiopulmonary adverse effects ensue. The precordial Doppler is noninvasive and acts as a constant, real-time audible monitor for VAE. However, it cannot predict VAE severity, and unlike TEE, it cannot detect paradoxical air, or analyze cardiac function.

Precordial Doppler beam placed across intracardiac chambers translates motion artifact from red blood cells and plasma into audible sounds. The acoustic echogenic properties of air bubbles are different from that of plasma and the cellular components of blood allowing for the detection of air bubbles moving along with the flow of blood. [29]. Optimal use of the precordial Doppler requires proper positioning and confirmation of the correct position. The precordial probe should be placed adjacent to the sternum (eg, at the 3^rd to 6^th intercostal space), on either the right or left side, which ever provides the clearer Doppler heart tones. In one study that compared Doppler probe placements in 46 patients who underwent elective craniotomy, adequate Doppler signals were obtained in all patients who had the probe placed at the left parasternal border, compared with 78 percent of patients with right parasternal placement [29].

We confirm correct placement of the Doppler probe by injecting approximately 10 mL of agitated saline through the CVC or peripheral intravenous (IV) line, listening for an obvious change in Doppler tone. If negative, we reposition the precordial Doppler, typically more midline, maintaining good cardiac auscultation, and repeat the test until position is confirmed.

The precordial Doppler probe should usually be placed and secured with tape after the patient is positioned for seated surgery, as the optimal site for the probe may change. If the patient is prone or lateral, the precordial Doppler probe should be appropriately padded with gauze or foam padding to avoid pressure point injury. This includes remembering to pad the cord. Optimal padding would avoid pressure on the probe against the patient's skin.

There are no specific contraindications to precordial Doppler monitoring.

Transesophageal echocardiography — TEE is the most sensitive monitor for VAE and can alert the anesthesiologist at the first sign of air entry. TEE can detect as little as 0.2 mL of air [30]. However, TEE is expensive, invasive, requires expertise to place and interpret, and requires that the clinician watch the ultrasound screen continuously. These issues limit the use of TEE in some institutions.

Contraindications to TEE (primarily related to esophageal pathology) are shown in a table and are discussed separately (table 2). (See "Transesophageal echocardiography: Indications, complications, and normal views", section on 'Safety of TEE examination'.)

Continuous use of TEE for the duration of surgery is usually not feasible. Over time during use, the tip of the TEE probe increases in temperature. The probe will stop working if a certain temperature threshold is exceeded as a safety precaution to minimize risk of thermal injury to the esophagus.

The safety of TEE in long cases with the neck flexed has not been established. Devices placed in the pharynx can obstruct venous drainage with the neck flexed, and can cause swelling of the tongue and soft tissues, with potential airway obstruction after extubation [31]. The clinician should evaluate the airway after the procedure is complete but prior to extubation in all patients who had a TEE probe in place intraoperatively. For those with excessive tongue swelling, the TEE probe can be removed but extubation should be delayed until swelling has diminished.

The TEE probe is placed after induction of anesthesia, and an examination is performed to assess cardiac function and if necessary, assess for patent foramen ovale (PFO). We perform a PFO diagnostic bubble test with Valsalva release in each patient, even those with previously confirmed PFO. We obtain a midesophageal four or five chamber (four chamber with aortic valve outlet) or bicaval view to monitor for VAE, paradoxical VAE, and cardiac function. If necessary, we adjust the TEE view after final patient positioning. (See "Intraoperative transesophageal echocardiography for noncardiac surgery" and "Intraoperative transesophageal echocardiography for noncardiac surgery", section on 'Neurosurgery with high risk of venous air embolism'.)

In high-risk patients in whom TEE is contraindicated, semi-continuous or intermittent transthoracic echocardiography could be used but this is logistically very difficult.

Mass spectrometry — Mass spectrometry (mass spec) was used in the past to quantify inspired and expired gas concentrations (including CO₂ and nitrogen) during anesthesia. In patients who inspire oxygen without air and with or without nitrous oxide, an increase in expired nitrogen could indicate VAE, since nitrogen in the embolized air would be expired and detected with mass spec.

Mass spec has largely been replaced by infrared spectroscopy for measuring inspired and expired gas concentration during anesthesia. Expired nitrogen is not detected by infrared spectroscopy, and is therefore not used to monitor for VAE.

Central venous catheter placement — In some institutions it is standard practice to place a CVC during procedures with high risk of VAE, with the goal of aspirating air should VAE occur. However, the benefits of CVC placement are theoretical and supported only by anecdotal evidence [4,32]. Reported success rates are variable, depending on the device. The most effective catheter may be the Bunegin-Albin multiorifice catheter (5.8 French, 14 gauge) [33,34]. In one study in dogs, 60 percent of an injected bolus of air was retrieved with aspiration of the Bunegin-Albin catheter placed with the tip near the mid right atrium, compared with approximately 6 percent aspirated via a standard multiorifice CVC [33]. The Bunegin-Albin catheter is available in 24 and 60 cm lengths and can be used for antecubital insertion [35].

We place CVCs for air aspiration for posterior fossa tumor surgery in the sitting position, but not for other types of surgery. Important considerations for CVC placement for air aspiration include the following:

●The insertion site for a CVC should be discussed with the surgeon. Internal jugular placement, which is most commonly used for other central line placements, may not be appropriate for some neurosurgical procedures. Alternative sites (eg, subclavian or antecubital vein) may be required. We routinely place multilumen antecubital central catheters, and have reported aspirating large volumes of air during VAE [4].

●We confirm placement of the catheter tip within 2 cm of the junction of the right atrium with the superior vena cava [36], using TEE with either a midesophageal four or five chamber view or a bicaval view. This requires placing the TEE probe prior to CVC insertion, with an assistant or echocardiographer available to reposition the catheter tip if necessary. Chest radiograph can also be used to confirm the catheter tip but takes longer.

●Help should be summoned if air aspiration is required. Aspiration of the catheter is labor intensive and can distract from other potentially more important therapeutic maneuvers (eg, fluid and vasopressor administration and change in patient position).

●There is no evidence that emergency insertion of a central catheter during a VAE is beneficial.

●We remove the CVC soon after surgery, either in the post-anesthesia care unit (PACU) or in the intensive care unit.

Use of nitrous oxide — We do not avoid the use of nitrous oxide for patients at high risk of VAE, though we turn it off and administer 100% oxygen if VAE occurs. There is a theoretical risk that nitrous oxide can worsen the effects of VAE by expanding air bubbles, and practice varies. However, several retrospective studies have shown that its use has no bearing on the incidence or severity of VAE [37-39].

MANAGEMENT OF INTRAOPERATIVE VAE — Management of intraoperative VAE is shown in a table (table 3).

●The most important initial step after recognizing VAE is to stop further air entry. This is accomplished by the surgeon, initially by flooding the wound with saline, and ultimately by identifying and repairing the vascular defect.

●Simultaneously, initial steps include administering 100% oxygen, discontinuing nitrous oxide, and rapid administration of intravenous (IV) fluid. Further management depends on the severity and clinical signs that develop. Not all VAE events may be clinically apparent. Most VAEs detected with intraoperative monitoring do not require major intervention (eg, position change, aborting the surgical procedure).

●If VAE progresses to the point at which vasopressors are necessary to support blood pressure, we aspirate the central venous catheter (CVC; if present).

●We urgently reposition the patient from a head up to supine position (if applicable), if any if the following occur:

•Significant hemodynamic compromise

•Air appears on the left side of the heart, or

•A neurologic deficit develops in an awake patient

Leveling the patient reduces or eliminates the pressure gradient between the vascular opening and the heart, thereby terminating VAE, and facilitates resuscitation. However, the decision to change position is not made lightly. Concerns include the risk of infection and interruption of surgery. However, in a review of eight cases of extreme VAE requiring position change, there were no cases of wound infection or adverse neurologic sequelae as a result of VAE [4].

●If hemodynamic compromise continues despite these maneuvers, or cardiac arrest occurs, resuscitation should proceed using advanced cardiac life support principles. (See "Intraoperative advanced cardiac life support (ACLS)".)

Once an episode of VAE resolves, the decision to proceed with surgery should be multidisciplinary, considering the severity of the event, likelihood of recurrence, urgency of the surgery, and patient factors. In the previously mentioned review of cases of extreme VAE, surgery was continued without incident in five of eight patients [4].

●Avoid changing the level of positive end-expiratory pressure (PEEP) – Older recommendations were to increase PEEP to prevent further cardiac entrainment of air. However, this strategy is now avoided because of the risk of further reducing cardiac preload in the setting of hemodynamic instability. In addition, abruptly discontinuing PEEP has been shown to exacerbate air entrainment [13].

●Bilateral jugular vein compression – Some authors apply pressure to the jugular veins if VAE occurs. Entrained air may return to the heart via jugular veins, and theoretically, compression of those veins can help slow the movement of air into the heart. Jugular compression can also be used to help the surgeon identify the leaking vascular site. We do not routinely perform jugular compression in this setting, for the following reasons: jugular compression can reduce cerebral perfusion by increasing intracranial pressure; care must be taken to avoid carotid artery compression and further reduction in cerebral blood flow; and carotid sinus pressure during the maneuver can cause significant bradycardia.

POSTOPERATIVE CARE/DISPOSITION — For most patients who experience intraoperative VAE, postoperative care is the same as it would be without having had a VAE. We consider postoperative intensive care for patients who would not have otherwise recovered in the intensive care unit (ICU) if the following occur:

●Severe or extreme VAE (ie, VAE requiring aggressive vasopressor support to sustain cardiac output), emergency change in patient position (from sitting or head up), or emergency abortion of the procedure

●Paradoxical VAE

●New unexpected neurologic deficits or seizure

●Need for hyperbaric oxygen therapy (HBOT)

HBOT is a less often used, but a known treatment for arterial air embolism [40]. HBOT has been used in isolated case reports in patients who suffered an intraoperative VAE during neurosurgery and who had significant arterial intracranial air. HBOT is indicated for patients with arterial intravascular air associated with hemodynamic instability, neurologic deficits, or other end-organ damage thought to be related to intraarterial air. (See "Air embolism", section on 'Hyperbaric oxygen'.)

OUTCOMES AFTER INTRAOPERATIVE VAE — With effective monitoring and rapid treatment, significant sequelae, even after severe VAE, are very rare. Most cases of intraoperative VAE do not result in severe hemodynamic instability or new neurologic changes, and patients can be observed closely in the operating room after allowing the surgeon to address possible sources of air entrainment [2]. However, arterial embolization after air entrance into the left heart can cause significant adverse outcomes and end-organ damage. Examples of relevant studies include the following:

●In a single institution review of 1792 procedures performed in the sitting position between 2000 and 2013, the rate of any detected VAE was 4.7 percent, whereas the rate of VAE requiring clinical intervention was 1.1 percent [2]. There were no intraoperative deaths, and two cases (0.1 percent) were aborted due to VAE. Patients who had general anesthesia were typically monitored with transesophageal echocardiography (TEE) and precordial Doppler, in addition to routine physiologic monitors.

●In another single institution review of 8 cases of extreme VAE during seated neurosurgery (ie, severe enough to require urgent repositioning to supine), in all cases the end-tidal carbon dioxide (ETCO₂) and blood pressure changes associated with VAE normalized quickly after repositioning, without persistent cardiac morbidity events or new neurologic deficits [4]. All patients were monitored with precordial Doppler and standard physiologic monitors; TEE was also used for craniotomies, but not for deep brain stimulator (DBS) placement.

A decrease in platelet count was reported in a case series of patients who had intraoperative VAE during seated craniotomy [41], and there is a case report of fatal severe coagulopathy after a massive intraoperative VAE [42].

SUMMARY AND RECOMMENDATIONS

●Mechanism of venous air embolism (VAE)

•Intraoperative VAE can occur when an opening is created in a vascular structure that is above the level of the heart and where pressure inside the vessel is subatmospheric. This creates a negative pressure gradient in the vascular structure, causing entrainment of air. (See 'Mechanism of air entry' above.)

•The mechanisms for some of the clinical effects of VAE (eg, pulmonary hypertension, bronchospasm, pulmonary edema) are not fully understood and may involve both the mechanical effects of air and release of inflammatory mediators. (See 'Mechanical and physiologic effects' above.)

●Incidence – VAE is most common in procedures performed in the sitting position. It is reported in up to 76 percent of suboccipital craniotomies performed in the sitting position. Severe VAE (ie, requiring an urgent change in the patient's position) is rare, occurring in 1 to 3 percent of sitting craniotomies. (See 'Incidence of VAE' above.)

●Clinical manifestations

•Minor VAEs detected by monitoring with transesophageal echocardiography (TEE), or precordial Doppler are often of no clinical consequence.

•Clinically relevant VAE typically presents with reduced end-tidal carbon dioxide (ETCO₂), followed by reduced blood pressure and/or increase in heart rate, and finally significant hemodynamic compromise which could include cardiac arrest. (See 'Clinical manifestations of VAE' above.)

●Risk of paradoxical air embolism – Patients with intracardiac shunt (eg, patent foramen ovale [PFO], atrial septal defect, ventricular septal defect) are theoretically at increased risk of paradoxical embolism with VAE, which can result in stroke, coronary artery embolism, or other end-organ embolism. We do not routinely request a preoperative echocardiogram to rule out intracardiac shunt, but we do perform a bubble test if a TEE is placed for monitoring. For patients with PFO, patient positioning should be discussed with the surgeon. (See 'Risk of paradoxical embolism' above.)

●Monitoring for VAE (see 'Monitoring for venous air embolism' above)

•For all patients who are at risk for VAE, we monitor with capnography and precordial Doppler. We use TEE as well for patients who have general anesthesia for high risk procedures, as shown in a table (table 1).

•The first signs of VAE are typically visible air bubbles on TEE, and simultaneously changes in Doppler sounds. Depending on the rapidity of progression and the patient’s ability to compensate, a drop in ETCO₂ follows; a significant drop in ETCO₂ usually precedes a drop in arterial blood pressure. Oxygen desaturation and cardiac arrythmias are later signs in most patients.

●Central venous catheter (CVC) for air aspiration – CVCs may be placed preoperatively to attempt air aspiration if VAE occurs, though their use is not well supported by evidence. We place CVCs for posterior fossa tumor surgery in the sitting position, but not for other types of surgery (table 1). (See 'Central venous catheter placement' above.)

●Management of VAE – Management of VAE is shown in a table (table 3).

•The most important first step is to stop further air entry (eg, by flooding the field with saline, and by repairing the entry site).

•Simultaneously, initial steps are to administer 100% oxygen, discontinue nitrous oxide, and administer intravenous (IV) fluid rapidly.

•We urgently reposition the patient supine if the following occur:

-Significant hemodynamic compromise

-Air appears on the left side of the heart, or

-A neurologic deficit develops in an awake patient