eMedicine Specialties > Emergency Medicine > Cardiovascular

Venous Air Embolism

Brenda Liz Natal, MD, Clinical Assistant Instructor and Staff Physician, Department of Emergency Medicine, Kings County Hospital and State University of New York Downstate, Brooklyn
Christopher I Doty, MD, FACEP, FAAEM, Assistant Professor of Emergency Medicine, Residency Program Director, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Updated: Jul 27, 2009

Introduction

Background

Venous air embolism (VAE), a subset of gas embolism, is an entity with the potential for severe morbidity and mortality. Venous air embolism is a predominantly iatrogenic complication^1,2 that occurs when atmospheric gas is introduced into the systemic venous system³ . In the past, this medical condition was mostly associated with neurosurgical procedures conducted in the sitting position.^4,5 More recently, venous air embolism has been associated with central venous catheterization,^3,6,7 penetrating and blunt chest trauma,^8,9 high-pressure mechanical ventilation,³ thoracocentesis,¹ hemodialysis,^3,7 and several other invasive vascular procedures. 

Venous air embolism (VAE) has also been observed during diagnostic studies, such as during radiocontrast injection for computerized tomography.^10,11 The use of gases such as carbon dioxide and nitrous oxide during medical procedures and exposure to nitrogen during diving accidents can also result in VAE.² Many cases of VAE are subclinical with no adverse outcome and thus go unreported. Usually, when symptoms are present, they are nonspecific, and a high index of clinical suspicion of possible venous air embolism is required to prompt investigations and initiate appropriate therapy.

Pathophysiology

Two preconditions must exist for venous air embolism to occur: (1) a direct communication between a source of air and the vasculature and (2) a pressure gradient favoring the passage of air into the circulation.^12,4

The key factors determining the degree of morbidity and mortality in venous air emboli are related to the volume of gas entrainment, the rate of accumulation, and the patient’s position at the time of the event.^1,6,11

Generally, small amounts of air are broken up in the capillary bed and absorbed from the circulation without producing symptoms. Traditionally, it has been estimated that more than 5 mL/kg of air displaced into the intravenous space is required for significant injury (shock or cardiac arrest) to occur.¹ However, complications have been reported with as little as 20 mL of air⁷ (the length of an unprimed IV infusion tubing) that was injected intravenously. The injection of 2 or 3 mL of air into the cerebral circulation can be fatal.¹³ Furthermore, as little as 0.5 mL of air in the left anterior descending coronary artery has been shown to cause ventricular fibrillation.^13,9 Basically, the closer the vein of entrainment is to the right heart, the smaller the lethal volume is.¹

Rapid entry or large volumes of air entering the systemic venous circulation puts a substantial strain on the right ventricle, especially if this results in a significant rise in pulmonary artery (PA) pressures. This increase in PA pressure can lead to right ventricular outflow obstruction and further compromise pulmonary venous return to the left heart. The diminished pulmonary venous return will lead to decreased left ventricular preload with resultant decreased cardiac output and eventual systemic cardiovascular collapse.^1,4,6  

With venous air embolism (VAE), resultant tachyarrhythmias are frequent, but bradyarrhythmias can also occur.^4,2  

The rapid ingress of large volumes of air (>0.30 mL/kg/min) into the venous circulatory system can overwhelm the air-filtering capacity of the pulmonary vessels, resulting in a myriad of cellular changes.³ The air embolism effects on the pulmonary vasculature can lead to serious inflammatory changes in the pulmonary vessels; these include direct endothelial damage and accumulation of platelets, fibrin, neutrophils, and lipid droplets.¹

Secondary injury as a result of the activation of complement and the release of mediators and free radicals can lead to capillary leakage and eventual noncardiogenic pulmonary edema.^1,7,3

Alteration in the resistance of the lung vessels and ventilation-perfusion mismatching can lead to intra-pulmonary right-to-left shunting and increased alveolar dead space with subsequent arterial hypoxia and hypercapnea.^1,4,11   

Arterial embolism as a complication of venous air embolism (VAE) can occur through direct passage of air into the arterial system via anomalous structures such as an atrial or ventricular septal defect, a patent foramen ovale, or pulmonary arterial-venous malformations. This can cause paradoxical embolization into the arterial tree.^1,4,9,2,3  The risk for a paradoxical embolus seems to be increased during procedures performed in the sitting position.^1,5

Air embolism has also been described as a potential cause of the systemic inflammatory response syndrome (case report), triggered by the release of endothelium derived cytokines.¹²

Frequency

United States

The nonspecific nature of the signs and symptoms of venous air embolism (VAE) as well as the difficulty in documenting the diagnosis does not allow the true incidence of VAE to be known. Interventional radiology literature reports an incidence of venous air embolism of 0.13% during the insertion and removal of central venous catheters despite using optimal positioning and techniques.¹⁴ The frequency of venous air embolism with central venous catheters based on a reported case series has also ranged from 1 in 47 to 1 in 3000.^15,2 The neurosurgical procedure-related complications of venous air embolism have been estimated to be between 10-80%.^16,2,17 Reports of venous air embolism in the setting of severe lung trauma have been estimated between 4-14%.^13,8,9,18,17

Mortality/Morbidity

The potentially life-threatening and catastrophic consequences of venous air embolism (VAE) are directly related to its effects on the affected organ system where the embolus lodges. VAE may be fatal and frequently carries high neurologic, respiratory, and cardiovascular morbidity. Catheter-associated VAE mortality rates have reached 30%.² In a case series of 61 patients with severe lung trauma, the mortality rate associated with concomitant VAE was 80% in the blunt trauma group and 48% in the penetrating trauma group.^8,18,17 The morbidity and mortality associated with traumatic VAE, as with nontraumatic VAE, depends not only on associated injuries but also on the volume and rate of air entry, underlying cardiac condition, and the patient's position.

Race

No racial predilection exists for venous air embolism.

Sex

No gender predilection exists for venous air embolism.

Age

No specific age predilection exists for venous air embolism.

Clinical

History

Most venous air emboli go unrecognized because their presentations are protean and mimic other cardiac, pulmonary, and neurologic dysfunctions. Because of the lack of specific signs and symptoms of venous air embolism (VAE), a high index of suspicion is necessary to establish the diagnosis and institute the appropriate treatment. The number of procedures that place patients at risk for VAE has increased, and these procedures occur across almost all clinical specialties. This must be considered to aid in the confirmation or ruling out of VAE. If venous air embolism is suspected, inquiry about the following key historical elements should be obtained:

• Recent surgical procedures especially neurosurgical, otolaryngological, cardiovascular, or orthopedic
• Scuba diving trips and a history of decompression injuries or decompression sickness
• Blunt or penetrating trauma to the head, face, neck, thorax, and/or abdomen
• Invasive therapeutic and/or diagnostic procedures such as central venous catheterization; lumbar puncture; high-pressure infusion of medications, blood products, and/or IV contrast agents
• Patients with HD access catheters or other indwelling central venous catheters
• Patients on positive pressure ventilation
• Peripartum/postpartum orogenital sex (air may enter veins of the myometrium)^7,4
• Ingestion of hydrogen peroxide (rare)

Physical

Clinical Presentation

Many cases of venous air embolism (VAE) are subclinical and do not result in untoward outcomes. However, severe cases are characterized by cardiovascular collapse and/or acute vascular insufficiency of several specific organs, including, but not limited to, the brain, spinal cord, heart, and skin. As mentioned earlier, the spectrum of effects is largely dependent on the rate and volume of entrained VAE.^1,6,11

Two additional contributing factors include whether or not the patient is spontaneously breathing (yielding negative thoracic pressure) or is under controlled positive pressure ventilation.¹ These two factors facilitate the entry of air down a pressure gradient. The clinical presentation is also dependent on the patient's body position at the time of the event. Generally, if the patient is in a sitting position, gas will travel retrograde via the internal jugular vein to the cerebral circulation, leading to neurologic symptoms secondary to increased intracranial pressure. In a recumbent position, gas proceeds into the right ventricle and pulmonary circulation, subsequently causing pulmonary hypertension and systemic hypotension.¹¹
 
An arterial air embolism can also form if passage of air occurred through a right-to-left shunt, as in the case of a patent foramen ovale.^2,3 The arterial air emboli can then lodge in the coronary or cerebral circulation, causing myocardial infarction or stroke.

Symptoms (awake patients)

• Acute dyspnea
• Continuous cough
• "Gasp" reflex (a classic gasp at times reported when a bolus of air enters the pulmonary circulation and causes acute hypoxemia)^1,2
• Dizziness/lightheadedness/vertigo
• Nausea
• Substernal chest pain
• Agitation/disorientation/sense of "impeding doom"

Signs

Cardiovascular

• Dysrhythmias (tachyarrhythmias/bradycardias)
• "Mill wheel" murmur - A temporary loud, machinerylike, churning sound due to blood mixing with air in the right ventricle, best heard over the precordium (a late sign){^9,11,2
• JVD
• Hypotension
• Myocardial ischemia
• Nonspecific ST-segment and T-wave changes and/or evidence of right heart strain^1,19,2
• Pulmonary artery hypertension
• Increased CVP
• Circulatory shock/cardiovascular collapse

Pulmonary

• Adventitious sounds (rales, wheezing)
• Tachypnea
• Hemoptysis
• Cyanosis
• Decreased end-tidal carbon dioxide, arterial oxygen saturation, and tension
• Hypercapnia
• Increased pulmonary vascular resistance and airway pressures
• Pulmonary edema
• Apnea

Neurological

• Acute altered mental status
• Seizures
• Transient/permanent focal deficits (weakness, paresthesias, paralysis of extremities)
• Loss of consciousness, collapse
• Coma (secondary to cerebral edema)

Ophthalmologic

• Funduscopic examination may reveal air bubbles in the retinal vessels.¹³

Skin

• Crepitus over superficial vessels (rarely seen in setting of massive air embolus)
• Livedo reticularis

The above hemodynamic, pulmonary, and neurologic complications primarily result from gas gaining entry into the systemic circulation, occluding the microcirculation and causing ischemic damage to these end organs. Animal studies have also suggested the presence of secondary tissue damage resulting from the release of inflammatory mediators and oxygen free radicals that occur in response to air embolism.

Causes

In order for venous air embolism (VAE) to occur, 2 physical preconditions for the entry of gas into the venous system must be met.

• A direct communication between a source of air/gas and the vasculature (incising of noncollapsed veins) must exist.^4,2  
• A pressure gradient (subatmospheric pressure in the vessels) favoring the passage of air into the circulation must be present.^4,2  

Classically, venous air embolism has been recognized as occurring in the context of decompression illness in divers, aviators, and astronauts. Barotrauma and air emboli complicate an estimated 7 of every 100,000 dives.²⁰ However, the most common cause of VAE is iatrogenic. 

• Surgical procedures are the primary cause of venous air emboli. Neurosurgical procedures, especially those performed in the Fowler’s (sitting) position, and otolaryngological interventions are the two most common surgeries complicated by venous air emboli.⁵
  • The incidence of mild or clinically silent venous air embolism (VAE) during neurosurgical procedures has been estimated to range between 10% in cervical laminectomy surgeries where the patients are in the prone position, and 80% during posterior fossa surgeries (eg, repair of cranial synostosis) where patients are placed in the Fowler’s position.^2,16,21,17
  • Venous air emboli pose a risk anytime the surgical wound is elevated more than 5 cm above the right atrium.² The presence of numerous, large, noncompressed, venous channels in the surgical field (especially during cervical procedures and craniotomies that breach the dural sinuses) also increase the risk of VAE.
  • Entrainment of air/gas facilitated by the patient's intraoperative position causing VAE, may result from other surgical procedures. These include, craniofacial surgery, dental implant surgery, vascular procedures (eg, endarterectomies), liver transplantation, orthopedic procedures (eg, hip replacement, spine surgery, arthroscopy), lateral decubitus thoracotomy, genitourinary surgeries in the Trendelenburg position, and surgeries involving tumors/malformations with high degree of vascularity or compromised vessels, as in the context of trauma.^1,7
• Obstetric/gynecological procedures (cesarean delivery) and laparoscopic surgeries each carry their own risk for venous air embolism. Although this risk is commonly not considered, they each have a reported associated incidence risk of VAE greater than 50%.¹ The risk of VAE during cesarean deliveries may be highest when the uterus is exteriorized. The risk of VAE in laparoscopic surgery may require an inadvertent opening of vascular channels through surgical manipulation rather than simply resulting from a complication of insufflation. Both of these surgical procedures have been associated with intraoperative mortality as a direct sequelae of air emboli.^1,22,23,24 Despite this, the potential for venous air embolism is often ignored in laparoscopic surgery and cesarean delivery.
• Venous air embolism may also result from the iatrogenic creation of a pressure gradient for air entry. Procedures causing such a pressure gradient include lumbar puncture (case report),^21,1 peripheral intravenous lines,¹ and central venous catheters^2,3,17 . 
• Venous air embolism is a potentially life-threatening and under-recognized complication of central venous catheterization (CVC), including central lines, pulmonary catheters, hemodialysis catheters⁷ and Hickman (long-term) catheters. As mentioned earlier, the frequency of VAE associated with CVC use ranges from 1 in 47 to 1 in 3000. The emboli may occur at any point during line insertion, maintenance, and/or removal.³ A pressure gradient of 5 cm H ₂ O between air and venous blood across a 14-gauge needle allows the entrance of air into the venous system at a rate of 100 mL per second.^{2,15,16,1,9,11}  Ingress of 300-500 mL of air at this rate can cause lethal effects.¹¹  A number of factors increase the risk of catheter-related VAE, including the following:
  • Fracture or detachment of catheter connections (accounts for 60-90%)^1,2
  • 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
  • Hypovolemia, which reduces central venous pressure
  • Upright positioning of the patient, which reduces central venous pressure
• Mechanical insufflation or infusion is another cause of venous air emboli. 
  • Several different procedures involve the use of insufflation, including arthroscopic procedures, CO ₂ hysteroscopy, laparoscopy, urethral procedures, and orogenital sexual activity during pregnancy (by entering veins of the myometrium during pregnancy and/or after delivery).^1,17  
  • Inadvertent infusion of air can also occur during the injection of IV contrast agents for CT scans,^10,25,11 angiography,² and cardiac catheterization, as well as during cardiac ablation procedures¹⁷ . Little information exists on the incidence and the complication rate associated with iatrogenic air embolization caused by injections of contrast medium during CT examinations; however, this is a potentially serious complication, which could be catastrophic. Few case reports exist, and all agree that the actual number of such cases is probably higher than reported.
• Positive pressure ventilation during mechanical ventilation places patients at risk for barotrauma and, subsequently, arterial and/or venous air emboli.^1,3 Entry of gas into the circulation may result if violation of pulmonary vascular integrity occurs at the same time alveoli rupture from overdistension of the airspaces. This complication can occur in the setting of various diagnoses; however, it is most frequently reported in patients with acute respiratory distress syndrome and in premature neonates with hyaline membrane disease. For these same reasons, SCUBA divers can also have VAE from alveolar distention.
• The occurrence of venous air embolism (VAE) has also been described in the setting of blunt and penetrating chest and abdominal trauma as well as in neck and craniofacial injuries.

Differential Diagnoses

Workup

Laboratory Studies

• Laboratory tests are neither sensitive nor specific for the diagnosis of venous air embolism. The only indication for obtaining routine laboratory tests is to evaluate the associated end-organ injury resulting from air embolism. 
• Extravasation of fluid into inflamed tissue may result in laboratory findings consistent with intravascular depletion.    
• Arterial blood gas samples often show hypoxemia, hypercapnia, and metabolic acidosis secondary to right-to-left pulmonary shunting.
• Patients may develop a clinical picture similar to that of classic pulmonary embolism, with hypoxia, decreased PCO ₂ levels, and respiratory alkalosis.

Imaging Studies

• Transesophageal echocardiography (TEE) has the highest sensitivity for detecting the presence of air in the right ventricular outflow tract or major pulmonary veins. It can detect as little as 0.02 mL/kg of air administered by bolus injection.^{1,2,17,5,9,21,13,11}  It also has the added advantage of identifying paradoxical air embolism (PAE), and Doppler allows audible detection of venous air embolism (VAE). Echocardiography, both TEE and transthoracic echocardiography (TTE) not only allow for the diagnosis of VAE but also aid in the diagnosis of cardiac anomalies, assessment of volume status, pulmonary hypertension, and cardiac contractility, thereby allowing exclusion of other causes of hypotension, dyspnea, and aiding in further patient management. The use of bedside TTE has become more common in emergency medicine. Its use in a case of VAE described by Maddukuri et al aided in the diagnosis and prompt initiation of appropriatetherapy.²⁶
• Precordial Doppler ultrasonography is the most sensitive noninvasive method for detecting venous air emboli. This modality is capable of detecting as little as 0.12 mL of embolized air (0.05 mL/kg).^1,21,11,17
• Transcranial Doppler ultrasonography is another imaging modality commonly used to detect cerebral microemboli.¹   
• Chest radiography may be normal or may show gas in the pulmonary arterial system, pulmonary arterial dilatation, focal oligemia (Westermark sign), and/or pulmonary edema.^9,11,17
• CT scans can detect air emboli in the central venous system (especially the axillary and subclavian veins), right ventricle, and/or pulmonary artery. Small (<1 mL) air defects, usually asymptomatic, occur during 10-25% of contrast-enhanced CT scans; thus, the specificity of this modality is best with large filling defects.^1,9   CT scans of the head may show intracerebral air, cerebral edema, or infarction. Chest CT in lung trauma may show underlying conditions such as pneumothorax, hemothorax, or emphysematous blebs that may have led to air embolism but is not helpful for initial diagnosis.
• MRI of the brain may show increased water concentration in affected tissues, but this finding alone may not be reliable for the detection of gas emboli.

Other Tests

• Electrocardiographic (ECG) – Low sensitivity for venous air embolism (VAE) detection. The findings closely resemble those seen with venous thromboembolism and include tachycardia, right ventricular strain pattern, and ST depression. Transient myocardial ischemia may also occur (severe bradycardia, ST elevation in inferior leads and ST depression in L1 and avL, observed 3 minutes post CVC removal (case report).^19,1
• End-tidal carbon dioxide (ETCO₂) – VAE leads to V/Q mismatching and increases in physiologic dead space. This produces a fall in end-tidal CO₂ (normal value is <5). A change in 2 mm Hg ETCO₂ can be an indicator of VAE. However, this finding is nonspecific and may also occur with other disease states, such as pulmonary embolism (PE), massive blood loss, hypotension, circulatory arrest, upper airway obstruction, mouth breathing, and/or disconnection from monitor. The detector also has a slow response time.^4,1,21,17,11
• End-tidal nitrogen (ETN₂) – Most sensitive gas-sensing VAE detection modality; measures increases in ETN₂ as low as 0.04%. Response time is much faster than ETCO₂ (30-90 s earlier). However, it does not detect subclinical VAE or decreases with hypotension and may falsely indicate resolution of VAE too prematurely.^27,1
• Pulse oximetry – Changes in oxygen saturation are late findings with VAE. Measurement is often skewed secondary to exposure to high fraction inspired oxygen. Like carbon dioxide measuring, it is on the lower end of sensitive measurements.¹
• Pulmonary artery catheter – Can detect increases in pulmonary artery pressures, which may be secondary to mechanical obstruction/vasoconstriction from the hypoxemia induced by the VAE. However, it is a relatively insensitive/nonspecific monitor of air entrainment (0.25 mL/kg).¹ The lumen catheter is also too small for air to be removed, thereby limiting its function.
• Central venous catheter – If in place, aspiration of air may help make the diagnosis. It is also helpful in monitoring central venous pressures, which may be increased in VAE.¹

Procedures

• Any procedure posing a risk for venous air embolism (VAE), if in progress, should be aborted immediately once VAE is suspected.
• During central venous catheterization (CVC) insertion/removal, one attempt at aspirating air back from line may be useful. Prior to aspiration, the tip of the central venous catheter should be optimally placed 2 cm below the junction of the SVC and the right atrium; however, it may need to be advanced to optimize results. If not already in place, the placement of a CVC (multiorifice) or PA catheter to attempt aspiration of air has been recommended by several authors.^4,13,1,27,17 When appropriately placed, it may be possible to aspirate approximately 50% of the entrained air with a right atrial catheter. Catheter removal should be performed with the patient supine or in a Trendelenburg position while holding his/her breath at the end of inspiration or during a Valsalva maneuver.^2,10,17
• In the event of circulatory collapse, CPR should be initiated in order to maintain cardiac output. CPR may also serve to break large air bubbles into smaller ones and force air out of the right ventricle into the pulmonary vessels, thus improving cardiac output.¹³  
• If an arrest is refractory to CPR, an immediate thoracotomy in the ED may be indicated. An emergency thoracotomy with clamping of the hilum of the injured lung is currently recommended for SAE-associated with unilateral lung injury. This prevents continued passage of air into the coronary, cerebral, and other systemic arteries.^9,13
• Other measures include cross-clamping the aorta, cardiac massage, and aspirating air from the left ventricle, aortic roots, and pulmonary veins.⁹

Treatment

Prehospital Care

If venous air embolism (VAE) is known about prior to ED presentation, these patients should be transported in the left lateral decubitus position.⁷

Emergency Department Care

Management of venous air embolism (VAE), once is suspected, includes identification of the source of air, prevention of further air entry (by clamping or disconnecting the circuit), a reduction in the volume of air entrained, and hemodynamic support.

• Administer 100% O ₂ and perform endotracheal intubation for severe respiratory distress or refractory hypoxemia or in a somnolent or comatose patient in order to maintain adequate oxygenation and ventilation. Institution of high flow (100%) O ₂ will help reduce the bubble's nitrogen content and therefore size.^{4,11,9,21,15,7,11,8,1}
• Immediately place the patient in the left lateral decubitus (Durant maneuver) and Trendelenburg position. This helps to prevent air from traveling through the right side of the heart into the pulmonary arteries, leading to right ventricular outflow obstruction (air lock). If CPR is required, place the patient in a supine and head-down position.^{7,11,1,9,21,11}
• Direct removal of air from the venous circulation by aspiration from a central venous catheter in the right atrium may be attempted. However, no current data support emergent catheter placement for air aspiration during an acute setting of VAE-induced hemodynamic instability.^4,11,1,9,11
• If necessary, initiate CPR. Other than maintaining cardiac output, CPR may also serve to break large air bubbles into smaller ones and force air out of the right ventricle into the pulmonary vessels, thus improving CO. Even without the need for CPR, this rationale holds for closed-chest massage. Animal studies have shown that the benefit of cardiac massage equals that of left lateral recumbency, as well as intracardiac aspiration of air.^4,1,9,11
• Consider transfer to a hyperbaric oxygen therapy (HBOT) facility. Indications for HBOT include neurological manifestations and cardiovascular instability. Potential benefits include compression of existing bubbles, establishing a high diffusion gradient to speed resolution of existing bubbles, improved oxygenation of ischemic tissues, and lowered intracranial pressure. Immediate HBOT, once venous air embolism (VAE) is diagnosed, is recommended; however, prognosis may still be good if therapy is initiated beyond 6 hours of event. Prompt transfer to an HBOT center has been reported to decrease the mortality rate in patients with cerebral air embolism. If transfer is necessary, ground transportation is preferred. If air transportation cannot be avoided, the lowest altitude should be sought.^{4,7,1,11,9,13,10,28}
• Supportive therapy should include fluid resuscitation (to increase intravascular volume, increase venous pressure and venous return). Also some evidence exists that gas emboli may cause a relative hemoconcentration, which increases viscosity and impairs the already compromised circulation. Hypovolemia is less tolerated than relative anemia. In animal studies, moderate hemodilution to a hematocrit of 30% reduces neurologic damage. Crystalloids may cause cerebral edema; therefore, colloids are preferred for hemodilution.^4,1,13
• The administration of vasopressors and mechanical ventilation are two other supportive measures that may necessary.^4,1,27 In a case report of a patient undergoing a craniotomy who showed cardiopulmonary findings suggestive of acute venous air embolism, inotropic treatment with ephedrine seemed to rapidly reverse the cardiopulmonary abnormalities. Early inotropic support of the right ventricle has been recommended if venous air embolism is suspected.²⁷
• In animal studies, the use of perfluorocarbons (FP-43) has been shown to enhance the reabsorption of bubbles and the solubility of gases, thereby decreasing both the neurologic and cardiovascular complications of systemic and coronary venous air embolism. These benefits, however, have not been validated in humans.¹

Consultations

Hyperbaric medicine

Follow-up

Further Inpatient Care

• Admit patients to the intensive care unit (ICU), as they may develop cardiopulmonary distress/failure following venous air embolism (VAE).

Transfer

• Consider transfer to a hyperbaric medicine center for symptomatic venous air embolism.

Deterrence/Prevention

The optimal management of venous air embolism (VAE) is prevention. 

• Minimizing the pressure gradient between the site of potential entry and the right atrium is essential in prevention of VAE.
• Measures to reduce the risk of air embolism during mechanical ventilation and central line insertion/removal/manipulation should be taken. With regard to these two procedures, the following interventions should be implemented:
  • Prevent barotraumas by minimizing airway pressures during mechanical ventilation.
  • Avoid PEEP as it impairs hemodynamic performance, does not protect against air embolism, and probably increases risk of paradoxical emboli.
  • Avoid and treat hypovolemia prior to catheter placement.
  • Occlude the needle hub during catheter insertion/removal.
  • Maintain all connections to the central line closed/locked when not in used (use Luer-lock syringes for blood draws from catheters).
  • During catheter insertion/removal, place the patient in the supine position with head lowered (insertion site should be 5 cm below right atrium). If the patient is awake he or she may assist by holding his or her breath or by doing a Valsalva maneuver, both of which can increase the central venous pressure

Miscellaneous

Medicolegal Pitfalls

• Failure to identify high-risk procedures and implement adequate measures to prevent venous air embolism (VAE) during these procedures
• Failure to recognize early signs and symptoms of venous air embolism
• Failure to provide optimal treatment for suspected/confirmed venous air embolism
• Failure to consider, diagnose, or treat VAE-associated complications, especially paradoxical embolism, which can lead to arterial embolism

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Keywords

VAE, venous air embolism, embolus, air embolism, venous air embolism causes, venous air embolism symptoms, venous air embolism treatment, AGE, arterial gas embolism, systemic air embolism, air embolism, gas embolism, paradoxical embolism, air lock

Contributor Information and Disclosures

Author

Brenda Liz Natal, MD, Clinical Assistant Instructor and Staff Physician, Department of Emergency Medicine, Kings County Hospital and State University of New York Downstate, Brooklyn
Brenda Liz Natal, MD is a member of the following medical societies: American College of Emergency Physicians and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Christopher I Doty, MD, FACEP, FAAEM, Assistant Professor of Emergency Medicine, Residency Program Director, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center
Christopher I Doty, MD, FACEP, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Daniel J Dire, MD, FACEP, FAAP, FAAEM, Clinical Associate Professor, Department of Emergency Medicine, University of Texas-Houston
Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, and Association of Military Surgeons of the US
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

David Eitel, MD, MBA, Associate Professor, Department of Emergency Medicine, York Hospital
David Eitel, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

David FM Brown, MD, Assistant Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Andrew G Wittenberg, MD, MPH, Allison J Richard, MD, and Steven A Conrad, MD, PhD, to the development and writing of this article.

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