AUTHOR AND EDITOR INFORMATION

Section 1 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Background

Venous air embolism (VAE), the entry of gas into the peripheral or central vasculature, can occur secondary to iatrogenic complications, trauma, and even certain recreational activities. Although many occurrences of VAE are believed to go unreported because they are asymptomatic, entrapment of large quantities of intravascular gas can lead to severe neurologic injury, cardiovascular collapse, and even death. The factors that determine the subsequent morbidity and mortality in VAE include the rate of air entrainment, the volume of air introduced, and the position of the patient at the time of the embolism.

Gas emboli are usually composed of air, but they can also occur with medically used gases such as carbon dioxide, nitrous oxide, and nitrogen. Although very small volumes of air can lead to severe sequelae, it is generally accepted that more than 50 mL of air can cause hypotension and dysrhythmias and more than 300 mL of air can be lethal.

Arterial gas embolism (AGE) is a separate but related entity that is not discussed in any detail in this article. AGE can occur through a patent foramen ovale (present in approximately 27% of the general population) or can form by gas movement across the alveolar-capillary membranes into the pulmonary venous circulation.

Pathophysiology

VAE results when a pressure gradient develops that favors the ingress of air into the venous system. Upon entry into the venous system, air is transported to the right atrium and ventricle. From there, it has the potential to continue on to the pulmonary arteries where it may cause interference with gas exchange, cardiac arrhythmias, pulmonary hypertension, and even cardiac failure and arrest. A large bolus of air entering the venous system can cause an air lock in the right atrium and ventricle, leading to outflow obstruction, decreased pulmonary venous return, and subsequent decreased left ventricular preload and cardiac output.

Intermediate amounts of air collect in the pulmonary circulation and produce a pulmonary vascular injury manifested by precapillary and postcapillary pulmonary vasoconstriction, pulmonary hypertension, endothelial injury, and permeability pulmonary edema. Subsequent ventilation-perfusion mismatch can cause right to left shunting and increased arterial hypoxia and hypercapnia.

Small amounts of air do not produce symptoms because the air is broken up and absorbed from the circulation. Although classical teaching states that more than 5 mL/kg of air (IV) is required for significant injury (including shock and cardiac arrest), patient complications secondary to as little as 20 mL of air (the length of an unprimed IV infusion set) have been reported. Further, as little as 0.5 mL of air in the left anterior descending coronary artery has been shown to lead to ventricular fibrillation.

The pathogenesis of pulmonary endothelial injury may have components of platelet-fibrin thrombi from the right ventricle, cytokine release, neutrophil, platelet, and complement activation at the microvascular air-blood interface, and injury mediated by lipid peroxidation and oxygen radicals.

Frequency

United States

The true incidence of VAE is unknown. Subclinical air embolism in hospitalized patients may be quite common. Frequency of clinically recognized VAE following central venous (CV) cannulation is less than 2%. Case report series (as mentioned above) have estimated VAE from central venous catheterization at 1 in 47 to 1 in 3000, and neurosurgical complications of VAE range from 10-80%.

Mortality/Morbidity

VAE is associated with significant morbidity and mortality. Morbidity can include lung injury, neurologic injury, cardiovascular ischemic injury, and ultimately cardiopulmonary collapse and arrest. Symptomatic VAE following CV catheterization has a mortality rate as high as 30%.

CLINICAL

Section 3 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

History

Signs and symptoms of VAE usually develop immediately following embolization. Severity of signs and symptoms are related to the degree of air entry into the body. The diagnosis can be a difficult one to make because of its similarity in presentation to pulmonary embolism (thromboembolic) and/or hypovolemic shock. Subsequently, physicians must maintain a high index of suspicion for this disease given the appropriate clinical scenario. The following historical events should be considered in taking a patient's history for suspected VAE:

• Recent surgery, especially neurosurgical, cardiovascular, or orthopedic procedures
• Blunt and penetrating trauma to the face, neck, chest, and/or abdomen
• Recent invasive procedures such as central venous catheterization or pressurized infusion of fluids, blood, or contrast
• Patients with indwelling central venous catheters
• Decompression injuries/sickness
• Orogenital sex during pregnancy or hydrogen peroxide ingestion (rare)
• Symptoms may include the following:
• • Dyspnea
  • Chest pain
  • Agitation or disorientation

Physical

Physical examination may reveal the following signs:

• Tachycardia
• Tachypnea
• Cyanosis
• Altered level of consciousness
• Hypotension
• Cardiac "mill wheel" murmur - A loud, churning, machinerylike murmur heard over the precordium (a late sign)
• Sudden loss of consciousness followed by convulsion in an intubated patient on positive-pressure ventilation
• Circulatory shock or sudden death (patients with severe VAE)

Causes

The primary cause of VAE is surgical procedures, especially neurosurgical procedures performed in the upright, sitting position. Anytime the operative site is more than 5 cm above the right atrium, VAE is a risk. Other surgical procedures that can lead to the infusion of air include obstetric/gynecologic procedures (cesarean section), craniofacial surgery, dental implant surgery, vascular procedures, liver transplantation, and orthopedic procedures (eg, hip replacement, arthroscopy). The frequency of reported VAE in surgical procedures ranges from 10% in cervical laminectomy up to 80% in posterior fossa surgery.

A second cause of VAE is iatrogenic creation of a pressure gradient for air entry. Examples include spinal needles in lumbar punctures (case report), peripheral intravenous lines, central venous catheters, pulmonary artery catheters, hemodialysis catheters, and long-term (Hickman) catheters. Most cases occur during catheter manipulation, disconnection, or removal. A pressure difference of 5 cm of H₂O across a 14-gauge needle allows 100 mL of air per second to enter the venous system. The frequency of reported VAE with central catheter use ranges from 1 in 47 to 1 in 3000.

A third cause of VAE is mechanical insufflation or infusion. Insufflation has been documented to occur during arthroscopic procedures, CO₂ hysteroscopy, laparoscopy, urethral insufflation, and orogenital sexual activity during pregnancy. Infusion air entry can occur during the injection of contrast agents for CT scans, angiography, and cardiac catheterization, and during cardiac ablation procedures.

A fourth cause of VAE is positive-pressure ventilation, which can occur during mechanical ventilation and SCUBA diving.

Finally, blunt and penetrating trauma to the chest, abdomen, neck, and face can lead to the entry of air and ultimately to VAE.

DIFFERENTIALS

Section 4 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Lab Studies

• Arterial blood gases are indicated and usually demonstrate hypoxemia, hypercapnia, and metabolic acidosis. Mild cases may demonstrate mild hypoxemia and hypocapnia.
• Other laboratory studies are nonspecific and are obtained as indicated by associated conditions.

Imaging Studies

• Transesophageal echocardiography is the most sensitive monitoring modality for VAE and can detect as little as 0.02 mL/kg of air. Precordial Doppler ultrasonography is also an effective monitoring technique and can detect as little as 0.25 mL of air. Transcranial Doppler is commonly used to help identify cerebral microemboli during neurosurgical and endovascular procedures.
• Chest radiography may be normal or may show one of the following signs:
• • Air in the pulmonary arterial system
  • Pulmonary arterial dilatation
  • Focal oligemia (Westermark sign)
  • Pulmonary edema

Other Tests

• Electrocardiographic (ECG) findings, if present, are the same as those found in venous thromboembolism:
• • Tachycardia
  • Right ventricular strain pattern
  • ST depression
• Increased dead space may be present and can be identified as an increased end-tidal to arterial blood carbon dioxide gradient (normal value is <5).
• If a central venous (CV) catheter is in place, aspiration of air may help establish the diagnosis. CV catheters can also be used to measure central venous pressure, which may be elevated in the case of VAE.
• Pulmonary artery (PA) catheters can detect increased PA pressure that may be caused by mechanical obstruction/vasoconstriction from the hypoxemia induced by VAE. However, this modality is not specific for VAE.
• Mass spectrometry for end-tidal nitrogen is also highly specific for air but is very limited in availability and practical use.

Procedures

• Once VAE is suspected, any central line procedure in progress should be terminated immediately, and the line should be clamped (or removed if it cannot be clamped). One attempt at aspirating air back from the line may be useful.
• If aspiration from a central catheter is going to be attempted, optimal placement of the tip is 2 cm below the junction of the superior vena cava and the right atrium. Catheters may have to be advanced for this to be successful. Some authors recommend placing a central venous catheter or PA catheter to attempt evacuation of air if one is not already in place.
• In circulatory collapse, CPR should be started to maintain cardiac output as well as to potentially break large air bubbles into smaller ones and force air out of the right ventricle into the pulmonary vessels. In arrest that is refractory to CPR, emergency thoracotomy may be indicated. Hilar injury and bronchovenous fistulae should be ruled out by the absence of bloody froth during positive-pressure ventilation, and then needle aspiration of intracardiac air from the ventricles should be performed. Consider cross-clamping the aorta in hypotensive patients.

TREATMENT

Section 6 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Emergency Department Care

Once VAE is suspected, any central line procedure in progress should be terminated immediately.

• Administer 100% oxygen and intubate for significant respiratory distress or refractory hypoxemia. Oxygen may reduce bubble size by increasing the gradient for nitrogen to move out.
• Promptly place patient in Trendelenburg (head down) position and rotate toward the left lateral decubitus position. This maneuver helps trap air in the apex of the ventricle, prevents its ejection into the pulmonary arterial system, and maintains right ventricular output.
• Maintain systemic arterial pressure with fluid resuscitation and vasopressors/beta-adrenergic agents if necessary.
• Consider transfer to a hyperbaric chamber. Potential benefits of this therapy include (1) compression of existing air bubbles, (2) establishment of a high diffusion gradient to speed dissolution of existing bubbles, and (3) improved oxygenation of ischemic tissues and lowered intracranial pressure.
• Circulatory collapse should be addressed with CPR and consideration of more invasive procedures as described above.

Consultations

Hyperbaric medicine for symptomatic venous air embolism syndrome.

FOLLOW-UP

Section 7 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Admit patients to the intensive care unit (ICU); pulmonary insufficiency may develop following VAE.

Deterrence/Prevention

• In general, prevention of VAE stems from decreasing the pressure gradient between the site of potential entry and the right atrium.
• With regard to central venous catheterization and manipulation of catheters, several general principles apply to preventing VAE:
• • Whenever possible, place patients in Trendelenburg position.
  • Keep patient agitation to a minimum.
  • Use closed catheterization systems when possible.
  • Constantly maintain vigilance to avoid opening the catheters during subsequent manipulation.
  • VAE also can occur following catheter removal and may be delayed for 30 minutes or more; initial dressing after removal should be occlusive.
  • Take particular care in patients with known right-to-left shunts, since paradoxical embolism to the arterial system can occur.

MISCELLANEOUS

Section 8 of 9  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to take precautions to prevent VAE during CV catheterization.
• Failure to recognize early signs of VAE following CV procedures.
• Failure to consider paradoxical embolism, which can lead to arterial gas embolism. Presentation may differ from the signs and symptoms of VAE and may present more similarly to cerebrovascular accident or acute coronary syndrome.

REFERENCES

Section 9 of 9

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• Miscellaneous
• References

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Article Last Updated: May 2, 2006