eMedicine Specialties > Emergency Medicine > Cardiovascular

Venous Air Embolism

Author: Andrew G Wittenberg, MD, MPH, Staff Physician, Department of Emergency Medicine, Los Angeles County-University of Southern California Hospital
Coauthor(s): Allison J Richard, MD, Instructor of Clinical Emergency Medicine, Keck School of Medicine, University of Southern California; Consulting Staff, Department of Emergency Medicine, LAC-USC Medical Center; Steven A Conrad, MD, PhD, Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center
Contributor Information and Disclosures

Updated: May 2, 2006

Introduction

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

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 H₂ O 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.

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