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Venous Air Embolism

  • Author: Brenda L Natal, MD, MPH; Chief Editor: Erik D Schraga, MD  more...
Updated: Dec 08, 2015


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 system.[3] 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] In addition, apparent cases of VAE resulting from pressurized, intravenous infusion of normal saline have been reported in professional football players.[12] 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 VAE is required to prompt investigations and initiate appropriate therapy.



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.[4, 13]

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 air[7] (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.[14] Furthermore, as little as 0.5 mL of air in the left anterior descending coronary artery has been shown to cause ventricular fibrillation.[9, 14] 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.[2, 4]

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, 3, 7]

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 hypercapnia.[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, 2, 3, 4, 9] 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.[13]



In order for venous air embolism (VAE) to occur, the following two 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. [2, 4]
  • A pressure gradient (subatmospheric pressure in the vessels) favoring the passage of air into the circulation must be present. [2, 4]

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.[15, 16]  However, the most common cause of VAE is iatrogenic.

Surgical procedures

Surgical procedures are the primary cause of VAE. Neurosurgical procedures, especially those performed in the Fowler’s (sitting) position, and otolaryngological interventions are the two most common surgeries complicated by VAE.[5]  Note the following:

  • The incidence of mild or clinically silent 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, 17, 18, 19, 20]
  • VAE poses 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]
  • A preliminary study by Longatti et al suggests that carbon dioxide field flooding (ie, carbox dioxide–enriched surgical microenvironment) reduces the hemodynamic effects of VAE occurring in the sitting position, which the investigators attribute to the better solubility and improved tolerance of the arterial carbon dioxide emboli compared to air emboli. [21]

Obstetric/gynecologic procedures, laparoscopy

Obstetric/gynecologic procedures (cesarean delivery) and laparoscopic surgeries each carry their own risk for VAE. 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.

Iatrogenic creation of a pressure gradient

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),[1, 19]  peripheral intravenous lines,[1]  and central venous catheters.[2, 3, 18, 25]

Central venous catheterization

Venous air embolism is a potentially life-threatening and under-recognized complication of central venous catheterization (CVC), including central lines, pulmonary catheters, hemodialysis catheters[7]  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 H2 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.[1, 2, 9, 11, 17, 26]  Ingress of 300-500 mL of air at this rate can cause lethal effects.[11, 25]

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

Mechanical insufflation or infusion is another cause of venous air emboli. Several different procedures involve the use of insufflation, including arthroscopic procedures, CO2 hysteroscopy, laparoscopy, urethral procedures, and orogenital sexual activity during pregnancy (by entering veins of the myometrium during pregnancy and/or after delivery).[1, 18]

Inadvertent infusion of air can also occur during the injection of IV contrast agents for CT scans,[10, 11, 27]  angiography,[2]  and cardiac catheterization, as well as during cardiac ablation procedures.[18, 28]  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

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.

Other causes

VAE has also been described in the setting of blunt and penetrating chest and abdominal trauma as well as in neck and craniofacial injuries.



United States statistics

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.[29] 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.[2, 26] The neurosurgical procedure-related complications of venous air embolism have been estimated to be between 10-80%.[2, 17, 18] Reports of venous air embolism in the setting of severe lung trauma have been estimated between 4-14%.[8, 9, 14, 18, 30]

Race-, sex-, and age-related demographics

No racial, sex, or specific age predilection exists for venous air embolism.



The presence of gyriform air on computed tomography brain scans appears to be a negative prognostic indicator in venous catheter-related cerebral air embolism.[31] Other potential predictors of unfavorable outcomes in patients with catheter-related venous air embolism (VAE) include older age of onset, an initial disturbance in consciousness, and the presence of hemparesis.[31]


The potentially life-threatening and catastrophic consequences of 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, 30]  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.

In a retrospective study of patients who were placed in a sitting position for neurosurgery, Ganslandt et al found a low rate of severe complications associated with VAE. In the study, 600 individuals underwent surgery for posterior fossa or cervical spinal disorders, with VAE occurring in 19% of these patients. However, only 3.3% of patients suffered severe VAE-associated complications, such as a drop in the partial pressure of oxygen or in blood pressure. Moreover, surgery had to be stopped in only 3 patients (0.5%) because the VAE could not be eliminated during surgery. No VAE-associated mortality occurred.[32]

Contributor Information and Disclosures

Brenda L Natal, MD, MPH Assistant Professor of Emergency Medicine, Simulation Director, Rutgers New Jersey Medical School; Attending Physician, Department of Emergency Medicine, University Hospital of Newark

Brenda L Natal, MD, MPH is a member of the following medical societies: American College of Emergency Physicians, American Medical Association

Disclosure: Nothing to disclose.


Christopher I Doty, MD, FAAEM, FACEP Associate Professor of Emergency Medicine, Residency Program Director, Vice-Chair for Education, Department of Emergency Medicine, University of Kentucky-Chandler Medical Center

Christopher I Doty, MD, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

David Eitel, MD, MBA Associate Professor, Department of Emergency Medicine, York Hospital; Physician Advisor for Case Management, Wellspan Health System, York

David Eitel, MD, MBA is a member of the following medical societies: American College of Emergency Physicians, American Society of Pediatric Nephrology, Society for Academic Emergency Medicine, Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Chief Editor

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Additional Contributors

Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center San Antonio

Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, American Academy of Emergency Medicine, American College of Emergency Physicians, Association of Military Surgeons of the US

Disclosure: Nothing to disclose.


The authors and editors of Medscape Drugs & Diseases 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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