eMedicine Specialties > Emergency Medicine > Cardiovascular

Venous Air Embolism

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
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
Contributor Information and Disclosures

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.

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