Venous Air Embolism Clinical Presentation

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)

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.

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, 21]} 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, 22, 17, 23]}
  • 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, 24, 25, 26]} 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),^{[22, 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 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 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, 27, 11]} angiography,^[2] and cardiac catheterization, as well as during cardiac ablation procedures.^{[17, 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 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.