DescriptionVenous air embolism (VAE) describes the entrapment of air or gas from the operative field or other communication with the environment into the vasculature, resulting in mechanical obstruction and secondary chemical and inflammatory mediators that impair gas exchange.
EpidemiologyIncidence
- Difficult to assess accurately due to the variable sensitivity of current detection methods and its subclinical presence
- Posterior fossa surgery: 80%
- OB-gynecologic surgeries: 1197%
- Laparoscopies: 69%
- Orthopedic surgeries: 57%
- Presence of a patent foramen ovale: 2035%
- Severe lung trauma: 414%
- Cervical laminectomy: 10%
- Insertion/removal of central line catheters with optimal positioning, technique: 0.13%
Morbidity/Mortality
Proportional to the volume and rate of air entry, patient position, and entry site, as well as underlying cardiac disease
Etiology/Risk Factors- Operative site above the heart (5 cm):
- Sitting craniotomies, posterior fossa procedures, craniosynostosis repair, upright posterior cervical surgery, radical neck dissection, thyroidectomy.
- Positioning (Trendelenburg, lateral decubitus, uterine displacement). THA, lateral decubitus thoracotomies, obstetric and genitourinary procedures
- Mechanical insufflations
- Laparoscopy, gastrointestinal endoscopy
- Blunt, penetrating chest trauma
- Vascular access
- Central, peripheral, arterial lines
- TPN, interventional radiology
- Pressure infusions/fluid irrigation
- Shoulder arthroscopy
- Rapid infusers
- Scuba diving, aviators, astronauts, and positive pressure ventilation
Physiology/Pathophysiology- Two requisites: Direct communication between the air source and vasculature, plus a pressure gradient favoring the passage of air into the circulation.
- Operative site >5 cm from the heart. Venous pressure exceeds atmospheric pressure, except when above the level of the heart. An injury to the vein allows air entry that travels to the right heart and then the lungs. This is increased with large, noncompressed venous channels, such as dural sinuses in neurosurgery.
- Mechanical insufflations: CO2 enters inadvertent open vascular channels from surgical manipulation. It is 20 times more dissolvable in blood than oxygen and significantly more than nitrogen, which may explain why, despite its high occurrence, it is often subclinical.
- Pressure infusions/fluid irrigation: When air is accidentally introduced into the system, it can subsequently be "driven" by the fluid pressure into veins or cancellous bony surface.
- Central vascular access: The equipment allows direct access to the vein during insertion or removal and when the patient is spontaneously ventilating, a negative pressure breath can provide the driving force. Inadvertent introduction of air into arterial lines, peripheral IVs, and other access is also a cause.
- Clinical manifestations result from mechanical and chemical pathophysiologic mechanisms, with the key factors being volume and rate of entrainment. The alveolar/capillary interface is capable of absorbing and exhaling gas from the circulation; when it occurs over a slow period, it is capable of withstanding large quantities. When this mechanism is overwhelmed (large amount and/or fast rate), symptoms result.
- Mechanical obstruction results from a gas-airlock in the right ventricular outflow tract (RVOT) or pulmonary circulation (V/Q mismatch: dead space being ventilated, but not perfused). Partial RVOT obstruction causes right heart strain (increased CVP, JVD; peaked P waves), decreased CO (increased wedge pressure; reduced MVO2, BP), with resultant cardiac and cerebral ischemia (tachyarrhythmias, ST changes). Complete RVOT obstruction results in heart failure, CV collapse, and possible death.
- Chemical pathways: Air in the right heart and pulmonary circulation trigger secondary injury from the activation of complement and inflammatory pathways (endothelin 1, platelet activator inhibitor, fibrin, neutrophils, lipid droplets, etc.). These result in pulmonary vasoconstriction/hypertension, microvascular permeability, platelet aggregation, noncardiogenic pulmonary edema, bronchoconstriction, and subsequent V/Q mismatch (shunting: Ventilation hindered, perfusion continues and returns non-oxygenated blood to the left heart circulation.).
- Paradoxical air embolism: The presence of a patent foramen ovale (2530% of the population) allows for a gas bubble to travel from the right-to-left side of the heart (bypasses lungs, direct delivery to cerebral and coronary arteries, resulting in ischemia or infarct).
Prevantative Measures- Patient positioning: The sitting position is utilized to provide adequate surgical conditions (visualization, reduced bleeding). Maintain a high level of suspicion, reduce the driving pressure gradient, and implement appropriate monitoring. Alternatives include the prone and park bench position (strongly consider with documented PFO).
- Hydration: Increases CVP, and reduces the negative pressure gradient at the level of insertion. Studies have suggested maintaining the CVP at 1015 cm H20. Consider zeroing the transducer at the level of the right atrium, and then elevating it to the surgical site to determine if a negative pressure gradient exists.
- Central line placement and removal should be performed in the Trendelenburg position (increases venous pressure at access site by gravity). During insertion and removal, consider occlusion of the needle hub/catheter, avoidance of deep inspiration when the patient is SV (avoids negative pressure/suction effect), and PEEP when the patient is being PPV. When Trendelenburg is contraindicated (increased ICP), consider temporary positioning during insertion of the guidewire or catheter, or raising the legs to increase venous return and pressure in the right atrium.
- PEEP: Theoretically, it increases intrathoracic pressure, thus reducing air entrainment into the surgical site (note: In patients with increased ICP, the goal is to reduce intrathoracic pressure to facilitate venous drainage of blood into the right atrium). Controversial, because it may increase the risk of paradoxical air embolism (increased intrathoracic, pulmonary vasculature pressures, facilitates flow through the PFO) and may exacerbate negative pressure when there is a sudden release. Consider PEEP when oxygenation needs to be improved, rather than to prevent a VAE.
- Avoidance of nitrous oxide is suggested particularly for sitting craniotomies. However, studies have not shown an increased incidence of VAE.
- If hemodynamic stability is recovered, may consider continuing with surgical procedure
- Consider continued intubation with positive pressure ventilation, vasopressors
- Consider central line placement for monitoring and therapy, if not already in place
Closed Claims Data
Air embolism comprised 8% (10/140) of IV catheter claims (All claims n = 6881).
- Deaths: N = 4
- Claims resulting in payment: 100%
- Payment range: $20,800$3,302,700