How is venous air embolism (VAE) detected and treated?

How is venous air embolism (VAE) detected and treated?

VAE is a potentially life-threatening event which must be detected and treated promptly. It is often associated with cases performed in the sitting position but it can occur under certain physiologic circumstances. In neurosurgical procedures, air may enter the venous system via non-collapsible venous channels such as the dural sinuses and diploic veins. When the head is elevated above the heart a pressure gradient can exist which facilitates air entrainment. In the sitting position, the incidence of VAE is almost 4 times higher than the incidence in other positions (45% vs. 12%). Air can also be entrained from the pin sites during a stereotactic biopsy in the semi-sitting position.

Monitoring for VAE generally includes a precordial Doppler, capnometry, central venous pressure (CVP) catheter, pulse oximeter, and esophageal stethoscope. When placed properly, as determined by rapid bolus fluid injec-tion through a CVP catheter, a precordial Doppler can detect 0.1 ml of air. Transesophageal echocardiography (TEE) is also sensitive for detecting and recognizing intra-cardiac air but is not generally used in this setting due to technical difficulty and cost. The CVP catheter is best located at the junction of the superior vena cava and the right atrium, where air collects after its entrainment into the venous system. It is a diagnostic device for detection or confirmation of VAE, rarely a therapeutic measure. It is of value when aspirating air from the right atrium in the rare instance of massive VAE creating an air lock. Multiorifice catheters are more efficacious for air aspiration than single-lumen catheters.

Pulmonary artery catheters may provide valuable infor-mation because pulmonary artery pressures rise during VAE. Unfortunately, pulmonary artery catheters are less efficient for air aspiration than CVP catheters. Continuous end-tidal carbon dioxide (ETCO₂) monitoring demon-strates a rapid decline as VAE ensues. Arterial PaCO₂ rises simultaneously, increasing the gradients between these two measurements. The difference rises as alveolar dead space increases. If minute ventilation remains constant, the divergence between PaCO₂ and ETCO₂ may represent a useful marker for the severity of VAE. Classically, the “mill wheel” murmur heard through an esophageal stethoscope is associated with intracardiac air. Once detected, VAE requires rapid treatment.

Surgeons must be alerted immediately when VAE is detected so that open sinuses may be identified and flooded with saline or closed surgically to halt the entrainment of air. In the absence of an obvious source of air entrainment, venous pressure in the head should be raised in an attempt to force blood through the concealed opening. This is accom-plished by lowering the head relative to the heart, manipulat-ing the table’s position, or occluding venous outflow from the head with jugular compression. N₂O administration should cease immediately. Rapid diffusion of N₂O into air bubbles will expand their volume, creating mechanical obstruction to flow, and hemodynamic compromise may ensue. Volume, inotropes, and vasopressor administration contribute to hemodynamic support, churning large air pockets into smaller ones to be carried out to the pul-monary blood vessels.

The application of PEEP in an attempt to increase CVP and decrease the magnitude of VAE is controversial. High levels of PEEP greatly increase the risk of hypotension in patients who are already intravascularly depleted. Furthermore, right atrial pressure may be increased in the face of lowered left atrial pressure, predisposing the patient to paradoxical air embolism through a patent foramen ovale. Application of PEEP should probably be limited to situations in which all other attempts at preventing con-tinuous VAE have failed. Even moderate amounts of VAE may result in decreased PaO₂. Initial treatment should be supportive with enhanced inspired oxygen concentrations guided by pulse oximetry and arterial blood gas determina-tions. Postoperatively, patients may develop an interstitial pulmonary process that usually resolves in 24–48 hours.