The first cases of vascular air embolism (VAE) in both pediatric and adult patients were first reported as early as the nineteenth century. VAE is the entrainment of air (or delivered gas) from the operative field or environment into the venous or arterial vasculature, producing systemic effects. Many cases are subclinical and go unreported. Historically, VAE is most often associated with sitting position craniotomies (posterior fossa) but we should also be suspicious of VAE during procedures where gas may be entrained under pressure, both within the peritoneal cavity or vascular access.
The two factors determining the ultimate morbidity and mortality associated with VAE are directly related to the volume of air entrainment and rate of accumulation. Many case reports of accidental intravascular delivery of air in adults show that a lethal volume has been described as between 200 and 300 mL (3–5 mL/kg). Many believe that the closer the vein of entrainment is to the right heart, the smaller the required lethal volume.
The rate of air entrainment is also important because the pulmonary circulation and alveolar interface allow for dissipation of intravascular gas. If entrainment is slow, the heart may be able to withstand large quantities of air despite entrainment over a prolonged time.
Not only negative pressure gradients but also positive pressure insufflations of gas may present a VAE hazard. Injection of gas into the uterine cavity for separation of placental membranes for a variety of laparoscopic procedures can increase the risk of a VAE.
Early animal experiments indicate that VAE increases microvascular permeability and release of platelet activation inhibitor, thus, precipitating systemic inflammatory response syndrome. These changes can lead to pulmonary edema and also cause toxic free radical damage to lung parenchyma. If the embolism is large (5 mL/kg), a gas air-lock can immediately occur, causing complete right ventricular outflow obstruction and cardiovascular collapse. Even with lesser volumes of emboli, the patient may have decreased cardiac output, hypotension, myocardial and cerebral ischemia, and even death. Air in the pulmonary circulation may lead to pulmonary vasoconstriction, bronchoconstriction, and an increase in ventilation/perfusion mismatch.
VAE may have cardiovascular, pulmonary, and neurologic consequences. Cardiovascularly, tachyarrhythmias are common and the ECG frequently shows ST-T wave changes. Blood pressure may decrease as cardiac output drops. Pulmonary artery pressures may increase as a result of increased filling pressures and reduction in cardiac output. The central venous pressure may increase as a consequence of right heart failure, resulting in jugular venous distention.
Pulmonary symptoms in awake patients include dyspnea, coughing, lightheadedness, and chest pain. As the patient gasps for air resulting from dyspnea, there can be a further reduction in intrathoracic pressure and hence more air entrainment. Pulmonary signs include rales, wheezing, and tachypnea. During anesthesia, decreases in ETCO2, SaO2, ...