Venous Air Embolism

Introduction

• VAE is when air enters the venous circulation and travels systemically, often disrupting hemodynamics and gas exchange.^1,2
• Over 90% of cases are iatrogenic, occurring during surgery or other medical procedures.¹
• The incidence of VAE in the general surgical population is unknown, as typically only patients undergoing surgery in the seated position are actively monitored for VAE.
• The incidence of VAE during sitting craniotomy is reported to be between 15 and 76%. Clinically significant hemodynamic changes occur in 1-3% of these cases.³
• Despite a low incidence, it is important that anesthesia providers understand VAE due to their role in preventing, monitoring, and treating potentially devastating consequences.

Risk Factors

• Surgical cases in the seated, sitting, or semi-sitting position with the operative site above the level of the heart increase the risk of iatrogenic VAE. Neurosurgical, otolaryngological, and laparoscopic procedures, as well as procedures requiring cardiopulmonary bypass, have traditionally been considered the highest-risk.^1-3
• Sitting intracranial procedures, particularly within the vascular posterior fossa, are high risk due to proximity to large venous sinuses, which are non-collapsable. VAE risk in these cases may be as high as 76% of patients with air detected on TEE. Although the incidence of clinically significant VAE is much lower.^3,4
• Upper cervical spine surgery, tumor resection near the posterior half of the sagittal sinus, and craniosynostosis cases also have an increased risk of VAE.^1-3
• Procedures that involve positive-pressure insufflation of air (i.e., pneumoperitoneum, endoscopy, etc.) can result in VAE if a conduit to vascular circulation exists or is created and/or significant absorption occurs.
• Other types of procedures with increased risk include lung biopsy, ablation, or resection, cardiopulmonary bypass, and central venous catheter placement.^2,5
• Hypovolemic patients are at higher risk of VAE due to lower central venous pressure.^1,2
• Spontaneous breathing (e.g., during deep-brain stimulator electrode placement) may increase the risk of VAE due to intermittent negative intrathoracic pressure.^1,3,4

Pathophysiology

• VAE occurs when air is entrained into venous circulation and travels to the right heart and pulmonary vasculature.
• Estimates of the amount of air that can cause fatality are from as little as 50 mL up to 500 mL.^2,3 Fast air entrainment may become fatal quickly at a small volume relative to air that is entrained at a very slow rate, allowing time for physiologic compensation.
• Air emboli can have both direct effects on hemodynamics and indirect effects leading to end-organ damage, as diagramed below (Figure 1).²
• Air can paradoxically embolize from the venous to arterial vasculature, leading to coronary, cerebral, or end-organ ischemia. Patients with a shunt, either intracardiac or intrapulmonary, may be at increased risk of arterial air embolism, although neither is a prerequisite for its occurrence.²

Detection

• The clinical presentation of VAE often mimics several other intraoperative emergencies, including pulmonary embolism and myocardial infarction, so a high degree of clinical suspicion is warranted in high-risk cases.^3,4
• Awake patients are more likely to show history and physical exam findings of VAE, including sudden cough, dyspnea, and chest pain. A “mill-wheel” murmur is characteristic on cardiac auscultation due to the interface of blood and air mixing in the right ventricle.^1-4
• Patients frequently become tachycardic to compensate for reduced cardiac output.³ However, the severity of hemodynamic changes does not correlate with the clinical severity of VAE.⁶
• Electrocardiography may show findings indicative of right heart strain or ischemia, including right bundle branch block and ST-segment changes, which may progress to arrhythmia.^2,4
• End-tidal carbon dioxide can rapidly fall during VAE, due to worsening ventilation-perfusion mismatch.^1-4 The embolism may block pulmonary circulation, leading to both increased dead space ventilation and lower effective pulmonary circulation. This mismatch is further exacerbated by hypoxic pulmonary vasoconstriction.
• Hypoxemia may be detected on pulse oximetry, and there may be evidence of both hypoxemia and hypercarbia on blood gas analysis. These tend to be later findings if they occur.³
• TEE is the most sensitive intraoperative monitoring modality and should be considered for patients and procedures at high risk for VAE.^2,4

• Precordial Doppler should also be considered in high-risk patients. Precordial Doppler offers continuous, noninvasive monitoring, albeit less sensitive and comprehensive than TEE. The probe should be placed at the left parasternal border, verified with agitated saline injection, and secured in place (Figure 3).³

Management

• Preventing additional air entry into venous circulation is the hallmark of VAE treatment. It is critical that the anesthesia provider immediately notify the surgeon of their suspicion so the surgeon may flood the surgical field with saline or apply bone wax to bony structures (i.e., pinion sites or bone incisions).^2-4
• If the patient has not progressed to cardiac arrest, initial measures include administering 100% oxygen (discontinue nitrous oxide if applicable) and administering vasopressors and inotropes, such as epinephrine, as needed for hemodynamic support. Additional intravenous (IV) access should be obtained as needed.³
• Additional IV fluids may be given to increase central venous pressure.^1-3
• In theory, air may be aspirated from the right heart through a central venous catheter. However, there is no clear clinical benefit, and this step should not delay hemodynamic support as above.^2-5
• Following hemodynamic stabilization and repair of the vascular defect, laboratory tests, formal echocardiography, and computed tomography imaging of the chest and brain may be considered to aid in diagnosis confirmation, degree of end-organ damage, and disposition planning.³
• If the patient has progressed to cardiac arrest, the anesthesia provider should call for help and begin advanced cardiac life support (ACLS).^2-4 If ACLS is required, urgent temporary closure of surgical incision sites and coordinated repositioning should be prioritized in clinical decision-making. It is difficult to perform ACLS in the seated position.
• HBOT be considered in patients with neurologic changes, hemodynamic compromise, or evidence of end-organ dysfunction, with most benefit occurring within 6 hours of onset. Increased oxygen tension may reduce the size of air embolism and increase oxygen delivery to tissues.^3-5