Venous Gas Embolism

Etiology

Approximately 90% of VGE cases are iatrogenic.[1] Most result from medical or surgical interventions that expose the venous circulation to external air or gas. Procedures in which the surgical wound is located above the phlebostatic axis, such as when the head is elevated or the patient is placed in the Fowler position, carry an increased risk of VGE.[2] The risk of VGE is greatest during neurosurgical interventions, particularly when performed in a sitting position for posterior fossa lesions.[3]

Minimally invasive neurosurgical procedures, including deep-brain stimulation and stereotactic surgeries, can also precipitate VGE. Craniosynostosis repair is a frequent complication in the pediatric population. Orthopedic procedures such as hip arthroplasty, obstetric interventions like placental removal and pregnancy termination, laparoscopic procedures involving positive-pressure insufflation, and ophthalmic surgeries such as vitrectomy have also been associated with VGE.[4]

Additional causes include intravascular catheter-related procedures, such as insertion or removal of central venous catheters and pressurized contrast injections for CT imaging. Contributing factors include failure to occlude the needle hub, detachment of catheter connections, deep inspiration during line manipulation, upright patient positioning, and hypovolemia.[5] Positive-pressure ventilation with alveolar overdistension and high positive end-expiratory pressure can introduce free air. Intraoperative irrigation with hydrogen peroxide and penetrating missile or nonmissile injuries may also result in VGE.

Deep-sea diving can induce nitrogen gas accumulation in the venous system. During ascent, decreasing ambient pressure allows nitrogen previously dissolved in the blood to form bubbles, which coalesce into emboli within the lower-pressure venous system.[6][7][8][9][10]

Epidemiology

The incidence of VGE has increased in parallel with the growing number of invasive medical procedures. Enhanced detection through end-tidal carbon dioxide (EtCO2) monitoring and Doppler techniques has contributed to higher reported rates of VGE. However, the true incidence is uncertain, as most VGE cases are subclinical and do not produce noticeable symptoms. Neurosurgical procedures carry the highest risk for VGE, attributable to upright patient positioning, the anatomical relationship of the brain to the heart, and the brain’s noncompressed venous system.

Pathophysiology

Three factors are crucial in the pathogenesis of VGE: the presence of a gas source, a direct and patent connection between the source and the venous system, and a pressure gradient that facilitates air entry into the veins.[11] This process may be exacerbated by hypovolemia, upright positioning greater than 45°, and increased intrathoracic pressure during mechanical ventilation.[12] A subatmospheric gradient of at least 5 cm H2O can promote ingress of air into the venous circulation.[13]

The rate and volume of air entry, as well as patient positioning, which determines cardiac orientation at the time of VGE, are pivotal. Symptomatic VGE typically requires the introduction of more than 5 mL/kg of air into the venous system, whereas even 1 to 2 mL of air injected into the central nervous system (CNS) can be fatal. Injection of 0.5 mL of air into the coronary arteries can induce ventricular fibrillation.

Air introduced closer to the right heart increases the risk of complications. Volumes of 50 to 100 mL can trigger hemodynamic instability, with 300 mL being usually fatal.[14] Bolus air can generate an "air lock," reducing right ventricular ejection fraction. Smaller volumes of air become trapped in the pulmonary arterioles, causing pulmonary arterial hypertension and acute right ventricular failure. Microbubbles may aggregate with neutrophils, fibrin, red blood cells, fat globules, and platelets, increasing pulmonary vascular permeability and the risk of pulmonary edema.

Paradoxical embolism occurs in approximately 14% of cases, often through a patent foramen ovale, ventricular septal defect, or pulmonary arteriovenous fistula, potentially resulting in stroke or mesenteric ischemia.[15][16][17] Intrapulmonary right-to-left shunting increases alveolar dead space, producing hypercapnia and arterial hypoxemia.[18]

Arterial embolism arises when air volume exceeds the filtering capacity of the pulmonary capillaries. Pulmonary overpressurization may also result in arterial gas embolism.[19] Air bubbles can activate the coagulation cascade, contributing to coagulopathy. Gas may enter the cerebral venous system retrogradely through the jugular veins due to their low specific weight and incomplete valve function.

History and Physical

VGE is a clinical diagnosis, with severity ranging from clinically silent episodes, occurring in approximately 10% of cases, to potentially lethal events, observed in up to 20% of cases. The volume and rate of air entrainment largely determine the clinical spectrum. The hallmark feature is the temporal relationship between symptom onset and the precipitating event. Recognition of VGE requires a high index of suspicion. Clinical presentation may be multispectral, with signs and symptoms referable to cardiovascular, pulmonary, or central nervous system damage, either individually or in combination.

Cardiovascular manifestations include anginal chest pain, a loud, machinery-like mill-wheel murmur, tachyarrhythmias or bradyarrhythmias, elevated jugular venous pressure, hypotension, acute right ventricular failure, myocardial ischemia or infarction, and cardiac arrest. Pulmonary features comprise cough, dyspnea, tachypnea, rales, wheezing, cyanosis, mild hemoptysis, and apnea. CNS involvement may present as headache, altered mental status, seizures, transient focal neurological deficits, ischemic strokes, or coma. Paradoxical air embolism can produce overlapping signs and symptoms characteristic of both venous and arterial gas embolism. The Tubingen scale provides a method for grading the clinical severity of VGE.[20]

Evaluation

Diagnostic evaluation of VGE relies on a combination of clinical and instrumental findings. An EtCO2 drop exceeding 3 mm Hg on capnography is an important clue. Measurement of nitrogen in expired air during 100% oxygen administration is highly suggestive of VGE. End-tidal nitrogen monitoring is highly sensitive and detects VGE more rapidly than EtCO2 measurement. However, this modality may fail to identify minute air volumes and can falsely suggest resolution.

Cardiac auscultation may reveal the classical mill-wheel murmur. Massive air embolism can produce palpable crepitus over superficial veins. Hemodynamic monitoring often demonstrates increased central venous pressure and pulmonary artery wedge pressure. Aspiration of air bubbles from a central venous catheter provides additional confirmation.

Electrocardiography may show patterns consistent with right ventricular strain, while chest radiography can reveal pulmonary edema. Arterial blood gas analysis typically demonstrates hypercapnia, hypoxemia, and metabolic acidosis. Fundoscopic examination may identify intraretinal gas bubbles.

CT with lung window or minimum intensity projection images and magnetic resonance imaging can detect air within dural venous sinuses and watershed cerebral infarctions, although vascular gas is often not visualized due to rapid resorption. The rate of air resorption is influenced by both the volume of gas and blood flow velocity, with CT offering rapid acquisition and broad availability.

Visualization of air within the right heart cavities via transthoracic echocardiography, considered the most sensitive though invasive method, is pathognomonic of VGE.[21] Precordial and transesophageal echocardiography, while operator-dependent, can also confirm the diagnosis and may reveal acute right ventricular dilation and pulmonary artery hypertension. Bedside point-of-care ultrasound offers an informative, rapid assessment.

Despite these methods, transesophageal and precordial Doppler monitoring may be technically challenging and logistically demanding. Meanwhile, EtCO2 measurement is nonspecific and correlates poorly with VGE severity. Automated alarms or centralized monitoring systems may improve detection efficiency.

Treatment / Management

Initial Management and Stabilization

Initial management of VGE focuses on maintaining airway, breathing, and circulation (ABC). Prevention of further air entry is critical and may be achieved through thorough saline irrigation, positioning the operative site below the level of the right atrium, application of the Valsalva maneuver, or jugular venous compression. Eliminating the source of gas, such as abdominal insufflation during laparoscopic procedures, is essential. Subsequent management aims to reduce the size of the embolus and restore normal blood flow by relieving the mechanical obstruction caused by intravascular air.

Interventions to Reduce Embolus Volume

Reduction of embolus size constitutes a key component of VGE management. Flooding the operative field with normal saline can limit further air entry and promote bubble dispersion. Administration of 100% oxygen should be initiated as early as possible to correct hypoxia and enhance nitrogen washout, creating a diffusion gradient that facilitates nitrogen egress from the gas embolus. Hyperbaric oxygen therapy further reduces bubble size by promoting nitrogen reabsorption, ideally within the first 4 to 6 hours. Intermittent jugular venous compression and elevation of positive end-expiratory pressure can assist in limiting bubble volume and improving hemodynamics. Discontinuation of nitrous oxide is essential due to its high solubility and potential to diffuse into intravascular air, enlarging emboli.

Techniques to Overcome Embolic Mechanical Obstruction

Relieving mechanical obstruction caused by intravascular air is a critical aspect of VGE management. The left lateral decubitus (Durant) and Trendelenburg positions are employed to overcome right ventricular air lock, which can impede ejection fraction. Therapeutic aspiration through a central venous catheter may remove entrained air, although pulmonary artery catheters are generally too narrow, and emergent central venous catheter placement is not supported if one is not already in place.[22][23][24]

Inotropic agents enhance myocardial contractility and preload, thereby improving cardiac output in the setting of elevated pulmonary vascular resistance. Chest compressions can displace air from the pulmonary outflow tract and fragment large intrachamber bubbles. Cardiopulmonary bypass or thoracotomy with pulmonary artery aspiration or hilar clamping may be lifesaving in cases of massive embolism, but these procedures carry significant morbidity and low survival rates. Adjunctive measures include lidocaine infusion, as recommended by the European Consensus Conference on Hyperbaric Medicine, and anticoagulation or antiplatelet therapy to prevent thrombus formation on the surface of air bubbles.

Differential Diagnosis

The differential diagnosis of VGE varies according to the predominant clinical presentation. When respiratory symptoms predominate, considerations include pulmonary embolism, tension pneumothorax, bronchospasm, and pulmonary edema. Cardiovascular presentations may mimic cardiogenic shock, acute myocardial failure, neurogenic or noncardiogenic pulmonary edema, and septic shock. Neurological manifestations should prompt evaluation for transient ischemic attack and acute ischemic stroke. Accurate differentiation among these conditions is essential to guide timely and appropriate management.

Prognosis

Most patients experience no complications when only minute amounts of air enter the venous system. In contrast, air entry into the CNS carries a grave prognosis. Outcomes are primarily influenced by the patient’s mental status, presence of neurological deficits, and age. VGE always carries the potential for life-threatening complications, particularly if air remains trapped within a vessel. Mortality rates of 30% to 80% have been reported following VGE associated with chest trauma. Surgeons performing procedures that require patients to assume the Fowler position or undergo carbon dioxide insufflation should maintain heightened vigilance, as VGE associated with such interventions is still observed in clinical practice.

Complications

VGE is a rare adverse event but can result in life-threatening consequences.[25] VGE associated with neurosurgical procedures may carry a mortality rate of up to 21%.