Excerpt from Venous Air Embolism

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Background

Venous air embolism (VAE), the entry of gas into the peripheral or central vasculature, can occur secondary to iatrogenic complications, trauma, and even certain recreational activities. Although many occurrences of VAE are believed to go unreported because they are asymptomatic, entrapment of large quantities of intravascular gas can lead to severe neurologic injury, cardiovascular collapse, and even death. The factors that determine the subsequent morbidity and mortality in VAE include the rate of air entrainment, the volume of air introduced, and the position of the patient at the time of the embolism.

Gas emboli are usually composed of air, but they can also occur with medically used gases such as carbon dioxide, nitrous oxide, and nitrogen. Although very small volumes of air can lead to severe sequelae, it is generally accepted that more than 50 mL of air can cause hypotension and dysrhythmias and more than 300 mL of air can be lethal.

Arterial gas embolism (AGE) is a separate but related entity that is not discussed in any detail in this article. AGE can occur through a patent foramen ovale (present in approximately 27% of the general population) or can form by gas movement across the alveolar-capillary membranes into the pulmonary venous circulation.

Pathophysiology

VAE results when a pressure gradient develops that favors the ingress of air into the venous system. Upon entry into the venous system, air is transported to the right atrium and ventricle. From there, it has the potential to continue on to the pulmonary arteries where it may cause interference with gas exchange, cardiac arrhythmias, pulmonary hypertension, and even cardiac failure and arrest. A large bolus of air entering the venous system can cause an air lock in the right atrium and ventricle, leading to outflow obstruction, decreased pulmonary venous return, and subsequent decreased left ventricular preload and cardiac output.

Intermediate amounts of air collect in the pulmonary circulation and produce a pulmonary vascular injury manifested by precapillary and postcapillary pulmonary vasoconstriction, pulmonary hypertension, endothelial injury, and permeability pulmonary edema. Subsequent ventilation-perfusion mismatch can cause right to left shunting and increased arterial hypoxia and hypercapnia.

Small amounts of air do not produce symptoms because the air is broken up and absorbed from the circulation. Although classical teaching states that more than 5 mL/kg of air (IV) is required for significant injury (including shock and cardiac arrest), patient complications secondary to as little as 20 mL of air (the length of an unprimed IV infusion set) have been reported. Further, as little as 0.5 mL of air in the left anterior descending coronary artery has been shown to lead to ventricular fibrillation.

The pathogenesis of pulmonary endothelial injury may have components of platelet-fibrin thrombi from the right ventricle, cytokine release, neutrophil, platelet, and complement activation at the microvascular air-blood interface, and injury mediated by lipid peroxidation and oxygen radicals.

Frequency

United States

The true incidence of VAE is unknown. Subclinical air embolism in hospitalized patients may be quite common. Frequency of clinically recognized VAE following central venous (CV) cannulation is less than 2%. Case report series (as mentioned above) have estimated VAE from central venous catheterization at 1 in 47 to 1 in 3000, and neurosurgical complications of VAE range from 10-80%.

Mortality/Morbidity

VAE is associated with significant morbidity and mortality. Morbidity can include lung injury, neurologic injury, cardiovascular ischemic injury, and ultimately cardiopulmonary collapse and arrest. Symptomatic VAE following CV catheterization has a mortality rate as high as 30%.

Please click here to view the full topic text: Venous Air Embolism