Air embolism
Air embolism is an uncommon but potentially catastrophic event which occurs as
a consequence of the entry of air into the vasculature. A venous, or pulmonary
air embolism occurs when air enters the systemic venous circulation and
travels to the right ventricle and/or pulmonary circulation. An arterial air
embolism results from introduction of air into the arterial system and can
produce ischemia of any organ with poor collateral circulation [
1,2,3].
This card will review the causes, pathophysiology, diagnosis, and treatment of
air embolism. Issues related to the embolization of thrombi, amniotic fluid,
fat, or tumor cells are discussed separately on designated cards.
ETIOLOGY ！ Two conditions must be present
for air embolism to occur:
• A direct communication between a source of air
and the vasculature must exist
• A pressure gradient favoring the passage of air
into the circulation (rather than bleeding from the vessel) must be present
Patients in the intensive care unit (ICU) are at particular risk for air
embolism because they are subjected to a number of procedures in which these
two conditions are commonly met (
show
table 1). Examples include surgery, instrumentation of the central venous
system, and positive pressure ventilation [
1,2].
Surgery ！ Venous air embolism most commonly
complicates neurosurgical and otolaryngological interventions because the
surgical incision is made at a level above the heart by a distance greater
than the central venous pressure. This is a particular problem if the patient
is placed in the Fowler's, or sitting position, which further increases
negative venous pressure relative to the atmosphere. The estimated incidence
of venous air embolism during neurosurgical procedures ranges from 10 percent
(for surgical patients in the prone position) to 80 percent (for patients
undergoing repair of cranial synostosis while in the Fowler's position) [
1,4,5,6,7].
Most episodes are clinically silent or result in mild, transient hypotension.
Penetrating chest injuries may produce a bronchopulmonary venous fistulae and
arterial air emboli. The mortality rate in one series of 9 patients with this
complication was 66 percent [
8].
Air embolism has also been reported following Nd:YAG laser treatment of
endobronchial lesions, likely due to coolant gas (which exits the bronchoscope
under high flow/high pressure conditions to cool the laser probe) entering the
pulmonary venules and gaining access to the systemic circulation [
2,9].
(
See
"Bronchoscopic laser resection"). Other surgical procedures
associated with air emboli are listed in Table 1 (
show
table 1).
Central venous catheterization ！ Venous air
embolism is a serious and often under-recognized complication of central
venous catheterization. The incidence of line-associated air embolism has
varied from 1 in 3000 to 1 in 47 in different reports [
10,11,12].
Venous air emboli can occur at the time of central line or pulmonary artery
catheter insertion, while the catheter is in place, or at the time of catheter
removal. (
See
"Indications for and placement of central venous catheters").
The risk of catheter-related venous air embolism is increased by a number of
factors [
2,12,13]:
• Fracture or detachment of catheter connections
(which accounts for 63 to 93 percent of episodes)
• Failure to occlude the needle hub and/or
catheter during insertion or removal
• Dysfunction of self-sealing valves in plastic
introducer sheaths
• Presence of a persistent catheter tract
following the removal of a central venous catheter
• Deep inspiration during insertion or removal,
which increases the magnitude of negative pressure within the thorax
• Hypovolemia, which reduces central venous
pressure
• Upright positioning of the patient, which
reduces central venous pressure
Barotrauma ！ Patients requiring positive
pressure ventilation are at risk for barotrauma and, as a consequence, both
arterial and venous air emboli. Gas may enter the circulation if violation of
pulmonary vascular integrity occurs concomitantly with alveolar rupture caused
by overdistension of the airspaces. This complication has been reported most
frequently in adult patients with the acute respiratory distress syndrome and
in premature neonates with respiratory distress syndrome (hyaline membrane
disease), but also occurs in patients with other diagnoses [
2,14,15,16,17].
Divers are also at risk for barotrauma, and one series estimated that
barotrauma and air embolism complicate approximately 7 of every 100,000 dives
[
18].
Rapid ascent without exhalation can result in expansion of gas in the lungs
and consequent alveolar rupture. If pulmonary veins tear as the alveoli
rupture, air can return to the left heart with oxygenated blood and can
embolize within the arterial system to produce tissue ischemia [
19,20].
(
See
"Complications of diving").
PATHOPHYSIOLOGY ！ Air introduced into the
venous circulation travels to the right heart and then usually lodges in the
pulmonary circulation, causing a venous air embolism. Arterial embolization
can result from several mechanisms [
1]:
• The direct passage of air into the arterial
system
• Paradoxical embolization through a septal
defect, patent foramen ovale, or pulmonary arterial-venous malformation
• Incomplete filtering of a large air embolus by
the pulmonary capillaries
Patients with a left-to-right shunt may suffer paradoxical air emboli
following initial emboli to the pulmonary circulation which raise right heart
pressures and reverse the direction of the shunt.
The effect of an air embolus depends both upon the rate and volume of air
introduced into the circulation. The capacity of the lung to filter
microbubbles of air from the venous circulation is exceeded when gas enters
the circulatory system at a rate greater than 0.30 mL/kg per minute in a
canine model; infusions at greater rates generally result in arterial emboli
and tissue ischemia [
21].
Large, rapid boluses of air are tolerated less well than slow infusions of
small amounts of air. It is estimated that 300 to 500 mL of gas introduced at
a rate of 100 mL/sec is a fatal dose for humans [
2,12].
This flow rate can be attained through a 14 gauge catheter with a pressure
gradient of only 5 cm H2O [
22].
Upright positioning places the patient at particular risk for entraining air
very rapidly into the venous circulation, since the venous pressure is below
atmospheric pressure in this setting [
2].
Hemodynamic complications of venous air embolism ！
Gas introduced into the venous circulation can cause cardiac dysfunction by
obstruction of the pulmonary outflow tract, pulmonary arterioles, or pulmonary
microcirculation. Obstruction of the pulmonary outflow tract ("air
lock") diminishes blood flow from the right heart and results in
increased central venous pressure and reductions in pulmonary and systemic
arterial pressures [
12].
Smaller bubbles within the pulmonary arterioles can impede blood flow directly
and result in vasoconstriction [
1,12].
As a result of these changes in the pulmonary vascular bed, the following
hemodynamic effects may be observed [
1,5,12]:
• Increased pulmonary vascular resistance
• Pulmonary artery hypertension
• Increased right ventricular pressure
• Initial brief increase (due to tachycardia)
followed by a decrease in cardiac output and systemic arterial pressure
• Myocardial ischemia, (secondary to hypoxia,
right ventricular overload, and/or air emboli to the coronary arterial
circulation)
Pulmonary complications of venous air embolism ！
Bubbles in the pulmonary microcirculation are associated with local
endothelial damage and the accumulation of platelets, fibrin, neutrophils, and
lipid droplets at the gas-fluid interface. Secondary injury to the endothelium
occurs due to the activation of complement and the release of mediators and
free radicals from neutrophils and other inflammatory cells; noncardiogenic
pulmonary edema and bronchoconstriction may result [
23,24,25,26,27].
A number of physiologic changes can ensue, including [
1,5,12,26,27,28]:
• Hypoxemia, due to alveolar flooding and
ventilation-perfusion mismatching
• Increased physiologic dead space, with a rise
in PaCO2 if ventilation is held constant
• Decreased lung compliance secondary to
pulmonary edema
• Increased airway resistance, postulated to be
due to release of bronchoconstricting mediators such as serotonin and
histamine from endothelium damaged by the air bubbles [
5]
Systemic complications of air embolism ！
Air bubbles in the microcirculation directly occlude blood flow and cause
ischemic damage to end-organs, such as the brain, spinal cord, heart, and skin
[
2,12].
Secondary tissue damage from the release of inflammatory mediators and oxygen
free radicals in response to air embolism has also been suggested by animal
experiments [
29].
CLINICAL FEATURES AND DIAGNOSIS ！ Minor
cases of air embolism occur frequently and are minimally symptomatic. Severe
cases are characterized by hemodynamic collapse and/or acute vascular
insufficiency of specific organs such as the brain or spinal cord.
Differentiation from pulmonary thromboemboli, acute myocardial infarction, or
cerebrovascular accident may be difficult. Dyspnea is an almost universal
finding, and may be accompanied by substernal chest pain and a subjective
sense of doom. Common signs and symptoms of air embolism are listed in Table 2
(
show
table 2) [
1,2,5,19].
Air embolism should be considered in the differential diagnosis of any patient
who has the sudden onset of cardiopulmonary or neurologic decompensation in a
clinical setting which puts the patient at risk for air embolism (
show
table 1). Disorders which should be considered in the differential
diagnosis of air embolism are listed in Table 3 [
12]
(
show
table 3).
Confirming the diagnosis of air embolism is difficult, and is complicated by
the fact that air may be rapidly absorbed from the circulation while
diagnostic tests are being arranged. Exclusion of other life-threatening
processes is generally required.
Some of the following techniques may be useful in supporting the clinical
diagnosis of air embolism:
Laboratory, hemodynamic, and chest x-ray
findings ！ A summary of common laboratory, hemodynamic, and chest x-ray
findings is shown in Table 4 (
show
table 4) [
1,2,12,30].
One study documented significant elevations in serum creatine kinase activity
in all of 22 divers with arterial air embolism, but not in 22 control divers [
31].
The sensitivity of elevated serum creatine kinase activity in other
populations with arterial air emboli has not been reported.
Echocardiography ！ Transthoracic and
transesophageal echocardiography have been used to document the presence of
air in the right ventricle and may show evidence of acute right ventricular
dilation and pulmonary artery hypertension consistent with air embolism [
3,32].
Continuous monitoring with echocardiography or transcranial Doppler techniques
have been used during high-risk surgical procedures to detect air embolism in
the preclinical phase [
33,34,35].
End-tidal CO2 monitoring ！ The worsening
of ventilation-perfusion matching and increase in physiologic dead space which
occur with venous air embolism produce a fall in end-tidal CO2 and may raise
intraoperative suspicion of the condition. However, this finding is
nonspecific and also occurs with pulmonary embolism, massive blood loss,
circulatory arrest, or disconnection from the anesthesia circuit [
36].
The combination of intraoperative echocardiography and end-tidal CO2
monitoring may increase intraoperative sensitivity in detecting preclinical
air emboli in high-risk patients [
5,34].
Pulmonary artery catheters ！ A rise in
pulmonary artery pressure may be observed when venous air embolism occurs in a
patient in whom a pulmonary artery catheter has been placed. However, this is
a nonspecific finding, with an estimated sensitivity of only 45 percent [
34].
Ventilation-perfusion scan ！
Ventilation-perfusion scan abnormalities which mimic those seen in pulmonary
thromboembolism may be seen in the setting of massive air embolism. However,
the perfusion defects due to air embolism resolve more rapidly, frequently
within 24 hours [
37].
Chest CT ！ Chest CT may detect air emboli
in the central venous system (especially the axillary and subclavian veins),
right ventricle, or pulmonary artery. The specificity of these findings is
greatest when large defects are detected because small (<1 mL),
asymptomatic air emboli occur during the performance of 10 to 25 percent of
contrast-enhanced CT scans if carefully sought [
38,39].
False positive studies may be more common when higher resolution or electron
beam CT scanners are used. (
See
"Principles of conventional and helical CT scanning" and
see
"Electron beam (ultrafast) computed tomography for the evaluation of
cardiac disease and function").
Pulmonary angiography ！ Pulmonary
angiography may be normal in patients who have suffered air embolism because
of rapid resorption of air between the time of presentation and the
performance of the procedure. If positive, vascular occlusion and/or findings
consistent with vasoconstriction may be seen, including
"corkscrewing" of vessels, tapering of vessels, and delayed emptying
of vessels in the affected versus the unaffected lung [
1].
TREATMENT ！ The primary aims of treatment
are identification of the source of air entry and prevention of further air
embolization, removal of embolized gas, and restoration of the circulation.
Supportive care (eg, the use of mechanical ventilation, vasopressors, volume
resuscitation as indicated) is the cornerstone of management, but several
active measures may also be helpful [
1,2,12].
Nitrogen washout ！ High-flow supplemental
oxygen increases the partial pressure of oxygen and decreases the partial
pressure of nitrogen in blood [
40].
This produces a positive pressure gradient for the diffusion of nitrogen from
the air bubbles to the blood, accelerating bubble resorption. In contrast,
nitrous oxide, when given during general anesthesia, can diffuse from blood to
air emboli, causing clinical deterioration as gas bubbles enlarge [
41].
Thus, nitrous oxide should be discontinued at the first suspicion of air
embolism.
Hyperbaric therapy ！ Patients with
continued evidence of cardiopulmonary compromise or neurologic deficits
generally should receive treatment with hyperbaric oxygen therapy (HBO) [
42].
HBO reduces air bubble size, accelerates nitrogen resorption, and increases
the oxygen content of arterial blood, potentially ameliorating ischemia.
Although prompt initiation of HBO is preferred, it may improve outcome even if
delayed up to 30 hours [
43].
No randomized controlled trials of HBO in air embolism have been conducted in
humans, and the potential benefits of HBO must be weighed against the
potential risks of transport to the HBO facility [
44].
(
See
"Hyperbaric oxygen therapy").
Patient positioning ！ Patients who develop
an "air lock" from a large gas bubble obstructing the right
ventricular outflow tract may benefit from maneuvers which float air emboli
into other areas of the ventricle. Both the left lateral decubitus position
(Durant's maneuver) and the Trendelenburg position can restore forward blood
flow by placing the right ventricular outflow tract inferior to the right
ventricular cavity, permitting air to migrate superiorly to a nonobstructing
position [
1,2,4,12].
Closed-chest cardiac massage ！
Closed-chest cardiac massage forces air out of the pulmonary outflow tract
into smaller pulmonary vessels, thus improving forward blood flow [
45,46].
This technique improved survival in dogs as effectively as positioning and
intracardiac aspiration of air [
45].
Aspiration of air from the venous circulation ！
Air has been successfully aspirated from the right ventricle via a
percutaneously introduced needle or a central venous catheter in several
experimental models and case reports [
12,45].
In general, however, these maneuvers are of limited benefit because the volume
of air recovered is less than 20 mL [
34].
Most authors recommend attempting to aspirate air only if a central venous
catheter is already in place [
2,12].
PROGNOSIS ！ Mortality in untreated
patients historically was reported to be in excess of 90 percent, but these
figures may have been biased by selective reporting of catastrophic cases.
With supportive therapy such as vasopressors, positioning, supplemental
oxygen, and closed-chest cardiac massage, mortality was reduced to
approximately 30 percent in a series form the 1960s [
46].
A later series of 16 patients with either arterial or venous air emboli
treated with HBO in the early 1980s reported a mortality rate of 7 percent,
with one-half of survivors experiencing complete recovery and the remaining
one-half suffering some residual deficits [
44].
PREVENTION ！ Efforts should be made to
reduce the risk of air embolism during mechanical ventilation and central line
placement. Measures towards this end include [
1,5,12]:
• Minimization of airway pressures in
mechanically ventilated patients to prevent barotrauma (
see
"Physiologic and pathophysiologic consequences of positive pressure
ventilation")
• Placing the patient in the Trendelenburg
position during central venous catheter insertion and removal
• Asking the patient to Valsalva or breath hold
at the time of central venous catheter insertion and removal
• Occluding the hub of the central venous
catheter during insertion
• Treating hypovolemia prior to catheter
placement, if possible
• Keeping all connections to a central line
closed and locked when not in use
