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J Emerg Trauma Shock. 2009 Sep-Dec; 2(3): 180185.

doi: 10.4103/0974-2700.55330
PMCID: PMC2776366

Acute management of vascular air embolism


Nissar Shaikh and Firdous Ummunisa
Department of Anesthesia/ICU, Hamad Medical Corporation, Doha, Qatar
Address for correspondence: Dr. Nissar Shaikh, E-mail: nissatfirdous99@gmail.com
Received January 28, 2009; Accepted February 15, 2009.
Copyright Journal of Emergencies, Trauma, and Shock
This is an open-access article distributed under the terms of the Creative Commons Attribution
License, which permits unrestricted use, distribution, and reproduction in any medium, provided
the original work is properly cited.

Abstract
Vascular air embolism (VAE) is known since early nineteenth century. It is the entrainment of
air or gas from operative field or other communications into the venous or arterial vasculature.
Exact incidence of VAE is difficult to estimate. High risk surgeries for VAE are sitting position
and posterior fossa neurosurgeries, cesarean section, laparoscopic, orthopedic, surgeries invasive
procedures, pulmonary overpressure syndrome, and decompression syndrome. Risk factors for
VAE are operative site 5 cm above the heart, creation of pressure gradient which will facilitate
entry of air into the circulation, orogenital sex during pregnancy, rapid ascent in scuba (self
contained underwater breathing apparatus) divers and barotrauma or chest trauma. Large bolus
of air can lead to right ventricular air lock and immediate fatality. In up to 35% patient, the
foramen ovale is patent which can cause paradoxical arterial air embolism. VAE affects
cardiovascular, pulmonary and central nervous system. High index of clinical suspicion is must
to diagnose VAE. The transesophgeal echocardiography is the most sensitive device which will
detect smallest amount of air in the circulation. Treatment of VAE is to prevent further
entrainment of air, reduce the volume of air entrained and haemodynamic support. Mortality of
VAE ranges from 48 to 80%. VAE can be prevented significantly by proper positioning during
surgery, optimal hydration, avoiding use of nitrous oxide, meticulous care during insertion,
removal of central venous catheter, proper guidance, and training of scuba divers.
Keywords: Vascular air embolism, high risk surgeries, pressure gradient, decompression
syndrome, transesopageal echocardiogram, hyperbaric oxygen, dysbarism

INTRODUCTION
Vascular air embolism (VAE) is known since early 19th Century but the interest and reporting of
VAE significantly increased in last three decade. Most of the episodes of VAE are preventable if
meticulous precaution taken or at least detected early and managed properly. It is important that
all acute care physicians should be aware of this medical emergency. VAE can be venous or
arterial, both condition can be differentiated by mechanism of air entry as well as site of
embolization. The venous or pulmonary air embolism is air entry in systemic venous circulation
reaching the right ventricle while arterial air embolism occurs due to entry of air in to the arterial
circulation and potentially life threatening as it can lead to circulatory deficiency in the body
organ with poor collateral circulation. Here we will review the VAE in the following subheadings.

DEFINITION
VAE is the entrainment of air (or exogenously delivered gas) from open operative field or
communication with environment into the venous or arterial vasculature, producing systemic
effects.[1] Or production of air bubbles in circulation due to dysbaric barotrauma in scuba (self
contained underwater breathing apparatus) divers, astronauts and aviators, air enters venous or
arterial circulation causing systemic air embolism.

EPIDEMIOLOGY
Exact incidence of VAE is difficult to know as the sub clinical cases will be unnoticed. VAE
probably most common embolic event to occur during the intra-operative period. In
neurosurgical patients the incidence of VAE varies from 10 to 80%.[2] While in obstetricgynaecological surgeries VAE can occur from 11 to 97% of the patients.[3] In laproscopic
surgical patients it is reported to occur in up to 69% of the patients.[4] In orthopedic surgeries the
incidence of VAE can be 57%.[5] During invasive monitoring catheter insertion the incidence of
VAE are less than 2%.[6] Approximately, 7% of penetrating chest trauma patient will have
VAE.[7] Few case reports of VAE after barotraumas[8] and use of pressure infuser bag.[9] In
scuba (self contained underwater breathing apparatus) divers air embolism is second common
fatal cause, the incidence are 7/100,000 dives.[10]

ETIOLOGY
As mentioned VAE is probably most common embolic event to occur during surgical
procedure.[11] First and primary etiology of VAE is surgical procedure where the operative site
is above the level of heart, such as sitting neurosurgical procedure, posterior fossa surgery,[12]
obstetric procedure,[13] and orthopedic surgeries. [14] Second etiological reason is iatrogenic
creation of pressure gradient which facilitate air entry into the circulation such as during
insertion of central venous catheter.[15] Third etiological cause is mechanical insufflations or
pressure infusion such as laparoscopic surgeries[16] and gastrointestinal endoscopies. [17]
Fourth reason for VAE is scuba diving, aviators, astronauts (due to dysbarism or changes in the

ambient barometric pressures) and positive pressure ventilation.[18] The other etiological factors
are blunt and penetrating trauma to chest[19] and head.[20]

RISK FACTORS
In most of VAE episodes there are clear risk factors.
1. When operative site is more than 5 cm above right atrium.
2. Numerous larger, noncompressed venous channels in the surgical field.
3. Creation of pressure gradient for air entry into the circulation. A pressure difference of 5
cm of H2O across a 14 gauge needle can allow 100 ml of air/sec to enter into the
circulation.[21]
4. Orogenital sex during pregnancy and puerperium, as there will be pelvic venous
congestion and larger capacity of vagina during pregnancy, there is great risk for
VAE.[22]
5. Barotrauma or trauma to chest causes alveolar rupture [Figure 1] into small vein and
capillaries leading to direct air entry into the circulation.[23]
6. During insertion and removal of central venous catheter the factors increasing the risk of
VAE such as fracture or detachment of catheter, failure to occlude the needle hub, deep
inspiration, hypovolumia, and up-right position.
7. Risk factors which increases the incidence of air embolism in scuba divers are, too rapid
ascent rate, diving for too long, diving at great depth, hard exercise at depth, dehydration,
old age, obesity, alcohol, and cold water.[24]
8. Risk factors for air embolism in aviator are bronchogenic cyst or cystic air filled lesion in
the lung.

PATHOPHYSIOLOGY
Smaller amount of air in the circulation does not cause any clinical manifestations as it is broken
and get absorbed from circulation.
Moderate amount of air causes pulmonary vascular injury leading to pulmonary hypertension
and permeability pulmonary edema.[25]
Large bolus of air in venous system can cause an air lock in right side of the heart leading to
right ventricular flow obstruction and death.[26]
In up to 35% of patient due to the presence of patent foramen ovale, the air passes from right side
to the left side of the heart and leading to systemic air emboliztion this is termed as paradoxical
embolism.[27] In such cases cerebral [Figure 2] and myocardial ischaemia [Figure 3] can result
from emboliztion of cerebral or coronary circulation.[28]
The fatal amount of air in human is reported to be either 200 and 300 ml bolus or 3-5 ml/kg.[29]

The pathophysiology of decompression syndrome in scuba divers is different from other


iatrogenic air embolism. These dysbaric changes affect more in divers than high altitude climbers
or astronauts as the density of water is 100 times more at the sea level and the ambient pressure
is linear to the depth of submergence; to understand the pulmonary overpressure syndrome and
decompression syndrome pathology we should know the law of physics concern with the partial
pressure of gases in relation to the ambient pressure and gas solubility. The ambient pressure
changes or dysbarism causes remarkable changes in the physiology of the breathing gases; (1)
according to Dalton's law, the partial pressure of the divers breathing gases increases
proportionally to the increase in ambient pressure as the depth increases; (2) these exposure to
the supernormal pressures of breathing gases will lead to proportionally supernormal amount of
these gases dissolved into the divers body tissues and this may lead to nitrogen narcosis or
oxygen toxicity.[30]
The third type of changes in the body of the divers occurs which can be explained by the Boyle's
law; that is the amount of gas compressed in the body cavities inversely related to the increased
ambient pressure. These gases will expand due to ascend and decrease in ambient pressure
leading to the barotrauma in non-distensible body tissues (in middle ear and sinuses) and
distensible body tissues (bowel and lung) leading to pulmonary overpressurization and
barotrauma which ultimately causes rupture of alveoli, pneumothorax, pneumomediastinum,
arterial air embolism and decompression syndrome.[31]
The gas bubbles at the capillary level causes direct endothelial injury leading to post capillary
constriction, platelets aggregation around the air bubbles with neutrophilic sequestration and
inflammatory changes.

CLINICAL MANIFESTATIONS
Presentation of VAE varies according to the nature, volume and speed of air entrainment into the
circulation. The main affected systems in VAE are cardiovascular, respiratory, and central
nervous system.
The cardiac manifestations are chest pain, bradyarrhythmias or tachyarrhythmias, increased
filling pressure due to right sided heart failure and in late stage typical mill-wheel murmur.
Electrocardiogram may show s-t segment changes or right ventricular strain pattern.[32]
The pulmonary changes include dyspnoea, tachypnoea and gasp reflex as a result of acute
hypoxaemia or even pulmonary edema. Patient may have reduced lung compliance, increased
dead space and acute shunting leading to hypoxaemia and hypercarbia.[33]
Neurological manifestations are due to two reasons; first the cardiovascular collapse causing
reduced cardiac output leading to cerebral hypo-perfusion, secondly direct paradoxical cerebral
embolism[26] may occur through patent foramen ovale.
In divers there will be two types of injuries. First one is due to changes that leads to expansion of
the breathing gases causing pulmonary over inflation syndrome; second type of injuries occur
due to changes in ambient pressure leading to bubble formation initially in the body tissue then

entering in to the circulation causing to decompression syndrome (DCS) or decompression


sickness.
The pulmonary over inflation syndrome ranges from minor parenchymal lung injury causing
local bleed, pneumothorax and less commonly but potentially dangerous, over expansion of
alveoli leading to rapture and entry of air into the pulmonary venoules and arterioles causing
systemic air embolism, clinically these can present as cerebrovascular accidents, paralysis,
convulsion, coma, and may be associated with cardiovascular instability.[31]
DCS is the clinical manifestation associated with liberation of gas originally held in the solution
into a free gas phase within the tissues as a result of decrease in the barometric pressures; these
bubbles finally reaches venules.
The DCS manifest as bends chokes and skinny bends [Figure 4]. The bends is boring pain in
major joints (hip, elbow, and knee) of the divers mostly due to increase in intramedullary
pressure at the ends of long bones and gas phase separation along ligaments and the tendon
sheath causing sever pain. Chokes is substernal burning, cough and shortness of breath with or
without haemodynamic instability. The main explanation for chokes is that the extreme high load
of venous gas emboli in the pulmonary artery leading to increased in pressure on right side of the
heart. Shinny bends are the coutaneous manifestation of DCS. The dangerous form of DCS is
affection of spinal cord leading to ascending paraesthesia and associated bowel and urinary
bladder dysfunction.[34]

DETECTION OF VASCULAR AIR EMBOLISM


High index of suspicion in high risk cases is the cornerstone for diagnosis of VAE.
VAE should be considered when unexplained hypotension or sudden decrease in end-tidal CO2
level occurs intraoperatively in high risk cases. If patient complains of short of breath during or
immediately after insertion or removal of central venous catheter. In cesarean section patients
who suddenly develops hypotension and hypoxia after delivery of the fetus.
Various monitoring devices can help in early detection of air in the vascular system.
The transesophageal echocardiography is the most sensitive monitoring; it can detect 0.02 ml/kg
of air injected by bolus administration or air bubbles as small as 5-10 microns.[35]
Precordial doppler ultrasound is the most sensitive non-invasive monitoring which can detect as
little as 0.05 ml/kg of air.[36]
End tidal nitrogen (ETN2) can show the changes 30-90 seconds earlier than end-tidal carbon
dioxide (ETCO2) changes.[37]
End-tidal carbon dioxide (ETCO2) is the most common and easily available monitoring, which
will reveal sudden decrease in level in event of VAE.[38]

Transcranial doppler[39] and ECG (Electrocardiogram) changes are also used to guide the
diagnosis of VAE. Pulmonary artery catheter will show rise in pulmonary artery pressure, its
sensitivity is only 15%. Ventilationperfusion scan findings are similar to those found in
pulmonary thromboembolism, however, air embolism causes perfusion defect which get resolved
rapidly usually within 24 hours. Computed Tomography (CT) chest will show air in central
venous system, ventricles, pulmonary artery or pneumothorax [Figure 1]. CT brain may show
intravascular air with or without infarction [Figure 2].[40]

DIFFERENTIAL DIAGNOSIS
VAE should be differentiated from acute coronary syndrome, cardiogenic shock, cerebrovascular
accidents, and pulmonary embolism.

TREATMENT
The goal of treatment in VAE is to prevent further air entry, reduction in volume of air entrained,
and haemodynamic support. Immediately covering the surgical field with saline soaked dressing
and if possible tilting the Table may help in preventing further air entrainment. In sitting position
surgeries, by jugular venous compression, it is documented that it limits or restrict the air entry
into chest circulation.[41]
Administration of 100% oxygen will maximize the patient's oxygenation as well as reduces
embolus volume by eliminating nitrogen.[42]
By maintaining the systemic arterial pressure with optimal fluid status and inotropic support to
the heart will help by keeping the patient stable[43] Air lock in right side of heart may be
relieved by partial left lateral decubitus position.[44]
Trendelenburg's position as a favorable placement to optimize haemodynamics is now
controversial.[45]
Aspiration of air from right atrium is possibly best treatment to improve the haemodynamic
parameters immediately and this can be done, with use of Bunegin-Albin multiorifice catheter up
to 60% success rate.[46]
Rapid cardiopulmonary resuscitation with chest compression demonstrated to be effective in
massive VAE which result in cardiac standstill.[47]
Hyperbaric oxygen therapy in the cases of VAE is beneficial as it causes compression of existing
air bubbles, by establishing a high diffusion gradient to speed dissolution of bubbles and by
improving oxygenation in the ischemic tissues.[48] In hyperbaric therapy, patient inspires 100%
oxygen at pressure above that of atmosphere at sea level with achieving an arterial partial
pressure of oxygen greater than 2000 mm of Hg. In decompression syndrome, patients should be
transported in supine position to minimize risk of cerebral embolization. The early compression
therapy has better results, as per Boyle's law, the compression by hyperbaric oxygen therapy will

decrease the bubble size. Most commonly initial schedule of recompression is for 5-hours with
intermittent air break. If sign and symptoms not relieved, therapy can be repeated once or twice
daily and most of the patients required one to three therapeutic sessions.[49]
Anticoagulation therapy with heparin in patients with air embolism decreases the severity of the
disease, if treated with heparin before air embolization.[50] As steroids do not have any effect on
cytotoxic brain edema which occurs in the patients with air emboilsm, the use of steroid is
controversial.[51] Interestingly, prophylactic lidocain is effective in reducing the gas embolism
effect on brain, it deceases brain edema in experimental animals. Various case reports suggesting
that the lignocain has beneficial effect in patient with decompression syndrome.[52]

MORBIDITY AND MORTALITY


Morbidity and mortality in VAE is directly related to volume of air entrainment, rate of
accumulation of air, and position of the patient at the time of VAE. Mortality of VAE ranges
from 48 to 80%.[53]

PREVENTION
Instead of sitting position for surgeries the alternative park bench position provides adequate
surgical conditions and to take extra-precautions and meticulous monitoring in patients with
documented right to left shunt.[54] During caesarean section, 15 degree left tilt position
facilitates entry of air into the circulation; hence institution of 50 degree reverse trendelenburg
position decreases the chances of VAE from 44 to 1%.[55] During insertion and removal of
central venous catheter one has to take care of all these risk factors for VAE to prevent its
occurrences.[56] Optimizing the volume status will prevent the wide gradient between right
atrium and entrain vein and hence decreasing the risk of VAE.[57] Avoidance of use of nitrous
oxide will help in preventing VAE.[42] The use of positive end expiratory pressure (PEEP) in
preventing VAE is controversial.[58]
The use of dive computers, published Tables and personal software algorithm recommended
limiting the dive duration, at given depth and prescribing maximum ascent and decompression
stops for various combinations of depth, dive time, and breathing gases which will be helpful in
preventing decompression sickness in divers.

CONCLUSION
Vascular air embolism (VAE) is preventable critical medical emergency. Apart from sitting
position neurosurgical procedures, VAE is common in obstetric and laproscopic surgeries. It is
the most feared complication in scuba divers. Small amount of air in the circulation get absorbed
but large bolus of air can cause air lock in the heart causing sudden death. Clinical manifestation
of VAE is mainly due to the involvement of respiratory, cardiovascular, and central nervous
system. In scuba divers, the barometric pressure changes will lead to change in breathing gas
solubility and expansion causing bubble formation in body tissue and circulation.

Paradoxical arterial air embolism occurs through patent foramen ovale causing significant endorgan damage. Precordial doppler ultrasound is the most sensitive method in detection of air
embolism, but high index of suspicion in the high risk patients and knowledge about VAE are
the corner stone for diagnosis of vascular air emboilsm. The goal of treatment of VAE is to
prevent further air entry in the circulation, reduction in volume of air entrained and
haemodynamic support. Aspiration of air from heart will immediately improve the haemodynaic
parameters, but use of Trendelenburg position is controversial. The early use of hyperbaric
oxygen therapy is vital in the treatment of VAE. To prevent occurrence of VAE the proper
positioning during surgery, optimal hydration, and meticulous precautions during insertion and
removal of central venous catheter is of vital importance. Use of diving computers, proper
training and knowledge will prevent the decompression syndrome in the scuba divers.

Footnotes
Source of Support: Nil
Conflict of Interest: None declared.

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