Vascular Gas Embolism

Reviewed and revised 28 August 2015

OVERVIEW

Vascular gas embolism (VGE) is the entrainment of air (or exogenously delivered gas) from a communication with the environment into the venous or arterial vasculature, producing systemic effects.

• Venous gas embolism involves gas entering the venous circulation with  embolism into pulmonary circulation causing right heart failure and cardiovascular compromise
• Arterial gas embolism involves gas entering the arterial circulation with embolism into distal capillary beds and resulting ischaemia

Most episodes of VGE are likely preventable

PATHOPHYSIOLOGY

VGE requires:

1. source of gas
2. communication between gas and circulatory system
3. pressure gradient allowing ingress of gas

Severity depends on:

1. Volume of gas (adult lethal volume is 200 to 300 ml, or ~3–5 ml/kg; the closer the vein of entrainment is to the right heart, the smaller the required lethal volume)
2. Rate of gas delivery (e.g. 100 mL/s; the lungs provide a route for dissipation of intravascular gas)

Venous gas embolism

• rapid, large volume VGE leads to immediate circulatory collapse due to “gas-air lock” phenomenon in the right ventricle; less severe cases precipitate RV failure due to mechanical effects as well as RV embolism triggering endothelin-1 release causing pulmonary hypertension
• Air entrainment into the pulmonary circulation may lead to pulmonary vasoconstriction, release of inflammatory mediators, bronchoconstriction, and an increase in V/Q mismatch
• Turbulent flow causes microbubble formation leading to platelet aggregation, resulting in an inflammatory response and SIRS
• Acute pulmonary edema can result from the above physical and chemical responses and free radical injury
• Gas can travel to arterial circulation via PFO and intra-pulmonary shunts (e.g. thebesian veins, bronchial vessels)

Arterial gas embolism

• entry of gas into aorta with distribution to organs, as a result of:
  • paradoxical embolism from the venous circulation via a patent foramen ovale (present in 20% of people) or other right-to-left shunt
  • overwhelming venous embolism that overcomes pulmonary filtration
  • direct entry into the aorta or other artery (e.g. cardiopulmonary bypass, ECMO, arterial cannulae)
• small emboli to skeletal muscle and viscera tolerated well
• cerebral and coronary embolisation can result in severe morbidity or death

CAUSE AND RISK FACTORS

Venous gas embolism

• high risk venous access patients
  • e.g. head up with central access, multiple infusion, rapid fluid transfusions under pressure, high negative inspiratory pressures during cannulation, extracorporeal supports (e.g. RRT, ECMO)
• any surgery where the operative field is above the heart and veins are large and held open by connective tissue is high risk
  • e.g. gas insufflation procedures, sitting craniotomy, posterior fossa craniotomy, spinal surgery, large bore venous lines, Caesarian section (traditional 15° left lateral tilt position during cesarean deliveries creates a gradient between the right side of the heart, which is at a lower level than the uterus), laparoscopic procedures (involves postive pressure gass inssufflation)
• other mechanisms
  • diagnostic procedures (e.g. epidural anaesthesia, lumbar puncture, contrast administration for imaging)
  • Hydrogen peroxide poisoning (portal venous gas)

Arterial gas embolism

• Cardiopulmonary bypass
• ECMO
• arterial cannulation
• intra-aortic balloon rupture
• pulmonary origin (e.g. decompression barotrauma, pneumothorax, trauma)

CLINICAL FEATURES

The spectrum is of presentation is diverse, ranging from subclinical to lethal

Venous gas embolism

• audible suction at time of gas entrainment (e.g. during cannulation)
• lightheadness, dizziness, dyspnoea, chest pain, anxiety (“sense of impending doom”), tachypnoea, tachycardia, altered mental state
• gasping in spontaneously breathing patients may lead to further air entrainment (higher negative inspiratory pressures)
• arrhythmias
• hypotension (especially during surgery performed in reverse Trendelenberg position)
• cardiovascular collapse
• ‘mill wheel’ murmur
• changes on bedside monitoring (see below)
• dyspnoea during or shortly after CVC insertion or removal

Arterial gas embolism

• neurological: delayed recovery from anaesthesia, altered mental state, focal neurological deficits, may mimic stroke
• other end organ dysfunction (e.g. acute coronary syndrome, spinal ischaemia, etc)

INVESTIGATIONS

Bedside (primarily of use for intra-operative monitoring)

• ETN2: sudden increase in ET nitrogen (VGE)
• ETCO2: increased dead space -> sudden fall in ETCO2 (VGE)
• ECG: tachyarrhythmias, AV block, right heart strain, T wave changes, ST changes (VGE or AGE)
• CVP: increase in CVP (VGE)
• PAC: increase in PCWP
• TOE: bubbles seen on TOE [VGE] (most sensitive monitoring device for VAE, can detect 0.02 ml/kg of air administered by bolus injection)
• Precordial Doppler: bubbles heard [VGE] (most sensitive noninvasive monitor for VAE, can detect 0.25 ml of air)
• Transcranial Doppler ultrasound (highly sensitive, in patients with PFO)
• fall in SpO2 (late sign)

Imaging

• CXR: normal, non-cardiogenic pulmonary oedema
• CT/ MRI brain: ischaemic injury not localised to single vascular territories [AGE]

MANAGEMENT

Goals

1. Maintain oxygenation and provide haemodynamic support
2. Minimise further air entrainment
3. Reduce size of embolism
4. Overcome mechanical obstruction caused by embolism

Resuscitation

• A – ETT
• B – FiO2 1.0
• C – CPR if required

Prevent further air entrainment

• identify and disable entry of gas
• flood field with saline and compress wound edges if surgical source
• volume expansion with IV fluids
• for VGE:
  • position operative site below RA then supine for cerebral protection; benefit of repositioning the patient is questionable but traditionally the Tredelenberg position or the Durant maneuver (placing the patient in a partial left lateral decubitus position) were suggested to relieve the air-lock in the right side of the heart
  • increase intrathoracic pressure -> Valsava (decrease VR)

Reduce size of embolism

• 100% O2 (prevents nitrogenation and therefore expansion of bubble)
• hyperbaric oxygen (optimal timing is uncertain; the sooner the better?)
• for VGE: aspirate blood if CVC in situ (won’t be effective unless tip is in RA)

Overcome mechanical obstruction

• for VGE: if air in RA – left lateral position will hopefully mean bubble travel superiorly allowing RV to empty
• inotropes
• bypass -> air can be aspirated from PA
• Chest compressions (even if not in cardiac arrest, CPR may help force air out of the pulmonary outflow tract into the smaller pulmonary vessels, thus improving forward blood flow)

Disposition

• admit to ICU/HDU
• discuss with family and patient
• document
• debrief
• case review and preventative strategies implemented

PREVENTION

Prevention during surgery:

• screening for PFO by transcranial Doppler for IV bubble administration or ECHO
• postioning (avoid sitting position)
• meticulous surgical technique
• reduce the height from operative site to RA
• hydration, keep CVP full
• pressure over jugular veins at high risk times
• use PEEP (not in sitting position as leads to increased likelihood of paradoxical embolism in patients with PFO)
• avoid N2O

Prevention during cannulation (e.g. CVCs, vascaths, PACs, etc)

• at insertion or removal of CVL keep RA above site
• avoid fracture or detachment of catheter connections
• occlude the needle hub or catheter during insertion or removal
• ensure functioning self-sealing valves in plastic introducer sheaths
• occlude persistent catheter tract following removal (if present)
• avoid deep inspiration during insertion or removal (increases negative intrathoracic pressure)
• correct hypovolemia (reduces CVP)
• avoid upright positioning of the patient (reduces CVP)
• Synchronise removal of the catheter with active exhalation in a cooperative patient;  apply PEEP if mechanically ventilated)
• Use Valsalva maneuver rather than breath holding during insertion/ removal in awake, cooperative patients (increases CVP)
• check lines for bubbles/air
• if high ICP or other contra-indication to head down position, use a transient Trendelenburg position during insertion of the guide wire or the catheter after the vein has been identified by the finder needle, and/or raising the legs by keeping pillows under the knees to increase the venous return and pressure in the right atrium

References and Links

litfl.com

• CCC — Hyperbaric oxygen

Journal articles

• Mirski MA, Lele AV, Fitzsimmons L, Toung TJ. Diagnosis and treatment of vascular air embolism. Anesthesiology. 106(1):164-77. 2007. [pubmed] [free full text]
• Muth CM, Shank ES. Gas embolism. The New England journal of medicine. 342(7):476-82. 2000. [pubmed]
• Sviri S, Woods WP, van Heerden PV. Air embolism–a case series and review. Critical Care and Resuscitation . 6(4):271-6. 2004. [pubmed] [free full text]
• van Hulst RA, Klein J, Lachmann B. Gas embolism: pathophysiology and treatment. Clinical physiology and functional imaging. 23(5):237-46. 2003. [pubmed]