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

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]

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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