Gas Embolism

What Is Cerebral Gas Embolism (CGE)?

Symptoms and signs of Gas Embolism, or the presence of bubbles of air (or any other gas) in the circulation, varies widely and its consequences range from mild discomfort (seen as microbubbles in decompression illness) to causing rapid death, particularly when caused by various invasive medical/surgical procedures, but occasionally also seen as diving accidents.

Upon entering the vascular system, gas bubbles follow the blood stream until they obstruct small vessels.

Depending on the access route, gas embolism may be classified as venous or arterial gas embolism. Diagnosis is based on the sudden occurrence of neurological and/or cardio-respiratory manifestations.


The London Hyperbaric unit at Whipps Cross Hospital and the East of England Hyperbaric unit at James Paget Hospital have 24/7 Consultant Anaesthetist cover to treat such cases. Speak directly to one of our consultants now on our 24/7 hotlines:

BartsHealth Hyperbaric Unit,

07999 292 999

James Paget University Hospital,
Great Yarmouth

01493 603 151

Origins of air or gas bubbles in the circulation

  • Intravascular Equipment

    • Intravenous access lines, fluids and giving sets, and any disconnection of these. (this includes insertion of peripheral as well a central lines and includes removal)
    • Arterial cannula flushed with air in the line
    • Angiographic accidents
    • Haemodialysis line disconnections and pump malfunctions
    • ECMO
  • Peri-operative

    • Neurosurgical
    • Vascular
    • Cardiac (i.e. open heart) or cardiopulmonary bypass systems
    • Thoracic
    • Orthopaedic (instruments using compressed air)
    • endoscopic procedures with gas insufflation
    • ophthalmic gas insufflation under pressure
  • Pulmonary Barotrauma

    • From sudden decompression, as a result of a diving accident
    • From barotrauma during mechanical ventilation
    • Blast injury, when close to an explosion
    • gunshot and chest stab wounds

Beware the Peri-procedural Stroke!

The pulmonary circulation generally filters bubbles in pulmonary arteries from the right ventricle and systemic veins. A right-to-left shunt in the heart can by-pass this filter, allowing bubbles to be pumped from left ventricle into aorta and its branches.

Bubbles in the pulmonary veins can travel to the left side of the heart, and reach the aorta, and thus the brain (and rest of the body). The effect may appear like a cerebro-vascular accident (stroke) from any other cause. Bubbles may be seen in cerebral arteries or veins and may even be described as pneumocephalus.

Once suspected, treatment for CGE must begin at once, the source identified and eliminated, life support be instituted as required and Hyperbaric Oxygen provided as quickly as possible.

Time is of the essence!

Once in the cerebral vessels, the effects of these bubbles are:

  • Mechanical obstruction to blood flow
  • Direct damage to endothelium. The bubble surface acts as a foreign substance and activates the coagulation cascade
  • Increased levels of C3a and C5a
  • Prostaglandin, leukotriene synthesis
  • Platelet and leukocyte activation, leading to ongoing impairment of microcirculation
  • Fibrin release and adhesion to endothelium
  • Vasospasm followed by vasodilatation
  • Damage to the blood brain barrier
  • Cerebral oedema and raised intracranial pressure

Mechanism of Action of Hyperbaric Oxygen Treatment

Pressures of 2.8 ATA are used, and with air-breaks in order to minimise oxygen toxicity. Further Hyperbaric Oxygen treatments are determined by the clinical progress of the individual patient and continued until resolution of all symptoms or failure to achieve further improvement.

There is no dispute about the applicability of Hyperbaric Oxygen in this condition, however, its recognition in clinical practice is difficult and very few cases are referred to Hyperbaric Medicine departments in good time. It is hardly ever too late to discuss the possibility of benefit though.

The rarity of air embolism in any one centre makes it unlikely that many Clinicians have seen how devastating CGE can be, nor what can be achieved by using Hyperbaric Oxygen in addition to conventional management.

Controlled trials are impossible to perform, since withholding Hyperbaric Oxygen from the control group would be highly unethical.

  • Reduces the size of bubbles (Boyle’s Law)
  • Removes nitrogen from bubbles by removing nitrogen from the blood and tissue (The hyperoxia produces enormous diffusion gradients for oxygen into the bubble and for nitrogen out of the bubble)
  • Improves oxygen delivery to tissues in the ischaemic penumbra
  • Reduces intra-cranial pressure by causing constriction of cerebral arteries
  • Hyperbaric oxygen inhibits membrane guanylate cyclase, which in turn inhibits b2 integrin adherence and decrease leukocyte stickiness
  • Protects against the effects of oxygen free-radicals (if given during reperfusion)

Laboratory Research:

Gorman, D., et al. (1987). “Redistribution of cerebral arterial gas emboli: A comparison of treatment regimens.” 9th International Symposium on Underwater and Hyperbaric Physiology Undersea and Hyperbaric Medical Sociaety, Bethesda, MD: 1031-1050.

Helps, S. C. and D. F. Gorman (1991). “Air embolism of the brain in rabbits pretreated with mechlorethamine.” Stroke 22(3): 351-354.

Helps, S., et al. (1990). “The effect of gas emboli on rabbit cerebral blood flow.” Stroke 21(1): 94-99.

Helps, S., et al. (1990). “Increasing doses of intracarotid air and cerebral blood flow in rabbits.” Stroke 21(9): 1340-1345.

Weenink, R. P., et al. (2012). “Animal models of cerebral arterial gas embolism.” J Neurosci Methods 205(2): 233-245.

Weenink, R. P., et al. (2013). “Hyperbaric oxygen does not improve cerebral function when started 2 or 4 hours after cerebral arterial gas embolism in swine.” Crit Care Med 41(7): 1719-1727. (KEEP IN MIND THAT THIS IS A VERY SEVERE INJURY TO THE BRAIN)


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