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Cerebral Gas Embolism advice

Cerebral Gas Embolism advice

If your interest is in connection with a current patient: YOU HAVE TO ACT NOW!!

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 (24/7) on 01493 603 151.

 

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.

Examples of the origins of air or gas bubbles in the circulation are:

Pulmonary barotrauma

  • From sudden decompression, as a result of a diving accident
  • From barotrauma during mechanical ventilation
  • Blast injury, when close to an explosion, thoracic trauma of other sorts.

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.

Peri-operative

  • Neurosurgical
  • Vascular
  • Cardiac (i.e. open heart) or cardiopulmonary bypass systems
  • Thoracic
  • Orthopaedic (instruments using compressed air)
  • Laparoscopic.

Cerebral Venous Gas Embolism (CVGE) is an equally dangerous variant of gas embolism with gas bubbles preferentially entering the cerebral venous circulation under certain circumstances, rather than following the flow of blood to the right side of the heart.

The main symptom is the sudden occurrence of ANY neurological and/or cardiovascular signs which can be instantaneous, delayed by just a few minutes or several hours after the causing event.

 

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 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.

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

Time is of the essence!

 

Mechanism of action of Hyperbaric Oxygen treatment

  • 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)

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.

Thank you for looking at our website.  If your interest is in connection with a current patient: YOU HAVE TO ACT NOW!!

If your interest is in connection with a previous patient, please register the case on the anonymous Gas Embolism website:

GasEmbolism.org

 

References

Bessereau J, Genotelle N, Chabbaut C, Huon A, Tabah A, Aboab J, et al. Long-term outcome of iatrogenic gas embolism. Intensive Care Medicine. 2010;36(7):1180-7.

Ploner F, Saltuari L, Marosi MJ, Dolif R, Salsa A. Cerebral air emboli with use of central venous catheter in mobile patient. Lancet. 1991;338:1331.

Schlimp CJ, Loimer T, Rieger M, Lederer W, Schmidts MB. The Potential of Venous Air Embolism Ascending Retrograde to the Brain. Journal of forensic sciences. 2005;50(4):906-9.

Blanc P, Boussuges A, Henriette K, Sainty J, Deleflie M. Iatrogenic cerebral air embolism: importance of an early hyperbaric oxygenation. Intensive Care Medicine. 2002;28:559-63.

Walker MB. Iatrogenic arterial gas embolism in Australia – a demographic perspective. Diving and Hyperbaric Medicine. 2006;36(3):158.

Trytko BE, Bennett MH. Arterial gas embolism: a review of cases at Prince of Wales Hospital, Sydney, 1996 to 2006. Anaesthesia and Intensive Care. 2008;36:60-4.

Fracasso T, Karger B, Schmidt PF, Reinbold WD, Pfeiffer H. Retrograde Venous Cerebral Air Embolism from Disconnected Central Venous Catheter: An Experimental Model. Journal of Forensic Science. 2011;56(S1):S101-S4.

Bothma PA, Brodbeck A, Smith B. Cerebral Venous Air Embolism Treated with Hyperbaric Oxygen: A Case report. Diving and Hyperbaric Medicine. 2012 June; 42(2):101-103.

Souday V, Radermacher P, Asfar P. Cerebral arterial gas embolism-a race against time! Crit Care Med. 2013 Jul;41(7):1817-9. PubMed PMID: 23774349.

Buompadre MC, Arroyo HA. Accidental cerebral venous gas embolism in a young patient with congenital heart disease. J Child Neurol. 2008;23:121-123.

Diving and Hyperbaric Medicine. 2013;44(4) December. Despite animal studies, HBOT is the treatment of choice for cerebral gas embolism.  PA Bothma, REA Heij

Br J Anaesth. 2013 Dec 18. (Editorial Epub ahead of print) PMID: 24355833).

Retrograde cerebral venous gas embolism: are we missing too many cases?     Bothma PA, Schlimp CJ.

 

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.” Stroke22(3): 351-354.

Helps, S., et al. (1990). “The effect of gas emboli on rabbit cerebral blood flow.” Stroke21(1): 94-99.

Helps, S., et al. (1990). “Increasing doses of intracarotid air and cerebral blood flow in rabbits.” Stroke21(9): 1340-1345.

Weenink, R. P., et al. (2012). “Animal models of cerebral arterial gas embolism.” J Neurosci Methods205(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 Med41(7): 1719-1727.

 

We are working in close collaboration with The London Hyperbaric Unit based at Whipps Cross Hospital, part of Barts health. If your patient is closer to Whipps Cross, you should contact them in the 1st instance in the interest of time.

BartsHealth Hyperbaric Unit, (London)  - Tel. 07736 898 066 or 07999 292 999.