Causes

The origin of air bubbles in the circulation can be as follows:

• Pulmonary barotrauma (from sudden decompression) Commercial and Sport Diving
  


• Intravascular equipment
  
• Intravenous fluids and giving sets, and CVP cannula disconnections
  
• Arterial cannula disconnections
  
• Angiographic accidents
  
• Haemodialysis line disconnections and pump malfunctions
  


• Peri-operative
  
• Neurosurgical (i.e. posterior cranial fossa)
  
• Vascular (i.e. arterial by-pass)
  
• Cardiac (i.e. open heart)
  
• Thoracic (i.e. pneumonectomy or lobectomy)
  


• Orthopaedic (instruments using compressed air)

Symptoms

The sudden occurrence of a combination of neurological and/or cardiovascular signs. It can be delayed by a few minutes to even several hours after the causing event.

Primary Injury

The pulmonary circulation generally filters bubbles in systemic veins. A right-to-left shunt in the heart can by-pass this filter. Bubbles in the pulmonary veins can travel rapidly through the left side of the heart, and reach the systemic arteries, and thus the brain. The effect may appear like a cerebrovascular accident (stroke) from any other cause.

Once in the cerebral vessels, the effects of bubbles are as follows:

• Obstruction to blood flow
  
• Direct damage to endothelium
  
• Platelet release and activation
  
• Fibrin release and adhesion to endothelium
  
• Vasospasm followed by vasodilatation
  
• Opening of the blood brain barrier

Cerebral oedema and raised intracranial pressure

Treatment

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

Hyperbaric Oxygen:

• Reduces the size of bubbles (Boyle’s Law)
  
• Removes nitrogen from bubbles, by removing nitrogen from the blood and tissue
  
• Improves oxygen delivery to tissues damaged by ischaemia
  
• Reduces intra-cranial pressure, by causing constriction of cerebral arteries
  

Pressures of 3 ATA are sometimes used, but for a maximum of one hour in the first instance, and with air-breaks in order to minimise oxygen toxicity. Further Hyperbaric Oxygen treatments are determined by the clinical progress of the individual patient. Treatment is continued until resolution of all symptoms or failure to achieve further improvement. Anti-convulsions may be necessary in some cases.

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.

Treatment

Hyperbaric Oxygen:

• Improves oxygen delivery to ischaemic tissues
  
• Reduces oedema, by causing constriction of local arterioles
  
• Accelerates wound healing
  
• Enhances the immune response of hypoxic tissues
  
• Protects against the effects of oxygen free-radicals (if given during reperfusion)
  

The rarity of each of these conditions in any one centre makes it unlikely that many surgeons have seen what can be achieved by using Hyperbaric Oxygen in addition to conventional management. Controlled trials are also difficult to perform, since the ethics of with-holding Hyperbaric Oxygen from the control group are doubtful.

Where Hyperbaric Oxygen helps to prevent the amputation of an extremity, its cost-effectiveness is likely to be high, considering the cost of supporting the patient who is so disabled. The close association of all specialists involved is essential.

Evidence / References

Kindwall E (ed), Hyperbaric Medicine Practice 2nd ed., Chapter 19.D.
Mathieu (ed.) – Handbook on Hyperbaric Medicine, 217-238. 2006