Air/Gas Embolism

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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 some cases of 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 effect on the brain is similar to thrombotic or ischaemic stroke, with infarction of vital areas if the circulation is not improved rapidly.

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

1. Pulmonary barotrauma,

1. From sudden decompression, e.g. as a result of a diving accident
2. From barotrauma during mechanical ventilation
3. Blast injury, when close to an explosion

2. Intravascular equipment.

1. 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)
2. Arterial cannula flushed with air in the line
3. Angiographic accidents
4. Haemodialysis line disconnections and pump malfunctions

3. Peri-operative

1. Neurosurgical
2. Vascular
3. Cardiac (i.e. open heart) or cardiopulmonary bypass systems
4. Thoracic
5. Orthopaedic (instruments using compressed air)

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 be 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.