Gas embolism occurs when gas bubbles enter arteries or veins. Arterial gas embolism (AGE) was classically described during submarine escape training, in which pulmonary barotrauma occurred during free ascent after breathing compressed gas at depth. Pulmonary barotrauma and gas embolism due to breath holding can occur after an ascent of as little as one meter. AGE has been attributed to normal ascent in divers with lung pathology such as bullous disease and asthma. Pulmonary barotrauma can also occur as a result of blast injury in or out of water, mechanical ventilation, penetrating chest trauma, chest tube placement and bronchoscopy.
Venous gas embolism (VGE) occurs commonly after compressed gas diving. Normally, VGE bubbles are trapped by the pulmonary capillaries and do not cause clinical symptoms. However, in large volumes, VGE can cause cough, dyspnea and pulmonary oedema, and may overwhelm the capacity of the pulmonary capillary network, allowing bubbles to enter the arterial circulation. VGE can also enter the left heart directly via an atrial septal defect or patent foramen ovale.
Causes of gas embolism other than diving include accidental intravenous air injection, cardiopulmonary bypass accidents, needle biopsy of the lung, haemodialysis, central venous catheter placement or disconnection, gastrointestinal endoscopy, hydrogen peroxide irrigation or ingestion, arthroscopy, cardiopulmonary resuscitation, percutaneous hepatic puncture, blowing air into the vagina during oro-genital sex and sexual intercourse after childbirth. Air embolism can occur during procedures in which the surgical site is under pressure (e.g. laparoscopy, transurethral surgery, vitrectomy, endoscopic vein harvesting and hysteroscopy). Massive VGE can occur due to passive entry of air into surgical wounds that are elevated above the level of the heart (such that the pressure in adjacent veins is sub-atmospheric). This has classically been described in sitting craniotomy, but has also occurred during cesarean section, prostatectomy using the radical perineal and retropubic approaches, spine surgery, hip replacement, liver resection, liver transplantation and insertion of dental implants.
Clinical deficits can occur after intra-arterial injection of only small volumes of air. Intravenous injection is often asymptomatic. Injection of up to 0.5-1 ml/kg has been tolerated in experimental animals. In humans, continuous IV infusion of oxygen at 10 ml/min has been reported as well tolerated, while 20 mL/min caused symptoms. Compared with constant infusions, injections of air are more likely to cause clinical abnormalities.
There are several possible mechanisms of injury, including intra-cardiac ‘vapour lock', with resulting hypotension or acute circulatory arrest, and direct arterial occlusion. Animal studies using a cranial window have demonstrated that bubbles can cause a progressive decline in cerebral blood flow even if without vessel occlusion. This effect appears to require neutrophils, and may be initiated by bubble-induced endothelial damage. In some cases of cerebral AGE there is clinical improvement followed by delayed deterioration a few hours later. Proposed mechanisms for this include oedema, bubble re-growth and secondary thrombotic occlusion.
Manifestations of arterial gas embolism include loss of consciousness, confusion, focal neurological deficits, cardiac arrhythmias or ischaemia. Venous gas embolism can manifest as hypotension, tachypnea, hypocapnia, pulmonary oedema or cardiac arrest. AGE in divers with a pre-existing inert gas load (due to a dive) can precipitate neurological manifestations that are more commonly seen with DCS, such as paraplegia due to spinal cord damage. While imaging studies sometimes reveal intravascular air, brain imaging is often normal even in the presence of severe neurological abnormalities. Findings that support the diagnosis of AGE include evidence of pulmonary barotrauma, and evidence of intravascular gas using ultrasound or direct observation (e.g. aspiration of gas from a central venous line).