Venous Air Embolism

Venous air embolism (VAE) is entrainment of air into the venous system through an open vein at a level higher than the heart, with air travelling to the right heart and pulmonary circulation. It can cause haemodynamic collapse.

Epidemiology. The incidence depends on the procedure: up to 25% to 75% on echocardiography in sitting position neurosurgery, 10% to 40% in posterior fossa surgery, and clinically significant events in about 1 in 100 to 1 in 1,000 laparoscopic, caesarean, orthopaedic and cardiac procedures. Lethal volume is estimated as 3 to 5 mL/kg, and rapid infusion of 100 mL/s can be fatal.

Risk factors. Operative site higher than the heart (neurosurgery in sitting position, head and neck, spine in prone position), hypovolaemia, central venous catheter insertion or removal, laparoscopy (gas insufflation), caesarean section, large veins open to atmosphere (dural sinuses), hysteroscopy and pressurised fluid lines.

Pathophysiology.

Air enters a vein when venous pressure falls under atmospheric pressure. In the right ventricle air forms a froth (airlock) that obstructs outflow and pulmonary vessels, causing pulmonary hypertension, right heart strain, reduced output and ventilation perfusion mismatch. Paradoxical embolism through a patent foramen ovale causes stroke.

Sudden fall in end tidal carbon dioxide, hypotension, tachycardia, arrhythmia, hypoxaemia, rising pulmonary artery pressure, a mill wheel murmur (rare and late), wheeze, chest pain in an awake patient, gasping and cardiac arrest.

Red flags.

• Abrupt fall in end tidal carbon dioxide (over 2 to 3 mmHg).
• Hypotension with hypoxaemia.
• Neurological deficit (paradoxical embolism).

Transoesophageal echocardiography is the most sensitive (detects 0.02 mL/kg). Precordial Doppler (right parasternal) is the most sensitive non-invasive test. Capnography change is a practical indicator. Aspiration of air from a central line confirms. Chest radiograph or CT shows air in the right heart.

Differential diagnosis.

• Pulmonary embolism.
• Cardiac tamponade.
• Anaphylaxis.
• Tension pneumothorax.
• Myocardial infarction.
• Haemorrhage.

Stop air entry: flood the surgical field with saline, cover the open vein with wet swabs, apply pressure to the neck veins (jugular compression), lower the surgical site to the level of the heart or lower, and close any open line.

Stop nitrous oxide, give 100% oxygen, and support circulation.

• Position the patient left lateral decubitus with head down (Durant manoeuvre) if feasible; this has limited evidence and should not delay other actions.
• Aspirate the air through a central line (a multi-orifice catheter positioned at the junction of superior vena cava and right atrium) if present.
• Fluid bolus 500 mL to 1 L crystalloid to raise venous pressure.
• Adrenaline: 10 to 100 microgram IV, then 0.02 to 0.2 microgram/kg/min; monitor ECG and arterial pressure; avoid excess in ischaemia.
• Noradrenaline: 0.05 to 0.5 microgram/kg/min; maximum 1 microgram/kg/min; monitor arterial pressure.
• Start chest compressions for arrest.

Hyperbaric oxygen (2.4 to 2.8 atmospheres absolute for 4 to 6 hours initially, by specialist) benefits cerebral or paradoxical embolism and sometimes massive VAE.

Prevention. Position the patient with the operative site as low as feasible, maintain euvolaemia, use positive end expiratory pressure with caution, use a central line for aspiration in sitting craniotomy, monitor with Doppler or transoesophageal echocardiography, and flush all lines of air. Place the patient flat for central line insertion and removal (supine or head down) with occlusive dressing for 24 hours after removal.

Monitoring. End tidal carbon dioxide, ECG, arterial pressure, saturation, and neurological examination after recovery.

Referral and escalation. Critical care and hyperbaric service. Neurology for neurological signs.