Describe the management of a patient you suspect of having developed an intraoperative air embolism
Air embolism is an iatrogenic ingress of air into the vascular system. Air is by far the most common gas which may cause embolism. However, embolism may occur following the use of other gases such as carbon dioxide (laparoscopy) and nitrous oxide. Venous air embolism is the most common. Arterial air embolism can occur as a result of air crossing into the systemic circulation via heart defects or pulmonary shunts. Other causes of arterial air embolism involve direct cannulation such as in cardiac surgery or angiography.
Air embolism should be suspected in any operation where large veins are exposed above the level of the heart; e.g. thyroid, mastectomy, head and neck surgery. Confirm if possible. Can bubbles be seen in the wound? Can froth be squeezed from the veins?
Signs and symptoms
• There is visible evidence of air being sucked into veins.
• Significant embolism leads to tachycardia, hypotension and tachypnoea.
• There is gasping respiration (if breathing spontaneously). A 10% obstruction to the pulmonary circulation can cause a gasp reflex.
• There is an unexplained fall in end-tidal (ET) CO2 due to an increase in physiological dead space and intrapulmonary shunting.
• ECG abnormalities described include signs of right ventricular strain, atrioventricular block, tachyarrhythmias, ST-segment elevation or depression, and non-specific T-wave changes.
• There is an unexplained fall in blood pressure or dysrhythmias. The compressible air causes obstruction to the right ventricular ejection at the level of the pulmonary outflow tract. This particularly occurs following a bolus air embolism. Slower infusions of air become trapped at the level of the pulmonary arterioles, causing pulmonary hypertension and subsequent right ventricular failure. More gradual air entrapment results in micro-emboli entering the circulation. These not only obstruct flow, but neutrophils, fibrin, red blood cells, fat globules and platelets build up around the bubble. The resulting ultrastructural damage leads to increased basement membrane permeability and pulmonary oedema.
• A change in heart sounds (‘mill wheel’ murmur) is a very late sign.
• Central venous pressure (CVP) is elevated in 25% of patients and pulmonary artery pressure (PAP) rises by 50%. Arterial blood gases may reveal hypoxaemia and, less commonly, hypercarbia.
• Doppler (if available) is exceedingly sensitive.
Differential diagnosis
• If respiratory symptoms predominate, consider pulmonary embolism, pneumothorax, bronchospasm and pulmonary oedema.
• If cardiovascular signs predominate, consider a cardiogenic shock, hypovolaemia, myocardial failure and septic shock.
Treatment
Immediate resuscitative measures should be initiated following the principles of ‘ABC’.
If blood pressure is normal:
1. The surgeon should squeeze the wound to prevent further air entry and/or flood the operative site with normal saline.
2. Occlude veins proximal to the site of entry.
3. Lower the operative site below the level of the heart.
4. Institute intravenous volume loading to elevated venous pressure.
5. Increase intrathoracic pressure with a Valsalva manoeuvre, thus reducing venous return.
6. If possible, express bubbles through the wound. If during laparoscopy, cease insufflation.
7. Give 100% oxygen. Stop nitrous oxide. Nitrous oxide is 34 times more soluble than nitrogen and will diffuse rapidly into the bubble, increasing its size. Administering 100% oxygen will increase the partial pressure of oxygen in the blood and tissues, favouring nitrogen diffusion out of bubbles and into alveoli, leading to nitrogen washout.
If blood pressure is reduced:
As above, plus:
• Cardiopulmonary resuscitation may be required.
• If a CVP line is in situ, try to aspirate air from the right atrium. The optimum site for the CVP catheter tip is in the right atrium 2cm below the junction with the superior vena cava.
• Place the patient in the left lateral decubitus position to overcome the airlock within the right ventricle by positioning it superior to the right ventricular outflow.
• Inotropic agents will increase cardiac contractility and may help improve cardiac output and systemic blood pressure, overcoming increased pulmonary vascular resistance. With a massive air embolism, air can be removed from the pulmonary artery at thoracotomy or the patient can be placed on cardiopulmonary bypass as a last resort.