Gas Embolism

• Neurosurgery
• Particularly sitting position for craniotomy
• Particularly if cranium and dura involved
• When looked for, there is venous air embolism in 100% of seated craniotomies


• Obstetrics
• Can occur in 40% of LSCS


• Laparoscopic surgery due to direct intravascular gas insufflation or CO₂ embolism


• Head and neck surgery, due to large areas of tissues exposed with vessels at sub-atmospheric pressure


• Orthopaedic surgery
• Cementing and reaming in long bone surgery e.g. 30% incidence in hip replacements
• Anterior cervical discectomy up to 10%
• Described during shoulder arthroscopy (BJA, 2000)
• Polytrauma patients


• Central line insertion, which is under the spotlight following a recent coroner's report on such a case

• Air crossing from venous to arterial circulation via cardiac or other transpulmonary shunts
• Direct cannulation of arterial vasculature e.g. cardiac surgery, angiography
• Carotid endarterectomy

• VAE has a broad range of clinical features that will depend on the volume of gas and rate of entrainment into the circulation, although cardiovascular features predominate


• In 'boluses' of air, the air embolus acts as an intra-cardiac air lock
• The air embolus prevents ejection of blood from the right ventricular outflow tract


• During slower 'infusions' of air, smaller bubbles instead become lodged in the pulmonary arterioles
• This leads to massively increased pulmonary vascular resistance, pulmonary hypertension and fulminant right heart failure
• There may also be ultrastructural damage as neutrophils are attracted to the cellular material which builds up around the bubbles, eventually leading to pulmonary oedema

• Tachypnoea
• Shortness of breath/difficulty in breathing
• Arterial desaturation
• Stepwise fall in EtCO₂ due to increase in physiological dead-space


• Differentials include pulmonary embolism, pulmonary oedema, bronchospasm, pneumothorax

• Chest pain
• Hypotension
• Tachycardia ± dysrhythmia


• Elevated CVP (25%) and/or PA pressure (50%)
• Precordial 'millwheel murmur'


• ECG
• Tachyarrhythmias
• AV nodal block
• Right ventricular strain pattern due to RV failure e.g. non-specific T-wave inversion
• Non-specific ST-segment and T-wave changes


• Differentials include haemorrhage/hypovolaemia, septic shock, cardiac failure, anaphylaxis

• The awake patient may notice light-headedness and a sense of impending doom
• The anaesthetised patient may demonstrate slow awakening
• Large emboli may cause:
• Altered mental status
• Focal neurological deficits
• Decreased conscious level

• End-arterial obstruction can cause significant tissue injury


• Coronary arteries - essentially mimics MI but may be a global phenomenon rather than territorial


• Cerebral arteries
• Initially headache, confusion, minor motor weakness
• Delayed awakening in the anaesthetists patient
• Progressing to disorientation, hemiparesis, convulsions and coma
• Abnormally cardiorespiratory patterns due to involvement of brainstem centres


• Coeliac axis; abdominal pain and gut ischaemia

• Consider screening patients for PFO prior to high-risk procedures
• Identify patients undergoing at-risk procedures associated with VAE
• Good communication e.g. during team brief

• Clear communication amongst the theatre team
• Use of monitoring devices (see below)
• Keep negative pressure gradient between operative site and RA to a minimum by maintaining high-normal RA and CVP
• IV fluid loading
• ± higher PEEP


• Meticulous intra-operative haemostasis
• Minimise time during which venous circulation is left open to atmospheric pressure


• Ensure CVC insertion site below level of RA (i.e. higher venous pressure) during procedure
• Ensure fluid administration sets are free from air

• Clinical features are a non-specific and late sign of VAE and therefore high risk cases necessitate use of detection devices
• They vary in their sensitivity and specificity to detect intracardiac air

• TOE is the most sensitive measure
• It allows localisation of air to a specific cardiac chamber, and allows assessment of cardiac function
• However, it is invasive, expensive, requires expertise and associated with complications e.g. oesophageal injury


• Precordial Doppler is the most sensitive non-invasive monitoring device for detection of VAE
• It is placed in the right parasternal region


• EtCO₂ will decrease with VAE due to an increase in dead-space ventilation
• Setting tight alarms may allow earlier detection
• Measuring EtN₂ is more sensitive and specific than EtCO₂, demonstrating a sudden increase in EtN₂ when nitrogen present in the air embolus is expelled by the lungs


• PA catheters are not sensitive, invasive and not routinely used


• An oesophageal stethoscope may detect the classic 'mill-wheel' murmur of VAE
• However, a significant volume of air has to be entrained before the murmur is heard and by that point there is often already cardiovascular collapse
• With more sensitive options available, it is seldom used


• CT or MR imaging may reveal intracerebral air and, subsequently, the development of hypodense lesions, which can be difficult to differentiate from cerebral infarction and is impractical for intra-operative use

VAE is an anaesthetic emergency, and I would seek senior anaesthetic support as well as making a rapid but thorough assessment of the patient

• The immediate management priorities are to:
1. Prevent further air ingress
2. Reduce the size of the embolus
3. Overcome mechanical RV obstruction

• Stop the surgeon, asking them to stop further air embolization by:
• Compressing or covering the surgical site, or
• Flooding the surgical site with saline, or
• Emptying the relevant cavity to reduce pressure e.g. uterine cavity during LSCS
• Stop insufflation of gas e.g. during laparoscopy


• Further air ingress can be reduced by increasing venous pressure:
• Position entry site lower than the heart
• Administer IV fluids
• Performing a Valsalva manoeuvre
• Increasing intrathoracic pressure e.g. adding PEEP

• Administer 100% oxygen
• Stop N₂O, which may increase the size of the gas bubble
• Aspirating air from the RA via CVC
• May be possible if large bubble, but requires CVC in situ with tip in RA
• Should not routinely insert a standard CVC to manage air embolus if not already in place

• Tilt head-down and left-lateral may prevent bubble embolising into pulmonary artery (Durant manoeuvre)
• Judicious use of fluid and inotropic agents to support the RV against a raised PVR
• E.g. Dobutamine 5 - 20μg/kg/min or adrenaline 0.05 - 0.1μg/kg/min

• Consider putative management options such as:
• CPB ± removal of air from the pulmonary artery via thoracotomy
• Hyperbaric oxygen therapy (BJA, 2018)
• IR-guided aspiration


• Discuss with senior colleagues about feasibility of continuing surgery
• Plan for HDU care post-operatively; may need organ support to manage the subsequent SIRS-like 'air embolism syndrome'


• Documentation in the notes
• Clinical incident form
• Fulfil duty of candour

• Lethal dose varies by volume of gas embolus relative to patient, and speed of air ingress
• In humans approximately 1ml/kg is lethal
• Rapid air entry is worse


• It carries a high morbidity and mortality
• 43% of survivors have neurological deficits at time of ICU discharge