Venous air embolism

Question 1

What are signs of venous air embolism under anaesthesia?

Answer 1

Depend on the rate & volume of air entrained & site (heart, brain, lungs particularly sensitive & small volumes of air can have significant complications)

5mL/kg considered large enough to cause “air-lock” effect in RVOT–> cardiovascular collapse
critical volume fatal in humans is unknown- estimated 200-300mL

Reduction in SpO2, reduction in EtCO2, bronchospasm, pulmonary oedema
Elevated PA pressure, elevated CVP
Air on cardiac TTE or TOE
Tachycardia, hypotension, CV collapse

Be vigilant particularly at key risk points of the procedure- culture of “speaking up” fostered, consider vascular gas embolism among interdepartmental SIM training

Look out for sudden:
hypoT (accumulating RV air–> RVOTO, acute RV failure which compromises LV output & –> CV collapse
tachycardia or bradycardia
arrhythmias or ischaemic changes on ecg (eg. air entrained into coronary circulation esp LAD)
cardiovascular collapse
pulmonary oedema or acute lung injury due to inflammatory cascade
reduced EtCO2 (due to headspace ventilation)
decreased SpO2
hypoxaemia & hypercarbia on the ABG depending on degree of V/Q mismatch
sudden sustained fall in BIS or cerebral oximetry
seizure activity
transient or persistent ST changes
“mill-wheel” splashing murmur of froth in cardiac chambers & great vessels (only with large emboli, low S&S)
may have failure to wake from GA (arterial air embolism may –> ischaemic stroke)

an awake pt: confusion, headache, stroke signs, chest pain/palpitations (may see arrhythmias or ischaemia on ecg), may pleural substernal-chest pain, tachypnoea, dyspnoea, cough, PAE typically causes signs of angina or embolic stroke. late sign= haemoptysis. abdo pain, bowel iscahemia.

May develop SIRS type syndrome & subsequent multi organ dysfunction

do not be falsely reassured by resolution of S&S (injury may be biphasic)

Question 2

What’s a paradoxical air embolism?

Answer 2

Where air entering the venous circulation moves to the arterial, eg. through an intracardiac shunt (eg, PFO) or via pulmonary circulation to heart

Question 3

What are the conditions required for gas embolisation to occur?
What are risk factors for venous air embolism?

Answer 3

source of gas, communication btwn this source & the venous or arterial system & a pressure gradient enabling the ingress of the gas. The size of the communication & the pressure gradient, volume & solubility of gas are of critical importance to the outcome- the body size is important.

Anaesthetic:

• negative pressure with spont respiration
• PEEP (paradoxical embolism)
• CVC
• pressurised infusions
• non-primed giving sets/inadvertent air injection.
• unrecognised epidural vein cannulation

Pt:

• trauma (blunt or penetrating)
• hypovolemia
• PFO
• ASD/VSD

Surgical:
procedures where operative site higher than RA & where vasculature exposed in a surgical field carries risk, addition of a pressure gradient btwn surgical site & R) heart increases the risk.
-sitting craniotomy (up to 100% incidence)
posterior fossa surgery
shoulder surgery
spinal surgery
laparoscopic surgery (CO2 embolism)
LSCS (40%)
exteriorisation of the uterus
hip arthroplasty (30%)
anterior cervical discectomy (10%)
cardiac surgery 5-25%
cardiopulmonary bypass
ECMO/insertion of assist devices
cardiac ablation
CEA
interventional radiology

Question 4

What are some preventive measures for venous air embolism? What steps may lead to early Dx & Rx?

Answer 4

Discuss high-risk surgical manoeuvres in pre-OT team briefing
Position the pt to minimise pressure gradients
Keep pt well-hydrated
Avoid N2O

Use of PPV, end tidal monitoring, central venous catheters, precordial doppler & TOE in high-risk procedures may aid early Dx & Mx

Question 5

What are the steps in management of venous air embolism?

Answer 5

1. PROMPT RECOGNITION:
   - Call for help, communicate the emergency & delegate
2. MINIMISE FURTHER AIR ENTRAINMENT:

Prevent further entrainment of gas by:

• flooding the field with irrigation fluid
• temporarily occluding the vessel
• ceasing insufflation
• decompressing any pressurised systems
• position operative site below heart
• stopping any procedures through which air may be entrained (eg. reaming of bones during ortho surgery)

3. SUPPORT AFFECTED ORGAN SYSTEMS
   - Secure airway if not already in place, ventilate w 100% O2 to maintain arterial oxygenation & facilitate de-nitrogenation & resorption of bubbles. Avoid N2O.

• maintain normovolaemia to optimise microcirciulation
• use Adr/other vasopressors/inotropes for haemodynamic support
• place L) lateral position if unconscious, trendelenburg no longer routinely recommended (risk worsening cerebral oedema, doesn’t keep bubbles from being distributed to systemic circulation)
• supine if awake or protected airway BUT if RVOTO by gas embolism, immediate placement into L) lateral decubitus & trendelenburg may relieve air lock & move air into RA
• if arrest, likely PEA or asystole

4. AIM TO HALT THE PROGRESS OF ALREADY ENTRAINED AIR
   - COULD CONSIDER aspirating CVC if in situ (emergent placement for this purpose isn’t evidence-based) & for venous gas embolism closed cardiac massage to break up large volumes of air in the cardiac chambers, forcing air into smaller vessels, improving blood flow.
5. DEFINITIVE Mx= HYPERBARIC O2:
   - after successful resus, consider hyperbaric O2 therapy & ICU

Question 6

What’s the role of PEEP in venous air embolism & when should it be used? concerns with it?

Answer 6

Can be considered along with 100% O2 only if needed to support oxygenation.
It may increase the risk of paradoxical embolism, impair venous return & with it’s sudden cessation may enhance air entrainment

Question 7

How much air in the coronaries may precipitate VF?

Answer 7

0.5mL

Question 8

When is hyperbaric oxygen considered & for how long should it be continued?

Answer 8

Consider for large paradoxical air embolism, continue it for up to 6 hrs or possibly more

Question 9

what proportion of the population have a PFO?

Answer 9

10-30%

Question 10

What is the level of risk for VAE with cardiac surgery? what measures of the modern surgical approach limit risk?

Answer 10

intermediate (5-25%)

cardiopulmonary bypass circuits with lower flow techniques

Question 11

What’s more sensitive for detecting VAE? TEE or precordial doppler? how do they compare with precordial or oesophageal stethoscope? transcranial doppler? pulmonary artery catheter?

Answer 11

TEE (can detect 0.02mL/kg venous air, while precordial doppler can detect 0.05mL/kg air), however TEE is invasive. It is the gold standard for detecting PFO & it can quantify the size of an embolus, has excellent sensitivity for VAE detection.

they have better sensitivity & specificity vs the precordial or oresophageal stethoscope which is also only able to detect mill wheel murmur with large emboli (1.5mL/kg air for precordial, 1.7mL/kg oesophageal)

both the precordial & transcranial doppler have good S&S for detecting venous air embolism- can test with agitated saline. However precordial affected by obesity, interference from diathermy, ambient noice. transcranial doppler requires a learning curve & has limited availability.

PAC can detect minimum volume 0.25mL/kg air, reasonably sensitive but limited specificity, risks with insertion, not conducive to aspirating air (can do via CVC), expensive

Question 12

What are some procedures during which VAE may occur?

Answer 12

seated craniotomy up to 100% (particularly posterior fossa procedures, most common for tutors near posterior saggital sinus)
lower incidence in p-fossa procedures not in sitting position

LSCS 40%- particularly during uterine exteriorisation, may not be clinically significant with LSCS but @ least one fatality has been reported for LSCS uterine exteriorisation

hip arthroplasty 30%

anterior cervical discectomy 10%

Question 13

with a pressure difference of 5cmH2O, how much air will be entrained per second via a 14g cannula?

Answer 13

100mL