Venous gas embolism blue book article and *hyperbaric medicine blue book article

Question 1

Why is the presentation of VGE so variable, from asymptomatic to cardiac arrest to catastrophic brain injury or death?

Answer 1

absolute quantity of gas varies
type of gas (most commonly air) varies
end location may be venous, pulmonary or arterial
the area impacted may have varying collateral circulation
metabolic requirements & susceptibility to vascular inflammatory changes vary

Question 2

How may venous gas embolism subsequently arterialise (paradoxical embolisation)?

Answer 2

via intra-cardiac (PFO, ASD) or intra-pulmonary (overwhelming the filtration capability of pulmonary capillaries or via intrapulm A-V anastomoses) shunting

Question 3

What types of procedures may risk direct arterial gas embolism?

Answer 3

cerebral angiography
open chamber cardiac surgery
bypass circuit accidents
extremely rarely via atrial-oesophageal fistulae

Question 4

What are the preconditions for entry of gas into the venous system? And what are other causes of venous gas embolism related to surgical procedures?

Answer 4

opening of non-collapsing veins to atmosphere
sub-atmospheric pressure within the vessels

situations where the surgical site is under pressure
surgical wound situated above the level of the heart, enabling passive air entry (eg. shoulder)
veins within a coagulated operative field may allow entry of air
air may enter through CVC or haemodialysis catheters, mainly on insertion removal but potentially due to detachments/breaks in the lines
myometrial veins during pregnancy & after delivery are particularly susceptible to air entrainment.

Question 5

Examples of non-collapsing veins?

Answer 5

epiploic
emissary
dural venous sinuses

Question 6

At what flow rates are the majority of bubbles able to be filtered by pulmonary capillaries?

Answer 6

up to 10mL/min

Question 7

What’s the sequence of events with a rapid or large volume of air entrained into venous circulation?

Answer 7

raised pulmonary artery pressure
increased RV preload
acute RV failure & reduced output
impaired pulmonary venous return/LV preload/CO & organ perfusion; cardiovascular collapse; tachy or bradyarrhythmias may develop

Due to the altered pulmonary resistance, R) -> L) intrapulmonary shunting & incr alveolar dead space ventilation, V/Q mismatch & hypoxaemia ensue

Question 8

How may cerebral arterial gas embolism (CAGE) occur?

Answer 8

direct injection of gas into cerebral arterial system during angiography or paradoxical embolism via intracardiac, intrapulmonary or other shunting.
pulmonary barotrauma can enable entry of gas into pulmonary veins, L) hear & subsequently cerebral circulation.

Question 9

Why & how is CAGE a biphasic phenomenon?

Answer 9

initial temporary neurologic dysfunction due to transient lodgement of bubbles in the cerebral circulation
most are cleared into the jugular veins (relatively high cerebral arterial systolic pressure, almost two-fold greater diameter of the venous end of a cerebral capillary cf the arterial end (bubbles sucked through capillaries into the veins))
Then, 65% get a secondary deterioration which may be several hrs later, due to interaction btwn gas bubbles & vessel walls (eg. endothelial damage, activation of clotting cascade)–> vascular inflammation, secondary thrombotic occlusions & oedema, secondary vasospasm.

Question 10

What happens if bubbles are distributed to brainstem?

Answer 10

cardiorespiratory arrest

frequently fatal

Question 11

What are some of the signs of cerebral gas embolism? and pulmonary?

Answer 11

Usually rapid onset: confusion, stupor, headache, vertigo, dizziness, focal neurological deficits (motor, sensory, speech, visual field defects mimicking stroke), gait disturbance, loss of consciousness.

Chest pain, shortness of breath, cardiac arrest.

Question 12

In which situations (which make up approximately 30% of cases of arterial gas embolism) is ischaemia, infarction & symptoms consistent with a stroke syndrome more likely to occur?

Answer 12

larger intra-arterial cerebral bubbles particularly within loop and anastomotic vessels which are subject to systolic pressure @ both ends or bubbles occupying many generations of arterioles

Question 13

How to prevent & diagnose vascular gas embolism?

Answer 13

Clinical diagnosis

High index of suspicion & attention to physiologic variables during procedures for which vascular embolism is a known risk

Consider surgical position, consider pre-op workup (eg. TTE or TOE to exclude PFO before seated craniotomy)

DISCUSS RISK PRIOR TO PROCEDURE & DURING TIME-OUT

Aim to maintain preload (minimise air entrainment)

Care re: pt positioning & monitoring (eg. lower threshold for art line)- head-down for CVCs, minimise time with open connections, pt should breathe all the way out when insert

Be attentive to the sound of sucking in of air or visible entrainment through lines or cannulae

Be vigilant particularly at key risk points of the procedure- maintain excellent communication with surgeon- 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)- may detect 0.5mL/kg venous air

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
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 & multi organ failure

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

Question 14

are cardiopulmonary symptoms (eg, tachypnoea, hypocapnia, pulmonary oedema, cardiac arrest) more common with venous or arterial air embolism?

Answer 14

venous

Question 15

How does symptom onset & type vary with arterial vs venous?

Answer 15

immediate onset if gas injected directly into arterial system- more often confusion, LOC, focal neurological deficits, cardiac arrhythmias or ischaemia.
venous air arterialising is a slower process; symptoms rely on increase in pulm artery pressures & incr R) heart pressures

Question 16

What’s the gold-standard for detection of air embolism? is there a threshold of intra-vascular air which is significant?

Answer 16

TOE (can detect as little as 0.02mL/kg of air)

no threshold since the outcome of vascular gas embolism depends on the vessels lodged into & other factors

Question 17

What’s the role of cerebral radiological imaging for CAGE?

Answer 17

only to exclude other causes that might present like AGE (eg. intracerebral haemorrhage)
high false -ve rate for CAGE even if severe neurological deficits, imaging should NOT be relied on for diagnosis
in cases highly suggestive of CAGE (eg. high-risk procedure), imaging is not recommended as it delays time to definitive Rx (recompression)

Question 18

Management for iatrogenic vascular gas embolism?

Answer 18

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 19

Is trendelenburg routinely recommended? why? what positions recommended in certain circumstances?

Answer 19

No. theories about mechanisms not experimentally confirmed, trendelenburg risks worsening cerebral oedema (a big risk given that large air emboli increase ICP from 12-52mmHg within 2 hrs of insult)

HOWEVER, if sudden RVOTO by gas embolism, immediate placement into L) lat decubitus & trendelenburg may relieve air-lock & move air into RA.

If the pt awake with protected airway, place supine
if unconscious with unsecured airway, lateral decubitus

Question 20

What’s the only definitive Rx for arterial gas embolism?

Answer 20

Hyperbaric oxygen treatment. There’s an AHA class 1 recommendation (level C evidence) for this indication

many studies show improved neurological outcomes, neurophysiological studies & neuro-psychometric testing among pts with arterial gas embolism treated with hyperbaric O2

Question 21

How soon after an air embolism event should hyperbaric oxygen be delivered? Is it, however, recommended for isolated venous gas embolisation?

Answer 21

ASAP- better neurological outcome if within 8 hrs of CAGE. Even if pt appears to have spontaneously recovered, early HBOT still recommended given can be biphasic, later benefits may occur with modulation of post-bubble vascular inflammatory changes.

Evidence for HBOT in isolated venous gas embolism is less clear; not recommended for asymptomatic venous gas embolism.

Question 22

How does HBOT work?

Answer 22

reduces gas bubble volume by increasing ambient pressure (Boyle’s law; P1V1=P2V2)
this allows the bubbles to be resolves or redistributed, restoring blood flow.

As per Henry’s law (C = kP), HBOT increases the solubility of the culprit gas, enabling resorption & increasing the amount of dissolved oxygen, improving tissue oxygenation.

Hyperoxia creates a diffusion gradient of O2 into gas bubble & N2 out (it eliminates inspired O2). Rate of bubble resolving depends on the diffusion of nitrogen out of the bubble & transport of dissolved gases to lungs.

HBOT also reduces leucocyte adhesion to damaged endothelium, reduces inflammation & limits ischaemia-reperfusion injury.

Question 23

What’s the dose for hyperbaric treatment of air embolism? why this dose? How many treatments?

Answer 23

compression with 282kPa, breathing 100% O2

this dose causes rapid bubble volume reduction, acceptable risk O2 toxicity & is safe for nurse attendant wrt nitrogen narcosis & decompression illness
short & cheap Rx

generally 1-3 treatments until response plateau reached & maintained

Question 24

What’s the recommendation for lignocaine in AGE? What dose use? possible mechanisms?

Answer 24

Class IIa AHA recommendation, level B evidence

Good evidence in animal studies.

If used, aim for a serum lignocaine [] of 2-6microg/mL, consistent with an anti arrhythmic effect

cerebral neuro protection, reduces leucocyte migration, modulates haemodynamic parameters

Question 25

*what’s 1atm in mmHg, PSI, bar, kPA?

Answer 25

downward pressure exerted by the weight of the atmosphere above
760mmHg
1.47psi
1.01 bar
101.3kPa

or 10msw

Question 26

what are typical treatment pressures for hyperbaric oxygen treatment?

Answer 26

100-180kPA

Question 27

What’s Henry’s Law? Boyle’s? Charles?

Answer 27

The amount of gas dissolved in a given volume of liquid is directly proportional to the partial pressure of that gas in equilibrium with that liquid

as pressure increases, the volume of a bubble/airspace decreases (p1v1=p2v2)- this is the basis for hyperbaric Rx of decompression illness (due to nitrogen bubbles) or CAGE but is the crux of middle ear barotrauma (relatively common complication of hyperbaric O2)

increased temp within chamber during pressurisation & decrease temp during decompression- hyperbaric chambers have air temp controls to control for these changes

Question 27

*What are physiological effects of hyperbaric O2 Rx?

Answer 27

• Increased DO2 (increases access of oxygen by tissues, via plasma)- role in decompression injury, arterial gas emboli, wound healing, acute crush injury, ischaemic grafts & flaps, arterial occlusions, severe blood loss anaemia
• wound healing- DO2, stimulates angiogenesis, vasculogenesis & mobilisation of stem cells (endothelial progenitor cells), anti-infective & anti-inflammatory effects
• reduced volume of gas bubbles (by raising ambient pressure & creating enormous diffusion gradient for O2 in & N2 out of the bubble)- beneficial for decompression illness (nitrogen coming out of solution & forming bubbles), or AGE
• peripheral vasoconstriction due to decreased NO (scavenged by ROS produced during hyperbaric hyperopia)- it reduces blood flow without compromising O2 supply, allows capillaries to absorb extra fluid, reduces oedema- useful therefore for crush injury, compartment syndrome, thermal burns, threatened flaps & grafts
• osmosis & reduction in oedema: O2 reduces oedema by ceasing the Na/K pump failure which happens with hypoxia (& subsequently –> oedema from loss of intracellular fluid)
• modulates ischaemia-reperfusion injury (decreased production & increased degradation of ROS), maximal benefit during the ischaemic phase
• infection control- useful in necrotising soft tissue infections, gas gangrene (inhibits the clostridial alpha-toxin), osteomyelitis, life or limb-threatening infections; HBOT is directly toxic to anaerobic bacteria & antibiotic to aerobic bacteria, has bacteriostatic & bactericidal effects on clostridia, E. coli & pseudomonas.

Question 28

*What proportion of the population have a PFO? what volume of gas (bolus) or continuous introduced into v venous system may generate intra-arterial bubbles?

Answer 28

30%

20mL bolus or 11mL/min

Question 29

*current indications for HBOT?

Answer 29

• Air or gas embolism
• Arterial insufficiencies
– Central retinal artery occlusion
– Enhancement of healing in selected problem wounds
-Carbon monoxide poisoning
• Clostridial myonecrosis (gas gangrene)
• Compromised grafts and flaps
• Acute traumatic ischaemia
• Decompression sickness
• Delayed radiation injuries (soft tissue and bony necrosis)
• Sudden sensorineural hearing loss
• Intracranial abscess
• Necrotising soft tissue infections
• Refractory osteomyelitis
• Severe anaemia
• Thermal burns

Question 30

*absolute contraindications to HBOT?

Answer 30

-Untreated pneumothorax is the only absolute contraindication to HBOT: intrapleural air may double or triple in volume on decompression as normal atmospheric pressure is approached.
Others listed in blue book article:
-Premature infants: due to susceptibility to retrolental fibroplasia, resulting in blindness
-Bleomycin: a chemotherapy agent used to treat a variety of tumours, which has been associated with irreversible restrictive lung disease. Oxygen breathing, even several years after the use of bleomycin, can cause severe interstitial pneumonitis leading to pulmonary fibrosis, and severe lung damage can occur.
-Disulfiram (Antabuse): blocks production of superoxide dismutase, a protective antioxidant which is the body’s major protection against oxygen toxicity
-Cisplatin: HBOT may increase the cytotoxic effect of the drug in tissues, ultimately impeding wound healing

Question 31

*relative contraindications to HBOT?

Answer 31

Pregnancy (now considered a reason to PURSUE HBOT in pregnancy)
Obstructive lung disease: Asthma, emphysema (may’ve pulmonary blebs or bullae) with CO2 retention
Recent ar or thoracic surgery
Upper respiratory tract infections
History of middle ear surgery or disorders
History of seizures or recent brain suegery- @ risk of complications due to CNS toxicity from high []O2
Uncontrolled fevers
Claustrophobia
Congenital spherocytosis
Optic neuritis

However, relative contraindications should NOT deter from use of HBOT to Rx severe neurological or other life or limb-threatening conditions

Question 31

*relative contraindications to HBOT?

Answer 31

Pregnancy
Asthma
Thoracic surgery
Emphysema with CO2 retention
Upper respiratory tract infections
History of middle ear surgery or disorders
History of seizures
Fevers
Congenital spherocytosis
Optic neuritis

Question 32

*complications of HBOT?

Answer 32

Claustrophobia
Hypoglycaemia
Middle ear barotrauma
Sinus squeeze
Oxygen toxicity seizure
Progressive myopia – typically reverses completely in days to weeks.
Cumulative pulmonary oxygen toxicity
Pulmonary barotrauma +/- air embolism
Exacerbation of congestive heart failure in patients with severe disease, due to:
a. Sinus bradycardia from stimulation of vagal activity and stimulation of a further measurable, nonoxygen dependent bradycardia that is associated with hyperbaric pressures.
b. Systemic vasoconstriction causing increased afterload.
Increased rate of maturation of cataracts with very long courses of HBOT.