Stroke Alert to the PACU

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The Pre-brief

As a rapid response team member or stroke team member, we are appropriately conditioned to evaluate for the most common types of strokes; the ischemic strokes caused by embolism of a blood clot and hemorrhagic strokes-but what about embolism of air?  While cerebral arterial gas embolism (CAGE) is uncommon, it is a diagnosis that must be considered in the patient who is immediately post-op or post-procedure as treatment differs from that of classic ischemic stroke.  CAGE is potentially devastating, often leading to disabling neurologic sequelae or death.  Outside of the realm of diving-related injuries, CAGE is iatrogenic and is likely underreported. It is imperative to keep CAGE on the differential diagnosis in a stroke-like patient in the peri-procedural time period.

Iatrogenic CAGE

While iatrogenic venous gas emboli likely occur on a regular basis, they are usually filtered by pulmonary capillaries and cause little to no clinical consequence.  Gas that travels to the left-sided circulation, on the other hand, can be injurious and especially so when affecting the brain.  Arterial gas emboli can occur directly from a procedural introduction or can be large volume venous emboli traveling across an atrial septal defect, patent foramen ovale, or another right to left shunt.  

Iatrogenic CAGE is a clinical diagnosis, with temporal proximity to a procedure or surgery being the critical element.  Symptoms starting immediately post-procedure should shoot CAGE to the top of the differential diagnosis.  Conversely, symptom onset further removed from a procedure makes CAGE less likely.  CAGE can manifest with transient loss of consciousness, focal neurologic deficits, aphasia, hemiparesis, and in extreme cases, coma.  While air can be evident on neuroimaging, this is not required to diagnose CAGE and the absence of air on neuroimaging should not exclude the diagnosis in an otherwise fitting clinical context.  

Non-contrast head CT of CAGE patient who became obtunded following dialysis

CAGE can occur as a complication from many procedures, with the more common culprits listed below in descending order of prevalence as reported by Hatling et al.

  1. Cardiopulmonary bypass
  2. Central venous catheter
  3. Lung biopsy
  4. ERCP
  5. Hemodialysis
  6. Mechanical ventilation
  7. Angiography

Classic teaching was to place patients with suspected CAGE in the Trendelenburg position in an effort to displace bubbles from cerebral circulation; however, this is no longer recommended given the deleterious effects of increased intracranial pressure caused by the Trendelenburg position.  In extreme cases of CAGE, cardiac arrest can occur as a result of a large volume of intra-cardiac air causing “vapor lock” and cessation of forwarding circulation of blood.  

Ischemia and Intimal Injury

Much of what we know regarding CAGE comes from historical research in submarine escape training (from which subjects unfortunately frequently had CAGE) and from animal models.2  In addition to the overt ischemia caused by bubble emboli, delayed injuries occur from a shearing effect that bubbles have on cerebrovascular intimal layers and from ischemia reperfusion injury.  The mechanical shearing effect bubbles have on vascular endothelial cells leads to a cascade in which there is an opening of transient receptor potential vanilloid (TRPV) channels, calcium influx, mitochondrial dysfunction, and subsequent cell death.  Not dissimilar from the “lucid interval” classically described with epidural hematoma, patients with CAGE often have transient improvement which is followed by a worsening decline in the hours thereafter.  This is thought to be due to progressive focal edema following the initial insult as well as ischemia-reperfusion injury.  Considering this, it is important to still pursue appropriate treatment in a suspected CAGE patient even with apparent spontaneous resolution of symptoms.    

Crushing Bubbles and CAGE Treatment

Treatment for iatrogenic CAGE is the same as for CAGE occurring in SCUBA divers, which is hyperbaric oxygen therapy (HBOT) to be initiated as soon as possible (immediate is ideal but patient may still benefit out to 24h).  The potential benefits a CAGE patient can gain from HBOT are as follows: 

  • Crushing bubbles-Following the inescapable laws of physics (Boyle’s Law in this case), bubble burden size is reduced during HBOT
  • Off gassing-The 100% O2 used in HBOT creates a gradient such that bubble size will also be reduced by off gassing to tissues.  In this vein, oxygen via facemask as an immediate, more accessible measure can also help, but to a lesser degree.
  • Oxygen for ischemic tissues-restoration of oxygenation to ischemic tissues
  • Blunting ischemia-reperfusion injury-Via pathways involving reactive oxygen species, neutrophil adhesion, and local vasoconstriction, HBOT has an overall blunting effect on ischemia-reperfusion injury

It is also of critical importance in the anesthetized patient to stop any inhaled nitrous, as this can cause bubbles to continue to grow even after the initial insult!

Of the previously explored adjunctive therapies (lidocaine, aspirin, NSAIDs, anticoagulation, steroids), lidocaine is the only therapy with reasonable data in support of its use.  It is not considered standard of care in CAGE, but a single dose of 1-2mg/kg IV can be considered.  

Lastly, just as in other types of major CNS injuries, it is important to avoid hyperthermia or hyperglycemia

The Debrief

  • In a peri-procedural, stroke-like patient, keep cerebral arterial gas embolism on the differential.
  • While intravascular air on neuroimaging is confirmatory, this is not always present.  CAGE is a clinical diagnosis with the timing of symptoms in association with a procedure (or diving) being key.
  • Physical bubble resorption as well as blunting of ischemia-reperfusion injury are how HBOT can be helpful in CAGE.
  • If feasible, treatment for CAGE is immediate HBOT

References

  1. Hatling D, Høgset A, Guttormsen AB, Müller B. Iatrogenic cerebral gas embolism-A systematic review of case reports. Acta Anaesthesiol Scand. 2019 Feb;63(2):154-160. doi: 10.1111/aas.13260. Epub 2018 Sep 10. PMID: 30203491.
  2. Moon RE. Hyperbaric treatment of air or gas embolism: current recommendations. Undersea Hyperb Med. 2019 Sep-Dec – Fourth Quarter;46(5):673-683. PMID: 31683367.
  3. Malik N, Claus PL, Illman JE, Kligerman SJ, Moynagh MR, Levin DL, Woodrum DA, Arani A, Arunachalam SP, Araoz PA. Air embolism: diagnosis and management. Future Cardiol. 2017 Jul;13(4):365-378. doi: 10.2217/fca-2017-0015. Epub 2017 Jun 23. PMID: 28644058.
  4. Francis A, Baynosa R. Ischaemia-reperfusion injury and hyperbaric oxygen pathways: a review of cellular mechanisms. Diving Hyperb Med. 2017 Jun;47(2):110-117. doi: 10.28920/dhm47.2.110-117. PMID: 28641323; PMCID: PMC6147229

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