This document discusses cerebral gas embolism, including two case studies. It covers the etiology, pathophysiology, clinical features, management, and prognosis of both arterial and venous gas embolism. Arterial embolism can result from direct gas entry into arteries or paradoxical embolism through a PFO. Venous embolism occurs when bubbles retrogradely ascend veins and enter the cerebral venous system. Clinical features include neurological deficits. Management involves laying the patient flat, hyperbaric oxygen therapy, and treating complications. Prognosis depends on factors like volume of air and speed of accumulation, with earlier treatment leading to better outcomes.

1. Cerebral Gas Embolism
Naresh Mullaguri MD
Neurocritical care

2. Disclosures
NONE

3. OBJECTIVES
❖ CASE SCENARIOS
❖ ETIOLOGY
❖ PATHOPHYSIOLOGY OF ARTERIAL AND VENOUS GAS EMBOLISM
❖ CLINICAL FEATURES
❖ MANAGEMENT
❖ PROGNOSIS

5. CASE 1
- 73-year-old man presented to the ER with acute onset left-
sided weakness, facial droop, and hemineglect. NIHSS was
16.
- 15 min before the onset of symptoms, he was undergoing
sclerotherapy for varicose veins.
- Computed tomographic angiography revealed an air
embolism within the right middle cerebral artery causing
occlusion of the superior branch of the middle cerebral
artery
- The patient was taken emergently to IR where the air
embolus was suctioned out by the neurointerventionalist.
- Echocardiogram revealed a left-to-right shunt consistent
with a PFO.
- The patient's National Institutes of Health stroke scale
score after than intervention dropped to 3.
- One week after discharge, the patient had mild dysarthria
and left facial weakness with resolution of all other
deficits.Belton 2016

6. NEUROIMAGING

7. CASE 2
- 32-year-old female was admitted to the medical intensive care unit from a long-term
acute care facility with a chief complaint of acute on chronic respiratory failure
requiring 100% FiO2.
- PMH - intravenous heroin and cocaine abuse, MSSA tricuspid valve (TV) infective
endocarditis on vancomycin, PFO, septic pulmonary embolism (PE) with cavitation,
tracheostomy with chronic ventilator dependence, multifocal cerebral infarction,
hepatitis C, nephrolithiasis, anxiety, and depression.
- Computerized tomography (CT) of the chest was unremarkable for PE, left lower
lobe collapse, and improving lung cavitation. She was being evaluated for valve and
PFO repair.

8. TTE with bubble study

9. - TTE showed normal EF, dilated RV, elevated RVSP (45 mm Hg) and RAP (15 mm Hg),
along with 4+ TR with a highly mobile TV vegetation.
- On day three, her oxygen requirements increased and required inhaled epoprostenol with a
good response. On day four, she developed hypotension with blood pressure of 78/43 mm
Hg.
- 1L of LR bolus was administered with a pressure bag into a midline peripheral access at
2315 pm. Bolus was finished at 1200 am and the patient’s neurological exam was
unremarkable.
- At 0025 am, she became unresponsive with a roving gaze, sluggishly reactive pupils,
decerebrate posturing, cyanotic with persistent hypotension requiring vasopressors.
- CT scan of the brain was obtained which showed diffuse arterial and venous cerebral
air embolism.

10. - She was laid flat and 100% oxygen was administered. Air embolism resolved by
the next day on the follow up CT scan of the brain but her neurological exam did
not improve.
- Her pupils were fixed and non-reactive the following day. She was managed
medically with hyperventilation, hyperosmolar therapy, and with head elevation.
- Magnetic resonance imaging (MRI) of the brain showed global anoxic injury and
flattening of the globe at the optic nerve insertion suggestive of intracranial
hypertension.
- She subsequently developed diabetes insipidus, which was managed with
vasopressin infusion. Given her poor prognosis, the family opted for comfort
measures and she died on day 4.

12. EPIDEMIOLOGY

13. - Documented cerebral gas emboli are rare, with the reported incidence of symptomatic cerebral
gas embolism requiring HBOT ranging from 2.5 per 100 000 hospital admissions in Paris and
Melbourne to even fewer according to reported data for the UK from the British Hyperbaric
Association
- Data about air embolism in general gained from the Case Mix Programme of the Intensive
Care National Audit And Research Centre reported 4.5 cases per 100 000 ICU admissions,
or six cases per year with an admission diagnosis of venous air embolism, arterial air
embolism, or both

14. ETIOLOGY

15. 25%
21%
15%
12%
11
%

18. PATHOPHYSIOLOGY

21. Microscopic bubbles can occur
● during the PFO test
● angiography (heart, brain)
● ECMO and heart-lung-machines
Macroscopic air embolism happens in
● Central venous access (push and pull!)
● Biopsies and other pulmonary procedures
● Endoscopy (mostly EGD)
● brain surgery (posterior fossa mainly due to the
sitting position)

22. Cerebral arterial gas embolism
1. Direct entry of gas into the cerebral arterial system (i.e. during
angiography)
2. Pulmonary barotrauma resulting in gas in the pulmonary veins
subsequently entering the left heart
3. Paradoxical emboli, whereby a venous embolism enters the arterial
system via an intracardiac right-to-left-shunt (e.g. patent foramen ovale)
or pulmonary arteriovenous malformations
4. By overwhelming the pulmonary capillary filter mechanism

23. Cerebral Venous air embolism
- Retrograde embolism, as a result of peripheral venous
air bubbles ascending against venous flow and entering
the cerebral venous system instead of the pulmonary
circulation.
- Bubble size is vital for retrograde embolism. Larger
the bubble greater the buoyancy and potential for
retrograde embolisation and subsequent infarction.
Lack of jugular venous valves is another risk factor.
- Mechanism can be potentiated by preexisting
pulmonary hypertension, severe tricuspid
regurgitation and venous stasis.

24. CLINICAL FEATURES
Mirski et al 2007

25. Wong et al 2017

26. MANAGEMENT

27. Mirski et al 2007

28. Mirski et al 2007

29. Muth et al 2000

30. Muth et al 2000

31. Recompression therapy with Hyperbaric Oxygen
- 100% FiO2 at higher atmospheric pressures. A PaO2 level of 2000mm Hg is achieved.
- Displaces N2 from the bubble. Higher O2 carrying capacity of Plasma helps with
ischemia.
- It may help prevent cerebral edema by reducing permeability of blood vessels while
supporting the integrity of blood brain barrier.
- It diminishes adherence of leukocytes to the damaged endothelium.
- First line therapy for Cerebral arterial gas embolism. Good prognosis when treated
early.
- Of 441 (78%) patients with arterial gas embolism, 346 recovered fully when treated with
HBOT, with only 20 (4%) dying, compared with 74 of 288 (26%) patients receiving no
recompression therapy fully recovering and 52% dying11; reports demonstrated its efficacy
even when treatment is delayed up to 21 hours.

32. Prognosis

33. - Earlier studies reported 80-90% morbidity and mortality, but this number has been more
recently reported at closer to 21% given earlier recognition and treatment when air embolism
suspected.
- Higher volumes of embolic air, rate of embolic air accumulation, importance of affected
cerebral territory, focal motor deficits (especially hemiparesis), presence of Babinski sign,
presence of gyriform air, initial disturbance of consciousness, older age, and retrograde
ascension of venous air have all been associated with worse prognosis.
Bessereau et al; cheng et al & Mirtchev et al