Keywords
air embolism - cerebral arterial air embolism - endovascular flow diversion
Introduction
Symptomatic cerebral arterial air embolism (CAAE) is an unusual complication of neurointervention
procedures with an incidence of 0.08% during cerebral angiographic procedures and
0.2% during therapeutic interventional procedures.[1] Early diagnosis and management can mitigate irreversible neurological deficits.
We hereby report a rare case of CAAE during endovascular treatment of left ophthalmic
internal carotid artery (ICA) aneurysm, which was detected timely and managed with
good clinical outcome.
Case Report
A 55-year-old female presented with intermittent headache and ptosis of the left eye
for 4 months and was diagnosed with an unruptured saccular aneurysm arising from the
left ophthalmic ICA ([Fig. 1]). Endovascular management in the form of flow diversion was planned and a flow diverter,
Silk 4 mm × 25 mm (Balt, California, United States), was deployed successfully. However,
postprocedural angiogram showed multiple filling defects in the branches of the left
middle cerebral artery (MCA) as well as mobile filling defects in the superior sagittal
sinus ([Fig. 2A, B]). Immediately, pressurized arterial flush lines connected to the long sheath, guide
catheter, and microcatheter were checked. The pressure bag connected to the long sheath
was found to be empty with air in the flush line tubing. The offending arterial line
was disconnected from the system. Blood was allowed to backflow through the side port,
by keeping the proximal end of the system vertical, to allow passive extrusion of
air bubbles by arterial pressure. The system was flushed and a fresh air-free pressure
bag was connected. FiO2 was raised to 100% oxygen and mean arterial pressure was raised
above 100 mm Hg. Rapid flushing of the long sheath and guiding catheter using heparinized
saline mixed with nimodipine was done. Left ICA check angiogram done after 30 minutes
showed normal opacification of the left MCA branches ([Fig. 2C, D]). An intraoperative cone-beam computed tomography (CT) confirmed air embolism ([Fig. 3A, B]). The patient was kept intubated and intravenous dexamethasone and mannitol, antiepileptics,
and sedatives were started. Hyperbaric oxygen therapy could not be offered due to
its unavailability. Noncontrast CT head done after 24 hours showed complete disappearance
of air foci from the cerebral vessels. The patient was extubated on postoperative
day 2 and had a Glasgow Coma Scale (GCS) of 11 (E2V3M6). There was mild right hemiparesis
with a power of 4/5 in the right upper and lower limbs. On postop day 4, GCS improved
to 15 with 5/5 power in all four limbs. Magnetic resonance imaging (MRI) done on postop
day 7 showed few acute infarcts in the left MCA territory ([Fig. 3C]). The patient was discharged with a modified Rankin score of 0 on postop day 8.
Follow-up MRI done after 2 weeks showed complete resolution of infarcts ([Fig. 3D]).
Fig. 1 (A) Left internal carotid artery (ICA) angiogram and (B) Three-dimensional rotational angiography (3D-RA) image showing saccular aneurysm
arising from the ophthalmic segment of the left ICA (arrows). Note hypoplastic left
A1 anterior cerebral artery (ACA).
Fig. 2 Post-flow diverter placement (A) anteroposterior and (B) lateral check angiogram of the left internal carotid artery (ICA) showed nonopacification
of the left middle cerebral artery (MCA) branches (asterisks) with mobile air foci
in superior sagittal sinus (white arrows in B). Preferential flow into hypoplastic
left A1 anterior cerebral artery (ACA) was seen due to MCA occlusion. (C) Repeat anteroposterior and (D) lateral check angiogram of the left ICA taken after 30 minutes showed normal opacification
of the left MCA branches (white arrows).
Fig. 3 (A) Intraoperative Xper computed tomography (CT) of head showing air emboli in the cortical
branches of the left middle cerebral artery (MCA) in the left high frontal sulcal
spaces. (B) Air bubbles are seen in the left ophthalmic internal carotid artery (ICA) aneurysm,
cavernous sinus, and bilateral pterygoid plexus (black arrows). Note flow diverter
in situ (inset). (C) Diffusion-weighted magnetic resonance imaging (DW-MRI) done on postprocedure day
7 showed multiple focal infarcts in the left MCA territory showing restricted diffusion
(black arrows). (D) Follow-up MRI after 2 weeks showed complete resolution of infarcts.
Discussion
CAAE can occur in several clinical situations such as trauma, central venous line
insertion, hemodialysis, endovascular interventions, phlebotomy, thoracentesis, cardiopulmonary
bypass, pneumoarthrography, neurosurgery, endoscopy, and scuba diving, etc.[2]
[3] There may be a direct inadvertent entry of air bubbles into the arterial system
through the flush system, or indirect entry of venous air into the arterial system,
that is, paradoxical embolism through a patent foramen ovale or pathological right-to-left
shunt-like cardiac septal defects, pulmonary arteriovenous malformation, etc.[4]
[5] Possible sources of air embolism during catheter angiography include sudden hypotension,
air bubbles in the syringes, improperly primed flush tubing, nondeairing of pressure
saline bag, emptied pressure saline bag, accidentally opened 3-way stopcock, loose
rotating hemostatic valves during injection, improperly deaired pressure injectors,
and, very rarely, rupture of an inadequately deaired balloon.[4] In our case, CAAE occurred when a 1-L normal saline bottle ran dry under pressurized
infusion, causing residual air to be inadvertently forced into the arterial system.
Although a blood transfusion intravenous set with an in-line filter was used, standard
filters are designed to trap macroaggregates and large air bubbles, not microbubbles,
which may still reach the cerebral circulation. This underscores the need for stricter
preventive strategies, including the use of dedicated in-line air-eliminating filters
during neurointerventional procedures involving pressurized infusions.[6] Such measures are crucial because occlusive air bubbles in cerebral arteries can
lead to ischemia, trigger platelet activation, and stimulate the release of vasoactive
substances, ultimately provoking a cascade of inflammatory responses.[5] Clinical features of CAAE include sudden depression in the level of consciousness,
seizures, or focal neurological deficits.[2]
[7] Paradoxical air embolism can cause cardiopulmonary compromise manifesting as arrhythmias,
hypotension, fall in EtCO2, and desaturation.[8] In our case, there was no change in cardiopulmonary parameters as air entry was
directly into the cerebral circulation.
The treatment of choice is hyperbaric oxygen therapy and should be initiated as early
as possible. It reduces the size of air emboli, promotes rapid absorption of air bubbles,
increases the partial pressure of oxygen, and improves perfusion.[1]
[5]
[9] However, the utilization of a hyperbaric chamber is limited by its availability.
Endovascular aspiration of larger occluding air bubbles with or without balloon-assisted
flow reversal can be done in selected patients with large vessel occlusion.[10]
[11]
[12] The prognosis of CAAE depends on numerous factors that is, the volume of air, entry
route of air, air delivery rates, collateral circulation, and hyperbaric oxygen therapy
onset.[8]
[13] Many of these patients show complete recovery; however, delay in diagnosis and intervention
may lead to permanent neurological deficits and mortality.[4]
Conclusion
Symptomatic cerebral air embolism is a rare but serious complication of endovascular
procedures, which can be avoided by preventive measures, early diagnosis, and appropriate
management.
