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Table of Contents    
Year : 2013  |  Volume : 61  |  Issue : 1  |  Page : 95-97

Massive cerebral air embolism during stent-assisted coiling of internal carotid artery aneurysm

1 Department of Neuroanesthesia, National Institute of Mental Health and Neurosciences, Bangalore, India
2 Department of Neuroradiology, National Institute of Mental Health and Neurosciences, Bangalore, India

Date of Submission21-Dec-2012
Date of Decision21-Jan-2013
Date of Acceptance27-Jan-2013
Date of Web Publication4-Mar-2013

Correspondence Address:
K. R. Madhusudan Reddy
Department of Neuroanesthesia, National Institute of Mental Health and Neurosciences, Bangalore
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.108045

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How to cite this article:
Surve RM, Reddy KM, Bansal S, Ramalingaiah A. Massive cerebral air embolism during stent-assisted coiling of internal carotid artery aneurysm. Neurol India 2013;61:95-7

How to cite this URL:
Surve RM, Reddy KM, Bansal S, Ramalingaiah A. Massive cerebral air embolism during stent-assisted coiling of internal carotid artery aneurysm. Neurol India [serial online] 2013 [cited 2021 Jan 26];61:95-7. Available from:


Massive cerebral arterial air embolism (CAAE) is a rare complication during neurointerventional procedures with a reported incidence of ~0.08%. [1] This report presents two such cases.

The clinical and radiological findings are given in [Table 1]. In both the patients, there was no desaturation throughout the procedure. Dexamethasone and mannitol was given to prevent cerebral edema and loading dose of phenytoin was administered for seizures prophylaxis. Both patients developed seizures within 24 h of Neurointensive Care Unit (NICU) stay. Case 1 received only benzodiazepine as treatment for seizures, whereas Case 2 received in addition low-dose thiopentone infusion for seizures and vasopressors to induce hypertension (systolic BP ≥ 150 mmHg). In Case 1, there was no improvement in the neurological status. She had tracheostomy and weaned from ventilator and later transferred to a general hospital in a severely disabled state. Case 2 improved completely and was extubated on day 3. The exact source of air entry could not be identified in Case 1 and it was assumed that air might have entered during hand injection of the contrast agent. In Case 2, the pressurized nimodepine arterial flush bottle was found empty.
Table 1: The clinical and radiological findings of case I and case II

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The commonest cause for CAAE is iatrogenic, and is associated with devastating consequences irrespective of the cause. However, we observed extremes of outcomes in our two patients who sustained massive CAAE. The possible reasons for this could have been: age of the patient and type of intracranial vessel occluded by air. Case 1 had complete occlusion of internal carotid artery (ICA) causing cerebral circulatory arrest, whereas in Case 2 only anterior cerebral artery (ACA) flow was compromised. Other important prognostic factor could be the volume of air entered. Case 1 had sudden bradycardia followed by severe hypotension and sudden drop in EtCO 2 , suggesting large amount of air entry in the cerebral circulation. In Case 2, the amount of air that entered the circulation was probably less as there was only a marginal fall in EtCO 2 without any episode of hypotension. Few important decisions taken in the management of Case 2 could have been responsible for the better outcome. After identifying the source of air entry and confirming air embolism, we tried to aspirate from the microcatheter. Also, repeated boluses of heparinized saline flush were given through the guiding catheter to break the air loculi to smaller bubbles and to facilitate air drainage. In the NICU, she was started on thiopentone infusion which has neuroprotective action and also vasopressors were administered to maintain adequate cerebral perfusion.

Although hyperbaric oxygen (HBO) therapy has been described as treatment for CAAE, [2] it is not widely available. We treated both the patients with 100% normobaric oxygen because of lack of access to an HBO chamber. Depending upon the severity, patient with CAAE can have varied presentation ranging from bradyarrhythmias to tachyarrythmias, hypotension, fall in EtCO 2 , and desaturation. [3] However, from our experience of these two patients, the most consistent finding seems to be the sudden change in the ECG rhythm and fall in EtCO 2 . CAAE is best diagnosed by intermittent check angiography during the procedure and postoperatively by computed tomography (CT) scan. However, diffusion-weighted magnetic resonance imaging (MRI) is the best tool for determining the prognosis. [4]

Various methods to prevent CAAE are described in the literature such as use of proper technique of flushing the catheters and promoting use of 1.2 μm air filters. [5],[6] Stress needs to be given on the implementation of these simple practices which can help in reducing the incidence of CAAE. Other preventive measures which need consideration are adequate illumination in the working area to visualize any obvious air entry. Air detecting devices with audiovisual alarm systems connected to the flushing lines might be helpful and is an avenue for innovation. Thus, we intend to emphasize on the fact that for prompt recognition of CAAE, one should have a high index of suspicion. Also, the lack of institutional protocols to prevent this avoidable complication or any breach in their implementation requires a serious reconsideration.[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
Figure 1: On angiogram, two saccular aneurysms seen in ophthalmic and cavernous segments of left ICA, shown by arrow heads (a) and non opacification of distal left ICA on AP view (b)

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Figure 2: Case 1: DynaCT brain shows air in the cortical arteries (a) ophthalmic artery (b) veins in the mastication space and nasal mucosa (c) and superior sagittal sinus (d)

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Figure 3: Case 1: CT brain 2 h post procedure shows specks of pneumocephalus (a) and diffusion-weighted MRI brain image shows multiple areas of restricted diffusion in both hemispheres; predominantly in the left hemisphere (b-d)

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Figure 4: Case 2: On DSA imaging, pre-embolization left ICA injection shows aneurysm in the cavernous segment (white arrows) and filling of both the ACA and MCA arteries on AP (a) and lateral views (b) Post - embolization ACA flow is obliterated on AP (c) and lateral views (d)

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Figure 5: Case 2: On right ICA injection both ACAs are not filling (a) DynaCT brain showing air in the cortical arteries and superior sagittal sinus (b and c) and restricted diffusion is seen as single hyperintense lesion in left hemisphere on MRI brain (d)

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  References Top

1.Gupta R, Vora N, Thomas A, Crammond D, Roth R, Jovin T, et al. Symptomatic cerebral air embolism during neuro-angiographic procedures: incidence and problem avoidance. Neurocritical Care 2007;7:241-6.  Back to cited text no. 1
2.Benson J, Adkinson C, Collier R. Hyperbaric oxygen therapy of iatrogenic cerebral arterial gas embolism. Undersea Hyperb Med 2003;30:117-26.  Back to cited text no. 2
3.Siviri S, Woods WP, Van Heerden PV. Air embolism; A case series and review. Crit Care Resusc 2004;6:271-6.  Back to cited text no. 3
4.Kenneth LW, Katarzyna JM, Adeeb A. Cerebral air embolism: Acute imaging. J Stroke Cerebrovasc Dis 1998;7:222-6.  Back to cited text no. 4
5.Markus H, Loh A, Israel D, Buckenham T, Clifton A, Brown MM. Microscopic air embolism during cerebral angiography and strategies for its avoidance. Lancet 1993;341:784-7.  Back to cited text no. 5
6.Bendszus M, Koltzenburg M, Bartsch AJ, Goldbrunner R, Gunther-Lengsfeld T, Weilbach FX, et al. Heparin and air filters reduce embolic events caused by intra-arterial cerebral angiography: A prospective, randomized trial. Circulation 2004;110:2210-5.  Back to cited text no. 6


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

  [Table 1]

This article has been cited by
1 Spontaneous Absorption of Cerebral Air Embolus Developed Accidentally during an Intra-arterial Procedure
Tae Ki Yang
Journal of Cerebrovascular and Endovascular Neurosurgery. 2016; 18(4): 391
[Pubmed] | [DOI]


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