Neuroradiology (2000) 42: 192±194
Ó Springer-Verlag 2000

D IA G N O S T I C NE UR OR A DI O LO G Y

Normal diffusion-weighted imaging
in cerebral air embolism complicating
angiography

T. Sayama
M. Mitani
T. Inamura
H. Yagi
M. Fukui

Received: 2 April 1999
Accepted: 12 July 1999

)

T. Sayama × T. Inamura ( ) × M. Fukui
Department of Neurosurgery,
Kyushu University Hospital,
3-1-1 Maidashi, Higashi-ku,
Fukuoka 812-82, Japan
e-mail: taka@ns.med.kyushu-u.ac.jp
Tel.: + 81-92-6 42 55 24
Fax: + 81-92-6 42 55 26
M. Mitani ´ H. Yagi
Department of Neurosurgery,
Yagi Hospital, Fukuoka, Japan

Abstract We report a case of cerebral air embolism resulting from accidental air infection during cerebral
angiography. A 60-year-old man was
accidentally injected with air via the
left subclavian artery. Angiography
demonstrated air within the basilar
artery. The patient showed signs of
posterior circulation ischaemia
(confusion, blindness, gaze palsy
and hemiparesis). However, MRI,
including diffusion-weighted imaging, showed no abnormality 4 h
later. The patient was treated with

hyperbaric oxygen within 5 h of the
embolism. All symptoms and signs
resolved completely within a week.
Key words Embolism, cerebral air ×
Magnetic resonance imaging,
diffusion-weighted image ×
Hyperbaric oxygen therapy

Introduction
Cerebral air embolism occasionally occurs in diving accidents or as a complication of positive-pressure mechanical ventilation [1, 2]. Multiple brain infarcts can be
seen on CT or MRI. Diffusion-weighted imaging (DWI)
is particularly useful for detection of early brain lesions
in stroke [3±6]. For cerebral air embolism, immediate
hyperbaric oxygen therapy is recommended as specific,
definitive treatment [7].
We report a case of cerebral air embolism due to accidental air injection during angiography, resulting in
severe neurological manifestations. MRI, including a
DWI sequence was performed, and immediate initiation
of hyperbaric oxygen therapy (HBOT) was accompanied by resolution of symptoms.

Case report
A 60-year-old man underwent cerebral angiography for a recurrent
cervical tumour. During angiography via the right subclavian artery, approximately 15 ml of air was accidentally injected due to a

Fig. 1 Approximately 15 ml of air was accidentally injected into
the left subclavian artery. The angiogram shows air within the basilar (arrow) and occipital (arrowhead) arteries

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Fig. 2 MRI demonstrated no abnormal signal 2 h after the embolism: left T1-weighted; centre T2-weighted; right diffusion-weighted
mechanical malfunction. The angiogram showed air within the
basilar artery (Fig. 1). Premedication with sedatives prior to angiography hindered assessment of the level of consciousness. Impairment of consciousness was prominent 2 h later. Examination
disclosed confusion, blindness with preserved light reflexes, a disturbance of horizontal eye movements, and left hemiparesis. MRI,
including DWI, showed no abnormal signal intensity. Cerebral air
embolism was diagnosed and the patient was transferred for
HBOT 4 h after the arterial air injection. HBOT was initiated immediately at 2.5 atm for 90 min, and the patient became alert and
showed improvement of the left hemiparesis the next day. His
blindness ameliorated after three further sessions of HBOT. All
neurological symptoms and signs resolved completely within a
week. T2-weighted MRI showed only a small focus of high signal in
the right frontal white matter, not seen on previous examinations.

Fig. 3 MRI showed no abnormal signal in area supplied by
the posterior circulation on
(left) T1- or T2-weighted images

Discussion
Cerebral air embolism can cause a variety of neurological disturbances: sudden loss of consciousness, nausea,
dizziness, seizures, limb weakness, paraesthesiae, visual
dysfunction and headache [1]. As imaging shows brain
infarcts which are not aetiologically specific [8±10], the
diagnosis should be made clinically when sudden neurological deficits follow events capable of introducing
air into vessels. In the present case, the complex of impaired consciousness, left hemiparesis, horizontal eyemovement disturbances and cortical blindness suggested involvement of the posterior circulation, which
corresponded well to the angiographic demonstration of
air in the basilar artery.
Echo-planar DWI generates images related to diffusion of water molecules [11±12]; in stroke, early cerebral
ischaemia can be detected even when T2-weighted
imaging shows no abnormality [13±17]. Specifically,

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DWI shows an increase in the amount of intracellular
water in the early phase of ischaemic stroke. Reuter et
al. [10] documented cerebral changes on MRI in six of
eight patients with arterial gas embolism [10]. However,
while our patient showed severe neurological deficits,
MRI, including DWI, showed no abnormality. As all
symptoms resolved within a week, any lesion caused by
the air embolism may have been too small to be demonstrated by DWI, and the amount of air ± 15 ml ±
might be considered relatively small.

In cerebral air embolism, biochemical actions at the
blood-gas interface can lead to alterations in haemostasis, endothelial damage and activation of leukocytes
[18, 19]. Immediate initiation of HBOT, typically at
2.5±3.0 atm for 2±4 h, has been the treatment of choice
[18]. It reduces the size of bubbles and helps to correct
hypoxia. In our patient, HBOT was given within 5 h of
the embolism, and repeated HBOT was accompanied by
complete resolution of all deficits, without abnormal
signal on MRI in the affected arterial territory.

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