Neurol Med Chir (Tokyo) 45, 627¿630, 2005

Acute Subdural Hematoma After Intra-arterial
Thrombolysis for Acute Ischemic Stroke
—Case Report—
Toshinari MEGURO, Hisato HIGASHI, and Ken NISHIMOTO
Department of Neurological Surgery, Sumitomo Besshi Hospital, Niihama, Ehime

Abstract
A 79-year-old man with a cardiac pacemaker for bradycardia fell down and presented with sudden onset
of right hemiplegia and aphasia. Initial computed tomography (CT) showed no cerebral infarction but
angiography revealed occlusion of the left middle cerebral artery (MCA). Local intra-arterial thrombolysis with tissue plasminogen activator (tPA; tisokinase, 1,600,000 units) was performed 3 hours after the
onset, and the MCA was partially recanalized. Further administration of tPA was suspended because of
nosebleed. However, the patient's neurological findings did not improve. His consciousness gradually
deteriorated to coma and quadriplegia with dilation of the left pupil 2.5 hours after thrombolysis. CT
disclosed marked mass effect with a left acute subdural hematoma and a small intracerebral hematoma
in the left frontal lobe. He underwent urgent craniotomy and removal of the subdural hematoma. The
subdural hematoma originated in a frontal cerebral contusion. He died of severe brain edema 2 days
after surgery. Acute subdural hematoma is a very rare complication of intra-arterial thrombolysis.
Presumably he had suffered head trauma at the first onset. Evidence of head trauma should be
considered a contraindication for the use of thrombolytic agents in a patient with acute stroke.
Key words:

acute subdural hematoma,

thrombolysis,

Introduction

tissue plasminogen activator,

stroke,

trauma

4, V: 1, M: 5) on the Glasgow Coma Scale. He
presented with right hemiplegia and aphasia.
According to his family he had had a small
nosebleed, but he did not show apparent external
injuries on admission.
Initial computed tomography (CT) showed no
signs of ischemic change (Fig. 1). Subsequent
cerebral angiography demonstrated occlusion of the
left middle cerebral artery (MCA) (Fig. 2A, B). The
patient received an intravenous bolus of heparin
(5,000 units). A microcatheter mounted on a guidewire was passed through the clot to the distal side,
where 80,000 units of tissue plasminogen activator
(tPA; tisokinase) were delivered by hand injection.
The microcatheter was then slowly withdrawn to
the proximal side of the clot and another 80,000
units of the tPA were injected. By this time, 3 hours
had passed from symptom onset and partial lysis of
the clot had occurred (Fig. 2C, D). Unfortunately,
we were forced to discontinue administration of tPA

Intra-arterial thrombolysis is an accepted treatment
for selected acute ischemic stroke. The most serious
complication of intra-arterial thrombolysis is intracranial hemorrhage, which mostly occurs as parenchymal hematoma or hemorrhagic infarction.2,3,10)
Acute subdural hematoma is extremely rare. We
report a case of acute subdural hemorrhage with
poor outcome as a complication of intra-arterial
thrombolysis.

Case Report
A 79-year-old man suddenly lost consciousness and
fell down at home. He was transferred to our
hospital 45 minutes later. He had undergone implantation of a cardiac pacemaker for bradycardia 12
years previously but had received no anticoagulant
therapy. On admission, his consciousness was 10 (E:

Received December 10, 2004;
Accepted May 23, 2005
Author's present address: T. Meguro, M.D., Department of Neurological Surgery, Hiroshima City Hospital, Hiroshima,
Hiroshima, Japan.

627

628

Fig. 1

Fig. 2

T. Meguro et al.

Initial computed tomography scans showing no signs of ischemic change.

Initial left carotid angiograms (A: anteroposterior view, B: lateral view) showing
occlusion of the left middle cerebral artery
from a cardiac embolus. Left carotid angiograms (C: anteroposterior view, D: lateral
view) after thrombolysis showing partial
lysis of the clot in the left middle cerebral
artery.

after the initial tPA injection because he had a
nosebleed. His nosebleed stopped spontaneously
before long, but subcutaneous hemorrhage in his
right forehead had become obvious. His neurological findings did not improve after the thrombolysis.
Second CT immediately after thrombolysis showed
hemorrhagic infarction in the territory of the

Fig. 3

Second computed tomography scans immediately after thrombolysis showing hemorrhagic infarction in the territory of the
recanalized middle cerebral artery and
intracerebral hemorrhage in the frontal
lobe.

Fig. 4

Third computed tomography scans 2.5
hours after thrombolysis disclosing left
acute subdural hematoma with marked
mass effect and brain shift.

recanalized MCA and intracerebral hemorrhage in
the frontal lobe, in which no microcatheter or guidewire had been inserted (Fig. 3).
The patient's consciousness gradually deteriorated to coma and quadriplegia with dilation of the left
pupil 2.5 hours after thrombolysis. Third CT disclosed a left acute subdural hematoma with marked
mass effect and brain shift (Fig. 4). He underwent
urgent craniotomy for evacuation of the subdural
hematoma. A large craniotomy flap was made on the
left. After evacuation of thick hematoma, the surface
of the brain around the sylvian fissure was found to
be edematous with partial subarachnoid hemorrhage. However, the arachnoid membrane in the

Neurol Med Chir (Tokyo) 45, December, 2005

Acute Subdural Hematoma Following Thrombolysis

Fig. 5

Computed tomography scans 8 hours after
the craniotomy demonstrating severe brain
swelling with shift of the whole left cerebral
hemisphere.

region was not damaged. The parenchymal and
arachnoid laceration was located on the anterior
surface of the frontal lobe, and communicated with
the subdural hematoma.
Postoperatively, the patient showed no improvement of neurological deficit. CT 8 hours after the
craniotomy demonstrated severe brain swelling
with shift of the whole left cerebral hemisphere
(Fig. 5). The patient died 2 days after the
craniotomy.

Discussion
Intravenous administration of thrombolytic agent
does not increase mortality or morbidity, despite a 2
to 2.5 fold increase in symptomatic intracranial
hemorrhage.5,8) A randomized trial of recombinant
pro-urokinase by intra-arterial thrombolysis showed
significant improvement in clinical outcome at 90
days. However, intracranial hemorrhage with
neurological deterioration within 24 hours occurred
in 10% of patients treated with recombinant prourokinase and 2% of control patients.2) Only hemorrhagic infarction or parenchymal hemorrhage has
been described as a complication of intravenous or
intra-arterial thrombolysis for acute ischemic stroke.
Acute subdural hematoma is one of the complications of thrombolysis for acute myocardial infarction, occurring in 0.1% to 0.2% of cases of thrombolytic therapy using intravenous recombinant tPA,
and is generally related to head trauma.4,6) CT is
essential to identify ischemic stroke, but not acute
myocardial infarction. Evidence of intracranial
hemorrhage on pretreatment CT is one of the most
important contraindications for the use of tPA in
patients with acute ischemic stroke.1)

Neurol Med Chir (Tokyo) 45, December, 2005

629

Our patient was bleeding a little at the nose when
he lost consciousness, but his nosebleed had
stopped, and he had no external injuries on arrival
to our hospital. Initial CT unfortunately did not
reveal any signs of intracranial bleeding. Cerebral
contusion appeared in the patient's left frontal lobe,
and acute subdural hematoma developed after the
thrombolysis. CT immediately after injury does not
always detect intracranial hemorrhage. Twenty-five
cases of traumatic intracerebral hematoma with
delayed onset, all identified with CT, were found
among 775 cases of acute head injury.9) It is possible
that patients with acute ischemic stroke had suffered
head trauma before onset. Late onset of intracranial
hemorrhage is one of the pitfalls of thrombolysis for
acute ischemic stroke, as the earlier the start of
thrombolysis from onset, the better the results.
Direct percutaneous transluminal angioplasty
(PTA) or clot retrieval in acute stroke is an additional or alternative option to thrombolysis for patients
with acute main trunk occlusion.7,11,12) Direct PTA or
clot retrieval without tPA or urokinase may be better
for the treatment of patients with acute ischemic
stroke who might have suffered head trauma.

Acknowledgment
We would like to thank Dr. Nobuyuki Hirotsune
(Department of Neurological Surgery, Hiroshima
City Hospital, Hiroshima) for helpful suggestions
and comments.

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Address reprint requests to: T. Meguro, M.D., Department
of Neurological Surgery, Hiroshima City Hospital,
7–33 Moto–machi, Naka–ku, Hiroshima, Hiroshima
730–8518, Japan.
e-mail: tmeguron＠hotmail.com

Neurol Med Chir (Tokyo) 45, December, 2005