(Stroke. 1997;28:1278-1282.)
© 1997 American Heart Association, Inc.
Articles |
From the Department of Neurosurgery, Showa General Hospital, Tokyo, Japan.
| Abstract |
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Methods We reviewed 30 patients with SAH of unverified etiology in whom initial CT scan showed a diffuse or anteriorly distributed subarachnoid blood clot. Ten of the patients had stenotic or occlusive lesions (SOCL) on initial angiography, and these were the main focus of this study.
Results Among the 10 patients with SOCL on initial angiography, the lesions were located on the anterior circulation in 6 and on the posterior circulation in 4. Ruptured dissecting aneurysms were confirmed by exploratory surgery or autopsy in 6 patients. Subsequent rupture occurred in 6 of the 10 patients (60%), and all 6 of these patients died as a result.
Conclusions The incidence (6/30) of dissecting aneurysms as the cause of SAH of unverified etiology was unexpectedly high, especially when initial angiography disclosed SOCL (6/10). The moribund patients with SOCL showed a high rate of rebleeding, and the untreated recurrent hemorrhages were fatal. Further MRI study is indicated for these patients to demonstrate the intramural hematoma. Compared with the devastating mortality caused by the subsequent ruptures, the extent of surgical morbidity was minor. Surgical intervention could therefore be justified when the following neuroradiological findings are present: (1) SOCL evident on angiography, (2) distribution of SAH on CT compatible with the location of the SOCL, and (3) intramural hematoma on MRI in the same region as the SOCL.
Key Words: aneurysm angiography dissection occlusion stenosis subarachnoid hemorrhage
| Introduction |
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| Subjects and Methods |
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| Results |
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CT Findings
Among 10 patients, 6 had diffuse subarachnoid clots and 3
had focal subarachnoid clots limited to the unilateral sylvian
cistern. The remaining patient was diagnosed as having SAH by lumbar
tap only. In the 9 patients with positive CT scans, the clot was
distributed predominantly in the cisterns adjacent to the SOCL.
Angiographic Findings
All the patients with SOCL met the following conditions: (1)
initial angiography was performed within 48 hours after onset, (2)
angiographic SOCL indicated single subtle luminal narrowing or vascular
occlusion at a point other than a vascular bifurcation, and (3)
adequate four-vessel studies disclosed absence of vasospasm and no
atherosclerotic changes in the other arterial systems. The
SOCL locations are listed in Table 1
(Fig 1
).
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MRI Findings
Among the 10 patients with SOCL, MRI findings were unavailable for
the first 4 patients (pre-MRI era.). The other 6 patients were
scheduled for investigation, but 4 with severe clinical grade did not
undergo MRI because of unstable vital signs and subsequent ruptures.
The 2 patients who underwent MRI study showed intramural hematomas (Fig 2A
and 2C
).
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Surgical Findings
On the basis of high rebleeding rate, exploratory surgery was
considered to be indicated when the following neuroradiological
findings were obtained: (1) SOCL evident on angiography, (2)
distribution of SAH compatible with the location of the SOCL on CT, and
(3) intramural hematoma in the same region as the SOCL on MRI. The
diagnosis of ruptured dissecting aneurysm was confirmed in all
the surgical cases (Fig 2B
and 2D
). In our series, surgical morbidity
and mortality were minor (0%). Wrapping or clip-reinforced wrapping
procedures were performed in our series. No subsequent ruptures were
observed during the follow-up period (41 to 95 months) (Table 1
).
Autopsy Findings
Among 3 autopsied patients, dissecting aneurysms were
verified on the basilar artery, vertebral artery, and internal carotid
artery, respectively. Fragmentation of the degenerated internal elastic
lamina was most commonly recognized on microscopic study. Multiple
intramural hemorrhages without luminal connections were also
observed in all patients (Fig 3A
and 3B
).
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| Discussion |
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Angiography does not always permit a definitive diagnosis because
luminal narrowing or vascular occlusion at a site other than a vascular
bifurcation is also seen in atherosclerotic or other vascular diseases.
It has been suggested that the pathognomonic sign for a dissecting
aneurysm is a double lumen, although this is infrequently
demonstrated.5 Angiographic signs may be understood in
terms of the status of thrombosis in the pseudolumen; thus, a double
lumen could result from minimum thrombosis, a pearl and string sign
could result from partial thrombosis, and subtle SOCL could result from
early progression of thrombosis. Although dissecting aneurysms
often demonstrate only subtle abnormalities in the acute stage, early
thrombosis might not necessarily indicate healing of the dissected
pseudolumen. This was demonstrated in our series and in other reported
cases4 5 6 7 8 9 10 11 12 13 14 15 (Table 1
). Cerebral vasospasm due to SAH
occasionally has the appearance of a string sign. Cerebral vasospasm
commonly occurs in multiple vessels and is hardly seen at the acute
stage. Differentiating SOCL from incidental atherosclerotic
stenosis may be important. Another definitive
diagnostic feature of arterial dissection is
intramural hematoma. MRI is very valuable when combined with
angiography because MRI can directly demonstrate the intramural
hematoma.16 In case 6 of our patients, a high-intensity
lesion with marked contrast enhancement on T1-weighted imaging along
the C1 portion of the right internal carotid artery was observed at the
subacute stage (Fig 2A
). In case 7, an isointense lesion along the
M1 segment of the right middle cerebral artery was observed at the
acute stage on proton-density imaging. In this case, T1-weighted
imaging was not diagnostic because of its inappropriate
slice position (Fig 2C
). In both cases, we clearly demonstrated
intramural hematoma, shown as a crescentic (case 6) or curvilinear
(case 7) isointensity to high-intensity structure in the lumen, in the
same region where SOCL were revealed angiographically. In our series,
there was no false-positive MRI demonstration of intramural hematoma in
cases without SOCL. With the use of MRI, we could successfully diagnose
dissecting aneurysms as the hemorrhagic sources among SAHs of
unverified etiology and discriminate them from atherosclerotic
stenosis.
Our experience and review of the literature suggested that these
lesions posed a significant risk of rebleeding if untreated. The
outcome in all patients presenting with a severe clinical grade was
fatal (Table 1
).4 5 6 7 8 9 10 11 12 13 14 15 When such lesions are encountered as
the likely cause of SAH, diagnosis with the aid of MRI and obliteration
of the dissected lesions are essential. Early surgery may be justified
to prevent rerupture: our series and a review of the literature
revealed a greater risk of subsequent rupture within the first week
(Table 1
).4 5 6 7 8 9 10 11 12 13 14 15 If a diagnosis of dissecting
aneurysm is highly suspected, trapping of the aneurysm
or proximal ligation of the artery with or without
extracranial-intracranial bypass surgery would be the optimal surgical
treatment for prevention of rebleeding, although the best surgical
procedure is still being debated.5
In conclusion, there was an unexpectedly high ratio (6/30) of dissecting aneurysms as the cause of SAH of unverified etiology. A substantial proportion (30%) of dissecting aneurysms showing only subtle angiographic SOCL in the acute stage was noted. There was a high mortality rate (6/10) due to subsequent rupture of such SOCL. We also demonstrated that patients with a severe clinical grade of SOCL showed a high rate of rebleeding and that untreated recurrent hemorrhages were fatal. Further MRI study is indicated for these patients to demonstrate the intramural hematoma. Compared with the devastating mortality caused by the subsequent ruptures, the extent of surgical morbidity was minor. Surgical intervention could therefore be justified when the following neuroradiological findings are present: (1) SOCL evident on angiography, (2) distribution of SAH on CT compatible with the location of the SOCL, and (3) intramural hematoma on MRI in the same region as the SOCL.
| Footnotes |
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Received February 6, 1997; revision received March 21, 1997; accepted March 21, 1997.
| References |
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