(Stroke. 1997;28:2078-2080.)
© 1997 American Heart Association, Inc.
Articles |
Intracranial Aneurysm Rupture Presenting as Delayed Stroke Secondary to Cerebral Vasospasm
From the Department of Neurosurgery, University of Minnesota, Minneapolis (E.S.N., D.Y.K.W.); Neurosurgery Service, Department of Veterans Affairs Medical Center, Minneapolis, Minn (E.S.N., D.Y.K.W.); and Neurosurgical and Spinal Surgery Associates, Rapid City, SD (L.A.S.).
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Abstract |
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Background Days after aneurysmal subarachnoid hemorrhage (SAH), cerebral vasospasm can result in the delayed appearance of ischemic neurological deficit identical to that produced by other causes of stroke. Despite the well-described, "classic" presentation of SAH, up to 25% of patients are initially misdiagnosed, and the initial hemorrhage from a ruptured aneurysm will not always bring the patient to medical attention.
Case Descriptions We report our experience with two patients who presented with signs and symptoms of ischemic stroke resulting from cerebral vasospasm that followed unrecognized rupture of a brain aneurysm. In one case, it was the recent complaint of significant headache and a prior history of SAH that led to the correct diagnosis. In the other case, a major rebleed occurred before the accurate diagnosis was recognized.
Conclusions It is critical to make the correct diagnosis of stroke due to vasospasm so that appropriate treatment can be instituted, thrombolytic and anticoagulant therapy can be avoided, and the unsecured aneurysm can be obliterated to prevent potentially catastrophic rebleeding.
Key Words: aneurysm • subarachnoid hemorrhage • thrombolysis • vasospasm
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Introduction |
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The clinical hallmark of subarachnoid hemorrhage (SAH) is severe headache, and typically this will prompt the patient to seek medical attention. There may be concomitant focal neurological deficit, depressed level of consciousness, or coma. Despite the well-described, "classic" presentation of SAH, up to 25% of patients are initially misdiagnosed after aneurysm rupture, and approximately 40% of patients describe a history of one or several significant headaches during the preceding weeks.1 2 3 4 We recently encountered two patients who presented days after unrecognized aneurysm rupture with symptoms of stroke secondary to delayed cerebral vasospasm. The clinical findings of cerebral vasospasm may be identical to those of other causes of stroke; therefore, prompt and accurate diagnosis may be difficult. Establishing the diagnosis of cerebral vasospasm due to aneurysm rupture is critical so that appropriate treatment measures can be instituted rapidly and potentially hazardous interventions such as anticoagulation and thrombolysis can be avoided.
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Case Reports |
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Case 1
This 37-year-old, left-handed woman presented with the sudden onset of left-sided weakness and speech difficulty. She was otherwise in excellent health but had complained of severe headaches during the previous week. Neurological examination revealed an expressive aphasia, marked left-sided hemiparesis, and nuchal rigidity. An emergency CT scan of the brain disclosed an ischemic stroke in the territory of the right middle cerebral artery. There was no evidence of hemorrhage. The patient was admitted to the hospital and started on aspirin therapy. Echocardiogram, duplex carotid ultrasound, and hematologic evaluation for a hypercoagulable state were unremarkable.
A cerebral angiogram demonstrated the presence of a right posterior
communicating artery aneurysm with local arterial
narrowing; however, it was not recognized that the patient's stroke
was related to delayed cerebral vasospasm from aneurysm rupture
(Fig 1
).
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The patient was transferred to a rehabilitation facility. One month later, she developed the sudden onset of lethargy and worsening left-sided weakness and then suffered a generalized seizure. An emergency CT scan revealed SAH with a large right temporal lobe hematoma. She was transferred to our institution, where a craniotomy was performed to evacuate the hematoma. The aneurysm was found to be the source of the bleeding and was clipped. Postoperatively, the patient recovered slowly and was transferred to a long-term care facility in poor condition.
Case 2
A 59-year-old, right-handed woman complained to her family of the
sudden onset of holocephalic headache but failed to seek medical
attention. She suffered from recurrent headaches for 4 days and then
developed left-sided weakness, worsening headache, and diminished level
of consciousness. Her medical history was notable for hypertension,
atherosclerotic coronary vascular disease, and a prior SAH of
uncertain etiology at age 30.
Neurological examination revealed the patient to be lethargic with
slurred speech and a moderate left-sided hemiparesis. An emergency CT
scan revealed hypodensity in the right parietal region, and MRI scan
confirmed an acute infarct of the right parietal lobe. The patient was
admitted to the hospital with a diagnosis of ischemic stroke,
and consideration was given to initiating intravenous
anticoagulation. Given the history of remote SAH, cerebral angiography
was performed and revealed an irregular, fusiform aneurysm of
the right middle cerebral artery with local spasm of the distal middle
cerebral artery (Fig 2). The current
stroke was not attributed to cerebral vasospasm, and the patient was
treated with aspirin therapy. Her level of consciousness deteriorated,
and she required mechanical ventilation.
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The patient was transferred to our institution for further care. Given the irregular aneurysm with local arterial spasm and the history of headache, the initial CT scan was re-reviewed and was found to show subtle evidence of hemorrhage around the aneurysm. Treatment with nimodipine and hypervolemic, hypertensive therapy was instituted, and the patient made a dramatic recovery. Three weeks later, repeated cerebral angiography showed resolution of the vasospasm. The patient was taken to the operating room, where the ruptured middle cerebral artery aneurysm was wrapped with muslin gauze. She recovered slowly and was subsequently discharged to home with moderate residual cognitive deficits.
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Discussion |
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Cerebral vasospasm occurs as a consequence of bleeding into the subarachnoid space. Vasospasm generally appears 3 to 4 days after hemorrhage, reaches a maximum at 1 week, and typically subsides by 2 weeks.5 Clinically, the onset of vasospasm may be heralded by an increase in headache, low-grade fever, worsening meningismus, or the development of hyponatremia.3 This may be followed by confusion or drowsiness and later by focal symptoms of ischemia corresponding to the involved arterial territories.
Stroke resulting from cerebral vasospasm may appear identical clinically to cerebral ischemia of other causes. However, the management of cerebral vasospasm is unique in that treatment must be directed at preventing aneurysm rerupture and ameliorating the arterial narrowing responsible for ischemia. After aneurysm rupture, the risk of potentially fatal rebleeding is approximately 20% over the ensuing 2 weeks and 6% during the first 48 hours.2 6 The rapid establishment of an accurate diagnosis is critical because surgical or endovascular obliteration of the aneurysm can prevent recurrent hemorrhage. In addition, hypertensive, hypervolemic, hemodilution therapy and balloon angioplasty can be lifesaving in the setting of cerebral vasospasm.2 7 8 9 Features suggesting the diagnosis of cerebral vasospasm in one or both of our patients included recent severe headaches, a history of prior SAH, young patient age, and the subtle finding of SAH on CT scan.
Although CT scan is very sensitive for the presence of acute blood, even an optimal study can miss SAH in at least 5% of cases.10 The probability of detecting blood on CT scan falls rapidly with time to 50% at 1 week, 30% at 2 weeks, and almost nil at 3 weeks; therefore, CT scan may fail to reveal evidence of hemorrhage if the patient presents days after SAH with delayed ischemia from vasopasm.10 11 For this reason, if any question of SAH exists, even if the CT scan fails to reveal hemorrhage, further evaluation is indicated.
Recently, magnetic resonance angiography (MRA) has been shown to reliably identify aneurysms greater than 4 mm in size, and MRI sequences have been developed that have greatly improved the ability of this imaging modality to identify acute and subacute SAH.12 13 14 15 Although lumbar puncture remains the gold standard for detecting SAH in the face of a negative CT scan, the acute stroke patient may be a candidate for thrombolytic therapy, and ideally an invasive procedure such as lumbar puncture should be avoided.3 11 16 In this setting, the combination of a normal CT scan with a negative emergency MRI/MRA study should exclude the presence of all but the smallest ruptured aneurysms. Nevertheless, in many hospitals it may be difficult or impossible to obtain a good-quality MRI/MRA study on an emergency basis, particularly if the patient is not perfectly cooperative. If high-quality MRI/MRA is unavailable or if uncertainty remains after these studies, a lumbar puncture to assay the cerebrospinal fluid should be considered.
To avoid potentially catastrophic rebleeding, anticoagulation and thrombolytic therapy should be strictly avoided after aneurysm rupture. Recent trials of thrombolytic therapy for ischemic stroke have emphasized very early institution of treatment to reduce the risk of hemorrhage and to maximize the potential for recovery.16 Because of this time constraint, subtle historical features suggesting SAH could be missed, and great care should be exercised to exclude the possibility of cerebral vasospasm as the cause of ischemia. If any question exists as to the possibility of a ruptured aneurysm, MRI/MRA or lumbar puncture should be considered before instituting such therapy.
Conclusion
In conclusion, cerebral vasospasm after SAH may result in
ischemic stroke indistinguishable on examination from stroke of
any other cause. Points that may be helpful in establishing the
diagnosis of vasospasm include a recent history of significant
headache, young patient age, the presence of blood in the
subarachnoid cisterns on CT scan, or a history of prior
intracranial hemorrhage. The importance of establishing the
correct diagnosis cannot be overstated because of the high rebleeding
rate of ruptured intracranial aneurysms and the fact that
anticoagulation and/or thrombolytic therapy, which
represent a mainstay of treatment for many causes of
ischemic stroke, may have disastrous consequences in the case
of aneurysm rupture. Other specific treatment modalities
including hypertensive, hypervolemic, hemodilution therapy and
balloon angioplasty may prove lifesaving in the face of cerebral
vasospasm. If any question exists based on clinical grounds and/or CT
scan, MRI/MRA or lumbar puncture should be considered to rule out
SAH.
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Footnotes |
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Reprint requests to E. Spencer Nussbaum, MD, UMHC Box 96, 420 Delaware St SE, Minneapolis, MN 55455.
Received April 14, 1997; revision received July 8, 1997; accepted July 8, 1997.
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References |
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