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|LETTER TO EDITOR
|Year : 2016 | Volume
| Issue : 7 | Page : 126-128
Vasospasm after iatrogenic subarachnoid hemorrhage
Sandeep Mohindra1, Amey Savardekar2, Ankur Kapoor1
1 Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, Punjab and Haryana, India
2 Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
|Date of Web Publication||3-Mar-2016|
Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh, Punjab and Haryana
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Mohindra S, Savardekar A, Kapoor A. Vasospasm after iatrogenic subarachnoid hemorrhage. Neurol India 2016;64, Suppl S1:126-8
The present communication describes a patient with a low-grade glioma, who had an intraoperative spillover of blood into the subarachnoid space and the lateral ventricles, leading to infarcts of the anterior and posterior cerebral arterial territories on the 14 th post-operative day. This is probably the first report describing vasospasm of major vessels of the circle of Willis following resection of a parenchymal tumor.
A 40-year-old woman presented with the symptomatology of raised ICP without any focal neurological deficits. Contrast-enhanced CT scan of the head showed a large hypodense, nonenhancing mass occupying the left frontal lobe, compressing the ipsilateral lateral ventricle and causing a massive midline shift [Figure 1]a. The patient underwent a left frontal craniotomy and a near-total tumor resection, via the transcortical approach. The tumor was soft, suckable, and gray in color. Just underneath the falx, bilateral anterior cerebral arteries were seen and were located at the medial limit of the tumor margins. The frontal horn of the left lateral ventricle got opened during tumor resection, but hemostasis at the tumor bed was accomplished easily. At closure, the brain was lax and pulsating well. The postoperative CT scan revealed subarachnoid bleed spilling into the perimesencephalic cisterns and intraventricular blood occupying bilateral lateral ventricles [Figure 1]b-d. During the convalescence period, another CT scan was done, which was unremarkable [Figure 2]a. After remaining asymptomatic until the 13 th postoperative day, the patient became unconscious and developed right hemiparesis on the 14 th postoperative day. CT scan at that time showed infarcts related to the arterial territories of the left anterior and posterior cerebral arteries [Figure 2]b and c. CT angiography confirmed the nonexistence of any aneurysmal pathology, but diffuse vasospasm of all major vessels of the circle of Willis was noteworthy [Figure 2]d and e. She underwent a tracheostomy and gradually improved in her consciousness, although she persisted with mild right hemiparesis and visual loss. The check CT scan showed resolution of the ventriculomegaly and decreased cerebral edema [Figure 2]f].
|Figure 1: CT scan (axial section, contrast enhanced) showing a nonenhancing mass involving the left frontal lobe. Obliteration of frontal horns of bilateral lateral ventricles indicates mass effect (a). CT scan (plain) showing blood trapped in the perimesencephalic and prepontine cisterns. Blood is also seen in the interhemispheric cistern, bilateral sylvian fissures and the third ventricle (b and c); and CT scan (plain) showing the blood-free tumor bed cavity and blood casts within bilateral lateral ventricles (d)|
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|Figure 2: Axial section of CT scan (plain) on the 4th postoperative day showing no remarkable findings (a); CT scan (plain) on the 14th postoperative day showing arterial infarcts related to the left anterior and posterior cerebral artery territories. Associated mass effect is evident in view of the obliterated occipital horn of the left lateral ventricle and the elevated bone flap (b and c); the CT angiogram did not reveal any vascular pathology except vasospam in the ACA and PCA vessels (d and e); CT scan (contrast enhanced) at 1 month of follow-up showing the decreased mass effect and the well-demarcated infarct (f)|
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Cerebral vasospasm after aneurysmal subarachnoid hemorrhage, traumatic SAH, or SAH following sellar surgery is widely described in literature. , Delayed ischemic neurological deficit following iatrogenic subarachnoid hemorrhage is rarely reported. During surgery, it is likely that a bleeder from a major vessel or a perforator, may get avulsed, leading to spillover of blood within the subarachnoid space. The thick layer of subarachnoid blood may cause vasospasm and delayed ischemic deficits. It is well established that the quantity of subarachnoid blood determines the onset of vasospasm and ischemic symptoms. It is the aneurysmal SAH that causes delayed neurological deficits. Traumatic SAH is known to disappear at a faster rate without causing any permanent deficits. Moreover, traumatic SAH causes cerebral hypodensities to appear in nonvascular territories. The present case highlights that major vascular territories may also get compromised and permanently damaged, even in nonaneurysmal iatrogenic subarachnoid hemorrhage. Such a subarachnoid bleed may occur after resection of a parenchymal tumor like a low-grade glioma. Literature describes a few cases of iatrogenic vasospasm where such a complication occurred after excision of a skull base tumor ,,,, or even after removal of brain stem lesions  [Table 1]. A higher incidence of vasospasm correlated with increased tumor size, total operative time, vessel encasement, vessel narrowing, and preoperative embolization.  Our case did not harbor any skull base tumors or brain stem lesions, and the postoperative vasospasm can be attributed solely to the spillover of blood in the subarachnoid space.
|Table 1: Reported cases of cerebral vasospasm after intracranial tumor resection (excluding the posterior fossa and the sellar - suprasellar region) |
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A postoperative CT scan is advisable after all intracranial surgeries to rule out an intracranial hematoma. The CT scans may detect this postoperative complication and alert the surgeon to deal effectively with its delayed sequel. The use of triple H therapy, nimodipine, or angioplasty to prevent these delayed ischemic deficits needs further evaluation.  It seems advisable to keep such postoperative patients admitted to the hospital for a longer duration and well-hydrated.
Iatrogenic subarachnoid hemorrhage following tumor resection may pose a real threat to the vascular territories, even the major ones. It is advisable to prevent such a subarachnoid bleed; during resection of a parenchymal tumor adequate hemostasis should be achieved and subarachnoid spillage of blood should be prevented. All intracranial surgeries should be followed by an immediate postoperative CT scan. A thick postoperative SAH may predispose all major vessels of the circle of Willis to severe vasospasm. The vasospasm may be severe enough to cause a major delayed neurological deficit.
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[Figure 1], [Figure 2]