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NI FEATURE: FACING ADVERSITY…TOMORROW IS ANOTHER DAY! - COMMENTARY
Year : 2019  |  Volume : 67  |  Issue : 3  |  Page : 862-866

Intra-operative, spontaneous subarachnoid hemorrhage during anterior temporal lobectomy for mesial temporal sclerosis: Video evidence and literature review


1 Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
2 Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
3 Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India

Date of Web Publication23-Jul-2019

Correspondence Address:
Dr. Bhaskara Rao Malla
Department of Neurosurgery National Institute of Mental Health and Neurosciences, Bengaluru - 560 029, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.263215

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How to cite this article:
Yeole U, Malla BR, Arivazhagan A, Shashidhar A, Deora H, Mundalamuri RC, Raghvendra K, Bharath RD, Sinha S. Intra-operative, spontaneous subarachnoid hemorrhage during anterior temporal lobectomy for mesial temporal sclerosis: Video evidence and literature review. Neurol India 2019;67:862-6

How to cite this URL:
Yeole U, Malla BR, Arivazhagan A, Shashidhar A, Deora H, Mundalamuri RC, Raghvendra K, Bharath RD, Sinha S. Intra-operative, spontaneous subarachnoid hemorrhage during anterior temporal lobectomy for mesial temporal sclerosis: Video evidence and literature review. Neurol India [serial online] 2019 [cited 2019 Aug 24];67:862-6. Available from: http://www.neurologyindia.com/text.asp?2019/67/3/862/263215




Sir,

The commonest cause of spontaneous subarachnoid hemorrhage (SAH) is an intracranial aneurysmal rupture.[1],[2] It is a clinical entity with a high rate of morbidity and mortality. However, there are 15-20% of cases in which the cause of SAH is not detectable in spite of extensive diagnostic imaging.[3] The other common causes for spontaneous SAH include arterio-venous malformation, anticoagulation status, brain tumors and rarely vasculitis. There are reports of spontaneous SAH intraoperatively while operating non-aneurysmal cases like gliomas, epilepsies and trans-sphenoidal surgeries. We are reporting an uncommon case of drug-resistant epilepsy with medial temporal sclerosis (MTS), who developed spontaneous SAH during surgery. The standard surgical treatment for MTS is anterior temporal lobectomy with amygdalo-hippocampectomy (ATL-AH). The procedure is uncommonly associated with post-operative complications like superior quadrantanopia, visual or verbal memory deficits for right and left temporal lobe, respectively, and rarely contralateral motor weakness. An occurrence of spontaneous SAH during ATL-AH has not been reported. A thorough search of literature for intraoperative SAH was also carried out to shed light on the possible factors or etiologies.

A 34-year old man presented with a history of uncontrolled complex partial seizures for the last 22 years. He was on appropriate dosages of sodium valproate, levetiracetam, zonisamide, and clobazam for the last 7 years. The seizure frequency was 2-3 episodes/week, each episode lasting for 5-10 seconds. He underwent a standard pre-surgical evaluation with magnetic resonance imaging (MRI) of the brain, video-electro-encephalography (V-EEG), psychiatric and neuropsychological assessment, and magnetoencephalography (MEG). There was concordance among all the modalities. The epileptogenic focus was localized to the right mesial temporal lobe [Figure 1]a and [Figure 1]b. He was a carrier of hepatitis B infection for the last nine years. Preoperative biochemical and hematological evaluation, including liver function tests and coagulation parameters, were normal. There was no other known co-morbidity or history of chronic medications.
Figure 1: Preoperative MRI Brain. (a) Axial FLAIR image showing a bulky hippocampus with hyperintense signal change in the parahippocampal gyrus. (b) T2 weighted coronal image showing loss of volume in the hippocampal region with dilatation of temporal horn of the lateral ventricle

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After informed consent, he was taken up for ATL-AH under general anesthesia. During induction of anesthesia and craniotomy, he was hemodynamically stable. After the durotomy, the brain was lax and pulsatile [Video 1]. After the initiation of corticectomy over the middle temporal gyrus, without any vascular injury, there was sudden development of spontaneous SAH over the posterior temporal surface, with gradual swelling and herniation of brain over the craniotomy edges. The procedure was abandoned in view of brain herniation. The dura was slit open at edges, duroplasty was performed with temporalis fascia graft, and the bone flap was placed in the abdominal wall. In the immediate post-operative period, under anesthesia, a plain computed tomographic (CT) scan of the brain was done to evaluate the extent and cause of SAH. The plain CT scan of the brain showed a diffuse SAH involving bilateral Sylvian fissures and basal cisterns [Figure 2]a. The patient was evaluated with a CT and MR angiography, and the next day with a digital subtraction angiogram (DSA) to look for a cause of SAH. All the imaging investigations ruled out any vascular abnormality [Figure 2]b, [Figure 2]c, [Figure 2]d, [Figure 2]e. As he was having a 10-year history of hepatitis B, the antibody workup for autoimmune vasculitis was done, which also was found to be negative. In spite of starting oral nimodipine in the immediate post-operative period, he developed clinical vasospasm on post-operative day 3 with a neurologic deficit in the form of left lower limb weakness. He received intra-arterial nimodipine injection for three consecutive days, after which the vasospasm was relieved and he was discharged in a stable neurologic condition without any deficits and no seizures occurred postoperatively. He was continued on anti-epileptic drugs (AEDs) and was on a regular follow up.
Figure 2: Postoperative radiological imaging. (a) CT brain plain axial image showing the post-decompressive craniectomy status with brain herniation through the craniectomy defect with right Sylvian SAH with bilateral occipital horn IVH. (b) DSA right carotid injection on antero-posterior view showing filling of internal cerebral and middle cerebral artery with no evident vascular abnormality. (c) DSA left carotid injection on antero-posterior view showing filling of internal cerebral, anterior cerebral and middle cerebral artery with no evident vascular abnormality. (d) MRI brain T2 weighted axial image showing dilatation of temporal horn with atrophy of mesial temporal lobe structures. (e) MRI brain coronal FLAIR image showing post-operative changes in middle temporal gyrus with dilatation of temporal horn and atrophy of mesial temporal structures

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At the last follow-up after 12 months, he remained seizure free. No epileptiform discharges were noted on routine scalp EEG. MRI images showed atrophy of medial temporal lobe structures on the operative side with dilatation of temporal horn of the lateral ventricle [Figure 3]a. The preoperative fluid attenuated inversion recovery (FLAIR) signal changes in the hippocampal region were not seen in the follow-up imaging. MR angiography did not reveal any vascular abnormality [Figure 3]b.
Figure 3: Follow up MRI brain with MR angiography at 6 months. (a) T1 axial image showing dilated temporal horn with atrophy of mesial temporal lobe structures. (b) MR angiography images of right internal carotid and middle cerebral artery showing normal vessel architecture without any abnormality

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This is a rare case report of intra-operative spontaneous SAH in a person with drug-resistant epilepsy due to MTS. SAH developed without any obvious identifiable vascular pathology or any underlying cause like vasculitis. Various causes have been reported in the literature for the development of SAH intra-operatively in other neurosurgical disorders. It is rare in itself to observe diffuse SAH in an epilepsy case, with herniation of brain through the craniotomy defect. Generally, in patients with drug-resistant epilepsy, the brain is lax and pulsatile, while brain atrophy is noted due to chronic seizures and its sequelae on the brain.

A complete search for all cases of intraoperative sub-arachnoid hemorrhage was carried out using the PubMed and Medline search engines using the keywords “Subarachnoid Hemorrhage”, “Intraoperative Subarachnoid Hemorrhage” and “Subarachnoid Hemorrhage and epilepsy”. All the available results were checked for relevance to the present cases, and only those cases that reported SAH in a non-aneurysmal setting were included. [Table 1] mentions all the cases of spontaneous intra-operative SAH with various underlying primary pathologies.
Table 1: Review of all the cases of intraoperative subarachnoid hemorrhage with no perioperative vascular anomaly diagnosed

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There are cases of hepatitis B induced autoimmune vasculitis, which lead to the development of SAH.[9] In extrahepatic manifestations of hepatitis B, there is deposition of immune complexes in small or medium-sized vessels with the development of vasculitis and they are generally positive for the antineutrophil cytoplasmic antibody (ANCA).[10] This immunological phenomenon secondary to hepatitis B virus (HBV) infection can be the cause for SAH. In our case, however, the vasculitis workup was negative for any autoimmune antibody. Intraoperative hemodynamic instability with post-induction hypertension, leading to an intraparenchymal hematoma is reported in one of the cases of epilepsy.[11] However, we did not notice any perioperative hemodynamic fluctuation in our case.

Valproic acid causes bone marrow suppression, with a decrease in platelets production and aggregation leading to thrombocytopenia. It is seen in 5-60% cases.[12] It can lead to prolongation of bleeding time because of its toxic effects on hematopoietic stem cells. The effect on platelets due to valproic acid is similar to NSAIDs with the involvement of cyclooxygenases and arachidonic acid and thromboxane A2 reduction.[13] Contradicting this, there are some reports that thrombocytopenia associated with valproic acid is clinically insignificant and may not be the cause of the perioperative increase in the bleeding. Although this coagulopathy associated with valproic acid is not a constant finding, certain factors like the duration of valproic acid administration, a dose of valproic acid, the pediatric age and the female gender have a stronger association.[14] Our patient was on valproic acid for a long time, but we did not notice any abnormality of platelet function historically, clinically or biochemically throughout the course of his illness.

The exact cause of spontaneous intra-operative SAH in our patient could not be conclusively linked to any etiology. We hypothesize that an autoimmune response in the background of hepatitis infection could be the cause for bleed. SAH led to the subsequent atrophy of mesial temporal structures, which may have been the cause of cessation of seizures at least during the 12-month follow-up period. Completion of ATL will be mandated in the case of recurrence of habitual seizures. Perhaps advanced methods of coagulation testing in the form of platelet aggregation time or thromboelastography (TEG) could have given us a clue. The serendipitous seizure freedom and the absence of residual deficits in this case prevented us from pursuing the control of seizures postoperatively.

Intraoperative spontaneous sub-arachnoid hemorrhage is a rare phenomenon in non-aneurysmal surgeries and thus needs to be studied in detail. Detailed preoperative evaluation including the study of the co-morbidities and drugs which may affect coagulation parameters, must be performed to prevent this complication.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

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2.
Lucke-Wold BP, Logsdon AF, Manoranjan B, Turner RC, McConnell E, Vates GE, et al. Aneurysmal subarachnoid hemorrhage and neuroinflammation: A comprehensive review. Int J Mol Sci 2016;17:497.  Back to cited text no. 2
    
3.
Rinkel GJ, Wijdicks EF, Vermeulen M, Ramos LM, Tanghe HL, Hasan D, et al. Nonaneurysmal perimesencephalic subarachnoid hemorrhage: CT and MR patterns that differ from aneurysmal rupture. Am J Roentgenol 1991;12:829-34.  Back to cited text no. 3
    
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Matsuno A, Yoshida S, Basugi N, Itoh S, Tanaka J. Severe subarachnoid hemorrhage during transsphenoidal surgery for pituitary adenoma. Surg Neurol 1993;39:276-8.  Back to cited text no. 7
    
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Kuroyanagi T, Kobayashi S, Takemae T, Kobayashi S. Subarachnoid hemorrhage, midbrain hemorrhage and thalamic infarction following transsphenoidal removal of a pituitary adenoma. A case report. Neurosurg Rev 1994;17:161-5.  Back to cited text no. 8
    
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Joshi U, Subedi R, Gajurel BP. Hepatitis B virus induced cytoplasmic antineutrophil cytoplasmic antibody-mediated vasculitis causing subarachnoid hemorrhage, acute transverse myelitis, and nephropathy: A case report. J Med Case Rep 2017;11:91.  Back to cited text no. 9
    
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Szupera Z, Mezei Z, Kis B, Gecse Á, Vécsei L, Telegdy G. The effects of valproate on the arachidonic acid metabolism of rat brain microvessels and of platelets. Eur J Pharmacol 2000;387:205-10.  Back to cited text no. 13
    
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