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Table of Contents    
LETTER TO EDITOR
Year : 2018  |  Volume : 66  |  Issue : 2  |  Page : 520-522

Remote contralateral side cerebral venous thrombosis following intracranial surgery: A rare complication in an unusual setting


1 Department of Neurosurgery, NIMHANS, Bangalore, Karnataka, India
2 Department of Neurology, NIMHANS, Bangalore, Karnataka, India
3 Department of NIIR, NIMHANS, Bangalore, Karnataka, India
4 Department of Neuropathology, NIMHANS, Bangalore, Karnataka, India

Date of Web Publication15-Mar-2018

Correspondence Address:
Dr. A Arivazhagan
Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Hosur road, Bangalore - 560 029, Karnataka
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.227318

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How to cite this article:
Arivazhagan A, Mundlamuri RC, Shreedhara A S, Bharath RD, Mahadevan A, Sinha S, Rao MB, Satishchandra P. Remote contralateral side cerebral venous thrombosis following intracranial surgery: A rare complication in an unusual setting. Neurol India 2018;66:520-2

How to cite this URL:
Arivazhagan A, Mundlamuri RC, Shreedhara A S, Bharath RD, Mahadevan A, Sinha S, Rao MB, Satishchandra P. Remote contralateral side cerebral venous thrombosis following intracranial surgery: A rare complication in an unusual setting. Neurol India [serial online] 2018 [cited 2019 Aug 23];66:520-2. Available from: http://www.neurologyindia.com/text.asp?2018/66/2/520/227318




Sir,

Cortical venous thrombosis (CVT), most often occurring as a spontaneous event secondary to procoagulant risk factors, is known to be precipitated by dehydration or by a cascade of events in the peri-partum period.[1],[2] Postoperative cortical venous thrombosis, as a consequence of venous injury in the operative field, is not an uncommon complication and has an incidence of 7%.[3] CVT is very rare, when the iatrogenic ones due to venous injury during surgery are excluded. We report a patient who developed CVT on the contralateral side of intracranial surgery and discuss the various factors which could have resulted in such a unique and previously unreported scenario.

A 22-year old gentleman, right-handed, had presented with drug resistant focal seizures of 11 year duration. The seizure semiology comprised of an aura of fear followed by impairment of consciousness, lip smacking, left upper limb tonic posturing and right upper limb automatisms, followed by forced head turning to the left side and secondary generalization. The seizures remained poorly controlled despite the administration of multiple anti-epileptic drugs, namely valproate (1000 mg/day), leviteracetam (1500 mg/day), clobazam (15 mg/day) and carbamazepine (1200 mg/day). There was a history of febrile seizures in the childhood. His diet was vegetarian and he had no history of alcohol intake, smoking or symptoms of gastrointestinal malabsorption. He had no history of cerebrovascular or cardiac disease in the past. He was evaluated for drug resistant epilepsy. MRI brain revealed atrophy of the right hippocampus with loss of architecture, and dilatation of the right temporal horn suggestive of right mesial temporal sclerosis [Figure 1]a. The video electroencephalogram (EEG) was suggestive of a seizure arising from the right anterior temporal region. Magnetoencephalography revealed significant clusters of dipole in the right mid and superior temporal regions. Routine blood investigations showed normal levels (Hemoglobin 13 gm/dl, total leucocytic count 6,400/dl, platelets 12.6 lakhs/cu.mm; international normalized ratio [INR] 0.94). A diagnosis of right mesial temporal sclerosis causing drug resistant epilepsy was made and he was advised surgery. The benefits and risks involved with the procedure were discussed in detail with the patient and his parents and after their consent, the patient underwent a right anterior temporal lobectomy and amygdalo-hippocampectomy. There was no significant blood loss or hemodynamic disturbances during surgery. The procedure was uneventful and he was fully conscious, had no complaints or neurological deficits immediately after the surgery. On postoperative day 1, routine computed tomographic (CT) scan of the brain was performed (around 16 hours after the surgery) which showed no post-operative hematoma at the site of surgery [Figure 1]b. There was evidence of curvilinear hyperdensity in the left parietal parasagittal region, which was perceived as subarachnoid blood [Figure 1]c and [Figure 1]d. A possibility of cortical venous thrombosis was considered, and an MRI of the brain was planned the next day. The patient was asymptomatic at this time. Around 32 hours after the surgery, at 3 AM in the morning, the patient developed one episode of right focal motor seizure involving the face and upper limb, which was controlled with intravenous phenytoin (800 mg). However, 6 hours later, he had another episode of right focal seizure and lapsed into altered sensorium. An urgent CT scan of the brain showed a large left parietal lobe hemorrhagic infarct with intraventricular bleed and mass effect [Figure 1]e and [Figure 1]f. There was no evidence of a filling defect in the dural venous sinuses. The reason for the hemorrhage was considered unrelated to the surgical procedure as it was remote and on the opposite side of the surgical site. He underwent an emergent left temporo-parieto-occipital decompressive craniectomy and augmentative duroplasty. Intraoperatively, the brain was tense and bulging; multiple thrombosed cortical veins were noted in the left parietal region [Figure 1]g. He was simultaneously worked up for coagulation disorders and his coagulation parameters (INR: 1.15, prothrombin time (PT): 15.7; activated partial thromboplastin time [APTT]: 36.1) were within normal limits. The patient was continued on anti edema measures. The option of starting heparin in the acute postoperative set up was discussed and he was started on heparin 5000 units QID about 24 hours after the second surgery. An MR venogram performed showed patent dural venous sinuses [Figure 1]h. He improved gradually in sensorium following surgery, with residual right hemiparesis. He was investigated to identify the exact cause of CVT in the immediate postoperative setting, which revealed a negative serum anti-nuclear antibody profile, a high serum homocysteine level (74.36 μmol/L) and a low serum vitamin B12 level (50 ng/L). He was treated with oral anticoagulants, vitamin supplement (B12, B6, folate) and rehabilitation. At discharge, he was obeying comands, with a persistent right hemiparesis of grade 3/5 proximally and 1/5 distally. At a nine-month follow up, he was seizure-free, had mild residual right hemiparesis, and has undergone a cranioplasty.
Figure 1: Compilation of the images depicting the sequence of events. Pre-operative fluid attenuated inversion recovery (FLAIR) coronal MRI (a) reveals right sided medial temporal sclerosis. Postoperative day 1 CT scan (b) reveals the anterior temporal lobectomy with evidence of hyperdense curvilinear structures (c and d) which was perceived as subarachnoid blood. Follow-up CT scan on postoperative day 2 (e and f) reveals a left parietal hemorrhagic infarct with an intraventricular extension, mass effect and subfalcine herniation. Intraoperative photograph during the left parietal decompressive craniectomy, (g) showed an edematous and bulging brain with thrombosed cortical veins in the left parietal region. Subsequently, magnetic resonance venogram (h) revealed patent dural venous sinuses

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Anterior temporal lobectomy with amygdalo-hippocampectomy is one of the commonest surgical procedures performed for drug resistant epilepsy, with a major complication rate of 4.1%, the most common ones being intracranial hematoma or infection.[4] Cortical venous thrombosis following intracranial surgery has been reported earlier and is most often due to the iatrogenic injury or coagulation of a draining cortical vein in the proximity of the surgical field.[5] However, in our case, any venous injury during the surgical procedure leading to CVT was comprehensively ruled out since the thrombosis of veins occurred remote from the surgical site, in the opposite hemisphere. Nevertheless, the temporal relationship of occurrence of CVT within a few hours after the surgical procedure, emphasizes the fact that the surgery had influenced the onset of CVT in some manner. Such a complication, namely, remote CVT following elective intracranial surgery has not been reported earlier to the best of our knowledge. We reviewed the various rare etiologies which can result in CVT.[1],[2] Steroids have been reported to increase the risk of CVT, more often in higher doses and when administered for a longer duration.[6] Our patient received dexamethasone in standard doses for a short period only in the peri-operative period, and therefore, administration of steroid would be an unlikely cause responsible for this complication. Cortical venous thrombosis has been reported following a lumbar puncture and/or administration of spinal anesthesia in some cases, possibly secondary to iatrogenic intracranial hypotension.[7],[8] Presicci et al., reported a child where both lumbar puncture and intravenous steroids could have played a role in causing CVT.[9] Our patient underwent a standard temporal lobectomy with a resultant cavity in the temporal region. However, this would not have caused intracranial hypotension. Therefore, we were not able to ascertain the etiology for the occurrence of CVT in this patient in the immediate postoperative period. Subsequent work up for procoagulant factors revealed the presence of hyperhomocysteinemia and a low serum vitamin B12 level. It is well known that these factors can increase the risk of CVT.[10] Hyperhomocysteinemia increases the risk of CVT with an odds ratio of 4.6 (95% confidence interval: 1.6–12.0).[1] The cause for hyper-homocysteinemia could be hereditary or acquired. In this case, the predisposing factors for hyper-homocysteinemia and low B12 levels could be a pure vegetarian diet and antiepileptic drugs. Various studies have reported that anticonvulsants like carbamazepine and valproate, especially in combination, can cause hyperhomocysteinemia.[11],[12] The peculiarity of our case was the onset of CVT in the perioperative period, which indicates that hemodynamic factors may have precipitated CVT in a patient with pre-existing risk factors. Previously, the onset of CVT due to conditions causing hemodynamic changes like dehydration, pregnancy, oral contraceptive drugs have been reported.[2] Our case highlights the possibility that a surgical procedure with its attendant hemodynamic changes and stress, albeit with a meticulous perioperative fluid management, can precipitate CVT in high risk individuals.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Saposnik G, Barinagarrementeria F, Brown RD, Bushnell CD, Cucchiara B, Cushman M, et al. Diagnosis and management of cerebral venous thrombosis: A statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2011;42:1158-92.  Back to cited text no. 1
    
2.
Saadatnia M, Fatehi F, Basiri K, Mousavi SA, Mehr GK. Cerebral venous sinus thrombosis risk factors. Int J Stroke 2009;4:111-23.  Back to cited text no. 2
    
3.
Agrawal D, Naik V. Postoperative cerebral venous infarction. J Pediatr Neurosci 2015;10:5-8.  Back to cited text no. 3
[PUBMED]  [Full text]  
4.
Mathon B, Navarro V, Bielle F, Nguyen-Michel V-H, Carpentier A, Baulac M, et al. Complications after surgery for mesial temporal lobe epilepsy associated with hippocampal sclerosis. World Neurosurg 2017;  Back to cited text no. 4
    
5.
Nakase H, Shin Y, Nakagawa I, Kimura R, Sakaki T. Clinical features of postoperative cerebral venous infarction. Acta Neurochir (Wien) 2005;147:621-6.  Back to cited text no. 5
    
6.
Kalanie H, Harandi AA, Alidaei S, Heidari D, Shahbeigi S, Ghorbani M. Venous thrombosis in multiple sclerosis patients after high-dose intravenous methylprednisolone: The preventive effect of enoxaparin. Thrombosis 2011;2011:785459.  Back to cited text no. 6
    
7.
Honig A, Eliahou R, Pikkel YY, Leker RR. Iatrogenic intracranial hypotension and cerebral venous thrombosis. J Neurol Sci 2016;366:191-4.  Back to cited text no. 7
    
8.
Costa BL, Shamasna M, Nunes J, Magalhães F, Peliz AJ. Cerebral venous thrombosis: An unexpected complication from spinal surgery. Eur Spine J 2014;23.  Back to cited text no. 8
    
9.
Presicci A, Garofoli V, Simone M, Campa MG, Lamanna AL, Margari L. Cerebral venous thrombosis after lumbar puncture and intravenous high dose corticosteroids: A case report of a childhood multiple sclerosis. Brain Dev 2013;35:602-5.  Back to cited text no. 9
    
10.
Dash D, Prasad K, Joseph L. Cerebral venous thrombosis: An Indian perspective. Neurol India 2015;63:318-28.  Back to cited text no. 10
[PUBMED]  [Full text]  
11.
Linnebank M, Moskau S, Semmler A, Widman G, Stoffel-Wagner B, Weller M, et al. Antiepileptic drugs interact with folate and vitamin B12 serum levels. Ann Neurol 2011;69:352-9.  Back to cited text no. 11
    
12.
Karabiber H, Sonmezgoz E, Ozerol E, Yakinci C, Otlu B, Yologlu S. Effects of valproate and carbamazepine on serum levels of homocysteine, vitamin B12, and folic acid. Brain Dev 2003;25:113-5.  Back to cited text no. 12
    


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