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NI FEATURE: FACING ADVERSITY…TOMORROW IS ANOTHER DAY! - LETTERS TO EDITOR
Year : 2019  |  Volume : 67  |  Issue : 3  |  Page : 861-862

Respiratory arrest immediately after thrombolysis for posterior circulation stroke


Stroke Center, Department of Neurosurgery, Tokorozawa Chuo Hospital, 3-18-1 Kusunokidai, Tokorozawa, Saitama, Japan

Date of Web Publication23-Jul-2019

Correspondence Address:
Dr. Hiroshi Nawashiro
Stroke Center, Tokorozawa Chuo Hospital, 3-18-1 Kusunokidai, Tokorozawa, Saitama - 359-0037
Japan
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.263202

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How to cite this article:
Nawashiro H. Respiratory arrest immediately after thrombolysis for posterior circulation stroke. Neurol India 2019;67:861-2

How to cite this URL:
Nawashiro H. Respiratory arrest immediately after thrombolysis for posterior circulation stroke. Neurol India [serial online] 2019 [cited 2019 Nov 15];67:861-2. Available from: http://www.neurologyindia.com/text.asp?2019/67/3/861/263202




Sir,

Timely reperfusion is the best way to improve outcomes of acute ischemic stroke. However, devastating neurological worsening could occur after intravenous thrombolysis. Recently, recurrent early ischemia after thrombolysis is known to be the most prevalent cause for an early neurological deterioration.[1],[2],[3] However, its mechanism remains unclear in most cases.

We have encountered two patients of posterior circulation stroke who presented with sudden respiratory arrest immediately after completion of 0.6 mg/kg alteplase administration.

A 61-year old man was admitted with the first episode of vertigo, ataxia, and dysarthria. The National Institutes of Health Stroke Scale (NIHSS) score was 5. The magnetic resonance imaging (MRI) of the head at admission showed scattered small high-intensity areas on diffusion-weighted images (DWI) in bilateral cerebellar hemispheres [Figure 1]a. Magnetic resonance angiography (MRA) revealed the absence of right and left vertebral arteries and basilar artery flow [Figure 1]b. A single alteplase dose of 0.6 mg/kg was administered intravenously 175 min after the symptom onset, with 10% given as a bolus, followed by continuous infusion of the remainder over 1 h. He suddenly became comatose and had a respiratory arrest after completion of alteplase administration. Head computed tomography (CT) showed no hemorrhage. Urgent rescue endovascular therapy was done within 6 h after the symptom onset using a direct aspiration, first pass technique, resulting in thrombolysis in cerebral infarction (TICI 2B) reperfusion [Figure 1]c; however, he was still comatose 30 days after the ictus.
Figure 1: (a), DWI of the first case on admission. (b), MRA of the first case on admission. (c), Right vertebral angiogram after rescue endovascular therapy. (d), DWI of the second case on admission. (e), MRA of the second case on admission. (f), Basiparallel anatomic scanning–MR imaging on admission. (g), DWI of the second case after neurological deterioration

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The second case was a 67-year old woman admitted with vertigo and dysarthria. The NIHSS score was 5. The initial head MRI showed a high-intensity area in the right cerebellar tonsil and hemisphere [Figure 1]d. MRA demonstrated right vertebral artery occlusion [Figure 1]e and basiparallel anatomic scanning (BPAS)–MR imaging clearly delineated the right vertebral artery [Figure 1]f. The combination of MRA with BPAS clarified the pathology of arterial occlusion.[4] An alteplase dose of 0.6 mg/kg was administered. She suddenly became comatose and had a respiratory arrest immediately after completion of alteplase administration. After supportive ventilation, she recovered consciousness and spontaneous respiration. The NIHSS score worsened to 10. The diffusion weighted image (DWI) after neurological deterioration revealed a new and a pronounced extension of high-signal-intensity areas [Figure 1]g. Her modified Rankin scale score, 30 days after stroke, was 3.

The temporal profile that neurological deterioration occurred immediately after completion of alteplase administration in both cases suggests a causative role of recombinant tissue plasminogen activator (rtPA).[3] Extension and migration of the unstable thrombi after rtPA administration for the treatment of large vessels occlusion could play a role in neurological deterioration after thrombolysis.[1],[2],[3] Registration of such cases will be meaningful.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
 » References Top

1.
Seners P, Hurford R, Tisserand M, Turc G, Legrand L, Naggara O, et al. Is unexplained early neurological deterioration after intravenous thrombolysis associated with thrombus extension? Stroke 2017;48:348-52.  Back to cited text no. 1
    
2.
Simonsen CZ, Schmitz ML, Madsen MH, Mikkelsen IK, Chandra RV, Leslie-Mazwi T, et al. Early neurological deterioration after thrombolysis: Clinical and imaging predictors. Int J Stroke 2016;11:776-82.  Back to cited text no. 2
    
3.
Georgiadis D, Engelter S, Tettenborn B, Hungerbühler H, Luethy R, Müller F, et al. Early recurrent ischemic stroke in stroke patients undergoing intravenous thrombolysis. Circulation 2006;114:237-41.  Back to cited text no. 3
    
4.
Takeuchi S, Wada K, Nagatani K, Nawashiro H. Differentiation between vertebral artery hypoplasia and occlusion. Intern Med 2012;51:345.  Back to cited text no. 4
    


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