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. 2020 Oct;15(7):733-742.
doi: 10.1177/1747493020937189. Epub 2020 Jun 26.

Cerebral ischemic and hemorrhagic complications of coronavirus disease 2019

Affiliations

Cerebral ischemic and hemorrhagic complications of coronavirus disease 2019

Ahmad Sweid et al. Int J Stroke. 2020 Oct.

Abstract

Background: The coronavirus disease 2019 is associated with neurological manifestations including stroke.

Objectives: We present a case series of coronavirus disease 2019 patients from two institutions with acute cerebrovascular pathologies. In addition, we present a pooled analysis of published data on large vessel occlusion in the setting of coronavirus disease 2019 and a concise summary of the pathophysiology of acute cerebrovascular disease in the setting of coronavirus disease 2019.

Methods: A retrospective study across two institutions was conducted between 20 March 2020 and 20 May 2020, for patients developing acute cerebrovascular disease and diagnosed with coronavirus disease 2019. We performed a literature review using the PubMed search engine.

Results: The total sample size was 22 patients. The mean age was 59.5 years, and 12 patients were female. The cerebrovascular pathologies were 17 cases of acute ischemic stroke, 3 cases of aneurysm rupture, and 2 cases of sinus thrombosis. Of the stroke and sinus thrombosis patients, the mean National Institute of Health Stroke Scale was 13.8 ± 8.0, and 16 (84.2%) patients underwent a mechanical thrombectomy procedure. A favorable thrombolysis in cerebral infarction score was achieved in all patients. Of the 16 patients that underwent a mechanical thrombectomy, the mortality incidence was five (31.3%). Of all patients (22), three (13.6%) patients developed hemorrhagic conversion requiring decompressive surgery. Eleven (50%) patients had a poor functional status (modified Rankin Score 3-6) at discharge, and the total mortality incidence was eight (36.4%).

Conclusions: Despite timely intervention and favorable reperfusion, the mortality rate in coronavirus disease 2019 patients with large vessel occlusion was high in our series and in the pooled analysis. Notable features were younger age group, involvement of both the arterial and venous vasculature, multivessel involvement, and complicated procedures due to the clot consistency and burden.

Keywords: Coronavirus disease 2019; angiotensin (1–7); angiotensin-converting enzyme 2; cerebral venous thrombosis; cerebrovascular disease; hypercoagulable; severe acute respiratory syndrome coronavirus 2; stroke; thrombectomy.

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Figures

Figure 1.
Figure 1.
Fifty-one-year-old male with no past medical concerns developed an acute neurological insult. On admission his NIHSS score was 15, head CT did not show any hemorrhage and tPA was given. The patient underwent a MT procedure within 3 h and 52 min. The patient had a right ICA occlusion from the cervical segment into the supraclinoid segment with a tandem M1 occlusion. The procedure was complicated by ICA re-occlusion and distal embolization occluding the A1. The insult progressed into complete infarct, and the patient passed away three days later. (a) Antero-posterior (AP) digital subtraction angiography (DCA) of a right ICA injection showing complete occlusion at cervical ICA segment; (b) AP DCA view showing an occlusion of the supraclinoid segment of the ICA; (c) AP DCA view showing an M1 occlusion; (d) AP DCA view showing re-occlusion of the cervical ICA segment; (e) AP DCA occlusion of the A1 segment either due to a distal embolization or a dissection; (f) final view showing revascularization of the ICA, M1, and A1 with a TICI 2B result by deploying intracranial and extracranial rescue stents; (g) non-contrast axial view of the brain, day 1 post mechanical thrombectomy showing the progression of the insult into a complete infarct; (h) all the devices in the room are draped; and (i) showing the powered air-purifying respirator used by operators.
Figure 2.
Figure 2.
Forty-four-year-old male experienced a sudden loss of consciousness following intense bouts of coughing. (a) and (b) He was diagnosed with ruptured 1.5 cm left PCOM aneurysm causing intraventricular, intracerebral, and subdural hemorrhage. (c) Lateral view of a follow-up DCA post-surgical aneurysm reconstruction and decompressive hemicraniectomy showing complete aneurysm obliteration. (d) Axial view of a non-contrast CT head day 1 post op shows decompression of the brain without a midline shift and a 3 cm epidural hematoma. (e) A follow-up non-contrast CT head four days post op showed increasing brain edema with midline shift, extensive bilateral cerebral infarcts with extension of the infarct into the bilateral occipital.
Figure 3.
Figure 3.
(a) and (b) Access route for the SARS-CoV-2 to the CNS via the olfactory route and hematogenous route via direct access or via a Trojan. (c) The hyperinflammatory, hypercoagulable state induced by SARS-CoV-2. (d) The downregulation of ACE2 receptor at the endothelium level. This blocks the conversion of angiotensin I and II into their active metabolites. The decline in Angiotensin (1–7) levels leads to loss of neuroprotective effect and sympathetic hyperactivity. ACE2: angiotensin-converting enzyme 2; ANG (1–7): angiotensin (1–7); SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.

References

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