CASE REPORT

Acute Ischemic Stroke Associated with COVID-19
Buse Cagla Ari
Department of Neurology, Medical Faculty, Bahcesehir University, Pendik Medical Park Hospital, Istanbul, Turkey

ABSTRACT
During the prevailing coronavirus disease 2019 (COVID-19) pandemic, the disease has started manifesting with some neurological symptoms. There have been reports on acute ischemic stroke, cerebral venous thrombosis, and intracerebral hemorrhage
associated with COVID-19. The plausible mechanism that causes these ischemic processes is called "sepsis-induced coagulopathy." A 40-year male patient, who was hospitalised due to COVID-19 pneumonia, developed sudden-onset motor aphasia and
right-sided hemiplegia. He was then placed in, with the diagnosis of acute ischemia, most probably associated with COVID-19,
considering that the patient's medical history was not remarkable for a relevant etiology, and all tests for the etiology of
ischemic stroke showed normal findings. The patient was placed on therapy with acetyl salicylic acid, 300 mg/day. It is
presumed that ischemic events occur by an increase in coagulopathy secondary to inflammation. COVID-19 causes ischemic
processes by inducing endothelial dysfunction and arterial or venous thrombosis.
Key Words: COVID-19, Stroke, Coagulopathy, Ischemia; SARS-CoV-2.
How to cite this article: Ari BC. Acute Ischemic Stroke Associated with COVID-19. J Coll Physicians Surg Pak 2021;
31(JCPSPCR):CR132-CR134.

INTRODUCTION
Coronavirus disease 2019 (COVID-19) caused by the severe
acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
presents with respiratory problems, but it can also manifest with
neurological symptoms as anosmia, seizures, and encephalopathy. There have been reports of cases with ischemic stroke,
cerebral venous thrombosis, and intracerebral hemorrhage.1,2
There is an increase in cerebrovascular events related to the
disease.3 The underlying pathophysiology has been defined as
"sepsis-induced coagulopathy(SIC)," which has been known as
the initial process of disseminated intravascular coagulation
(DIC). The systemic inflammatory response induced by infection
aggravates coagulopathy, and results in organ failure, and
ischemia by causing endothelial dysfunction.3,4 So far, a few
cases of acute ischemic stroke associated with COVID-19 have
been reported, but the actual underlying mechanism has not
been clarified yet. The current report aims to increase the awareness of the neurological manifestations of COVID-19.

CASE REPORT
A 40-year male patient presented with fever, shortness of
breath, and cough that started a week before admission. On
examination, he had dyspnea (respiratory rate, 28/min), fever
(37.6oC), and hypoxemia (oxygen saturation on room air = 80%).
Correspondence to: Dr. Buse Cagla Ari, Department of
Neurology, Medical Faculty, Bahcesehir University, Pendik
Medical Park Hospital, Istanbul, Turkey
E-mail: juvelia@gmail.com
.....................................................
Received: December 22, 2020; Revised: March 02, 2021;

Accepted: April 18, 2021
DOI: https://doi.org/10.29271/jcpsp.2021.JCPSPCR.CR132
132

In the laboratory, procalcitonin was 0.59 ng/ml, C-reactive
protein (CRP) was 265.1 mg/L, ferritin was 1180.5 µg/l, troponin
was 19.2 ng/l, D-dimer was 1280 µg/dl, prothrombin time (PT)
was 16.1 seconds, and fibrinogen was 661 mg/dl. The complete
blood count revealed leukocytosis (9.22×109/L), lymphopenia
(1.04×109/L), and thrombocytopenia (100×109/L). Thoracic
computed tomography (CT) revealed bilateral consolidation in
the upper, middle, and lower zones of the lungs, accompanied
by air bronchograms and infiltration, mainly of lung
parenchyma in subpleural areas with ground glass opacity in
the middle and upper zones (Figure 1). The patient was diagnosed with COVID-19 upon detection of SARS-CoV-2 in reverse
transcriptase-polymerase chain reaction (RT-PCR) analysis of
the throat swab sample, and was placed on therapy with
azithromycin 250 mg/day, favipiravir 600 mg/day followed by
the loading dose. He was provided with continuous positive
airway pressure ventilation support to relieve respiratory
distress. During his stay in the hospital, he developed motor
aphasia, forced deviation of the head and eyes to the left, right
homonymous hemianopsia, right central facial paralysis, right
hemiplegia, brisk deep tendon reflexes in right extremities, and
extensor plantar response in the right foot on the fifth day of
admission. The National Institutes of Health Stroke Scale
(NIHSS) score was 16. Blood pressure was 135/80 mm/Hg. Electrocardiogram revealed a normal sinus rhythm. We observed an
acute diffusion restriction in the area supplied by the upper division of the left middle cerebral artery (MCA) in multiple resonance imaging (MRI) (Figure 2). The patient was not treated with
intravenous (iv) thrombolytic therapy as he was already on
therapy with enoxaparin 12,000 IU/day. We continued the
existing therapy with low-molecular-weight heparin (LMWH),
and added acetyl salicylic acid 300 mg/day with the diagnosis of
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Buse Cagla Ari

acute ischemic stroke. Cranial and cervical CT angiography
showed no findings suggestive of a vascular occlusion. His
cholesterol levels and HbA1c were within normal ranges. He
tested negative for the vasculitis workup. Transthoracic echocardiography (ECHO) revealed normal findings. The history was
not remarkable for any disease or drug use. He was considered
to have acute ischemic stroke secondary to COVID-19, considering the nature of existing clinical symptoms and the lack of
findings that would suggest other causes of stroke. He was
connected to the mechanical ventilator upon a further decline in
th
the consciousness level. On the 10 day, his consciousness
level improved, and muscle strength increased to 3/5 in the
upper and 2/5 in the lower limbs.

Figure 1: A single axial image from the thorax CT scan of the patient
demonstrating ground-glass opacity on basal parts of the lungs bilaterally.

with COVID-19-related stroke. It has also been observed that
patients with comorbid conditions exhibit a more aggressive
disease course and are prone to ischemic events.5,6 Our patient
did not have a risk factor, tested negative in the young stroke
panel, and the tests to detect etiology identified no factor to
cause coagulopathy. To the best of our knowledge, the present
patient was one of the first cases of large-vessel artery ischemia
secondary to COVID-19, younger than 50-year, and that did not
have any risk factors.7,8
A proposed mechanism of ischemic events in COVID-19 is the
release of cytokines due to the activation of an inflammatory
cascade secondary to hypoxia.9 An increase in interleukin (IL)
levels causes the activation of endothelial and mononuclear
cells, thereby increasing thrombin production, accelerating
atherosclerosis, and resulting in stroke.8,10 Our patient had
refractory hypoxia, and oxygen saturation did not reach the
desired level, despite supplementation. It was, therefore,
thought that a hypoxic state and inflammation might cause an
ischemic stroke. SIC occurs after the development of the
disease that leads to DIC with an increase in D-dimer and
fibrinogen levels. SIC causes abnormalities in the coagulation
cascade, resulting in prolonged prothrombin time (PT),
increased D-dimer levels, and thrombocytopenia. COVID-19
triggers a systemic inflammatory response that lead to endothelial dysfunction and thrombosis.3 PT was prolonged, and Ddimer and fibrinogen levels were increased in our patient. The
therapy with LMWH was, therefore, continued.
An issue that struck our mind was, even though our patient was
on LMWH treatment, he had a stroke. Therefore, it could be
concluded that LMWH therapy might not be effective enough to
protect the patients from cerebrovascular events. As a result,
for future approaches, at the onset of the COVID-19, it could be a
rational suggestion to add anti-aggregants apart from LMWH.
In conclusion, the cerebrovascular events' pathophysiology
secondary to COVID-19 is still unknown, and further studies are
required to elucidate the actual mechanism.
ACKNOWLEDGEMENT:
This case report was written at Neurology Department, Siirt
Research and Training Hospital, Turkey
PATIENT’S CONSENT:
The informed consent was provided from the patient.
CONFLICT OF INTEREST:
The author declared no conflict of interest.
AUTHOR’S CONTRIBUTION:
BCA: Conceived, designed the manuscript, and did editing.

Figure 2: Axial diffusion-weighted images (DWI) and apparent diffusion
coefficient (ADC) images on MRI of the patient. It demonstrates increased
signal in the territory of the upper division of left middle cerebral artery
(MCA) on A and B.

DISCUSSION
Recent studies have reported a mean age of 71 years in patients
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