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ORIGINAL ARTICLE Table of Contents  
Ahead of print publication
Clinical course and outcome of stroke patients at a tertiary health care center during SARS-COV-2 pandemic in North India: A single-center study

1 Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India
2 Department of Cardiovascular and Thoracic Surgery, King George's Medical University, Lucknow, Uttar Pradesh, India
3 Department of Internal Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India
4 Department of Plastic Surgery, King George's Medical University, Lucknow, Uttar Pradesh, India

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Date of Submission13-Jun-2022
Date of Decision12-Jul-2022
Date of Acceptance21-Jul-2022
Date of Web Publication27-Oct-2022


Background: SARS-COV-2 is primarily a respiratory illness. However, beyond respiratory illness and associated acute and long-term medical complications, it manifests as stroke, including acute ischemic stroke and hemorrhagic stroke. Clinical evidence reported the occurrence of both venous and arterial thromboembolic complications in SARS-COV-2 positive patients due to hypercoagulable state, hyperinflammatory response, cardiomyopathy, and endothelial inflammation. Materials and Methods: This is a retrospective, single-center cohort study, which includes confirmed SARS-COV-2-positive patients hospitalized between March 2021 and February 2022. Clinical and biochemical data were analyzed. Noncontrast computed tomography of the brain was performed to assess the area and type of stroke. Results: Among all the included 703 patients with SARS-COV-2, 42 patients developed stroke. SARS-COV-2 patients who developed stroke were older and had multiple comorbidities. Patients had higher quick sequential organ failure assessment (qSOFA) score on hospitalization (P < 0.05), higher in-hospital mortality, and had poor clinical outcomes (P < 0.0001). In multivariate regression analysis, there were higher odds of in-hospital mortality linked with higher qSOFA scores (odds ratio 4.47, 95% confidence interval 1.21–16.5; P = 0.025). SARS-COV-2 patients developing stroke had high total leukocyte counts, high neutrophil counts, low platelet counts, low lymphocyte counts, raised C-reactive protein, raised ferritin levels, raised interleukin-6, raised fibrinogen, and D-dimer as compared to those without stroke. Conclusion: Patients with SARS-COV-2 who developed stroke had more severe clinical symptoms, poor clinical outcomes, and higher in-hospital mortality rates compared to those without stroke.

Keywords: SARS-COV-2, stroke, thrombo-embolism

How to cite this URL:
Atam V, Kumar S, Rahul K, Kumar B, Gupta H, Sonkar SK, Patel ML, Kumar A, Singh A, Yadav A. Clinical course and outcome of stroke patients at a tertiary health care center during SARS-COV-2 pandemic in North India: A single-center study. J Appl Sci Clin Pract [Epub ahead of print] [cited 2023 Feb 4]. Available from: http://www.jascp.org/preprintarticle.asp?id=358989

  Introduction Top

Coronavirus disease 2019 (SARS-COV-2) was first detected in December 2019 in Wuhan, China and was declared a global pandemic by the World Health Organization as of March 11, 2020. Till now, SARS-COV-2 disease has affected more than 50 million individuals and caused more than 6 million fatalities worldwide. SARS-COV-2 is primarily a respiratory illness, the disease being characterized by fever, dry cough, dyspnea, and hypoxia with interstitial pneumonia being detected on chest X-ray or computed tomography scan of the thorax.[1],[2] However, beyond respiratory illness and associated acute- and long-term medical complications, it manifests as stroke including acute ischemic stroke (AIS) and hemorrhagic stroke [Figure 1] and [Figure 2].[3],[4] Hypercoagulable state, hyperinflammatory response, cardiomyopathy, endothelial inflammation, and injury from direct viral invasion can occur during the infectious phase and can lead to thromboembolic events resulting in cerebral ischemia.[5],[6],[7] One-third of patients with SARS-COV-2 positive can have neurological manifestations with the higher frequency seen in those with more severe infection. Studies evaluating these manifestations have demonstrated a variety of presentations and complications.[4] AIS has been reported as both presenting features and as a complication of SARS-COV-2. However, the most common neurological manifestations were dizziness (16.8%), headache (13.1%), and encephalopathy (2.8%). About 5.9% of SARS-COV-2-positive patients who developed stroke were older with multiple comorbidities including hypertension, diabetes mellitus, cardiovascular diseases, respiratory disease, and more severe pneumonia.[8],[9]
Figure 1: NCCT brain in SARS-COV-2 patient showing areas of ischemic infract (Department of Radiodiagnosis, King George's Medical University, India). NCCT: Noncontrast computed tomography scan of the brain

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Figure 2: NCCT brain in SARS-COV-2 patient showing areas of hemorrhagic stroke (Department of Radiodiagnosis, King George's Medical University, India). NCCT: Noncontrast computed tomography of brain

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Our present narrative aims to determine the incidence of ischemic and hemorrhagic stroke in SARS-COV-2-positive patients, assess the frequency of symptoms that lead to hospital admissions among SARS-COV-2-positive patients who had an ischemic or hemorrhagic stroke, assess the risk factors for ischemic and hemorrhagic stroke in SARSCOV-2 positive patients, assess the clinical and laboratory data of stroke patients in comparison to those who did not develop stroke and to assess the clinical outcome and mortality in SARS-COV-2-positive patients.

  Materials and Methods Top

A single-center, retrospective study was conducted on patients admitted to Coronavirus Disease Hospital (SARS-COV-2 Hospital) of King George's Medical University, the largest designated Medical Center for SARS-COV-2 in Northern India, from March 2021 to February 2022. This institution facilitates tertiary level care, admitting patients from urban as well as rural areas. Laboratory confirmation of SARS-COV-2 was performed by the real-time reverse transcriptase polymerase chain reaction (rt-PCR). The study was approved by KGMU Hospital Ethics Committee (Institutional Review Board ID: KGMU-COVID 03/20200188). Written informed consent was waived by the Ethics Committee of the University Hospital for emerging infectious diseases.

Data collection

Demographic, clinical, laboratory, management, and outcome data were obtained from patients' electronic medical records and analyzed. Clinical outcomes were followed up to 3 months after being discharged. We defined the clinical endpoint as severe events comprising of all-cause death, admission to intensive care unit (ICU), and mechanical ventilation.

Study population

The study included all patients, over the age of 18, hospitalized for SARS-COV-2 positive by real-time rt-PCR assay of nasopharyngeal and oropharyngeal swabs between March 2021 and February 2022. A total of 42 patients were identified, who developed new-onset stroke during the course of hospitalization and were stratified as a study group. Data from the study group were compared by control groups, without a history of stroke for hospitalizations, critical care services, intubation, and mortality data. Baseline demographic, laboratory data, and clinical outcomes in these groups were also studied.

Statistical analysis

The continuous variables were described as mean (standard deviation [SD]) if they were normally distributed or medians (interquartile range [IQR]) if not normally distributed and compared using Mann–Whitney U-test. The categorical variables were delineated as n (%) and compared by χ2 test and Fisher's exact test. Propensity score matching of patients with and without a history of stroke was performed using a 1:4 matching algorithm with a caliper distance of 0.2 of the SD of the logit of the propensity score and controls used only once. Matching was performed using age, sex, history of smoking, and comorbidities including hypertension, diabetes mellitus, cardiovascular diseases, and malignant tumor. The matched cohorts were then compared using the Pearson χ2 test for categorical clinical outcomes and Cox-regression test for the composite endpoint. The hazard ratio and the 95% confidence interval (CI) are also reported. All the statistical analyses were performed using the IBM SPSS Statistics for Windows, Version 22.0. IBM Corp., Armonk, NY. Two-tailed P < 0.05 was statistically significant.

  Results Top

Clinical features of the study group

This study included a total of 745 SARS-COV-2-positive confirmed patients, of which 42 developed stroke during hospitalization (study group). The mean age of the study group was 68.4 ± 13.6 years and 19 (45.23%) were male in this group. In the control group, mean age was 45.9 ± 17.9 years and 375 (53.4%) were male. Baseline characteristics such as age, sex, associated comorbid conditions, clinical data, laboratory reports, and clinical outcome are listed in [Table 1].
Table 1: Baseline characteristics, risk factors, clinical data, laboratory parameters, and clinical outcome of study group and control group of SARS-COV 2 patients with and without stroke

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On comparing both the study and control groups, patients in the study group were observed with middle age as well as older age (68.4 ± 13.6 vs. 45.9 ± 17.9 years; P < 0.001) and had significantly higher comorbidities such as hypertension, chronic kidney disease, heart failure, diabetes mellitus, obstructive pulmonary disease, liver disease, ischemic heart disease, obesity, and history of smoking.

Laboratory findings among the study group

Noncontrast computed tomography of the brain (NCCT brain) was performed in stroke patients to look for the areas of the infarction [Figure 1] and [Figure 2]. SARS-COV-2 patients who developed stroke during hospitalization were found to have a hypercoagulable state as evidenced by raised C-reactive protein (CRP) (124 vs. 89 mg/L, P < 0.01), ferritin levels (989 vs. 763 ug/L, P < 0.001), fibrinogen (10 vs. 5 g/L, P < 0.023), and D-dimer (1760 vs. 786 ng/ml, P < 0.001). Other findings were increased total leukocyte counts (11.2 vs. 8.5 × 109/L; P = 0.437), higher neutrophil counts (4.8 vs. 3.9 × 109/L; P = 0.005), lower platelet counts (2.01 vs. 2.22 × 109/L; P = 0.025), lower lymphocytes (1.1 vs. 1.8 × 109/L; P < 0.001) in comparison to those without stroke. Interleukin-6 (IL-6) (21.55 pg/ml with IQR 6.46–93.55, P < 0.001) and lactate dehydrogenase (LDH) (296 units/L, P < 0.001) were also found significantly on the higher side of the study group.

Treatment, complications, and outcomes of the study group

The study group was found to have more acute respiratory distress syndrome and the requirement for noninvasive and invasive ventilation. Outcomes were compared among both the groups and it was observed that unmatched analysis showed statistically higher ICU admission rates (12% vs. 1.9%, P < 0.001), endotracheal intubation (6% vs. 2.4%, P < 0.001, and mortality (15% vs. 3.9%, P < 0.001) among the study group. However, among 42 patients in the study, group 2 patients developed hemorrhagic stroke (4.76%) while 40 patients developed ischemic stroke (95.23%). The type of stroke, either ischemic or hemorrhagic was not associated with the severity of SARS-COV-2 (hazards ratio, 22.265 [95% CI, 0.028–34012.867], P = 0.385). In addition, the severity of prior stroke before infection, assessed by the modified Rankin Scale (mRA), was not associated with the clinical composite endpoint of SARS-COV-2, comparing patients with severe stroke disability (mRA, 3–5) to those with mild impairment (mRA, 0–2; hazards ratio, 0.506 [95% CI, 0.114–2.254]; P = 0.372). A poor outcome was observed among the study group with a lesser number of discharges and higher mortality rates than the control group. The patients who were discharged had a higher score of 3–5 on mRA.

  Discussion Top

This retrospective study included 703 patients with laboratory-confirmed SARS-COV-2. SARS-COV-2 positive patients were older, had high quick sequential organ failure assessment (qSOFA) scores on admission and had a higher rate of cerebrovascular disorders compared to patients without SARS-COV-2. During hospitalization, SARS-COV-2-positive patients had a higher incidence of neurological complaints with prolonged hospital length of stay and increased in-hospital mortality rates. A total of 42 (5.64%) patients with confirmed SARS-COV-2 developed stroke, including either hemorrhagic or AIS during the initial period of hospitalization [Figure 1] and [Figure 2]. Similar findings were also observed by Li et al. with 4.6% of AIS and 0.5% intracerebral hemorrhage in SARS-COV-2 patients.[8] Qureshi et al. in their study reported 4.9% SARS-COV-2 patients with AIS.[10] In a systematic review of 212 studies on the neurological manifestations of SARS-COV-2, stroke was reported in 0.5%‒5.9% of patients.[11] In a meta-analysis of 108571 SARS-COV-2 patients, ischemic stroke was diagnosed in 1328 patients (1.22%).[12] In our study, patients with SARS-COV-2 stroke were older and had various comorbid conditions such as hypertension, diabetes mellitus, ischemic heart disease, and had severe infection than SARS-COV-2 patients without stroke. In addition, patients with SARS-COV-2 had significant differences in laboratory values on admission, including blood count analysis, acute-phase proteins, and coagulation profiles. High qSOFA score, thrombocytopenia and increased LDH levels, increased D-dimer and CRP were found to have potential risk factors for a poor prognosis at an early stage. Studies have also found that SOFA and qSOFA scores were associated with high in-hospital mortality, raised D-dimer, and older age with more comorbidities in patients with SARS-COV-2 patients.[13] The qSOFA is a bedside evaluation scale that identifies patients with suspected infection who are at greater risk for a poor outcome outside the intensive care unit, and it can be rapidly performed by the clinician without the need for laboratory analysis.[14] In our study, most patients admitted with SARSCOV-2 suffered stroke occurring few days later. Ischemic stroke was the most common stroke subtype and was frequently characterized by either single or multiple cerebral infarctions lesions. Young patients with stroke who were SARS-COV-2 positive suffered from more severe stroke, and stroke was more often caused by large artery occlusion. Several studies have also reported young patients without vascular risk factors admitted for large-artery stroke during the SARSCOV-2 pandemic.[15],[16] Zheng et al. in their study showed that elderly people with comorbidities are more likely to be infected and develop severe symptoms of SARSCOV-2 and these patients had a high risk of developing stroke. Underlying coronary artery disease was found to aggravate pneumonia in SARS-COV-2 patients and increase the severity of symptoms.[17] Patients with underlying pulmonary disease and coronary artery disease were found to have severe pneumonia in SARS-COV-2 and had an increase in the severity of symptoms, resulting in a hypercoagulable state.[18]

Common presenting complaints of patients in the study group were olfactory disturbances, taste changes, headache, nausea, vomiting, sleep disturbances, vertigo, seizures, myalgia, and altered conscious levels. These findings were also reported by Giacomelli et al. and Bohmwald et al. in their study.[19],[20] Aggarwal et al. in their cohort of six studies showed that there is a 2.5-fold increase in odds of severe SARS-COV-2 infection in patients with a previous history of stroke.[21] Similarly, Qin et al. in their study showed that after propensity score matching, patients with a history of stroke had a higher risk of severe events including high mortality, critical care admission, intubations, and lower rates of discharge.[22] Similar findings were observed in our study. Stroke mechanisms in COVID-19 could include various processes, including the release of pro-inflammatory cytokines which have direct effect on plaque rupture through local inflammation and activation of coagulation factors or cardio-embolism from virus-related cardiac injury.[23],[24],[25] Moreover, a direct effect of the virus on endothelial cells or on heart tissue has also been found in studies considering that the receptor for SARS-COV-2, the angiotensin-converting enzyme-2 is expressed on vascular endothelial cells and myocytes.[26],[27],[28],[29],[30] In our study, we observed several indexes of altered coagulability in patients with SARS-COV-2 compared to patients without SARS-COV-2. Prothrombin time and d-dimer were increased in the former group, including inflammatory markers like as CRP and IL-6. Serum ferritin level and fibrinogen were also found to be significantly raised suggestively of hypercoagulable state. These findings of marker profiles are consistent with what has been observed in disseminated intravascular coagulation and may play an important role in stroke incidence and severity in SARS-COV-2 patients.[31] Abnormal coagulation parameters have been also shown to be associated with poor prognosis in patients with SARS-COV-2-positive associated pneumonia.[32] Anti-inflammatory responses post stroke facilitate infection, which is in itself an important independent contributor to poor outcomes.[33] It was noted that most patients with stroke had a higher number of neutrophils and elevated inflammatory markers suggesting that SARSCOV-2 might induce a greater cytokine storm and generate a series of immune responses. The continuous and uncontrolled activation of the immune system caused by the viral infection, with subsequent excessive cytokine release or ''cytokine storm'' has been implicated in brain damage during SARS-COV-2 infection. Cytokines/chemokines promote atherosclerosis, plaque rupture, and superimposed thrombosis.[34],[35]

Various manifestations of myocardial injury including viral myocarditis, myocardial dysfunction due to cytokine storm, coronary artery disease, and stress cardiomyopathy due to the stimulation of the sympathetic nervous system may lead to cardiac arrhythmias and intracardiac thrombus formation, possibly exacerbated by the hypercoagulable state and could increase the risk of cardioembolic stroke.[36],[37] Moreover, more severe lymphopenia was found in patients with a history of stroke and an increased neutrophil-to-lymphocyte ratio, a well-known marker of systemic inflammation and infection.[38] These laboratory findings indicate that inflammatory mechanisms might play a crucial role in developing and progressing SARS-COV-2 in stroke survivors. In our study, raised levels of D-dimer and lower platelet counts were also found in patients with stroke, this phenomenon reminds us of the necessity to titrate the antithrombotic and anti-platelet medication regimen according to the platelet counts or coagulation function in patients with stroke. Patients ofSARS-COV-2 with stroke experienced worse clinical outcomes than those without stroke, given that patients with stroke were older and had a higher prevalence of smoking, hypertension, and cardiovascular disease, which were the important predictors of poor SARS-COV-2 outcomes.[39]

We do acknowledge that this study entails some limitations. First, being a single-center retrospective study design, not all laboratory tests were performed on all patients, including high-sensitivity cardiac Troponin I and ILs and other inflammatory markers. Therefore, their role could have not been thoroughly assessed in this study. Second, extraction of data from medical records and lack of long-term outcomes, as some patients still need to be followed up for their clinical course and status of recovery from illness. Thus, continued observations and follow-up of this patient population with SARS-COV-2will be crucial. Third, interpretation of our findings could be limited by sample size and by the single-center design. Nevertheless, we hope these results will hopefully provide guidance for clinicians to understand the whole picture of the disease and are more conducive to the management of patients. To the best of our knowledge, this is the largest retrospective cohort study among patients with SARS-COV-2 who developed stroke at our institute in the northern part of India with a definite outcome.

  Conclusion Top

It was found that patients with confirmed SARS-COV-2 disease were predisposed to neurological manifestations including ischemic stroke due to hypercoagulable states through a number of mechanisms. They had worse clinical outcomes and significantly higher in-hospital mortality rates. This risk was higher in those infected severely and those with preexisting cardiovascular risk factors and multiple comorbidities. Most stroke was ischemic and there was an increase in large vessel occlusion and multiple territory infarcts suggesting that increased thrombosis and thromboembolism could be important factors.

Key take-home messages

  1. Abnormal coagulation profile and series of continuous and uncontrolled activation of the immune system caused by the viral infection with subsequent excessive cytokine release or ''cytokine storm'' leading to thrombo-embolic phenomena have been implicated in brain damage during SARS-COV-2 infection
  2. Patients with confirmed SARS-COV-2 disease are predisposed to neurological manifestations including ischemic and hemorrhagic stroke
  3. SARS-COV-2 patients with stroke had worse clinical outcomes and significantly higher in-hospital mortality rate
  4. SARS-COV-2 has affected the practice of all primary care physicians. Knowledge of its complications including stroke will improve time management and proper referral of the patients to higher centers.

Key points/new information

  1. In this study cohort, we found that patients who sustain stroke in the setting of SARS-COV-2 may potentially suffer poorer outcomes proportionate to the severity of infection
  2. If further investigations into SARS-COV-2-related thrombogenesis are carried out, it may lay a foundation for the understanding of future infection or inflammation-induced hypercoagulability and shall be more conducive to developing treatment strategies for such patients with stroke.


We would like to thank all the health-care professionals working devotedly in the SARS-COV-2 designated hospitals and ICUs worldwide.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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  [Full text]  

Correspondence Address:
Kumar Rahul,
Department of Cardiovascular and Thoracic Surgery, King George's Medical University, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jascp.jascp_29_22


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