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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 3  |  Issue : 2  |  Page : 40-42

Is COVID-19 infection also a silent killer?: A case of acute stroke


1 Department of Neurology, Apollo Multispeciality Hospitals, Kolkata, West Bengal, India
2 Department of Cardiology, Apollo Multispeciality Hospitals, Kolkata, West Bengal, India
3 Department of Neurology, Rabindranath Tagore International Institute of Cardiac Sciences, Kolkata, West Bengal, India

Date of Submission13-Feb-2022
Date of Decision25-Mar-2022
Date of Acceptance26-Mar-2022
Date of Web Publication20-May-2022

Correspondence Address:
Dr. Debabrata Chakraborty
64/4A/9, Beliaghata Main Road, Kolkata - 700 010, West Bengal
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jopcs.jopcs_2_22

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  Abstract 


A 59-year-old male had multiple comorbidities such as diabetes, dilated cardiomyopathy, hypertension, ischemic heart disease, and chronic obstructive pulmonary disease. He presented with dyspnea and had ground-glass opacity in the lungs. It was during the pandemic of COVID-19 so repeated Reverse transcription polymerase chain reaction (RT-PCR) was done, but all were negative. He got stabilized within 5 days and we planned discharge. Suddenly, he had right hemiplegia and developed altered sensorium. He had NIH Stroke Scale/Score of 28 and computed tomography-Alberta Stroke Program Early Computed Tomography Score of 10. We used tenecteplase (0.25 mg/kg bodyweight) for thrombolysis within 20 min of onset and planned mechanical thrombectomy for the occlusion of internal carotid artery and beyond. However, in magnetic resonance imaging of the brain, he had an established infarct in the left middle cerebral artery (MCA) territory (within this short time) without significant DWI/FLAIR mismatch. Hence, we continued conservative management. We incidentally detected him to have COVID-19 infection positivity on that day, but all inflammatory and coagulation parameters were normal on that day and later. His monitor did not reveal arrhythmia (during the event and later) and echocardiography failed to reveal evidence of culprit lesion. He had a rapid clinical decline, required hemicraniectomy but expired within 2 days. COVID-19 infection may have negative reports initially, but malignant MCA infarct with normal inflammatory markers makes our case special. The rapidity with which stroke developed underscores the severe nature of the disease process, the absence of arrhythmias (in this in-house stroke), and normal coagulation parameters hints that the exact mechanism of stroke in this type of infection is still an enigma.

Keywords: Acute stroke, COVID-19 infection, malignant middle cerebral artery infarct, thrombolysis


How to cite this article:
Chakraborty D, Mondal PC, Sundar K, Dingal SK. Is COVID-19 infection also a silent killer?: A case of acute stroke. J Prim Care Spec 2022;3:40-2

How to cite this URL:
Chakraborty D, Mondal PC, Sundar K, Dingal SK. Is COVID-19 infection also a silent killer?: A case of acute stroke. J Prim Care Spec [serial online] 2022 [cited 2022 Oct 3];3:40-2. Available from: https://www.jpcsonline.org/text.asp?2022/3/2/40/345643




  Introduction Top


Epidemiological knowledge of infection is very important in clinical medicine. Even though investigations are not supportive, it is important to diagnose based on the clinical experience, keeping present disease prevalence in the community in mind. We report such an incident when repeated tests proved the absence of COVID-19 infection. Finally, when the report came positive, it brought with it a catastrophe.


  Case Report Top


A 59-year-old male was a known case of ischemic heart disease, hypertension, diabetes mellitus, and dilated cardiomyopathy. He had presented with effort intolerance and shortness of breath for 5 days. At the emergency room, he was alert, cooperative with tachypnea, and maintained a saturation of 98% with 2 L of oxygen supplementation/minute. His other vital parameters were within normal limits. He presented during the pandemic of COVID-19 surge and was under high suspicion of contracting the disease. Although his computed tomography (CT) scan of the chest revealed mild ground-glass opacity, repeated RT-PCR tests for COVID were negative. We started dual antiplatelet (aspirin and clopidogrel) and heparin 2500 units subcutaneously twice daily (he had renal impairment), along with standard medications for respiratory care. We brought his respiratory distress and high blood sugar level under control. He got stabilized gradually within 7 days. One fine morning, as he was talking with his doctor comfortably, suddenly had slurring of speech and fell down on the bed. He had a blood pressure of 130/80 mmHg, a pulse rate of 100/min (sinus rhythm). On examination, he was drowsy, pupils were of normal size and reaction, and other brainstem reflexes were normal and had no movement of the right upper and lower limbs. His NIH Stroke Scale/Score was 28 and CT scan of the brain revealed the Alberta Stroke Program Early Computed Tomography Score of 10. We immediately thrombolyzed him with injection tenecteplase (TNK) with a bolus dose of 0.25/kg bodyweight (20 min from the onset). MRA of the brain and neck (just after the bolus dose of TNK) revealed a large evolving infarct in the territory of the left middle cerebral artery (MCA) (involving basal ganglia, frontal, temporal, parietal, and left insula) [Figure 1]. There was no flow-related enhancement seen in the intracranial part of the left internal carotid artery, left MCA, and A1 segment of the left anterior cerebral artery. He was well within the window period for endovascular therapy but had already established infarct in this short time (had no significant DWI/FLAIR mismatch). So, we continued with conservative treatment.
Figure 1: A large acute infarct in the territory of the left middle cerebral artery (involving basal ganglia, frontal, temporal, parietal, and left insula). There was no flow-related enhancement seen in the intracranial part of the left internal carotid artery, left middle cerebral artery, and A1 segment of the left anterior cerebral artery

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His blood parameters on that day revealed: hemoglobin level of 18.5 g%, total leukocyte count of 9300/cubic mm, platelet count of 2.5 lakh/cubic mm, international normalized ratio of 1.3, D-dimer of 1703 ng/ml, activated partial thromboplastin time of 26.8 s (control of 29 s), C-reactive protein of 5 mg/dl, erythrocyte sedimentation rate of 3 mm/1st h, lactate dehydrogenase 269 U/L, pro-calcitonin of 0.2 ng/ml, creatinine of 1.5 mg%; random blood sugar was 200 mg%; liver function and electrolytes were normal around the event. We detected him to have COVID-19 RT-PCR positive on the day of the event.

His Glasgow Coma Scale deteriorated by evening (same day of the event) and repeat CT scan revealed malignant left MCA territory infarct with significant edema and mass effect [Figure 2]. He underwent decompressive hemicraniectomy in the night itself. However, from the next day, he progressively deteriorated and expired after 2 days.
Figure 2: Malignant left middle cerebral artery territory infarct with significant edema, mass effect, and midline shift

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  Discussion Top


Our patient had the first two COVID-19 results negative, but the third one positive. Hence, serial tests are the call of the day in suspected cases. Interestingly, they have noted that patients with a first negative RT-PCR test for COVID-19 had higher inflammation markers (median of 6 days) compared to patients with a positive first test.[1] Our case was odd as inflammatory markers were unremarkable even on the 6th day of symptom onset and remained within limits post stroke. His coagulation parameters were never grossly deranged during illness. The patient was under continuous monitor in our hospital and had no arrhythmogenic event either. Hence, it is possible that the patient had some other mechanism of the thrombotic state which is COVID-19 related or unrelated (he had significant stroke risk factors). He was on dual antiplatelet and anticoagulant (heparin), so we could not detect his true thrombotic status at any point in time.

COVID-19-associated coagulopathy is related to increased cytokines, activation of platelets, endothelial dysfunction, complement activation, hemostasis, and alteration in coagulation parameters (increased factor VIII).[2],[3] The systemic inflammatory response, mild disseminated intravascular-hypercoagulability, immunothrombosis, and genetic predisposition are other contributors in the thromboembolic episodes.[2],[3]

In COVID-19 infection, proteolytic coagulation factors convert inactive coagulation factors into the active form.[2] The plasminogen activator inhibitor-1 (PAI-1) is elevated, so it inhibits tissue plasminogen activator more than normal.[2] Hence, the conversion of plasminogen to plasmin is reduced (tissue plasminogen facilitates the conversion). Hence, plasmin degrades less fibrin matrix of the thrombus, exerting lesser thrombolytic action.

Thrombolysis might have also activated the coagulation cascade in our case. The procoagulant activation in stroke patients treated with recombinant tissue plasminogen activator may be explained by the exposure of clot-bound thrombin and factor Xa as the clot undergoes lysis.[4]

Decisions to use treatments such as corticosteroids (indispensable to tackle the inflammatory process in COVID-19) cannot be based only on the RT-PCR test results.[1] However, our patient had normal inflammatory markers and steroid itself has a prothrombotic state (activate coagulation system directly inhibit fibrinolysis by activation of PAI-1 and von Willebrand factor).[5] Hence, it was not introduced even after the COVID-positive result.


  Conclusion Top


The patient had risk factors for stroke and must have been having poor collaterals owing to his comorbidities. However, the COVID-19 infection must have played a significant role in forming an outstanding thrombogenic atmosphere, causing a malignant infarct in such a short time (even mechanical thrombectomy was less likely to make much difference). We need to be extra cautious in this type of case scenario, both for detection of the infection and acute management. The need to do serial RT-PCR for COVID-19 in doubtful cases is needless to reiterate. Etiopathogenesis and treatment response in acute stroke and such infection are different; a new management strategy/protocol (like novel immune-thrombosis targeted interventions) needs to be decided soon!

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.

Acknowledgment

We acknowledge the faith patient and his family kept on us during difficult times.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Lascarrou JB, Colin G, LeThuaut A, Serck N, Ohana M, Sauneuf B. Predictors of negative first SARS-CoV-2 RT-PCR despite final diagnosis of COVID-19 and association with outcome. Sci Rep 2021;11:2388.  Back to cited text no. 1
    
2.
Loo J, Spittle DA, Newnham M. COVID-19, immunothrombosis and venous thromboembolism: Biological mechanisms. Thorax 2021;76:412-20.  Back to cited text no. 2
    
3.
Mullaguri N, Hepburn M, Gebel JM Jr., Itrat A, George P, Newey CR. COVID-19 disease and hypercoagulability leading to acute ischemic stroke. Neurohospitalist 2021;11:131-6.  Back to cited text no. 3
    
4.
Fassbender K, Dempfle CE, Mielke O, Schwartz A, Daffertshofer M, Eschenfelder C, et al. Changes in coagulation and fibrinolysis markers in acute ischemic stroke treated with recombinant tissue plasminogen activator. Stroke 1999;30:2101-4.  Back to cited text no. 4
    
5.
van Zaane B, Nur E, Squizzato A, Gerdes VE, Büller HR, Dekkers OM, et al. Systematic review on the effect of glucocorticoid use on procoagulant, anti-coagulant and fibrinolytic factors. J Thromb Haemost 2010;8:2483-93.  Back to cited text no. 5
    


    Figures

  [Figure 1], [Figure 2]



 

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