key: cord-1051324-ax57pmdz
authors: Shtaya, Anan; Trippier, Sarah; Ghatala, Rita; Cluckie, Gillian; Zhang, Liqun
title: Comment on “Stroke in patients with SARS‑CoV‑2 infection: case series” from a London hospital experience
date: 2020-07-25
journal: J Neurol
DOI: 10.1007/s00415-020-10105-0
sha: 95d8fb8efeb372c9a17a888515ef253efae2b2ea
doc_id: 1051324
cord_uid: ax57pmdz

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We read with interest Morassi et al. case series, [2] where they and others [1, 3] reported stroke as a complication of severe COVID-19 infection. The effect of COVID-19 on acute stroke patients (ischaemic and haemorrhagic) who may catch the disease concomitantly with stroke or after stroke but not as a cause of severe COVID-19 disease is not known. Therefore, we detail the demographic, clinical, radiological, laboratory results, treatment and outcomes of 22 consecutive COVID-19-positive (confirmed by reverse-transcriptase polymerase chain reaction (RT-PCR)) stroke patients diagnosed during the lockdown period 23rd March to 1st May 2020 inclusive at a tertiary London neuroscience centre. The mean age is 70.3 ± 2.2 years (range 49-83 years old, 14 (64%) males and 8 (36%) females). We classified these patients into (i) hospital acquired COVID-19; those who developed COVID-19 in the hospital while being treated for stroke, (ii) community acquired COVID-19; patients who had COVID-19 symptoms in the community shortly before attending the hospital with stroke and (iii) stroke as a direct complication of COVID-19; patients who were treated in intensive care with obvious prothrombotic state. Table 1 cases 1-5 are hospital acquired COVID-19, this category of patients has not been described before. These were the patients being treated for stroke in mid-March 2020, when wearing personal protective equipment (PPE) was not recommended for staff looking after non-COVID-19

patients. In addition, relative visiting rules were not restricted. Cases 2-5 had high poor functional status before hospital admission and high frailty score on admission. They presented with mild fever at the time of testing and normal chest X-ray. They received oxygen therapy by nasal canulae for their COVID-19 and did not require or proceed for intensive care input. Cases two and three were discharged home at similar level of function as before and the others deceased. It is interesting to note the two discharged patients had minimum elevation of high-sensitivity C-reactive protein (CRP). None of these patients had worsening of stroke symptoms.

Twelve community acquired COVID-19 patients (Cases 6-17) developed stroke within 72 h of showing COVID-19 symptoms. Ten patients presented with fever, six had also cough, three patients had severe hypoxia on admission (87% on 15 L O 2 in case 7, 70% on 15 L O 2 in case 16 and 89% on 15 L O 2 in case 17). These three patients are care home residents, have high pre-admission mRS and frailty score. Cases 6-8, 10-12, 14-15 and 17 had confirmed large vessels stroke. Two cases (13 and 16) were clinically unstable on admission and diagnosed without brain imaging. Cases 6, 9-14 and 17 of ischaemic stroke patients with known symptom onset presented late (> 4.5 hr). Case nine had intraventricular haemorrhage due to a suspected arterio-venous malformation (AVM). We noted that the majority of the patients who died had high CRP. Patients who had hypoxia and abnormal chest X-ray at presentation except case 14, did not survive. Difficult to ascertain whether patients of community acquired COVID-19 developed stroke as a different disease process or as a result of COVID-19. The patients' pre-morbid status and clinical findings in this group suggest that perhaps these patients developed stroke as an additional disease to their COVID-19 infection.

We report five cases (18-22) where patients had severe COVID-19 disease and developed (apart from case 22 which is a stroke mimic) multiorgan failure and large vessel stroke. These patients are middle age males with pre-admission mRS of zero and very low frailty score. Presenting /L symptoms were typically of COVID-19. All shared chest radiographs abnormalities. They also had abnormally low oxygen saturation on admission and all needed intubation, ventilation and intensive care management. Apart from the stroke mimic case, all had high D-Dimer, ferritin and CRP. These cases share pro-thrombotic characteristics with most of the cases of Morassi et al. [2] . They all received full anticoagulation with low molecular weight heparin. Four out of these patients had CT pulmonary angiogram with no major pulmonary emboli (PE), suggesting PE may not be the major cause of their death. Further studies into this subpopulation are needed. We included all COVID-19 stroke patients diagnosed within the period 23rd March and 1st May 2020. However, not all COVID-19 patients had brain scans and, therefore, the number of cases who were diagnosed with stroke due to severe COVID-19 disease may be underestimated. We present the management and outcome of a full spectrum of COVID-19-stroke patients in a tertiary centre. A pro-thrombotic state was found in severe COVID-19 patients, who did not do well, and stroke may be a late complication in these patients. Classifying COVID-19-stroke patients the way we did may help understand the disease and guide management.

Funding Anan Shtaya is the recipient of a Clinical Lectureship from National Institute for Health and Research (NIHR), England, UK. No dedicated fund was used to do this study.

Conflicts of interest The authors declare that they have no conflict of interest.

Ethical approval Consents have been obtained from patients, next of kin or legal representative. No identifiable data is presented. The reference ranges are as follows: activated partial thromboplastin time ratio, albumin, 35-50 g/L; 0.85-1.15; D-dimer, 21-300 ng/ml; ferritin, 30-400 µg/ml; fibrinogen, 1.6-4.8 mg/dl; highsensitivity C-reactive protein, 0-5 mg/L; lymphocyte count, 1.1-4.0 × 10 9 /L, platelet count, 150-450 × 10 9 /L, prothrombin time/INR ratio, 0.8-1.1; white-cell count, 4-11 × 10 9 /L.

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