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Immunosuppression for intracranial vasculitis associated with SARS-CoV-2: therapeutic implications for COVID-19 cerebrovascular pathology
  1. Luke Dixon1,
  2. Charles Coughlan2,
  3. Kushan Karunaratne3,
  4. Nikolaos Gorgoraptis3,4,
  5. James Varley3,
  6. James Husselbee2,
  7. Dermot Mallon1,
  8. Roseita Carroll2,
  9. Brynmor Jones1,
  10. Claire Boynton2,
  11. Jane Pritchard3,
  12. Taryn Youngstein5,
  13. Justin Mason6,
  14. Carolyn Gabriel3
  1. 1Department of Imaging, Imperial College Healthcare NHS Trust, London, UK
  2. 2Department of Anaesthetics, Imperial College Healthcare NHS Trust, London, UK
  3. 3Department of Neurology, Imperial College Healthcare NHS Trust, London, UK
  4. 4Department of Brain Sciences, Imperial College London, London, UK
  5. 5Department of Rheumatology, Imperial College Healthcare NHS Trust, London, UK
  6. 6National Heart and Lung Institute, Imperial College London, London, UK
  1. Correspondence to Dr Luke Dixon, Department of Imaging, Imperial College Healthcare NHS Trust, London, London, UK; luke.dixon1{at}nhs.net

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Introduction

Acute cerebrovascular disease, particularly ischaemic stroke, has emerged as a serious complication of COVID-19.1 However, the mechanism and optimal management of this remain incompletely understood. In the pulmonary and cardiac circulation, there is evidence that thrombotic complications may relate to endothelial inflammation and injury but evidence for this in the cerebrovascular system is limited.2 We demonstrate direct imaging evidence of vasculitis in a patient with COVID-19 complicated by multiple territory ischaemic strokes which responded to steroids and targeted interleukin-1 (IL-1) and interleukin-6 (IL-6) inhibition.

Case report

A 64-year-old man with type 2 diabetes mellitus, hypertension, hypercholesterolaemia and ischaemic heart disease was admitted with a 5-day history of dry cough and fever. He was diagnosed with COVID-19 pneumonia requiring early intubation, mechanical ventilation, inotropic support and haemofiltration for acute kidney injury. Blood tests showed lymphopenia (0.6×109/L), elevated C-reactive protein (196 mg/L), renal dysfunction (creatinine 156 μmol/L) and raised D-dimer (>20 000 µg/L). Given this, and his need for continuous renal replacement therapy, the patient was systemically heparinised. SARS-CoV-2 infection was confirmed with nasopharyngeal swab reverse-transcriptase PCR testing.

On day 24 of admission, following a sedation hold, he was not appropriately responsive with Glasgow Coma Scale 8 (E4, V2, M2) and episodic clonic movements of the proximal upper limbs. The patient was on aspirin and intravenous heparin at this time.

MRI brain demonstrated abnormal signal, variable restricted diffusion and peripheral enhancement in the left occipital and right parietal, occipital and temporal lobes (figure 1). Appearances were consistent with multiple subacute infarcts in the right middle cerebral artery …

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Footnotes

  • Contributors LD, CC, CB and CG conceived the case report. CC obtained written consent from the patient’s next-of-kin. LD, CC, KK, NG, JV and JH cowrote the first draft. LD, DM and BJ sourced and reported high-quality images for this study. RC, CB, JP, TY, JM and CG revised the manuscript for important intellectual content. All authors have read and approve the final version of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient consent for publication Next of kin consent obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.