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Incidence, predictors and clinical characteristics of orolingual angio-oedema complicating thrombolysis with tissue plasminogen activator for ischaemic stroke
  1. Robert Hurford1,2,
  2. Sean Rezvani1,
  3. Mohammad Kreimei1,
  4. Annie Herbert3,4,
  5. Andy Vail1,3,
  6. Adrian R Parry-Jones1,2,
  7. Chris Douglass2,
  8. Jane Molloy2,
  9. Hana Alachkar5,
  10. Pippa J Tyrrell1,2,
  11. Craig J Smith1,2
  1. 1Stroke and Vascular Research Centre, Institute of Cardiovascular Sciences, University of Manchester, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Trust, Manchester, UK
  2. 2Comprehensive Stroke Centre, Greater Manchester Neurosciences Centre, Salford Royal NHS Foundation Trust, Manchester, UK
  3. 3Health Sciences Research Group, University of Manchester, Manchester, UK
  4. 4Centre for Paediatric Epidemiology and Biostatistics, University College London Institute of Child Health, London, UK
  5. 5Department of Immunology, Salford Royal NHS Foundation Trust, Manchester, UK
  1. Correspondence to
    Dr Craig J Smith, Room C238, Clinical Sciences Building, Manchester Academic Health Science Centre, Salford Royal NHS Foundation Trust, Manchester M6 8HD, UK; craig.smith{at}srft.nhs.uk

Abstract

Background Orolingual angio-oedema is a recognised complication of tissue plasminogen activator (tPA) for ischaemic stroke. We investigated its incidence, clinical characteristics and relationship with other factors in patients receiving tPA at a UK centre.

Methods 530 consecutive patients (median age 70 years) receiving tPA treatment for confirmed ischaemic stroke were included. Cases were defined as those developing angio-oedema within 24 h of initiation of tPA. Angio-oedema was retrospectively classified as mild, moderate or severe using predefined criteria. The primary analysis was the association between prior ACE inhibitor (ACE-I) treatment and angio-oedema.

Results Orolingual angio-oedema was observed in 42 patients (7.9%; 95% CI 5.5% to 10.6%), ranging from 5 to 189 min after initiation of tPA (median 65 min). 12% of the angio-oedema cases were severe (1% of all patients treated with tPA), requiring urgent advanced airway management. 172 patients (33%) were taking ACE-I. In multifactorial analyses, only prior ACE-I treatment remained a significant independent predictor of angio-oedema (odds ratio (OR) 2.3; 95% CI 1.1 to 4.7).

Conclusions Angio-oedema occurs more frequently than previously reported and is associated with preceding ACE-I treatment. Angio-oedema may be delayed and progress to life-threatening airway compromise, which has implications for the assessment and delivery of thrombolysis.

  • Stroke
  • Cerebrovascular Disease

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