English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

A 63-year-old man presented to the emergency department with a 5-day history of a cool, painful lef leg, new onset of paresthesia of the lef leg and foot, and severe shortness of breath. The patient had no personal or family history of thrombotic events and no personal history or symptoms of arrythmia. He was a nonsmoker with no symptoms or prior documentation of peripheral vascular, coronary or cerebrovascular disease. He had a history of obesity and hypertension controlled with a single agent. Two rapid point-of-care tests were negative for SARS-CoV-2 earlier on the day of presentation (Abbott ID NOW isothermal nucleic acid test). The patient had received his first dose of the ChAdOx1 nCoV-19 vaccine 20 days before the onset of his symptoms. Upon presentation, we noted that the patient was obese (body mass index 41.8) and hypoxic (oxygen saturation 85% on room air, normal > 90%). His lef foot was cold, pale and insensate, with decreased motor function and absent arterial Doppler signals (Rutherford IIB acute limb ischemia).1 Laboratory investigations showed thrombocytopenia (platelets 36 [normal 150– 400] × 109/L), D-Dimer > 10 000 (normal ≤ 50) ng/mL fibrinogenequivalent units, fibrinogen 1.4 (normal 1.6–4.1) g/L and international normalized ratio 1.3 (normal 0.9–1.1). A computed tomography angiogram showed lef popliteal artery occlusion with no visible tibial vessels, even on delayed imaging. It also showed bilateral segmental pulmonary artery thrombi and thrombus adherent to the wall of the infrarenal aorta (Figure 1). We started therapeutic anticoagulation with intravenous unfractionated heparin. Emergency surgical thrombectomy of the popliteal artery and all tibial arteries yielded a large amount of thrombus. We infused tissue plasminogen activator into the tibial arteries intraoperatively. We obtained good antegrade and retrograde flow, with marked pedal hyperemia and normal triphasic arterial Doppler signals upon reperfusion. Intraoperatively, the patient was intermittently hypoxic, consistent with his substantial pulmonary artery thrombus. KEY POINTS • Vaccine-induced immune thrombotic thrombocytopenia (VITT) must be considered in any patient presenting with thrombosis and thrombocytopenia afer recently receiving a vaccine for SARS-CoV-2 that uses an adenovirus vector (ChAdOx1 nCoV-19 Oxford–AstraZeneca or Ad26.COV2.S Johnson & Johnson–Janssen). • The clinical presentation and pathobiology of VITT are similar to those of heparin-induced thrombocytopenia (HIT), but in VITT, an immunoglobulin G (IgG) antibody against platelet factor 4 triggers platelet activation, thrombosis and thrombocytopenia. • Commonly used rapid assays for HIT, such as the latexenhanced immunoassay, can be falsely negative in patients with VITT; however, enzyme-linked immunosorbent assays for HIT and serotonin-release assays can be used to detect and confirm VITT, respectively. • If VITT is suspected, heparin should be discontinued and replaced with an alternate anticoagulant; platelet transfusion should be avoided and intravenous immunoglobulin should be considered in patients who present with clinically worrisome features.

cmaj. canadian medical association journal

Limb ischemia and pulmonary artery thrombosis after the ChAdOx1 nCoV-19 (Oxford–AstraZeneca) vaccine: a case of vaccine-induced immune thrombotic thrombocytopenia