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

Abstract

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] × 10 9 /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).

Inflammation and Platelet Activation After COVID-19 Vaccines - Possible Mechanisms Behind Vaccine-Induced Immune Thrombocytopenia and Thrombosis

“…VITT is characterized by multiple thromboses at unusual sites most often as cerebral venous sinus thrombosis (CVST) and splanchnic vein thromboses combined with thrombocytopenia, increased D-dimer and often decreased fibrinogen ( 1 , 2 , 7 – 9 , 11 ). VITT is occasionally complicated by arterial thrombosis as ischemic stroke, myocardial infarction or limb ischemia ( 3 , 12 , 13 ).…”

Recognizing, managing and reporting vaccine-induced immune thrombotic thrombocytopenia

“…Michelle Sholzberg MDCM MSc, Donald M. Arnold MD MSc, Andreas Laupacis MD MSc n Cite as: CMAJ 2021. doi: 10.1503/cmaj.210882; early-released May 14, 2021 See related article at www.cmaj.ca/lookup/doi/10.1503/cmaj.210795 I n a related case report, Jones and colleagues describe a 63-year-old man who developed thromboses in his popliteal and pulmonary arteries. 1 The patient's thromboses were likely caused by vaccine-induced immune thrombotic thrombocytopenia (VITT), a rare complication of the ChAdOx1 nCoV-19 (Oxford-AstraZeneca) vaccine, which he had received 20 days previously. 1 We discuss some important lessons clinicians can learn from this case.…”

“…1 The patient's thromboses were likely caused by vaccine-induced immune thrombotic thrombocytopenia (VITT), a rare complication of the ChAdOx1 nCoV-19 (Oxford-AstraZeneca) vaccine, which he had received 20 days previously. 1 We discuss some important lessons clinicians can learn from this case.…”

“…It is theoretically possible that heparin will exacerbate VITT because VITT antibodies may react with circulating PF4-heparin complexes. [1][2][3][4][5][6][7][8][10][11][12] Therefore, thrombosis should instead be managed with nonheparin anticoagulants, such as argatroban, fondaparinux or a direct oral anticoagulant. Management is made more challenging if the VITT-associated thrombosis is complicated by hemorrhage, particularly for patients with cerebral venous sinus thrombosis or stroke.…”

Untangling the Intricacies of Infection, Thrombosis, Vaccination, and Antiphospholipid Antibodies for COVID-19

“…Nevertheless, the latter authors have rightfully acknowledged the potential for other causes of thrombosis and thrombocytopenia and have urged caution in the nature of investigations required including the search for antiphospholipid syndrome. Many case reports of a similar event among those receiving adenovirus-vectored vaccine have emerged both in media and scientific journals [117][118][119][120][121][122][123][124][125][126][127][128][129][130][131][132]. Typical features include thrombocytopenia, increases in circulating D-dimer, and low fibrinogen levels.…”