key: cord-0867106-senzcbvp
authors: Al Rawahi, Bader; BaTaher, Hashem; Jaffer, Zoheb; Al‐Balushi, Aya; Al‐Mazrouqi, Asma; Al‐Balushi, Noof
title: Vaccine‐induced immune thrombotic thrombocytopenia following AstraZeneca (ChAdOx1 nCOV19) vaccine–A case report
date: 2021-08-24
journal: Res Pract Thromb Haemost
DOI: 10.1002/rth2.12578
sha: 197d945b8101ffa52b58de4217546419e23bee81
doc_id: 867106
cord_uid: senzcbvp

Vaccination with ChAdOx1 nCov‐19 can result in vaccine‐induced immune thrombotic thrombocytopenia (VITT). This phenomenon mimics heparin‐induced thrombocytopenia (HIT), yet it does not require heparin as a trigger. HIT screen/ELISA along with optical density and functional assay are useful in diagnosis. A 64‐year‐old man presented to the emergency department with intermittent fever and persistent, dull, nonspecific abdominal pain 7 days after the first dose of ChAdOx1 nCov‐19 vaccine. Laboratory results showed significantly reduced platelet count, acute kidney injury, and low basal cortisol. He underwent investigations including computed tomography angiography, which revealed multiple sites of arterial and venous thrombosis. We present the first reported case of VITT at our institution and in Oman. This case highlights the potentially life‐threatening complication associated with ChAdOx1 nCov‐19 vaccine, clinical presentation, diagnostic approach, and treatment.

under the age of 55 years, and cerebral venous thrombosis or other thrombosis seems to occur 4 to 16 days after vaccination. [2] [3] [4] [5] This phenomenon mimics autoimmune heparin-induced thrombocytopenia (HIT), yet it does not require heparin as a trigger. The Paul Ehrlich Institute demonstrated that affected individuals in Germany have antibodies against platelet factor 4 (PF4)/heparin complex that induces massive platelet activation, reducing the platelet count and causing thrombosis. [3] [4] [5] [6] [7] In the following case, we present the first reported VITT case from our institution and in Oman. This case highlights the potentially life-threatening complication associated with ChAdOx1 nCov-19 vaccine, clinical presentation, diagnostic approach, and treatment. are not available in Oman and therefore were not performed.

For management, he was initiated on an argatroban infusion (to target aPTT ratio between 1.5 and 2.5 of normal) as a nonheparin anticoagulation for 3 days as his renal function further deteriorated and did not permit for fondaparinux or direct oral anticoagulants.

Anticoagulation was started despite the adrenal hemorrhages.

As the renal function improved significantly, anticoagulation was changed to fondaparinux for 4 days until the patient's platelet count improved, then shifted to rivaroxaban at the time of discharge. We also treated him with intravenous immunoglobulin 0.5 gm/kg for 4 days (total of 2 gm given over 4 days). The platelets were 114 000 per cubic millimeter at the day of discharge (Figure 2 ). The management was tailored according to the case at hand and recommended interim guidelines. 8-10 Two week later, repeated blood work showed complete recovery of the platelet count (216 000/mm 2 ), reduction in D-dimer (ie, 5.6 mg/L and a decline in the HIT ELISA OD to 0.99.

As far as his hypoadrenalism was concerned, he was initially given stress doses of hydrocortisone during the acute phase (ie, the first 3 days) followed by a maintenance regimen. There were no bleeding complications to anticoagulation during admission or follow-up.

In summary, our patient presented 7 days after ChAdOx1 nCov-19 vaccine with severe thrombocytopenia and multiple arterial and venous thromboses. Therefore, the main differential was VITT caused by the AstraZeneca vaccine. This was confirmed with a strongly positive HIT ELISA highly suggestive of spontaneous HIT (without heparin exposure). He had the full spectrum of VITT complicated by hypoadrenalism. Prompt and adequate intervention was 

during the course of admission shows improvement after initiation of treatment established, and he recovered with a platelet count improved to nor-

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