A Puzzling Diagnosis of Cerebral Vein Thrombosis in a COVID-19-Vaccinated Patient.

Cerebral vein thrombosis (CVT) is a rare condition equivalent to deep vein thrombosis of the intracranial veins. Delayed diagnosis will result in severe and disabling complications. We report a case of a 59-year-old man with CVT with no significant past medical or surgical history. On admission, he reported right-sided numbness and weakness concerns, preceded by the sudden onset of bilateral vision loss and dysarthria. Magnetic resonance imaging and computed tomography scans confirmed the diagnosis of CVT. The most interesting relative risk factor was flying overseas twice a month for the last 10 years; each flight was longer than eight hours. Another possible contributing factor to our patient's condition was polycythemia, with a hemoglobin level of 19, but the most questionable and puzzling is the recent coronavirus disease 2019 (COVID-19) vaccination two months, eight months, and one year prior to admission. Our case highlights a rare COVID-19 vaccine-related CVT diagnosis and that close monitoring for new symptoms and signs is vital to prevent life-threatening complications, herniation, and hemorrhagic transformation.

Spontaneous HIT syndrome: Knee replacement, infection, and parallels with vaccine-induced immune thrombotic thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is characterized clinically by thrombocytopenia, hypercoagulability, and increased thrombosis risk, and serologically by platelet-activating anti-platelet factor 4 (PF4)/heparin antibodies. Heparin-"induced" acknowledges that HIT is usually triggered by a proximate immunizing exposure to heparin. However, certain non-heparin medications (pentosan polysulfate, hypersulfated chondroitin sulfate, fondaparinux) can trigger "HIT". Further, naturally-occurring polyanions (bacterial lipopolysaccharide, DNA/RNA) can interact with PF4 to recapitulate HIT antigens. Indeed, immunologic presensitization to naturally-occurring polyanions could explain why HIT more closely resembles a secondary, rather than a primary, immune response. In 2008 it was first reported that a HIT-mimicking disorder can occur without any preceding exposure to heparin or polyanionic medications. Termed "spontaneous HIT syndrome", two subtypes are recognized: (a) surgical (post-orthopedic, especially post-total knee arthroplasty, and (b) medical (usually post-infectious). Recently, COVID-19 adenoviral vector vaccination has been associated with a thrombotic thrombocytopenic disorder associated with positive PF4-dependent enzyme-immunoassays and serum-induced platelet activation that is maximal when PF4 is added. Vaccine-induced immune thrombotic thrombocytopenia (VITT) features unusual thromboses (cerebral venous thrombosis, splanchnic vein thrombosis) similar to those seen in spontaneous HIT syndrome. The emerging concept is that classic HIT reflects platelet-activating anti-PF4/heparin antibodies whereas spontaneous HIT syndrome and other atypical "autoimmune HIT" presentations (delayed-onset HIT, persisting HIT, heparin "flush" HIT) reflect heparin-independent platelet-activating anti-PF4 antibodies-although the precise relationships between PF4 epitope targets and the clinical syndromes remain to be determined. Treatment of spontaneous HIT syndrome includes non-heparin anticoagulation (direct oral Xa inhibitors favored over direct thrombin inhibitors) and high-dose immunoglobulin.