Sex: F
Vaccine: COVID19
Symptoms: Activated partial thromboplastin time, Angiogram, Blood fibrinogen, Blood lactate dehydrogenase, Blood smear test
Clinical narrative: VACCINE-INDUCED THROMBOTIC THROMBOCYTOPENIA; This spontaneous report was received from literature. This report concerned a 43 year old female. The patient's weight, height, and medical history were not reported. The patient received covid-19 vaccine ad26.cov2.s (dose series 1) (suspension for injection, intramuscular, batch number was not reported) dose, start therapy date were not reported for covid-19 prophylaxis. No concomitant medications were reported. On an unspecified date, the patient experienced vaccine-induced thrombotic thrombocytopenia (dose series 1), and was hospitalized (date unspecified). Treatment medications (dates unspecified) included: apixaban, rituximab, immunoglobulin human normal, fondaparinux, and dexamethasone. The patient received the Johnson and Johnson COVID-19 vaccine 10 days before admission. Initial complete blood count (CBC) revealed a white blood cell count of 7.1 × 103/?L, hemoglobin of 15.4 g/dL, hematocrit of 44.9%, platelets of 73 × 103/?L, and mean corpuscular volume of 103.2 fL. Moreover, the prothrombin time was 11.9 s; the international normalized ratio was 1.1; the partial prothrombin time was 25.9 s; the absolute reticulocyte count was 0.113 × 106/mm3; fibrinogen level was 331 mg/dL; d-dimer level was 4.3 ?gFEU/mL; lactate dehydrogenase level was 175 units/L; and haptoglobin level was 182 mg/dL. A CBC obtained a month before the admission was normal. The blood smear was reviewed by the hematology team, revealing stomatocytes, few spherocytes, and no schistocytes or platelet clumping. The head CT of the patient, obtained the following day, revealed an evolving left ICA infarct with petechial hemorrhagic transformation in the anterior inferior basal ganglia and progression with rightward midline with early left uncal and transtentorial herniations. The patient was placed on hypertonic saline and given two units of platelets with minimal improvements in platelet count, i.e., from 75 to 78 × 103/?L. Venous Doppler of her lower extremities revealed a DVT of the right femoral vein and right popliteal vein. She underwent decompressive hemicraniectomy and expansile duraplasty with neurosurgery. She had an inferior vena cava filter placed, given her DVT and inability to receive therapeutic anticoagulation due to a major stroke with hemorrhagic conversion. As there was high suspicion of VITT, heparin-induced thrombocytopenia (HIT) antibodies were also measured from the serotonin release assay. A full hypercoagulable workup testing reported negative indications for antiphospholipid syndrome, factor V Leiden mutation, prothrombin II mutation, proteins C and S, antithrombin III, JAK2 mutation, and paroxysmal nocturnal hematuria. Given the high suspicion of VITT and contraindication to therapeutic anticoagulation, the patient was given intravenous immunoglobulin (IVIG) at 1 g/kg daily for 2 days. As observed, there was no initial improvement in the platelet count. She was then given 10 mg of dexamethasone 3 times a day for concerns of laryngeal edema, exhibiting some improvement in platelet count (i.e., to 91 × 103/?L) the next day. She was subsequently extubated, and her PF-4 antibody results came back positive, with an optical density (OD) of 1.58. She was given an additional dose of IVIG, which steadily increased the platelet count to 137 × 103/?L, but the patient was still unable to receive a full dose of anticoagulation. Therefore, she was started on a 4-day course of 40 mg dexamethasone daily and given a dose of 1000 mg rituximab for long-term control. The patient's platelet count eventually normalized to 173 × 103/?L, and a prophylactic dose of non-heparincontaining anticoagulation with 2.5 mg fondaparinux daily was started. A repeated assessment of HIT antibodies reported an elevated OD of 1.642 for PF-4 antibodies. The patient was given a total of four doses of rituximab weekly and was successfully able to start therapeutic anticoagulation with 7.5 mg of fondaparinux; she was then discharged to a rehabilitation facility. Two months after her initial presentation, the anticoagulation agent was changed to 5 mg apixaban twice a day. A year and a half after the initial diagnosis, the patient's d-dimer levels normalized, but her HIT antibodies were still weakly positive at OD 0.388. It was only 2 years after the original diagnosis that the patient's HIT antibody test came back negative. Anticoagulation was reduced accordingly to a prophylactic dose of 2.5 mg apixaban twice a day (BID). The action taken with covid-19 vaccine ad26.cov2.s was not applicable. The patient recovered from vaccine-induced thrombotic thrombocytopenia. Conclusion: While the development of VITT is rare, it corresponds with increased morbidity and mortality. Thus, a high level of suspicion followed by prompt investigation and treatment initiation of anticoagulation and IVIG are warranted for better patient outcomes. Many VITT patients are at a high risk of life-threatening hemorrhage from thrombosis and thrombocytopenia, warranting further investigation into refractory VITT cases. This report was serious (Hospitalization Caused / Prolonged, and Other Medically Important Condition). This case, from the same reporter is linked to 20200510360 and 20231035978.; Sender's Comments: V0: Thrombosis with thrombocytopenia syndrome : The event has an unknown/unclear temporal relationship, and is labeled. There is no information on any other factors potentially associated with the event. Therefore, this event is considered consistent with vaccine administration.