scholarly journals An Update on COVID-19 Vaccine Induced Thrombotic Thrombocytopenia Syndrome and Some Management Recommendations

Molecules ◽  
2021 ◽  
Vol 26 (16) ◽  
pp. 5004
Author(s):  
Amin Islam ◽  
Mohammed Sheraz Bashir ◽  
Kevin Joyce ◽  
Harunor Rashid ◽  
Ismail Laher ◽  
...  
Keyword(s):  
Sinus Thrombosis ◽  
Cerebral Venous Sinus Thrombosis ◽  
Thromboembolic Events ◽  
Patient Exposure ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Younger Patients ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Management Recommendations

The thrombotic thrombocytopenia syndrome (TTS), a complication of COVID-19 vaccines, involves thrombosis (often cerebral venous sinus thrombosis) and thrombocytopenia with occasional pulmonary embolism and arterial ischemia. TTS appears to mostly affect females aged between 20 and 50 years old, with no predisposing risk factors conclusively identified so far. Cases are characterized by thrombocytopenia, higher levels of D-dimers than commonly observed in venous thromboembolic events, inexplicably low fibrinogen levels and worsening thrombosis. Hyper fibrinolysis associated with bleeding can also occur. Antibodies that bind platelet factor 4, similar to those associated with heparin-induced thrombocytopenia, have also been identified but in the absence of patient exposure to heparin treatment. A number of countries have now suspended the use of adenovirus-vectored vaccines for younger individuals. The prevailing opinion of most experts is that the risk of developing COVID-19 disease, including thrombosis, far exceeds the extremely low risk of TTS associated with highly efficacious vaccines. Mass vaccination should continue but with caution. Vaccines that are more likely to cause TTS (e.g., Vaxzevria manufactured by AstraZeneca) should be avoided in younger patients for whom an alternative vaccine is available.

scholarly journals Prothrombotic immune thrombocytopenia after COVID-19 vaccine

Blood ◽  
2021 ◽  
Author(s):  
Andreas Tiede ◽  
Ulrich J Sachs ◽  
Andreas Czwalinna ◽  
Sonja Werwitzke ◽  
Rolf Bikker ◽  
...  
Keyword(s):  
Healthy Donor ◽  
Immune Thrombocytopenia ◽  
Sinus Thrombosis ◽  
Clinical Manifestations ◽  
Cerebral Venous Sinus Thrombosis ◽  
Dependent Manner ◽  
Thromboembolic Events ◽  
Platelet Factor ◽  
Vein Thrombosis ◽  
Heparin Anticoagulation

We report five cases of prothrombotic immune thrombocytopenia after exposure to the ChAdOx1 vaccine (AZD1222, Vaxzevria) against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients presented 5 to 11 days after first vaccination. The spectrum of clinical manifestations included cerebral venous sinus thrombosis (CVST), splanchnic vein thrombosis (SVT), arterial cerebral thromboembolism, and thrombotic microangiopathy (TMA). All patients had thrombocytopenia and markedly elevated D-Dimer. Autoantibodies against platelet factor 4 (PF4) were detected in all patients although they had never been exposed to heparin. Immunoglobulin from patient sera bound to healthy donor platelets in an AZD1222-dependant manner, suppressed by heparin. Aggregation of healthy donor platelets by patient sera was demonstrated in the presence of buffer or AZD1222 and was also suppressed by heparin. Anticoagulation alone or in combination with eculizumab or intravenous immunoglobulin (IVIG) resolved the pathology in three patients. Two patients had thromboembolic events despite anticoagulation at a time when platelets were increasing after IVIG. In summary, an unexpected autoimmune prothrombotic disorder is described after vaccination with AZD1222. It is characterized by thrombocytopenia and anti-PF4 antibodies binding to platelets in AZD1222-dependent manner. Initial clinical experience suggests a risk of unusual and severe thromboembolic events.

Heparin-Induced Thrombocytopenia Antibodies Do Not Predict Adverse Outcomes in End-Stage Renal Disease Patients on Dialysis.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3517-3517
Author(s):  
Lars M. Asmis ◽  
Jodi B. Segal ◽  
Laura C. Plantinga ◽  
Nancy E. Fink ◽  
Jonathan S. Kerman ◽  
...  
Keyword(s):  
Risk Factor ◽  
Platelet Count ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Thromboembolic Events ◽  
Heparin Induced Thrombocytopenia ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Stage Renal Disease ◽  
End Stage

Abstract Introduction: Heparin-induced thrombocytopenia (HIT) is a syndrome in which anti-platelet factor 4/heparin antibodies (HITab) and thrombocytopenia develop after heparin exposure. While HIT is an established risk factor for arterial and venous thromboses, HITab, in the absence of thrombocytopenia, may also be a prothrombotic risk factor. As patients with chronic kidney disease on hemodialysis are chronically exposed to heparin, we hypothesized that the presence of HITab may contribute to the high rates of thrombotic disease and mortality in these patients. Patients and methods: We analyzed data from the CHOICE study, a prospective cohort study of incident dialysis patients. Clinical data were available from medical record review. Arterial cardiovascular events and events of vascular access occlusion were validated by chart review and adjudication. Venous thromboembolic events were defined by ICD-9 codes. Thrombocytopenia was defined as a platelet count <150,000/mm3 or a >50% decline from a previous platelet count. Median duration of follow-up is 2.7 years. We measured HITab using a commercial ELISA assay in stored serum obtained 6 months after cohort enrollment of 740 participants (596 on hemodialysis, 144 on peritoneal dialysis). ELISA results were corrected for inter-plate variability. A positive HITab test associated with thrombocytopenia in the subsequent three months was considered compatible with HIT. We used techniques of logistic regression and of survival analysis with adjustment for potential confounders in our analyses. Results: 10.3% of all patients were positive for HITab at six months. HITab positivity was not associated with thrombocytopenia. HITab did not predict subsequent outcomes including cardiovascular (hazard ratio (HR) 0.96, 95% confidence interval (CI) 0.65–1.41), vascular access occlusive (HR 0.82, CI 0.40–1.71), or venous thromboembolic events (HR 1.39, CI 0.17–11.5) and did not predict mortality (HR 1.00, CI 0.66–1.53). 9 patients (1.2%) had results compatible with HIT (thrombocytopenia + HITab). 1 patient with HIT (0.13%) had venous thrombosis yielding a hazard ratio of 13.7 (CI 1.63–115.5) for HIT and thrombosis. Conclusions: HITab seropositivity after six months of dialysis is frequent, but is not associated with thrombocytopenia. In end-stage renal disease patients treated by dialysis HITab seropositivity in the absence of thrombocytopenia is not an independent risk factor for cardiovascular morbidity or mortality. However, HIT may occur in this patient population and is associated with thrombosis.

Delayed-Onset Heparin-Induced Thrombocytopenia With Cerebral Venous Sinus Thrombosis Following Total Knee Arthroplasty: Case Report

2021 ◽  
pp. 194187442110429
Author(s):  
Megan M. J. Bauman ◽  
Ryan M. Naylor ◽  
Ashley R. Santilli ◽  
Eelco F. Wijdicks
Keyword(s):  
Total Knee Arthroplasty ◽  
Knee Arthroplasty ◽  
Sinus Thrombosis ◽  
Cerebral Venous Sinus Thrombosis ◽  
Venous Sinus ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Venous Sinus Thrombosis ◽  
Delayed Onset ◽  
Total Knee

Heparin-induced thrombocytopenia (HIT) is a prothrombotic state caused by autoantibodies against platelet factor 4 (PF4)-heparin complexes. Although HIT typically presents 5-10 days after the initiation of heparin, thrombosis and thrombocytopenia may occur up to several weeks following heparin withdrawal, so-called delayed-onset HIT. Although rare, there have been isolated reports of HIT-induced cerebral venous sinus thrombosis (CVST), which carry high rates of morbidity and mortality. There is a need to further characterize the etiology, clinical presentation, treatment paradigms, and outcomes of patients with HIT-induced CVST. Here, we present the case of a 57-year old female who presented to the emergency department with a headache and seizure 11 days following a right total knee arthroplasty for which she received 3 post-operative doses of enoxaparin. Work-up demonstrated acute intracerebral hemorrhage (ICH), CVST, and thrombocytopenia. Intravenous heparin resulted in rapidly deteriorating platelet count and subsequent serologic testing confirmed the diagnosis of HIT. Treatment with bivalirudin was initiated, the HIT resolved, and the patient was discharged home on hospital day 19 with long-term anticoagulation mediated by warfarin. At 3-month follow up, the patient had mild upper motor neuron pattern weakness and was living independently. This case depicts a rare case of delayed-onset HIT and CVST, highlights the importance of establishing a fluid treatment plan for managing HIT-induced CVST, and illustrates the importance of employing rapid anticoagulation despite acute ICH to achieve a desirable clinical outcome.

scholarly journals Refractory Heparin-Induced Thrombocytopenia With Cerebral Venous Sinus Thrombosis Treated With IVIg, Steroids, and a Combination of Anticoagulants: A Case Report

2019 ◽  
Vol 7 ◽  
pp. 232470961983232 ◽  
Author(s):  
Mia Gonzales ◽  
Amrish Pipalia ◽  
Andrew Weil
Keyword(s):  
Sinus Thrombosis ◽  
Cerebral Venous Sinus Thrombosis ◽  
Venous Sinus ◽  
Small Subset ◽  
Severe Thrombocytopenia ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Venous Sinus Thrombosis ◽  
Increased Risk ◽  
Risk For Thrombosis

Heparin-induced thrombocytopenia (HIT) type II is caused by antibody production that bind complexes between heparin and platelet factor 4 leading to platelet consumption and thrombosis. In a small subset of cases referred to as autoimmune HIT, the antibodies activate platelets even in the absence of heparin. Refractory HIT is a type of autoimmune HIT in which thrombocytopenia persists for weeks after heparin discontinuation and carries increased risk for thrombosis and more severe thrombocytopenia. We present a case of refractory HIT with cerebral venous sinus thrombosis (CVST) that was successfully treated with a change in anticoagulant alongside steroids and a second trial of intravenous immunoglobulin (IVIg).

scholarly journals Cerebral venous sinus thrombosis secondary to ChAdOx-1 nCov-19 vaccine

2021 ◽  
Vol 14 (12) ◽  
pp. e246200
Author(s):  
Syed Noman Atta ◽  
Nariman Othman ◽  
Munir Babar
Keyword(s):  
Sinus Thrombosis ◽  
Rare Condition ◽  
Cerebral Venous Sinus Thrombosis ◽  
Platelet Factor 4 ◽  
Prior History ◽  
Cerebral Veins ◽  
Thromboembolic Events ◽  
Platelet Factor ◽  
Venous Sinus Thrombosis ◽  
History Of

Thrombosis and thrombocytopaenia secondary to ChAdOx-1 nCov-19 vaccine is a new phenomenon that usually occurs after the first dose of vaccine. Most of these patients are healthy without any prior history of thromboembolic events or heparin use. Hall marks of this condition include detectable antibodies to platelet factor 4 and thrombosis at atypical sites particularly cerebral veins and sinuses mimicking atypical heparin induced thrombocytopaenia. We describe a case of a patient who was diagnosed with this rare condition and treated successfully.

scholarly journals Thrombocytopenia and Intracranial Venous Sinus Thrombosis after “COVID-19 Vaccine AstraZeneca” Exposure

2021 ◽  
Vol 10 (8) ◽  
pp. 1599
Author(s):  
Marc E. Wolf ◽  
Beate Luz ◽  
Ludwig Niehaus ◽  
Pervinder Bhogal ◽  
Hansjörg Bäzner ◽  
...  
Keyword(s):  
Sinus Thrombosis ◽  
Clinical Manifestations ◽  
Venous Sinus ◽  
European Medicines Agency ◽  
Coagulation Disorder ◽  
Platelet Factor ◽  
Venous Sinus Thrombosis ◽  
Antiplatelet Antibodies ◽  
Imaging Results ◽  
Venous Thromboembolic Events

Background: As of 8 April 2021, a total of 2.9 million people have died with or from the coronavirus infection causing COVID-19 (Corona Virus Disease 2019). On 29 January 2021, the European Medicines Agency (EMA) approved a COVID-19 vaccine developed by Oxford University and AstraZeneca (AZD1222, ChAdOx1 nCoV-19, COVID-19 vaccine AstraZeneca, Vaxzevria, Covishield). While the vaccine prevents severe course of and death from COVID-19, the observation of pulmonary, abdominal, and intracranial venous thromboembolic events has raised concerns. Objective: To describe the clinical manifestations and the concerning management of patients with cranial venous sinus thrombosis following first exposure to the “COVID-19 vaccine AstraZeneca”. Methods: Patient files, laboratory findings, and diagnostic imaging results, and endovascular interventions of three concerning patients were evaluated in retrospect. Results: Three women with intracranial venous sinus thrombosis after their first vaccination with “COVID-19 vaccine AstraZeneca” were encountered. Patient #1 was 22 years old and developed headaches four days after the vaccination. On day 7, she experienced a generalized epileptic seizure. Patient #2 was 46 years old. She presented with severe headaches, hemianopia to the right, and mild aphasia 13 days after the vaccination. MRI showed a left occipital intracerebral hemorrhage. Patient #3 was 36 years old and presented 17 days after the vaccination with acute somnolence and right-hand hemiparesis. The three patients were diagnosed with extensive venous sinus thrombosis. They were managed by heparinization and endovascular recanalization of their venous sinuses. They shared similar findings: elevated levels of D-dimers, platelet factor 4 antiplatelet antibodies, corona spike protein antibodies, combined with thrombocytopenia. Under treatment with low-molecular-weight heparin, platelet counts normalized within several days. Conclusion: Early observations insinuate that the exposure to the “COVID-19 vaccine AstraZeneca” might trigger the expression of antiplatelet antibodies, resulting in a condition with thrombocytopenia and venous thrombotic events (e.g., intracranial venous sinus thrombosis). These patients’ treatment should address the thrombo-embolic manifestations, the coagulation disorder, and the underlying immunological phenomena.

scholarly journals Recurrence of Upper Extremity Deep Vein Thrombosis Secondary to COVID-19

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 878
Author(s):  
Yesha H. Parekh ◽  
Nicole J. Altomare ◽  
Erin P. McDonnell ◽  
Martin J. Blaser ◽  
Payal D. Parikh
Keyword(s):  
Deep Vein Thrombosis ◽  
Lower Extremity ◽  
Upper Extremity ◽  
Thromboembolic Events ◽  
Vein Thrombosis ◽  
Venous Thromboembolic Events ◽  
Venous Thromboembolic ◽  
Deep Vein

Infection with SARS-CoV-2 leading to COVID-19 induces hyperinflammatory and hypercoagulable states, resulting in arterial and venous thromboembolic events. Deep vein thrombosis (DVT) has been well reported in COVID-19 patients. While most DVTs occur in a lower extremity, involvement of the upper extremity is uncommon. In this report, we describe the first reported patient with an upper extremity DVT recurrence secondary to COVID-19 infection.

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