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Theodore E Warkentin - One of the best experts on this subject based on the ideXlab platform.
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cerebral venous sinus thrombosis associated with spontaneous heparin induced thrombocytopenia syndrome after total knee arthroplasty
Platelets, 2021Co-Authors: Steven R Hwang, Theodore E Warkentin, Yuxiang Wang, Erika L Weil, Anand Padmanabhan, Rajiv K PruthiAbstract:Spontaneous heparin-induced thrombocytopenia (HIT) syndrome, characterized by clinical and serologic features of HIT despite the absence of proximate heparin exposure, can be triggered by total knee arthroplasty (TKA). A 56-year-old female receiving aspirin thromboprophylaxis post-TKA presented with aphasia and thrombocytopenia on post-operative day 11. Imaging studies revealed cerebral venous sinus thrombosis (CVST) and intravenous bivalirudin was initiated. Her serum tested strong-positive for IgG anti-PF4/polyanion complexes and serotonin-release assay in the presence and absence of heparin; strong-positive IgG-specific chemiluminescent immunoassay; and moderate-positive latex immunoturbidimetric assay. Two 65 g doses of IVIG were administered. With the improvement of her platelet count, she was transitioned from bivalirudin to warfarin. At one-year follow-up, she remained free of recurrent thrombosis and neurologically stable with a normal platelet count. Previous reports of post-TKA spontaneous HIT syndrome include venous/arterial thrombosis and Adrenal Hemorrhage, and this report of CVST expands the clinical spectrum of this rare complication of orthopedic surgery.
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heparin induced thrombocytopenia presenting as bilateral Adrenal Hemorrhages
The New England Journal of Medicine, 2015Co-Authors: Theodore E Warkentin, Eric L Safyan, Loriann LinkinsAbstract:Two cases are described in which Adrenal Hemorrhage was misdiagnosed as the result of too much anticoagulation when the cause was Adrenal-vein thrombosis mediated by anti–platelet factor 4 antibodies.
Rajiv K Pruthi - One of the best experts on this subject based on the ideXlab platform.
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cerebral venous sinus thrombosis associated with spontaneous heparin induced thrombocytopenia syndrome after total knee arthroplasty
Platelets, 2021Co-Authors: Steven R Hwang, Theodore E Warkentin, Yuxiang Wang, Erika L Weil, Anand Padmanabhan, Rajiv K PruthiAbstract:Spontaneous heparin-induced thrombocytopenia (HIT) syndrome, characterized by clinical and serologic features of HIT despite the absence of proximate heparin exposure, can be triggered by total knee arthroplasty (TKA). A 56-year-old female receiving aspirin thromboprophylaxis post-TKA presented with aphasia and thrombocytopenia on post-operative day 11. Imaging studies revealed cerebral venous sinus thrombosis (CVST) and intravenous bivalirudin was initiated. Her serum tested strong-positive for IgG anti-PF4/polyanion complexes and serotonin-release assay in the presence and absence of heparin; strong-positive IgG-specific chemiluminescent immunoassay; and moderate-positive latex immunoturbidimetric assay. Two 65 g doses of IVIG were administered. With the improvement of her platelet count, she was transitioned from bivalirudin to warfarin. At one-year follow-up, she remained free of recurrent thrombosis and neurologically stable with a normal platelet count. Previous reports of post-TKA spontaneous HIT syndrome include venous/arterial thrombosis and Adrenal Hemorrhage, and this report of CVST expands the clinical spectrum of this rare complication of orthopedic surgery.
Traci L Hedrick - One of the best experts on this subject based on the ideXlab platform.
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bilateral Adrenal Hemorrhage the unrecognized cause of hemodynamic collapse associated with heparin induced thrombocytopenia
Critical Care Medicine, 2011Co-Authors: Laura H Rosenberger, Philip W Smith, Robert G Sawyer, John B Hanks, Reid B Adams, Traci L HedrickAbstract:Heparin-induced thrombocytopenia (HIT) is a common, well-documented adverse effect of treatment with heparin resulting in paradoxical arterial and venous thromboses. HIT occurs in up to 1% of patients receiving unfractionated heparin for postoperative antithrombotic prophylaxis, most frequently in orthopedic patients (4.8%) and more often with unfractionated heparin (4.8%) than with low molecular weight heparin (0.6%) (1, 2). HIT is an antibody-mediated effect in which an antibody forms against heparin when bound to a protein called platelet factor 4. These antibodies, predominantly immunoglobulin G class, can then attach directly to the heparin–platelet factor 4 complex. The antibody then binds to the FcγIIa platelet surface receptor, resulting in platelet activation, consumption, and thrombocytopenia in the clinical syndrome of HIT. The resulting immune complexes stimulate excessive thrombin formation, causing thrombosis, defining HIT with thrombosis syndrome (1). HIT antibody seroconversion typically occurs between days 5 and 10 following heparin initiation, and thrombocytopenia occurs between days 5 and 14 (2). HIT should be suspected with recent heparin use, a platelet drop of >50% from baseline or to <100 K/µL, evidence of new thrombosis or extension of an old thrombus, and an absence of other causes of thrombocytopenia. To confirm HIT, a heparin–platelet factor 4 enzyme-linked immunosorbent assay (HIT antibody) or a serotonin release assay should be obtained (3). In contradistinction to other drug-induced thrombocytopenias that lead to a risk of Hemorrhage, thrombocytopenia in HIT leads to an acquired hypercoagulability syndrome secondary to platelet activation and thrombin generation. This environment promotes serious arterial and venous thromboses, including our reported complication of bilateral Adrenal Hemorrhage (BAH) secondary to venous occlusion (2). These prothrombotic complications necessitate immediate discontinuation of heparin and initiation of a thrombin inhibitor. We present a case of HIT complicated by BAH from venous thrombosis that led to hemodynamic collapse with subsequent acute renal failure and myocardial infarction.
Loriann Linkins - One of the best experts on this subject based on the ideXlab platform.
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heparin induced thrombocytopenia presenting as bilateral Adrenal Hemorrhages
The New England Journal of Medicine, 2015Co-Authors: Theodore E Warkentin, Eric L Safyan, Loriann LinkinsAbstract:Two cases are described in which Adrenal Hemorrhage was misdiagnosed as the result of too much anticoagulation when the cause was Adrenal-vein thrombosis mediated by anti–platelet factor 4 antibodies.
Livia Hegerova - One of the best experts on this subject based on the ideXlab platform.
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Heparin-induced thrombocytopenia presenting as splenic Hemorrhage following cardiac surgery: a case report
Thrombosis Journal, 2021Co-Authors: Joseph Ferry, Samuel Youssef, Livia HegerovaAbstract:Background Heparin-induced thrombocytopenia with thrombosis (HITT) is a paradoxical prothrombotic complication of anticoagulant therapy. As many as 3% of patients undergoing cardiac surgery develop clinical HIT presenting as thrombocytopenia with or without thrombosis within 5–10 days of heparin exposure. Thrombotic complications associated with HIT carry a mortality rate of 5–10%. Case presentation We report a case of atraumatic splenic Hemorrhage due to splenic vein thrombosis as the main indicator of HIT following cardiac surgery in a 62-year-old woman. She presented to the emergency department on day nine following coronary artery bypass graft surgery with acute weakness, dizziness, and malaise. Her evaluation in the emergency department found anemia and thrombocytopenia. A coagulation profile revealed a markedly elevated d-dimer. She underwent a computed tomography scan of the chest, abdomen and pelvis for suspected bleed and was found to have splenic vein thrombosis, right atrial filling defects consistent with atrial thrombus and mild to moderate hemoperitoneum. Surgical consultation was obtained due to splenic Hemorrhage. Hematology was consulted on post-operative day 10, however, she unfortunately developed left sided weakness concerning for stroke. A magnetic resonance imaging scan of the brain demonstrated infarct involving distribution of the right anterior cerebral artery. A transesophageal echocardiogram demonstrated a large immobile thrombus within the right atrium with a second, mobile thrombus arising from the left tricuspid valve annulus. Due to a 4Ts score of 7 and markedly positive platelet factor 4 (PF4) IgG antibody a serotonin release assay was not performed given the high probability of HIT. She was cautiously treated with bivalirudin and was transitioned to warfarin anticoagulation. In the following days her platelet count recovered and 3 months later a transthoracic echocardiogram revealed solution of the intracardiac thrombi. Conclusions Atraumatic splenic Hemorrhage is an unusual presentation of HIT that is reminiscent of the rare bilateral Adrenal Hemorrhage due to Adrenal necrosis that also occurs in HIT. Alternative anticoagulation is the mainstay of therapy for HIT despite Hemorrhage, given the underlying acquired hypercoagulability. Despite similarities of the presentation between splenic Hemorrhage and bilateral Adrenal Hemorrhage, splenic Hemorrhage is rarely described in the literature. HIT should be considered in patients presenting with thrombocytopenia following cardiac surgery.