Central venous catheters and upper-extremity deep-vein thrombosis complicating immune heparin-induced thrombocytopenia

Hong, Aaron; Cook, Deborah J.; Sigouin, Christopher; Warkentin, Theodore E.

doi:10.1182/blood-2002-05-1448

Cited by 156 publications

(91 citation statements)

References 15 publications

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“…We postulate that the difference stems from the increased propensity of HIT-related thrombosis to occur in areas of vascular injury. 14 The strengths of our study include its large size, which increases the generalizability of its results and avoids the biases inherent in small, single-center studies. As with any administrative dataset, the NIS may include coding errors related to underdiagnosis and overdiagnosis (eg, a HIT/ HITT diagnosis carried forward from prior episodes).…”

Section: Discussionmentioning

confidence: 99%

Medical and Economic Burden of Heparin‐Induced Thrombocytopenia: A Retrospective Nationwide Inpatient Sample (NIS) Study

Pathak

Bhatt

Karmacharya

et al. 2017

Journal of Hospital Medicine

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In recent years, US hospitals have switched from use of unfractionated heparin to use of low-molecular-weight heparin, which is associated with lower risk of heparin-induced thrombocytopenia (HIT). In the study reported here, we retrospectively searched the Nationwide Inpatient Sample (NIS) for patients who were at least 18 years old and received a diagnosis of HIT between 2009 and 2011. Our goal was to get an updated perspective on the incidence and economic impact of HIT. We calculated the incidence of HIT overall and in subgroups of patients who underwent cardiac, vascular, or orthopedic surgery. We compared characteristics of patients with and without HIT and compared characteristics of patients with HIT with thrombosis (HITT) and HIT patients without thrombosis. Of 98,636,364 hospitalizations, 72,515 (0.07%) involved HIT. Arterial and venous thromboses were identified in 24,880 (34.3%) of HIT cases. Men were slightly more likely to have a HIT diagnosis (50.1%), but women had higher rates of HIT after cardiac surgery (odds ratio [OR], 1.41; 95% confidence interval [CI], 1.26-1.58) and vascular surgery (OR, 1.42; 95% CI, 1.29-1.57). Rates of HIT were 0.53% (95% CI, 0.51%-0.54%) after cardiac surgery, 0.28% (95% CI, 0.28%-0.29%) after vascular surgery, and 0.05% (95% CI, 0.05%-0.06%) after orthopedic surgery. HIT and HITT cases were significantly (P < 0.001) more likely than non-HIT cases to be fatal (9.63% and 12.28% vs 2.19%), and they had significantly higher costs and longer inpatient stays. HIT and especially HITT are associated with increased mortality, costs, and length of stay. Journal of Hospital Medicine 2017;12:94-97.

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Section: Discussionmentioning

confidence: 99%

Medical and Economic Burden of Heparin‐Induced Thrombocytopenia: A Retrospective Nationwide Inpatient Sample (NIS) Study

Pathak

Bhatt

Karmacharya

et al. 2017

Journal of Hospital Medicine

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“…11,12 In view of the low incidence of CAT in this patient population, and the risk of bleeding during periods of thrombocytopenia, routine prophylactic anticoagulation or aspirin does not appear to be warranted. In a retrospective study, Hong et al 13 showed that central venous catheters contribute to the development of upper extremity DVT among patients with HIT. In our series, one patient developed HIT who presented with CAT.…”

Section: Discussionmentioning

confidence: 99%

Low risk of symptomatic venous thromboembolic events during growth factor administration for PBSC mobilization

Naina

Pruthi

Inwards

et al. 2010

Bone Marrow Transplant

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The use of erythropoietic agents has been associated with an increased risk of venous thromboembolic events (VTEs), especially in patients with underlying malignancies. However, it is not known whether there is an increased risk of VTE associated with granulocyte growth factors. We reviewed 621 patients undergoing PBSC mobilization using granulocyte growth factors, alone or in combination with CY. Patients with a diagnosis of AL amyloidosis (AL: 114; 18%), multiple myeloma (MM: 278; 44%) Hodgkin lymphoma (HL: 20; 3%) or nonHodgkin lymphoma (NHL: 209; 33%) were included. Symptomatic VTE occurred in six (0.97%) patients: two AL, two MM and two NHL. Of the six patients, two had pulmonary embolism, one developed deep vein thrombosis and three developed symptomatic catheter related thrombosis. Two patients with AL had heparin-induced thrombocytopenia and thrombosis. We found a low incidence of VTE among patients undergoing PBSC mobilization.

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“…For example, recent arterial surgery or severe atherosclerosis is associated with arterial thrombosis in HIT, while a central venous catheter predisposes to development of upper limb DVT in patients with HIT. 88,91 Inherited prothrombotic risk disorders such as factor V Leiden have not been shown to be play a major role in explaining HIT-associated thrombosis, although a contributory role in specific circumstances remains plausible. 92 Venous limb gangrene is another manifestation of HIT, which usually occurs as a result of warfarin-induced microthrombosis due to an altered procoagulant-anticoagulant balance.…”

Section: Heparin-induced Thrombocytopenia 2611mentioning

confidence: 99%

Heparin-induced thrombocytopenia: a historical perspective

Kelton

Warkentin

2008

Blood

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168

113

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Heparin was discovered 90 years ago, 1 and within 2 decades it was being widely used as an anticoagulant. 2 The numerous advantages of heparin lend to its broad use including its immediate onset of action, relatively short half-life (ϳ60 minutes), simple laboratory monitoring (aPTT), ability to be reversed (using protamine), and low cost. Despite a long experience of using heparin, the counterintuitive notion that an anticoagulant could be intensely prothrombotic took almost 4 decades to become recognized.Our understanding of heparin-induced thrombocytopenia (HIT) has increased considerably and to a large measure exemplifies the best of translational research. Sometimes, basic studies investigating the pathophysiology of HIT lead to clinical insights. In other instances, clinical observations prompted basic studies. Together, these basic and applied investigations have dramatically enhanced our understanding of the pathogenesis and treatment of HIT. Heparin-induced arterial embolismOn June 1, 1957, at the Fifth Scientific Meeting of the International Society of Angiology in New York, Rodger E. Weismann, an Assistant Professor of Clinical Surgery at the Dartmouth Medical School, and his Resident in Surgery, Dr Richard W. Tobin, described 10 patients who developed arterial embolism during systemic heparin therapy. 3 The first reported embolic event was a femoral artery embolic occlusion, which occurred in a 62-year-old woman who was receiving heparin because of a deep-vein thrombosis (DVT). Three days after successful femoral embolectomy, and while continuing to receive heparin, she developed sudden occlusion of the distal aorta requiring distal aortic and bilateral iliac embolectomies. 3 Multiple thromboemboli were observed in 9 of the 10 patients reported. Six patients died as a result of the thromboembolism, and 2 survivors underwent above-knee amputation. 3 The clots were described as "pale, soft, salmon-colored" and were composed mostly of fibrin, platelets, and leukocytes. The arterial emboli began on average 10 days after commencing heparin treatment.An additional 11 patients were described 5 years later by Roberts and colleagues. 4 These vascular surgeons noted the paradox of "unexplained arterial embolization [occurring] for the first time while being treated with heparin for some condition that could not of itself reasonably be expected to cause arterial emboli. All patients had been receiving heparin for 10 days or more when the initial embolus occurred." Thus, both groups 3,4 noted the temporal hallmark of HIT, a delay of approximately 1 week from initiation of heparin to onset of its thrombotic manifestations. Heparin-induced thrombocytopeniaRoutine platelet count measurements were not routinely performed until the 1970s. This may explain why thrombocytopenia was not reported in the first 24 patients with heparin-induced arterial emboli. [3][4][5][6] In 1969, the term "heparin-induced thrombocytopenia" was used by Natelson 7 to describe a 78-year-old man with pulmonary embolism who developed severe t...

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Central venous catheters and upper-extremity deep-vein thrombosis complicating immune heparin-induced thrombocytopenia

Cited by 156 publications

References 15 publications

Medical and Economic Burden of Heparin‐Induced Thrombocytopenia: A Retrospective Nationwide Inpatient Sample (NIS) Study

Medical and Economic Burden of Heparin‐Induced Thrombocytopenia: A Retrospective Nationwide Inpatient Sample (NIS) Study

Low risk of symptomatic venous thromboembolic events during growth factor administration for PBSC mobilization

Heparin-induced thrombocytopenia: a historical perspective

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